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15.1: Case Study: Muscles and Movement

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• Page ID 16809

• Suzanne Wakim & Mandeep Grewal
• Butte College

Case Study: Needing to Relax

The dog in Figure \(\PageIndex{3}\) is expressing his interest in something—perhaps a piece of food—by using the neck muscles to tilt its head in an adorable fashion. Humans also sometimes tilt their heads to express interest. But imagine how disturbing and painful it would be if your neck tilted involuntarily, without you being able to control it! Forty-three-year-old Nasir, unfortunately, knows just how debilitating this can be. Nasir uses they, them, and their pronouns.

Nasir has a rare condition called cervical dystonia, which is also called spasmodic torticollis. In this condition, the muscles in the neck contract involuntarily, often causing the person’s head to twist to one side. The illustration in Figure \(\PageIndex{2}\) shows one type of abnormal head positioning that can be caused by cervical dystonia. The muscles may contract in a sustained fashion, holding the head and neck in one position, or they may spasm repeatedly, causing jerky movements of the head and neck.

Cervical dystonia is painful and can significantly interfere with individuals' ability to carry out their usual daily activities. In Nasir’s case, they can no longer drive a car, because their uncontrollable head and neck movements and abnormal head positioning prevent them from navigating the road safely. Nasir also has severe neck and shoulder pain much of the time.

Although it can be caused by an injury, there is no known cause of cervical dystonia—and there is also no cure. Fortunately for Nasir and other cervical dystonia sufferers, though, there is a treatment that can significantly reduce symptoms in many people. You may be surprised to learn that this treatment is the same substance that, when injected into the face, is used for cosmetic purposes to reduce wrinkles!

The substance is botulinum toxin, one preparation of which may be familiar to you by its brand name: Botox. It is a neurotoxin produced by the bacterium Clostridium botulinum , and can cause a life-threatening illness called botulism. However, when injected in very small amounts by a skilled medical professional, botulinum toxins have some safe and effective uses. In addition to cervical dystonia, botulinum toxins can be used to treat other disorders involving the muscular system, such as strabismus (misalignment of the eyes), eye twitches, excessive muscle contraction due to neurological conditions like cerebral palsy; and even overactive bladder.

Botulinum toxin has its effect on the muscular system by inhibiting muscle contractions. When used to treat wrinkles, it relaxes the muscles of the face, lessening the appearance of wrinkles. When used to treat cervical dystonia and other disorders involving excessive muscle contraction, it reduces abnormal contractions.

In this chapter, you will learn about the muscles of the body, how they contract to produce movements and carry out their functions, and some disorders that affect the muscular system. At the end of the chapter, you will find out if botulinum toxin helped relieve Nasir’s cervical dystonia, and how this toxin works to inhibit muscle contraction.

Chapter Overview: Muscular System

In this chapter, you will learn about the muscular system, which carries out both voluntary body movements and involuntary contractions of internal organs and structures. Specifically, you will learn about:

• The different types of muscle tissue—skeletal, cardiac, and smooth muscle—and their different characteristics and functions
• How muscle cells are specialized to contract and cause voluntary and involuntary movements
• The ways in which muscle contraction is controlled
• How skeletal muscles can grow or shrink, causing changes in strength
• The structure and organization of skeletal muscles (including the different types of muscle fibers) and how actin and myosin filaments move across each other, according to the sliding filament theory, to cause muscle contraction
• How cardiac muscle tissue in the heart contracts to pump blood through the body
• Smooth muscle tissue that makes up internal organs and structures, such as the digestive system, blood vessels, and uterus
• The physical and mental health benefits of aerobic and anaerobic exercise, such as running and weight lifting
• How individuals vary in their response to exercise
• Disorders of the muscular system, including musculoskeletal disorders (such as strains and carpal tunnel syndrome) and neuromuscular disorders (such as muscular dystrophy, myasthenia gravis, and Parkinson’s disease)

As you read the chapter, think about the following questions:

• How is the contraction of skeletal muscles controlled?
• Botulinum toxin works on the cellular and molecular levels to inhibit muscle contraction. Based on what you learn about how muscle contraction works, can you think of some ways it could potentially be inhibited?
• What is one disorder involving a lack of sufficient muscle contraction? Why does it occur?

