impaired judgement and problem solving abilities examples

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• Mild cognitive impairment (MCI)

Mild cognitive impairment (MCI) is the stage between the expected decline in memory and thinking that happens with age and the more serious decline of dementia. MCI may include problems with memory, language or judgment.

People with MCI may be aware that their memory or mental function has "slipped." Family and close friends also may notice changes. But these changes aren't bad enough to impact daily life or affect usual activities.

MCI may increase the risk of dementia caused by Alzheimer's disease or other brain disorders. But some people with mild cognitive impairment might never get worse. And some eventually get better.

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The brain, like the rest of the body, changes with age. Many people notice they become more forgetful as they age. It may take longer to think of a word or to recall a person's name.

If concerns with mental function go beyond what's expected, the symptoms may be due to mild cognitive impairment (MCI). MCI may be the cause of changes in thinking if:

• You forget things more often.
• You miss appointments or social events.
• You lose your train of thought. Or you can't follow the plot of a book or movie.
• You have trouble following a conversation.
• You find it hard to make decisions, finish a task or follow instructions.
• You start to have trouble finding your way around places you know well.
• You begin to have poor judgment.
• Your family and friends notice any of these changes.

If you have MCI , you also may experience:

• Depression.
• A short temper and aggression.
• A lack of interest.

When to see a doctor

Talk to your health care provider if you or someone close to you notices you're having problems with memory or thinking. This may include trouble recalling recent events or having trouble thinking clearly.

• Changes in brain structure with MCI and Alzheimer's disease

Some changes in brain structure — such as the decrease in size of the brain's memory center (hippocampus) — are typical with aging. However, this reduction in size is greater in those with mild cognitive impairment and even more dramatic in people with Alzheimer's disease.

• Brain shrinkage in MCI and Alzheimer's disease

Dementia causes the brain to lose mass, especially in critical areas. Note the difference in size between a healthy brain (top), a mild cognitive impairment brain (middle) and an Alzheimer's disease brain (bottom).

There's no single cause of mild cognitive impairment (MCI), although MCI may be due to early Alzheimer's disease. There's no single outcome for the disorder. Symptoms of MCI may remain stable for years. Or MCI may progress to Alzheimer's disease dementia or another type of dementia. In some cases, MCI may improve over time.

MCI often involves the same types of brain changes seen in Alzheimer's disease or other forms of dementia. In MCI , those changes occur at a lesser degree. Some of these changes have been seen in autopsy studies of people with MCI .

These changes include:

• Clumps of beta-amyloid protein, called plaques, and tangles of tau proteins that are seen in Alzheimer's disease.
• Microscopic clumps of a protein called Lewy bodies. These clumps are associated with Parkinson's disease, dementia with Lewy bodies and some cases of Alzheimer's disease.
• Small strokes or reduced blood flow through brain blood vessels.

Brain-imaging studies show that the following changes may be associated with MCI :

• Decreased size of the hippocampus, a brain region important for memory.
• Increased size of the brain's fluid-filled spaces, known as ventricles.
• Reduced use of glucose in key brain regions. Glucose is the sugar that's the main source of energy for cells.

Risk factors

The strongest risk factors for MCI are:

• Increasing age.
• Having a form of a gene known as APOE e4 . This gene also is linked to Alzheimer's disease. But having the gene doesn't guarantee that you'll have a decline in thinking and memory.

Other medical conditions and lifestyle factors have been linked to an increased risk of changes in thinking, including:

• High blood pressure.
• High cholesterol.
• Obstructive sleep apnea.
• Lack of physical exercise.
• Low education level.
• Lack of mentally or socially stimulating activities.

Complications

People with MCI have an increased risk — but not a certainty — of developing dementia. Overall, about 1% to 3% of older adults develop dementia every year. Studies suggest that around 10% to 15% of people with MCI go on to develop dementia each year.

Mild cognitive impairment can't be prevented. But research has found some lifestyle factors may lower the risk of getting MCI . Studies show that these steps may help prevent MCI :

• Don't drink large amounts of alcohol.
• Limit exposure to air pollution.
• Reduce your risk of a head injury.
• Don't smoke.
• Manage health conditions such as diabetes, high blood pressure, obesity and depression.
• Practice good sleep hygiene and manage any sleep problems.
• Eat a healthy diet full of nutrients. Include fruits and vegetables and foods low in saturated fats.
• Stay social with friends and family.
• Exercise at a moderate to vigorous intensity most days of the week.
• Wear a hearing aid if you have hearing loss.
• Stimulate your mind with puzzles, games and memory training.

Mild cognitive impairment (MCI) care at Mayo Clinic

• Knopman DS, et al. Alzheimer disease. Nature Reviews. Disease Primers. 2021; doi:10.1038/s41572-021-00269-y.
• Jankovic J, et al., eds. Alzheimer disease and other dementias. In: Bradley and Daroff's Neurology in Clinical Practice. 8th ed. Elsevier; 2022. https://www.clinicalkey.com. Accessed Sept. 21, 2022.
• Zhuang L, et al. Cognitive assessment tools for mild cognitive impairment screening. Journal of Neurology. 2021; doi:10.1007/s00415-019-09506-7.
• What is mild cognitive impairment? National Institute on Aging. https://www.nia.nih.gov/health/what-mild-cognitive-impairment. Accessed Sept. 21, 2022.
• Mild cognitive impairment (MCI). Alzheimer's Association. https://www.alz.org/alzheimers-dementia/what-is-dementia/related_conditions/mild-cognitive-impairment. Accessed Sept. 21, 2022.
• Lewis JE, et al. The effects of twenty-one nutrients and phytonutrients on cognitive function: A narrative review. Journal of Clinical and Translational Research. 2021; doi:10.18053/jctres.07.202104.014.
• Kellerman RD, et al. Alzheimer's disease. In: Conn's Current Therapy 2022. Elsevier; 2022. https://www.clinicalkey.com. Accessed Sept. 21, 2022.
• Ferri FF. Mild cognitive impairment. In: Ferri's Clinical Advisor 2023. Elsevier; 2023. https://www.clinicalkey.com. Accessed Sept. 21, 2022.
• Petersen RC, et al. Practice guideline update summary: Mild cognitive impairment: Report of the Guideline Development, Dissemination, and Implementation Subcommittee of the American Academy of Neurology. Neurology. 2018; doi:10.1212/WNL.0000000000004826.
• Budson AE, et al. Subjective cognitive decline, mild cognitive impairment and dementia. In: Memory Loss, Alzheimer's Disease, and Dementia. 3rd ed. Elsevier; 2022. https://www.clinicalkey.com. Accessed Sept. 21, 2022.
• Cognitive impairment in older adults: Screening. U.S. Preventive Services Task Force recommendation statement. https://www.uspreventiveservicestaskforce.org/uspstf/recommendation/cognitive-impairment-in-older-adults-screening. Accessed Sept. 21, 2022.
• Levenson JL, ed. Dementia. In: The American Psychiatric Association Publishing Textbook of Psychosomatic Medicine and Consultation-Liaison Psychiatry. 3rd ed. American Psychiatric Association Publishing; 2019. https://psychiatryonline.org. Accessed Sept. 21, 2022.
• Livingston G, et al. Dementia prevention, intervention, and care: 2020 report of the Lancet Commission. The Lancet. 2020; doi:10.1016/S0140-6736(20)30367-6.
• Cummings J, et al. Alzheimer's disease drug development pipeline: 2022. Alzheimer's and Dementia. 2022; doi:10.1002/trc2.12295.
• Memory, forgetfulness and aging: What's normal and what's not? National Institute on Aging. https://www.nia.nih.gov/health/memory-forgetfulness-and-aging-whats-normal-and-whats-not. Accessed Sept. 26, 2022.
• Ami T. Allscripts EPSi. Mayo Clinic. April 21, 2022.
• Alzheimer's disease research centers. National Institute on Aging. https://www.nia.nih.gov/health/alzheimers-disease-research-centers#minnesota. Accessed Sept. 26, 2022.
• About the Alzheimer's Consortium. Arizona Alzheimer's Consortium. https://azalz.org/about/#institutes. Accessed Sept. 26, 2022.
• Shi M, et al. Impact of anti-amyloid-β monoclonal antibodies on the pathology and clinical profile of Alzheimer's disease: A focus on aducanumab and lecanemab. Frontiers in Aging and Neuroscience. 2022; doi:10.3389/fnagi.2022.870517.
• Graff-Radford J (expert opinion). Mayo Clinic. Sept. 30, 2022.
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What Should You Do When Your Judgment Is Impaired?

When your ability to act in your best interests is compromised, you need a plan..

Posted November 22, 2013

There’s a supreme irony here. If your judgment is temporarily impaired, then—now afflicted with such a deficit—how could you possibly know it was impaired? And realistically, how could you even be expected to act prudently in a state where cautiousness or circumspection may totally elude you?

These are tough questions. But still, it’s unquestionably true that at one time or another all of us have found ourselves in such an untenable situation. In fact, if you look at some of the worst decisions you’ve ever made, did you not make them when your common sense was, well, “offline”? Times when you just couldn’t access the knowledge or past experience that, doubtless, would have let you know that you were about to step on a land mine—or fall headfirst over a precipice? In other words, there are various circumstances when you should have known better than to say or do something that almost certainly would get you into trouble. But in that crucial instant, you didn’t . . . or couldn’t.

So how can you avoid the pitfalls that your momentarily “logged off” mind may topple you into (as in, “What in the world were you thinking of when you did that?!”)?

The first thing to do is determine your personal risk factors for such a lapse in judgment. Traditional twelve-step programs for addiction —each in their own way focusing on what can catapult an individual back into their dysfunctional behavior—employs the term HALT to abort the downwards progression. This useful acronym alludes to the four main threats to maintaining abstinence from one’s drug of choice. That is, it’s essential for the addict to be mindful of the contingencies most commonly linked to losing control and resorting, yet again, to one’s particular addiction. So, to “unpack” the acronym, the “H” in HALT stands for getting too Hungry, the “A” for becoming too Angry, the “L” for feeling too Lonely, and the “T” for being in a state of fatigue—that is, too Tired.

In such situations, it’s crucial to mindfully “halt” (or stop in your tracks), and to contemplate what’s going on inside yourself. For when you’re in any of these negative states, you’re at increased risk for relapsing back into your addiction (whether it’s related to a substance, activity, or an unhealthy, harmful relationship). In such hazardous moments, recovering addicts are advised to immediately get in touch with their sponsor or another program member, or to go to a 12-step meeting—and, if possible, both .

But the great majority of us aren’t members of a 12-step program—either because the religious dogma usually attached to it doesn’t much appeal to us, or (more likely) because our problems don’t really pertain to addiction. Still, the HALT model, even though it doesn’t address all the problematic situations we’re vulnerable to, represents a good starting point. If we can become more aware of just what mental or emotional states put us at risk for acting foolishly, recklessly, or otherwise ill-advisedly, we may be able to avoid doing something we’ll later regret. Consequently, it’s helpful to make a list of what—for us personally—exemplify cues or clues that we’re in danger of acting contrary to our best interests. And then to determinedly revisit this list with sufficient frequency that it enters our head almost automatically before our judgment becomes so clouded that it’s no longer to be trusted.

For this self-protective internal mechanism to work, we need to maintain at least a glimmer of self-recognition when we’re in a mental—or emotional —state that threatens to vex us with sudden amnesia for our well-memorized (i.e., overlearned) catalog of cautions. Which is to say that we have to be on guard for those times, people, and places when our optimal cerebral functioning may become compromised. Situations in which our higher neo-cortical operations are beginning to falter and our far more primitive reptilian (or "dinosaur") brain is on the verge of taking over.

Of course, if in such cases we have a “back up,” we’re that much more likely to withstand any internal pressure to act contrary to our better judgment. So you might think of giving a copy of your list of hazardous situations to a trusted friend, spouse, or parent(s), or in certain instances, your son or daughter. If your emotions are so strong that they’re beginning to overwhelm you—if you’re well on your way to tumbling down your own private rabbit hole—then there’s a good chance that the other person, forewarned of your susceptibilities and “authorized” to act on your behalf, can catch you before you fall. Similar to sponsors in 12-step programs, they might prevent you from doing something that could return to haunt you.

So, once you’re able to identify the precipitants (or “usual suspects”) of past imprudences or indiscretions, it’s wise to let trusted others know about them. And your vulnerability may go well beyond your being in a state of excess hunger, anger , loneliness , or tiredness. In fact, if you’re in any heightened emotional state, your ability to accurately evaluate your situation will be weakened. For example, if you’re extremely anxious you may be tempted to avoid dealing with something that’s critical to handle, or to do something impulsive that could make matters much worse. If you’re overcome with anger, you may be sorely tempted to verbally strike out at someone, which could do irreparable damage to the relationship—or maybe get you fired. And if you’re depressed to the point of being suicidal , without altering your catastrophic thoughts or talking to someone who can offer you sympathy and reassurance, your very life may be at stake.

It’s now established scientific fact that emotions must come into play if you’re to intelligently decide among various alternatives, or be sufficiently motivated to take action on things affecting your welfare. And your emotions, at least those experienced to a mild or moderate degree, typically guide your behavior in positive ways. But whenever your emotions are so pronounced—and stressful —that they literally preempt your rational mind, you need to “retreat” to your list, stopping (or “halting”) yourself in your mental/emotional tracks. Then you can work on productively modifying your negatively distorted self-talk . Or, if that’s no longer feasible, contact a friend or engage in a distracting activity that will lessen your anxiety , anger, guilt , depression , humiliation , or shame .

Finally, if your problems are related to an addiction and you’re about to succumb to your drug of choice, or are already “under the influence,” you need to access something deep inside yourself to circumvent further craving or use—or get in touch with an understanding, compassionate person or professional to help you better cope with your temporary crisis. At times when you can no longer trust yourself, you need to have enough “sanity” left to reach out to another whom you can trust.

Remember, it’s okay to make mistakes. That’s inevitable, and it’s also how you learn to do better next time. But it’s less acceptable to continue to make the same mistakes once you’ve learned what caused them initially. So when your judgment is beginning to go south, look to your list to locate the origin of its degradation. Then do what’s needed to reverse direction.

NOTE: If you think any of the ideas in this piece might be of interest to others, please consider sending them the link. If, additionally, you’d like to explore other posts I’ve done for Psychology Today , click here .

© 2013 Leon F. Seltzer, Ph.D. All Rights Reserved.

---I invite readers to join me on Facebook , and to follow my miscellaneous musings on Twitter .

Leon F. Seltzer, Ph.D. , is the author of Paradoxical Strategies in Psychotherapy and The Vision of Melville and Conrad . He holds doctorates in English and Psychology. His posts have received over 53 million views.

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Cognitive impairment

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• Cognitive impairment is not an illness, but it can signal other medical conditions.
• Signs of cognitive impairment can include memory loss, mood swings and behavioural changes.
• There are ways to treat and prevent cognitive impairment and its complications

What is cognitive impairment?

Cognitive impairment is when you have problems remembering things and solving problems. Cognitive impairment is not an illness. It can be caused by many conditions.  

You may struggle with:

• remembering things
• paying attention
• speaking or understanding
• recognising people, places or things
• experiencing new places and situations — you may become overwhelmed

Cognitive impairment can come and go. This is often called delirium . Delirium can be a sign of serious medical problems.

Cognitive impairment can go from mild to severe.

What are the symptoms of cognitive impairment?

If someone you know has cognitive impairment, you may notice:

• they sometimes feel confused , agitated or distressed
• a change in their speech or behaviours
• that they struggle to finish their daily tasks

What causes cognitive impairment?

There are many causes of cognitive impairment. Some causes of short-term or reversible cognitive impairment are:

• head injury
• anxiety or depression
• recreational use of alcohol and/or drugs
• vitamin deficiency
• dehydration
• reactions to medicines

Some causes of cognitive impairment that lasts forever are:

• brain injury
• intellectual disability

CHECK YOUR SYMPTOMS — Use the Symptom Checker and find out if you need to seek medical help.

When should I see my doctor?

If you, or someone you know is showing signs of cognitive impairment, see your doctor. They can help find out the cause, rule out any serious conditions, and help arrange treatment.

FIND A HEALTH SERVICE — The Service Finder can help you find doctors, pharmacies, hospitals and other health services.

ASK YOUR DOCTOR — Preparing for an appointment? Use the Question Builder for general tips on what to ask your GP or specialist.

How is cognitive impairment diagnosed?

To work out if you have cognitive impairment, your doctor might ask questions to test your:

• concentration
• understanding

They may also ask your family or carers questions. This is because they may have noticed changes in your behaviour over time. Doctors may also examine you, and do more tests to try to find the cause.

How is cognitive impairment treated?

Treatment will depend on what is causing your cognitive impairment. Exercise, healthy sleep and relaxation techniques may also help. You may find familiar objects comforting.

Not every older person has cognitive impairment. But cognitive impairment is more common in older people.

What are the complications of cognitive impairment?

People who have delirium and confusion have a higher chance of falls and injuries . It’s important to avoid dangerous activities like driving.

Can cognitive impairment be prevented?

Sometimes, cognitive impairment can be prevented.

A doctor can give advice on preventing cognitive impairment. They can also refer you for more help, such as:

• physiotherapy
• occupational therapy

For people with long-term cognitive impairment, there are ways to prevent delirium, confusion and other complications.

Resources and Support

You can learn more about cognitive impairment on the Caring for Cognitive Impairment website .

You can also call the healthdirect helpline on 1800 022 222 (known as NURSE-ON-CALL in Victoria). A registered nurse is available to speak with 24 hours a day, 7 days a week.

Learn more here about the development and quality assurance of healthdirect content .

Last reviewed: November 2022

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Mild Cognitive Impairment | Dementia Australia

Memory loss has long been accepted as a normal part of ageing. Recently there has been increasing recognition that some people experience a level of memory loss greater than that usually experienced with ageing, but without other signs of dementia. This has been termed Mild Cognitive Impairment (MCI). As MCI has only recently been defined, there is limited research on it and there is much that we do not yet understand.

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An estimated two-thirds of Australians living in residential aged care live with moderate to severe cognitive impairment, so what are the requirements for dementia specific training for aged care workers?  

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Cognitive screening and assessment Why is an assessment for cognitive impairment and dementia so important?  It is because an early diagnosis means early access to support, information and medication.   There is no single definitive test for diagnosing dementia. Assessment will account for behavioural, functional and psychosocial changes, together with radiological and laboratory tests. The assessment process may take three to six months to achieve.

Planning: early stages | Dementia Australia

Helping someone at the early stages of losing capacity Many of the people who are losing capacity have mild cognitive impairment or are in the early stage of dementia. While each person’s experience will be different, it will be a challenging and confronting time for most people. The person losing capacity may not be aware of this happening to them. They may be confused, resentful or angry about this being suggested. Alternatively, they could be aware of it happening and respond with a range of emotions – such as acceptance, depression, confusion, anger or grief.

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These resources will help you gain a better understanding of caring for people with cognitive impairment

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During COVID-19, people with cognitive impairment may be further disoriented by the use of personal protective equipment (PPE) and find instructions such as social distancing hard to follow. There may be restrictions on family and carers who are usually there to support them.  

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This resource describes what to expect when going to hospital, information about informed consent and what to do if something doesn't go to plan. The Easy English version of this guide is available here

Changes in thinking and memory - Cancer Council Victoria

You may notice changes in the way you think and remember information. This is called cancer-related cognitive impairment, 'cancer fog' or 'chemo brain'. 

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When any person, particularly an older adult, accesses a healthcare service, there is a need for health professionals to not only treat their prioritising health concerns but also recognise and treat any other comorbidities they may have concurrently (or consequently) developed during their stay. One such comorbidity that may occur during a hospital stay is delirium. Any patient who has had surgery, is in pain, has moved beds multiple times or is dehydrated is at risk of delirium.

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Overview ME/CFS is a complex and debilitating condition, characterised by profound fatigue following exertion (not relieved by sleep or rest), unrefreshing sleep and cognitive impairment. Secondary symptoms may include gastrointestinal disorders, muscle and joint pain and immune impairments. Post exertional malaise (PEM) is suggested as a cardinal feature of ME/CFS.1, 2

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Cognitive Problem Symptoms, Causes and Effects Ad PsychGuides independently researches, tests, and reviews products and services which may benefit our readers. Where indicated by "Medically Reviewed by", Healthcare professionals review articles for medical accuracy. If you buy something through our links, or engage with a provider, we may earn a commission.

Cognitive disorders often begin subtly but progress until they significantly impede the affected individual’s quality of life. It is important to understand the various cognitive disorders, their symptoms and relevant treatment options.

What Are the Types of Cognitive Disorders?

Cognitive disorders are a part of the neurocognitive disorder classification in the fifth edition of the Diagnostic and Statistical Manual of Mental Disorders (DSM-V). Cognitive disorders are defined as any disorder that significantly impairs the cognitive function of an individual to the point where normal functioning in society is impossible without treatment. Some common cognitive disorders include:

• Developmental disorders
• Motor skill disorders
• Substance-induced cognitive impairment

Alzheimer’s disease, one of the most common cognitive disorders, affects approximately 5.1 million Americans.

What Causes a Cognitive Disorder?

Like most mental disorders, cognitive disorders are caused by a variety of factors. Some are due to hormonal imbalances in the womb, others to genetic predisposition and still others to environmental factors. Common environmental causes of cognitive disorders include a lack of proper nutrients and interaction during vulnerable stages of cognitive development, particularly during infancy.

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Other common causes of cognitive disorder include substance abuse and physical injury. When an area of the brain that determines cognitive function is damaged, either by the excessive use of drugs, by alcohol or from physical trauma , those neurophysiological changes can result in cognitive dysfunction.

What Are the Signs of Cognitive Disorder?

Cognitive disorder signs vary according to the particular disorder, but some common signs and symptoms overlap in most disorders. Some of the most common signs of cognitive disorder include:

• Poor motor coordination
• Loss of short-term or long-term memory
• Identity confusion
• Impaired judgment

Some cognitive disorders develop in stages and symptoms increase in severity the further the disease progresses. Alzheimer’s disease, for example, begins with the patient showing very minor signs of forgetfulness. Sufferers may forget names they know well, or they may have trouble remembering what they did recently. The initial symptoms of early-onset Alzheimer’s disease are often indistinguishable from normal memory errors. However, as the disease progresses, the affected person’s memory becomes persistently impaired. They may have rare moments of clarity, but life is generally lived in a state of confusion.

If you or a loved one is experiencing any of these symptoms, call our toll-free hotline today at . We are available 24/7 to take your call and to help you find the information you need.

Emotional Symptoms of Cognitive Problems

Cognitive problems manifest in a variety of ways, with emotional imbalance being one of the most common symptoms. Cognitive impairment is frustrating, and those suffering from it often react with emotional outbursts, making it difficult for friends and family to help. Others may push people away in an attempt to isolate themselves, only making the problem worse. Other cognitive disorders have the opposite effect, causing the person to have dulled or nonexistent emotions.

Physical Symptoms of Cognitive Problems

Cognition problems often manifest in the form of visible outward symptoms. The affected person may appear dazed and confused, and their eyes may have a glazed appearance. Motor coordination is often affected in both neurological and psychological cognitive disorders, and the person may have unusual mannerisms or simply a lack of balance and normal posture.

Short-Term and Long-Term Effects of Cognitive Instability

Cognitive instability comes with both short- and long-term effects. Some common short-term effects include memory loss, a state of confusion and a lack of coordination. Long-term effects include the increasing loss of declarative memory, such as forgetting names and significant faces, and a general lack of emotional stability and control over one’s actions.

Is There a Test or Self-Assessment I Can Do?

Various memory and cognitive function tests are available online, but it is important to understand that these tests can only give you a general idea concerning some of the symptoms that a person with a cognitive disorder may experience. A full medical exam is necessary to impart an official diagnosis, and you should consult a doctor before you begin any form of treatment plan.

Medication: Drug Options for Cognitive Issues

Fortunately, various options are available when it comes to drugs for cognitive issues. While most cognitive disorders cannot be cured permanently, the symptoms that make life difficult can be treated and managed to improve your quality of life. From supplements and drugs engineered to reduce memory loss and improve cognitive function to those that help with the depression and anxiety that can often result from cognitive impairment, the drug options for cognitive issues are many.

Cognitive Drugs: Possible Options

The most widely used drugs for cognitive disorders are antidepressants and drugs that prevent the further decay of memory. Such drugs can make it possible to extend the awareness of a person affected by cognitive issues by many years. To determine which drugs would be most effective for a given situation, you need to undergo a full medical assessment.

Medication Side Effects

All medicines come with their own set of side effects, and cognitive disorder treatments are no different. Many of these drugs are powerful, and it can result in drowsiness, insomnia and upset stomach, to name but a few of the common side effects. To determine whether a particular drug is worth taking in exchange for its side effects, you should work closely with a medical professional.

Drug Addiction, Dependence and Withdrawal

Cognitive dysfunction can make a person feel hopeless, and they may turn to unfortunate sources in an effort to regain some control over their mental state. Commonly abused substances include alcohol, illegal narcotics and prescription drugs. Stimulants are a commonly abused drug for those who are dealing with cognitive issues that impair the sharpness of their mental processes. It is also possible to become addicted to legitimately prescribed medication that was initially aimed at treating a cognitive disorder. Individuals with cognitive impairment may become dependent on their medications and suffer withdrawal if they attempt to get off them without proper medical supervision.

If you or a loved one is addicted to medication for a cognitive disorder, help is available. Call our 24/7 hotline at for information on how you can get free of your addiction while managing the symptoms of your cognitive disorder.

Medication Overdose

Medication overdose is a serious issue that often results from dependence on a prescribed medication, including those for cognitive disorders. When a medication stops being effective, many individuals increase their dosage without consulting their doctor in an attempt to make the drug work again. Taking more than the prescribed amount of medication can easily result in drug overdose and have life-threatening consequences.

Depression and Cognitive Problems

Cognitive disorders and depression are heavily linked, and many depression-related illnesses result in at least mild cognitive dysfunction. Not being able to think clearly or remember fully can naturally lead to depression if the affected person feels like they have lost something they will never be able to get back. In cases where depression and cognitive problems are linked and the depression lasts longer than a few months, doctors may prescribe an antidepressant or other lifestyle changes to combat the effects of depression.

