clinical presentation of mental health problems

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To determine a diagnosis and check for related complications, you may have:

• A physical exam. Your doctor will try to rule out physical problems that could cause your symptoms.
• Lab tests. These may include, for example, a check of your thyroid function or a screening for alcohol and drugs.
• A psychological evaluation. A doctor or mental health professional talks to you about your symptoms, thoughts, feelings and behavior patterns. You may be asked to fill out a questionnaire to help answer these questions.

Determining which mental illness you have

Sometimes it's difficult to find out which mental illness may be causing your symptoms. But taking the time and effort to get an accurate diagnosis will help determine the appropriate treatment. The more information you have, the more you will be prepared to work with your mental health professional in understanding what your symptoms may represent.

The defining symptoms for each mental illness are detailed in the Diagnostic and Statistical Manual of Mental Disorders (DSM-5), published by the American Psychiatric Association. This manual is used by mental health professionals to diagnose mental conditions and by insurance companies to reimburse for treatment.

Classes of mental illness

The main classes of mental illness are:

• Neurodevelopmental disorders. This class covers a wide range of problems that usually begin in infancy or childhood, often before the child begins grade school. Examples include autism spectrum disorder, attention-deficit/hyperactivity disorder (ADHD) and learning disorders.
• Schizophrenia spectrum and other psychotic disorders. Psychotic disorders cause detachment from reality — such as delusions, hallucinations, and disorganized thinking and speech. The most notable example is schizophrenia, although other classes of disorders can be associated with detachment from reality at times.
• Bipolar and related disorders. This class includes disorders with alternating episodes of mania — periods of excessive activity, energy and excitement — and depression.
• Depressive disorders. These include disorders that affect how you feel emotionally, such as the level of sadness and happiness, and they can disrupt your ability to function. Examples include major depressive disorder and premenstrual dysphoric disorder.
• Anxiety disorders. Anxiety is an emotion characterized by the anticipation of future danger or misfortune, along with excessive worrying. It can include behavior aimed at avoiding situations that cause anxiety. This class includes generalized anxiety disorder, panic disorder and phobias.
• Obsessive-compulsive and related disorders. These disorders involve preoccupations or obsessions and repetitive thoughts and actions. Examples include obsessive-compulsive disorder, hoarding disorder and hair-pulling disorder (trichotillomania).
• Trauma- and stressor-related disorders. These are adjustment disorders in which a person has trouble coping during or after a stressful life event. Examples include post-traumatic stress disorder (PTSD) and acute stress disorder.
• Dissociative disorders. These are disorders in which your sense of self is disrupted, such as with dissociative identity disorder and dissociative amnesia.
• Somatic symptom and related disorders. A person with one of these disorders may have physical symptoms that cause major emotional distress and problems functioning. There may or may not be another diagnosed medical condition associated with these symptoms, but the reaction to the symptoms is not normal. The disorders include somatic symptom disorder, illness anxiety disorder and factitious disorder.
• Feeding and eating disorders. These disorders include disturbances related to eating that impact nutrition and health, such as anorexia nervosa and binge-eating disorder.
• Elimination disorders. These disorders relate to the inappropriate elimination of urine or stool by accident or on purpose. Bed-wetting (enuresis) is an example.
• Sleep-wake disorders. These are disorders of sleep severe enough to require clinical attention, such as insomnia, sleep apnea and restless legs syndrome.
• Sexual dysfunctions. These include disorders of sexual response, such as premature ejaculation and female orgasmic disorder.
• Gender dysphoria. This refers to the distress that accompanies a person's stated desire to be another gender.
• Disruptive, impulse-control and conduct disorders. These disorders include problems with emotional and behavioral self-control, such as kleptomania or intermittent explosive disorder.
• Substance-related and addictive disorders. These include problems associated with the excessive use of alcohol, caffeine, tobacco and drugs. This class also includes gambling disorder.
• Neurocognitive disorders. Neurocognitive disorders affect your ability to think and reason. These acquired (rather than developmental) cognitive problems include delirium, as well as neurocognitive disorders due to conditions or diseases such as traumatic brain injury or Alzheimer's disease.
• Personality disorders. A personality disorder involves a lasting pattern of emotional instability and unhealthy behavior that causes problems in your life and relationships. Examples include borderline, antisocial and narcissistic personality disorders.
• Paraphilic disorders. These disorders include sexual interest that causes personal distress or impairment or causes potential or actual harm to another person. Examples are sexual sadism disorder, voyeuristic disorder and pedophilic disorder.
• Other mental disorders. This class includes mental disorders that are due to other medical conditions or that don't meet the full criteria for one of the above disorders.

Your treatment depends on the type of mental illness you have, its severity and what works best for you. In many cases, a combination of treatments works best.

If you have a mild mental illness with well-controlled symptoms, treatment from your primary care provider may be sufficient. However, often a team approach is appropriate to make sure all your psychiatric, medical and social needs are met. This is especially important for severe mental illnesses, such as schizophrenia.

Your treatment team

Your treatment team may include your:

• Family or primary care doctor
• Nurse practitioner
• Physician assistant
• Psychiatrist, a medical doctor who diagnoses and treats mental illnesses
• Psychotherapist, such as a psychologist or a licensed counselor
• Social worker
• Family members

Medications

Although psychiatric medications don't cure mental illness, they can often significantly improve symptoms. Psychiatric medications can also help make other treatments, such as psychotherapy, more effective. The best medications for you will depend on your particular situation and how your body responds to the medication.

Some of the most commonly used classes of prescription psychiatric medications include:

• Antidepressants. Antidepressants are used to treat depression, anxiety and sometimes other conditions. They can help improve symptoms such as sadness, hopelessness, lack of energy, difficulty concentrating and lack of interest in activities. Antidepressants are not addictive and do not cause dependency.
• Anti-anxiety medications. These drugs are used to treat anxiety disorders, such as generalized anxiety disorder or panic disorder. They may also help reduce agitation and insomnia. Long-term anti-anxiety drugs typically are antidepressants that also work for anxiety. Fast-acting anti-anxiety drugs help with short-term relief, but they also have the potential to cause dependency, so ideally they'd be used short term.
• Mood-stabilizing medications. Mood stabilizers are most commonly used to treat bipolar disorders, which involves alternating episodes of mania and depression. Sometimes mood stabilizers are used with antidepressants to treat depression.
• Antipsychotic medications. Antipsychotic drugs are typically used to treat psychotic disorders, such as schizophrenia. Antipsychotic medications may also be used to treat bipolar disorders or used with antidepressants to treat depression.
• Psychotherapy

Psychotherapy, also called talk therapy, involves talking about your condition and related issues with a mental health professional. During psychotherapy, you learn about your condition and your moods, feelings, thoughts and behavior. With the insights and knowledge you gain, you can learn coping and stress management skills.

There are many types of psychotherapy, each with its own approach to improving your mental well-being. Psychotherapy often can be successfully completed in a few months, but in some cases, long-term treatment may be needed. It can take place one-on-one, in a group or with family members.

When choosing a therapist, you should feel comfortable and be confident that he or she is capable of listening and hearing what you have to say. Also, it's important that your therapist understands the life journey that has helped shape who you are and how you live in the world.

Brain-stimulation treatments

Brain-stimulation treatments are sometimes used for depression and other mental health disorders. They're generally reserved for situations in which medications and psychotherapy haven't worked. They include electroconvulsive therapy, repetitive transcranial magnetic stimulation, deep brain stimulation and vagus nerve stimulation.

Make sure you understand all the risks and benefits of any recommended treatment.

Hospital and residential treatment programs

Sometimes mental illness becomes so severe that you need care in a psychiatric hospital. This is generally recommended when you can't care for yourself properly or when you're in immediate danger of harming yourself or someone else.

Options include 24-hour inpatient care, partial or day hospitalization, or residential treatment, which offers a temporary supportive place to live. Another option may be intensive outpatient treatment.

Substance misuse treatment

Problems with substance use commonly occur along with mental illness. Often it interferes with treatment and worsens mental illness. If you can't stop using drugs or alcohol on your own, you need treatment. Talk to your doctor about treatment options.

Participating in your own care

Working together, you and your primary care provider or mental health professional can decide which treatment may be best, depending on your symptoms and their severity, your personal preferences, medication side effects, and other factors. In some cases, a mental illness may be so severe that a doctor or loved one may need to guide your care until you're well enough to participate in decision-making.

More Information

• Mental health providers: Tips on finding one
• Deep brain stimulation
• Electroconvulsive therapy (ECT)
• Transcranial magnetic stimulation
• Vagus nerve stimulation

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Lifestyle and home remedies

In most cases, a mental illness won't get better if you try to treat it on your own without professional care. But you can do some things for yourself that will build on your treatment plan:

• Stick to your treatment plan. Don't skip therapy sessions. Even if you're feeling better, don't skip your medications. If you stop, symptoms may come back. And you could have withdrawal-like symptoms if you stop a medication too suddenly. If you have bothersome drug side effects or other problems with treatment, talk to your doctor before making changes.
• Avoid alcohol and drug use. Using alcohol or recreational drugs can make it difficult to treat a mental illness. If you're addicted, quitting can be a real challenge. If you can't quit on your own, see your doctor or find a support group to help you.
• Stay active. Exercise can help you manage symptoms of depression, stress and anxiety. Physical activity can also counteract the effects of some psychiatric medications that may cause weight gain. Consider walking, swimming, gardening or any form of physical activity that you enjoy. Even light physical activity can make a difference.
• Make healthy choices. Maintaining a regular schedule that includes sufficient sleep, healthy eating and regular physical activity are important to your mental health.
• Don't make important decisions when your symptoms are severe. Avoid decision-making when you're in the depth of mental illness symptoms, since you may not be thinking clearly.
• Determine priorities. You may reduce the impact of your mental illness by managing time and energy. Cut back on obligations when necessary and set reasonable goals. Give yourself permission to do less when symptoms are worse. You may find it helpful to make a list of daily tasks or use a planner to structure your time and stay organized.
• Learn to adopt a positive attitude. Focusing on the positive things in your life can make your life better and may even improve your health. Try to accept changes when they occur, and keep problems in perspective. Stress management techniques, including relaxation methods, may help.

Coping and support

Coping with a mental illness is challenging. Talk to your doctor or therapist about improving your coping skills, and consider these tips:

• Learn about your mental illness. Your doctor or therapist can provide you with information or may recommend classes, books or websites. Include your family, too — this can help the people who care about you understand what you're going through and learn how they can help.
• Join a support group. Connecting with others facing similar challenges may help you cope. Support groups for mental illness are available in many communities and online. One good place to start is the National Alliance on Mental Illness.
• Stay connected with friends and family. Try to participate in social activities, and get together with family or friends regularly. Ask for help when you need it, and be upfront with your loved ones about how you're doing.
• Keep a journal. Or jot down brief thoughts or record symptoms on a smartphone app. Keeping track of your personal life and sharing information with your therapist can help you identify what triggers or improves your symptoms. It's also a healthy way to explore and express pain, anger, fear and other emotions.

Preparing for your appointment

Whether you schedule an appointment with your primary care provider to talk about mental health concerns or you're referred to a mental health professional, such as a psychiatrist or psychologist, take steps to prepare for your appointment.

If possible, take a family member or friend along. Someone who has known you for a long time may be able to share important information, with your permission.

What you can do

Before your appointment, make a list of:

• Any symptoms you or people close to you have noticed, and for how long
• Key personal information, including traumatic events in your past and any current, major stressors
• Your medical information, including other physical or mental health conditions
• Any medications, vitamins, herbal products or other supplements you take, and their dosages
• Questions to ask your doctor or mental health professional

Questions to ask may include:

• What type of mental illness might I have?
• Why can't I get over mental illness on my own?
• How do you treat my type of mental illness?
• Will talk therapy help?
• Are there medications that might help?
• How long will treatment take?
• What can I do to help myself?
• Do you have any brochures or other printed material that I can have?
• What websites do you recommend?

Don't hesitate to ask any other questions during your appointment.

What to expect from your doctor

During your appointment, your doctor or mental health professional is likely to ask you questions about your mood, thoughts and behavior, such as:

• When did you first notice symptoms?
• How is your daily life affected by your symptoms?
• What treatment, if any, have you had for mental illness?
• What have you tried on your own to feel better or control your symptoms?
• What things make you feel worse?
• Have family members or friends commented on your mood or behavior?
• Do you have blood relatives with a mental illness?
• What do you hope to gain from treatment?
• What medications or over-the-counter herbs and supplements do you take?
• Do you drink alcohol or use recreational drugs?

Your doctor or mental health professional will ask additional questions based on your responses, symptoms and needs. Preparing and anticipating questions will help you make the most of your time with the doctor.

• Diagnostic and Statistical Manual of Mental Disorders DSM-5. 5th ed. Arlington, Va.: American Psychiatric Association; 2013. https://dsm.psychiatryonline.org. Accessed April 8, 2019.
• Dual diagnosis. National Alliance on Mental Illness. https://www.nami.org/Learn-More/Mental-Health-Conditions/Related-Conditions/Dual-Diagnosis. Accessed April 8, 2019.
• Practice Guidelines for the Psychiatric Evaluation of Adults. 3rd ed. Arlington, Va.: American Psychiatric Association; 2013. http://psychiatryonline.org. Accessed April 1, 2019.
• Understanding psychotherapy and how it works. American Psychological Association. https://www.apa.org/helpcenter/understanding-psychotherapy. Accessed April 1, 2019.
• Asher GN, et al. Complementary therapies for mental health disorders. Medical Clinics of North America. 2017;101:847.
• Complementary health approaches. National Alliance on Mental Illness. https://www.nami.org/Learn-More/Treatment/Complementary-Health-Approaches. Accessed April 4, 2019.
• Warning signs of mental illness. American Psychiatric Association. https://www.psychiatry.org/patients-families/warning-signs-of-mental-illness. Accessed April 4, 2019.
• Helping a loved one cope with mental illness. American Psychiatric Association. https://www.psychiatry.org/patients-families/helping-a-loved-one-cope-with-a-mental-illness. Accessed April 4, 2019.
• What is mental illness? American Psychiatric Association. https://www.psychiatry.org/patients-families/what-is-mental-illness. Accessed April 4, 2019.
• For friends and family members. MentalHealth.gov. https://www.mentalhealth.gov/talk/friends-family-members. Accessed April 4, 2019.
• For people with mental health problems. MentalHealth.gov. https://www.mentalhealth.gov/talk/people-mental-health-problems. Accessed April 4, 2019.
• Brain stimulation therapies. National Institute of Mental Health. https://www.nimh.nih.gov/health/topics/brain-stimulation-therapies/brain-stimulation-therapies.shtml. Accessed April 4, 2019.
• Mental health medications. National Institute of Mental Health. https://www.nimh.nih.gov/health/topics/mental-health-medications/index.shtml. Accessed April 4, 2019.
• Psychotherapies. National Institute of Mental Health. https://www.nimh.nih.gov/health/topics/psychotherapies/index.shtml. Accessed April 4, 2019.
• Muesham D, et al. The embodied mind: A review on functional genomic and neurological correlates of mind-body therapies. Neuroscience and Biobehavioral Reviews. 2017;73:165.
• Suicide in America: Frequently asked questions. National Institute of Mental Health. https://www.nimh.nih.gov/health/publications/suicide-faq/index.shtml. Accessed April 10, 2019.
• Types of mental health professionals. National Alliance on Mental Illness. https://www.nami.org/Learn-More/Treatment/Types-of-Mental-Health-Professionals. Accessed April 8, 2019.
• Risk and protective factors. Substance Abuse and Mental Health Services Administration. Accessed April 8, 2019.
• Newman L, et al. Early origins of mental disorder — Risk factors in the perinatal and infant period. BMC Psychiatry. 2016;16:270.
• Treatment settings. National Alliance on Mental Illness. https://www.nami.org/Learn-More/Treatment/Treatment-Settings. Accessed April 10, 2019.
• Hall-Flavin DK (expert opinion). Mayo Clinic, Rochester, Minn. May 18, 2019.
• Intervention: Help a loved one overcome addiction
• Mental health: Overcoming the stigma of mental illness

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What Is Clinical Depression?

Symptoms of clinical depression include feelings of sadness and a lack of energy

Nancy Schimelpfening, MS is the administrator for the non-profit depression support group Depression Sanctuary. Nancy has a lifetime of experience with depression, experiencing firsthand how devastating this illness can be.

Daniel B. Block, MD, is an award-winning, board-certified psychiatrist who operates a private practice in Pennsylvania.

Verywell / Catherine Song

Depression is one of the most common mental health disorders. In fact, it's estimated that 1 in 5 adults in the United States have received a depression diagnosis in their lifetime.

Depression exists on a continuum of severity, ranging from relatively mild, transient states of low mood to severe, long-term symptoms that have a major impact on a person’s quality of life. Depression is often described as being mild , moderate , or severe. When a person’s symptoms have reached the chronic end of the spectrum and require professional treatment, it's typically referred to as clinical depression.

Although depression can take on many forms and may be categorized in several different ways, there are two primary types of clinical depression as defined by the Diagnostic and Statistical Manual of Mental Disorders (DSM–5): major depressive disorder (unipolar depression) and the depressive phase of bipolar disorder.

Symptoms of Clinical Depression

People experience depression in different ways. Some people only have a few symptoms, while others have many. Some symptoms might get better over time while others may get worse.

It’s important to work with your mental health care team to identify which depression symptoms you experience and determine the best approach to treating them. For each type of clinical depression, as well as the various subtypes, there are some symptoms or features that are common in those who experience it. 

Major Depression

Also known as major depressive disorder or unipolar depression, this form is what most people think of when they hear “depression.” Major depression is typically characterized by the following symptoms:

• Sadness, feelings of emptiness
• Loss of enjoyment of hobbies, work, other activities
• Appetite changes, weight loss or gain
• Trouble sleeping (too much or too little)
• Feeling "slowed down" or being excessively agitated
• Tiredness, fatigue, lack of energy
• Physical symptoms and pain (such as body aches, stomach upset, headaches)
• Feelings of worthlessness or guilt
• Problems with concentration or focus
• Inability to make decisions or poor decision-making
• Thinking about death or dying ; planning or attempting suicide

If you are having suicidal thoughts, contact the National Suicide Prevention Lifeline at 988 for support and assistance from a trained counselor. If you or a loved one are in immediate danger, call 911.

For more mental health resources, see our National Helpline Database .

Psychotic Depression

Psychotic depression is considered part of the unipolar depression spectrum at its most severe and not a separate form of depression. People who have mental health conditions that cause them to experience hallucinations or delusions may also have a form of depression.

Psychotic depression can manifest with hallucinations that are focused on death or being gravely ill. Delusions also might be related to other major life stressors, such as losing a job or being poverty stricken.

Depressive Phase of Bipolar Disorder

Clinical depression can also be a feature of another mental health condition called bipolar disorder . People with bipolar disorder tend to alternate between periods of depression and periods of greatly elevated mood called mania . 