Attributions

• Whisky's 2nd Birthday by Kelly Hunter , CC BY 2.0 via Flickr
• Gray 1194 by Henry Gray , public domain via Wikimedia Commons
• Text adapted from Human Biology by CK-12 licensed CC BY-NC 3.0

Want to create or adapt books like this? Learn more about how Pressbooks supports open publishing practices.

12.1 Case Study: Muscles and Movement

Created by CK-12 Foundation/Adapted by Christine Miller

Case Study: Needing to Relax

This dog (Figure 12.1.1) is expressing his interest in something — perhaps a piece of food — by using the neck muscles to tilt its head in an adorable fashion. Humans also sometimes tilt their heads to express interest. But imagine how disturbing and painful it would be if your neck tilted involuntarily, without you being able to control it! Forty-three year old Edward unfortunately knows just how debilitating this can be.

Edward has a rare condition called cervical dystonia , which is also called spasmodic torticollis. In this condition, the muscles in the neck contract involuntarily, often causing the person’s head to twist to one side. Figure 12.1.2 shows one type of abnormal head positioning that can be caused by cervical dystonia. The muscles may contract in a sustained fashion, holding the head and neck in one position, or they may spasm repeatedly, causing jerky movements of the head and neck.

Cervical dystonia is painful and can significantly interfere with a person’s ability to carry out their usual daily activities. In Edward’s case, he can no longer drive a car, because his uncontrollable head and neck movements and abnormal head positioning prevent him from navigating the road safely. He also has severe neck and shoulder pain much of the time.

Although it can be caused by an injury, there is no known cause of cervical dystonia — and there is also no cure. Fortunately for Edward, and others who suffer from cervical dystonia,  there is a treatment that can significantly reduce symptoms in many people. You may be surprised to learn that this treatment is the same substance which, when injected into the face, is used for cosmetic purposes to reduce wrinkles!

The substance is botulinum toxin, one preparation of which may be familiar to you by its brand name — Botox . It is a neurotoxin produced by the bacterium  Clostridium botulinum , and can cause a life-threatening illness called botulism . However, when injected in very small amounts by a skilled medical professional, botulinum toxins have some safe and effective uses. In addition to cervical dystonia, botulinum toxins can be used to treat other disorders involving the muscular system, such as strabismus (misalignment of the eyes); eye twitches; excessive muscle contraction due to neurological conditions like cerebral palsy; and even overactive bladder.

Botulinum toxin has its effect on the muscular system by inhibiting muscle contractions. When used to treat wrinkles, it relaxes the muscles of the face, lessening the appearance of wrinkles. When used to treat cervical dystonia and other disorders involving excessive muscle contraction, it reduces the abnormal contractions.

In this chapter, you will learn about the muscles of the body, how they contract to produce movements and carry out their functions, and some disorders that affect the muscular system. At the end of the chapter, you will find out if botulinum toxin helped relieve Edward’s cervical dystonia, and how this toxin works to inhibit muscle contraction.

Chapter Overview: Muscular System

In this chapter, you will learn about the muscular system, which carries out both voluntary body movements and involuntary contractions of internal organs and structures. Specifically, you will learn about:

• The different types of muscle tissue — skeletal, cardiac, and smooth muscle — and their different characteristics and functions.
• How muscle cells are specialized to contract and cause voluntary and involuntary movements.
• The ways in which muscle contraction is controlled.
• How skeletal muscles can grow or shrink, causing changes in strength.
• The structure and organization of skeletal muscles, including the different types of muscle fibres, and how actin and myosin filaments move across each other — according to the sliding filament theory — to cause muscle contraction.
• Cardiac muscle tissue in the heart that contracts to pump blood through the body.
• Smooth muscle tissue that makes up internal organs and structures, such as the digestive system, blood vessels, and uterus.
• The physical and mental health benefits of aerobic and anaerobic exercise, such as running and weight lifting.
• How individuals vary in their response to exercise.
• Disorders of the muscular system, including musculoskeletal disorders (such as strains and carpal tunnel syndrome) and neuromuscular disorders (such as muscular dystrophy, myasthenia gravis, and Parkinson’s disease).