Dual Diagnosis: Addiction and Cognitive Disorders

Addiction and cognitive disorders have a high comorbidity rate. In fact, many researchers believe that addiction is a form of cognitive impairment and may be the result of atypical neural activity. Cognitive impairment also comes as a result of substance abuse, and research shows that adults with alcoholism are 10 times more likely than the general population to have ADHD .

Getting Help for a Cognitive Issue

If you need help finding information on cognitive issues, whether for yourself or for a loved one, we can help. Call our 24/7 hotline at for more information on cognitive disorders, comorbidity with substance abuse and the various treatment options available to you. It is never too late to seek help, and our friendly representatives would love to help you begin on your path to mental and physical wellness.

Additional Resources

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Interview Questions

Comprehensive Interview Guide: 60+ Professions Explored in Detail

26 Good Examples of Problem Solving (Interview Answers)

By Biron Clark

Published: November 15, 2023

Employers like to hire people who can solve problems and work well under pressure. A job rarely goes 100% according to plan, so hiring managers will be more likely to hire you if you seem like you can handle unexpected challenges while staying calm and logical in your approach.

But how do they measure this?

They’re going to ask you interview questions about these problem solving skills, and they might also look for examples of problem solving on your resume and cover letter. So coming up, I’m going to share a list of examples of problem solving, whether you’re an experienced job seeker or recent graduate.

Then I’ll share sample interview answers to, “Give an example of a time you used logic to solve a problem?”

Problem-Solving Defined

It is the ability to identify the problem, prioritize based on gravity and urgency, analyze the root cause, gather relevant information, develop and evaluate viable solutions, decide on the most effective and logical solution, and plan and execute implementation. 

Problem-solving also involves critical thinking, communication, listening, creativity, research, data gathering, risk assessment, continuous learning, decision-making, and other soft and technical skills.

Solving problems not only prevent losses or damages but also boosts self-confidence and reputation when you successfully execute it. The spotlight shines on you when people see you handle issues with ease and savvy despite the challenges. Your ability and potential to be a future leader that can take on more significant roles and tackle bigger setbacks shine through. Problem-solving is a skill you can master by learning from others and acquiring wisdom from their and your own experiences. 

It takes a village to come up with solutions, but a good problem solver can steer the team towards the best choice and implement it to achieve the desired result.

Watch: 26 Good Examples of Problem Solving

Examples of problem solving scenarios in the workplace.

• Correcting a mistake at work, whether it was made by you or someone else
• Overcoming a delay at work through problem solving and communication
• Resolving an issue with a difficult or upset customer
• Overcoming issues related to a limited budget, and still delivering good work through the use of creative problem solving
• Overcoming a scheduling/staffing shortage in the department to still deliver excellent work
• Troubleshooting and resolving technical issues
• Handling and resolving a conflict with a coworker
• Solving any problems related to money, customer billing, accounting and bookkeeping, etc.
• Taking initiative when another team member overlooked or missed something important
• Taking initiative to meet with your superior to discuss a problem before it became potentially worse
• Solving a safety issue at work or reporting the issue to those who could solve it
• Using problem solving abilities to reduce/eliminate a company expense
• Finding a way to make the company more profitable through new service or product offerings, new pricing ideas, promotion and sale ideas, etc.
• Changing how a process, team, or task is organized to make it more efficient
• Using creative thinking to come up with a solution that the company hasn’t used before
• Performing research to collect data and information to find a new solution to a problem
• Boosting a company or team’s performance by improving some aspect of communication among employees
• Finding a new piece of data that can guide a company’s decisions or strategy better in a certain area

Problem Solving Examples for Recent Grads/Entry Level Job Seekers

• Coordinating work between team members in a class project
• Reassigning a missing team member’s work to other group members in a class project
• Adjusting your workflow on a project to accommodate a tight deadline
• Speaking to your professor to get help when you were struggling or unsure about a project
• Asking classmates, peers, or professors for help in an area of struggle
• Talking to your academic advisor to brainstorm solutions to a problem you were facing
• Researching solutions to an academic problem online, via Google or other methods
• Using problem solving and creative thinking to obtain an internship or other work opportunity during school after struggling at first

You can share all of the examples above when you’re asked questions about problem solving in your interview. As you can see, even if you have no professional work experience, it’s possible to think back to problems and unexpected challenges that you faced in your studies and discuss how you solved them.

Interview Answers to “Give an Example of an Occasion When You Used Logic to Solve a Problem”

Now, let’s look at some sample interview answers to, “Give me an example of a time you used logic to solve a problem,” since you’re likely to hear this interview question in all sorts of industries.

Example Answer 1:

At my current job, I recently solved a problem where a client was upset about our software pricing. They had misunderstood the sales representative who explained pricing originally, and when their package renewed for its second month, they called to complain about the invoice. I apologized for the confusion and then spoke to our billing team to see what type of solution we could come up with. We decided that the best course of action was to offer a long-term pricing package that would provide a discount. This not only solved the problem but got the customer to agree to a longer-term contract, which means we’ll keep their business for at least one year now, and they’re happy with the pricing. I feel I got the best possible outcome and the way I chose to solve the problem was effective.

Example Answer 2:

In my last job, I had to do quite a bit of problem solving related to our shift scheduling. We had four people quit within a week and the department was severely understaffed. I coordinated a ramp-up of our hiring efforts, I got approval from the department head to offer bonuses for overtime work, and then I found eight employees who were willing to do overtime this month. I think the key problem solving skills here were taking initiative, communicating clearly, and reacting quickly to solve this problem before it became an even bigger issue.

Example Answer 3:

In my current marketing role, my manager asked me to come up with a solution to our declining social media engagement. I assessed our current strategy and recent results, analyzed what some of our top competitors were doing, and then came up with an exact blueprint we could follow this year to emulate our best competitors but also stand out and develop a unique voice as a brand. I feel this is a good example of using logic to solve a problem because it was based on analysis and observation of competitors, rather than guessing or quickly reacting to the situation without reliable data. I always use logic and data to solve problems when possible. The project turned out to be a success and we increased our social media engagement by an average of 82% by the end of the year.

Answering Questions About Problem Solving with the STAR Method

When you answer interview questions about problem solving scenarios, or if you decide to demonstrate your problem solving skills in a cover letter (which is a good idea any time the job description mention problem solving as a necessary skill), I recommend using the STAR method to tell your story.

STAR stands for:

It’s a simple way of walking the listener or reader through the story in a way that will make sense to them. So before jumping in and talking about the problem that needed solving, make sure to describe the general situation. What job/company were you working at? When was this? Then, you can describe the task at hand and the problem that needed solving. After this, describe the course of action you chose and why. Ideally, show that you evaluated all the information you could given the time you had, and made a decision based on logic and fact.

Finally, describe a positive result you got.

Whether you’re answering interview questions about problem solving or writing a cover letter, you should only choose examples where you got a positive result and successfully solved the issue.

Example answer:

Situation : We had an irate client who was a social media influencer and had impossible delivery time demands we could not meet. She spoke negatively about us in her vlog and asked her followers to boycott our products. (Task : To develop an official statement to explain our company’s side, clarify the issue, and prevent it from getting out of hand). Action : I drafted a statement that balanced empathy, understanding, and utmost customer service with facts, logic, and fairness. It was direct, simple, succinct, and phrased to highlight our brand values while addressing the issue in a logical yet sensitive way.   We also tapped our influencer partners to subtly and indirectly share their positive experiences with our brand so we could counter the negative content being shared online.  Result : We got the results we worked for through proper communication and a positive and strategic campaign. The irate client agreed to have a dialogue with us. She apologized to us, and we reaffirmed our commitment to delivering quality service to all. We assured her that she can reach out to us anytime regarding her purchases and that we’d gladly accommodate her requests whenever possible. She also retracted her negative statements in her vlog and urged her followers to keep supporting our brand.

What Are Good Outcomes of Problem Solving?

Whenever you answer interview questions about problem solving or share examples of problem solving in a cover letter, you want to be sure you’re sharing a positive outcome.

Below are good outcomes of problem solving:

• Saving the company time or money
• Making the company money
• Pleasing/keeping a customer
• Obtaining new customers
• Solving a safety issue
• Solving a staffing/scheduling issue
• Solving a logistical issue
• Solving a company hiring issue
• Solving a technical/software issue
• Making a process more efficient and faster for the company
• Creating a new business process to make the company more profitable
• Improving the company’s brand/image/reputation
• Getting the company positive reviews from customers/clients

Every employer wants to make more money, save money, and save time. If you can assess your problem solving experience and think about how you’ve helped past employers in those three areas, then that’s a great start. That’s where I recommend you begin looking for stories of times you had to solve problems.

Tips to Improve Your Problem Solving Skills

Throughout your career, you’re going to get hired for better jobs and earn more money if you can show employers that you’re a problem solver. So to improve your problem solving skills, I recommend always analyzing a problem and situation before acting. When discussing problem solving with employers, you never want to sound like you rush or make impulsive decisions. They want to see fact-based or data-based decisions when you solve problems.

Next, to get better at solving problems, analyze the outcomes of past solutions you came up with. You can recognize what works and what doesn’t. Think about how you can get better at researching and analyzing a situation, but also how you can get better at communicating, deciding the right people in the organization to talk to and “pull in” to help you if needed, etc.

Finally, practice staying calm even in stressful situations. Take a few minutes to walk outside if needed. Step away from your phone and computer to clear your head. A work problem is rarely so urgent that you cannot take five minutes to think (with the possible exception of safety problems), and you’ll get better outcomes if you solve problems by acting logically instead of rushing to react in a panic.

You can use all of the ideas above to describe your problem solving skills when asked interview questions about the topic. If you say that you do the things above, employers will be impressed when they assess your problem solving ability.

If you practice the tips above, you’ll be ready to share detailed, impressive stories and problem solving examples that will make hiring managers want to offer you the job. Every employer appreciates a problem solver, whether solving problems is a requirement listed on the job description or not. And you never know which hiring manager or interviewer will ask you about a time you solved a problem, so you should always be ready to discuss this when applying for a job.

Related interview questions & answers:

• How do you handle stress?
• How do you handle conflict?
• Tell me about a time when you failed

About the Author

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Toward an Understanding of Decision Making in Severe Mental Illness

• Ricardo Cáceda , M.D., Ph.D. ,
• Charles B. Nemeroff , M.D., Ph.D. , and
• Philip D. Harvey , Ph.D.

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A commonality of patients with major psychiatric disorders is their propensity to make poor decisions, which is intimately related to poor real-life outcomes. The authors reviewed the literature on decision making as applied to severe psychiatric disorders, with particular focus on advances in cognitive neuroscience. Deficits in reward sensitivity, avoidance learning, and temporal discounting are reported in depression. Besides abnormalities in hedonic capacity, other cognitive distortions required for flexible control of behavior occur in patients with bipolar disorder and schizophrenia. A conceptual framework of abnormal decision making in mental illness could generate targeted interventions to improve quality of life and clinical outcomes.

In this paper, a theoretical reconceptualization of some of the critical characteristics of severe mental illness is presented as an extension of previous conceptualizations that have focused on cognitive factors as central components of psychiatric disorders. 1 Psychiatric disorders are defined by abnormalities of thought, affect, and impulse control. Arguably, the greatest functional impact of these illnesses on the lives of the mentally ill and society are not related to the symptoms of delusions, hallucinations, or depressed mood, but simply to making poor decisions. These decisions can contribute to behaviors such as nonadherence to medications or outpatient appointments, failing to exercise, poor diet, using drugs, or engaging in unprotected sex. Downstream consequences of poor decisions include worsening of symptoms, reduced life satisfaction, impaired everyday functioning, relapse and rehospitalization, clashes with law enforcement, poor physical health, and even more tragic outcomes such as accidental death, homicide, or suicide.

In many cases flawed decision making in mental illness is a product of the deficits in basic neuropsychological processes, including impaired attention, working memory, or response inhibition. Flawed decision making has a pervasive presence in clinical outcomes. For example, adherence rates for antidepressants, mood stabilizers, antipsychotics, or stimulants range between 30%−50%. More than half of the patients with severe mental illness are affected by substance use disorders. Forty percent of schizophrenic patients, regardless of medication regimen, suffer from metabolic syndrome. Thus, addressing impaired decision-making processes should provide a valuable strategy to improve everyday functioning through an alteration of health status and treatment outcomes in psychiatric patients. In this monograph, the concepts used to characterize decision making are reviewed followed by a review of the known neural substrates that mediate the various elements of decision making. Last, the application of a decision-making approach to understanding some of the morbidity associated with mental illness is described.

Defining Decision Making

A decision problem is defined by the actions or options among which one must choose, the possible outcomes or consequences of these actions, and the contingencies or conditional probabilities that relate outcomes to actions. Herbert Simon, a Nobel laureate, decomposed the task of rational decision making in three steps: (1) identification and delineation of all alternatives, (2) determination of the consequences of each alternative, and (3) a comparison of the accuracy and efficiency of each of these sets of consequences. Decision making is a constant process in modern life, that takes place from when we wake up until we decide to go to bed. Different disciplines, including psychology, psychiatry, neuroscience, economics, and neuroeconomics attempt to systematize the understanding of decision making.

Decision-making research paradigms range from electrophysiological to behavioral experiments (from insects to humans), lesion studies, and brain imaging. The paradigms used include monetary or nonmonetary positive- and negative-reinforcing stimuli (e.g., food, juice squirts, electric shocks) in order to assess an individual’s reactions and choices. These paradigms allow for the exploration and characterization of interactions between individuals using economic principles ( Table 1 ).

One of the many psychological theories focused on understanding behavior, drive theory, posits that organisms have needs, the primary needs related to survival, such as food and shelter, and secondary needs related to the organism’s well-being and comfort. The goal of satisfaction of these needs drives organisms to action and represents the underlying motivation for behavior. When a need is satisfied, the drive is reduced and the person returns to a state of homeostasis and relaxation. An opposing view is promulgated in Skinnerian models, which deny the existence of inner nonobservable phenomena, including motivation. Skinner defined operant conditioning and decision making as processes in which behavior is solely determined by its consequences, wherein organisms learn through experience to behave in ways in order to obtain rewards and avoid punishment. Thus, decision making is intrinsically related to previous experiences and their consequences.

Cognitive Control

Cognitive control refers to the ability to flexibly direct behavior in accordance with a variety of goals, and constitutes the ability to represent, maintain, and update the rules that guide behavior in a context-appropriate manner. Cognitive control functions include error detection and correction mechanisms, conflict resolution, response inhibition, task-switching, and emotion regulation. Although cognitive control functions were initially deemed to be a frontal cortex function, research in the last two decades has identified a “cognitive control network” that includes the dorsolateral prefrontal cortex (DLPFC), medial prefrontal cortex (mPFC), anterior cingulate cortex (ACC), parietal cortex, motor areas, and cerebellum. 2 – 5 Recent meta analyses of a very large number of published functional magnetic resonance imaging (fMRI) datasets demonstrated that a superordinate frontal-cingulate-parietal-subcortical cognitive control system is engaged during the performance of a range of executive function tasks. 6 Functional connectivity has revealed that coordinated temporal activation across the network of prefrontal and posterior brain regions is associated with better performance on cognitive control tasks. 7 Impairments in the cognitive control system are seen in a variety of psychiatric disorders. For instance, deficits in emotion regulation are central to borderline personality and mood disorders, attention biases to negative stimuli are hallmark of anxiety disorders. Moreover, global impairments in cognitive control associated with deficits in attention, memory, language comprehension, and emotional processing are characteristic of schizophrenia, and responsible for this disorder’s most disheartening clinical challenges (e.g., disorganization, negative symptoms) and functional outcome.

Reward and Value

A considerable amount of neuroscience research has been performed using the learning paradigm classical conditioning. Classical conditioning, prototypically illustrated by Pavlov’s experiments, refers to the development of an automatic association between two co-occurring, previously independent stimuli. The classic example is a dog’s association of hearing a bell and the presentation of food thereby inducing salivation to subsequent sounding of the bell in the absence of the food stimulus. Seminal studies by Schultz et al. 8 examined brain responses during classical conditioning and showed increased phasic responses in the ventral tegmental area (VTA) dopaminergic neurons in primates when presented with an unexpected pleasurable stimulus or reward. These brain responses were subsequently evoked by a conditioned stimulus after pairings with the reward. Further, the activation of dopamine neurons decreased with extinction trials when the expected reward was omitted. Subsequent observations showed that these neurons actually fire in anticipation of future rewards. Thus, dopaminergic neurons seem to encode the likelihood of a rewarding outcome and generate a continuous update of its prediction accuracy. Dopamine is therefore believed to provide a teaching signal to parts of the brain responsible for acquiring new behaviors. Notably, serotonin closely interacts with dopamine along two different axes: reward (dopamine)-punishment (serotonin) and behavioral activation (dopamine) inhibition (serotonin). 9 The role of serotonin seems to counteract impulsivity, possibly by enhancing aversion and increasing behavioral inhibition. Although dopamine promotes behavioral activation to seek rewards, serotonin serves to inhibit actions when punishment may occur.

Neuroimaging experiments have identified dopaminergic projection areas, the orbitofrontal cortex (OFC) and ventral striatum [including the nucleus accumbens (NAcc)], as sites active during the learning, retention, and extinction conditions during reward processing. 10 These two structures constitute the brain reward valuation system, which has been posited to mediate representation of a common neural currency. 11 Ventral striatal activation correlates with reward magnitude, whereas mPFC activation correlates with the probability of receiving a reward, reward anticipation, and saliency. However, the calculation of the different facets of reward and value are distributed along several brain regions, including the posterior cingulate cortex (PCC), ACC, the temporoparietal junction, including the inferior parietal lobule, superior temporal gyrus and anterior insula, and the left posterior parietal cortex. 12

Risk, Uncertainty, and Ambiguity

Expected value, initially defined by Pascal, is the product of the payoff and estimated probability of occurrence of a possible choice, and represents a common internal currency that individuals use to compare and choose between different options to utilize resources (i.e., buying drugs versus groceries and medications).

The value of an item to an individual depends on the risk context. Thus, in an environment where the consequences of choices are certain and constant ( Figure 1A , Figure 1B ), the option with the highest value would be the preferred one. 13 However, since this situation is rarely encountered, expected value alone is often a poor predictor of choice. Risk is present when multiple possible outcomes can occur with well-defined or estimable probabilities ( Figure 1C , Table 2 ). In economic models, risk is considered a cost and has to be weighed against the expected value of a decision. Sensitivity to risk is evidenced as risk aversion or risk-seeking behaviors. The incorporation of risk with reward or payoff led Bernoulli to posit the idea of subjective value or utility. Utility is the subjective assessment of the value of a reward; it is dynamic and can be influenced by the physiologic state of the individual (hunger, thirst, or sleep) and the context (home, inpatient unit, or prison). For instance, the challenge of keeping sobriety and taking prescribed medications is quite different for patients receiving ambulatory or inpatient care.

A) Stable environment; B) changing environment; C) stochastic environment; D) unknown environment; and E) interactive environment (Adapted From 13 )

A more accurate analysis of real life situations requires the consideration of the interaction of uncertainty × context. Uncertainty refers to the lack of knowledge about the outcome of a decision and it can be associated with risk or ambiguity ( Table 2 ). Ambiguity occurs in the presence of multiple outcomes whose probabilities are unknown or not well-defined, hence, the expected value cannot be calculated ( Figure 1D ). Ambiguity is a more common real world situation and is even more aversion-provoking than risk. In the latter part of the last century, Kahneman and Tversky 14 developed prospect theory , which explains how humans calculate value nonlinearly. This view, supported by findings of nonlinear striatum activity, explains phenomena such as larger aversive response to losses compared with favorable response to comparable gains, strong preference for certainty, and cognitive biases as the framing effect (i.e., inconsistent choices dependent on whether a question is presented in terms of gains or losses). 14

Risky choice tasks, such as facing a large reward associated with an unlikely outcome, versus a small reward associated with a more probable outcome, lead to OFC activation. 15 Additionally, increased insular activation occurs when choosing riskier outcomes over safer outcomes 10 , 16 and amygdalar activation appears in anticipation of loss or punishment. 17 Gambling tasks revealed expected risk to be proportional to activation in the insula, lateral OFC, and midbrain, 18 and choices that maximized gains or minimized losses were predicted by activation in the ventromedial PFC (VMPFC) or anterior insula, respectively 19 Of these regions, the insula and the dorsomedial PFC (DMPFC) 20 have been shown to be predictive of uncertainty related to monetary 21 and nonmonetary stimuli. 22 , 23 In summary, the data support the view that the cognitive processing of uncertainty is related to the DMPFC, whereas the affective reaction is associated with the OFC and insula. Much of the data presented in this paper originates from fMRI. These data are usually obtained from the comparison of brain activation of a condition of interest and an adequate control, which is reflected in statistical maps that can be visualized as activation of particular brain regions or circuits. However, sensory perception, motor function, and cognition are the product of a coordinated action of several neural processes that occur below the temporal or spatial resolution of fMRI. Thus, it is important to avoid the temptation of assigning discrete mental operations to specific brain regions or circuits. Last, a practical example of abnormalities in uncertainty processing is the anticipatory anxiety found in panic disorder. Panic attacks can be such terrifying and helplessness-inducing experiences that patients live in fear of the next attack, uncertain when it will occur, thereby leading to progressively restricted lifestyles as futile attempts to prevent them.

Strategic Uncertainty

An even more realistic scenario when considering decision making in a social context is interaction with other individuals. Figure 1E shows the interaction between two individuals. In this type of interaction a decision maker needs to consider not only the inherent risk but also what the other person is likely to do, and how his/her own actions will affect others (strategic uncertainty). Strategic uncertainty can be studied with economic games that target the interaction between two or more people such as the prisoners’ dilemma, the stag hunt, or the ultimatum game ( Table 1 ). Paranoia is a prime example of a mental state that strongly influences the view of others and their attributed intentions, and consequently the patient’s own decision making that frequently leads to violence or isolation.

Game Theory

Game theory attempts to predict the strategies that a group of decision makers will converge on as they try to maximize their own profits. It rests on two basic assumptions: first, individuals only seek to maximize their own profit; and second, to achieve this they behave rationally. Nash equilibrium refers to a set of strategies from which no individual player can increase his payoff unilaterally. However, results from experiments in both human and nonhuman primates have systematically violated predictions from the Nash equilibrium. In humans, decision making in social contexts is not purely driven by self-interest, but also by considerations about the well-being of other individuals. Therefore, to better characterize decision making in social contexts, socially oriented emotions such as spite, fairness, and altruism need to be considered. The relevance of decision making within social contexts cannot be overestimated. For example, guilt is frequently found in abusive relationships in depressed patients; grandiosity and recklessness explain many of the interpersonal conflicts during mania; and paranoia and auditory hallucinations found in psychosis can strain interpersonal interactions to the point of violence.

Temporal Discounting

An additional dimension in decision making is time. We do not assign the same subjective value to rewards obtained in the present or in the future. Temporal or delay discounting is an operational measure of delayed gratification and has been shown to be altered in a number of conditions marked by impulsivity. This refers to the decrease in the subjective value of a commodity as the product of its amount and the delay to receive it. 24 For instance, if someone would prefer $80 now instead of $100 in 1 year, it could be said that the temporally distant $100 are discounted to an immediate value of $80. In a classical experiment, Mischel and collaborators presented preschool children the choice of one treat (cookie or candy) immediately, or having to wait several minutes for two treats. 25 This task was remarkably predictive of the childrens future life achievements. Children who preferred delayed larger rewards tended to be more intelligent, better able to concentrate, and more tolerant to frustration; and as adolescents had higher social-emotional and cognitive function ratings, including academic performance. 25 Later follow up showed that the ability to wait as a preschooler predicted higher education achievements, and less risk for crack cocaine use. 26 This capacity to delay gratification has been associated with effective self-regulation through the use of abstract rather than consummatory strategies, as well as shifting of attention. Furthermore, in adolescents, a greater ability to delay gratification was associated with such characteristics as being responsible, productive, ethically consistent, interested in intellectual matters, overly controlled, and higher IQ, whereas those adolescents who were not able to delay gratification were characterized as rebellious, unpredictable, self-indulgent, or hostile. 27

Temporal discounting is the outcome of opposing trends. The first, an instinctive response of craving immediate fulfillment of desires or needs, is linked to activation of medial OFC and subcortical structures, mainly the ventral striatum (VS). 28 The second, executive function, paradigm of cold cognition, reasoning, and planning, is associated with the activity of the right DLPFC and posterior parietal cortex. 29 The role of the PFC is further illustrated by the overwhelming preference for immediate rewards in patients with prefrontal damage in the so-called “ environmental-dependency syndrome.” 30 Activity in the mPFC, ventral striatum, and PCC are directly proportional to a reward magnitude, but inversely to the delay in time in which it is expected. 31 An attempt to separate the risk component in temporal discounting showed frontal pole, PCC, and the parahippocampal gyri to be associated with purely temporal computation. 32 Furthermore, when risky choices are dissociated from temporal ones, the former are associated with activation in DLPFC and posterior parietal cortex, whereas the later indicated activation of the PCC and the striatum. 33 These results suggest that cognitive processing of temporal discounting needs to integrate an element of risk and visualization of the future.

Emotions and Decision Making

A traditional dichotomous view of hot emotion versus cold cognition has been refuted by research in neuroscience, psychology, and economics over the last decades. Emotion does not equate with irrationality, but is an altogether component of the decision-making process. Not surprisingly, the wide range of various emotions explains why is unrealistic to project all emotions into a one-dimensional category of pleasure versus pain. 34 Loewenstein and Lerner construe emotions according to their place along the time course of the decision process, including deliberation about a choice and the posterior reaction to the outcome. 35 They distinguish between anticipated and immediate emotions, with immediate emotions further classified into incidental and integrated emotions. Anticipated emotions are those believed to occur following a given decision outcome. This is also known as effective forecasting and typical examples are regret or disappointment. On the other hand, immediate emotions are those experienced while the individual is pondering a choice. Immediate emotions are either incidental emotions caused by factors, which are not related to the decision problem at hand, or integral emotions, which are caused by the decision problem itself.