In the depressive phase, symptoms can be very similar major depression. During the manic phase , symptoms at the opposite end of the spectrum are more likely, such as:

• Increased energy
• Sleeplessness
• Irritability
• Rapid speech
• Hypersexual behavior
• Racing thoughts
• Grandiose ideas
• Greatly increased activity
• Impulsivity
• Poor judgment

Other forms of depression are classified a bit differently, often because they occur in specific situations or require different treatment approaches. 

Postpartum Depression

Postpartum depression is depression that occurs after a person gives birth and can persist well into the first year postpartum. While it is common and treatable, it needs to be promptly and correctly diagnosed. While many new parents experience ups and downs when caring for a new baby (especially on little sleep) the typical stress and anxiety of the newborn stage usually last only a few weeks, whereas postpartum depression is more serious and can last long after the birth of a child. 

Premenstrual Dysphoric Disorder (PMDD)

With PMDD , people who have a menstrual cycle become depressed prior to the onset of their period. Hormonal changes can cause mild menstrual symptoms (PMS) in anyone who has periods, but it’s not the same as PMDD. In PMDD, symptoms are more intense, persistent, and require treatment. 

Seasonal Affective Disorder (SAD)

Some people experience bouts of depression at certain times of the year, most often in the dark winter months (though it can occur at any time of year). It's referred to as seasonal affective disorder.

The lack of sunlight has been associated with low mood for a number of reasons, including vitamin D deficiency and an increased likelihood that someone will be spending more time alone or at home (potentially due to colder weather and shorter days). Several holidays and celebrations also occur during this time of the year, which can contribute to depression and anxiety in some people.

Dysthymia (Persistent Depressive Disorder)

If you have an episode of depression that lasts two years or more, you may be diagnosed with dysthymia . Sometimes, major depression also develops or alternates with periods of persistent depression. 

Situational Depression

Many people will experience a period of depression in their lifetime in response to a specific event. Losing a job, caring for a parent or child who is ill, getting divorced, or experiencing a trauma such as a robbery, car accident, or a house fire are just a few examples of stressors that could lead to situational depression .

Unlike more persistent forms of depression, situational depression can usually be treated and improves in response to positive change in a person’s situation, such as getting a new job and having social support, counseling, and in some cases, medication. 

The DSM-5 also mentions other forms of depression classified as atypical . If you are having symptoms of depression, the doctors and mental health professionals you’re working with will evaluate your symptoms carefully.

You may experience more than one form of depression in your lifetime. If you are a parent or young person, newer entries in the DSM-5 also categorize forms of depression that are more specific to children and teens. 

Depression in Children and Teens

It used to be believed that children couldn’t be depressed, but we now know that’s not true. Children, teens, and young adults can experience depression, but it may not look the same as it does in adults. 

Children may not yet have the language skills and emotional awareness to express exactly what they are feeling. An adult who is depressed may feel profound sadness , whereas a depressed child may appear angry, frustrated, and irritable. 

Symptoms of depression in school-aged children and teens may interfere with school work, social activities, or friendships. For example, a child who is depressed may begin to make poor grades in school, lose interest in after school activities like sports, or no longer want to hang out with friends. 

As with teens and adults, children who are experiencing depression may also have trouble sleeping, lose their appetite, or have unexplained physical symptoms such as headaches and stomachaches. 

If you're concerned that your child or teen is depressed, talk to your pediatrician. There are some medical conditions that can cause depression which will need to be ruled out . If your child is diagnosed with depression, finding the appropriate treatment is critical to their well-being. 

You can help by putting together a network of mental health professionals, doctors, teams at school, as well as friends and people in the community, who can support your family as you learn about managing your child’s depression. 

Different types of clinical depression include major depressive disorder, psychotic depression, depressive phases of bipolar disorder, postpartum depression, premenstrual dysphoric disorder, and seasonal affective disorder. Depression can also occur in children, although symptoms may present somewhat differently than in adults.

Causes of Clinical Depression

The causes of depression are not completely understood, but it’s believed that there are several key factors, including genetics and environment, that make a person more likely to become depressed.

Some Common Causes of Depression

Researchers have particularly been interested in investigating whether depression is an inherited condition. A major theory is that certain genetic changes make neurotransmitters (mood-regulating chemicals in the brain) ineffective or scarce. 

The other major component is environmental triggers which may make a person who is genetically predisposed to depression more likely to develop it. Certain factors that make it more likely a person will experience clinical depression include:

• A family history of depression (especially a parent or sibling)
• Experiencing a traumatic event or major life change (such as loss of a job, death or serious illness of a spouse, divorce)
• Financial troubles (such as debt and worries about paying for big expenses)
• Being very ill or injured (such as from cancer or a car accident), needing to have surgery or undergo medical treatment, or having to manage a chronic and/or progressive health condition (such as multiple sclerosis)
• Caring for a loved one (spouse, child, parent) who has a major illness, injury, or disability
• Taking certain medications that can cause symptoms associated with depression (including medications used to treat depression)
• Using illegal drugs and/or misusing alcohol 

If you have experienced a form of depression before, you may be more likely to experience it again or develop another form in response to certain stressors or life changes (such as having a baby). 

Diagnosis of Clinical Depression

Your doctor may be the first health care professional to talk to you about depression. If you feel depressed, your doctor may want to start by ruling out medical conditions, such as thyroid disorders, that can cause depression symptoms. While your primary care doctor can diagnose clinical depression, they may want also you to be evaluated by someone with psychological expertise.

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If you will be taking medication to treat depression, your doctor may refer you to a psychiatrist . This type of doctor has special training for prescribing and monitoring medications used to treat mental health conditions. They can make sure that the medication you are taking for depression is the best fit for the form you have and that the dose is the safest and most effective for you.

Co-Occurring Conditions

In addition to physical medical conditions that can cause symptoms of depression or increase the likelihood someone will become depressed, there are also several other mental health conditions that people with depression may be diagnosed with.

When a person who has depression also has another mental health condition, it's referred to as a "co-occurring" condition. Common co-occurring conditions in people with clinical depression include:

• Anxiety disorders
• Obsessive-compulsive disorde r (OCD)
• Post-traumatic stress disorder (PTSD)
• Attention deficit and hyperactivity disorder (ADHD)
• Autism spectrum disorders
• Eating disorders and body dysmorphia
• Alcohol and drug use disorders

Sleep disorders, irritable bowel syndrome (IBS), headaches, chronic pain, and fibromyalgia are other conditions that may co-occur with depression.

Treatment for Clinical Depression

There are several different ways to treat depression . You may need to try different approaches or combine more than one method. What works well for one person with depression may not work for someone else. Your health care team will inform you of the options that are safe for you. 

If your symptoms are severe or your mental health team feels you are at risk of hurting yourself or someone else, you may need to start treating your depression in the hospital, an inpatient mental health care facility, and/or take part in outpatient treatment programs.

Keep in mind that the process can take time. You also may need to adjust the way you manage your depression symptoms in response to changes in your life.

One of the first-line treatments for clinical depression is medication. There are several different types of antidepressants , however, those belonging to a class called selective serotonin reuptake inhibitors (SSRIs) are the most frequently prescribed. 

SSRIs such as Prozac (fluoxetine), Zoloft (sertraline), Lexapro (escitalopram), and Paxil (paroxetine) are generally preferred by both doctors and patients because they tend to have fewer and less bothersome side effects compared to older classes of antidepressants. Other major classes of antidepressants include:

• Serotonin and norepinephrine reuptake inhibitors ( SNRIs ) such as Effexor (venlafaxine), Cymbalta (duloxetine), and Pristiq (desvenlafaxine).
• Monoamine oxidase inhibitors ( MAOIs ) such as Marplan (isocarboxazid), Nardil (phenelzine), and Parnate (tranylcypromine). MAOIs are not safe to use with SSRIs.
• Atypical antidepressants such as Wellbutrin (bupropion).
• Tricyclic antidepressants such as Tofranil (imipramine) and Elavil (amitriptyline). Tricyclics are of an older class of antidepressant medications that are not prescribed as often due to their side effects.

Your doctor or psychiatrist may recommend you take more than one type of antidepressant or add another pharmaceutical treatment, such as anti-anxiety medications , to your routine.

Antidepressants can worsen some mental health conditions . For this reason, it’s very important to work closely with your doctor and therapist to ensure you have the most accurate diagnosis, and that the treatment you choose is a safe and effective way to manage your symptoms.

Before you start taking antidepressants, you should know that it can take some time for the medication to work. Your doctor or psychiatrist will likely have you try taking the medication for a certain period of time—usually several weeks or months—before adjusting the dose or trying a different medication. 

After starting an antidepressant it can take several weeks for you to feel a difference in your symptoms. It may also take weeks for side effects to resolve.

Even if you have side effects or don't feel your medication is working, do not stop taking it suddenly. This can cause withdrawal, which can be serious. Talk to your doctor if you want to stop taking your antidepressant.

If your doctor wants you to switch to a different medication, they will instruct you to gradually lower your dose over several weeks. Tapering off antidepressants can help prevent symptoms of withdrawal. 

In some cases, your doctor may start you on a new medication while you are still slowly reducing your dose of your old one. If you are changing antidepressants or adjusting to a new dose, it’s very important that you stay in touch with your mental health care team. 

The health care provider prescribing medication will discuss the risks and benefits with you. There may be some circumstances when taking a particular drug to treat depression would not be advised or you may need an adjusted dose.

For example, if you are pregnant or breastfeeding, your doctor will talk to you about any risks associated with the medications you take or are considering taking. They will help you evaluate the risks and benefits of each decision.

Children, teens, and young adults with depression may have serious side effects when taking certain antidepressants. People under the age of 25 taking these medications can be at an increased risk of worsening symptoms, including suicidal ideation.

Research has indicated that the risk of attempting suicide can also be markedly increased, which is why these medications get a black box warning from the FDA. 

Psychotherapy

Psychotherapy is another popular choice for treating depression, both on its own and combined with antidepressants. Psychotherapy involves working with a therapist, either by yourself or with a group, to talk through how you feel, your experiences, and how you view yourself and the world.

Together, you may be able to identify certain underlying causes or triggers that influence your depression. Once you are aware of them, you can begin to work on effective coping strategies. 

One example is cognitive-behavioral therapy , which research has found can be effective for treating depression.   Other studies indicate the combination of medication and psychotherapy may be the most effective treatment, as each method targets depression in a different way.

When both are used together, the underlying chemical imbalance and individual psychological factors can be addressed.  

If you have depression, therapy can help you better understand yourself and your depression symptoms. It’s also an essential component of your support system. If you are taking antidepressant medications, a psychiatrist can help by monitoring your dose to ensure it continues to work well and be safe.

There can be barriers to accessing therapy, such as a lack of providers where you live, not having reliable transportation, and cost. A relatively new option you may want to learn more about is using an internet connection or cellphone to communicate with a mental health provider. These options may also be more appealing to teens with depression.

Therapists can use email or text messaging, video chatting, or voice calls to connect with people who need help managing depression. You can also download mental health apps on your smartphone or tablet to help you track your symptoms or communicate with your provider. There are even some apps that offer interactive self-help resources and games to help you practice new coping skills, like mindfulness.

Treatment for clinical depression typically involves the use of medications, psychotherapy, or a combination of the two. 

Alternative and Complementary Treatment

You may choose to explore complementary or alternative therapies for depression. One of the most common is an herbal supplement called St. John’s wort . 

The FDA has not officially approved St. John’s wort to treat depression, but it is often suggested by alternative health practitioners. Research has indicated that St. John’s wort may be beneficial for some people who have symptoms of depression.   

The supplement comes in various doses and preparations and can be purchased over-the-counter and at most health food stores. There is no standard dose and you may want to work with a practitioner as you undertake some “trial and error” to determine the dose that feels right for you. 

Similar to how prescription medications affect neurotransmitter levels, St. John’s wort may influence the levels of a specific neurotransmitter called serotonin in the brain. When people have too little serotonin, they can feel depressed. Increasing the amount of serotonin can help improve symptoms. However, having too much serotonin can lead to a serious condition called serotonin syndrome . 

If you are taking a medication that carries a risk of increasing your serotonin levels too much, your doctor will teach you about the signs of serotonin syndrome to watch for. They will also want you to make sure that you never take more than one medication, herb, or supplement that can raise your serotonin levels at the same time (including St. John’s wort). 

While St. John’s wort may be helpful for some people with mild-to-moderate depression, it can also interact with a number of prescription medications. If you are already taking an antidepressant, do not start taking St. John’s wort until you’ve discussed it with your doctor.  

Coping With Clinical Depression

Clinical depression can be disabling and may make it difficult to function normally at work, school, and home. Medication and therapy can be valuable components of depression treatment, but each individual person with depression will need to find their own ways of coping with the condition. 

If you have depression, there are a variety of avenues you can explore to help you manage your symptoms. Depending on your lifestyle, physical health, and preferences, you can work with your mental health care team to develop the strategies that work best and feel like a good fit for you.

Physical Activity

Research has shown that the physical and mental symptoms of depression may benefit from getting your body moving. When you exercise, your body releases endorphins, which can boost your mood. Regular physical activity also helps keep your muscles and bones strong, improves cardiovascular health, and promotes a healthy weight.

Exercise not only helps keep your body and mind in working order, but it can give you the opportunity to connect with others.

Even if you prefer working out alone, going to the gym or taking your dog for a stroll through the park can help lessen feelings of isolation that come with depression. Other ideas include joining a community sports team or taking a group fitness, dance, or yoga class.

Hobbies and Creativity

A major symptom of depression is losing interest in hobbies or activities you used to enjoy. Motivation and focus can be challenged when you have depression. It's not easy, but finding ways to keep your mind engaged is an important part of learning to cope with depression.

You may find it helpful to start with a hobby or activity you already know you like and try to give yourself small milestones to work toward. While you may not feel up to teaching yourself an entirely new skill if you’re depressed, keeping your mind engaged without putting too much pressure on yourself can be a healthy strategy for coping . It can also help you reconnect with the parts of your life you might feel you have “lost” to depression or even find an entirely new interest or hobby.

If you enjoy being creative, you may find these activities help you deal with your depression symptoms. It can also be an opportunity for you to express how you are feeling in a new way. You may even be able to use your creativity as part of your therapy. 

Kids especially benefit from using creative expression to help them communicate and understand feelings of depression. Other creative outlets such as reading and making music can be coping strategies, though they may be difficult to stick with if you are having trouble focusing.

You can also use these activities as a way to encourage yourself if you are having a hard time leaving the house or have not had an interest in social activities.

For example, one day you may find a quiet afternoon alone at an art gallery or museum feels doable. On another day, you may feel up to seeing a movie or attending a concert or theatrical performance with a friend. 

Self-Care and Staying Connected

Depression can make it very hard to take care of yourself physically, emotionally, mentally, and spiritually. If you are struggling with self-care such as showering or cleaning your home , buying groceries, working, or other day-to-day pursuits, you may feel guilty and ashamed. 

It can feel impossible to ask for help, but even making small, healthy changes can make coping with depression symptoms more manageable. Having help tidying up your room, getting your trash taken out, stocking up your kitchen with easy-to-prepare meals, and making sure you can get to your doctor or therapy appointments are just a few ideas. 

It’s also important to stay connected to others . Depression can be incredibly isolating. In fact, you may feel like you need to stay far away from other people–even the people you love most. 

Sometimes, especially when you are first diagnosed, you may not feel ready to talk to your loved ones about your depression. At first, it might be easier to explore how you are feeling with other people who are going through the same process. 

Start by asking your doctor or therapist about support groups in your local community. If you don’t have a wide network of support or you do not feel ready to talk to people face-to-face, you may find it helpful to seek out online depression support groups .

Message boards, forums, and social media groups can be a place to share experiences that may feel less intense for you, as it provides a little distance and sense of anonymity. 

Online support networks may continue to be valuable to you even after you have opened up about your depression with your loved ones and have the support of your mental health team. Whether you are primarily connecting with others in-person or talk to them online, the most important thing is that you feel safe doing so.

A Word From Verywell

If you or a loved one has clinical depression, you may be overwhelmed by all the different aspects of living with mental illness there are to consider. While everyone's experience with depression will be unique, there are some commonalities when it comes to symptoms, causes, and treatment.

You will want to discuss your specific symptoms with your mental health care team. They will help you find the safest and most effective treatment for you, which may include medication, therapy, or both.

Your support network, whether in-person or online, can be there for you as you learn to cope with the symptoms of depression. When you're depressed, it can be hard to ask others for help. It's important to remember that you don't need to address all the different aspects of living with depression at the same time—and you don't have to face it alone.

Centers for Disease Control and Prevention.  National, State-Level, and County-Level Prevalence Estimates of Adults Aged ≥18 Years Self-Reporting a Lifetime Diagnosis of Depression — United States, 2020 .

Harvard Health Publishing. What causes depression? Harvard Health.

Mental Health America. Co-Occurring Disorders And Depression .

ADAA. Co-Occurring Disorders . Anxiety and Depression Association of America website.

DeRubeis RJ, Hollon SD, Amsterdam JD, et al. Cognitive therapy vs medications in the treatment of moderate to severe depression .  Arch Gen Psychiatry.  2005;62(4):409–416. doi:10.1001/archpsyc.62.4.409

Arnow BA, Constantino MJ. Effectiveness of psychotherapy and combination treatment for chronic depression .  Journal of Clinical Psychology . 2003;59(8):893-905. doi:10.1002/jclp.10181

Ng QX, Venkatanarayanan N, Ho CYX. Clinical use of Hypericum perforatum (St John’s wort) in depression: A meta-analysis .  Journal of Affective Disorders . 2017;210:211-221. doi:10.1016/j.jad.2016.12.048

Harvard Health Publishing. Exercise is an all-natural treatment to fight depression . Harvard Health.

American Psychological Association. Depression .

National Alliance on Mental Illness. Depression overview .

The National Institute of Mental Health Information Resource Center. Depression .

By Nancy Schimelpfening Nancy Schimelpfening, MS is the administrator for the non-profit depression support group Depression Sanctuary. Nancy has a lifetime of experience with depression, experiencing firsthand how devastating this illness can be.  

About Mental Health

What is mental health?

Mental health includes our emotional, psychological, and social well-being. It affects how we think, feel, and act. It also helps determine how we handle stress, relate to others, and make healthy choices. 1 Mental health is important at every stage of life, from childhood and adolescence through adulthood.

Why is mental health important for overall health?

Mental and physical health are equally important components of overall health.  For example, depression increases the risk for many types of physical health problems, particularly long-lasting conditions like diabetes , heart disease , and stroke. Similarly, the presence of chronic conditions can increase the risk for mental illness. 2

Can your mental health change over time?

Yes, it’s important to remember that a person’s mental health can change over time, depending on many factors.  When the demands placed on a person exceed their resources and coping abilities, their mental health could be impacted. For example, if someone is working long hours, caring for a relative, or experiencing economic hardship, they may experience poor mental health.

How common are mental illnesses?

Mental illnesses are among the most common health conditions in the United States.

• More than 1 in 5 US adults live with a mental illness.
• Over 1 in 5 youth (ages 13-18) either currently or at some point during their life, have had a seriously debilitating mental illness. 5
• About 1 in 25 U.S. adults lives with a serious mental illness, such as schizophrenia, bipolar disorder, or major depression. 6

What causes mental illness?