As you read the chapter, think about the following questions:

• How is the contraction of skeletal muscles controlled?
• Botulinum toxin works on the cellular and molecular level to inhibit muscle contraction. Based on what you learn about how muscle contraction works, can you think of some ways it could potentially be inhibited?
• What is one disorder involving a lack of sufficient muscle contraction? Why does it occur?

Attributions

Figure 12.1.1

Whiskey’s 2nd Birthday by Kelly Hunter on Flickr is used under a CC BY 2.0 (https://creativecommons.org/licenses/by/2.0/) license.

Figure 12.1.2

1024px-Dystonia2010 by James Heilman, MD on Wikimedia Commons is used under a  CC BY-SA 3.0 (https://creativecommons.org/licenses/by-sa/3.0) license.

Botulism [online article]. (2018, January 10). World Health Organization (WHO). https://www.who.int/news-room/fact-sheets/detail/botulism

Mayo Clinic Staff. (n.d.) Cervical dystonia [online article]. MayoClinic.org. https://www.mayoclinic.org/diseases-conditions/cervical-dystonia/symptoms-causes/syc-20354123

A drug prepared from the bacterial toxin botulin, used medically to treat certain muscular conditions and cosmetically to remove wrinkles by temporarily paralyzing facial muscles.

A soft tissue that composes muscles in animal bodies, and gives rise to muscles' ability to contract. This is opposed to other components or tissues in muscle such as tendons or perimysium.

Actions which take place according to the one's desire or are under control.

Actions which are not under one's conscious control.

Voluntary, striated muscle that is attached to bones of the skeleton and helps the body move.

Involuntary, striated muscle found only in the walls of the heart; also called myocardium.

An involuntary, nonstriated muscle that is found in the walls of internal organs such as the stomach.

Human Biology Copyright © 2020 by Christine Miller is licensed under a Creative Commons Attribution-NonCommercial 4.0 International License , except where otherwise noted.

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Duchenne muscular dystrophy: Case report and review

Rupam sinha.

1 Department of Oral Medicine and Radiology, Haldia Institute of Dental Sciences and Research, Haldia, West Bengal, India

Soumyabrata Sarkar

Tanya khaitan, soumyajit dutta.

Muscular dystrophies are a clinically and heterogeneous group of disorders that all share clinical characteristics of progressive muscular weakness. Duchenne muscular dystrophy (DMD) is the most common X-linked disorder muscular dystrophy in children, presenting in early childhood and characterized by proximal muscle weakness and calf hypertrophy in affected boys. There is usually delay in motor development and eventually wheelchair confinement followed by premature death from cardiac or respiratory complications. Treatment modalities such as corticosteroid therapy and use of intermittent positive pressure ventilation have provided improvements in function, ambulation, quality of life, and life expectancy, although novel therapies still aim to provide a cure for this devastating disorder. Here, we present a case of DMD in a 12-year-old male with remarkable clinical and oral manifestations.

Introduction

Duchenne muscular dystrophy (DMD) is an atypical inherited musculoskeletal disorder which shows clinical characteristics of progressive muscular weakness at an early stage and pathologic features of fibrosis and fatty replacement, particularly late in the disease course. It is a recessive X-linked disorder occurring 1 in every 3500 live male births and named after a French neurologist Guillaume Benjamin Amand Duchenne in 1860.[ 1 ]

It is the most common and severe form of muscular dystrophy, beginning at 3–5 years of age and characterized by proximal muscle weakness and calf hypertrophy in affected boys.[ 1 , 2 ] DMD has a very high mutation rate with distinctive and relentless clinical presentation. Patients usually become wheelchair-bound by the age of 12 and die in their late teens to early twenties.[ 2 , 3 ] According to PubMed literature, approximately 150 cases have been reported till date. Here, we present a rare case of DMD in a 12-year-old child.

Case Report

A 12-year-old male patient reported to the department with chief complaint of painful decayed tooth in the lower right jaw region. His parents gave medical history of repeated falls, fatigue, muscle weakness, and inability to climb stairs. There was no history of muscular pain and cranial nerve involvement. His intelligence quotient was claimed to be in the normal range. Patient's family history revealed that one of his maternal uncles died of the same illness at a young age.