On the other hand, Pfister and Bohm classify emotion according to its function emphasizing emotion’s role in decision-making processes. They consider four categories: information, speed, relevance , and commitment . 36 The information function provides evaluative information which weighs in preference construction. Emotions such as joy or distress inform about the degree of (un)pleasantness of choices and consequences. They allow one to map a diversity of experiences on a one-dimensional scale of pleasure and pain. The speed function enables rapid choice and action under time pressure. Affect programs for negative emotions such as fear and disgust trigger immediate avoidance responses. 37 These mechanisms are highly stimulus-specific and presumably have evolved under evolutionary selection pressure. The somatic-marker hypothesis 38 maintains that these kinds of affective signals, originating in bodily states and acquired by learning from previous experiences, act as markers about the valence of current experiences. Somatic markers operate automatically and obligatorily, influencing behavior even before a conscious intention is generated. The relevance function focuses attention on particular aspects of potential relevance for the decision-maker. Emotions such as regret or envy constitute a particular appraisal, which implies particular evaluations as well as particular action tendencies. The commitment function enables social coordination by committing people to stick to decisions, even against their short-term self-interest. Guilt, altruism, love, or hate guide decision making in strategic choice situations. Overall, emotions do not have a uniform influence on decision making, but seem to be rather dependent on the context and in the individual circumstances. An example of the pervasive effect of emotion in mental illness is given by the abnormalities in reward processing found in anhedonia and depression ( Table 3 ). 39

Unconscious Decision Making

Unconscious knowledge refers to that revealed by task performance alone, subjects being unaware that they are accessing it, whereas we speak of conscious knowledge when subjects are aware of possessing and accessing it. 40 It ranges from basic perceptual processing to spontaneous problem solving. Even though attention to the unconscious had already been studied before Freud, his work had considerable impact on the 20th century’s research on unconscious knowledge. 41 Unconscious or subliminal processing has been described in visual, auditory, somatosensory, and olfactory information. Experimental methods used to tap unconscious processes, include studying subjects who are unaware of the stimuli, because they are too weak, brief, complex, or are masked (i.e., subliminal perception). Other approaches examine states of complete unconsciousness (i.e., sleep, coma, and anesthesia), inability to be conscious of certain kinds of stimuli (i.e., blindsight, hemineglect, and prosopagnosia), or when attention has been diverted to another demanding task.

Examples of cognitive processes found to run at the unconscious level include task-set preparation, conflict detection/resolution, motivation, and error detection. (For detailed reviews see 42 , 43 .) Several “high-level” (prefrontal) cognitive functions, such as response inhibition and task-switching, space integration of multiple unconscious stimuli, 44 ensemble statistics, 45 and play recognition in expert chess players 46 have been observed to be influenced and modulated by subliminal stimuli. Priming research has shown that subliminal information can affect behavior and brain activity for a considerable amount of time, even 24 hours. 47 Last, although controversial, unconscious thought theory, with limitations and detractors, attempts to account for the existence of what it calls “the unconscious” in the empiric observations of people seeming to make better decisions when they leave it to “the unconscious” to do the job. 48

Decision Making in Mental Illness

Psychiatric disorders encompass a wide variety of nosological presentations traditionally classified as disorders of thought, affect, or impulse control. The pathophysiology of the vast majority of psychiatric disorders is complex and not well understood. There is a trend in psychiatry to explain mental illness with common denominators across diagnostic boundaries. One common element in severe mental illness is pervasive bad decision making (i.e., not taking medications, paying heed to command hallucinations, or attempting suicide). Despite the ubiquity of decision making in daily life, it has been largely neglected in the diagnosis and management of mental illness. Individuals’ choices are intimately related to disease outcome (hospitalization, incarceration, or suicide), which have been largely unchanged despite decades of research in neuroscience, psychology, and psychiatry.

Major depressive disorder (MDD) is characterized by two primary affective symptoms: sustained negative affect and reduced positive affect. 49 In general, decisions during depressed states are tainted by negative affect and distorted negative cognitions, 50 although some research suggests that mild levels of depression may be associated with more realistic self-assessments even in psychotic patients. 51 A number of studies have used monetary and nonmonetary paradigms to evaluate the reward system in depression. A consistent pattern of reduced activation of the ventral striatum, dorsal striatum, and VMPFC 52 – 54 in response to positive reward stimuli has been reported, but see also for discrepant results. 55 A real life consequence of altered reward processing in depression was demonstrated in a report of economic social interaction using the ultimatum game in which participants were asked to accept or reject a wide range of offers. Depressed patients exhibited a more negative emotional reaction to unfair offers, despite accepting more of these offers than controls. 56 Thus, depression appears to have a dual effect on the processing of reward and value: induction of excessive emotional responses and reduced willingness to reject unfair offers.

There is considerable evidence that monoamine systems, including doparnine (DA) and serotonin, are altered in depression. 57 Considerable monoamine loss is observed in high-risk states for depression. 58 In particular, DA neurotransmission in major depressive disorder (MDD) seems to be diminished, either by decreased DA release or intracellular signaling processing. These DA-related disturbances improve by treatment with antidepressants, presumably by acting on serotonergic or noradrenergic circuits, which then affect DA function. 57 Furthermore, DA receptor binding and amphetamine response in depression are correlated with altered brain activation in the ventrolateral PFC, OFC, caudate, and putamen. 59 Overall, depression seems to be associated with an alteration of the prefrontal control over the striatum leading to a dysfunctional frontostriatal connectivity. The impact of the frontostriatal system dysfunction in depression can be further understood considering the role of two circuits: the medial prefrontal cortex-ventral striatum, which underlies motivation, and the OFC-ventromedial caudate, considered to intervene in affective processing. 60 , 61

In addition of serotonin’s role in impulsive aggression, 62 – 64 abnormal serotonin function has been linked to psychopathologies associated with negative affects such as depression and anxiety. 65 – 68 In contrast to impulsivity, depression is characterized by reduced behavioral vigor and enhanced aversive processing, with increased sensitivity to negative stimuli. 69 However, both impulsivity and depression have been associated with low serotonergic tone, based primarily on the therapeutic efficacy of selective serotonin reuptake inhibitors (SSRIs) and observations that central serotonin depletion through dietary manipulation can induce depressive relapse. 70 , 71 Indeed, patients with depression show reduced tryptophan levels, 72 abnormal serotonin receptor function, 73 abnormal serotonin transporter function, 74 and elevated brain serotonin turnover. 75 However, the relationship between depression and serotonin is less clear-cut than that between impulsivity and serotonin. It is possible that the link between depression and serotonin might be indirect and mediated by associative learning 76 and/or disinhibition of negative thoughts. 77 Overall, a number of psychiatric disorders seem to disrupt the delicate balance between serotonin and dopamine, reflecting alterations in reward, risk assessment, and social interaction. This view is supported by the wide pharmacological profiles of the major psychotropics, such as antidepressants, antipsychotics, and even drugs of abuse.

Anhedonia, which is the loss of pleasure or interest in previously rewarding stimuli, is a key pathological element of MDD and predicts antidepressant response. 78 Anhedonia is associated with disruption of the frontostriatal valuation system and reward processing ( Figure 2 ). Anhedonic depressed patients exhibit reduced caudate 52 and OFC volume. 79 Decreased activation of the ventral striatum during reward selection, anticipation, and feedback are found in monetary tasks in nonmedicated anhedonic depressed patients. 80 Exploration of anhedonia in healthy volunteers showed decreased striatal activation and overactivation of the VMPFC during reward processing. 81

The bottom highlighted area shows the brain reward valuation system: ventral tegmental area (VTA) projections, ventral striatum (VS), and orbitofrontal cortex (OFC). The top highlighted area shows the substrates of executive function: dorsolateral prefrontal cortex (DLPFC) and posterior parietal cortex. The middle highlighted area shows two brain regions involved in emotion and intuition processing: amygdala and insula.

There is debate as to whether anhedonia in depressed patients represents the inability to experience pleasure and engage in rewarding activities, or the inability to sustain positive affect. Neuroimaging data support both hypotheses. Epstein et al. 80 reported that unmedicated depressed patients exhibited decreased ventral striatum and DMPFC activation with positive stimuli. Additionally, the magnitude of ventral striatum deactivation correlated with decreased interest and pleasure during daily activities. In contrast, Heller et al., 39 using an emotion regulation task found that depressed individuals were able to up-regulate positive affect, but failed to sustain NAcc activity over time. This diminished capacity to maintain positive affect was associated with decreased connectivity between the NAcc and mPFC. This concatenation of results points to an altered valuation system (frontostriatal circuit) in anhedonia, likely at the PFC level. This would be consistent with the therapeutic effects of psychotherapy such as cognitive behavioral therapy (CBT), which aims to identify and change dysfunctional patterns of thought and behavior. Furthermore, different forms of psychotherapy (e.g., interpersonal, behavioral activation, and cognitive behavioral therapy), for depression have shown normalization of PFC and striatum activity during reward tasks. 81 , 82

Development

Depressed adolescents exhibit similar alterations of the reward system as their adult counterparts. Children between 9 and 17 years old with MDD had reduced neural response than controls in the caudate, OFC, ACC, and amygdala, as well as higher neuroactivation in the DLPFC and frontal pole during decision and outcome phases in a monetary reward task. 83 In addition, diminished caudate activation was correlated with lower subjective positive affect during follow-up. 83 The same group also reported that pretreatment striatal and medial PFC reactivity during a monetary reward task were predictive of response to cognitive-behavioral therapy (CBT) or pharmacological treatment. Relative to control subjects, adult individuals exposed to childhood adversity reported elevated symptoms of anhedonia and depression, rated the reward cues less positively, and displayed a weaker response to reward cues in the left globus pallidus. 84 Additionally, the combination of adverse early life experience and the short polymorphism of the serotonin transporter gene enhances negativity bias (perceiving more danger and risk than reward) and physiological reactivity to negative experiences. 49

On the other hand, depression in older adults presents with unique cognitive characteristics. Individuals are guided by the same essential set of socioemotional goals throughout life, such as seeking novelty, feeling needed, and expanding one’s horizons. However, the relative priority of different sets of goals changes as a function of age. Typically, despite being at risk for loss of loved ones, function, finances, and status, older adults endorse better well-being than younger counterparts. This apparent paradox is explained by the Socioemotional Selectivity theory 85 , which states that according to the perception of time left to live, an individual’s perceived limitations on time lead to reorganizations of goals thereby prioritizing those with emotional meaning over those that maximize long-term payoffs in the distant future. This is believed to occur through more effective cognitive control over negative affect which reflects in effective emotion regulation mediated by the ventral PFC. 86 However, in the less frequent cases when depression occurs in older adults, it is typically associated with vascular insults that affect the PFC function. Because late onset depression is usually secondary to the loss of coping cognitive mechanisms in the elderly, it tends to be treatment resistant and have poorer outcomes.

Suicide is the most catastrophic outcome of depression and other psychiatric disorders, and is associated with reduced serotonergic neurotransmission, particularly within the VMPFC, including increased expression of serotonin 1 and 2 receptors 87 and binding of the presynaptic serotonin 2 receptor in the VMPFC 88 (for review, see 89 ). This dearth of serotonin is thought to impair executive function, predisposing patients to become more impulsive, rigid in their thinking, and poorer decision-makers. Deficits in executive function and problem-solving are greater in depressed individuals with a history of suicide attempts or even suicidal ideation compared with depressed controls. 90 Impaired decision making, reflected in poor performance in the Iowa Gambling Task (IGT), which is designed to mimic complex and uncertain decision making, is found in individuals with a past history of suicide attempts, 91 in particular, in those that used violent methods. 92 Euthymic patients with a history of suicide attempts showed significant deficits in executive function: impaired visuospatial conceptualization, inhibition, and visual attention (or reading fluency) suggestive of generalized PFC dysfunction, both DLPFC and VMPFC. 93 It is possible that executive function deficits may be more specific to suicidal behavior rather than to any specific psychiatric diagnosis because this observation holds true for suicidal patients with depression, bipolar disorder, and even temporal lobe epilepsy. Last, poor inhibition is found in suicide attempters when compared with patients with only suicidal ideation, 94 and greater cognitive executive function impairments are found in depressed patients with suicidal ideation compared with those without it. 95 However, individuals with a history of suicide attempts show poorer inhibition but better problem-solving ability than suicide ideators. 94 There is evidence that at least a subgroup of suicide attempters have deficits in self-regulation and temporal discounting. Depressed suicide attempters 60 years or older showed deficits in probabilistic reversal learning suggesting that this population makes present focused decisions, ignoring past experiences. 96 In a similar elderly sample, Dombrovski et al. 97 showed decreased temporal discounting in high-lethality suicide attempters compared with low lethality ones.

Anxiety is the natural response to risk and uncertainty, both of which are frequently found in everyday life (see Figure 1 ). The amygdala plays a central role in mediating an anxiogenic response to unpredictability. 98 Additionally, the insula is a key structure involved in the prediction of risk, 18 and the DLPFC is positively correlated with risk aversion. 99

Fear and anxiety are closely related, and share common cognitive and physiological properties. 100 Fear response is evoked by specific stimuli and tends to be transient, decreasing once a threat has dissipated. Anxiety may be experienced in the absence of a direct threat and typically persists over a longer period of time. However, anxiety is commonly conceptualized as a state of sustained fear. 101 Fear conditioning has been a most successful research model to understand the biology of anxiety. Animal and human research on fear conditioning has highlighted the central role of the amygdala in fear acquisition, storage, and expression. 101 – 103 The amygdala’s projections to different parts of the brain have been associated with specific functions. For instance, projections to the brainstem and hypothalamus mediate autonomic fear expression, projections to the ventral striatum mediate the use of actions to cope with fear, 102 hippocampal projections are involved in contextually dependent expression of fear, 104 and connectivity to the VMPFC is required for inhibition or control of conditioned fear and storage of extinction memory 5 , 104 , 105

Two principal information-processing biases are characteristic of anxiety: (1) a bias to attend toward threat-related information, and (2) a bias toward negative interpretation of ambiguous stimuli. 106 Anxiety is associated with faster response times when detecting a threat or negative stimuli or identifying a target cued by a threat stimulus, and slower response times when detecting a neutral stimulus or reporting neutral information in the presence of a threat stimulus. 107 – 109 This attentional bias reflects both facilitated detection of threat-related stimuli and difficulty in disengaging attention from negative stimuli, 107 and seems to be related to both the engagement of preattentive amygdala-dependent threat evaluation processes 110 and impaired prefrontal control mechanisms typically engaged during attentional competition and control. 111 Consistent with this view, high trait anxiety is associated with increased amygdala activity to attended as well as unattended threat stimuli 112 and decreased prefrontal activation under conditions of attention competition, 111 , 112 even in the absence of threat-related stimuli. 113

Anxious individuals unrealistically judge negative outcomes to be more likely than positive ones. 114 – 116 Higher trait anxiety is associated with heightened amygdala blood-oxygen-level-dependent (BOLD)-responses during passive viewing of neutral faces 117 and a tendency to interpret neutral faces more negatively. 118 For instance, anxious individuals tend to interpret ambiguous emotional facial expressions, 119 face-voice pairings, 120 and homophones 121 as more negative in valence than less-anxious individuals.

Anxiety as a trait has been amply studied in healthy subjects. Trait anxiety, worry, and social anxiety in healthy participants are predictive of heightened risk aversion. 122 – 124 In turn, heightened arousal to risky choices or increased interoceptive awareness of arousal responses (or an interaction of the two) may lead anxious individuals to be more risk averse. Trait anxiety is also associated with greater susceptibility to the framing effect (i.e., reacting differently whether a choice is presented in terms of gain or loss). 125

The circuitry involved in the learning and regulation of conditioned fear is altered in healthy individuals with the anxiety trait and in patients suffering from anxiety disorders. Trait anxiety is associated with heightened amygdala activation as well as elevated fear expression during fear acquisition. 126 , 127 Anxiety also impairs extinction learning and retention 126 – 128 as well as the regulation of emotional responses via intentional cognitive strategies. 107 , 129 Patients with panic disorder show an increased generalization of conditioned fear to similar stimuli. 130 Atrophy of the hippocampus in posttraumatic stress disorder patients suggests that contextual modulation of fear may also be altered in anxiety. 131

Although clinical data are still limited, 105 there is clear evidence of negative attentional biases in several anxiety disorders including generalized anxiety disorder, posttraumatic stress disorder, social and specific phobias, and obsessive-compulsive disorder (for review see 107 ). Amygdala hyper-responsivity while attending to, evaluating, and anticipating negative stimuli may heighten the cognitive and affective responses to a potential threat in anxious individuals. Thus, the everyday decisions made by individuals suffering from anxiety disorders to avoid exaggerated perceived threats can have a profound impact on the ability to function adaptively.

Bipolar Disorder

Bipolar disorder and schizophrenia share impairments in similar cognitive areas including attention, processing speed, verbal memory, learning, and executive function, although bipolar disorder deficits are usually less severe. 132 These cognitive impairments represent a substantial clinical problem in up to 60% of bipolar disorder patients 133 and can be found in depressed, manic, and mixed episodes as well as in the euthymic state. This pervasive impairment in cognitive function in bipolar disorder suggests it may be a trait marker associated with genetic vulnerability.

A real life consequence of these cognitive deficits is functional impairment in several spheres including independent living, social relationships, and vocational success. For instance, 20% of patients with bipolar disorder are married in contrast to 60% of the general population; approximately 60% of bipolar patients are unemployed compared with 6% in the general population; and 19%−58% are not living independently. 134 These functional impairments are present at the time of the first episode and persist over time. 135

In addition to the pervasive alterations in the cognitive sphere, emotion processing is markedly disrupted in patients suffering from bipolar disorder. It has been proposed that central to bipolar disease is a heightened processing of positive emotion regardless of the context. 136 A recent meta-analysis identified significant deficits in theory of mind and emotion processing in euthymic bipolar patients. 137 Emotion processing in depressed bipolar patients appears to involve a partially overlapping neural network with that of major depression, but with distinct roles of the VLPFC and thalamus. 138 Thus, bipolar patients are impaired in their ability to identify other individuals’ emotions and intentions, with a resultant impact on everyday functioning.

Despite these deficits in cognition and emotion processing, the findings on decision making are heterogeneous in bipolar disorder. For instance, manic or hypomanic patients tend to make suboptimal choices in the Cambridge Gambling Task, 139 they are more sensitive to error processing during a two choice prediction task, 140 they show steep temporal discounting, 141 and deficits in response disinhibition and inattention ( 142 , but see also 143 , 144 ). These deficits are not exclusive to mania, since depressed bipolar patients evidence deficits in reward processing, short-term memory, and sensitivity to negative feedback. 145 Moreover, euthymic patients with bipolar disorder also display moderate to severe deficits in a wide variety of executive function measures including category fluency, mental manipulation, verbal learning, abstraction, set-shifting, sustained attention, response inhibition, and psychomotor speed ( 146 – 148 , but see also 91 , 149 , 150 ). Furthermore, even first degree relatives of bipolar disorder patients show executive function deficits (i.e., attentional set shifting). 151 In addition to moderate to severe neuropsychological impairments, there seems to be specific cognitive and decision making biases in bipolar patients including impulsivity, exaggerated positive emotion, and deficits in risk assessment and reward processing. The weights of these cognitive and decision-making impairments are evident in the somber functional outcomes of patients with bipolar disorder.

Schizophrenia

Schizophrenia is a severe psychiatric disorder that afflicts approximately 1% of the population worldwide. It is characterized by alterations in higher function including thought, perception, mood, and behavior. The majority of people with schizophrenia do not attain “normal” milestones in social functioning, productivity, residence, and self-care. For instance, less than 20% of schizophrenic patients are responsible for their housing, almost 80% are unemployed, and less than 15% are married or in stable relationships. 152 This functional impairment occurs despite adequate symptom control that is attained by 30%−70% of patients. A large body of evidence has demonstrated significant cognitive dysfunction in schizophrenia, which is associated with disorganization, negative symptoms, and impaired functional outcome. 153 Information-processing deficits in schizophrenia are described in attention, working memory, inhibition, and context processing. 154 Context-processing deficits are associated with working memory impairments and dopaminergic tone in the PFC ( Table 3 ). 155 Moreover, both cognitive control and social cognition (e.g., theory of mind) deficits are disease outcome predictors and suitable candidates for therapeutic interventions. 152 , 156 It is no surprise that this faulty information processing in schizophrenic patients translates into impaired risk assessment, 75 , 76 reward processing, 157 and temporal discounting. 158 , 159 The latter are correlated with working memory deficits. 159 , 160

A pervasive clinical challenge in schizophrenia is the elevated comorbidity with substance abuse disorders. Approximately half of schizophrenic patients present a lifetime history of substance abuse disorders, 161 and 75%−90% are current smokers. 162 , 163 These extraordinary high rates of substance-use comorbidity may be explained by disrupted reward processing. 164 Thus, patients with schizophrenia who are smokers display a stronger subjective response and intensity of demands to smoking than the general population smokers. 165 , 166 In sum, patients with schizophrenia exhibit global cognitive control dysfunction that is reflected in specific deficits in risk assessment, reward processing, and temporal discounting. These impairments are translated in the devastating functional toll of this disorder.

Possible Interventions

There are already successful therapeutic approaches focused on improving cognition and decision-making capabilities of psychiatric patients: cognitive remediation and variations of cognitive-behavioral therapy (CBT), which aim to enhance emotional cognitive control and decision-making skills. Cognitive remediation is based on enhancing specific cognitive processes in order to modify the course and morbidities of disease. Recent advances in cognitive remediation strategies and delivery methods have notably increased the success of this intervention. 167 These advances include (1) the development of multidimensional tests of executive functioning that drill and practice with low-level cognitive demands, (2) the dynamic adjustment of difficulty in order to maintain a constant difficulty level, and (3) the development of understanding the minimum effective dose and optimal spacing of practice trials. Successful examples are found in areas as diverse as schizophrenia, 168 bipolar disorder, 169 attention deficit hyperactivity disorder (ADHD), 170 dyslexia, 171 traumatic brain injury, 172 and stroke. 173 In these studies, cognitive remediation was associated with improvement in hyperactivity, organizational skills, affect, sustained attention, and temporal discounting. 174 Moreover, improvements induced by cognitive remediation correlate with discrete changes in neural activity, 175 noneffortful auditory evoked potentials, 176 peripheral biomarkers as brain-derived neurotrophic factor (BDNF), 177 as well as improvements in everyday functioning. Furthermore, considering the close association between cognitive impairments and poor functional outcome, cognitive remediation aimed at social cognitive impairments has proven effective in enhancing social functioning. Social cognitive remediation programs are either targeted to a specific social cognitive domain (e.g., emotion perception), or broad-based, combining a variety of psychosocial approaches, including cognitive remediation, social skills training, and social cognitive skill building. 178 , 179 Both approaches have proved effective in improving social cognitive processes in schizophrenia. 180 , 181

Two examples of the successful adaptation of cognitive-behavioral therapy to enhance decision making are dialectical behavior therapy and problem-solving therapy. Dialectical behavior therapy (DBT) was the first psychological treatment for borderline personality disorder tested in a clinical trial. 182 It is specifically designed to target the emotion dysregulation (mood instability) and to reduce impulsive behaviors (in other words, enhancing emotional cognitive control). It applies behavioral analysis to incidents leading to self-injury and overdoses, teaching patients alternative ways to handle dysphoric emotions. DBT has been used successfully in patients with borderline personality disorder, eating disorders, and parasuicidal behavior. Problem-solving therapy (PST) is a cognitive-behavioral intervention that focuses on training in adaptive problem-solving attitudes and skills. 183 It aims to reduce and prevent psychopathology and enhance positive well-being by helping individuals cope more effectively with stressful problems in living. PST is based on a relational/problem-solving model of stress and well-being (psychological, social, and health functioning) in which social problem solving (i.e., real-life problem solving) is assumed to play an important role as a mediator and a moderator of the relationship between stressful life events (major negative events as well as daily problems) and well-being. It has proven effective for the treatment of depression. 184

Conclusions

It is not surprising that severe mental illness affects patients’ lives not only because of the cardinal disease symptoms, but also by impairing their ability to make functional and healthy decisions. This impairment may be related to disorganization or global deficits in attention, working memory, and language, such as those observed in schizophrenia and bipolar disorder. However, it can be subtler and lead to abnormal risk assessment or reward processing as found in depression. These pervasive deficits translate into medication and medical appointment nonadherence, poor diet and exercise, and drug use, which in turn leads to poor quality of life and clinical outcomes such as relapse, hospitalization, death, and incarceration.

A multidisciplinary approach to how the brain makes decisions may provide a new theory of thought with quantifiable parameters that can increase understanding of mental processes (decision making) in health and disease. The study of two particular constructs, reward and temporal discounting, has shed light on our understanding of severe mental illness. The utilization of additional paradigms can further lead to interventions to address every day situations that patients with mental illness face. The consideration of decision-making patterns in the assessment and manag e ment of patients with mental illness might yield evidence-based interventions with real life impact such as cognitive remediation.

Dr. Cáceda receives funding from the Arsht Foundation, the Community Alliance Against AIDS, the National Institute on Alcohol Abuse and Alcoholism, the National Institute on Drug Abuse, and NIMH. Dr. Nemeroff receives research/grant support from the Agency for Healthcare Research and Quality and NIH; he has served as a consultant to Allergan, Lilly, Roche, Shire, SK Pharma, Takeda, and Xhale; he is a shareholder with CeNeRx BioPharma, NovaDel Pharma, PharmaNeuroBoost, Reevax Pharma, and Xhale; he holds patents for a method and devices for transdermal delivery of lithium and for a method of assessing antidepressant drug therapy through transport inhibition of monoamine neurotransmitters by ex vivo assay; he has served on the scientific advisory boards of the American Foundation for Suicide Prevention, the Anxiety Disorders Association of America; AstraZeneca, CeNeRx BioPharma, NARSAD, PharmaNeuroBoost, Skyland Trail, and Xhale; he has served on the board of directors for the American Foundation for Suicide Prevention, the Anxiety and Depression Association of America, Gratitude America, Mt. Cook Pharma, NovaDel, and Skyland Trail; he has received royalties from American Psychiatric Publishing; and he has received other financial support from AstraZeneca, BioPharma, CeNeRx, NovaDel Pharma, PharmaNeuroBoost, Reevax Pharma, and Xhale. Dr. Harvey has received consulting fees from Abbott Laboratories, Amgen, Bristol-Myers Squibb, Genentech, Johnson and Johnson, PharmaNeuroBoost, Sunovion Pharma, and Takeda Pharma.