There is no single cause for mental illness. A number of factors can contribute to risk for mental illness, such as

• Adverse Childhood Experiences , such as trauma or a history of abuse (for example, child abuse, sexual assault, witnessing violence, etc.)
• Experiences related to other ongoing (chronic) medical conditions, such as a traumatic brain injury , cancer, or diabetes
• Biological factors or chemical imbalances in the brain
• Use of alcohol or drugs
• Having feelings of loneliness or isolation

People can experience different types of mental illnesses or disorders, and they can often occur at the same time. Mental illnesses can occur over a short period of time or be episodic. This means that the mental illness comes and goes with discrete beginnings and ends. Mental illness can also be ongoing or long-lasting.

There are more than 200 types of mental illness. Some of the main types of mental illness and disorders are listed here .

• Strengthening Mental Health Promotion . Fact sheet no. 220. Geneva, Switzerland: World Health Organization.
• Chronic Illness & Mental Health . Bethesda, MD: National Institutes of Health, National Institute of Mental Health. 2015.
• Kessler RC, Angermeyer M, Anthony JC, et al. Lifetime prevalence and age-of-onset distributions of mental disorders in the World Health Organization’s World Mental Health Survey Initiative. World Psychiatry. 2007;6(3):168-176.
• Key substance use and mental health indicators in the United States: Results from the 2015 National Survey on Drug Use and Health. Rockville, MD: Center for Behavioral Health Statistics and Quality. Substance Abuse and Mental Health Services Administration. 2016.
• Merikangas KR, He J, Burstein M, et al. Lifetime Prevalence of Mental Disorders in US Adolescents: Results from the National Comorbidity Study-Adolescent Supplement (NCS-A). Journal of the American Academy of Child and Adolescent Psychiatry. 2010;49(10):980-989. doi:10.1016/j.jaac.2010.05.017.
• Health & Education Statistics . Bethesda, MD: National Institute of Mental Health. National Institutes of Health. 2016.
• Kessler RC, Chiu WT, Demler O, Walters EE. Prevalence, Severity, and Comorbidity of Twelve-month DSM-IV Disorders in the National Comorbidity Survey Replication (NCS-R). Archives of general psychiatry. 2005;62(6):617-627. doi:10.1001/archpsyc.62.6.617.Substance Abuse and Mental Health Services Administration, Center for Behavioral Health Statistics and Quality. (2016). Key substance use and mental health indicators in the United States: Results from the 2015 National Survey on Drug Use and Health. Rockville, MD.
• Rui P, Hing E, Okeyode T.  National Ambulatory Medical Care Survey: 2014 State and National Summary Tables. Atlanta, GA: National Center for Health Statistics. Centers for Disease Control and Prevention. 2014.
• Web-based Injury Statistics Query and Reporting System (WISQARS) . Atlanta, GA: National Center for Injury Prevention and Control. Centers for Disease Control and Prevention. 2015.
• Insel, T.R. Assessing the Economic Costs of Serious Mental Illness. Am J Psychiatry. 2008 Jun;165(6):663-5. doi: 10.1176/appi.ajp.2008.08030366.
• HCUP Facts and Figures: Statistics on Hospital-based Care in the United States, 2009. Rockville, MD: Agency for Healthcare Research and Quality. 2009.
• Reeves, WC et al. CDC Report: Mental Illness Surveillance Among Adults in the United States. MMWR Morb Mortal Wkly Rep 2011;60(03);1-32.
• Parks, J., et al. Morbidity and Mortality in People with Serious Mental Illness. Alexandria, VA: National Association of State Mental Health Program Directors Council. 2006.

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Introduction

Somatic symptom and related disorders, clinical features and studies of pediatric somatic symptom and related disorders, somatic symptom and related disorders and the ed, treatment strategies, adverse effects of psychiatric medications, antipsychotic adverse effects, neuroleptic malignant syndrome, serotonin syndrome, children with special needs, autism spectrum and developmental disorders, mental health screening, the advantages of the ed setting, feasibility and acceptability of ed mental health screening, ed mental health screens, lead authors, american academy of pediatrics committee on pediatric emergency medicine, 2014–2015, former members and liaisons, 2013-2015, american college of emergency physicians pediatric emergency medicine committee, 2013–2014, former committee members, evaluation and management of children with acute mental health or behavioral problems. part ii: recognition of clinically challenging mental health related conditions presenting with medical or uncertain symptoms.

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Thomas H. Chun , Sharon E. Mace , Emily R. Katz , AMERICAN ACADEMY OF PEDIATRICS Committee on Pediatric Emergency Medicine , AMERICAN COLLEGE OF EMERGENCY PHYSICIANS Pediatric Emergency Medicine Committee; Evaluation and Management of Children With Acute Mental Health or Behavioral Problems. Part II: Recognition of Clinically Challenging Mental Health Related Conditions Presenting With Medical or Uncertain Symptoms. Pediatrics September 2016; 138 (3): e20161573. 10.1542/peds.2016-1573

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Part I of this clinical report ( http://www.pediatrics.org/cgi/doi/10.1542/peds.2016-1570 ) discusses the common clinical issues that may be encountered in caring for children and adolescents presenting to the emergency department (ED) or primary care setting with a mental health condition or emergency and includes the following:

Medical clearance of pediatric psychiatric patients

Suicidal ideation and suicide attempts

Involuntary hospitalization

Restraint of the agitated patient

Verbal restraint

Chemical restraint

Physical restraint

Coordination with the medical home

Part II discusses the challenges a pediatric clinician may face when evaluating patients with a mental health condition, which may be contributing to or a complicating factor for a medical or indeterminate clinical presentation. Topics covered include the following:

Somatic symptom and related disorders

Adverse effects of psychiatric medications

Antipsychotic adverse effects

Neuroleptic malignant syndrome

Serotonin syndrome

Children with special needs (autism spectrum disorders [ASDs] and developmental disorders [DDs])

Mental health screening

The report is written primarily from the perspective of ED clinicians, but it is intended for all clinicians who care for children and adolescents with acute mental health and behavioral problems. An executive summary of this clinical report can be found at http://www.pediatrics.org/cgi/doi/10.1542/peds.2016-1574 .

The Diagnostic and Statistical Manual of Mental Disorders, Fifth Edition recognizes 7 distinct somatic symptom and related disorders, including somatic symptom disorder, illness anxiety disorder, conversion disorder (functional neurologic symptom disorder), psychological factors affecting other medical conditions, factitious disorder, other specified somatic symptom and related disorder, and unspecified somatic symptom and related disorder. 1 Each disorder has specific diagnostic criteria, which apply to both adults and children and which are not adjusted for children. All these disorders refer to an individual’s subjective experience of physical symptoms. These diagnoses can also be applied to situations in which the level of distress or disability is thought to be disproportionate to what is typically associated with the physical findings. For example, when a medical condition is present, if the physical problems do not fully explain the reported symptoms or severity, a somatic symptom and related disorder may apply. 2  

Additional criteria for somatic symptom disorders include the requirement that the complaints or fixations are not associated with material gain, nor are they intentionally produced. 3 Symptoms that are intentionally created are classified as factitious disorders; those that result in material gain are categorized as malingering. Lastly, the symptoms result in significant impairment in psychosocial functioning (eg, relationships with family or friends, academic or occupational difficulties). 1  

Epidemiologic studies have found that somatic symptom and related disorders are both common and a significant contributor to health care usage and costs. In adult primary care populations, between 10% and 15% of patients have a diagnosis of 1 of these disorders. 4 Among children and adolescents, recurrent abdominal pain and headaches account for 5% and between 20% and 55% of pediatric office visits, respectively; 10% of adolescents report frequent headaches, chest pain, nausea, and fatigue. 5 Patients with somatic symptom and related disorders use all types of medical services (eg, primary, specialty, ED, and mental health care) more frequently, 4 , 6 , – 8 are more likely to “doctor shop,” 4 and in 2005, were estimated to have incrementally added $265 billion to the cost of health care in the United States. 9  

The clinical presentations of somatic symptom and related disorders are myriad, most often involving neurologic, pain, autonomic, or gastrointestinal tract symptoms ( Table 1 ). Children and adolescents often report such symptoms 10 , 11 and often have multiple visits for these symptoms in primary care and other settings. 3 , 5 , 12 , 13 Vague, poorly described complaints, recent or current stressful events, symptoms that fluctuate with activity or stress, and lack of physical findings and laboratory abnormalities are common. 3  

Common Symptoms of Somatic Symptom and Related Disorders 14  

Symptoms of pediatric somatic symptom and related disorders often do not meet strict Diagnostic and Statistical Manual of Mental Disorders, Fifth Edition diagnostic criteria and defy categorization. Other difficulties in caring for patients with these disorders in the ED are that few patients will have received a formal diagnosis, and ED clinicians rarely have access to sufficient clinical information to confirm the diagnosis. 15 , – 17 In addition, the diagnosis of a “psychosomatic” illness can be stigmatizing to patients and families, resulting in them feeling unheard, disrespected, and defensive about their symptoms. 5 For these and other reasons, some prefer the term “medically unexplained symptoms”. 2 , 6 , 18 , 19  

Several studies, including 1 performed jointly in the Pediatric Research in Office Settings and Ambulatory Sentinel Practice Network collaboratives, have identified demographic and risk factors associated with pediatric somatic symptom and related disorders. 2 , 8 , 20 , 21 Patients who are adolescents, female, from minority ethnicities, from nonintact families, or from urban dwellings; who have past histories of psychological trauma; whose parents have lower education levels; and who have other family members with somatic symptom and related disorders are more likely to present with unexplained medical symptoms. Such patients are also at much higher risk of comorbid psychiatric problems. 8  

Other studies have approached this topic by investigating the prevalence of and relationships between psychiatric conditions in patients with unexplained medical symptoms. Emiroğlu et al 22 studied 31 patients referred to a pediatric neurology clinic for headache, vertigo, and syncope. When comprehensive testing did not reveal an identifiable medical cause for their symptoms, the patients were interviewed by a child psychiatrist. A large majority (93.5%) were found to have a diagnosable disorder according to Diagnostic and Statistical Manual of Mental Disorders, Fourth Edition criteria, the most common being mood and somatic symptom and related disorders. Other pediatric headache studies have found similar results. 23 , 24 Guidetti et al 25 followed patients for 8 years after referral to a pediatric neurology headache clinic. At follow-up, persistence or worsening of headaches was highly associated with the presence of comorbid psychiatric conditions, and resolution of headaches strongly correlated with the absence of mental health conditions. In this study, the most common mental health conditions were anxiety disorders and depression.

Other studies in other settings echo these findings. In a pediatric cardiology clinic study, Tunaoglu et al 26 reported a prevalence of 74% for psychiatric disorders, primarily depression, anxiety, and somatic symptom and related disorders, in patients referred for chest pain with normal medical workups. Campo et al 27 recruited patients from a pediatric primary care office. Using standardized psychiatric interviews, they found that patients with recurrent abdominal pain were significantly more likely to be diagnosed with anxiety (79%) and depressive disorders (43%) than controls. In a study from a pediatric rheumatology clinic, Kashikar-Zuck et al 28 also conducted standardized psychiatric interviews among patients with juvenile fibromyalgia. A high prevalence of current and lifetime anxiety and mood disorders was detected in this population.

Somatic symptom and related disorders are a particularly vexing problem in the ED because of the potential harm to patients that may result from diagnostic uncertainty. It is understandable that a patient with 1 of these disorders might undergo extensive, invasive testing such as a lumbar puncture, be exposed to radiographic studies with ionizing radiation, or be given potent medications to treat their symptoms, which in turn could result in significant respiratory, cardiac, central nervous system (CNS), or hematologic adverse effects, potentially necessitating additional medications or procedures such as endotracheal intubation and mechanical ventilation to treat these adverse effects.

Psychogenic nonepileptic seizures (PNES, previously called “pseudoseizures”) in pediatric ED patients are an illustrative example of this conundrum. In their review of identified PNES patients (the authors recognize that PNES is often unrecognized and underdiagnosed in the ED), Selbst and Clancy 29 found that all had multiple previous ED visits, 8 of 10 patients had been prescribed anticonvulsants in the past, 6 received anticonvulsants either in the ED or before arrival in the ED by prehospital personnel, all but 1 had invasive procedures and testing, and 8 were admitted to the hospital. Other studies have found similar rates of extensive medical testing in children with PNES. 30 Accurate diagnosis and appropriate referrals for these patients may be important, as Wyllie et al 31 found that on follow-up, 72% of patients’ PNES had resolved after psychiatric treatment. A particularly challenging problem when treating potential PNES in the ED is that some of these patients will have both a true seizure disorder and PNES, making airway management and the decision to give anticonvulsants for apparent seizure activity difficult and complex for ED physicians.

Several studies have investigated the impact of somatic symptom and related disorders on emergency department patients. Knockaert et al 32 prospectively enrolled 578 adult patients presenting to a Belgian ED with chest pain. Although the majority of these patients were found to have a cardiac or pulmonary disease as the etiology of their chest pain, the authors classified “somatization disorder” as the third leading cause (9.2%) of these ED visits. Another interesting finding from this study was that somatization disorder was more common among patients who were self-referred to the ED and those brought by ambulance. Although formal psychiatric evaluation was not performed on all patients, and classification as somatization disorder was based on the available clinical information and the final discharge diagnoses, the authors believe that their methods underestimated the true prevalence. Other studies have found a higher prevalence of mental health disorders among adult ED patients with chest pain. 17  

Lipsitz et al 33 studied 32 pediatric ED patients who presented with chest pain and for whom no medical cause was found. Using a semistructured Diagnostic and Statistical Manual of Mental Disorders, Fourth Edition interview to detect anxiety disorders, they found that 81% met diagnostic criteria for an anxiety disorder, with 28% meeting full criteria for panic disorder. Other pain symptoms such as headaches, abdominal pain, and back pain were common in these children, as were impaired quality of life and multiple domains of daily functioning. In a secondary analysis of a larger study on maternal and pediatric mental health problems, Dang et al 34 explored the relationship between mothers’ somatic symptoms and subsequent pediatric ED use for their child. Maternal somatic symptoms were assessed with the Patient Health Questionnaire 15, a validated measure for inquiring about common somatic problems in outpatient settings. After covariates were adjusted for, mothers with high somatic symptom scores reported higher rates of depression symptoms, difficulty caring for themselves and their child, and a greater use of the ED for their child (odds ratio, 1.8; 95% confidence interval [CI], 0.99–3.38; P = .055).

Although there are no known studies of interventions for pediatric ED patients, Abbass et al 35 performed an intriguing prospective study of adult ED patients with suspected somatic symptom and related disorders. If the treating ED physician made a provisional diagnosis of somatization after completing the medical evaluation of the patient, a referral was made for an outpatient mental health evaluation and intensive, short-term psychotherapy. The mental health evaluation and treatment typically took place a few weeks after the ED visit, with patients receiving a mean of 3.8 psychotherapy sessions (range: 1–25 sessions). After the psychotherapy intervention, at 1-year follow-up, they found a mean reduction of 3.2 ED (69%) visits per patient (SD, 6.4; 95% CI, 1.3–5.0; P < .001), compared with the year before the index ED visit. In addition, at follow-up patients reported significant improvement in their somatic symptoms and high satisfaction with the psychotherapeutic referral and intervention. Although this was not a randomized controlled trial, patients who were referred to psychotherapy but did not attend treatment did not show any changes in their ED use at 1 year follow-up.

Medically unexplained symptoms are extremely frustrating for patients, families, and medical providers. Parents and children often think that they are not being listened to and that physicians have misdiagnosed the problem, or potential causes of the symptoms have not been adequately evaluated. 2 , 10 These feelings can be intense and may be rooted in a fear that a medical illness is being missed, frustration over the lack of success in resolving the symptoms, the stigma of being labeled or perceived as “psychosomatic,” or difficulty in acknowledging that psychological and physical symptoms may be related. 18  

Prognosis often is unpredictable. In some cases, the episode can be brief and resolve. In other cases, the course is chronic and difficult to treat. The chronicity of the symptoms and previous response to treatment may be informative about the likely treatment course. Most experts agree that an empathetic, consistent, multidisciplinary, long-term treatment plan is helpful for chronic cases. 2 , 5 , 10 , 18 This may include various psychotherapies (eg, cognitive–behavioral, rehabilitative, operant interventions, self-management strategies, and family or group therapy), consistent communication between all treating providers, and comprehensive treatment of comorbid psychiatric conditions. 2  

Although these treatment modalities are not practical or possible for the ED setting, there are some strategies that are applicable and may be helpful. Experts suggest the following 2 , 5 , 18 :

Provide reassurance : First and foremost, it is important to convey to the patient and family that the patient’s symptoms are being heard and taken seriously. Taking time to obtain a detailed history and comprehensive physical examination can help accomplish this goal. Some children and families may be reassured by the knowledge that their symptoms are not life or limb threatening. In addition, eliciting and addressing the child’s and family’s anxiety and fears about the patient’s symptoms may be both clinically illuminating for the ED provider and comforting to the patient and family. It may also be important to reaffirm that their ED and outpatient providers are working and will continue to work with them to continue to evaluate and treat their symptoms.

Communicate : Strategies to improve communication include emphasizing collaboration between the patient, family, and all caregivers; identifying common goals and outcomes; and introducing the idea of working on improving functioning in addition to working toward symptom resolution. In addition, educating the patient and family about the limitations of the ED setting, as well as the benefits of other settings for evaluation and treatment, may be helpful. Lastly, exploring the patient and family’s openness to the possibility that the symptoms may be psychologically related may be an important first step. Determining and using terms such as stress, temperament, anxiety, “nerves,” and other terms that are acceptable to the patient and family may assist in this goal.

Coordinate care : Contacting and communicating with all involved care providers may be time consuming but is important in implementing a cohesive, comprehensive evaluation and treatment plan and may have the added benefit of providing reassurance to the patient and family as well as decreasing frustration and improving satisfaction.

The use of all psychotropic medications in pediatric populations over the last 2 decades has markedly increased. 36 , 37 Antipsychotic use, in particular, has shown large increases. 38 Especially notable is their burgeoning off-label use, 39 , – 41 including in preschool-aged children. 42 , – 44 Given the frequency and multiple medication regimens with which psychotropic agents are being prescribed, 36 ED clinicians are likely to encounter children and adolescents taking 1 or many of these medications. This section focuses on the clinical problems and diagnostic and treatment dilemmas one may encounter in the ED when caring for pediatric patients on antipsychotics and antidepressants.

An additional important consideration for ED clinicians is that many commonly used medications not typically thought of as psychotropic agents have dopaminergic and serotonergic properties similar to those of antipsychotics and antidepressants. For example, drugs used as antiemetics and for migraines (ie, prochlorperazine, metoclopramide, promethazine, and trimethobenzamide) are phenothiazines, the same type of medications as first-generation, “typical” antipsychotics. Droperidol, which has been used as an antiemetic and for agitation, is a butyrophenone, the same class as the antipsychotic haloperidol. 45 The number and scope of medications with serotonergic effects are surprising and are detailed in this section. Either alone or in combination with psychotropic serotonergic drugs, these medications can result in serotonin toxicity. Given how frequently these medications are used in clinical practice, familiarizing oneself with them and their potential adverse effects may be beneficial to ED clinicians.