On general physical examination, the child had an obese appearance and presented with difficulty in standing, walking, getting up from sitting position and climbing stairs, proximal weakness, calf hypertrophy, hamstring muscle contracture, and positive Gower's sign [Figures ​ [Figures1 1 and ​ and2]. 2 ]. There was no thinning and twitching of muscles, muscle tone, and cranial nerve examination was also found to be normal. Intraoral examination revealed anterior open bite, left posterior cross bite, enlarged tongue, crowding in lower anteriors, decayed 46, and poor oral hygiene status [ Figure 3 ].

Clinical photograph of the patient

Proximal muscle weakness of upper and lower limbs and calf hypertrophy

Intraoral photograph showing no abnormality except for carious 46

The patient was subjected to radiological and laboratory investigations. Panoramic radiography revealed no abnormality except for grossly carious 46 indicative of chronic periapical abscess [ Figure 4 ]. Serological analysis showed creatine kinase (CK) level to be elevated to 7342 U/L, lactate dehydrogenase to 595 μg/dl, and alanine transaminase level to 124 U/L. On electromyographic examination, interference pattern analysis revealed myopathic pattern in the right vastus lateralis suggestive of primary muscle disease. Deltoid muscle biopsy revealed positivity for alpha, beta, gamma, delta-sarcoglycan and negativity for DYS1, DY2, and DYS3. Based on the history, clinical examination and investigations, a diagnosis of DMD was established.

Orthopantomograph showing no abnormality

The child was advised to consult a pediatrician regarding his general and physical health status. He was counseled to undergo daily physiotherapy, steroid therapy, and regular assessment for progressive muscle and cardiac/respiratory damage. With regard to dental therapy, pulpectomy for 46 and oral prophylaxis was performed. The patient was kept under periodic recall to prevent any further dental complications.

DMD is the most common muscle dystrophy in India as well as the world, caused by mutations in dystrophin gene as a result of which the body is unable to synthesize the protein dystrophin required for muscle contraction. Every time the muscle contracts, muscle damage occurs which is repaired but with deficient protein resulting in repaired muscle which is also a damaged one. This continuous succession of damage and repair and eventually replacement of muscle with fibrofatty tissue is responsible for the clinical signs of progressive muscle wasting and degeneration that is usually evident by 3–4 years.[ 1 , 4 ]

DMD is caused by mutations in the DMD gene encoding a protein called dystrophin, which localizes to the cytoplasmic face of the sarcolemma of the skeletal muscle, forming one component of a large glycoprotein complex (dystrophin-associated glycoprotein complex). Dystrophin consists of an N-terminal actin-binding domain, 24 spectrin-like repeat units interspersed by four hinge regions, followed by a cysteine-rich domain and a C-terminal domain. The cysteine-rich domain binds to laminin-2 through alpha and beta-dystroglycan, and therefore acts as mechanical link between actin in the cytoskeleton and the extracellular matrix. The DMD gene contains 79 exons but accounts for only 0.6% of the gene; the rest made of large introns. The large size of the DMD gene makes it susceptible to mutations, leading to loss of function of dystrophin, resulting in a prematurely truncated, and unstable dystrophin protein. The majority of mutations are intragenic deletions, which account for 65–72% of all DMD patients. The precise mechanism of how dystrophin deficiency leads to degeneration of muscle fibers remains unclear. The absence of dystrophin at the plasma membrane leads to delocalization of dystrophin-associated proteins from the membrane, disruption of the cytoskeleton with resultant membrane instability and increased susceptibility to mechanical stress. In addition, altered membrane permeability and abnormal calcium homeostasis are thought to play a role, with increased cytosolic calcium concentration leading to activation of proteases such as calpains.[ 3 ]