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Improving Our Understanding of Impaired Social Problem-Solving in Children and Adolescents with Conduct Problems: Implications for Cognitive Behavioral Therapy

• Published: 14 February 2022
• Volume 25 , pages 552–572, ( 2022 )

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• Walter Matthys   ORCID: orcid.org/0000-0002-8887-0785 1 &
• Dennis J. L. G. Schutter   ORCID: orcid.org/0000-0003-0738-1865 2  

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In cognitive behavioral therapy (CBT) children and adolescents with conduct problems learn social problem-solving skills that enable them to behave in more independent and situation appropriate ways. Empirical studies on psychological functions show that the effectiveness of CBT may be further improved by putting more emphasis on (1) recognition of the type of social situations that are problematic, (2) recognition of facial expressions in view of initiating social problem-solving, (3) effortful emotion regulation and emotion awareness, (4) behavioral inhibition and working memory, (5) interpretation of the social problem, (6) affective empathy, (7) generation of appropriate solutions, (8) outcome expectations and moral beliefs, and (9) decision-making. To improve effectiveness, CBT could be tailored to the individual child’s or adolescent’s impairments of these psychological functions which may depend on the type of conduct problems and their associated problems.

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Matthys, W., Schutter, D.J.L.G. Improving Our Understanding of Impaired Social Problem-Solving in Children and Adolescents with Conduct Problems: Implications for Cognitive Behavioral Therapy. Clin Child Fam Psychol Rev 25 , 552–572 (2022). https://doi.org/10.1007/s10567-021-00376-y

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Cognitive impairment in hospital is often associated with adverse outcomes, such as falls. For some people with cognitive impairment and for their carers and families, a hospital stay can be a negative experience. Staff may struggle to provide the right care in the absence of appropriate education and training.

The first step to making a person’s stay safer is to understand the different forms of cognitive impairment, the people who are at risk, and what steps can be taken to reduce harm. 

Cognitive impairment:

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Understanding what each person is experiencing will help you to communicate with that person and provide the right care.

Cognitive impairment can affect us all. People with cognitive impairment may be our patients, our parents, our loved ones, or us.

Common conditions associated with cognitive impairment 

Dementia and delirium  are the two most common forms of cognitive impairment among older people admitted to hospital. While they are not a normal part of getting old,  these conditions commonly affect older people. As our population ages, the number of people with delirium and dementia in hospital will increase.

Dementia causes progressive cognitive impairment, affecting memory, judgement, language and the ability to perform everyday tasks. Alzheimer’s disease is the most common type of dementia. Dementia is predominately a disorder related to age but can affect people younger than 65 years old. This is known as younger onset dementia.

Delirium is an acute disturbance of consciousness, attention and cognition that tends to fluctuate during the course of the day. It can be a treatable medical emergency. Delirium is common in hospitals but is often not detected or is misdiagnosed. Delirium can be treated if diagnosed early and even prevented with the right care following a hospital admission.People with dementia are at a greater risk of developing delirium.

People may also be cognitively impaired due to either:

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Any form of cognitive impairment needs to recognised, understood and acted on.

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To search for products and suppliers of modifications in your local area visit the Independent Living Centres Australia website.

Cognitive and thinking skills

Cognitive or thinking skills can be hard for people if their disability affects the way their brain processes information, for example, people with intellectual disabilities, acquired brain injuries, specific learning disabilities, autism spectrum disorders, psychiatric disorders, dementia or other neurological conditions. Poor cognitive and thinking skills can lead to stress, social withdrawal and poor work performance. This can cause people to feel frustrated with themselves and others, become overwhelmed and easily confused when trying to learn new information. As a result, people can withdraw from others and underperform in their role at work.

The processes affected by cognitive or thinking skills include critical thinking, problem solving, attention, concentration and memory, organisation and planning. These processes and some suggested workplace solutions and adjustments are provided below.

Original and creative thinking

Original or creative thinking means the ability to question the common way of doing things and form new ideas or approaches to solve a problem or meet a need. It involves higher-level brain functioning, incorporating the use of intuition, making unusual connections or associations, imagination, objectivity and the willingness to take risks.

Workplace adjustments and solutions

• fostering a friendly, open work environment, where verbal and written input from workers regarding operations, work processes and methods is valued and encouraged
• establishing a buddy program with a co-worker to provide mentoring and prompting for workers with a cognitive impairment

Problem Solving

Problem solving is the ability to find answers to problems using an organised thought process.

Critical thinking

Critical thinking refers to the mental process of analysing information accurately, precisely, comprehensively and without bias. Both problem solving and critical thinking involve gathering of information, defining the issue and breaking it down into smaller sections to action through to an outcome or solution.

• prompts, reminders and checklists can assist people with problem solving as they can be used to assess the situation and provide information about the problem, such as what has been done, when and what is next
• aids like graphic organisers can help people with problem solving. These enable the removal of most of the words and focus on connections or links between ideas using only key words and images. This allows people to look at the whole problem as well as the interrelated smaller issues. Graphic organisers have many names including visual maps, mind mapping, and visual organisers.

Attention, concentration and remembering work tasks

Attention is the process of selectively concentrating thinking on one aspect or task whilst ignoring other things, so thinking in an intended direction. The ability to maintain attention and concentration to focus on learning new information and/or focus on carrying out tasks and activities is a general work requirement across all industries.

The ability to remember work tasks and activities is also a necessary requirement across workplaces.

It is important to recognise that difficulty maintaining attention/concentration or remembering can be related to disability and that understanding and support at work should be made available. Memory issues in particular can affect job performance and safety in the workplace.

Workplace solutions and adjustments

• avoid or eliminate distractions and do not multitask as this will divide attention
• break down job tasks into small steps and use visual prompts for each step to assist with refocus and continuation with tasks
• use a pin-up board/white board to display task flow charts
• use ‘to do’ lists which can be ticked off as completed to help with tracking actions
• schedule regular breaks to accommodate a reduced attention span
• schedule the early part of the working day for ‘attention demanding’ tasks or activities, with less demanding tasks scheduled later in the day
• rotate between tasks to increase interest
• establish a buddy program with a co-worker to provide extra support and encouragement to keep on task
• establish a set work routine to make it easier to remember and allow time to adjust if the routine alters
• minimise potential distractions to concentration, for example, partition off the workspace, have a workstation away from other colleagues and reduce noise or other distracting factors
• incorporate the use of acronyms and mnemonics which can be short poems or sayings used to remember information
• foster a healthy lifestyle for workers, for example, be conscious of stress levels in the workplace, encourage physical fitness and, if food or meals are provided, make healthy foods available

There are also different aids and products that can help prompt memory:

• clocks, watches and timers with built-in prompts
• colour coding
• electronic organisers

Organising, planning and managing time

Difficulties associated with organisation, planning and the ability to effectively judge and manage time can adversely affect job performance, as they are important skills for efficiency and effectiveness in the workplace. The ability to prepare and organise daily work requirements or tasks provides structure or a semblance of order to each working day and can reduce stress levels. Examples include not being prepared at meetings, poor punctuality due to lack of travel planning or limited reliability as an employee.

• establish a buddy system with a co-worker to provide extra support and guidance
• various organising and timing devices are available including calendars, watches and timers with prompts

Support Services

For all cognition deficits, other supports such as job coaches, skills trainers and mentors can assist people with problem solving and critical thinking skill development in the workplace. Strategies may include role playing, reviewing information with the employee or presenting information in a way that is more easily understood, such as through Easy English translation. A cognition and communication specialist, such as a speech pathologist, may be helpful in identifying any barriers through an assessment.

Specialist employment agencies who provide coaching and support on the job for people with disability may be able to assist a person to learn how to problem solve at work. Find a provider near you.

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Cognitive Problems After Traumatic Brain Injury

What is cognition?

Cognition is the act of knowing or thinking. It includes the ability to choose, understand, remember and use information. Cognition includes:

• Attention and concentration.
• Processing and understanding information.
• Communication.
• Planning, organizing, and assembling.
• Reasoning, problem-solving, decision-making, and judgment.
• Controlling impulses and desires and being patient.

How does TBI affect cognition and what can be done about it?

After a TBI it is common for people to have problems with attention, concentration, speech and language, learning and memory, reasoning, planning and problem-solving.

Attention and concentration problems

A person with TBI may be unable to focus, pay attention, or attend to more than one thing at a time. This may result in:

• Restlessness and being easily distracted.
• Difficulty finishing a project or working on more than one task at a time.
• Problems carrying on long conversations or sitting still for long periods of time.

Since attention skills are considered a “building block” of higher level skills (such as memory and reasoning), people with attention or concentration problems often show signs of other cognitive problems as well.

What can be done to improve attention and concentration?

• Decrease the distractions. For example, work in a quiet room.
• Focus on one task at a time.
• Begin practicing attention skills on simple, yet practical activities (such as reading a paragraph or adding numbers) in a quiet room. Gradually make the tasks harder (read a short story or balance a checkbook) or work in a more noisy environment.
• Take breaks when you get tired.

Problems with processing and understanding information

After brain injury, a person’s ability to process and understand information often slows down, resulting in the following problems:

• Taking longer to grasp what others are saying.
• Taking more time to understand and follow directions.
• Having trouble following television shows, movies, etc.
• Taking longer to read and understand written information including books, newspapers or magazines.
• Being slower to react. This is especially important for driving, which may become unsafe if the person cannot react fast enough to stop signs, traffic lights or other warning signs. Individuals with TBI should not drive until their visual skills and reaction time have been tested by a specialist.
• Being slower to carry out physical tasks, including routine activities like getting dressed or cooking.

What can be done to improve the ability to process and understand information?

• Place your full attention on what you are trying to understand. Decrease distractions.
• Allow more time to think about the information before moving on.
• Re-read information as needed. Take notes and summarize in your own words.
• If needed, ask people to repeat themselves, to say something in a different way, or to speak slower. Repeat what you just heard to make sure you understood it correctly.

Language and communication problems

Communication problems can cause persons with TBI to have difficulty understanding and expressing information in some of the following ways:

• Difficulty thinking of the right word.
• Trouble starting or following conversations or understanding what others say.
• Rambling or getting off topic easily.
• Difficulty with more complex language skills, such as expressing thoughts in an organized manner.
• Trouble communicating thoughts and feelings using facial expressions, tone of voice and body language (non-verbal communication).
• Having problems reading others’ emotions and not responding appropriately to another person’s feelings or to the social situation.
• Misunderstanding jokes or sarcasm.

What can be done to improve language and communication?

Work with a speech therapist to identify areas that need work. Communication problems can keep improving for a long time after the injury.

How family members can help:

• Use kind words and a gentle tone of voice. Be careful not to “talk down” to the person.
• When talking with the injured person, ask every so often if he or she understands what you are saying, or ask the person a question to determine if he or she understood what you said.
• Do not speak too fast or say too much at once.
• Develop a signal (like raising a finger) that will let the injured person know when he or she has gotten off topic. Practice this ahead of time. If signals don’t work, try saying “We were talking about…”
• Limit conversations to one person at a time.

Problems learning and remembering new information

• Persons with TBI may have trouble learning and remembering new information and events.
• They may have difficulty remembering events that happened several weeks or months before the injury (although this often comes back over time). Persons with TBI are usually able to remember events that happened long ago.
• They may have problems remembering entire events or conversations. Therefore, the mind tries to “fill in the gaps” of missing information and recalls things that did not actually happen. Sometimes bits and pieces from several situ¬ations are remembered as one event. These false memories are not lies.

What can be done to improve memory problems?

• Put together a structured routine of daily tasks and activities.
• Be organized and have a set location for keeping things.
• Learn to use memory aids such as memory notebooks, calendars, daily schedules, daily task lists, computer reminder programs and cue cards.
• Devote time and attention to review and practice new information often.
• Be well rested and try to reduce anxiety as much as possible.
• Speak with your doctor about how medications may affect your memory.

Planning and Organization Problems

• Persons with TBI may have difficulty planning their day and scheduling appointments.
• They may have trouble with tasks that require multiple steps done in a particular order, such as laundry or cooking.

What can be done to improve planning and organization?

• Make a list of things that need to be done and when. List them in order of what should be done first.
• Break down activities into smaller steps.
• When figuring out what steps you need to do first to complete an activity, think of the end goal and work backwards.

Problems with reasoning, problem-solving and judgment

• Individuals with TBI may have difficulty recognizing when there is a problem, which is the first step in problem-solving.
• They may have trouble analyzing information or changing the way they are thinking (being flexible).
• When solving problems, they may have difficulty deciding the best solution, or get stuck on one solution and not consider other, better options.
• They may make quick decisions without thinking about the consequences, or not use the best judgment.

What can be done to improve reasoning and problem-solving?

• A speech therapist or psychologist experienced in cognitive rehabilitation can teach an organized approach for daily problem-solving.
• Work through a step-by-step problem-solving strategy in writing: define the problem; brain¬storm possible solutions; list the pros and cons of each solution; pick a solution to try; evalu¬ate the success of the solution; and try another solution if the first one doesn’t work.

Inappropriate, embarrassing or impulsive behavior

Individuals with brain injuries may lack self-control and self-awareness, and as a result they may behave inappropriately or impulsively (without thinking it through) in social situations.

• They may deny they have cognitive problems, even if these are obvious to others.
• They may say hurtful or insensitive things, act out of place, or behave in inconsiderate ways.
• They may lack awareness of social boundaries and others’ feelings, such as being too personal with people they don’t know well or not realizing when they have made someone uncomfortable.

What causes it?

• Impulsive and socially inappropriate behavior results from decreased reasoning abilities and lack of control. The injured person may not reason that “If I say or do this, something bad is going to happen.”
• Self-awareness requires complex thinking skills that are often weakened after brain injury.

What can be done about it?

Things family members can do:

• Think ahead about situations that might bring about poor judgment.
• Give realistic, supportive feedback as you observe inappropriate behavior.
• Provide clear expectations for desirable behavior before events.
• Plan and rehearse social interactions so they will be predictable and consistent.
• Establish verbal and non-verbal cues to signal the person to “stop and think.” For example, you could hold up your hand to signal “stop,” shake your head “no,” or say a special word you have both agreed on. Practice this ahead of time.
• If undesired behavior occurs, stop whatever activity you are doing. For example, if you are at the mall, return home immediately.

Cognitive outcome/recovery and rehabilitation

Cognition is usually evaluated by a neuropsychologist. Since there are many factors that can affect how someone will improve cognitively, it is very difficult to predict how much someone will recover. With practice, cognitive problems usually improve to some degree.

Cognitive rehabilitation is therapy to improve cognitive skills and has two main approaches, remediation and compensation:

• Remediation focuses on improving skills that have been lost or impaired.
• Compensation helps you learn to use different ways to achieve a goal.

Discuss your concerns with your physician or treatment provider.

You should discuss any questions or concerns you have with a physiatrist (rehabilitation specialist) or the rehabilitation team. It is important to mention new problems as they develop. New problems could be the result of medication or require further evaluation.

Recommended reading

• Managing Cognitive Issues, in Making Life Work after Head Injury , South Carolina Department of Disabilities and Special Needs.
• Guideposts to Recognition: Cognition, Memory and Brain Injury, in The Road to Rehabilitation , Brain Injury Association of America.
• Cognitive and Communication Disorders , in TBI Resource Guide, Centre for Neuro Skills.
• Cognitive Rehabilitation , Brain Injury Resource Center.

Source Our health information content is based on research evidence and/or professional consensus and has been reviewed and approved by an editorial team of experts from the TBI Model Systems.

Authorship Cognitive Problems after TBI was developed by Dawn Neumann, PhD and Anthony Lequerica, PhD, in collaboration with the Model Systems Knowledge Translation Center. Portions of this document were adapted from materials developed by the Rocky Mountain Regional Brain Injury System, the UAB TBI Model System, the Mayo Clinic TBI Model System, the New York TBI Model System, and from Picking up the pieces after TBI: A guide for Family Members , by Angelle M. Sander, PhD, Baylor College of Medicine (2002).

Cognitive Problems after TBI was developed by Dawn Neumann, PhD and Anthony Lequerica, PhD, in collaboration with the Model Systems Knowledge Translation Center. Portions of this document were adapted from materials developed by the Rocky Mountain Regional Brain Injury System, the UAB TBI Model System, the Mayo Clinic TBI Model System, the New York TBI Model System, and from Picking up the Pieces after TBI: A Guide for Family Members , by Angelle M. Sander, PhD, Baylor College of Medicine (2002). Copyright © 2010 by University of Washington/MSKTC. 

Please check the MSKTC site for any recent updates on this article.

• Add new comment

Comments (87)

Please remember, we are not able to give medical or legal advice. If you have medical concerns, please consult your doctor. All posted comments are the views and opinions of the poster only.

Anonymous replied on Fri, 10/13/2023 - 2:22am Permalink

Hey folks. I was walking in a sidewalk and a van hit me throwing me ten feet. Subdural hematoma, subarachnoid hemorrhaging and basil skull fracture. When this happened in 1996, I wasn’t given enough cognitive rehab therapy and became homeless with my four cats. Things became a lot better when Brain InjurySpecialists stepped in to help me. I’m now working on being an advocate, as professional journals estimate 50% of homeless people have brain injuries. It’s a frickin leaning process, but find ways to keep yourself going!!! Music, books, friends, look at the stars or clouds in the sky every night….

Learn as much as you can. I’m now facing being abused by brain injury rehab people, and no one is listening. I also just learned that I don’t need a cognitive behavioral therapist, but a cognitive REHAB therapist. Another reason to get a lawyer.

Believe in yourself people. There’s got to be a purpose in what we are dealing with. Life events happen sometime that we don’t cause or deserve, but just have to deal with. ✌️and hope for you all…..

Zack replied on Wed, 10/27/2021 - 8:38pm Permalink

I suffered two minor brain injuries when I was younger, one at 19 and one at 23, and then a major TBI at the age of 29. I experience virtually everything listed on this page and sadly no medicine seems to help. There are many days I just want to give up on living. Been 9 years now since the major TBI and things have only improved slightly. Hard to face the fact the rest of my life will be miserable. Worst of all, the U.S. government refuses to give me disability, claiming that I just dont want to work.

Anonymous replied on Sun, 05/10/2020 - 7:26pm Permalink

I have many cognitive problems, but I didn't have a TBI, I have been diagnosed with schizophrenia, I have read that schizophrenia can cause many cognitive problems, my problems are with language comprehension, I can't understand so many things, I can't understand movies, TV shows, audiobooks, books, comic books etc., it's very hard for me to live with these problems, I have improved over the years, but I still can't understand very well.

Zack replied on Wed, 10/27/2021 - 8:41pm Permalink

I have a friend who was diagnosed with Schizophrenia 20 years ago and he discovered that improvement meant finding a very specific combination of medicines at very specific dosages. Every persons body is different so you might want to ask your doctor to adjust your medicine and add or remove medicines. My friend also went through 3 doctors before finding one that would really work with him. Sadly too many in the medical community only follow textbook recommendations and do not tailor their medical treatments to the individual needs of each person.

Anonymous replied on Wed, 02/19/2020 - 2:55pm Permalink

Hell my wife is a nurse and she calls me insensitive for forgetting thing, wont listen to me when i talk and wont let me finish without distracting me, then i get lost. Can deal with explosive emotional outbursts, angger, im isolated and alone.

Anonymous replied on Thu, 02/06/2020 - 6:48pm Permalink

Are there support groups for family members? My son's girlfriends, mother, has TBI. Her mom can be erratic and controlling of her daughter, making her cry multiple times a week and question herself as a good person. I'm not sure if all her mom's behavior is due to the TBI, but I have experienced first hand her mom's irrational behavior and I try to be understanding... but there should be boundaries. I think it would be great for my son and his girlfriend to go to a support group where they can get help in understanding and dealing what is going on. They are in Washington at college... does anyone have any suggestions?

Mrs. Y replied on Fri, 01/10/2020 - 3:45pm Permalink

Much of the advice here in my opinion is going to leave your family member with a TBI potentially more ashamed and more embarrassed.

For example it states if the undesired behavior occurs to leave the space immediately. Additionally raise a finger at them if they get off topic so they know.

My husband had initially tried these sort of tactics with me and it hurt my feelings. Instead now he employs a gentler approach of patience and loving guidance which has worked much better and avoids making me feel ashamed if I’ve gotten off topic (no fingers waggling in my face) instead he kindly redirects the conversation back.

If I’ve done something inappropriate no more being marched out of the public space in front of everyone like a child instead he handles it calmly, waits until the space is clear and provides clear simple options (one of which is always to go home and rest).

The advice in this column isn’t very good. Your family member is hopefully someone you love who is hurt so treat them like it, not like someone who is sick and can be bossed around.

5yrsPostTBI replied on Fri, 02/05/2021 - 1:42pm Permalink

Your husband sounds like a sweet heart and you are very lucky to have him. I strongly believe there should be a guide for friends, family, coworkers, etc. on how to approach those whom they know with TBI and what to expect.

Karyn replied on Thu, 12/26/2019 - 7:59am Permalink

I suffered a concussion on 9/3/19, I have difficulty with almost all of the things above. My short term memory is really bad, but I can remember in detail what happened or events in my life from 20 years ago. The only things that have gotten better are the dizzyness and balance, which lasted 10 or 11 weeks. My family doesn't fully understand what is happening to me. My daughter had a concussion 2 years ago and her symptoms only lasted 6 weeks, she has said that my injury is far worse. My neurologist is helpful, but workman's comp has been delaying my therapies until I undergo an ime exam. They have never approved speech therapy which was recommended by my neurologist and physical therapist. I'm extremely depressed to the point that I don't shower every day, and this is very unlike me. I also have herniated discs in my cervical spine and fear that I will regress without the help I truly need. The list goes on and on.

Leslie replied on Sun, 02/14/2021 - 11:34am Permalink

Karyn, if workers comp is not working with you and denying treatments, you might look for a workers comp lawyer to help you navigate. Unfortunately this is a common occurrence. I got really lucky with my workers comp rep. Also, know that somewhere on the order of 30% of those who suffer concussion (which is a TBI) don’t recover right away. You aren’t alone and it’s not because of anything you have done. I can recommend the book conquering concussion by Dr. Mary Esty for both you and family members to read at least the first 100 pages - which include examples of others and common post concussion symptoms. that helped me understand why so many simple things- like doing my dishes or laundry were so hard after injury due to the effects on executive function. Good luck!

Seri replied on Wed, 12/11/2019 - 2:26am Permalink

My injury occurred in 2008, due to a brain tumor. I have someone in particular in my life (gym trainer), who says after I forget, misunderstood, get appointments incorrect. or don't follow through on things, that my TBI is just an excuse. They have known me since being released from the hospital PT program to rehabilitate on my own. They say I should be doing this, or that, every week now...every time the blow up at me getting upset or p****d off at me...and in public--the gym. I am a higher-functioning TBI survivor, but I have cognitive issues. I paraphrased this explanation for the sake of spaced time. My questions for the community is, am I doing something wrong? I'm so frustrated that I'm no longer mentally sharp, depression is working hard on me. I must be doing something wrong they keep hounding me. Thanks for any feedback.

Laura replied on Thu, 03/21/2019 - 7:14pm Permalink

I experienced my TBI in September 2016. My main question for those of you who might read this: what have been your issues with hearing after your TBI? I was non-hearing for 3-4 months when I learned to lip read and some ASL. Then sound came back slightly but heavily distorted. With more issues than I’m explain here. I can’t hear music. I hear it but it registers as jumbled noise. I’d be very curious if someone has similar issues. From what I can tell it may always be this way or slowly get better with time. Thoughts? Similar experiences? Find me on Twitter @popwatching I’d love to discuss. Thanks.

S replied on Sun, 11/07/2021 - 10:55am Permalink

After a TBI I was diagnosed with central auditory processing disorder (CAPD). I have trouble hearing sound correctly and a bunch of other cognitive issues that come with TBI induced CAPD. I highly recommend the book, When the Brain Can't Hear: Unraveling the Mystery of Auditory Processing Disorder. by. Teri James Bellis. Hopefully this will help you, it helped me a lot.

Cynthia replied on Wed, 05/01/2019 - 5:07pm Permalink

I had a car accident with a TBI on April 6. I was taken from the scene of a Total loss accident when hit by a Semi Truck that totaled my 3 month old brand new SUV. 55k. and put in the tow truck driver vehicle. I was last wandering in Portland for a few hours until my son found me after going to the tow yard and finding they let me leave and had been gone over 3 or 4 hours after they towed my vehicle to the tow lot. I don’t remember the next 48 hours. My son had to come and find me wandering around Portland. I was covered from head to foot with mud had no phone or identification nothing. The chp shouldn’t have let me go with the tow truck driver and the tow driver shouldn’t have let me walk away without my phone, wallet and purse at the tow yard. I did hit the left side of my head very hard and have hearing loss in that ear . I have had headaches and severe nausea and have felt the most tired I’ve felt in In my life. I can fall asleep during a conversation and then when I wake up and I am still talking but not making any sense and don’t know what I was talking about. I’m sorry you got hurt. I am not having the same issues as you with sound except it is just harder to hear. Mine are more with balance, memory, headache, cognitive, vision, memory, communication, speech, balance and speech. .

Laura replied on Fri, 05/03/2019 - 11:50am Permalink

Thank you for replying Cynthia. I’m so very sorry that happened to you and I agree you shouldn’t have been allowed to leave the scene. That’s very scary. I’m so glad your son found you. Have you had medical care since? I’m assuming you have since you know it’s a TBI. I was in a coma for 3 weeks and in the hospital for nearly 4 months so I had a lot of care (physical therapy, speech therapy, neuropsychological therapy, occupational therapy and I’ve seen ENTs and audiologists). I hope you are getting plenty of care, Cynthia. Because even though you weren’t in a coma like me TBIs are serious.

Cass replied on Mon, 04/15/2019 - 6:09pm Permalink

I’m sorry that your hearing has not returned. Mine has taken quite some time but is still not 100%. I would recommend seeing an ENT to determine the best plan.

