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Facioscapulohumeral muscular dystrophy

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Last Updated: 02 July 2021

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Facioscapulohumeral muscular dystrophy

Other namesLandouzy-Dejerine muscular dystrophy, FSHMD, FSH
SpecialtyNeurology
SymptomsFacial weakness, scapular winging, foot drop
Usual onsetAdolescence
DurationLong term
TypesFSHD1, FSHD2
CausesGenetic (inherited or new mutation)
Diagnostic methodGenetic testing
Differential diagnosisLimb-girdle muscular dystrophy (especially calpainopathy ), Pompe disease , Mitochondrial myopathy , Polymyositis
ManagementPhysical therapy, bracing, orthopedic surgery
Frequency1 in 8333 to 1 in 15000

Facioscapulohumeral muscular dystrophy affects upper body muscles. It is not the same as Duchenne muscular dystrophy and Becker muscular dystrophy, which affect the lower body. Facioscapulohumeral muscular dystrophy is a genetic disease due to chromosome mutation. It appears in both men and women. It may develop in children if either parent carries gene for disorder. In 10% to 30% of cases, parents do not carry gene. Facioscapulohumeral muscular dystrophy is one of the most common forms of muscle dystrophy affecting 1 in 15 000 to 1 in 20 000 adults in the United States. It affects men and women equally. Facioscapulohumeral muscular dystrophy mainly affects face, shoulder, and upper arm muscles. However, it can also affect muscles around the pelvis, hips, and lower leg. Symptoms can appear after birth, but often they do not appear until age 10 to 26. However, it is not uncommon for symptoms to appear much later in life. In some cases, symptoms never develop. Symptoms are most often mild and very slowly become worse. Muscle weakness of face is common, and may include: shoulder. Muscle weakness causes deformities such as pronounced shoulder blades and sloping shoulders. People have difficulty raising their arms because of shoulder and arm muscle weakness. Weakness in the lower legs is possible as the disorder gets worse. This interferes with the ability to play sports because of decreased strength and poor balance. Weakness can be severe enough to interfere with walking. A small percentage of people use a wheelchair. Chronic pain is present in 50% to 80% of people with this type of muscular dystrophy. Hearing loss and abnormal heart rhythms may occur but are rare. Physical exam will show weakness of face and shoulder muscles as well as scapular winging. Weakness of back muscles can cause scoliosis, while weakness of abdominal muscles can BE cause of sagging belly. High blood pressure may BE note, but is usually mild. Eye exam may show changes in blood vessels in the back of the eye. Creatine kinase test DNA testing, Electrocardiogram EMG fluorescein angiography, Genetic testing of chromosome 4 Hearing tests, Muscle biopsy visual exam, Cardiac testing X - rays of spine to determine if there is scoliosis Pulmonary function tests bharucha - Goebel DX. Muscular dystrophies. In: Kliegman RM, Geme JW, Blum NJ, Shah SS, Tasker RC, Wilson KM, eds. Nelson Textbook of Pediatrics. 21 ed. Philadelphia, PA: Elsevier; 2020: chap 627. Preston DC, Shapiro BE. Proximal, distal, and generalized weakness. In: Daroff RB, Jankovic J, Mazziotta JC, Pomeroy SL, eds. Bradley's Neurology in Clinical Practice. 7 ed. Philadelphia, PA: Elsevier; 2016: chap 27. Warner WC, Sawyer JR. Neuromuscular disorders. In: Azar FM, Beaty JH, Canale, eds. Campbell's Operative Orthopaedics. 13 ed. Philadelphia, PA: Elsevier; 2017: chap 35.

* Please keep in mind that all text is machine-generated, we do not bear any responsibility, and you should always get advice from professionals before taking any actions.