Antipsychotics are prescribed for various childhood disorders, including oppositional–defiant disorder, conduct disorder, attention-deficit/hyperactivity disorder, and ASDs. 46 , – 49 These medications have also been used as antiemetics and antipruritics and to treat headaches, hiccups, and various neurologic disorders such as Parkinson disease, hemiballismus, ballismus, Tourette syndrome, and Huntington chorea. 50 , 51  

The common adverse effects of antipsychotics can be conceptualized and organized around the CNS neurotransmitters on which they act. 45 , 50 , – 54   Table 2 lists the common adverse effects of antipsychotics and the medications with which they are most commonly associated.

Antipsychotic Adverse Symptoms

It is important to note that antipsychotics have other clinically significant effects, including “black box” warnings from the US Food and Drug Administration (FDA) for thioridazine and droperidol because of their potential to cause dysrhythmias. Almost all antipsychotics cause some degree of QT c prolongation because of a quinidinelike effect. For most of the medications, however, the degree of QT c prolongation is small, which has given rise to a debate about the actual risk of dysrhythmias and torsades de pointes with antipsychotics administered in their usual doses and routes of administration. 45 , 47 , 48 , 55 , – 60 Of note, intravenous (IV) haloperidol has been studied 61 but carries an FDA non–black box warning because of deaths associated with high doses and IV administration. 62 Therefore, experts suggest that intramuscular dosing of antipsychotics in the ED is the parental preferred route of administration. Table 3 details the factors that are thought to increase the risk of QT c prolongation and sudden death. 48 , 51 , 63 , 64 , Table 4 lists the degree of QT c prolongation for common antipsychotics. 65  

Risk Factors for QT c Prolongation or Dysrhythmias With Antipsychotic Use

QT c Prolongation Associated With Antipsychotics

Cardiac: Black Box Warning

Both thioridazine and droperidol have been issued FDA black box warnings for a potential association with prolonged QT interval, torsades de pointes, and sudden death. Since then, several studies have disputed this risk with droperidol. 55 , – 60 A large retrospective review of 2468 patients given droperidol in the ED found that no cardiovascular event occurred that did not have an alternative explanation, and only 6 serious adverse events occurred, with 1 cardiac arrest in a patient with a normal QT interval out of 2468 patients (0.2% = 6/2468). 56 A pediatric study also suggested the safety and efficacy of droperidol when used to treat agitation, nausea and vomiting, headache, and pain. 66 Thus, “although droperidol can be associated with prolongation of the QT interval, there is not convincing evidence that the drug causes severe cardiac events.” 60 Despite these and other studies, since the black box warning was issued, use of droperidol has declined exponentially. 67 , 68  

Acute extrapyramidal syndromes associated with antipsychotic medications include acute dystonia, akathisia, and a Parkinsonian syndrome. Acute dystonia is characterized by involuntary motor tics or spasms usually involving the face, the extraocular muscles (oculogyric crisis), and the neck, back, and limb muscles and tends to occur after the first few doses of medication or after an increase in dosage. Laryngeal dystonia is a rare, potentially life-threatening adverse event that presents as a choking sensation, difficulty breathing, or stridor. 45 , 48  

Akathisia is a subjective feeling of restlessness, which generally occurs within the first few days of antipsychotic medication administration. Akathisia is found in up to 25% of patients 51 and has also been reported in patients receiving a single, standard dose (10 mg) of prochlorperazine. Both acute dystonia and acute akathisia tend to occur early in the course of treatment (ie, days to weeks after beginning an antipsychotic) and are easily reversed. To minimize these adverse effects, some advocate coadministering 25 to 50 mg of diphenhydramine or 1 to 2 mg of benztropine when giving an antipsychotic. 69 Others prefer to treat with anticholinergic agents (ie, diphenhydramine or benztropine) only if acute symptoms occur, followed by 2 days of oral therapy, given the prolonged half-life of antipsychotics.

The delayed-onset neurologic syndromes are Parkinsonism and tardive dyskinesia. The hallmarks of Parkinsonism are shuffling gait, cogwheel muscle rigidity, mask facies, bradykinesia or akinesia, pill-rolling tremors, and cognitive impairment. These symptoms are found in up to 13% of patients and generally occur weeks to months after the patient starts antipsychotic therapy. 51 Drug-induced Parkinsonism syndrome is often treated by adding an anticholinergic agent, adding a dopaminergic agonist (eg, amantadine), or decreasing the dosage of a typical antipsychotic or switching to an atypical antipsychotic. Considering the diagnosis of drug-induced Parkinsonism may be important, because early diagnosis and rapid withdrawal of the antipsychotic drug may improve the possibility of complete recovery. 50 Tardive dyskinesia is characterized by rapid involuntary facial movements (eg, blinking, grimacing, chewing, or tongue movements) and extremity or truncal movements. Respiratory dyskinesia is often undiagnosed, can lead to recurrent aspiration pneumonia, and includes orofacial dyskinesia, dysphonia, dyspnea, and respiratory alkalosis. 45 Tardive dyskinesia occurs in 5% of young patients per year and is more common with older, “typical” antipsychotics. 50  

Although antipsychotic medications have been noted to lower the seizure threshold in a dose-dependent manner, antipsychotic medication–induced seizures are rare (usually <1%) when therapeutic doses are used, except for clozapine, which has a 5% incidence of seizures at high dosages. 45 , 51  

Adverse effects, such as weight gain, hyperglycemia, and hyperlipidemia, are common, especially with second-generation, “atypical” antipsychotics. 45 , 50 , 51 , 70 Antipsychotics vary in their metabolic adverse effects, with the highest risk associated with clozapine and olanzapine, an intermediate risk with quetiapine, risperidone, and chlorpromazine, and the lowest risk with haloperidol, ziprasidone, and aripiprazole. 53  

Agranulocytosis is a potential adverse effect of the atypical antipsychotic drug clozapine. Patients on clozapine regularly have complete blood cell counts performed, usually weekly or monthly, to monitor for this adverse effect. Other adverse effects of various atypical antipsychotics include somnolence, anxiety, agitation, oral hypoesthesia, headache, nausea, vomiting, insomnia, and tremor. 51  

Neuroleptic malignant syndrome (NMS) is a potentially lethal syndrome consisting of the tetrad of mental status changes, fever, hypertonicity or rigidity, and autonomic dysfunction. It is presumed to be attributable to a lack of dopaminergic activity in the CNS, although hyperactivity of the sympathetic nervous system may also be involved. The deficiency of central dopaminergic activity can be attributable to dopamine antagonists or dopamine receptor blockade, dysfunction of the dopamine receptors, or withdrawal of dopamine agonists. 50 , 71 , 72  

With the increasing use of antipsychotic medications in the pediatric population, clinicians caring for children and adolescents may encounter this syndrome. 73 Given that NMS can be difficult to recognize and attenuated or incomplete presentations are possible, NMS is challenging to diagnose. 71 , 74 The incidence of NMS has been difficult to determine, with estimates ranging from 0.02% to 3%. 45 , 71 , 75 Fortunately, mortality from NMS has decreased from 76% in the 1960s to <10% to 15% more recently. 72 , 76 , – 78 Experts suggest considering NMS in the differential diagnosis of patients presenting with fever and altered mental status who are taking or may have taken an antipsychotic. 74  

NMS affects patients of all ages, with an apparent predominance in young adults and male patients (2:1). 73 , 79 , – 81 It is unclear whether these are truly risk factors or reflect the patient population with the greatest use of antipsychotic medications. 75 Coadministration of psychotropic agents seems to be an especially high risk factor for precipitating NMS; in 1 study, more than half of people with reported NMS cases were taking concomitant psychotropic agents. 77 Other risk factors include dehydration, physical exhaustion, preexisting organic brain disease, and the use of long-acting depot antipsychotics. Neither duration of exposure to the drug nor toxic overdoses of antipsychotics appear to be associated with NMS. In addition, reintroducing the original precipitating drug may not lead to a reoccurrence of NMS, although patients with a history of NMS are at increased risk of recurrence. 76 , 77 The onset of NMS generally occurs within 7 days of starting or increasing antipsychotics and may last for 5 to 10 days even after the initiating agent is stopped. With depot forms of antipsychotics, however, onset of NMS symptoms may be more insidious and may last longer, up to 15 to 30 days. 71 , 76 , 82  

It was initially thought that newer atypical antipsychotics, which have both serotonin and dopamine-blocking properties, would not cause NMS because of their lower activity at dopamine receptors and their greater antiserotoninergic activity. This has not turned out to be the case. Both second-generation atypical antipsychotics and the third-generation aripiprazole, which has partial dopamine agonist activity, have all been implicated in causing NMS. 76 , 79 , 83 , – 87  

Despite its name, NMS can also be triggered by the administration or withdrawal of other, nonantipsychotic medications. Administration of tricyclic antidepressants, selective serotonin reuptake inhibitors (SSRIs), and lithium have been associated with NMS. 75 NMS also has been associated with the abrupt withdrawal of medications (eg, dopaminergic drugs used to treat Parkinson disease, such as levodopa, as well as baclofen, amantadine, some antipsychotics, and some antidepressants). 74 Lastly, the introduction to this section enumerates some of the medications commonly thought to be antiemetics or antimigraine therapies. They are, in fact, phenothiazines (ie, the same class of medications as first-generation, typical antipsychotics), but because of the clinical conditions for which they are used, they may not be suspected for being at risk for triggering NMS.

Pathophysiology

The cause of NMS is postulated to be a lack of dopaminergic activity in the CNS, principally affecting the D 2 receptors. Dopamine D 2 receptor antagonism leads to the manifestations of the NMS. Blockade of D 2 receptors in the hypothalamus produces an increased set point and loss of heat-dissipating mechanisms. Antagonism of the D 2 receptors in the nigrostriatal pathways and spinal cord via extrapyramidal pathways produces muscle rigidity and tremor. In the periphery, the increased release of calcium from the sarcoplasmic reticulum causes increased contractility, leading to muscle rigidity, increased heat production (with worsening of hyperthermia), and muscle cell breakdown with elevated creatine kinase and rhabdomyolysis. In addition, D 2 receptor antagonism by eliminating tonic inhibition of the sympathetic nervous system leads to sympathoadrenal hyperactivity and autonomic instability. 72 , 75  

Clinical Presentation

The hallmarks of NMS are hyperthermia, altered mental status, muscle rigidity, and autonomic instability. Manifestations of autonomic dysfunction, which may occur before other symptoms, include fever up to 41°C or higher, tachycardia, blood pressure instability, diaphoresis, pallor, cardiac dysrhythmia, diaphoresis, sialorrhea, and dysphagia. 71 , 88  

The most common neurologic finding is lead pipe rigidity, although akinesia, dyskinesia, or waxy flexibility may be present. 45 , 77 The alteration in mental status often takes the form of delirium but varies from alert mutism to agitation to stupor to coma. 50 , 76 Motor abnormalities may include rigidity, akinesia, intermittent tremors, and involuntary movements. Other less common neurologic or neuromuscular signs include a positive Babinski, chorea, seizures, opisthotonos, trismus, and oculogyric crisis. 76 , 86  

Complications include renal failure from rhabdomyolysis, thromboemboli, dysrhythmias, cardiovascular collapse, and respiratory failure from aspiration pneumonia or tachypneic hypoventilation caused by diminished chest wall compliance from muscle rigidity, which may result in endotracheal intubation and ventilatory support. 50 , 71  

Because there are no pathognomonic clinical or laboratory criteria, NMS is a clinical diagnosis. The differential diagnosis for NMS is broad and is outlined in Table 5 . An important component of the diagnosis is a history of antipsychotic use or withdrawal of a dopaminergic agent. 45 , 86 Numerous diagnostic criteria have been proposed, which have included the classic clinical symptoms and other supplemental criteria. 1 , 79 , 81 , 88 Additional proposed criteria include elevated creatine kinase, 81 leukocytosis, incontinence, dysphagia, mutism, and metabolic acidosis. 1 , 79 , 81  

Differential Diagnosis of NMS 72 , 89  

Recently, a Delphi panel of international NMS experts convened to discuss NMS diagnostic criteria. 90 Although its purpose was not to create a new set of criteria, the results reflect consensus on the relative importance of individual clinical and diagnostic features for making a diagnosis of NMS. On a 100-point scoring system (ie, the total number of points sum up to 100), each clinical feature of NMS was assigned a number of “priority points.” The point system is not meant to be used as a method for making the diagnosis of NMS; that is, there is no threshold number of points that indicate the presence or absence of NMS. Rather, it is meant to help clinicians determine which features of NMS are more important in making the diagnosis. The greater the number of points assigned, the greater the significance of the feature in making the diagnosis of NMS. The Delphi panel made the following assignments: exposure to dopamine antagonist or withdrawal of dopamine agonist within 3 days (20 points), hyperthermia (>100.4°F oral on ≥2 occasions [18 points]), rigidity (17 points), mental status alteration (13 points), creatine kinase elevation (≥4 times upper limit of normal [10 points]), sympathetic nervous system lability (10 points), hypermetabolism (5 points), and negative workup for infectious, toxic, metabolic, or neurologic causes (7 points). Sympathetic nervous system lability was defined as 2 or more of the following: elevated (systolic or diastolic ≥25% of baseline) or fluctuations (≥20 mm Hg diastolic or ≥25 mm Hg systolic change within 24 hours) in blood pressure, diaphoresis, or urinary incontinence. Hypermetabolism was defined as a heart rate increase ≥25% above baseline and respiratory rate ≥50% above baseline.

Leukocytosis, generally in the range of 15 000 to 30 000 cells per cubic millimeter, and electrolyte findings consistent with dehydration may be present. The etiology of elevated alkaline phosphatase, lactic dehydrogenase, and transaminases indicating impaired liver function is unknown but may be secondary to acute fatty liver changes from the hyperpyrexia. An elevated serum aldolase and creatine kinase, often greater than 16 000 IU/L, may be attributable to severe, sustained muscle contractions. The elevated creatine kinase may lead to rhabdomyolysis, acute myoglobinuria, and renal failure. A nonspecific common finding is the presence of a low serum iron concentration in patients with NMS. 77 , 86 , 91 If a lumbar puncture is performed, the cerebrospinal fluid results may be normal or have nonspecific findings. Findings on an EEG, if obtained, are variable. The EEG results may be normal or demonstrate findings of a nonspecific encephalopathy, such as diffuse slowing. 71 , 76 There are no specific findings on postmortem histopathology of the brain. 71  

Differentiating NMS from serotonin syndrome and other toxidromes can be challenging. Clinical features that may help are detailed in Table 7 and the section on serotonin syndrome.

Management of NMS involves primarily supportive care and removal of the initiating agent. If NMS is triggered by the abrupt withdrawal of an anti-Parkinsonism drug, reintroduction of the drug may be considered. 72 Cardiorespiratory compromise may be managed with standard, supportive measures. Dehydration or elevated creatine kinase and rhabdomyolysis may be treated with IV fluids. If renal failure occurs, hemodialysis may be necessary (however, dialysis does not remove antipsychotics that are protein bound). For agitation, experts suggest benzodiazepines as the first-line agent. Fever can be treated with external cooling measures, such as cooling blankets. 72 , 75  

Suggestions for NMS treatment are based on case reports and clinical experience, not rigorous clinical trials, limiting the strength of the evidence base. The most frequently administered drugs have been dantrolene, bromocriptine, and amantadine. Dantrolene decreases muscle rigidity, and thermogenesis caused by the tonic contraction of muscles. It blocks the release of calcium from smooth muscle cells’ sarcoplasmic reticulum, uncoupling actin and myosin chains, resulting in muscle relaxation. Commonly used dosages in NMS are 1 mg/kg by IV push followed by 0.25 to 0.75 mg/kg every 6 hours. The drug may be continued until symptoms resolve or a maximum of 10 mg/kg is reached. 72 , 77  

The utility of CNS dopaminergic agents is unclear and controversial. Therefore, consultation with a toxicologist or poison control center may be helpful. Bromocriptine is a centrally acting dopamine agonist. Experts suggest an initial dosage of 1.25 to 2.5 mg twice a day, which may be increased to 10 mg 3 times a day. Muscle rigidity usually responds quickly to bromocriptine, but fever, blood pressure, and creatine kinase levels may take several days to normalize. Amantadine has dopaminergic and anticholinergic effects. A common starting dosage is 100 mg orally, with a maximum dosage of 200 mg twice a day. 72 , 77 , 86 Benzodiazepines are often used for agitation and rigidity. Electroconvulsive therapy has been used in some pharmacotherapy-resistant cases. 72 , 77  

ED clinicians may not have seen or treated many cases of NMS. Potential resources for caring for these patients include toxicologists, a poison control center, and the NMS Information Service, which can be accessed through its Web site ( http://www.nmsis.org/index.asp ). Staffed by NMS experts, the NMS Information Service provides information, education, and phone consultation regarding the diagnosis and treatment of NMS.

Serotonin syndrome occurs in all ages, from infants and children to older adults. It has even been reported in newborn infants as a result of in utero exposure. 92 The incidence of and mortality from serotonin syndrome have been increasing and may escalate in the future 93 , 94 because of the growing number and use of proserotonergic medications, such as SSRIs, other classes of psychiatric medications (eg, other antidepressants and anxiolytics), antibiotics, opiate analgesics, antiemetics, anticonvulsants, antimigraine drugs, anti-Parkinsonism drugs, muscle relaxants, and weight-reduction or bariatric medications ( Table 6 ). In addition to prescription medications, a wide variety of over-the-counter medications, herbal and dietary supplements, and drugs of abuse have all been associated with serotonin syndrome. 95  

Medications and Other Agents Associated With Serotonin Syndrome

This is not an all-inclusive list but gives an overview of the wide range of agents that can trigger the serotonin syndrome. Drugs are listed by their therapeutic category. This list is not intended to endorse any given drug or product.