Laura replied on Fri, 05/03/2019 - 11:59am Permalink

Cass, thank you so much for your reply. Much appreciated. Yes, I have been to an ENT and audiologists. I have been to neurologists that specialize in brain injury. So far what I “hear” the most from them is healing takes time. And every TBI is unique so there’s no guarantee my hearing will improve more than it already has. Right now I’m just reaching out to fellow survivors (like yourself) for if they’ve had similar experiences. I haven’t given up on the medical community though. I’m still pursuing those avenues as well. Thanks again, Cass. I hope you’re well.

donna replied on Tue, 03/19/2019 - 12:53am Permalink

what do you do when you don't have contacts anymore because the resources ran out yrs. ago to pay facilitators to come and help for a short period of time but now the medicaid I'm forced to use won't pay the very people that helped me before when car insurance pd. the bills of the psychologist and chiropractor. so now I'm in constant pain from lower back down legs and have a terrible time being able to clear my house to be livable again and after I lost my doctors..I have no social life at all

Anonymous replied on Sun, 02/10/2019 - 5:00pm Permalink

I am 31 I had a bad tbi and many many bad concussions after. I saw so many specialists and nothing. Then I saw dr Cantu in concord the #1 concussion specialist and found out a lot. I had an mri and found out I had a hole in my brain and the left side is deteriorating. Cte has proven side effects there’s 4 stages. The fourth is suicidal thoughts that hit like a freight train. There’s two medication that save our lives. Allow us to focus work and be sane. Zoloft is made for tbi and time release adderal. It will change your life it did mine. If anyone ever needs anything please reach out to a dr and also look up cte side effects. Anger impulsive depression suicide. It can be managed.

Crystal replied on Tue, 10/01/2019 - 1:03pm Permalink

I'm so sorry to hear your story. I'm here looking for answers for my sister. She had a concussion almost two years ago she fell and broke her orbital bone, woke up to a pool of blood. They said she had a concussion but from the time this happened until now no one can tell her what's wrong. I read everyone's story and yours sounds similar to hers. I need a good Dr. To take her to we are in Maryland. She keeps saying the Drs looked at the MRI but didn't see anything. Anyone that talks to her knows something is wrong. She has trouble finding words . reading, forming sentences, she can't remember how to spell. She says she see things differently than everyone else. I'm very worried for her. She's sad she feels alone no one can hold a full conversation with her. If anyone knows a Dr in md that will take on a patient that doesn't have insurance and pays cash please let me know. I miss my sister and im concerned she's slipping into a deep depression from this. She cries all of the time. It's so sad. She was an awesome bartender, she taught me now she can't remember how to pour. I hope this reaches someone that can help me help her because her husband isn't willing to help. They had just gotten married when this happened and he seems done dealing with it. If anyone can help please contact me. Thank you in advance.

Darleen replied on Wed, 12/12/2018 - 5:57pm Permalink

I can't believe this website has been here all this time and I never ran into it. Some much information that I had to walk away for a little bit, but I'll be reading more each day. Anyway one of the things that I wonder about is that I've been diagnosis with bipolar disorder and I'm wonder if that's a misdiagnosis or more likely a result of the injury. The accident happened when I was 29 and I never had a history of mental illness until after the accident. Sure there were ups and downs but not to the degree I had in the following years. Now I take an anti seizure, anti anxiety and respirone to control paranoia. After reading the information on this website definitely going to have a few doctors look more closely at my case management. Of course going to remain on my present meds :p but I'm curious to find out how much is contacted here and if there is more I can do to improve my cognitive ability.

Mary replied on Fri, 03/01/2019 - 2:12pm Permalink

I was curious if you told your doctor? Are they looking into it more? Just wondering if so how they went about it and what your outcome was?

Terri replied on Mon, 02/04/2019 - 7:51pm Permalink

I had a TBI and brain surgery in 2015. I'm having trouble. Nobody has patience to deal with me. I get so frustrated. Hearing loss and trouble grasping what people are asking me. What do I do?

Jackie replied on Thu, 08/08/2019 - 8:20am Permalink

My grandson is the same ,he is living with me because he was with he’s mum and stepdad. I understand it difficult for you .you must seek help special if you have no one to ack on your behalf! Need to learn new ways to deal with thing . I feel for you as I do my grandson.

Lana replied on Mon, 03/18/2019 - 10:16pm Permalink

Have your doctor refer you to a good speech therapist and occupational therapist. They can help you work throught it. Also see a neuropsychologist for testing and diagnosis. You have to push and advocate for yourself. I found a lot of healthcare professionals will blow you off.

Teri replied on Sun, 04/07/2019 - 1:47am Permalink

Very true I have found the same thing my saving grace was stumbling across a article like this I went back to the neurologist that said there was nothing I could do but wait and asked for referral to the Speech Therapist she was so wonderful and has helped my come along way #Gratefull

Tom replied on Mon, 10/29/2018 - 11:01pm Permalink

Thank you for sharing I have found my people. You all are Mental Warriors and I am so thankful for sharing. Thank you Thank you Thank you I am so great full for my following experiences:

When I was 5 years old I fell out of a tree house, hospitalized with concussion and broken left wrist. When I was 13 I wiped out on a skateboard going 30 – 40 mph trying to break a speed record, hospitalized with a concussion When I was 16 I broke my jaw in baseball taking a line drive hit from the pitching mound back to my right jaw, hospitalized with a concussion and broken jaw in two places.

Brain Injuries When I was 4 years old I fell directly on the basement floor on my head from a monkey bar. Only fell a few feet guess I was warming up. At 5, I went head first into a glass front door, hospitalized with several stitches in back of my neck. At 7 years old on my bike I ran into a car, went to doctor with bleeding tong and was told to eat nothing but jello and broth for 2 weeks. At 9 years old, I had a PTSD incident At 14 years old I had debilitating migraines and doctors could not find anything. When I was 48, I was in a car accident (totaled car) with whiplash

Played HS and College Football

I have had memory problems, processing problems, comprehension issues, migraines and headaches my whole life. I

I have been diagnosed with Neuropathy, Neuro Fatigue, Digentitive Disk Disease, Depression, insomnia, Tinnitus, Sleep Apnea, Bi Polar, Chronic pain and fatigue, Roasa, IBS, RA, Migraines, Digenitive Disk Disease, Hiatal Hernia, GERD, acid reflux, tarsal tunnel syndrome, social isolation, and entering Parkinson’s with stiff muscels and joints, internal shaking,

At 55 I am jobless, broke and trying to survive. In 2015 I started eating clean, meditating, affirmations, exercise (lost 80 lbs.) but nothing working so far.

ACTION PLAN: Eat a plant exclusive lifestyle Read High Performance Habits (this does help but I have lost steam which I know you understand) Sell stuff to pay rent Start Walking in am Check out app Brain HQ Get approved for disability Create Web Page

Love you all thoughts and prayers

Laurie replied on Sat, 12/29/2018 - 9:17am Permalink

As I was reading your post... I could so relate!! I am 53 and after this last concussion I started to realize just how many concussions I have had diagnosed and undiagnosed. I also have identified with several of your diagnosis! Thank yoh for sharing... and I appreciate your positive perspective on “internally not giving up”. Blessings back at ya!!

Jennifer Kerber replied on Wed, 08/29/2018 - 3:56am Permalink

I'm 4.5 years post my brain injury: swelling of the brain, seizures, global damage affecting all areas of my life. The official term is encephalopathy, I think.

I've been doing well, using helping tools but in the last six months, my family and I have noticed a dramatic decrease in long-term and especially short-term/current memory abilities. Have any studies/research determined that brain damage can worsen with age? With anything else?

I was tested for seizures and dementia and both came back negative but I forget what I did this morning, yesterday, going to my daughter's graduation and Disneyland in late June. I have absolutely no memory of being there.

Up to about 4 years post-coma, I had both long and short-term memory problems but not nearly as bad as now.

I appreciate ANY help!

Thank you in advance, Jennifer Kerber

Katleho Makhubela replied on Wed, 06/27/2018 - 3:54am Permalink

Hi everyone,

I wanted to ask what I can do, where I can go, or who to talk to.

I suffered an accident when I was a child with my mother in the same car. All I can remember was we were driving home and the next thing the windows shattered. My mom called someone to tow the car and we didn't go to the hospital. I had bumped my head and thought little of it, my injury healed. Ever since then, I've had problems, -- making friends, keeping a girlfriend, interacting with my family, focusing on one task. I've had it rough. By Gods grace, I'm still alive. In 2014, I was involved in another accident, a car almost hit me at some club. I just remember jumping over the car, barely surviving.

Where can I go for help?

Cathy replied on Tue, 12/31/2019 - 10:16am Permalink

I'm traveling the post concussion syndrome road with continued cognitive issues that at first were being completely attributed to visual processing problems until I saw a neuro optemetrist. Based on how conversations and interactions are also fatiguing she thought I should also see a speech therapist maybe...a guess on her part which was a decent one. The speech therapist identified mild cognitive impairment and is now suggesting I see a concussion specialist. I have seen a neurologist in the past who prescribed some medication, but he is lacking in follow up care. I sense concussion specialists, speech/language therapists, and it looks like maybe neuropsychologists(?) are good routes to go. That's the key is finding the people with the right knowledge and skill set. Day by day, one foot in front of the other, we move forward.

Billie Sackett replied on Mon, 03/19/2018 - 3:51pm Permalink

I have bicycle accident last September during our steam engines days in my hometown all I remember is riding the bike and the next thing I knew I was heading in the ambulance to the hospital. Now I can't remembering anything I do during the day or who I talk to my short term memory is gone and seems nobody understands please help with information or books I can read to help me understand or any resource in southeast mn close to Rochester mn as groups or resources and people to talk to and living enviroments Im raising my nine year old daughter that witnessed the accident .

Laura replied on Thu, 03/21/2019 - 1:53pm Permalink

Here’s a continuation on my earlier comment on resources. You had ask for book recommendations. Here are a few:“Brain Survival Kit: 365 Tips, Tools & Tricks to Deal with Cognitive Function Loss” by Cheryle Sullivan, MD

“The Traumatized Brain: A Family Guide to Understanding Mood, Memory and Behavior after Brain Injury” (a Johns Hopkins Press Health Book)

“To Root and to Rise: Accepting Brain Injury” by Carol J Starr

“101 Tips for Recovering from Traumatic Brain Injury: Practical Advice for TBI Survivors, Caregivers and Teachers” by Kelly Bouldin Darmofal (she also has a memoir)

All on Amazon.

Laura replied on Thu, 03/21/2019 - 1:48pm Permalink

Billie, I too experienced a TBI, and other life threatening injuries in a car accident in September 2016 (ironically a year before you). I was in a coma for 3 weeks. In the hospital for 4 months. It’s been a long road. I can’t live independently anymore, my hearing is incredibly compromised, etc. However, I’m writing to you to give you resources, hopefully. I’m in MN as well. We have the MN Brain Injury Alliance (located in Roseville, MN but they have many online resources), this page has some good resources: http://www.braininjurymn.org/consumerguide/index.php

You mentioned you’re close to Rochester,MN. Therefore, Mayo. Check out them if you haven’t, especially: https://www.mayo.edu/research/centers-programs/traumatic-brain-injury-mo...

Also, check out this website. It lists TBI resources within a 100 miles of Rochester. 2 are Mayo-related so they’re close. The rest are probably too far. https://www.brainline.org/resource-directory/state/MN

I hope you find this helpful and not overbearing (that’s not my intent).

Jessica replied on Sun, 12/31/2017 - 12:48am Permalink

I took a swan dive and landed on concrete to get my TBI. I didn't even realize how bad my mind was until a few years ago (about 10 years after the accident, when the seizures became noticeable). People just assumed I was a kid with a poor attention span who didn't react well to others. After very extensive research, I know now how complicated things really are. As much as I wish I could go back to being ignorant and thinking I'm just vapid, it's nice to know there is some kind of explanation for my memory, emotional, and other cognitive problems. And I'm both happy I'm not alone in this, and sad that others are suffering as well (likely worse than I am).

Anonymous replied on Wed, 06/14/2017 - 7:45am Permalink

Anonymous replied on Sun, 06/04/2017 - 8:41am Permalink

Anonymous replied on Wed, 05/24/2017 - 5:58pm Permalink

Anonymous replied on Tue, 04/11/2017 - 11:07pm Permalink

Anonymous replied on Sun, 03/05/2017 - 9:39pm Permalink

Isabel replied on Sun, 05/05/2019 - 10:33pm Permalink

Wow, What an attitude....great stuff... you sure are an inspiration and someone to learn from. God speed.

Jennifer Wilkinson replied on Mon, 04/16/2018 - 12:03am Permalink

Thank you for sharing your thoughts. You have helped me to identify some of the issues I have been feeling but unable to sort out.

I wish you well. J

Anonymous replied on Thu, 12/14/2017 - 8:44am Permalink

I have been reading through all of the comments and yours has really inspired me. I am a licensed electrician and a class A CDL driver. I received my head injury when a case of liquids fell out of the back of my truck hitting me on the head. It has really changed my life to where I just gave up. I did not think things were going to get better but I have a little hope now. Like you I really don't believe anyone will hire me even if I get better but I need to concentrate on getting better then start that battle. I also walk with a cane now and my PT wants me to have a walker. It really sucks that I educated myself and climbed the chain to get where I was just to get knocked back down to learn it all over again but I am willing to tackle it now so I can get back on my feet to continue on with life. Thank You.

Meredith replied on Tue, 12/19/2017 - 1:03pm Permalink

Thanks for sharing all that! I just wanted to recommend a resource for you. It’s the Department of Rehab in your state! They can really help you get back to work after a TBI. Good luck!

Anonymous replied on Thu, 03/02/2017 - 11:00pm Permalink

Anonymous replied on Wed, 01/04/2017 - 12:11am Permalink

You all can write. I am just getting to know someone who cannot read or write . He remembers things almost photographically. He has a very limited vocab. People assume he is on drugs. He is highly intelligent but unable to express properly. He had a traumatic brain injury in a lacrosse game, was resuscitated 3 times, and woke from a coma 2 months later, at 13, and even now at 40 cannot formulate sentences, etc. He has a very high IQ, but is unable to use it.

bohdih replied on Sat, 01/20/2018 - 1:08am Permalink

I had a jerk response to your description of your new friend, he can, I believe -use his hi IQ, or you wouldn't be aware of it.. ugh, I don't know how to explain but you are a good student, he is teaching you many great lessons about life. keep sharing, be his voice ...

Anonymous replied on Tue, 12/27/2016 - 6:58pm Permalink

My son has most of the same symptoms from a motorcycle accident. I can say for certain that your girlfriend needs a reality check and needs to thank the Lord that you are here and can have any relationship with your son. Your brain has had massive injuries that are probably still healing and you need love and support. If you would like to speak with me or my son for support, you can email me your contact info. Tdrawdy aol.com

Anonymous replied on Thu, 12/22/2016 - 4:33pm Permalink

2013, landed on left side of helmet after hitting side of car turning left in front of me. I was thrown from the motorcycle, doing 30, went maybe 12 feet up in air, landed in street. Had a daydream about floating down a silver river, all happy, beautiful...then a voice said if I kept going, I wouldn't be able to come back. Opened my eyes, and the girl that wrecked me was looking down at me. I didn't try to get up, wasn't sure how bad I was hurt. Called my girlfriend on cell phone and told her I was in wreck. She showed up about the same time as ambulance, wasn't far from home. I thought I was fine, but I couldn't understand why the girl turned left in front of me like that...kept asking why she did that over and over, many times. Got a CT scan and X-rays a the ER. Doctor said I was fine, and told me to take the day off of work. I was working as an RN in an ICU, had been an RN for 20 years. Went home, and don't really remember much for a week..maybe more? Girlfriend said I seemed ok at first, slept for almost 3 days, only getting up to use bathroom. It is mostly just darkness to me, that time, There are bits and pieces, but I rely on my girlfriend to tell me how I was acting. She knew something was wrong with me when I started hallucinating, hearing and seeing things that weren't there, saying strange things...she was afraid to call an ambulance because she thought I would fight them and get hurt worse. Finally, after a few days, she talked me into going to see my doctor. I was sent to a neurologist, optometrist, (left pupil anisocorea), neuropsychologist, endocrinologist, occupational therapy, speech therapy, foot doctor, (had multiple fractures of left foot), knee doctor, shoulder doctor, (torn meniscus, rotator cuff injury), ophthalmology ended up doing surgery on my right eye for a displaced intraocular lense. Anyway, I had to have a lot of stuff done, and I still have frequent migraines, cognitive problems, and visual working memory deficit, (don't remember what I see). I was never allowed to go back to work, and lost my job, had to go on food stamps, long term disability insurance, ( a nightmare), finally was a approved for 100% SSDI, because my doctors didn't think I could work at ANY job that required working regular hours. So, now it is three and a half years later, and my court case with the pizza delivery driver is still pending. I nearly lost my home, I can't stand florescent lighting or looking at computer screens for very long. My balance is lousy, and I have to wear prism glasses because of a midline shift in my brain. I have to take multiple medications, and testosterone replacement, because my pituitary gland was damaged. I have had three surgeries, one on my eye, one on my knee, and one on my shoulder. People say I seem fine, but then after they spend some time with me, they start to notice that I am off a bit...can't remember directions, can't understand things, can't multitask, slow reactions. Sometimes I feel sorry for myself, and cry when no one is around, because my life is so far away from what I wanted it to be, and I feel helpless. I try not to be sad though, because there are a lot of people in the world that are far worse off than I am, and I have people around me that still love me, even though I am not quite who I was. I hope to sell my house and move to the country someday, perhaps learn to make furniture in a little shop, or try to learn blacksmithing. I like to make things, but I tire easily, and sometimes cannot function because of the pain in my head, and ringing in my ears. If I could do something at my own pace, maybe sell some things, if they turn out nice, that could keep me busy. My main goals are to never give up hope, keep trying, doing the best I can to improve myself, not dwell upon what might have been, play the cards I've been dealt, to love, and to be loved.

Jackie replied on Thu, 08/08/2019 - 8:29am Permalink

You sound loved , stay kind to those that love you . We are all dealt a hand in life and those that make it learn to live with what ever life throughs at us . You can do it .

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• Dement Neuropsychol
• v.14(2); Apr-Jun 2020

Language: English | Portuguese

Daily functioning and dementia

Atividades da vida diária e demência, gabriele cipriani.

1 MD,Versilia Hospital, Neurology Unit, Lido di Camaiore (Lu), Italy.

2 MD, Versilia Hospital, Psychiatry Unit, Lido di Camaiore (Lu), Italy.

Sabrina Danti

3 PhD, Clinical and Health Psychology Unit, Hospital of Pontedera, Pontedera (PI), Italy.

Lucia Picchi

4 PsyD, Clinical Psychology Unit, Hospital of Leghorn, Leghorn (LI), Italy.

Angelo Nuti

Mario di fiorino.

Author contributions. Gabriele Cipriani, Angelo Nuti, Mario Di Fiorino: conceptualization; Sabrina Danti: conceptualization, investigation. Lucia Picchi: conceptualization, supervision.

Dementia is characterized by a decline in memory, language, problem-solving and in other cognitive domains that affect a person’s ability to perform everyday activities and social functioning. It is consistently agreed that cognitive impairment is an important risk factor for developing functional disabilities in patients with dementia. Functional status can be conceptualized as the ability to perform self-care, self- maintenance and physical activity. A person with dementia usually requires help with more complex tasks, such as managing bills and finances, or simply maintaining a household. Good functional performance is fundamental for elderly people to maintain independency and avoid institutionalization. The purpose of this review is to describe functional changes in demented patients, evaluating the variability in subgroups of dementias.

Demência é caracterizada por declínio na memória, linguagem, resolução de problemas e de outros domínios cognitivos que afetam a capacidade de realização de atividades cotidianas e atividades sociais. É consensual que o comprometimento cognitivo é um importante fator de risco para o desenvolvimento de incapacidades funcionais em pacientes com demência. O status funcional pode ser conceituado como a capacidade de realizar autocuidado, automanutenção e atividade física. Uma pessoa com demência geralmente requer ajuda para tarefas mais complexas, como gerenciar contas e finanças, ou simplesmente realizar atividades domésticas. Um bom desempenho funcional é fundamental para que os idosos mantenham a independência e evitem a institucionalização. O objetivo desta revisão é delinear alterações funcionais em pacientes com demência, valorizando os subgrupos variados de demências.

Dementia constitutes a multifactorial process 1 that is always associated with cognitive decline and impaired functioning. As the disease progresses, people living with dementia experience, in addition to impaired cognitive functions, gradual dysfunction and loss of individual autonomies. Besides decline in memory and/or other cognitive domains, the criteria for diagnosis of dementia require loss of functional reserve and pejoration in functional status. 2 An important quality of life component from elderly people’s perspective is functional indepen dence. When older people show functional loss, they experience a variety of negative outcomes, such as higher rates of use of hospital services, institutionalization, and increased risk of death. 3 The progression of healthy aging to dementia must be considered a continuum, both in terms of the slow manifestation of the impairment of cognitive functions, as well as functional limitation. 4 Originally, mild cognitive impairment (MCI) was considered a condition in which someone has minor cognitive decline, not severe enough to interfere significantly with daily life and function. As a result, some authors proposed introducing minor functional disability among the criteria for diagnosing MCI. 5 However, many years can separate the onset of disease, perceived only through mild impairments in everyday living, the evolution from the date of clinical diagnosis and the earliest functional deficits as patients advance to mild dementia, are often difficult to characterize. 6 Furthermore, there are age and gender differences in functional limitations. Subjects with a low level of formal education can show early deficits in cognitive performances, as well as functional abilities. 7 Data regarding differences in functional limitations by dementia subtype are limited and conflicting. The aim of this literature review is to describe functional disabilities in dementia and to understand the individual variability of limitations in the heterogeneity of the disease.

A literature review (Cochrane Library and PubMed databases) was carried out (only upper time limit: 2019) on daily functioning and dementia. We retrieved: 207 articles by using the search terms “activities of daily living” and “dementia”; 47 articles using the terms “instrumental activities of daily living” and “dementia”; 18 articles using the terms “daily functioning” and “dementia”; and 21 articles using the terms “functional abilities” and “dementia”. Publications found through this indexed search were reviewed and manually screened to identify relevant studies. We manually added relevant articles identified through other sources (i.e. Google Scholar and key journals). At the end of the process, 81 articles and chapters of books were included in our qualitative evidence synthesis.

FUNCTIONAL ASSESSMENT: ACTIVITIES OF DAILY LIVING AND INSTRUMENTAL ACTIVITIES OF DAILY LIVING

Useful screening techniques or instruments can provide valuable clinical and psychosocial information and can expedite the efficient assessment of patients once they are routinely utilized. Therefore, the assessment of functional disability and its severity must be carried out through measurement scales both in the general population and in dementia. 8 , 9 The instruments for assessing functional ability are divided into two levels, from the more basic (Activities of Daily Living - ADLs) to the more advanced activities necessary for self-care (Instrumental Activities of Daily Living IADLs). The activities that fall into the category of ADLs, involve all tasks that are needed to be performed in order for the patient to survive comfortably: mobility, toilet and bathing/continence, personal hygiene, dressing, and feeding; IADLs, on the other hand, are more complex than ADLs. They include transportation, shopping, preparing meals, managing households, managing finances, using communication devices, and managing medication. Performance of basic and instrumental activities of daily living depends upon the integrity of different cognitive (e.g., reasoning, planning), motor (e.g., balance, dexterity), and perceptual (including sensory) functions. Nevertheless, at present there is no “gold standard” available for ADL and IADL assessment in dementia, despite the fact that functional decline is an essential part of the diagnostic criteria for dementia. 10 , 11 In clinical practice, information about everyday activities is typically ascertained by asking a patient or his/her caregiver to report everyday functioning. It has been suggested that family caregivers who are depressed and feel burdened may be inaccurate and underestimate the patient’s actual functional capacity. 12 According to Loewenstein et al., 12 caregivers significantly overestimate the ability of impaired dementia patients to tell time, identify currency, make change for a purchase, and utilize eating utensils. The selection of a functional assessment instrument typically depends upon the severity of the dementia population being evaluated. Many assessment tools are available to help the clinician detect and monitor improvement in IADLs and ADLs in the elderly. The Katz ADL Index 13 was first developed in an effort to find a way to assess function and how it changes over time in the elderly. It is an ordinal index designed to assess physical functioning using a dichotomous rating (dependent/independent) of six ADLs in hierarchical order of decreasing difficulty as follows: bathing, dressing, toileting, transferring, continence, and feeding, rated on a scale of independence. An appropriate instrument for assessing independent living skills was developed by Lawton and Brody in 1969 to assess the more complex ADLs necessary for living in the community: eight domains of function for women (ability to telephone, shopping, food preparation, housekeeping, laundry, mode of transportation, responsibility for own medication, ability to handle finances), but only five for men (food preparation, housekeeping, and laundry were excluded). 14 The administration time of the Lawton IADL is 10-15 minutes and it is easy to administer. The patient or a knowledgeable family member or caregiver may provide answers. The higher the score, the greater the person’s abilities. A summary score ranges from 0 (low function, dependent) to 8 (high function, independent) for women, and 0 through 5 for men. As the items of the Lawton IADL scale conform to a formal hierarchy, the most “difficult” items such as “shopping” and “food preparation” can act as sensitive indicators of impending disability in the other activities. 15 Fields et al. 16 found that when using a caregiver-report measure, problems in bathing and grooming appeared first, whereas eating was the last to be affected. Elderly aged 80 or older are more than twice as likely to have limitations than those aged 65 to 74. The impairment of individual activities develops sequentially (i.e., housework, transportation, shopping, meal preparation, finances). 17 IADL impairment is reported to develop earlier in dementia and has a higher prevalence, and stronger correlations with cognition than ADL, 18 whereas basic ADL declines are often not present until later dementia stages. 19 One study demonstrated that diminishing IADLs predicted a clinical diagnosis of dementia 10 years beforehand and suggested it as an early screening tool. 10 Among all ADLs, bathing impairment may be associated with the highest risk of future institutionalization. 20

RELATIONSHIP BETWEEN FUNCTIONAL IMPAIRMENT AND COGNITIVE DECLINE

Cognition is a term referring to the mental processes involved in gaining knowledge and comprehension. These processes include thinking, knowing, remembering, judging and problem-solving. These cognitive domains are closely associated with the ability to perform everyday functions. 21 Longitudinal studies of persons at risk for dementia have demonstrated the initial clinical presentation of the disease is one in which there are cognitive deficits measurable with performance-based tests, but with no evident deficit in activities of daily living. According to anecdotal reports, many of those with poor performances on mental status examinations may exhibit an essentially normal life. For this reason, it is essential to establish the degree of correlation between performance on a cognitive test and ability to function in daily life. While functional assessment typically addresses specific content areas, neuropsychological assessment normally focuses on patterns of relatively impaired and preserved generic, cognitive, perceptual, and motor abilities, such as language, memory, spatial ability, problem-solving ability, and perceptual-motor skills. The relationship between these two domains is complex, since a particular functional content area usually involves a number of the specific skills typically evaluated by neuropsychological tests. Neuropsychological assessment can be a reasonably good predictor of those activities of daily living that place relatively heavy demands on reasoning, memory, and related intellectual abilities. Executive function 22 and memory have been shown to have specific relationships to functional limitations. Individuals with marked executive dysfunction are likely to have significant difficulty carrying out such complex tasks as managing a complicated medication regimen, preparing a meal involving multiple ingredients and steps, or balancing a check-book. 23 Barberger-Gateau et al. 9 performed a study identifying which IADL items are more specifically related to cognitive impairment as assessed by the MMSE, in a representative sample of French elderly community dwellers. The authors affirmed that, when age, sex, educational level, and all Lawton’s scale items are simultaneously taken into account, only items A (telephone), G (medication) and H (budget), plus F (transportation) for women, are significant. More recently, Brown et al. 24 investigated whether the MMSE was associated with functional performance as measured by the Functional Independence Measure (FIM) 25 (the FIM is an 18-item, clinician-reported scale that assesses function in six areas including self-care, continence, mobility, transfers, communication, and cognition). The MMSE scores derived for inpatients with suspected dementia were significantly associated with the inpatients’ total FIM and cognition subscale scores. The Short Portable Mental Status Questionnaire (SPMSQ), 26 a mental status test that emphasizes memory, orientation, and calculation, was deemed an inadequate predictor of self-care capacity in nursing home patients. 27 A strong association was found between the MMSE and the Disability Assessment for Dementia (DAD), 28 in particular DAD total score. 29 There was an association between functional status and visuospatial performances among AD samples. 30 A significant and specific relationship was found between measures of visual object form discrimination and the adequacy of performance of IADLs that require visual processing; no similar relations emerged between other visual perceptual abilities and IADLs. 31 Damage to the frontal lobe, the prefrontal cortex in particular, was associated with problems in successful completion of goal-directed behaviour and with a variety of neuropsychiatric syndromes: Instrumental Activities of Daily Living (IADLs) such as using transportation, managing financial matters, and organizing a household require the planning strategy and adjustment capacities of the dorsolateral prefrontal cortex. 32 Executive dysfunction serves as a predictor of IADL impairment both in dementia and, in general, in geriatric patients. 33 Abilities that fall under executive function include goal planning, initiating and executing actions, multitasking, switching between tasks, monitoring, and inhibiting habitual behaviours when presented with unexpected events. 34 Mariani et al. affirmed that performance of tasks such as shopping and medication management, is mainly related to more severe cognitive dysfunction and lower executive abilities, supporting the connection between executive function, global cognition, and IADLs. 35 Mayo et al. 36 hypothesized that there is a relationship between judgment/problem solving and functional status: findings showed that cognition moderated a strong relationship between functional status and judgment/problem solving among individuals with dementia, with lower reported functional performance predicting poorer judgment/problem solving.