Affected boys clinically present with difficulty in running or getting up from the ground, frequent falls, or toe-walking. Patients have a waddling gait, calf enlargement, and lumbar lordosis which disappear on sitting. There is weakness of the proximal muscles of the lower limb as in which a patient uses his hands and arms to “walk” up their own body from a squatting position due to lack of hip and thigh muscle strength suggestive of Gower's sign.[ 5 ] In this case, the affected child clinically presented with signs of delayed motor development, difficulty in walking and climbing stairs, positive Gower's sign, and muscle weakness. Oral manifestations include wide dental arches, large tongue, delayed eruption, open bite, and retrognathic facial morphology. The development of malocclusion in these patients is linked to the involvement of the orofacial muscles by the disease which was apparent in the present case.[ 4 , 5 ]

Diagnosis is confirmed by high serum marker levels of CK, muscle biopsy, electromyography, and genetic analysis. The increased permeability of the sarcolemma damaged due to repeated contractions in DMD patients leads to leakage of proteins, such as CK into the plasma resulting in elevated levels of CK in the serum, characteristic in DMD patients. Other enzymes such as alanine transaminase, aspartate transaminase, aldolase, and lactate dehydrogenase are also raised.[ 2 , 6 ] In this case, serum markers such as CK, lactate dehydrogenase, and alanine transaminase levels were markedly increased. Muscle biopsy and electromyography also revealed positive results.

Current management of DMD involves physiotherapy and corticosteroid therapy which delays loss of ambulation 1–3 years but does not cure the disease which was provided in our case. However, corticosteroids are associated with significant side effects, including weight gain, decreased bone mineralization, Cushing syndrome, and behavioral disturbances. Alternate regimens have been tried, although the efficacy of these regimens in comparison to daily dosing is incompletely studied.[ 7 , 8 ] A growing number of reports suggest that treatment before the age of 5 years is especially beneficial, though the data to support early use are limited.[ 7 ] Recent treatment modalities include gene therapy and stem cell therapy which appear very promising and suggest that an upregulation of dystrophin-like protein has beneficial effects. Prenatal counseling and genetic tests like multiplex ligation-dependent probe amplification are being used to offer hope in this progressive and eventually fatal muscle dystrophy to prolong and improve the quality of patient's life.[ 9 , 10 ]

Declaration of patient consent

The authors certify that they have obtained all appropriate patient consent forms. In the form the patient(s) has/have given his/her/their consent for his/her/their images and other clinical information to be reported in the journal. The patients understand that their names and initials will not be published and due efforts will be made to conceal their identity, but anonymity cannot be guaranteed.

Financial support and sponsorship

Conflicts of interest.

There are no conflicts of interest.