Serotonin syndrome occurs in approximately 16% to 18% of patients who overdose with an SSRI. 93 The true incidence of serotonin syndrome is difficult to estimate, given that many instances are probably undiagnosed or misdiagnosed. 96 , 97 Variable clinical manifestations (eg, lack of the classic triad of symptoms), wide spectrum of disease from mild to life-threatening, symptoms that are easily misattributed to the patient’s underlying mental condition (eg, anxiety and akathisia), lack of awareness of the disorder, and the vast number of medications, other agents, and combinations of medicines or agents that can cause serotonin syndrome all may contribute to missed diagnoses. 93 , 97 , 98  

In the CNS, serotonin (5-hydroxytryptamine) regulates temperature, attention, and behavior. Peripherally, serotonin modulates gastrointestinal tract motility, vasoconstriction, bronchoconstriction, and platelet aggregation. Seven families of serotonin receptors have been identified, with serotonin syndrome resulting from excess CNS serotonin, 98 , 99 primarily caused by overstimulation of serotonin 2A receptors. 100 , 101  

Excessive serotonin activity may result from myriad mechanisms, including increased release of serotonin (eg, cocaine, amphetamines), increased production of serotonin (eg, L-tryptophan in stimulant products), inhibiting reuptake of synaptic serotonin (eg, tricyclic antidepressants, SSRIs), decreased neuronal metabolism of serotonin via inhibition of monoamine oxidase inhibitors, direct stimulation of serotonin receptors (eg, lysergic acid diethylamide, migraine drugs such as sumatriptan, buspirone), and increased postsynaptic receptor responsivity (eg, lithium). 93 , 95  

A single dose of a single proserotonergic agent may precipitate serotonin syndrome. However, many cases occur after exposure to 2 or more drugs that increase the serotonin activity. Examples of combinations of proserotonergic medications causing serotonin syndrome include reports of SSRIs and fentanyl (given during procedural sedation), 102 erythromycin, 96 and St John’s wort (an over-the-counter herbal supplement). 95 In addition, serotonin syndrome has also been reported in a patient withdrawing from a serotonergic agent. 100  

The clinical triad of the serotonin syndrome consists of mental status changes, autonomic hyperactivity, and neuromuscular abnormalities. One of the greatest challenges of this diagnosis is its extremely variable presentation. Many patients do not exhibit all these clinical characteristics. 103 Some patients will have severe symptoms, such as high fever (up to 41.1°C), severe hypertension, and tachycardia that may deteriorate into hypotension, shock, agitated delirium, muscular rigidity, and hypertonicity. Mild cases may range from tremor and diarrhea to tachycardia and hypertension but no fever. Symptom onset is generally rapid, often within minutes of exposure to the precipitating agent, with most patients presenting within 6 to 24 hours. 100  

Agitated delirium is the most common form of mental status change, although this too has a wide spectrum of severity, including mild agitation, hypervigilance, slightly pressured speech, and easy startle. Diaphoresis, shivering, mydriasis, increased bowel sounds, and diarrhea are common signs of autonomic dysfunction. 95 , 100 Myoclonus is the most common neuromuscular finding, 98 but other abnormalities are possible, including muscular rigidity, hypertonicity (which may in turn contribute to hyperthermia), hyperreflexia and clonus (which are more pronounced in the lower than the upper extremities), horizontal ocular clonus, tremor, and akathisia. In some cases, muscle hypertonicity may be so severe that it overpowers and obscures tremor and hyperreflexia.

Significant morbidity and mortality are associated with serotonin syndrome. Severe cases are characterized by rhabdomyolysis with an elevated creatine kinase, metabolic acidosis, elevated serum aminotransferase, renal failure with an elevated serum creatinine, seizures, and disseminated intravascular coagulopathy. Approximately one-quarter of patients are treated with intubation, mechanical ventilation, and admission to an ICU. The mortality rate is approximately 11%, with the most common cause of death being inadequate management of hyperthermia. 98  

The differential diagnosis of serotonin syndrome includes other disorders precipitated by medications or drug toxicity reactions (eg, NMS and malignant hyperthermia, anticholinergic syndrome, and withdrawal syndromes including delirium tremens); CNS disorders spanning infection (meningitis, encephalitis), tumors, and seizures; and psychiatric disorders such as acute catatonia.

Differentiating between serotonin syndrome and other medication-induced syndromes can be challenging and may be important, given that treatment may differ depending on the underlying etiology. Table 7 details both the similar and differentiating features of these syndromes. The most common clinical finding of serotonin syndrome is myoclonus, which occurs in slightly more than half (57%) of cases. 98 Some experts believe that clonus and hyperreflexia are “highly diagnostic for the serotonin syndrome and their occurrence in the setting of serotonergic drug use establishes the diagnosis.” 100  

Differentiation of the Drug Toxicity Syndromes

All of these drug toxicity syndromes can present with altered mental status, autonomic dysfunction, and neuromuscular abnormalities as manifested by abnormal vital signs including fever, hypertension, and tachycardia. Treatment in all 4 syndromes may include removing the precipitating agent and providing supportive care. Other specific therapy may differ depending on the disorder. Not all patients will have all the classic signs and symptoms. For example, a patient with mild serotonin syndrome may be afebrile but have tachycardia and hypertension. Typical findings are listed in this table.

Anticholinergic syndrome described as “Red as a beet, dry as a bone, hot as a hare, blind as a bat, mad as a hatter, full as a flask.”

As with NMS, there are no pathognomonic laboratory or radiographic findings of serotonin syndrome. Testing may be obtained on the basis of clinical suspicion and may include a complete blood cell count, electrolytes, serum urea nitrogen, creatinine, arterial blood gas (checking respiratory status and for metabolic acidosis), hepatic transaminases, creatine kinase, urinalysis, toxicology screens, coagulation studies, electrocardiography, EEG, and brain imaging studies.

Clinical diagnostic criteria for serotonin syndrome have been proposed. 104 , 105 Hunter criteria 104 have a higher sensitivity (84% vs 75%) and specificity (97% vs 96%) than Sternbach criteria. 105 In addition, the use of the Sternbach criteria may exclude mild, early, or subacute serotonin syndrome. Others prefer modified Dunkley criteria. 100 , 104 According to the modified Dunkley criteria, the diagnosis can be made if the patient has taken a serotonergic drug within the last 5 weeks and has any of the following: tremor and hyperreflexia; spontaneous clonus; muscle rigidity, temperature >38°C, and either ocular clonus or inducible clonus; ocular clonus and either agitation or diaphoresis; or inducible clonus and either agitation or diaphoresis. 100 Other variations of these diagnostic criteria have been proposed. They all include a serotonergic drug having been started or the dosage increased and other possible etiologies (eg, NMS, substance abuse, withdrawal, infection, other toxidromes) having been ruled out, plus the presence of specific signs and symptoms. 95 , 106 , 107  

Treatment often involves discontinuing the precipitating agent and providing supportive care. Supportive care may include treatment of agitation (eg, benzodiazepines), amelioration of hyperthermia, and management of the autonomic instability (eg, IV fluids and other agents to address abnormal vital signs). In addition, for those with severe serotonin syndrome (eg, temperature >41.1°C), emergency sedation, neuromuscular paralysis, and intubation may be considered. Physical restraints may be detrimental, because they may exacerbate isometric contractions, thereby worsening hyperthermia and lactic acidosis and increasing mortality. 98  

In severe cases, serotonin 2A antagonists may be considered, with cyproheptadine being most commonly used. The adult dosage of cyproheptadine is usually 12 to 24 mg over 24 hours, typically starting with 12 mg, followed by 2 mg every 2 hours for continuing symptoms, and a maintenance dose of 8 mg every 6 hours, given orally. There is no parenteral form, but tablets have been crushed and administered via a nasogastric tube. The pediatric dosage is usually 0.25 mg/kg per day, divided into 2 or 3 doses daily, up to a maximum of 12 mg. Chlorpromazine, an antagonist of serotonin 2A receptors as well, is available in a parenteral form but has the disadvantage that it can cause hypotension and may increase muscle rigidity, decrease the seizure threshold, and worsen NMS. 98 Both drugs may be effective, 108 but cyproheptadine is preferred by most experts. 99 , 100  

Low dosages of direct-acting sympathomimetic amines (eg, phenylephrine, norepinephrine, and epinephrine) or short-acting drugs such as esmolol or nitroprusside have been used to manage fluctuating blood pressure and heart rate. Use of indirect agents (eg, dopamine) may not be efficacious, because the mechanism of action of these drugs includes intracellular metabolism via catecholamine-O-methyl transferase to metabolize the dopamine to epinephrine and norepinephrine, which may result in overshooting the desired effect.

Management of hyperthermia often involves terminating the extreme muscle activity. In addition to treating agitation, benzodiazepines may be useful in controlling muscular activity in moderate cases. In severe cases, paralysis with nondepolarizing drugs (eg, vecuronium or rocuronium) and intubation may be considered. Some experts suggest that succinylcholine may be risky with these patients, secondary to hyperkalemia and rhabdomyolysis, which may be present and ultimately result in dysrhythmias. Because the fever of NMS is secondary to muscular hyperactivity and not effects on the hypothalamic thermoregulation set point, antipyretics typically are not efficacious. 96 , 99 , 108  

Patients with serotonin syndrome can deteriorate rapidly; therefore, close observation and preparation for rapid intervention may be considered. In milder cases, evaluation, observation, and discharge with close, additional outpatient management may be considered. As mentioned previously, discussing these patients’ care with a toxicologist or poison control center may be helpful.

In recent years, there has been a sharp increase in the incidence of ASDs and DDs, 109 with corresponding interest and growth in treatment strategies. Investigated therapeutic modalities include psychobehavioral therapies, 110 , – 115 psychopharmacology, 116 , – 118 occupational and language therapies, 119 , – 121 and complementary and alternative medicines. 122 Unfortunately, many studies have had methodologic limitations (eg, small sample sizes, variability in study populations, methods or interventions used, and outcomes measures) and are not applicable to the medical setting. 123 , – 125 Three evidence-based reviews of this topic conclude that there is adequate evidence for only a limited number of therapies (eg, pharmacotherapy), although several other strategies show promise (eg, early and intensive behavioral therapy, social skills training, and visual communication systems). 125 , – 128 Given these limitations, the strategies discussed below are based primarily on expert, consensus opinion.

ASD-DD–Sensitive Care Resources

A wide range of ED health professionals can champion, organize, design, and coordinate ASD-sensitive ED care, including physicians, nurses, nursing assistants, nurse practitioners and physician assistants, social workers, and child life specialists. Non-ED professionals who may be helpful include developmental–behavioral pediatricians, child psychologists and psychiatrists, special education teachers, speech–language therapists, and occupational therapists.

Often, the most important ASD-DD “experts” to consult are the child’s parents. Parents of children with ASDs or DDs know what strategies work with their children (eg, which words, actions, or stimuli calm and help their child and which have the opposite effect). Parents can also be “interpreters” for ED clinicians, deciphering the significance of their child’s actions and behaviors and facilitating communication with their child. Spending some time asking parents about their child is likely to be a productive, efficient method for tailoring effective ED care for these patients.

Strategies for ASD-DD–Sensitive ED Care

Typical strategies for caring for children with ASD-DD are listed in Table 8 . 128 Children with ASD-DD are often hypersensitive to environmental stimuli (eg, light, sound, and activity). Simple solutions include using a quiet office or counseling room (if available) instead of a loud, stimulating examination room. If this type of patient space is not available, an alternative solution may be to use a quiet examination room, away from the busy, noisy areas of the ED, with dimmed lighting (eg, turning off some lights or using a single lamp).

Nonpharmacologic Strategies for Caring for Children With ASD-DD

Studies have demonstrated that visual communication systems (VCSs) can improve communication with children with language disabilities. 129 , – 132 VCS products are the most commonly used communication adjuncts and are widely available. There are numerous commercial or free and print and electronic products (eg, Web sites, “apps,” devices). A visual schedule ( Fig 1 ) exemplifies how a VCS can be used to prepare a child with ASD-DD for an upcoming event or activity. Visual schedules help children organize themselves, understand what will happen next, highlight or introduce activities that are unfamiliar to them, and create smoother transitions, all of which may decrease children’s anxiety.

Digital photograph visual schedule. Photo credit: Thomas H. Chun, MD, MPH, FAAP.

If a child has his or her own personal VCS, it may be advantageous to use the VCS, because the child will be familiar with pictures. A potential disadvantage of a personal VCS is that the set of images may not have the necessary medical pictures. A simple and inexpensive solution to this problem is to create a custom set of images of the ED setting. This can easily be done with clip art or digital photography images, which are then printed and laminated. If digital photography is used, taking pictures of the ED staff, equipment, and commonly performed procedures is a simple method for creating a customized VCS for your setting ( Fig 2 ).

Clip art visual schedule.

Transitions are often problematic for children with ASD-DD, including changing from 1 activity to the next, moving from 1 setting to another (especially new settings), and breaks or deviations from their usual routines. For these reasons, a medical visit may be upsetting or unsettling to these children. Fortunately, many parents are familiar with anticipating and planning for these types of transitions. For example, these parents talk to their children before a new experience, describe what will happen and the sequence of events, and explain what might be upsetting to the children and how they will handle these stressful situations. Preparing children with ASD-DD for a medical visit ideally begins before or while en route to the visit and is an ongoing process once they arrive.

Anticipating and building breaks in a schedule may be helpful. Many children with ASD-DD are able to remain on task for only short periods of time. Regular, brief breaks in the schedule may be helpful to these children. As time consuming as it may be, in the total calculus of planning the ED visit this may still be a time-neutral strategy relative to the time consumed by unsuccessful strategies. At the least, this strategy is likely to be more satisfactory to children, their parents, and ED clinicians.

Desensitization strategies that are used with all children (eg, gradually approaching and engaging with children, bending down to interact at children’s level, allowing children to play with medical instruments or to use them on you or their parent first, distracting them with a toy or game, and having children held or comforted by parents while they are examined) also may help with children with ASD-DD. For some, however, the same strategies may benefit from significant augmentation, literally breaking each step down into several incremental, smaller steps. It may take several visits and interactions and multiple attempts before children will allow you to approach and examine them. Other children with ASD-DD are very sensitive about their personal space. Starting at the periphery (ie, toes and fingers) and slowly moving centrally may help relax children and facilitate the examination. These types of desensitization strategies have been successfully used for phlebotomy attempts in children with ASD-DD. 133  

Many children with ASD-DD find value in occupational therapy (OT). OT techniques that are directly applicable to medical settings involve sensory integration and tasks that can be used as distraction techniques. Children with ASD-DD have variable responses to touch, with some finding it soothing and others becoming distressed by touch. Some find “deep pressure” (ie, the feeling of weight on their bodies) relaxing, but others respond to light touch. Devices such as weighted blankets or shawls for deep pressure and gentle massaging devices for light touch frequently are used. These products can be purchased through OT supply vendors, but simple substitutes can be found easily in medical settings. For example, a radiology lead vest or apron is an easy facsimile of a weighted blanket. Gently stroking the child with gauze or cast underpadding provides an excellent light touch massage.

Distraction may be a useful adjunct in children with ASD-DD. Occupying a child’s hands or body with “fidget toys” is a typical strategy. OT devices (eg, grip strengthening and manual dexterity devices, devices to improve balance) also may serve this function. With appropriate supervision, simple substitutes for these devices are also easily made (eg, a loosely wound roll of gauze or cast underpadding can be a substitute for a squeeze toy). Rocking in a rocking chair or nylon folding sports stadium seat also can calm children ( Fig 3 ).

Example of rocking in a sports chair. Photo credit: Thomas H. Chun, MD, MPH, FAAP.

Psychopharmacology and ASD-DD

There are no rigorous evidence-based guidelines regarding psychotropic medications for children with ASD-DD. Although there is strong evidence for the use of psychotropic medications in ASD-DD, 116 , 117 , 125 there are no controlled trials of these medications for acute agitation or sedation. Currently, there are no known contraindications to using common sedating medications for children with ASD-DD, although some experts believe that atypical medication responses may be more common (eg, idiosyncratic, disinhibition, or paradoxical reactions). Inquiring about the previous reaction to medications often is helpful, as may be beginning with lower medication dosages to observe and determine the child’s response to the medication. 134  

For a discussion of mental health screening strategies in primary care settings, please refer to the American Academy of Pediatrics clinical report on screening for behavioral and emotional problems . 135  

The ED may be an ideal setting for screening and identifying high-risk, difficult-to-reach pediatric populations with mental health problems. Many teenagers either do not have a primary care provider or face significant barriers to accessing such health care. For these adolescents, the ED often is their main or only source of medical care. 136 , 137 Other high-risk groups for mental health and substance use problems are homeless adolescents and school dropouts, 138 , – 143 both of whom disproportionately seek medical care in the ED.

Finally, male adolescents may preferentially seek care in EDs because they are less likely to participate in primary or mental health care. 144 , 145  

Several rapid, efficient, and accurate ED mental health screening tools have been developed and show promising results. As few as 2 screening questions have been found to be helpful in detecting depression in both adult and pediatric ED settings as well as problematic adolescent alcohol use. 146 , – 148 A 4-question adolescent suicide screen has been shown to have good sensitivity, specificity, and predictive value across a range of teenagers seeking care in the ED and can be accurately administered by non–mental health professionals. 149 , – 151 Similarly, an 8-question screen was shown to have excellent predictive characteristics for detecting posttraumatic stress symptoms in children who sustained traffic-related injuries. 152  

Given the clinical and time pressures of the ED setting, it is important that mental health screening be acceptable to adolescents, their parents, and ED clinicians. Numerous studies have shown the acceptability of such screening. Teenagers and parents both report favorable attitudes toward mental health screening during an ED visit. 153 , 154 In this study, suicide and drug and alcohol screening rated as more important than other mental health problems. Female adolescents and their parents, more than male adolescents, expressed positive views on screening. In another study, both teenagers and their caregivers perceived ED depression screening as a sign of caring and concern for the adolescent. 155 Suicide screening has been found to be acceptable to 60% to 66% of patients and parents, with 96% of participants agreeing that suicide screening is appropriate in the ED. 149 , 150 , 156  

What do ED clinicians think about mental health screening in the ED? Is such screening acceptable to them? Perceived and real barriers to such screening exist, including lack of training, time constraints, and increasing ED patients’ length of stay. Williams et al 154 investigated this question and found that 99% of physicians and 97% of nurses stated that a brief, validated screening tool did not interfere with patient care. In addition, research staff endorsed “no difficulty” in administering the screen to 73% of participants. Lastly, a significant and important finding of the study by Horowitz et al 149 was that real-time evaluation of positive suicide screens did not increase ED patients’ length of stay.

Many mental health screening tools have been developed or tested in the ED setting. Although not validated in general ED populations, they have the potential to increase ED mental health screening. One example is an abbreviated version of the Home, Education/School, Activities, Drugs, Depression, Sexuality, Suicide, Safety (HEADDSSS) mnemonic for adolescent psychosocial assessment, which was adapted for and tested in an ED. 157 The Home, Education, Activities and Peers, Drugs and Alcohol, Suicidality, Emotions and Behaviors, Discharge Resources (HEADS-ED) was found to be reliable and accurate, with good concurrent and predictive validity for future psychiatric evaluation and hospitalization. 158  

Horowitz et al 149 , 151 , 159 have performed several studies on ED suicide screening, most recently by using multiple logistic regression modeling to determine which suicide screening questions best screen for and identify occult suicidal youth. 150 A 4-question model was found to optimize sensitivity (97%; 95% CI, 91%–99%), specificity (88%; 95% CI, 84%–91%), and negative predictive value (99%, 95% CI, 98%–99%) for ED patients presenting with both psychiatric and nonpsychiatric conditions. The 4 domains of suicidal ideation are current suicidal ideation, past suicide attempts, current wish to die, and current thoughts of being better off dead. Given the prevalence of suicidal ideation and attempts and the morbidity and mortality associated with attempts, screening patients with unclear or high risk of suicide (eg, those presenting with ingestions, acute intoxication, single-car motor vehicle crashes, and significant falls) also may be important.