RELATIONSHIPS BETWEEN FUNCTIONAL DECLINE AND BEHAVIOURAL DISTURBANCE

Performance on cognitive testing predicts only a modest proportion of the variance in functional abilities in persons with cognitive impairment, indicating that other variables also predict function. Behavioural disturbances, such as apathy, 37 depression, 38 and delusions, 39 are frequent bothersome characteristics of people living with dementia that increase with disease severity. Additional problem behaviours among late-stage dementia patients include wandering, 40 disruptive vocalizations, 41 and inappropriate sexual behaviours. 42 An understanding of which neuropsychiatric symptoms are most strongly associated with functional disability may encourage health care providers and loved ones to vigilantly monitor for their presence and aggressively treat these symptoms to reduce their potentially modifiable effects on function. One study strongly indicated the close relationship between behavioural and functional impairment, especially for IADLs that deteriorate in the early stages of the disease and are hierarchically more complex than ADLs. 43 Given the consistent associations between behavioural disturbances and functional disability, researchers have attempted to determine their relative strengths in predicting everyday functioning in persons with cognitive impairment. 44 The development and severity of behavioural disorders are not always correlated with poor cognitive symptoms and functional disability; changes in behaviour may be determined by other factors, such as the variety of clinical signs and symptoms of dementia, personality traits of patients, the social support required and available, and the capacity to manage stress of caregiver. 45 Associations have been reported between behavioural disturbance and ADLs, such as toileting and hygiene, 46 and IADLs, such as managing medications and finances. 44 Different types of neuro-behavioural changes have been associated with functional disability. 47 Some features of apathy and depression overlap. In persons with cognitive impairment, apathy may be more common than depression, which is characterized by guilt, sad mood, hopelessness and poor self-concept. Apathy is characterized by loss of interest, social withdrawal, and generally decreased motivation, initiation, and persistence in the absence of low mood or depressive thought patterns. Apathy has been associated with impairments in planning, initiating and executing IADLs, 43 while depression was only associated with impaired initiation and planning. Depression has been shown to be a strong predictor of functional difficulty. 48 Depression reduction was associated with benefits to non-mood outcomes of importance to patients who had dementia and their caregivers. 49 The most striking benefit involved ADLs, with stabilization, and perhaps some reversal of ADL decline. Anxiety and aberrant motor disturbance may also be an important risk factor for functional disability. 50

ALZHEIMER’S DISEASE

Alzheimer’s disease (AD) is an age-related progressive neurodegenerative disorder representing the most common form of dementia, that ultimately leads to death due to complications of the disease or to age-related mortality. Its prevalence increases exponentially between the age of 65 and 85 years. 51 The diagnosis of AD requires that patients display both cognitive and functional deterioration. There is robust evidence and consensus that the onset of the symptoms of AD is so insidious that neither family nor patient can pinpoint the exact date of onset. It is now clear that there is continuum from psychosomatic individuals, to those with MCI, to patients with dementia, and that the pathological hallmarks of the disease are present years before cognitive symptoms are recognized. 52 , 53 Functional impairment is a core symptom of AD, significantly impacting the quality of life of persons with AD as well as of their family members and caregivers. 29 Data support the concept that decline in cognition is later reflected in functional deficits. 54 Researchers have studied the temporal relationship of cognitive deficit and functional impairment in AD. The correlation observed supports the hypothesis that, as disease progresses, cognition becomes more clearly related to function and the two measures become more strongly associated. IADLs, specifically finance and medications or outings, are the first to decline with memory deterioration and evolving of behavioural changes; decline in ADLs follows when, gradually, dementia progresses and becomes severe and executive dysfunction becomes evident. 55

Furthermore, IADLs requiring higher neuropsychological functioning seem to be more severely affected than ADLs. 56 Observations suggest that the influence of poor cognitive function on impairments in everyday activities becomes more significant as the disease progresses from MCI to the early symptoms of dementia, and then to the severe form of AD, with the magnitude of correlations depending on the complexity of the functional task. 57 , 58

FRONTOTEMPORAL DEMENTIA

Frontotemporal dementia (FTD) was first described by Arnold Pick (1851-1924), a Czech psychiatrist, neurologist and neuropathologist, in 1892. It covers a wide range of different conditions, representing a group of neurodegenerative dementias affecting the frontal and/or temporal lobes relatively selectively, even in later stages of the disease. It is most often diagnosed between the ages of 45 and 65. Therefore, FTD has a substantially greater impact on work, family, and economic burden faced by families than AD. There are three subtypes of FTD: the behavioural-variant FTD (bvFTD), the most common presentation of the three variants, characterized by behaviour changes, emotional blunting, loss of empathy, and personality decline, progressive non-fluent aphasia (PNFA) characterized by agrammatism, effortful speech, alexia, and agraphia, semantic dementia (SD) with loss of semantic knowledge and inability to match certain words with their images or meanings. 59 FTD impinges markedly on everyday function, but studies evaluating functional status in the course of FTD are sparse. Functional difficulties depend on the clinical subtype of dementia and its severity. These differences are recognizable even after controlling for age, education, and disease duration. 60 The bvFTD patients proved the most impaired group and this deficit was particularly evident in ADLs. The PNFA group, despite being the least impaired overall, had subtle, but definite, problems beyond language-based IADLs. Similarly, the SD group was not only affected in language-based activities, but impairment extended to IADLs, such as “leisure and house chores,” “going on an outing,” and “meal preparation.” It should be highlighted that bvFTD may sometimes have a catastrophic effect on ADLs, which may not be reflected in cognitive test scores. 61 Patients with SD remain relatively independent in everyday tasks for a much longer period of time, in line with a much more protracted disease progression. 62 With worsening of the disease, functional outcomes become similar in all FTD variants. 63 Stereotypical behaviour and ADL decline are associated with disability in patients with bvFTD. 63 However, little is known about the rate of deterioration of functional activities in FTD patients over a 12-month period and if the decline is associated with changes on general tests of cognitive function. 62 The rate of deterioration for bvFTD and PNFA patients are more marked than those reported in studies of AD patients, whereas SD patients decline at a similar rate to AD. 64 , 65 Some authors have investigated the relationship between emotion and social skills assessed by ADL scales. 66 In fact, decision-making may be affected by the inability to use emotional cues to bias behaviour in social situations. The researchers demonstrated that the ability to perform ADLs is independent of impaired emotion in FTD.

DEMENTIA WITH LEWY BODIES

Dementia with Lewy bodies (DLB) is a progressive, degenerative dementia of unknown aetiology and complex clinical picture. Fluctuating cognitive function is a relatively specific feature of a person with DLB; other clinical features are recurrent visual hallucinations, behavioural problems, extrapyramidal symptoms (typically including rigidity, bradykinesia, and gait instability), and changes in autonomic body functions, such as blood pressure control, temperature regulation, and bladder and bowel function. 67 It is characterized by cellular inclusions called Lewy bodies in the cytoplasm of cortical neurons, the limbic system and brainstem structures. Lewy bodies are abnormal, eosinophilic spherical structures, resulting in neuronal cytoplasmic inclusions composed of aggregates of alpha-synuclein, a synaptic protein. Little is known about how much individual cognitive, behavioural and motor problems influence functional performance in patients suffering from DLB. In the elderly with motor disorders, functional impairment is particularly significant, especially for continence and walking 68 (up to 75% of DLB patients are reported to have extrapyramidal motor symptoms during the illness). Differences in functional changes between people with DLB and AD tend to manifest in the early stages of the diseases, whereas these difference tend to disappear in advanced stages. According to Stavitsky et al., 69 at first evaluation, patients with DLB were significantly more impaired on measures of ADL and showed greater dependence on caregivers, but functional changes over time were similar in the two groups. Similarly, another study found no differences in the frequency of development of severe functional impairment between patients with AD and those with DLB. 70 In DLB, motor disability best predicts IADL ratings, with severity of cognitive impairment adding predictive value. 71 An explanation is that motor disability in DLB serves as a proxy for the general integrity of the basal ganglia, and cognitive impairment associated with basal ganglia dysfunction (e.g., executive dysfunction) contributes to the IADL deficits in DLB.

PARKINSON’S DISEASE DEMENTIA

Parkinson’s disease (PD) is a long-term, progressive, degenerative nervous system disorder that affects a wide range of functions. It is generally accepted that the main pathological feature of this condition is damaged dopaminergic nigrostriatal pathways with decreased concentration of dopamine in the compact zone of the substantia nigra. Resting tremor is the most common clinical feature. Bradykinesia, rigidity and postural instability are often detectable. It is now recognized that PD is much more than a motor disorder. In the course of the illness, autonomic symptoms, anxiety, mood disorder and cognitive changes are often observed. 71 PD patients may have deficits in multiple cognitive areas from the initial stages of the disease progressing ranging from subtle symptoms (mild cognitive impairment in PD - PD-MCI) to clear cognitive alterations (PD dementia - PDD). PDD has been increasingly better recognized, probably because persons with PD survive for longer than before owing to modern treatment. Different cognitive profiles may exist within PD, but cognitive deficits associated with PD mainly involve executive functions, memory, attention and visuo-spatial functions, but other cognitive functions may also be impaired, often as a secondary consequence of the primary executive disorder. 72 The aetiology of dementia in PD has not yet been fully established. The rate of early disability in PD patients is associated with declining cognitive function. 73 We know that dysfunction in everyday activities occurs early in the course of the disease and its detection is important for patients to fully understand their substantial difficulties in daily life. For example, people with PD show compromise in housekeeping, managing money, and preparing meals. 74 While it has been well documented that the extrapyramidal syndrome is associated with impairment in basic ADLs, 75 , 76 Rasovska and Rektorova also observed highly significant correlations between IADL and functional disability. 77 Axial non-dopaminergic symptoms (such as postural instability and gait difficulty) influence IADLs; this is more evident in PDD patients than in persons suffering from PD without dementia. 77 However, a recent study demonstrated that cognitive deficits contribute to a greater functional decline in ADL performance. 78 More specific to PD than AD is impairment of executive functions as the hallmark feature of cognitive dysfunction. 79 Patients with PD showing executive impairment scored lower on instrumental self-maintenance, the use of new devices, and life management compared to those not presenting executive function impairments. 73 Financial capacity represents a cognitive set of knowledge and skills that has a special characteristic as an IADL. It correlates poorly with motor function and is usually clearly compromised in persons with PDD. 80 Disability in IADLs is particularly correlated with PD duration. 79

PROGRESSIVE SUPRANUCLEAR PALSY

Steele, Richardson and Olszewski first described progressive supranuclear palsy (PSP). It is an uncommon degenerative neurological disorder representing the most common form of atypical parkinsonian syndrome. It is a debilitating disease. Symptoms usually emerge at50-60 years of age, with onset ranging from the early forties to late eighties. PSP symptoms include progressive, early-onset postural instability, frequent (unexplained) falls, impaired eye movement (vertical supranuclear gaze palsy), axial (involving neck or trunk) rigidity and speech/swallowing difficulties. Clinically, the presence or absence of functional impairment may dictate a diagnosis of dementia or MCI, respectively. 81 Affected individuals frequently experience personality changes and memory and executive attention deficits. 82 Mood and behavioural changes may occur. People with PSP may become irritable, depressed or apathetic; they may also become more impulsive in their decision-making. 83 Functional disability is high in patients with early-stage PSP. 84 Duff et al. 84 examined functional profiles of patients with early-stage PSP: 100% of the participants in their study underperformed on all scales, suggesting at least some functional disability.

HUNTINGTON’S DISEASE

Huntington’s disease (HD), sometimes called Huntington’s chorea, is an incurable, lethal, genetically inherited neurodegenerative disorder caused by an expansion of a repeating cytosine-adenine-guanine (CAG) triplet series in the huntingtin gene on the short arm of chromosome 4, resulting in impairment of multiple domains. The illness is characterized by motor, cognitive, and psychiatric symptoms, which begin insidiously and progress over many years, until the death of the individual. It is thought that the variability in disease severity and rate of progression among people with HD is linked to the genetic mutation causing the disease. Patients and their families note the progression of the disease in different ways, as symptoms are present at different times from person to person; however, it is difficult to divide physical and mental traits. 85 The cognitive deficits can precede the appearance of motor symptoms by as much as 20 years, although they most often emerge in the 10 years leading up to clinical diagnosis of the disease. Because the disease affects the frontal lobes of the brain, planning ability, judgment and decision-making are affected; memory appears especially affected, with problems occurring for both verbal and non-verbal memory; motor functions are disrupted, which interferes with speech and coordination. 85 Individuals with mildly deteriorating conditions may be able to carry on their ‘normal’ life for many years and continue to function well in their job and with hobbies and activities, but at some point they will become disabled and need help to carry out activities of daily living. The most common functional declines show relationships with behavioural changes, motor functioning, and cognitive deficits. In particular, the latter deficits are responsible for functional losses in managing finances, working performance and driving. 86 Certain changes in cognitive abilities are characteristic of HD and can significantly affect the lives of individuals with the disease. For example, cognitive changes may affect the ability of a person with HD to work, manage a household or properly care for him or herself regardless of motor impairment. 87 Furthermore, in the early stages of HD (duration 0 to 5 years), cognitive deterioration is considered an important factor that determines the loss of functional ability. 88 The role of emotional changes needs further elucidation. Regarding neuropsychological performance and depressive symptomatology, these are considered predictive factors of functional disability. 86 Behavioural problems associated with the disease are thought to contribute significantly to dysautonomia in daily functions: the significant loss of motivation, absence of initiative, and irascibility present in some Huntington’s chorea individuals may affect their ability to perform basic activities of daily living, even if cognitive and motor functioning remain intact. 87

VASCULAR DEMENTIA

Vascular dementia (VaD) is an umbrella term for a group of conditions that recognize vascular brain damage of ischemic, haemorrhagic, or hypoxic type as a common pathophysiological event. Its prevalence increases exponentially with age and its risk doubles every 5.3 years. Clinical 37 manifestation may be cortical or subcortical. Cortical manifestations include cognitive and behavioural symptoms, with or without sensory or motor deficits. Subcortical VaD patients have sensory and motor deficits, gait disorders, dysphagia, dysarthria, extrapyramidal signs, urinary incontinence, emotional lability, impairment of attention and executive function with slowing of information processing. Frequently, small infarcts remain clinically “silent”, producing no apparent symptoms, while larger infarcts are more likely to produce impairment. This is especially true for subcortical white matter ischemic events, which may not produce cognitive dysfunction until a particular threshold has been exceeded. 89 There is limited information on functional limitations in VaD. This fact may, in part, be due to the clinical heterogeneity in subgroups of patients. 34 Functional status among people with VaD is often conditioned by sensory and motor deficits, but other underlying factors such as perceptual and mood changes, apathy, and even urinary incontinence, have a negative impact on both ADLs and IADLs. In addition, the co-presence of other diseases such as diabetes, peripheral arteriopathies, and heart failure further reduces functional capacity in VaD patients. 55 Therefore, it is not easy to ascertain the main origin of disability in everyday functioning. Individuals with VaD have significant limitations in ADLs (eating, toileting, and transferring) and in IADLs (grocery shopping and cooking). 55 IADLs are typically affected at earlier stages with worsening of memory and the development of behavioural disturbances, followed by a progressive decline in ADLs as executive function becomes more affected at later stages of the dementia. 10 People suffering from VaD present functional impairment that differs from that presented by AD patients. However, in the scientific literature, there are data that contradict this assertion; in fact, some authors claim that the rate of progression of ADL deficits in VaD is slower than in AD, but that the impairment is qualitatively similar. 34 Researchers have observed worse performance in almost all variables of both ADLs and IADLs in patients with subcortical ischemic vascular disease compared to those with AD: the fully adjusted model indicated that patients with subcortical ischemic vascular disease had worse performance in toilet use among ADLs and in laundry and ability to handle finances among IADLs than patients with AD. 90 Associations between specific cognitive domains and functional disability have been studied and show that executive functions consistently predict everyday functioning in cognitively impaired older adults with VaD. This is especially true for IADL dysfunction in patients with VaD due to small vessel disease. 91 , 92 Given the consistency of reports indicating frequent and prominent executive dysfunction among patients with VaD allied to the increasing evidence of its functional significance, evaluations of executive abilities are recommended for VaD patients, particularly those with VaD due to small vessel disease. 34 Jefferson, et al. 93 highlight the impact of executive processes on functional performance, such as using means of transport or managing money. Tasks such as cooking, housekeeping and managing finances are the most vulnerable to cognitive decline. Disturbances in ADLs may be considered unidimensional, but their clinical repercussion might vary according to the hierarchy or importance of the function affected. Changes in executive functioning and memory over a one-year period were predictive of IADL and ADL changes. 93 Functional impairment is more severely impaired among those subjects with both cortical infarcts and white matter ischemia, but the differences were largely quantitative rather than qualitative. This finding was not observed for both basic and instrumental activities, as significant group differences were evident only on the more complex instrumental behaviours such as managing money and shopping. 89

CONCLUSIONS

Dementia goes beyond cognitive impairment, also encompassing functional disability. With disease worsening, physical, cognitive and clinical problems accumulate and the pattern of loss follows a distinct progression. The first areas requiring external support in functional status are the IADLs and, over time, there is a need for support in performing ADLs. Expected functional decline may be an even more important issue for families than cognitive decline. Cognitive impairment is a condition with a high impact on the aetiology of disability, independently of other clinical variables, while impairment in functions of daily living worsens with clinical stage of dementia. However, data indicate that disability is significantly affected by comorbidity. Behavioural symptoms also play a role in deteriorating function. Executive function is a high complexity cognitive domain which comprises several functions required for the efficient execution of a cognitive process, enabling active retrieval of the information stored in long-term memory. A correlation between dysexecutive syndrome and poor functional status has been observed. Furthermore, it is clear that executive functioning measures are able to predict functional outcome. Knowing the stages of functional decline in dementia can help clinicians to make decisions regarding patients, considering that dementia affects each patient differently. It is important to make the necessary lifestyle adaptations, while remaining flexible about meeting needs as they evolve. Clinicians should be able to assess functional performance, where this information is integral to understanding health and for the optimal provision of clinical care and implementation of individual measures of rehabilitation designed to improve executive function. 94

This study was conducted at the Versilia Hospital, Neurology Unit, Lido di Camaiore (Lu), Italy.

ORIGINAL RESEARCH article

Impaired reasoning and problem-solving in individuals with language impairment due to aphasia or language delay.

• 1 VA Northern California Health Care System, Martinez, CA, USA
• 2 Palo Alto University, Palo Alto, CA, USA
• 3 Center for Mind and Brain, University of California, Davis, Davis, CA, USA
• 4 National Research University Higher School of Economics, Moscow, Russian Federation

The precise nature of the relationship between language and thought is an intriguing and challenging area of inquiry for scientists across many disciplines. In the realm of neuropsychology, research has investigated the inter-dependence of language and thought by testing individuals with compromised language abilities and observing whether performance in other cognitive domains is diminished. One group of such individuals is patients with aphasia who have an impairment in speech and language arising from a brain injury, such as a stroke. Our previous research has shown that the degree of language impairment in these individuals is strongly associated with the degree of impairment on complex reasoning tasks, such as the Wisconsin Card Sorting Task (WCST) and Raven’s Matrices. In the current study, we present new data from a large group of individuals with aphasia that show a dissociation in performance between putatively non-verbal tasks on the Wechsler Adult Intelligence Scale (WAIS) that require differing degrees of reasoning (Picture Completion vs. Picture Arrangement tasks). We also present an update and replication of our previous findings with the WCST showing that individuals with the most profound core language deficits (i.e., impaired comprehension and disordered language output) are particularly impaired on problem-solving tasks. In the second part of the paper, we present findings from a neurologically intact individual known as “Chelsea” who was not exposed to language due to an unaddressed hearing loss that was present since birth. At the age of 32, she was fitted with hearing aids and exposed to spoken and signed language for the first time, but she was only able to acquire a limited language capacity. Chelsea was tested on a series of standardized neuropsychological measures, including reasoning and problem-solving tasks. She was able to perform well on a number of visuospatial tasks but was disproportionately impaired on tasks that required reasoning, such as Raven’s Matrices and the WAIS Picture Arrangement task. Together, these findings suggest that language supports complex reasoning, possibly due to the facilitative role of verbal working memory and inner speech in higher mental processes.

Introduction

To what extent is thought dependent on language? This question has been pondered by philosophers and scientists alike for millenia. When asked about the nature of thinking, Socrates stated: “The soul when thinking appears to me to be just talking" ( Jowett, 1892 , p. 252). Many individuals echo this same subjective experience of an internal dialog that often accompanies their thoughts ( Hurlburt, 1990 ; Hurlburt and Heavey, 2001 ; Carruthers, 2002 ), but how can we objectively study the relationship between language and thought? A number of efforts to address this question experimentally have made use of data from a range of sources, including animals, young children, healthy adults, and language-impaired individuals ( Watson, 1920 , 1924 ; Piaget, 1967 ; Kertesz and McCabe, 1975 ; Vygotsky, 1978 ; Hjelmquist, 1989 ; Hurlburt, 1990 ; Halford et al., 1998 ; Hermer-Vazquez et al., 1999 ; Kinsbourne, 2000 ; Varley and Siegal, 2000 ; Kuczaj and Hendry, 2003 ; Wheeler, 2004 ; Machery, 2005 ; Clark, 2006 ; Penn et al., 2008 ; Carpendale et al., 2009 ; for a review, see Perrone-Bertolotti et al., 2014 ). In the current paper, we focus on the role that language plays in reasoning and problem-solving in particular. First, we review prior work in this area from a range of sources and then describe our current research focused on studying the relationship between language and reasoning in individuals with varying degrees of language impairment.

Evidence from a number of animal studies clearly demonstrate remarkable reasoning and problem-solving abilities in non-human species ( Blaisdell et al., 2006 ; Taylor et al., 2009 ; Smirnova et al., 2015 ), but it is argued that such abilities have reached a higher level in humans ( Premack, 1983 , 2007 ; O’Brien and Opie, 2002 ; Penn et al., 2008 ). Since abstract, symbolic language reaches its apex in humans as well, it has been suggested that these abilities are causally related, that is, our language system facilitates logical reasoning in some way ( Sokolov, 1968/1972 ; Premack, 1983 ; Carruthers, 2002 ; O’Brien and Opie, 2002 ; Bermudez, 2003 ; Gentner, 2003 ; Kuczaj and Hendry, 2003 ; Goel and Dolan, 2004 ). Interestingly, it has been shown that chimpanzees who receive language-training have superior reasoning and problem-solving skills compared to language-naïve chimpanzees ( Premack, 1983 ), supporting the notion that representational language facilitates advanced reasoning.