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Case Studies: Answers

Case 1: Acute joint disease 1 The most crucial piece of information is that the patient is well. The diagnosis to rule out in every case is septic arthritis, and this seems unlikely in this scenario. However, his diabetes is a risk factor for infection, and a careful history of the previous injury might reveal a route of entry for bacteria. Although sports injuries can cause recurrent problems, acute flares of swelling and pain are unusual in the absence of a clear precipitating event. His psoriasis may indicate the development of a large-joint psoriatic arthropathy, but psoriasis is also a risk factor for gout, and his alcohol intake would certainly put him at risk of this. 2 The combination of a painful red eye and arthropathy raises the possibility of anterior uveitis or scleritis in association with one of the following: Reiter’s syndrome (check for a history of urethritis or gastrointestinal upset, circinate balanitis, keratoderma blennorrhagica). Enteropathic arthropathy (history of abdominal pain or bloody diarrhoea, erythema nodosum). Ankylosing spondylitis (inflammatory back pain). 3 Joint fluid aspiration to rule out septic arthritis and to diagnose gout. 4 First-line treatment for gout is a non-steroidal anti-inflammatory drug (NSAID). If he continues to experience attacks, a urate-lowering therapy such as allopurinol should be considered. All patients with gout should attempt lifestyle modification. In this instance, a reduction in his alcohol intake is crucial. Additional risk factors in his diet would also need to be addressed. See Chapter 27 for further details. Case 2: Initial management of polytrauma 1 ABC: A Check airway with cervical spine control. B Breathing: give 100% oxygen at 15 l/min; check for pneumothorax. C Circulation: introduce two wide-bore cannulae. Take bloods for cross-match, haemoglobin, glucose, urea and electrolytes, and drug screen. 2 Distal neurovascular status. 3 The fracture is open and potentially contaminated. The wound must therefore be opened and cleaned. All contaminating material should be washed out, and dead tissue excised. If it is not possible to be sure that the wound is clean, then it should not be closed. The wound should be packed and then inspected daily until it is clean. The fracture needs to be reduced, and then held. The operation should be covered by prophylactic antibiotics. The patient should be mobilised as soon as practicable. 4 Options include intramedullary nail with locking screws; plate and screws; external fixator (Ilizarov or conventional); balanced traction; plaster or brace. An intramedullary nail allows secure fixation and early mobilisation but infection is a dangerous complication. A plate with screws needs a much longer incision, but will also give secure fixation. An external fixator is very difficult to apply, especially in the thigh where the soft tissues are deep so the pins rub on the muscle. Traction is safe but takes many weeks with the patient languishing in a hospital bed. A plaster or brace would be almost impossible to fit to a thigh so that the fracture could be held. See Chapters 42 and 48 for further details. Case 3: Rheumatoid arthritis 1 No, but enough to make the diagnosis! The diagnostic criteria stipulate at least four of the following: Morning stiffness: duration >1 hour (for >6 weeks). Arthritis of at least three joints: soft tissue swelling (for >6 weeks). Arthritis of hand joints: MCPs, PIPs or wrist (for>6 weeks). Symmetrical arthritis: at least one area (for >6 weeks). Rheumatoid nodules. Positive rheumatoid factor. Radiographic changes: periarticular erosions. 2 Rhematoid factor positivity is associated with more severe disease and a higher incidence of extra-articular manifestations. 3 Methotrexate is effective and generally well tolerated. Side effects include nausea and oral ulcers. Regular blood tests are used to screen for myelosuppression and hepatitis. An idiosyncratic (and reversible) allergic alveolitis/pneumonitis can occur and pre-treatment lung function testing and chest X-ray is advised. Pregnancy is contraindicated as methotrexate is a folic acid antagonist. 4 Differential diagnoses: Respiratory disease: – Pleural effusion – Pulmonary fibrosis – Allergic alveolitis due to methotrexate therapy – Bronchiolitis obliterans (rare) – Cryptogenic organising pneumonia (rare). Investigations include arterial blood gases, chest X-ray and lung function testing. Symptomatic anaemia: – Anaemia of chronic disease – Gastrointestinal blood loss due to NSAID use – Myelosuppression due to methotrexate therapy – Associated B12 deficiency (pernicious anaemia). Investigations include haematinics and endoscopy. 5 Causes include:

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Case Studies in Management of Muscle Cramps

Affiliation.

• 1 Toronto General Hospital / University Health Network, Krembil Brain Institute, University of Toronto, 200 Elizabeth Street, 5ES-306, Toronto, Ontario M6S 4E6, Canada. Electronic address: [email protected].
• PMID: 32703476
• DOI: 10.1016/j.ncl.2020.03.011

Muscle cramps, defined as a painful contraction of a muscle or muscle group, are a common symptom most people have experienced throughout their lifespan. In some cases cramps can be frequent, severe, and disabling, thus requiring medical assessment and intervention. Physiologic states such as pregnancy and exercise are associated with excessive muscle cramps, as are numerous medical and neurologic conditions, medications such as diuretics and statins, and peripheral nerve hyperexcitability syndromes. Treatment options for muscle cramps are limited, although recent studies have shown that mexiletine could be a safe and efficient alternative for patients with amyotrophic lateral sclerosis.

Keywords: Charley horse; Contraction; Hyperexcitability; Muscle cramps; Spasms.

Copyright © 2020 Elsevier Inc. All rights reserved.

Publication types

• Case Reports
• Research Support, Non-U.S. Gov't
• Disease Management*
• Mexiletine / therapeutic use
• Middle Aged
• Muscle Cramp / diagnosis*
• Muscle Cramp / physiopathology
• Muscle Cramp / therapy*
• Voltage-Gated Sodium Channel Blockers / therapeutic use
• Young Adult
• Voltage-Gated Sodium Channel Blockers