Both depression and alcohol abuse may be screened for with 2 questions. Rutman et al 147 found that the 2 questions “During the past month, have you often been bothered by feeling down, depressed, or hopeless?” and “During the past month, have you often been bothered by little interest or pleasure in doing things?” were 78% sensitive (95% CI, 73%–84%) and 82% specific (95% CI, 77%–87%) for adolescent depression. These 2 questions have similar screening properties in adult ED patients as well. 146 Both Newton et al and the National Institute of Alcohol Abuse and Alcoholism (NIAAA) have developed 2-question screens for problematic teenage alcohol use. 148 , 160 Newton et al also believe that a single question may efficiently screen for marijuana use. They used the following questions: “In the past year, have you sometimes been under the influence of alcohol in situations where you could have caused an accident or gotten hurt?”, “Have there often been times when you have a lot more to drink than you intended to have?”, and “In the past year, how often have your used cannabis: 0 to 1 time, or greater than 2 times?” Teenagers who answer “yes” to 1 alcohol question or to the marijuana question have an eightfold and sevenfold increased risk of having a substance use disorder, respectively. The 2 NIAAA questions vary according to the patient’s age and explore the patient’s and their friends’ experience with alcohol. The NIAAA currently is investigating the reliability as well as the concurrent, convergent, discriminant, and predictive validity of this screen. 161  

Computerized screening may add advantages and efficiency to ED mental health screening. They can be administered with little ED clinician time or effort and have been used successfully in both pediatric and general ED settings for general health and mental health screening, alcohol use, 162 , – 164 interpersonal and intimate partner violence, 165 , 166 weapons, 167 injury prevention, 168 and HIV risk behaviors. 169 Adolescents not only rated these screens as highly acceptable but also may prefer such health interventions. 170 , – 172 Fein and Pailler 140 , 173 have developed and implemented an electronic tool for universal screening of ED adolescent physical and mental health risks. The screen was presented to patients by a nurse or medical technician. After the screen was scored, the adolescent’s results were printed out and reviewed by the treating physicians. This method resulted in a 68% increase in identification of psychiatric illnesses and subsequently a 47% increase in mental health assessments.

autism spectrum disorder

confidence interval

central nervous system

developmental disorder

emergency department

US Food and Drug Administration

intravenous

National Institute of Alcohol Abuse and Alcoholism

neuroleptic malignant syndrome

occupational therapy

psychogenic nonepileptic seizures

selective serotonin reuptake inhibitor

visual communication system

This document is copyrighted and is property of the American Academy of Pediatrics and its Board of Directors. All authors have filed conflict of interest statements with the American Academy of Pediatrics. Any conflicts have been resolved through a process approved by the Board of Directors. The American Academy of Pediatrics has neither solicited nor accepted any commercial involvement in the development of the content of this publication.

Clinical reports from the American Academy of Pediatrics benefit from expertise and resources of liaisons and internal (AAP) and external reviewers. However, clinical reports from the American Academy of Pediatrics may not reflect the views of the liaisons or the organizations or government agencies that they represent.

The guidance in this report does not indicate an exclusive course of treatment or serve as a standard of medical care. Variations, taking into account individual circumstances, may be appropriate.

All clinical reports from the American Academy of Pediatrics automatically expire 5 years after publication unless reaffirmed, revised, or retired at or before that time.

FINANCIAL DISCLOSURE: The authors have indicated they have no financial relationships relevant to this article to disclose.

FUNDING: No external funding.

POTENTIAL CONFLICT OF INTEREST: The authors have indicated they have no potential conflicts of interest to disclose.

Thomas H. Chun, MD, MPH, FAAP

Sharon E. Mace, MD, FAAP, FACEP

Emily R. Katz, MD, FAAP

Joan E. Shook, MD, MBA, FAAP, Chairperson

James M. Callahan, MD, FAAP

Gregory P. Conners, MD, MPH, MBA, FAAP

Edward E. Conway Jr, MD, MS, FAAP

Nanette C. Dudley, MD, FAAP

Toni K. Gross, MD, MPH, FAAP

Natalie E. Lane, MD, FAAP

Charles G. Macias, MD, MPH, FAAP

Nathan L. Timm, MD, FAAP

Kim Bullock, MD – American Academy of Family Physicians

Elizabeth Edgerton, MD, MPH, FAAP – Maternal and Child Health Bureau

Tamar Magarik Haro – AAP Department of Federal Affairs

Madeline Joseph, MD, FACEP, FAAP – American College of Emergency Physicians

Angela Mickalide, PhD, MCHES – EMSC National Resource Center

Brian R. Moore, MD, FAAP – National Association of EMS Physicians

Katherine E. Remick, MD, FAAP – National Association of Emergency Medical Technicians

Sally K. Snow, RN, BSN, CPEN, FAEN – Emergency Nurses Association

David W. Tuggle, MD, FAAP – American College of Surgeons

Cynthia Wright-Johnson, MSN, RNC – National Association of State EMS Officials

Alice D. Ackerman, MD, MBA, FAAP

Lee Benjamin, MD, FACEP, FAAP - American College of Physicians

Susan M. Fuchs, MD, FAAP

Marc H. Gorelick, MD, MSCE, FAAP

Paul Sirbaugh, DO, MBA, FAAP - National Association of Emergency Medical Technicians

Joseph L. Wright, MD, MPH, FAAP

Lee S. Benjamin, MD, FACEP, ChairpersonKiyetta Alade, MD

Joseph Arms, MD

Jahn T. Avarello, MD, FACEP

Steven Baldwin, MD

Isabel A. Barata, MD, FACEP, FAAP

Kathleen Brown, MD, FACEP

Richard M. Cantor, MD, FACEP

Ariel Cohen, MD

Ann Marie Dietrich, MD, FACEP

Paul J. Eakin, MD

Marianne Gausche-Hill, MD, FACEP, FAAP

Michael Gerardi, MD, FACEP, FAAP

Charles J. Graham, MD, FACEP

Doug K. Holtzman, MD, FACEP

Jeffrey Hom, MD, FACEP

Paul Ishimine, MD, FACEP

Hasmig Jinivizian, MD

Madeline Joseph, MD, FACEP

Sanjay Mehta, MD, MEd, FACEP

Aderonke Ojo, MD, MBBS

Audrey Z. Paul, MD, PhD

Denis R. Pauze, MD, FACEP

Nadia M. Pearson, DO

Brett Rosen, MD

W. Scott Russell, MD, FACEP

Mohsen Saidinejad, MD

Gerald R. Schwartz, MD, FACEP

Harold A. Sloas, DOOrel Swenson, MD

Jonathan H. Valente, MD, FACEP

Muhammad Waseem, MD, MS

Paula J. Whiteman, MD, FACEP

Dale Woolridge, MD, PhD, FACEP

Carrie DeMoor, MD

James M. Dy, MD

Sean Fox, MD

Robert J. Hoffman, MD, FACEP

Mark Hostetler, MD, FACEP

David Markenson, MD, MBA, FACEP

Annalise Sorrentino, MD, FACEP

Michael Witt, MD, MPH, FACEP

Dan Sullivan

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Reasons for hope

Solutions for the mental health crisis emerge through innovative research, diagnostics and treatments

By Nina Bai

Illustration by Jules Julien

Photography by Leslie Williamson

It’s the spring of hope for mental health, astir with novel discoveries, life-changing therapies and more openness than ever before — yet, for many, it feels like the winter of despair. The pandemic years, that crucible of stress, isolation and uncertainty, fueled and exposed mental health problems. In 2022, nearly 1 in 4 American adults (about 59 million people) said they experienced a mental illness in the previous year, but only half of those afflicted reported receiving any mental health treatment.

Among children and adolescents, the prevalence of mental illness, which had been steadily creeping upward, jumped during the pandemic, according to the U.S. Substance Abuse and Mental Health Services Administration. In 2019, 15.7% of American adolescents aged 12-17 reported experiencing a major depressive episode in the past year. In 2022, that number was 19.5%. That same year, 13.4% of adolescents — just over 1 in 8 — seriously thought about killing themselves.   

And even as the pandemic has stoked demand for mental health care, it also has worn down the mental health workforce, already short-handed, with early retirements and widespread burnout. Access to affordable, effective interventions remains a daunting barrier. People face long waiting lists and lack of insurance coverage. Many treatable conditions remain undiagnosed because people lack a way to obtain assessments. 

Yet, below this perfect storm of mental health crisis, there is a strong undercurrent of hope that begins in the lab. Research is leading the way toward treatments that are more effective, more personalized and more accessible.

“The manner in which we know the brain now, compared with what we knew in previous decades, is incredibly different,” said Victor Carrión , MD, the John A. Turner, MD, Endowed Professor for Child and Adolescent Psychiatry and vice chair of the department of psychiatry and behavioral sciences.

Direct impact on patients

New imaging technologies allow researchers to see the neural circuitry that goes awry in neuropsychiatric disorders, lab-grown clumps of brain tissue — known as organoids — can simulate the impact of genetics in autism, and artificial intelligence can surmise signals that predict the onset of depression and anxiety.

Moreover, these discoveries, rather than moving slowly through specialist silos, can now rapidly inform new treatments. “Collaboration is vital for translation, and our departmental awards and programs promote and emphasize synergy between research and clinical practice,” said Laura Roberts , MD, the Katharine Dexter McCormick and Stanley McCormick Memorial Professor and chair of the department of psychiatry and behavioral sciences.

“Our bench scientists doing tremendous research also work alongside our clinicians to make sure that new knowledge translates to the clinical setting and has a direct impact on patient care,” she said.

Researchers developing transcranial magnetic stimulation, for example, work with clinicians who treat patients with severe depression to design clinical trials, and their techniques are informed by teams inventing new ways to measure the flow of brain signals and those building virtual reality models of the brain.

A clearer understanding of the biology of mental health disorders not only leads to breakthrough treatments — but just as powerfully, helps dissipate stigma.

“There’s been a large shift in stigma in the past 25 years,” said Heather Gotham , PhD, clinical professor of psychiatry and behavioral sciences, who leads the coordination of a nationwide network of centers dedicated to implementing evidence-based mental health care.

The Mental Health Technology Transfer Center Network, funded by the Substance Abuse and Mental Health Services Administration, offers training in preventing school violence, substance use in the workplace, adolescent depression and more, and it offers support for mental health providers seeing refugees and asylum seekers.

“Collaboration is vital for translation, and our departmental awards and programs promote and emphasize synergy between research and clinical practice.” Laura Roberts, the Katharine Dexter McCormick and Stanley McCormick Memorial Professor and chair of the department of psychiatry and behavioral sciences

“One thing that’s made a difference is the greater understanding that mental health disorders and substance use disorders are chronic, relapsing disorders of the body, just like diabetes and heart disease,” Gotham said.

With this new awareness, more people want to be mental health literate. In the past few years, Gotham has seen a surge of interest, from a broader community, in the network’s online courses — from teachers, for example, who want to be more responsive to the needs of students and reduce stigma in the classroom.

Less stigma also means more money for research and mental health services. Funding for mental health has become a rare bipartisan issue. In 2022, Congress passed the Bipartisan Safer Communities Act, which has provided $245 million to fund mental health services like training for school personnel, first responders and law enforcement and expanding the 988 suicide and crisis lifeline.

Stanford Medicine researchers know that to make the most impact with their discoveries they must reach those who need help the most — through online symptom screenings, virtual therapy, group therapy, inclusive clinical trials and community interventions.

They are training mental health professionals locally and globally in new evidence-based techniques. Providers in more than 38 countries, for example, have been trained in cue-centered therapy, a 15-week treatment program developed at Stanford Medicine to help children and teens recover from chronic trauma. Recently, pro bono training in cue-centered therapy was provided to clinicians in Ukraine.

What gives Roberts hope is that a more open conversation on mental health is drawing together experts from different fields with a shared purpose. “It used to be that clinicians would stay in their clinical practice and refer to journals for new research, and researchers would stay in the lab and never see a patient — and we don’t have that now,” she said. “I see more openness and more flexibility from the current generation of researchers and clinicians.”

Read on in this issue of Stanford Medicine to learn about some of the ways Stanford Medicine researchers and clinicians are advancing the understanding of mental health and sharing that knowledge.

Nina Bai is a science writer in the Stanford Medicine Office of Communications.

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MODULE 3: CLINICAL ASSESSMENT, PROBLEMS, AND TREATMENT

Clinical assessment, problems, and treatment.

This module aligns with APNA’s “Clinical Decision Making” specific core nursing content (American Psychiatric Nurses Association Education Council, Undergraduate Branch, 2022).

Module Outline

• Using the nursing process to guide mental health nursing care

Module Learning Outcomes

• Describe the nursing process
• Discuss various treatment options

The Nursing Process

Traditionally, the nursing process involves assessment, diagnosis, planning outcomes, implementation, and evaluation (ADPIE). However, you may remember from the Introduction, this text will focus on Problems (see the Introduction for explanation). An interview with the patient will allow the nurse to gather crucial information for the assessment. When interacting with patients, it is imperative to be aware of the potential for t ransference and countertransference. Transference is the process through which patients transfer attitudes to the nurse. They may be positive and include friendly, affectionate feelings, or negative, and include hostile and angry feelings. Countertransference is a similar attitude transfer, but from the nurse to the patient.

Read more about the nursing process here: https://www.ncbi.nlm.nih.gov/books/NBK499937/  (Toney-Butler & Thayer, 2022).

The nursing process is used to guide mental health nursing care. The first step of the nursing process is an assessment. In general, the nurse is gathering data, including:

• allergies and code status
• list of current medications (dose, frequency, route)
• current assessment of presenting signs/symptoms, any effects on daily functioning
• pertinent physical, surgical, and psychosocial history
• cultural, spiritual, sexual, and gender identity

An initial assessment serves as a baseline to inform future needs. The assessment involves the collection of subjective data (i.e., information from the patient or caregiver) and objective data (i.e., measurable data such as vital signs, intake and output, height and weight, and nurse’s assessment). This collection of information involves critical thinking about the client’s skills, abilities, personality characteristics, cognitive and emotional functioning, the social context in terms of environmental stressors that are faced, and cultural factors particular to them such as their language or ethnicity. Lastly, it is important to note that clinical assessment is ongoing.

Mental Health  Assessment

Specific to a mental health assessment, a nurse would also incorporate additional attention to a mental status examination.  A mental status examination is used to organize the information collected during the interview and systematically evaluate the patient through a series of questions assessing appearance and behavior. The latter includes grooming and body posture, thought processes and content to include disorganized speech or thought and false beliefs, mood and affect such that whether the person feels hopeless or elated, intellectual functioning to include speech and memory, and awareness of surroundings to include where the person is and what the day and time are. The exam covers areas not normally part of the interview and allows the mental health professional to determine which areas need to be examined further. See Voss and Das’s (2021) resource for further explanation of the mental status examination.

Additional Assessment Resources

• Nurses can utilize Dr. Leininger’s Sunrise Enabler (Transcultural Nursing Society, 2022) as a tool to help guide assessment.
• For a new admission , students might find Toney-Butler and Unison-Pace’s (2021) resource helpful.

Nursing students will notice patients’ medical records may often contain several diagnoses (e.g., medical and psychological). Diagnoses serve as a communication tool to members of the healthcare team and relay the patient’s health needs as well as to insurance providers. Specific to mental health needs, the American Psychiatric Association (APA) publishes the most widely used classification system in the United States (i.e., Diagnostic and Statistical Manual of Mental Disorders  (DSM) (APA, 2022).  The DSM is currently in its 5th edition Text-Revision (DSM-5-TR) and is produced by the American Psychiatric Association (APA, 2022). The DSM-5-TR is used to formally document the presence of a mental health diagnosis.

Nurses can use nursing diagnoses to document patient health needs. Nursing diagnoses are apart from medical diagnoses. The North American Nursing Diagnosis Association (NANDA) provides an official list of nursing diagnoses.  Nursing diagnoses are used to describe actual or potential health problems related to a patient, family, or community (Toney-Butler & Thayer, 2022). Remember from Maslow’s Hierarchy of Needs that basic needs should be met before higher level needs (Toney-Butler & Thayer, 2022). Nursing students can typically find NANDA’s nursing diagnoses within a fundamental or medical surgical nursing text.

This text will focus on the problem statement of the nursing diagnosis. For example, in the nursing diagnosis statement: Anxiety related to situational crisis as evidenced by statement of “I feel overwhelmed by the loss of my job!” Anxiety is the identified problem.

Watch “How to write a diagnosis.mov” (hawknurse, 2010) for further explanation of nursing diagnoses.

Planning Outcomes

Planning outcomes, sometimes seen written as “goals”, are created to establish a positive health outcome. The patient’s outcomes should be formed with the patient to ensure patient-centered care (Quality and Safety Education for Nurses, 2020).

Outcomes/goals should be S.M.A.R.T .:

• Measurable or Meaningful
• Attainable or Action-Oriented
• Realistic or Results-Oriented
• Timely or Time-Oriented

Implementation

• Explore the Dimensions of Wellness Wheel above to gather ideas patients can help create mental health wellness throughout many aspects of their lives.

Cognitive therapy/CBT

Complementary alternative medicine (cam), electroconvulsive therapy.

Electroconvulsive therapy (ECT) is a procedure wherein an electric stimulus is used to produce a generalized seizure. Patients are placed on a padded bed and administered a muscle relaxant to avoid injury during the seizures. ECT is not typically a first-line treatment option.

 Psychosurgery

Another option to treat mental disorders is to perform brain surgeries. In the past, we have conducted trephination and lobotomies, neither of which are used today. Today’s techniques are much more sophisticated and have been used to treat schizophrenia, depression, and some personality and anxiety disorders. However, critics cite obvious ethical issues with conducting such surgeries as well as scientific issues.

Transcranial Magnetic Stimulation 

Transcranial magnetic stimulation (TMS) is a non-invasive procedure that uses low or high-intensity magnetic fields to stimulate brain tissue (Mann & Malhi, 2022). Repetitive transcranial magnetic stimulation (rTMS) refers to utilizing repetitive TMS pulses to a specific region of the brain (Mann & Malhi, 2022). TMS can be performed outpatient. The patient is alert and will feel a tapping sensation. Possible side effects include headache, neck pain, local pain, and transient tinnitus (Mann & Malhi, 2022). These side effects are typically mild and resolve in a short period of time (Mann & Malhi, 2022). Seizures are rare with higher incidence for those having epilepsy (Mann & Malhi, 2022).

Psychopharmacology

Nami’s resources.

Review the  National Alliance on Mental Illness (NAMI) webpage for an overview of the above mental health treatments (NAMI, 2022a).

The final step in the nursing process is evaluation of interventions towards achievement of the outcomes ( Toney-Butler & Thayer, 2022). Evaluation is imperative as it provides information to maintain, modify, add additional, and/or stop current interventions.

Key Takeaways

You should have learned the following in this section:

• Traditionally, the nursing process (ADPIE) is used to develop a nursing plan of care.
• Nursing diagnoses are not medical diagnoses. NANDA nursing diagnoses are used to form nursing care plans that can be complementary to or apart from medical diagnoses. In this text, we will focus on the identified problem of the nursing diagnosis
• The nursing process is an ongoing process to evaluate the patient’s progress towards a state of holistic health.

Transference is the process through which patients transfer attitudes to the nurse. These attitudes may be positive and include friendly, affectionate feelings, or negative, and include hostile and angry feelings.