Data from children also suggest that language plays an important role in thought and reasoning ( Behrend et al., 1989 ; Gentner and Loewenstein, 2002 ; Gentner, 2003 ; Loewenstein and Gentner, 2005 ; Lidstone et al., 2012 ). Vygotsky (1978 , 2012 ) argued that young children first use overt speech to work through problems in conjunction with elders, then learn to speak to themselves privately while working through problems on their own, and eventually internalize that overt speech into private, covert speech while problem-solving. Piaget also believed that children’s private speech supported thinking and was related to the development of reasoning ability ( Piaget, 1926 , 1967 ). Young children verbalize overtly when performing cognitively demanding tasks, but by 14–17 years of age, children report using an inner speech strategy ( Winsler and Naglieri, 2003 ). Experimental evidence for these ideas comes from studies showing that problem-solving performance in children is associated with the use of private speech: Fernyhough and Fradley (2005) showed that the use of self-regulating statements in children correlated with performance on the Tower of London puzzle task (see also Winsler et al., 2009 ). Similarly, it has been shown that children exhibit increased self-directed and private speech when performing a difficult task and that children who exhibit more self-directed speech are better able to solve problems ( Berk and Garvin, 1984 ; Berk, 1986 ; Behrend et al., 1989 ; Winsler et al., 1997 ). Finally, others such as Hermer-Vazquez et al. (1999) have shown that children’s ability to perform a problem-solving task involving spatial orientation is related to their level of language competence (but see Learmonth et al., 2008 ).

Other work has approached the study of the relationship between language and reasoning by assessing cognitive functioning in individuals with varying degrees of language impairment ( Kinsbourne, 2000 ; Varley and Siegal, 2000 ). A series of findings have shown that individuals with aphasia (an impairment in language due to brain injury) show deficits in reasoning and problem-solving (e.g., Weinstein and Teuber, 1957 ; Piercy, 1964 ; De Renzi et al., 1966 ; Archibald et al., 1967 ; Basso et al., 1973 ; Edwards et al., 1976 ; Borod et al., 1982 ; Larrabee, 1986 ; Hjelmquist, 1989 ; Hamsher, 1991 ; Baldo et al., 2005 , 2010 ; but see Kinsbourne and Warrington, 1963 ; Basso et al., 1973 ). Moreover, a large number of these studies have shown that the degree of aphasia severity is correlated with the level of cognitive impairment ( De Renzi et al., 1966 ; Archibald et al., 1967 ; Edwards et al., 1976 ; Borod et al., 1982 ; Larrabee, 1986 ; Vilkki, 1988 ; Baldo et al., 2005 , 2010 ; but see Basso et al., 1973 ; Helm-Estabrooks, 2002 ). In particular, individuals with severe comprehension deficits such as those with Wernicke’s aphasia appear to be especially impaired on problem-solving and reasoning tasks ( Kertesz and McCabe, 1975 ; Hjelmquist, 1989 ; Baldo et al., 2005 ), a finding not simply explained by a failure to understand task instructions.

In our work, we have examined the role of language in reasoning by comparing large groups of stroke patients with and without aphasia on standardized tests of non-verbal reasoning and problem-solving. Such tests require the ability to recognize/represent a problem, use available information to test possible solutions, and monitor the veracity of those solutions. By “non-verbal,” we refer to the fact that these tasks do not require a spoken response and have no/minimal language comprehension requirements. For example, Baldo et al. (2005) tested 41 right and left hemisphere stroke patients with a wide range of aphasia severity on the Wisconsin Card Sorting Test (WCST; Heaton et al., 1993 ) and showed that problem-solving performance was significantly related to the degree of patients’ language impairment. Interestingly, performance was most strongly related to patients’ comprehension scores in particular, suggesting that core language processes are most important for successful problem-solving. In an effort to establish discriminant validity (i.e., to show that the relationship between language scores and performance on the WCST was not simply a matter of overall cognitive impairment), we also showed that there was no relationship between patients’ language scores and performance on Block Design, a non-verbal test of visuospatial functioning that is minimally dependent on reasoning. This dissociation reinforces the idea that individuals with aphasia, particularly those with core language impairments, have difficulty on tasks involving reasoning that are not explained by a general cognitive impairment.

Similarly, we have shown that aphasic individuals also exhibit poor performance on another test of non-verbal reasoning, Raven’s Coloured Progressive Matrices ( Baldo et al., 2010 ). Importantly, there was a significant interaction in performance on this test such that individuals with aphasia were disproportionately impaired on Raven’s items that required relational reasoning relative to those items that only required visual-pattern completion (see Figure 1 for examples; Bunge et al., 2005 ; Crone et al., 2009 ). Again, the specificity of these findings bolster the conclusion that decrements in reasoning in particular are associated with language impairment following stroke, rather than such deficits being part of a more general cognitive impairment.

FIGURE 1. Examples of the types of problems on Raven’s Matrices: (A) visual-pattern completion and (B) relational reasoning. These are not actual items from the test due to copyright issues and to maintain test security.

In the current paper, we sought to extend our previous findings by testing the relationship between aphasia severity and reasoning using a series of putatively non-verbal tasks from a commonly administered instrument, the Wechsler Adult Intelligence Scale (WAIS; Experiment 1A). We also sought to replicate and extend our previous findings with the WCST in a larger and more homogeneous patient sample that included left hemisphere-injured patients only (Experiment 1B). Rather than focus solely on aphasia subtypes, which can be problematic due to the multi-dimensional nature of these syndromes ( Caramazza and McCloskey, 1988 ; Coltheart, 2004 ), we also assessed the relationship between reasoning performance and specific language sub-processes (e.g., auditory comprehension, repetition). In the second part of this paper, we describe findings from a unique individual whose language impairment derives not from aphasia but from the fact that she was not exposed to language until the age of 32 due to an unaddressed hearing loss (Experiment 2). Together, these data provide further insights into the close relationship between language and reasoning.

Experiment 1A: Reasoning Performance in Aphasic Individuals on the WAIS

In a further effort to understand the role of language in reasoning, we conducted an analysis of aphasic patients’ performance on the Picture Completion and Picture Arrangement subtests of the WAIS-R and WAIS-III ( Wechsler, 1981 , 1997 ). These standardized tasks were chosen for comparison because they both require visual perception and attention with no/minimal language or motor requirements, but differ with respect to the amount of reasoning required ( Ryan and Paolo, 2001 ; Tulsky et al., 2003 ). A previous study ( Varley, 1998 ) used the Picture Arrangement task as a measure of causal reasoning in aphasia and reported that one of the two aphasic individuals tested showed impaired performance; however, there was concern that visual impairments could have contributed to performance. Given these equivocal results, it was of interest to compare performance on the Picture Arrangement task to performance on the Picture Completion task, which also involves visual perception and attention but a smaller reasoning component. Also, we analyzed performance from a large sample of well-characterized left hemisphere patients with a range of language disturbance and no known visual disturbance. Our prediction was that aphasic individuals would be disproportionately impaired on the more reasoning-intensive Picture Arrangement task, relative to Picture Completion and that patients’ comprehension scores would be most strongly correlated with performance.

Participants

A retrospective analysis was performed on data from 60 individuals (17 female) in our database who met strict inclusion/exclusion criteria: history of a single left hemisphere stroke, at least 6 months post-stroke (to ensure that behaviors had stabilized), native English-speaking (by age 5), right-handed, 8 th grade education or higher, and no prior neurologic or severe psychiatric history. The determination of language impairment was made with the Western Aphasia Battery (WAB; Kertesz, 1982 , 2006 ), which also provides scores for language sub-processes (fluency, comprehension, naming, etc.) as well as an aphasia subtype diagnosis (i.e., Broca’s, Wernicke’s, conduction aphasia, etc.). Individuals that score above the cut-off for normal language on the WAB (93.7 out of 100 points possible) are considered non-aphasic according to the WAB manual and norms. Based on this cut-off, our sample included 37 individuals with aphasia and 23 non-aphasic individuals. The aphasic individuals included 17 individuals with anomic aphasia, nine with Broca’s aphasia, five with conduction aphasia, five with Wernicke’s aphasia, and one individual who was unclassifiable. Patients’ mean age ± SD was 61.7 ± 11.0 years for the aphasic individuals and 59.6 ± 10.9 years for non-aphasic individuals; mean education was 14.6 ± 2.3 years for the aphasic individuals and 15.8 ± 3.0 years for non-aphasic individuals; mean months post-stroke was 44.4 ± 46.9 months for aphasic individuals and 41.7 ± 48.3 months for non-aphasic individuals; and mean lesion volume was 136.1cc ± 71.6 for aphasic individuals and 31.5cc ± 29.0 for non-aphasic individuals. Finally, the aphasic group included eight women and the non-aphasic group included six women.

Materials and Procedures

Participants were administered the Picture Completion and Picture Arrangement subtests from the WAIS-R or WAIS-III. The Picture Completion task requires examinees to point to something missing in a series of drawings of increasing difficulty (e.g., a number missing from a keypad). The Picture Arrangement task requires examinees to rearrange a series of pictures so that they tell a story, like the tiles in a comic strip (e.g., a series of pictures showing different stages of people cooking a meal). While both tasks require visuo-spatial perception and attention, the Picture Arrangement task puts a greater burden on reasoning ability ( Varley, 1998 ; Tulsky et al., 2003 ). The tasks were administered and scored in the standard manner according to the WAIS manual. Because the data were collected over a period of years, some participants were administered the Picture Completion and Picture Arrangement subtests from the WAIS-R and others, the WAIS-III. In order to combine data from the WAIS-R and WAIS-III, scores were adjusted according to Gläscher et al. (2009) , which involved converting the WAIS-R raw scores to WAIS-III raw scores by adding the mean difference to each subtest (-0.4 for Picture Completion and -0.6 for Picture Arrangement). Last, we also analyzed data from the Benton Face Recognition Task ( Benton et al., 1983 ) for these 60 individuals. The Benton Face Recognition Task is a visuo-perceptual task in which examinees are asked to point to which of six faces on the bottom of the page is the same person as the face on top. Despite being called a face recognition task, it is simply a face-matching task involving non-famous faces with no delay.

An analysis of covariance (ANCOVA) was used to compare aphasic and non-aphasic individuals’ raw scores on the different tasks with age, years of education, months post-stroke, and lesion volume included as covariates. Partial correlation coefficients (two-tailed) were computed to relate reasoning performance to WAB subtest scores for speech fluency, object naming, repetition, and auditory comprehension, with the same nuisance factors as control variables. The WAB fluency score is a rating from 0 to 10 of an individual’s spontaneous speech based on fluency of speech, grammatical competence, and paraphasic errors; the WAB naming subtest involves naming a series of 20 physically presented items (e.g., ball, cup); the WAB repetition subtest requires examinees to repeat 15 items that include single words, phrases, and sentences; and the WAB auditory comprehension score is based on yes/no questions, single-word recognition (both physical object-word matching and picture-word matching), and sequential commands.

As predicted, the ANCOVA showed that aphasic individuals performed significantly poorer than non-aphasic individuals on the Picture Arrangement task, F (1,54) = 6.25, p = 0.04 ( M ± SD = 34.8 ± 21.7% vs. 60.8 ± 22.3%, respectively), but the groups did not differ statistically on the Picture Completion task (49.0 ± 19.1% vs. 68.5 ± 14.6%, respectively), F (1,54) = 1.51, p = 0.24 (see Figure 2 ), controlling for age, education, months post-stroke, and lesion volume. Again, these results suggest that language impairment is related to reduced performance on tasks that place a greater demand on reasoning ability, even when that task does not require any overt language production. As in our previous work, the most severely language-compromised individuals in the sample, those with Wernicke’s aphasia, had the numerically lowest performance on the Picture Arrangement (reasoning) task. In keeping with this result and similar to our previous findings, partial correlations revealed significant relationships between scores on the Picture Arrangement task and comprehension, r (58) = 0.27, p = 0.04, as well as repetition, r (58) = 0.28, p = 0.03, but not with naming or fluency ( p s > 0.05). The same pattern held true when we repeated the partial correlation analyses with the sub-sample of aphasic individuals only, with comprehension and repetition alone showing marginally significant correlations of 0.33 ( p = 0.07) and 0.32 ( p = 0.08), respectively. With respect to normative cut-offs based on age-adjusted norms provided by the WAIS manual, 13.5% of the aphasic individuals performed in the significantly impaired range on the Picture Arrangement task (age-adjusted scale score of 4 or lower) but only a single individual in the non-aphasic subgroup. On the Picture Completion task, 18.9% of aphasic individuals performed in the significantly impaired range and none of the non-aphasic individuals.

FIGURE 2. Performance of aphasic and non-aphasic stroke patients on the WAIS Picture Completion and Picture Arrangement subtests, and the Benton Face Recognition (Matching) Task. The raw data (number of points attained on each task) were converted to a percentage of total points possible for each task in order to compare the results across tasks. Standard deviation bars are shown.

As can be seen in Figure 2 , aphasic individuals exhibited numerically (though not statistically) poorer performance than non-aphasic individuals on the Picture Completion task as well. For this reason, we additionally analyzed performance from these same 60 individuals on another standardized test of visuospatial functioning that does not involve reasoning, the Benton Face Recognition Task. On this more purely visual-perceptual task, aphasic and non-aphasic individuals performed comparably as revealed by ANCOVA, F (1,54) = 0.72, p = 0.40 ( M ± SD = 81 ± 9.4% vs. 84 ± 7.7%, respectively; see Figure 2 ).

These findings are consistent with the notion that language facilitates reasoning. Specific correlations between problem-solving performance and comprehension and repetition further suggest that core language processes (as opposed to output processes such as fluency and naming) are most strongly related to performance. It should be emphasized that poor performance cannot simply be explained by individuals with severe language impairments misunderstanding the task, as they are able to demonstrate their understanding of task instructions in the initial trials, before it becomes more difficult. In the Discussion, we explore potential explanations of the observed relationship between compromised core language and impaired reasoning as they relate to the supportive role of inner speech and working memory.

Experiment 1B: WCST Performance in Individuals with Aphasia

We previously showed that performance on the WCST, a standardized measure of problem-solving and reasoning, was impaired in aphasic individuals and also correlated with a number of critical language variables ( Baldo et al., 2005 ). However, our paper included a relatively small sample and a heterogeneous group of both right and left hemisphere patients. Therefore, we sought to replicate our previous findings in a larger sample of patients whose lesions were restricted to the left hemisphere, in order to confirm our previous findings of a relationship between language impairment and problem-solving performance.

A retrospective data analysis was conducted on data from 81 chronic left hemisphere stroke patients from our database (23 female) who met the same strict inclusion/exclusion criteria described above in Experiment 1A. Seventeen of these patients were also included in Baldo et al. (2005) . Based on the WAB, 35 patients were non-aphasic (i.e., scored within normal limits) and 46 patients were aphasic. This latter group included 20 individuals with anomic aphasia, 12 with Broca’s aphasia, seven with conduction aphasia, two with transcortical sensory aphasia, and five with Wernicke’s aphasia. Patients’ mean age ± SD was 60.6 ± 11.6 years for the aphasic individuals and 60.5 ± 10.3 years for non-aphasic individuals; mean education was 14.3 ± 2.7 years for the aphasic individuals and 15.3 ± 2.8 years for non-aphasic individuals; mean months post-stroke was 48.5 ± 50.5 months for aphasic individuals and 44.7 ± 53.2 months for non-aphasic individuals; and mean lesion volume was 126.2cc ± 67.1 in aphasic individuals and 35.1cc ± 43.6 in non-aphasic individuals. Finally, the aphasic group included 12 women and the non-aphasic group included 11 women.

The WCST requires examinees to match test cards with different arrays of 1–4 items (e.g., two triangles) drawn in different colors to one of four key cards with similar arrays. Participants are not told how to match the test cards to the key cards but are provided with feedback from the examiner ( correct or incorrect ) after each move. Unbeknownst to the examinee, the examiner repeatedly changes the sorting category after a set number of trials, and the examinee must recognize this switch and modify their sorting behavior based on the feedback. As an indication of adequate comprehension of task instructions, only a single individual with Wernicke’s aphasia was unable to sort at least 1 category.

Aphasic and non-aphasic individuals’ raw scores were compared with an ANCOVA using age, years of education, months post-stroke, and lesion volume as covariates as above. In addition, individuals’ praxis subtest scores from the WAB were included as an extra covariate to ensure that poor performance was not related to ideomotor apraxia ( Basso et al., 1981 ; a subset of 10 individuals in the sample scored below 80% correct on the praxis subtest). Partial correlation coefficients (two-tailed) were computed with the same nuisance factors, in order to test the relationship between problem-solving performance on the WCST and language processes including speech fluency, naming, repetition, and auditory comprehension.

Confirming our 2005 findings, the left hemisphere stroke patients with aphasia performed poorly on the WCST, completing an average of just 2.6 out of 6 possible category sorts ( SD = 2.1), compared to non-aphasic left hemisphere stroke patients who completed an average of 4.4 out of 6 category sorts ( SD = 1.9). An ANCOVA confirmed that this difference was significant, F (1,64) = 4.16, p = 0.04, correcting for age, education, praxis, and months post-onset. The size of patients’ lesions, another potential confound, was available for 79 of the patients and did not change the results when included as an additional covariate.

As in our previous studies, aphasic individuals with the most severe comprehension deficits, those with Wernicke’s and transcortical sensory aphasia, were particularly impaired and were the only subgroups significantly impaired relative to the non-aphasic group, Dunnett’s T3 (equal variances not assumed), p s < 0.001 (see Figure 3 ). As shown, individuals with milder comprehension impairments (i.e., Broca’s, anomic, and conduction aphasia) performed in the moderately impaired range on the WCST task. Since aphasia subtypes can be problematic as they are multi-determined syndromes, we also analyzed WCST performance in relation to specific language subprocesses as measured by the WAB, including speech fluency, auditory comprehension, repetition, and naming. Partial correlations revealed that overall performance on the WCST based on the number of categories sorted was significantly related to auditory comprehension alone, r (65) = 0.46, p < 0.001. The same was true when the partial correlation analyses were repeated using data from only the aphasic individuals rather than the entire sample: only auditory comprehension significantly correlated with WCST performance, r (37) = 0.41, p = 0.01.

FIGURE 3. Wisconsin Card Sorting Task (WCST) performance is shown for the number of categories completed, based on aphasia subtype. Individuals with severe comprehension deficits (Wernicke’s and TC Sensory aphasia) sorted the fewest number of categories on the WCST. Performance in individuals with milder deficits overlapped with that of non-aphasic individuals. TC Sensory, transcortical sensory aphasia. Standard deviation bars are shown.

These new findings on the WCST reinforce our previous work showing that many individuals with aphasia exhibit difficulties on putatively non-verbal problem-solving tasks and thus suggest a relationship between the presence of language deficits and the degree of impairment in problem-solving capacity. Furthermore, individuals with the most severe language impairments (those with transcortical sensory and Wernicke’s aphasia) performed worse overall, and correlational data showed a significant relationship between comprehension scores and problem-solving performance. These latter findings again suggest that core language processes (as opposed to production processes such as fluency) are most significantly related to problem-solving performance.

In short, we have conducted a series of large-scale studies comparing reasoning/problem-solving in aphasic vs. non-aphasic individuals that suggest a supportive role of language in these abilities. Although concerns about potentially confounding factors such as lesion size and overall cognitive impairment were addressed, one could still argue that brain-injured individuals are not the ideal population for addressing the issue of language and cognition. Thus, we now turn to complementary data obtained from a healthy adult with a severely restricted language capacity.

Experiment 2: Reasoning in a Deaf Individual with Impaired Language

Another way to examine the role that language plays in reasoning and problem-solving is by assessing cognition in healthy individuals with compromised language abilities. This can happen, for example, in deaf individuals who are not exposed to language until they are older ( Siegal et al., 2001 ; Morgan and Kegl, 2006 ). One of the authors (ND) has worked with such an individual (pseudonym “Chelsea”) who had an untreated, congenital hearing loss and was not exposed to language or any formal education until the age of 32. In Experiment 2, we describe Chelsea’s performance on non-verbal measures of reasoning in comparison to her performance on other cognitively demanding tasks that do not involve reasoning. Data from this unique individual parallel findings in aphasic individuals and offer additional insights into the role that language plays in reasoning and problem-solving.

Data were collected from a single case whose pseudonym is “Chelsea,” as well as her parents and two sisters who served as controls. Chelsea was born with a severe to profound sensorineural hearing loss that went unaddressed due to being raised in a rural setting with limited resources ( Dronkers, 1987 ; Glusker, 1987 ; Glusker et al., 1990 ; Curtiss, 2014 ). Her mother had a viral illness while pregnant with Chelsea that is associated with congenital deafness, but a definitive cause of her sensorineural hearing loss was not established. She was raised in a supportive home with her parents and six siblings, and she functioned normally according to family report: carrying out household chores, taking care of younger siblings, etc. As an infant/toddler, she achieved all developmental milestones at a normal rate and at a pace similar to her siblings (e.g., sitting, crawling, standing, walking, etc.), with the exception of language. According to family report, there were no home-signs used to communicate with Chelsea, but rather she relied on pointing, gestures, and miming to indicate her needs. Home visits and videotapes of the family interacting with Chelsea (without researchers present) confirmed the apparent lack of any home-signing system (see Curtiss, 2014 ).

At the age of 32, Chelsea was evaluated by a number of medical providers and was fitted with bilateral hearing aids that allowed her to hear speech for the first time. She started receiving instruction in both spoken English and Signing Exact English by a licensed speech pathologist. CT and MRI as well as EEG studies conducted at the time were all normal. The neurologist who evaluated her over several sessions reported that she showed no evidence of neurologic disabilities except for a single neurologic sign of mild hyperreflexia on the left side ( Glusker et al., 1990 and personal communication).

After being fitted with bilateral hearing aids, Chelsea gradually began acquiring spoken and receptive language, and she achieved a good command of the English lexicon (i.e., production and comprehension of single words; Curtiss, 2014 ). However, her ability to process syntax, both in production and comprehension, was extremely limited. Not surprisingly, she was difficult to understand and converse with. Examples of Chelsea’s spontaneous speech are provided in Table 1 . In contrast, she demonstrated relatively preserved pragmatics, including normal body language, prosody, facial expressions, gesture, etc. ( Dronkers, 1987 ; Dronkers et al., 1998 ; Curtiss, 2014 ). Curtiss (2014) concluded that Chelsea’s case provides clear evidence that there exists a critical period for acquiring grammar but not for acquiring other aspects of language such as the lexicon, which continues to grow in Chelsea’s case.

TABLE 1. Examples of Chelsea’s spontaneous speech.

Cognitive performance data from Chelsea’s parents and two sisters are also reported here for comparison. Her mother and father were tested at ages 52 and 62, and had 6th and 9th grade educations, respectively. While not as restricted in their schooling as Chelsea, her parents’ performance offers an informative comparison. Her two sisters were tested at ages 33 and 36, and had 12 and 13 years of education, respectively.

Chelsea was administered Raven’s Coloured Progressive Matrices and the WAIS-R Performance subtests at several time points from age 32–41. Raven’s Coloured Progressive Matrices includes a series of 36 non-speeded trials in which examinees have to point to 1 of 6 visual patches that best completes a visual pattern or sequence. She was also administered the WAIS-R Performance subtests, which represent the putatively non-verbal portion of the WAIS and are the preferred means of assessing intellectual functioning in hearing-impaired individuals ( Braden, 1992 ). The subtests include Picture Completion, Picture Arrangement, Block Design, Object Assembly, and Digit-Symbol. As described above, the WAIS-R Picture Completion task involves identifying a missing object in a picture, and the Picture Arrangement task involves rearranging a series of pictures so that they tell a story. Block Design requires examinees to rearrange red and white colored cubes to match a pattern printed in a stimulus book, and performance is based on both speed and accuracy. Object Assembly is a series of jigsaw puzzles that begin with very simple ones and get progressively harder. Last, the Digit-Symbol test involves speeded writing of symbols that correspond to numbers provided in a legend at the top of the page.

Serving as controls, Chelsea’s parents and two of her sisters were also administered the WAIS-R and Raven’s Matrices at a single time point that occurred between Chelsea’s 2nd and 3rd testing sessions. Her family was administered the Raven’s Standard Progressive Matrices, a more advanced version for adults whereas Chelsea was administered a simpler version, the Raven’s Coloured Progessive Matrices, which is administered to children. The data described below for all testing are presented as percentiles based on age-corrected, published norms.

Consistent with our findings in aphasic individuals, Chelsea showed a large discrepancy in performance between the Picture Completion and Picture Arrangement subtests of the WAIS-R. This discrepancy is even more striking in Chelsea than in the aphasic individuals: her performance on the Picture Completion task ranged from the average to high average range across five different administrations, while her performance on the Picture Arrangement task was consistently in the impaired range (based on age-adjusted WAIS-R norms; see Figure 4 ). Importantly, she was able to solve the first item on the Picture Arrangement task, indicating that she understood the task instructions. Furthermore, her poor performance on the Picture Arrangement task was not explained by exceeding time limits on the task, as she rearranged the cards (incorrectly) with time to spare. In contrast to Chelsea’s performance, her parents’ and two sisters’ scores were all in the average to high average range on both of these tasks.

FIGURE 4. Chelsea’s discrepant performance on the WAIS-R Picture Completion vs. Picture Arrangement tasks across several different testing sessions.

Chelsea performed in the average to high average range on two other non-verbal WAIS-R subtests that are less dependent on reasoning, Block Design and Object Assembly. Like the Picture Arrangement and Completion tasks, these subtests also require visual perceptual processing and attention as well as a manual response. On the other non-verbal subtest of the WAIS-R, the Digit-Symbol test, Chelsea initially performed in the impaired range as it requires speeded writing with a pencil, to which she was not accustomed, but by the last administration, she performed in the average range. This striking contrast in Chelsea’s performance across WAIS-R subtests lends further support to the idea that language competence is related to reasoning performance; if Chelsea’s poor performance were due to her lack of formal education or some other general cognitive impairment, one would expect to see consistently impaired performance across all WAIS subtests.

Chelsea was also tested on the Raven’s Coloured Progressive Matrices at four different time-points. Similar to findings in the aphasic individuals described above, Chelsea performed in the impaired range on this test. Figure 5 shows her performance in relation to that of her two sisters and parents who all performed in the normal range based on normative percentiles. Importantly, just as with our findings in aphasic individuals described above, Chelsea showed a dissociation across different types of Raven’s items, correctly solving 100% of items requiring visual-pattern completion but only 20% of those requiring relational reasoning.

FIGURE 5. Chelsea’s performance on Raven’s Coloured Progressive Matrices at four different time points (normed percentiles ranged from <0.01 -9th percentile) and her family’s performance on a single administration of Raven’s Standard Matrices. Note that Chelsea’s scores on the first two administrations are difficult to see since they approach the x-axis at 0. The normal cut-off at the 10th percentile is shown.

In summary, Chelsea, a congenitally deaf individual with poor language skills, showed disproportionately impaired performance on standardized neuropsychological tasks that involved reasoning. Based on her pattern of performance as well as a comparison with other family members who also had limited educational backgrounds, we conclude that her impaired reasoning skills may be in part due to her restricted language abilities.

In this paper, we have argued that there is a close relationship between language competence and the ability to reason and problem-solve. We have come to this conclusion based on our own work and the work of others showing that individuals with impaired language, particularly those with core language deficits (i.e., impaired comprehension and disordered language output), exhibit diminished performance on tests of reasoning and problem-solving ( Piercy, 1964 ; De Renzi et al., 1966 ; Borod et al., 1982 ; Larrabee, 1986 ; Hjelmquist, 1989 ; Hamsher, 1991 ; Baldo et al., 2005 , 2010 ). Specifically, we described data from a series of studies in which we compared the performance of aphasic (i.e., language-impaired) and non-aphasic stroke patients on a variety of reasoning and problem-solving tasks, such as the WCST and non-verbal subtests of the WAIS. In these analyses, the aphasic group as a whole was disproportionately impaired on reasoning tasks relative to the non-aphasic group, but the two groups showed comparable performance on other cognitively demanding tasks that did not involve reasoning. In the second part of the paper, we described complementary findings from a case of a healthy individual with delayed exposure to language due to an unaddressed congenital deafness. She, too, exhibited marked impairment on tasks of reasoning that stood in stark contrast to her ability to perform in the average to high average range on numerous cognitive tasks that did not involve reasoning. Taken together, these data are highly suggestive of an important role for language in reasoning and problem-solving.

Our findings in language-impaired individuals are consistent with previous studies in non-human animals and children that also suggest an association between language and reasoning. With respect to animal research, studies have shown that language-training in non-human primates facilitates problem-solving performance ( Premack, 1983 , 2007 ). Thompson et al. (1997) further showed that this facilitation is likely due to the learned ability of these animals to associate a token with an abstract relation, much like language provides us with words that can singly represent other propositional knowledge. In studies with children, it has been shown that the level of language competence and the use of private speech are directly related to problem-solving performance ( Berk and Garvin, 1984 ; Berk, 1986 ; Winsler et al., 1997 ; Hermer-Vazquez et al., 1999 ; Fernyhough and Fradley, 2005 ; Carpendale et al., 2009 ). Vygotsky (1978 , 2012 ) championed this idea that language plays a role in children’s development of reasoning skills: initially overt speech and dialoguing with elders is used to work through problems and is later internalized and becomes covert or inner speech. Before him, Piaget (1967) believed that language, while not critical for most stages of development, did play a role in formal operations when abstract reasoning emerges. In support of this idea, performance on Piagetian tasks involving formal operations is impaired in language-delayed individuals, while performance on tasks involving concrete operations is relatively intact ( Furth, 1966 ; Furth and Youniss, 1971 ; Twilling, 1984 ). This dissociation between concrete and formal operations was also exhibited by Chelsea, the deaf individual with language impairment described above.

If we accept the idea that language facilitates problem-solving and reasoning in some way, this still leaves the question: what is the mechanism underlying this relationship? The answer to this question remains elusive and was not the focus of our investigations reported above, but a number of data points are instructive. First, prior work from our group and others have shown that articulatory suppression in healthy individuals (e.g., vocalizing nonsense syllables or irrelevant speech while doing a task) is disruptive to performance on reasoning/problem-solving tasks, suggesting that some form of verbal mediation (e.g., talking to oneself) facilitates reasoning and problem-solving ( Hermer-Vazquez et al., 1999 ; Baldo et al., 2005 ; Wallace et al., 2009 ; Lidstone et al., 2010 ; but see Learmonth et al., 2008 ; Bek et al., 2010 ; Forgeot d’Arc and Ramus, 2011 ). Importantly, control conditions with non-verbal distraction (e.g., tapping a rhythm) are much less disruptive, showing that the effect is specific to verbal disruption, not a general disruption of attention or some other process. Furthermore, as in children, it has been shown that when healthy adults think out loud on a reasoning task, performance can improve (see Fox and Charness, 2010 ). Such studies in healthy individuals provide a causal link between language and reasoning.

In keeping with this idea, Sokolov (1968/1972 ) described studies in which individuals doing mental arithmetic and repeating words had recordable muscle activity in the articulators (e.g., tongue, lips, etc.), suggesting that such inner speech is literally that—covert vocalization. More recent studies measuring muscular activity show incredible specificity: when participants silently read the letter “P,” muscular activity was detected in their lips and when they silently read the letter “T,” muscular activity was detected in their tongue ( McGuigan and Dollins, 1989 ; but see discussion below regarding dissociations of covert and overt speech). Sokolov concluded: “Inner speech emerges as a rather intricate phenomenon, where thought and language are bound in a single, indissoluble complex acting as the speech mechanism of thinking” (p. 1; also see Clark, 2006 ). Similarly, Carruthers (2002) echoes this notion: “Central cognition may also deploy the resources of the language system to generate representations of natural language sentences (in “inner speech”), which can similarly be of use in a variety of conceptual reasoning tasks” (p. 658).

A more systematically studied concept that can be invoked to explain the role of verbal mediation or inner speech is verbal working memory ( Baddeley and Logie, 1999 ; Baddeley, 2000 ; Al-Namlah et al., 2006 ; Marvel and Desmond, 2012 ; Perrone-Bertolotti et al., 2014 ). It may be that this mechanism underlies successful problem-solving performance, as it provides a real-time rehearsal and updating of relevant information that can provide cognitive flexibility on reasoning and problem-solving tasks ( Jonides, 2000 ; Emerson and Miyake, 2003 ; Carpendale et al., 2009 ). Verbal working memory may also facilitate problem-solving/reasoning by focusing attention and supporting self-cueing and self-monitoring ( Clark, 2005 ; Unsworth and Engle, 2007 ; Forgeot d’Arc and Ramus, 2011 ). Verbal working memory, as measured by tasks such as repetition, is impaired in many aphasic individuals ( Brown, 1975 ; Goodglass, 1992 ; Kohler et al., 1998 ; Baldo et al., 2012 ), and we have shown that patients’ repetition scores correlate with the percent of perseverative errors on the WCST and performance on Raven’s Matrices ( Baldo et al., 2005 , 2010 ).

In our current findings described above, repetition impairment, along with comprehension impairment, was related to poor performance on the Picture Arrangement (reasoning) task, although comprehension alone was most strongly related to performance on the WCST. Moreover, we also found that individuals with transcortical sensory aphasia (who have impaired comprehension but relatively preserved repetition) were greatly impaired in their reasoning performance, suggesting that core language (rather than simple repetition) is most strongly related to reasoning performance. By “core language,” we refer to the ability to both formulate and comprehend meaningful language. That is, while posterior patients with Wernicke’s/transcortical sensory aphasia (and global aphasics as well) are defined in part based on their poor comprehension, they also have a corresponding inability to produce meaningful language. Presumably, this limited ability to produce meaningful, overt language is paralleled by a limited ability to produce meaningful inner speech, a supposition which has only just recently begun to be tested more systematically (see Fama et al., 2014 ; Hayward et al., 2014 , discussed below). Our speculation is that disordered inner speech is central to the reasoning performance decrements we observe in many language-impaired individuals. Such suppositions need to be explored in future studies to assess the extent to which inner speech is disordered in different aphasic subgroups and demonstrate how this relates to impaired reasoning ( Kinsbourne, 2000 ).

Interesting insights on the role of inner speech in reasoning come from Jill Bolte Taylor, the neuroanatomist who suffered a left hemisphere stroke and later recounted her subjective experiences ( Taylor, 2008 ; Morin, 2009 ). Taylor describes a striking loss of inner speech that accompanied her aphasia and negatively impacted her ability to reason and think through problems:

The most notable difference between my pre- and post-stroke cognitive experience was the dramatic silence that had taken residency inside my head. I just didn’t think in the same way. Communication with the external world was out. Language with linear processing was out. But thinking in pictures was in (pp. 75–76).

A similar parallel between overt and covert language loss in aphasia has also been described in other case studies of severe aphasia ( Lecours and Joanette, 1980 ; Kertesz, 1988 ).

In contrast, individuals whose aphasia is more related to production deficits (e.g., Broca’s aphasia, anomic aphasia) appear to retain some capacity to generate inner speech, which might explain their residual reasoning ability. Although difficult to study, evidence for this capacity comes from two recent studies that assessed inner speech and the tip-of-the-tongue phenomenon in a group of aphasic individuals who had primarily output production deficits ( Fama et al., 2014 ; Hayward et al., 2014 ). In Fama et al. (2014) , 82% of the aphasic individuals reported hearing the words they wanted in their head but being unable to articulate them. Both Fama et al. (2014) and Hayward et al. (2014) reported anatomical and functional dissociations that mirrored the patients’ self-reports, such as fMRI activity in brain regions associated with phonological access (in left superior temporal cortex) when patients had this subjective experience. Single cases with such a dissociation between inner speech and overt language capacity have also been reported ( Lecours and Joanette, 1980 ; Hanley and McDonnell, 1997 ).

Findings from the current study stand in seeming contrast to a handful of smaller case studies that have concluded that language is not critical for reasoning. For example, Varley and Siegal (2000) reported a case study of an individual with agrammatic aphasia who was trained to understand and then pass a theory of mind (perspective-taking) test. Another study by this group ( Bek et al., 2010 ) tested five individuals with aphasia on a spatial-landmark conjunction task used previously to show the reliance of such tasks on language ( Hermer-Vazquez et al., 1999 ). They found that language was not critical for performance, but they also concluded that such tasks are likely “assisted by” language (p. 656), consistent with our position. Last, Apperly et al. (2006) showed that a severely aphasic individual was able to pass first- and second-order false belief (theory of mind) tasks, again concluding that grammar is not a requisite for such performance.

One likely explanation for differing conclusions about the role of language in reasoning between our work and others’ is a difference in the types of patients investigated. What we refer to as “severe aphasia” is a syndrome in which patients have core language deficits: they cannot generate meaningful language, they are far below chance on simple word-picture matching tasks, and they have difficulty understanding simple sentences. In the case studies described above, the use of the term “severe aphasia” refers to primarily agrammatic patients who are well above chance on basic language tasks such as single word-picture matching vs. our severely aphasic patients who score in the very impaired range on such tasks. Our studies also include individuals with severe agrammatism, and these individuals do relatively well on our reasoning tasks. We believe they do well because their core language is less impaired and they may thus possess relatively preserved inner speech (see discussion of overt vs. covert speech above). In our opinion, the individuals who provide the best test of the role of language in reasoning are patients with severe, core language impairments who have an inability to generate meaningful language (e.g., individuals with chronic Wernicke’s aphasia) and who likely have disordered inner speech. These types of patients are more rare (relative to agrammatic patients), and it has taken many years to be able to analyze data from a group of such individuals.

Another explanation for the different conclusions reached by previous case studies of language and reasoning is the types of tasks employed. Most of these previous case studies focused on theory of mind/perspective-taking tasks, whereas we have focused on standardized neuropsychological tasks of reasoning and problem-solving like the WCST. Interestingly, in Apperly et al. (2006) , the individual with severe aphasia who was able to perform false belief tasks was greatly impaired on executive functioning tests that included the WCST. Similarly, Varley (1998) reported impaired performance on the WAIS Picture Arrangement (reasoning) task in a fluent aphasic patient who was able to pass theory of mind tasks. These dissociations suggest that the two types of tasks likely tap distinct functions. False-belief tasks, including theory of mind, do not require the same degree of planning, self-monitoring, and online processing as the standardized neuropsychological tasks used to test reasoning and problem-solving in our studies described above. It is perhaps for this reason that performance on these latter types of tasks is more strongly related to language ability.

At the same time, a number of other studies on theory of mind in children and in delayed language learners have shown that performance is related to language competence ( de Villiers and Pyers, 2002 ; Hale and Tager-Flusberg, 2003 ; Schick et al., 2007 ; Pyers and Senghas, 2009 ; see de Villiers, 2007 ; Carpendale et al., 2009 for reviews). In an interesting experimental paper, theory of mind performance was shown to be disrupted in adults under conditions of articulatory suppression (verbal shadowing) but not tapping ( Newton and de Villiers, 2007 ). However, there is debate as to the precise nature of the role that language competence plays in theory of mind tasks ( de Villiers, 2007 ). Although we have not collected data on theory of mind tasks with our aphasic patients, our case study described above, Chelsea, was tested on a spatial perspective-taking task that involved minimal verbal instructions and required a simple pointing response. She was able to understand the task and comply with instructions when asked to point to the picture that matched the visual scene in front of her. However, she failed when asked to point to the picture that matched the scene in front of the examiner (who sat to her side). Given her excellent spatial skills on tasks such as the WAIS Block Design and Object Assembly subtests, this poor performance was more likely due to her inability to take another’s perspective but could also have been due to her impaired language-understanding. A similar problem arises when attempting to test aphasic individuals on theory of mind tasks: the instructions themselves necessitate a minimal level of language competence, even when the task is visually presented. To the extent that a patient can understand the instructions on a theory of mind task, even a visually presented one, likely indicates that their language is not completely impaired. Indeed, it would be impossible for us to successfully convey instructions for theory of mind tasks to the severely aphasic individuals that were most impaired on our reasoning tasks described above.

To ensure that we did not overlook any “exceptional” cases in our large datasets, we inspected our data for single individuals demonstrating a dissociation between core language and reasoning, that is, individuals with a severe impairment in comprehension/lexical-semantics such as those with Wernicke’s aphasia who nonetheless showed preserved reasoning. On the WCST problem-solving task, 70% of patients were able to sort between 2 and 6 categories (out of a possible 6) and not a single patient with severe language impairment was among this group. All of the individuals with Wernicke’s or transcortical sensory aphasia (i.e., patients with severe core language impairments) sorted 0–1 categories. On the WAIS Picture Arrangement task, 9 of the top 10 performers were non-aphasic (within normal limits on the WAB language battery), with the 10th patient being an individual with mild anomic aphasia. There was one individual with Wernicke’s aphasia who scored 70% correct on the task (moderately impaired), and the other three individuals with Wernicke’s aphasia were in the bottom 10 performers. In contrast, many of the Broca’s/agrammatic individuals in our study were able to perform well on both the WCST and Picture Arrangement tasks (exceptions were those Broca’s/agrammatic individuals with more severe comprehension deficits), similar to the previous case studies of agrammatic aphasia. Thus, we would concur with previous studies suggesting an independence of grammar and reasoning (e.g., Varley and Siegal, 2000 ), but suggest that core language processes such as those most typically affected in Wernicke’s aphasia play an important role in reasoning. As suggested above, further work is needed to further explore these dissociations among different aphasic subgroups.

It should be noted that we are not claiming here that intelligence, or thought more generally, is necessarily dependent on language (also see Carruthers, 2012 ). Rather, we restrict our claims to higher-level reasoning/problem-solving, that is, the kind of thought normally facilitated by verbal mediation or inner speech ( Sokolov, 1968/1972 ; Carruthers, 2002 ; Evans, 2008 ). This distinction has been made by Evans (2008) who contrasts a heuristic, quick and dirty system that “rapidly contextualize[s] problems with prior knowledge and belief” vs. a slow and serial system that is engaged during “conscious effortful analytic reasoning” (p. 261). He argues that the former is a non-verbal system that we share with other animals, while the latter system is dependent on language and is unique to humans.

Nor are we making the claim that language is absolutely indispensable to reasoning—we have rather argued throughout this paper that language can “facilitate” and is “supportive” of higher-level reasoning capacity. Even Ratliff and Newcombe (2008) who were skeptical of the original Hermer-Vazquez et al. (1999) shadowing study on reasoning and language reported that the original findings hold up to a certain degree. They concluded that, although language may not be “crucial” to reasoning, it is “helpful.” Similarly, Forgeot d’Arc and Ramus (2011) showed that verbal shadowing impaired performance overall on a non-verbal task involving belief attribution but that performance was still above chance. Although they felt their data supported the idea that belief attribution is independent from language, they also concluded that language acts as “an additional tool to keep relevant information in short-term memory” (p. 984). Similarly, Varley (2014) concluded that “language resources may often be deployed to scaffold performance on a range of problems” by way of supporting short- and long-term memory (p. 242). Again, this is consistent with the idea that language can serve a facilitatory role in online processes that support reasoning performance.

Finally, we are not suggesting that the use of inner speech and language to support reasoning is somehow predetermined; it is apparently a learned phenomenon ( Vygotsky, 2012 ) that can vary across individuals. Interesting cross-cultural research has also shown that the use of inner speech, while facilitatory for non-verbal reasoning in European–Americans (healthy individuals), can be disruptive for non-verbal reasoning in East Asian–American participants on particular tasks ( Kim, 2002 ). This finding makes the intriguing prediction that reasoning performance in East Asian patients with aphasia would not show a similar pattern of disruption as in our current study which included predominantly European–American patients. We are currently investigating this prediction with a cross-linguistic study of aphasia in collaboration with colleagues in Taiwan. It is likely that the degree to which language is invoked to support reasoning within and across cultures depends on the type of task involved (e.g., supportive strategies for particular tasks in one culture may be more visual-spatial while in another, more verbal). More experimental work in this intriguing area of investigation is clearly needed.

Brain imaging studies have also provided novel insights into the relationship between language/inner speech and cognition (for a review, see Girbau, 2007 ; Morin and Hamper, 2012 ). Consistent with our findings, Pillay et al. (2014) found that posterior brain regions overlapping with Wernicke’s area, including the left posterior superior temporal gyrus and inferior parietal cortex, were most closely related to pre-articulatory phonological access (what they and others have used as a stand-in for inner speech). However, some recent functional imaging studies in healthy individuals have suggested that language areas can dissociate from higher-level cognitive processes ( Monti et al., 2007 ; Willems et al., 2010 ; Fedorenko et al., 2011 ). In our work, we have shown that lesions involving language areas in the left hemisphere (most consistently, left posterior temporal cortex) are associated with decreased performance on reasoning and problem-solving tasks ( Baldo et al., 2005 , 2010 ). In Baldo et al. (2010) , we found a dissociation between brain regions associated with performance on the visual-pattern completion items on Raven’s Matrices vs. performance on the relational reasoning items: the former was associated with visual association regions in left inferior temporo-occipital cortex and the latter, with left posterior middle and superior temporal cortex (a critical language zone). Still, caution is warranted in drawing strong conclusions from lesion data as there is also the possibility that distinct but overlapping networks underlie language and reasoning processes in the brain ( Kertesz, 1988 ; Baldo et al., 2010 ).

In short, a range of philosophical inquiries and experimental evidence supports the idea that language and reasoning are highly inter-dependent. Further experimental investigations of this relationship are needed in order to establish more evidence for a causal role of language in reasoning ( Varley, 2014 ), especially with respect to the putative role that inner speech plays as a mediating mechanism. We conclude here with an elegant description by O’Brien and Opie (2002) of the relationship between language and cognition:

Natural language thereby becomes a powerful cognitive tool… one that can regulate the sequencing of thought, via the constant interplay between networks that encode linguistic signals and those that encode thoughts… Such causal loops catch up language and thought in a tight web of mutual influence that extends our cognitive capacities well beyond those of infra-verbal organisms (p. 327).

Conflict of Interest Statement

The authors declare that the research was conducted in the absence of any commercial or financial relationships that could be construed as a potential conflict of interest.

Acknowledgments

This material is based on work supported in part by the U.S. Department of Veterans Affairs, Office of Research & Development Rehabilitation R&D and CSR&D Programs, NIH/NINDS 5 P01 NS040813, NIH/NIDCD 5 R01 DC00216, and a subsidy granted to the National Research University Higher School of Economics, by the Government of the Russian Federation for the implementation of the Global Competitiveness Program. The contents reported within do not represent the views of the Department of Veterans Affairs or the United States Government. All of the research described herein was carried out in a manner consistent with the Helsinki Declaration. Written consent was obtained from all study participants, and the study was approved by the local Institutional Review Board. We would like to thank Christine Chiarello, Catherine O’Connor, Susan Curtiss, and Peter Glusker for their work in evaluating the case of Chelsea. We would like to thank Lisa LeJeune for her assistance with data compilation. We would also like to thank our lab colleagues as well as two reviewers for their feedback on earlier versions of this paper. Finally, we would like to thank all of the research volunteers who took part in our studies.

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Keywords : reasoning, problem-solving, aphasia, language delay, deafness, thought, language, inner speech

Citation: Baldo JV, Paulraj SR, Curran BC and Dronkers NF (2015) Impaired reasoning and problem-solving in individuals with language impairment due to aphasia or language delay. Front. Psychol. 6:1523. doi: 10.3389/fpsyg.2015.01523

Received: 08 May 2015; Accepted: 22 September 2015; Published: 26 October 2015.

Reviewed by:

Copyright © 2015 Baldo, Paulraj, Curran and Dronkers. This is an open-access article distributed under the terms of the Creative Commons Attribution License (CC BY) . The use, distribution or reproduction in other forums is permitted, provided the original author(s) or licensor are credited and that the original publication in this journal is cited, in accordance with accepted academic practice. No use, distribution or reproduction is permitted which does not comply with these terms.

*Correspondence: Juliana V. Baldo, [email protected]

Disclaimer: All claims expressed in this article are solely those of the authors and do not necessarily represent those of their affiliated organizations, or those of the publisher, the editors and the reviewers. Any product that may be evaluated in this article or claim that may be made by its manufacturer is not guaranteed or endorsed by the publisher.

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Examples of Visual Spatial Problems in People With Dementia

Visuospatial Refers to Vision and Perception Skills

Dementia affects more than just the ability to remember things. It also can impact visuospatial abilities and skills.

Visual-spatial problems in dementia are common. This article discusses what visual spacial difficulties are and how they affect people with dementia.

What Are Visuospatial Abilities?

Also referred to as "visual-spatial" and "visuo-spatial," visuospatial abilities consist of the ability to understand what we see around us and interpret spatial relationships. In other words, this includes both the images we see ( visual ), as well as our perception of the size and location of our surroundings ( spatial ).

How Dementia Affects Visuospatial Abilities

Depth perception.

Dementia can affect depth perception, making it more difficult to navigate tasks such as going downstairs and thus increasing the risk of falls . Activities of daily living such as getting into a bathtub, getting dressed or feeding oneself can also become more challenging.

Increased Risk of Wandering

Persons with dementia can also become easily lost and wander , even in very familiar environments. They might not recognize the path home that they've taken every day for many years, or be able to locate the bathroom in the middle of the night.

Recognizing Faces and Locating Objects

Visuospatial changes may also contribute, along with the cognitive symptoms of dementia, to the inability to recognize faces or find objects that are in plain sight.

Difficulty Driving

Driving may become more difficult as dementia develops, in part because of changes in the ability to understand spatial relationships. For example, navigating a turn, changing lanes, or parking a car could become a significant challenge due to a decline in visuospatial abilities. As dementia progresses, the difficult decision to quit driving usually must be made.

The ability to read may also decline, in part due to visuospatial changes and a decline inability to remember how to read or comprehend the meaning of the words.

Research on Visuospatial Ability and Other Kinds of Dementia

Visuospatial ability is affected in multiple types of dementia, including in the very early stages of Alzheimer's disease. Interestingly, several research studies have concluded that visuospatial changes are especially prevalent in Lewy body dementia, which includes dementia with Lewy bodies and Parkinson's disease dementia . One study noted that poor performance on visuospatial tests was connected with a faster rate of decline in persons with Lewy body dementia.

In addition, research demonstrated that visuospatial deficits have been correlated with an increase in hallucinations in Lewy body dementia . Hallucinations are one of the hallmarks of Lewy body dementia, making this connection with visuospatial ability intriguing and identifying it as an area for further research.

Visuospatial changes have also been regularly found in vascular dementia.

Interestingly, visuospatial abilities appear to vary in different types of frontotemporal dementia, with some research suggesting that it is less affected in behavioral variant frontotemporal dementia (also known as Pick's disease) and more impacted in corticobasal degeneration .

How Visuospatial Ability Is Measured

Certain cognitive tests include sections that help identify visuospatial impairments. These tasks include the clock drawing test , the task of drawing intersecting shapes (required on the MMSE) or copying a complex figure and the ability to recognize an object, such as a pencil or watch.

Additionally, the Visual Object and Space Perception (VOSP) test was designed to specifically assess visuospatial ability and can be helpful in identifying impairment in this area.

A Word From Verywell

It's important to understand that several types of dementia impact visuospatial abilities. This knowledge can help explain why some people living with dementia fall easily, seem to misjudge distances, get lost easily and struggle with driving skills.

Additionally, while we can't change how the brain processes visuospatial information in dementia, scheduling regular vision checks at the eye doctor can help ensure that vision is functioning optimally and any glasses are of the correct prescription.  

Frequently Asked Questions

Visuospatial problems are difficulties understanding what we see around us and interpreting spatial relationships. This can include trouble recognizing faces, locating objects, reading, depth perception, and navigating movements. Visuospatial difficulties can be especially dangerous when it comes to driving a car, particularly with making turns and parking.  

Spacial disorientation is often one of the first symptoms of dementia. It involves being confused about your surroundings and can affect a person's ability to remember directions and recognize previously familiar locations. Spatial disorientation is one reason people with Alzheimer's are more likely to wander and get lost.

While any form of dementia can affect vision, it is more common in some types of dementia than others. Vision problems are more likely to occur with:

• Alzheimer's
• Lewy body dementia
• Posterior cortical atrophy
• Vascular dementia

Visual agnosia is the total or partial loss of recognizing and identifying familiar objects and/or people by sight. This can be a common symptom of dementia as the condition progresses.

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D’Antonio F, Boccia M, Di Vita A, et al. Visual hallucinations in Lewy body disease: pathophysiological insights from phenomenology .  J Neurol . 2022;269(7):3636-3652. doi:10.1007/s00415-022-10983-6

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Puthusseryppady V, Emrich-Mills L, Lowry E, Patel M, Hornberger M. Spatial disorientation in Alzheimer's disease: the missing path from virtual reality to real world . Front Aging Neurosci . 2020;12:550514. doi:10.3389/fnagi.2020.550514

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By Esther Heerema, MSW Esther Heerema, MSW, shares practical tips gained from working with hundreds of people whose lives are touched by Alzheimer's disease and other kinds of dementia.