Countertransference is the process through which a healthcare provider transfers attitudes to the patient. These attitudes may be positive and include friendly, affectionate feelings, or negative, and include hostile and angry feelings.

The outward expression of one's mood.

MENTAL HEALTH IS A VERB Copyright © 2023 by Jake Bush and Jill Van Der Like is licensed under a Creative Commons Attribution-NonCommercial-ShareAlike 4.0 International License , except where otherwise noted.

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Choosing Meaningful Actions to Support Clinicians’ Mental Health

Why it matters.

During Mental Health Awareness Month — and every month of the year — it is vital to help destigmatize getting mental health support when it is needed.

May is  Mental Health Awareness Month in the US, and we have all seen the well-intended sentiments and gestures this time of year that can ring hollow for some working in health care. A table full of pizzas is offered to nurses who do not have time to eat due to staffing shortages. Doctors who are expected to see more patients in less time get free pens stamped with their health system’s logo. Clinic staff receiving pay cuts see inspiration-themed posters freshly mounted on the walls. Hospital workers stressed near their breaking points get commemorative medals.

Many of us have made such missteps and may have seen the resulting disillusionment and disaffection that is made more complicated by the pervasive threats to clinician mental health. Given this reality, it can be paralyzing for employers to determine how best to support employees. But any health care organization can take important steps to support mental health. For example, regardless of organization size or resources, one meaningful and achievable action is to remove job and credentialing application-related barriers to clinicians seeking mental health care.

Most health care organizations ask clinical applicants — including nurses, doctors, respiratory therapists, podiatrists, and pharmacists — if they have or have had a mental health diagnosis or have ever sought mental health care even if having that diagnosis has not in any way affected their ability to do their job . Employers originally asked such questions in the misguided belief that clinicians with a mental health diagnosis would worsen patient care.

There is no evidence that these questions improve quality or safety, but their presence on job and credentialing applications  deters clinicians from seeking and receiving mental health care . This worry may seem misplaced, but it is unsurprising given that clinicians cannot practice without going through these processes.

When health care organizations remove these questions from their job and credentialing applications it helps physicians, nurses, and other clinicians overcome this common barrier to receiving care. When taking this step, our organizations can also add an explicit statement of support for people seeking the care they need. An expert consensus group from the Institute for Healthcare Improvement (IHI)  Leadership Alliance developed this example: “It is common for clinicians to feel overwhelmed from time to time and to seek help when appropriate. We emphasize the importance of well-being and appropriate treatment and support for all health conditions.”

A recent high-profile initiative to remove these care-deterring questions from license applications came out of Massachusetts, where  every hospital, health system, and local health plan is eliminating such questions . Smaller, local successes are crucial, and Mental Health Awareness Month is the perfect time to start.

If you are unsure where to begin, you do not have to go it alone. Join colleagues across the country working to reduce barriers to clinicians seeking mental health care. Use the tools developed by and for clinicians as part of the IHI  Leadership Alliance   Helping Healthcare Heal Coalition to educate peers, professional society members, medical boards, and health care institutions about these issues. The Coalition’s  publicly available resources include a sample email to send to your medical staff office or credentialing committee recommending this change. There are also talking points, a slide presentation with speaker notes, an FAQ document, and references supporting this work.

All health care organizations can help physicians, nurses, and other clinicians overcome barriers to seeking and receiving mental health care. Tools are available right now to help you make this meaningful change before this Mental Health Awareness Month has passed.

Eileen Barrett, MD, MPH, practices internal medicine on the Navajo Nation.

If you or someone you know may be considering suicide or are in crisis, please  call or text 988 to reach the Suicide & Crisis Lifeline .

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5 Reasons to Include Psychosis in Mental Health Awareness

Let's not leave psychosis out of this may's mental health awareness campaigns..

Posted May 1, 2024 | Reviewed by Davia Sills

• What Is Psychosis?
• Find counselling to treat psychosis
• Psychosis is common; as many as 1 in 10 may experience a psychotic symptom in their lifetime.
• Tragically, research strongly links schizophrenia to risk of suicide.
• A meta-analysis found 57 percent of individuals who had a first episode of psychosis recovered; there is hope.

May 1st marks the beginning of Mental Health Awareness Month. Never before have we in America seen such an acceptance of the realities of emotional pain and the healing that can come from reaching out for help. Still, amid anti- stigma campaigns focused on difficulties such as depression and anxiety , there is one area that often remains unacknowledged: the experiences of those living with psychosis and schizophrenia.

We can change this. What follows are five reasons that mental health awareness must include these experiences.

1. Psychosis and Schizophrenia Are Common.

While a diagnosis of schizophrenia only affects one in 100 people, the lifetime prevalence of experiences associated with psychosis may affect as many as 1 in 10 people (Beavan et al., 2011). Still, psychosis remains a topic that is not often talked about in our culture, leading many who are suffering from it to feel quite alone.

2. People Need to Know That There Is Hope.

Historically, conditions involving psychosis were seen as a sort of "kiss of death" diagnosis. Yet, with innovative treatments, research is finding that an overwhelming majority of people who experience psychosis in their lifetime recover. A meta-analysis of studies involving a total of 12,301 participants experiencing a first episode of psychosis found that 58 percent made a full recovery, with a greater proportion achieving remission each year (Lally et al., 2017).

3. Misunderstanding Is Dangerous.

Despite positive outcomes overall, a recent research study featuring a review of medical records found that schizophrenia was more frequently linked to suicide than any other mental health condition (Song et al., 2020). More recent onset of the illness is linked to a higher risk of suicide (Popovic et al., 2014). Clinicians hypothesize that this may be due to a loss of hope. Through education , we can dispel the dangerous myth that schizophrenia represents a hopeless situation and show that recovery is possible.

4. Acceptance Saves Lives.

Research shows that social isolation is a major risk factor for suicidal ideation in individuals living with schizophrenia (Bornheimer et al., 2020). By spreading awareness and moving toward acceptance, we may be able to overcome the unfortunate reality of isolation experienced by those with schizophrenia instead by embracing these individuals and the many strengths they have to share.

5. Early Identification of Psychosis Can Make All the Difference.

Early identification of psychosis has been shown to strongly improve outcomes (McGorry, 2015). In the case of schizophrenia, some research suggests that untreated psychosis can result in more grey matter being lost in the brain. Some experts believe intervention within the early years of psychosis to be just as critical and make just as big a difference as if treatment is delivered within the first 30 minutes of a stroke. By increasing awareness of psychosis, we may also enhance identification and intervention for a better quality of life and chances of recovery.

Beavan, V., Read, J., & Cartwright, C. (2011). The prevalence of voice-hearers in the general population: a literature review. Journal of Mental Health , 20 (3), 281-292.

Blumer, D. (2002). The illness of Vincent van Gogh. American Journal of Psychiatry , 159 (4), 519-526.

Bornheimer, L. A., Li, J., Im, V., Taylor, M., & Himle, J. A. (2020). The role of social isolation in the relationships between psychosis and suicidal ideation. Clinical Social Work Journal , 48 , 54-62.

Lally, J., Ajnakina, O., Stubbs, B., Cullinane, M., Murphy, K. C., Gaughran, F., & Murray, R. M. (2017). Remission and recovery from first-episode psychosis in adults: systematic review and meta-analysis of long-term outcome studies. The British Journal of Psychiatry , 211 (6), 350-358.

McGorry, P. D. (2015). Early intervention in psychosis: obvious, effective, overdue. The Journal of nervous and mental disease , 203 (5), 310-318.

Popovic, D., Benabarre, A., Crespo, J. M., Goikolea, J. M., González‐Pinto, A., Gutiérrez‐Rojas, L., & Vieta, E. (2014). Risk factors for suicide in schizophrenia: systematic review and clinical recommendations. Acta Psychiatrica Scandinavica , 130 (6), 418-426.

Song, Y., Rhee, S. J., Lee, H., Kim, M. J., Shin, D., & Ahn, Y. M. (2020). Comparison of suicide risk by mental illness: a retrospective review of 14-year electronic medical records. Journal of Korean medical science , 35 (47).

Jennifer Gerlach, LCSW, is a psychotherapist based in Southern Illinois who specializes in psychosis, mood disorders, and young adult mental health.

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This article is part of the research topic.

Insights in Sleep, Behavior and Mental Health: Volume II

Rett Syndrome: A Review of Clinical Manifestations and Therapeutic Approaches Provisionally Accepted

• 1 University of North Carolina Hospitals, United States

The final, formatted version of the article will be published soon.

Rett syndrome (RTT) is a severe X-linked dominant neurodevelopmental disorder predominantly affecting females (Tascini et al., 2022) and over 90% of these patients mutations linked to the methyl-CpG-binding protein 2 (MeCP2) gene (Zoghbi 2005, Weaving et al., 2005). Although the syndrome is well noted for the classic repetitive hand motion with decline in speech, patients may have a wide range of cognitive and motor impairments. Typical comorbidities in RTT are characterized by poor growth, seizures, disrupted sleep, hyperventilation, breath holding spells, feeding difficulties, scoliosis, and behavioral issues (Gold et al., 2018). This paper aims to provide a brief overview of RTT, focusing on the clinical features of sleep and epilepsy, effects on childhood development, and available emerging treatment options. Sleep disturbances, epilepsy, and developmental regression can have profound effects on the quality of life in affected individuals. Current management strategies focus on a multidisciplinary approach to address symptoms and enhance overall well-being of individuals with RTT.

Keywords: Rett, Neurodevelopment disorders, sleep disorder, Epilepsy, Developmental Disabilities

Received: 19 Jan 2024; Accepted: 02 May 2024.

Copyright: © 2024 Bricker and Vaughn. 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: Mx. Katelyn Bricker, University of North Carolina Hospitals, Chapel Hill, United States Mx. Bradley Vaughn, University of North Carolina Hospitals, Chapel Hill, United States

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Perspectives from the Inaugural “Spinal CSF Leak: Bridging the Gap” Conference: A Convergence of Clinical and Patient Expertise

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BACKGROUND AND PURPOSE: The inaugural “Spinal CSF Leak: Bridging the Gap” Conference was organized to address the complexities of diagnosing and treating spinal CSF leaks. This event aimed to converge the perspectives of clinicians, researchers, and patients with a patient-centered focus to explore the intricacies of spinal CSF leaks across 3 main domains: diagnosis, treatment, and aftercare.

MATERIALS AND METHODS: Physician and patient speakers were invited to discuss the varied clinical presentations and diagnostic challenges of spinal CSF leaks, which often lead to misdiagnosis or delayed treatment. Patient narratives were interwoven with discussions on advanced radiologic techniques and clinical assessments. Treatment-focused sessions highlighted patient experiences with various therapeutic options, including epidural blood patches, surgical interventions, and percutaneous and endovascular therapies. The intricacies of immediate and long-term postprocedural management were explored.

RESULTS: Key outcomes from the conference included the recognition of the need for increased access to specialized CSF leak care for patients and heightened awareness among health care providers, especially for atypical symptoms and presentations. Discussions underscored the variability in individual treatment responses and the necessity for personalized diagnostic and treatment algorithms. Postprocedural challenges such as managing incomplete symptom relief and rebound intracranial hypertension were also addressed, emphasizing the need for effective patient monitoring and follow-up care infrastructures.

CONCLUSIONS: The conference highlighted the need for adaptable diagnostic protocols, collaborative multidisciplinary care, and enhanced patient support. These elements are vital for improving the recognition, diagnosis, and management of spinal CSF leaks, thereby optimizing patient outcomes and quality of life. The event established a foundation for future advancements in spinal CSF leak management, advocating for a patient-centered model that harmonizes procedural expertise with an in-depth understanding of patient experiences.

• ABBREVIATIONS:

The inaugural “Spinal CSF Leak: Bridging the Gap” Conference, held on November 11, 2023, highlighted collective insights shared by a diverse cohort of clinicians, researchers and, crucially, patients. The goal of this conference was to foster a nuanced, patient-centered understanding of the diagnosis and treatment of spinal CSF leak (SCSFL), a condition that has historically posed profound challenges to both patients and physicians.

SCSFL may be spontaneous, resulting in the syndrome of spontaneous intracranial hypotension, or may be caused by an intentional or unintentional dural puncture, producing acute or chronic post-dural puncture headache (PDPH). SCSFL frequently present a diagnostic conundrum due to ambiguous clinical presentations combined with a relative lack of recognition in the medical community. Many patients with SCSFL are initially misdiagnosed, leading to delays in care, inappropriate treatments, and degrading patient trust in the medical system. 1 ⇓ - 3 This mismanagement is superimposed on a condition which, when left untreated, can cause immense disability and suffering. 4

This conference was designed not only to feature physician experts in the field but to provide a platform for a diverse group of patients to synthesize their experiences in a didactic format and highlight their journey throughout SCSFL care. A variety of perspectives were presented, converging on a proposed framework that balanced cutting-edge diagnostic and treatment techniques with a patient-centered approach. The conference was divided into 3 sessions: diagnosis, treatment, and aftercare.

• MATERIALS AND METHODS

Content from lectures at the conference was reviewed and synthesized with current literature to summarize the major themes pertaining to SCSFL care. Patient lectures and video compilations were recorded and transcribed using a large language model (GPT-4) to convert patient narratives into written form. Recommendations were abstracted from the content of the conference and summarized by the authors.

The Patient Perspective.

The conference opened with a narrative shared by a patient detailing their decade-long struggle with undiagnosed symptoms of a SCSFL. At 11 years of age, the patient had a fall, which led to a diagnosis of postconcussion headaches, and at 15 years of age underwent corrective surgery for scoliosis. The patient developed worsening in orthostatic symptoms postoperatively, initially attributed to a postconcussion syndrome. It was not until a potential chronic surgical leak was identified by a subspecialist years later that the patient received epidural patching and symptom relief. This patient’s journey highlights the potentially disabling delay in diagnosis commonly experienced by patients with SCSFL. This narrative emphasized the need for heightened awareness of SCSFL among health care providers for younger demographics, in whom the condition is often unexpected and the diagnosis challenging.

Another perspective was shared by a patient with a PhD and professional background in trauma therapy who had a CSF-venous fistula (CVF). Given this unique position, he shed light on the psychological challenges accompanying undiagnosed or misdiagnosed SCSFL, including the emotional toll and mental health implications of living with chronic, unexplained symptoms. Additionally, he suggested techniques for patients to process trauma associated with a SCSFL diagnosis and treatment to reclaim their health autonomy. This narrative advocated an enhanced, empathetic, and comprehensive approach by health care professionals to address the mental health aspects inherent in the patient journey of SCSFL. Specifically, it stressed the importance of the patient-provider relationship in SCSFL care, extending beyond diagnostic and therapeutic procedures. This aspect is particularly important for procedural neuroradiologists, who often perform procedures in isolation and without a framework for continuity of care.

Clinical Challenges

The complexity of diagnosing SCSFL hinges on the wide spectrum of clinical presentations that often lead to misdiagnosis or delayed treatment ( Table ). The classic clinical presentation of SCSFL is characterized by an orthostatic headache. The headaches themselves can have nuanced features, which should be addressed via a thorough history. Patients also frequently describe acephalgic symptoms including fatigue, tinnitus, ear fullness, light sensitivity, cognitive dysfunction. and neck pain, and often experience worsening of symptoms during the day. 5 Patients with acephalgic symptomatology may be particularly susceptible to misdiagnosis and inappropriately dismissed if a classic orthostatic headache is not described.

Differential diagnoses in patients presenting with SCSFL

Patients with SCSFL are frequently misdiagnosed with migraine. Chronic migraine is characterized by headaches on >15 days per month for at least 3 months, with at least one-half of these days demonstrating unilateral throbbing pain, physical activity exacerbation, light and noise sensitivity, or nausea. 6 Chronic migraine evolves across time with increased frequency of attacks, while SCSFL symptoms often begin suddenly. Cephalgia in SCSFL is typically orthostatic and worsens as the day progresses, while migraine attacks often occur in the morning. Patients may also be frequently misdiagnosed with postconcussion headaches, because some SCSFL leaks are precipitated by trauma. 7 However, the postconcussion syndrome more commonly presents with migraine-like, nonorthostatic headaches and cognitive issues. 8

Postural orthostatic tachycardia syndrome (POTS) is a condition predominantly affecting young women and is characterized by an abnormal heart rate increase on standing. 6 Many patients with POTS also have headache; however, most POTS headaches are nonorthostatic and resemble migraine, while orthostatic headache and neck stiffness are more common in SCSFL. 9

SCSFL can be radiographically misdiagnosed as Chiari I morphology due to potential presence of cerebellar tonsillar ectopia in both conditions. Scrutiny of the posterior fossa structures on brain MR imaging aids in the reliable differentiation of these 2 entities. 2 , 10 While patients with both SCSFL and Chiari I can present with occipital headaches and neck pain, patients with Chiari I do not commonly have orthostatic headaches but may experience lightheadedness or fainting. 11

Connective tissue disorders (CTD) are common in patients with SCSFL. 12 Patients with CTD often exhibit chronic, debilitating symptoms that are challenging to treat due to multifactorial etiologies. For instance, mast cell dysfunction has been linked to CTD, causing disordered immune/inflammatory responses. 13 Patients may undergo evaluation for Ehler Danlos syndrome, small fiber neuropathy, and/or craniocervical instability, and pinpointing a specific diagnosis is often difficult. In designing diagnostic and treatment strategies for such patients, the interplay of these various disorders must be considered.

It is the synthesis of both clinical and radiographic clues that leads to diagnostic optimization for patients with SCSFL. Discussing patients in a formal, multidisciplinary conference incorporating expertise from neurologists, neurosurgeons, and neuroradiologists can be critically important in this regard. 14

Radiologic Challenges

In SCSFL, brain MR imaging classically demonstrates diffuse pachymeningeal enhancement, subdural collections, venous/pituitary engorgement, and/or sagging of the posterior fossa structures. However, a proportion of brain MR imaging studies will be interpreted as having normal findings in patients with proved SCSFL. 15 Some patients experience normalization of brain MR imaging findings with time, despite persistent symptoms and a localizable dural defect or CVF ( Fig 1 ). 16 It is, therefore, crucial to obtain all prior imaging for patients presenting with symptoms of SCSFL, particularly imaging available close to the onset of symptoms. Some patients may have their examinations incorrectly interpreted as having normal findings, particularly when these changes are subtle ( Fig 2 ). 17 Findings of others are truly normal even with careful scrutinization for subtle MR imaging findings. This outcome is particularly true of patients with PDPH, in whom findings of brain imaging are frequently normal, particularly in the chronic period despite known dural puncture and new headache symptoms. 18 , 19

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Normalization of MR imaging findings across time despite persistent spinal CSF leaks. A , Sagittal T1 noncontrast MR imaging in 2018 demonstrates sagging of posterior fossa structures ( bracket ), engorgement of the pituitary gland, and narrowed suprasellar distance ( arrow ). B , Axial FLAIR MR imaging in 2018 demonstrates a diffuse, thin subdural collection ( arrows ). Sagittal ( C ) and axial ( D ) T2 MR imaging of the cervical spine in 2018 shows a cervicothoracic ventral epidural fluid collection ( arrows ). The patient underwent a dorsal nontargeted epidural blood patch in 2018 with partial relief of symptoms. E , Sagittal T1 noncontrast MR imaging in 2023 demonstrates resolution of brain sag, pituitary engorgement, and narrowing of the suprasellar interval. F , Axial FLAIR MR imaging in 2023 with resolution of the subdural collection. Sagittal ( G ) and axial ( H ) T2 MR imaging of the cervical spine in 2023 shows persistence of the cervicothoracic ventral epidural fluid collection. I . Intraoperative photograph later in 2023, with a ventral dural defect identified at T2–T3 ( arrows ). After repair, the patient had substantial symptom improvement, with the Headache Impact Test score improving from 68 to 48 (Headache Impact Test: range, 36–78).

Brain MR imaging findings incorrectly reported as normal in a patient with spontaneous intracranial hypotension. A , Sagittal T1 postcontrast MR imaging demonstrates mild narrowing of the suprasellar (1 mm, dotted arrow ), mamillopontine (4.8 mm, dashed arrow ), and prepontine (3 mm, solid arrow ) distances. B , No pachymeningeal thickening or subdural collection on axial T1 postcontrast MR imaging. C , Left-lateral decubitus dynamic CTM detected a CVF arising from the left T7–8 neural foramen ( arrow ).

The Bern Score is a probabilistic scoring system reflecting the likelihood of localizing a leak or CVF on myelography ( Fig 3 ). 20 ⇓ - 22 It is derived from the sum of points ascribed to certain observations on brain MR imaging and can help radiologists avoid inappropriately characterizing an abnormal examination having abnormal findings as having normal findings. 17 However, a recent study by Houk et al 23 demonstrated that the Bern Score does not correlate with clinical headache severity. This finding challenges the hypothesis that symptoms in SCSFL are directly related to sagging/traction on meningeal layers and/or venous engorgement. Understanding the specific role of brain MR imaging findings and Bern Score applications and limitations is critical to appropriately triage patients with suspected SCSFL.

The Bern score. A, Sagittal T1 noncontrast MR imaging demonstrating the suprasellar interval ( solid line , normal, >4 mm), mamillopontine interval ( dotted line , normal, >6.5 mm), and prepontine interval ( dashed line , normal, >5 mm). B , Sagittal T1 postcontrast MR imaging illustrates a normal flat appearance of the upward margin of the transverse sinus ( arrow ). C , Coronal FLAIR MR imaging with bilateral subdural fluid collections ( arrows ). D , Sagittal T1 postcontrast image demonstrates abnormal venous engorgement evidenced by an abnormal convex upward margin ( solid arrow ), as well as diffuse pachymeningeal enhancement ( dotted arrows ). The presence of a narrowed suprasellar interval, venous engorgement, or pachymeningeal enhancement are ascribed 2 points each, while a narrowed mamillopontine interval, prepontine interval, or the presence of subdural collections are ascribed 1 point each. A combined score of ≤2 equates to low probability, a score of 3 or 4 equates to moderate probability, and a score of ≥5 equates to high probability of localizing a CSF leak or venous fistula on subsequent myelography. 20

CVFs are not visible on conventional CT myelography (CTM) and thus have long evaded detection, with the first formal description published in 2014. 35 Dynamic lateral decubitus CT or fluoroscopic myelography (with or without digital subtraction, digital subtraction myelography [DSM]) producing densely layering contrast along the lateral thecal sac is key to localizing CVF. 14 Provocative maneuvers such as resisted inspiration can also enhance fistula conspicuity. 24 , 25 Whether DSM or CTM is performed for CVF localization depends on institutional resources and expertise. Newer CT technology, specifically photon-counting CT, has been shown to increase the sensitivity for small CVFs by using ultra-high-resolution imaging with 0.2-mm slices at lower radiation doses. 26

In the case of dural defects or ruptured meningeal diverticula, conventional, nondynamic CTM will confirm the presence of an extradural collection but lacks the temporal resolution for precise leak localization. Furthermore, heavily T2-weighted, noncontrast 3D MR imaging of the spine is noninferior to conventional CTM for the detection of epidural fluid collections. 27 , 28 Thus, conventional CTM is likely of limited utility in the work-up of suspected SCSFL. Additionally, CTM exposes patients to radiation and a dural puncture, risking the development of PDPH.

We recommend that patients with suspected SCSFL undergo contrast-enhanced brain MR imaging and heavily T2-weighted MR imaging of the entire spine before an invasive procedure. The Bern Score should be calculated to assess the potential yield of myelography, and spinal MR imaging should be scrutinized for the presence of any epidural fluid. This work-up strategy maximizes information for procedural planning and patient counseling. 12 In patients with a high clinical suspicion of SCSFL but a low Bern score and no spinal epidural fluid, a trial of empiric epidural blood patching is a useful treatment strategy, potentially providing symptom relief while minimizing the risk to the patient. 29

The experience of undergoing an epidural blood patch was highlighted in a video montage of patient testimonials. These personal accounts detailed the effects of the procedure, ranging from marked relief to minimal or short-lived symptom improvement. Some patients described intense pain during the procedure, while others noted minimal discomfort. Patients expressed a range of emotions, from gratitude for the relief provided to frustration and disappointment in cases in which symptoms persisted or recurred. Their narratives underscored the complexity and variability of patient responses to this treatment, emphasizing the need for individualized care and the importance of patient-provider communication in managing expectations and outcomes of the procedure.

A family medicine physician who experienced an SCSFL shared her unique perspective as both a doctor and patient. In 2020, she developed a sudden-onset severe headache following a cough, which only improved on lying down, leading to suspicion of an SCSFL. Despite her medical background, she was unfamiliar with this condition and, like many patients, had to educate herself. She underwent epidural blood patching, which provided only partial relief. Communication with specialists led to a recommendation for surgery due to a suspected ventral dural defect. However, like many patients with SCSFL, she faced challenges obtaining definitive treatment, requiring approval for an out-of-network referral and interstate travel for the procedure. She ultimately underwent surgical repair. The postoperative period was daunting, marked by the challenge of recovering away from her medical team. The surgery successfully alleviated her headaches; however, returning to work as a physician proved challenging due to persistent back pain, requiring an extended medical leave. More than 2 years postsurgery, she still experiences back pain, a condition she accepts as a trade-off for freedom from debilitating head pain. Her experience underscores the importance of having a support network while undergoing treatment and the reality of living with long-term effects of invasive medical interventions.

Percutaneous and Endovascular Therapies

Image-guided percutaneous treatments for SCSFL include image-guided injection of autologous blood and/or fibrin sealant into the epidural space, ideally targeted to the localized dural defect or CVF. 30 Patching can close the leak without surgical intervention, particularly when performed near symptom onset. However, as a leak persists into the chronic period, the likelihood that surgery will be required for definitive management increases. 31 Thus, prompt recognition of an SCSFL is critical to maximize the success of percutaneous patching. Nontargeted epidural blood patching can be performed using a 2-level thoracolumbar interlaminar approach and ideally injecting at least 20 mL of autologous blood. 32 , 33 Targeted patching is performed when a leak is localized and may be performed with fluoroscopy or CT guidance. When a ventral leak is identified, a far-lateral transforaminal approach may allow injection directly into the ventral epidural space ( Fig 4 ). 34 Guidelines for post-patch management vary widely across institutions, especially regarding the duration of bed rest and activity restrictions. In most centers, patients are advised to lie flat for 24–72 hours postpatch and avoid bending, lifting, or twisting for 6 weeks. Because there is a relative lack of high-quality evidence supporting specific recommendations, guidance provided is often based on expert opinion and physiologic principles.

A 35-year-old man with spontaneous intracranial hypotension who underwent 2 prior nontargeted dorsal epidural blood patches. Sagittal ( A ) and axial ( B ) T2-weighted MR imaging sequences demonstrate a ventral epidural fluid collection ( arrows ). C , Prone dynamic CTM detected contrast extravasating from the subarachnoid into the ventral epidural space at T1-2, consistent with a ventral dural defect ( arrow ). D , Procedural image from a CT-guided epidural blood and fibrin patch using a 15-cm 22-ga spinal needle via a far-lateral transforaminal approach to target the ventral epidural space adjacent to the defect ( arrow ). Postinjection sagittal ( E ) and axial (F ) images demonstrate spread of injected blood and fibrin glue along the ventral epidural space ( arrows ). Posttreatment sagittal T2 ( G ) and axial 3D T2 fat-saturated MR imaging ( H ) with resolution of the epidural fluid collection.

Initially described treatment for CVF included surgical ligation of the associated nerve root. 35 More recently, both transvenous embolization with liquid embolic agents and percutaneous occlusion with fibrin sealant have been described with success rates of >50%. 36 , 37 At institutions equipped with such treatment modalities, an initial trial of either transvenous embolization or fibrin occlusion may be attempted before surgical ligation. If these procedures fail to relieve the patient’s symptoms, surgical intervention should be considered.

Surgical Treatment

Advancements in radiology, particularly DSM and dynamic CTM, have revolutionized the surgical approach to spinal CSF leaks, enabling a precise identification of the leak type and location and allowing minimally invasive approaches. 38 Such techniques can include a hemilaminectomy performed under microscopic visualization using tubular retractors placed through small incisions, thereby reducing postoperative pain.

Surgical strategies for repair of ventral dural defects have evolved with time. Rather than requiring an anterior approach with corpectomy and potential thoracotomy, ventral dural defects may be repaired using a transdural, posterior approach, improving patient outcomes and recovery time ( Fig 5 ). 39 , 40 Defects may be closed with direct suturing, collagen patches, or fat/muscle grafts.

A 49-year-old man with a history of spontaneous intracranial hypotension, with persistent symptoms after 3 epidural blood patches. A , Axial SWI with hypointense signal along the cerebellar folia ( arrows ), consistent with superficial siderosis, a rare complication of chronic CSF leak. B , Axial T2-weighted MR imaging demonstrates a ventral epidural fluid collection ( arrows ). C , Axial noncontrast CT image shows a small osteophyte ( arrows ) along the ventral canal at T6–7. D , Prone dynamic CTM demonstrates extravasation of contrast from the subarachnoid space into the ventral epidural space at T6–7 ( arrows ), consistent with a ventral dural defect. E , Intraoperative photograph during repair of the ventral dural defect ( arrows ) at T6–7, accessed via hemilaminectomy, posterior durotomy, and lateral mobilization of the cord after dentate ligament resection .

Iatrogenic leaks can also require surgical intervention. Post-dural puncture pseudomeningoceles, also known as arachnoid “blebs,” have been reported to cause symptoms of SCSFL and can be repaired using minimally invasive surgical approaches. 41 , 42 Treatment of a CVF can include ligation of the fistula alone versus transection of the involved nerve root. The postoperative length of the hospital stay can vary, influenced by the surgical approach and patient-specific factors such as rebound intracranial hypertension (RIH).

A recent study identified substantial gaps in the evidence for the efficacy of epidural patching and surgery in the treatment of SCSFL. 43 Thus, there are opportunities for future research in this area, which could be supported by patient registries and multicenter collaborations.

Posttreatment

Patient perspective: recovery..

A patient discussed her personal journey navigating the recovery process from a SCSFL. She shared her experience with a difficult-to-localize leak, and the many procedures were required before the leak was durably repaired. She described the challenge of undertaking recovery without locally available comprehensive care. She noted that for many patients who lived for years with SCSFL, recovery becomes an existential experience, questioning the meaning of healing and reckoning with a new reality that, while potentially characterized by meaningful clinical improvement, may look nothing like a prior normal life.

She reported that uncertainty is typical during the recovery process, even after successful treatment. Some techniques used to cope with her evolving posttreatment state included tracking symptoms, which helped her take a long view of ongoing severity or resolution, and using talk therapy to process the trauma of living with a SCSFL for so many years.

As noted in her talk, current quaternary referral programs are unable to provide sustained, holistic, comprehensive care to address not only diagnosis and treatment but the recovery process as well. She concluded with a call to action for those in the medical community to consider that although a leak may be closed, it does not mean that the patient’s symptoms have been fully addressed.

Patient Perspective When Treatments Fail: Living with a Leak

Another patient shared her experience with a chronic SCSFL in a presentation focused on acceptance and adaptation, highlighting practical tools and home modifications that have aided in managing daily life. Her journey began with a lumbar puncture performed with an 18-ga cutting needle, leading to a chronic PDPH that significantly impacted her daily activities. After undergoing several rounds of epidural patching, she experienced temporary relief before relapsing. She emphasized the challenges of living with an invisible illness, the emotional toll of acceptance, and the importance of therapy in coping with the condition. She described her fluctuating “uptime,” the duration she could spend upright, and how it shaped her living situation and reliance on family and friends.

She detailed various assistive devices and modifications in her home, including a spill-proof cup for drinking while lying down, a tool for picking up items, comfortable pillows for sleep support, and accessible kitchen and bathroom equipment. She stressed the importance of creating a living environment tailored to the unique needs of individuals with SCSFL. This presentation offered a glimpse into the possibilities of independent living for those affected by long-term SCSFL, while simultaneously providing physicians a firsthand look at the modifications and adaptations required for daily living when available treatment options are inadequate.

Because treatment of SCSFLs can alter CSF homeostasis, RIH occurs in some cases. The symptoms of RIH include headaches different in character from the original SCSFL headache, often described as frontally located and worse when lying down rather than standing; patients may also experience symptoms of visual disturbances, nausea, and pulsatile tinnitus. 44 The morphology and caliber of the transverse venous sinuses, including unilateral hypoplasia and/or stenosis, have been linked to the development of RIH, suggesting a link between venous and CSF dynamics underpinning patient symptomatology. 45

The diagnosis of RIH involves clinical assessment and sometimes imaging studies to rule out other causes of increased intracranial pressure. Papilledema may or may not be present and can appear before symptoms occur. In some cases, patients may have had untreated idiopathic intracranial hypertension resulting in eventual dural dehiscence and subsequent SCSFL. 46 These patients can experience marked intracranial hypertension after leak repair. Management can be challenging and typically focuses on symptom relief while allowing gradual CSF pressure homeostasis. Treatment options include medication to reduce production of CSF or relieve pain, and in severe cases, CSF diversion may be necessary. RIH can present acutely in the immediate posttreatment period or be delayed. 47 The course of RIH varies, with some patients experiencing a resolution of symptoms with time, while others may require ongoing management. It is important for clinicians to monitor patients closely after SCSFL treatment to identify and manage RIH promptly. Critically, a clinical follow-up infrastructure is needed to optimize symptomatic management for patients in the acute and chronic posttreatment period.

Final Patient Presentation: What Doctors Should Know

The concluding patient talk of the day was a montage of personal experiences and insights from individuals living with SCSFL, detailing struggles with a debilitating condition affecting their daily lives, ambitions, and relationships. The speakers discussed the isolating nature of SCSFL and the need for self-advocacy when pursuing treatment. Some patients expressed the disappointment of having normal imaging findings despite severe symptoms and the relief experienced when procedures confirmed a leak. Above all, they spoke to doctors directly, noting that patients suffer more when providers are unable or unwilling to listen to them and urging physicians to believe their patients.

While the understanding of optimal diagnostic strategies and treatments for SCSFL has rapidly increased in the past several years, these techniques are limited to a few institutions, leaving many patients underserved. Additionally, these advances are not stand-alone solutions. Patient experiences offer key clinical insights instrumental in refining diagnostic acumen, which is of particular value to the procedurally inclined neuroradiologist. Neuroradiologists are uniquely situated to advocate for the patient with SCSFL because they may be the first to suggest the condition on the basis of imaging and often have procedural skills required to localize and treat the leak. We advocate a patient-centered model, in which these skills are combined with a deeper, nuanced understanding of clinical presentations in the pre- and posttreatment period.

Discussions at the Bridging the Gap Conference illuminated several key topics for future focus. One such area is the need for a standardized-yet-flexible diagnostic protocol. Variability in clinical presentations and often-subtle radiographic findings necessitate a protocol adaptable to the nuances of individual cases. This process should integrate the latest radiologic techniques with thorough clinical assessment, incorporating patient history as a critical component in the diagnostic process. Specifically, key historical features including any prior intended or unintended dural puncture, how and when symptoms started, and the nature of the symptoms should be ascertained.

Another focal point of the conference was the need for collaborative, multidisciplinary care teams. Such teams, composed of neuroradiologists, neurologists, headache/pain specialists, neurosurgeons, and other health care professionals, are essential for providing comprehensive care that addresses all facets of SCSFL diagnosis, treatment, and recovery. The value of this approach was evident through shared patient narratives in which multidisciplinary teams were often critical to achieving a correct diagnosis and effective treatment plan. Moreover, these teams can serve as a platform for ongoing education and awareness-building within the medical community, further improving the recognition and understanding of SCSFL.

The conference also highlighted the importance of patient support and advocacy. Patients’ narratives and questions revealed common themes of physical, emotional, and psychological distress, often exacerbated by the struggle for diagnosis and effective treatment. This outcome underscores the need for health care providers to adopt a holistic approach, going beyond addressing physical symptoms in isolation. Providing emotional and psychological support, ensuring clear and empathetic communication, and fostering patient empowerment and education are key to improving the overall quality of life for individuals with SCSFL. Additionally, strengthening informed patient support networks and advocacy groups can provide crucial resources and a sense of community for those affected by this condition.

Attendees of the conference reported high levels of satisfaction with the content. A postconference survey was administered to patient attendees who were asked to rate their level of satisfaction with the content on a 5-point Likert Scale: 63% of responders reported being “very satisfied” with the content, while the remaining 36% reported being “satisfied.” A CME evaluation form administered to physician attendees showed similar positive feedback, with 90.9% of physicians stating they would change the way they practice because of attending the conference.

The conference is planned to recur annually. A principal goal for the conference in the coming years includes the advocacy of patient-centered research through incorporation of a peer-reviewed scientific abstract-submission process. As the scope of the conference grows, we aim to incorporate additional institutions and more varied health care specialties/perspectives to increase both the breadth and depth of discussion surrounding optimal care of patients with SCSFL.

• CONCLUSIONS

The Bridging the Gap Conference provided not only a comprehensive overview of the current state of SCSFL diagnosis and treatment but also set the stage for future advancements in this field. The ideal forward-focal points in SCSFL care include developing adaptable diagnostic protocols, fostering multidisciplinary care teams, and enhancing patient support and advocacy. These steps are essential for bridging the existing gaps in the understanding and management of spinal CSF leaks, ultimately leading to improved patient outcomes and quality of life.

The “Spinal CSF Leak: Bridging the Gap” Study Group comprises: Nick Stevens, Deborah Friedman, John Reiman, Jessica Houk, Jill Rau, Ian R. Carroll, Wouter Schievink, Claudia Perez Sandhu, Terri Baker, Lalani Carlton Jones, Prem Subramanian, Ilene Ruhoy, Jodi Ettenberg, Danielle Wilhour.

Financial support for this conference was provided by the Spinal CSF Leak Foundation and the University of Colorado Departments of Neuroradiology, Neurosurgery, and Neurology.

Disclosure forms provided by the authors are available with the full text and PDF of this article at www.ajnr.org .

Indicates open access to non-subscribers at www.ajnr.org

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• © 2024 by American Journal of Neuroradiology

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