* Please keep in mind that all text is machine-generated, we do not bear any responsibility, and you should always get advice from professionals before taking any actions

Signs and symptoms

Age of onset, progression, and severity of facioscalpulohumeral muscular Dystrophy vary a great deal. Usually, symptoms develop during teen years, with most people noticing some problems by age 20, although weakness in some muscles can begin as early as infancy and as late as 50s. In some people, disease can be so mild that no symptoms are notice. In these cases, disease may be diagnosed only after another, more affected member of the family comes to medical attention. People with FSHD often do not go to the doctor until their shoulder or leg muscles become involved and they experience difficulty reaching over their heads or going up and down stairs. When questioned closely, many people can remember having symptoms in childhood, such as shoulder blades that stick out or trouble throwing ball. Very often, people say they have never been able to whistle or blow up balloon, or that they have had trouble drinking through straw, but they may not associate these problems with muscular dystrophy. Fshd does not affect sensation, nor does it affect ability to control bladder and bowels, or sexual function. In most people with FSHD, disease progresses very slowly. It can take as long as 30 years for a disease to become seriously disabling, and that does not happen to everyone. Estimates are that about 20% of people with FSHD eventually use a wheelchair at least some of the time. For more on corrective measures for some of these symptoms, see Medical Management.

* Please keep in mind that all text is machine-generated, we do not bear any responsibility, and you should always get advice from professionals before taking any actions.

* Please keep in mind that all text is machine-generated, we do not bear any responsibility, and you should always get advice from professionals before taking any actions

Genetics

Table

ConditionSize of DNA Deletion (in kilobase pairs)
NormalGreater than 51 base pairs
BorderlineBetween 36 and 50 base pairs
AffectedLess than 35 base pairs

Facioscapulohumeral muscular dystrophy is an inherited neuromuscular disorder that causes weakness, most prominently of muscles in the face, shoulder blades, and upper arms. It often progresses to cause widespread muscle weakness, and it can also cause loss of hearing. The region of human chromosomes that cause FSHD contains a section with multiple identical units of DNA called D4Z4 repeats. The number of D4Z4 repeat units in the general population varies from 11 to 100. Each repeat contains a copy of a gene called DUX4. This gene is used during fetal development, but in adulthood, DNA in this region is normally condense, or packed tightly together, which prevents cellular machinery from reading DUX4 gene. As a result, no protein is made from it once fetal development is complete. In approximately 95% of patients with FSHD, D4Z4 allele is contract, meaning that multiple D4Z4 units are lose. This de - condenses DNA and reactivates DUX4 gene, allowing aberrant production of DUX4 protein. Synthesis of DUX4 transcripts and protein is toxic to muscle cells. In most patients with FSHD, one D4Z4 allele is contracted to between 1 and 10 repeat units and the other D4Z4 allele has normal number, condition term FSHD1. There is an inverse relationship between onset and clinical severity of FSHD, and size of pathogenic D4Z4 repeat units. Individuals with one to three repeat D4Z4 units are typically at the severe end of the disease spectrum. With four to 10 repeat units, clinical variation ranges from asymptomatic to severely affected. Allele with 10 to 11 D4Z4 repeats is considered borderline. Many FSHD researchers now believe that elevation of DUX4 protein causes symptoms of FSHD. In less than 5% of people with FSHD, D4Z4 region is of normal length, condition term FSHD2. In these individuals, mutations in different gene, called SMCHD1, cause DNA in vicinity of D4Z4 repeat to be spread out, allowing DUX4 gene to be read and protein to be produce. Fshd1 is inherited in autosomal dominant pattern, meaning it takes only one mutation to cause disorder. This altered piece of DNA also occurs spontaneously in a child as he or she develops in the womb, which accounts for 10% to 30% of FSHD1 cases. Inheritance of FSHD2 is not fully established and, in most cases, may require mutations in SMCHD1 on chromosome 18. Approximately 60% of FSHD2 cases appear to be sporadic. For help in understanding your family's specific situation and planning for future children, it is best to meet with genetic counselor.

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Table2

ConditionSize of DNA Deletion (in CTG repeats)
NormalLess than 38 repeats
BorderlineBetween 39 and 49 repeats
AffectedMild 50 to approximately 150 Classic approximately 100 to 1000 Congenital greater than 2000

Table3

ConditionSize of DNA Deletion (in kilobase pairs)
NormalLess than 175 base pairs
BorderlineBetween 177-372 base pairs
AffectedGreater than 372 base pairs
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Pathophysiology

The mutation causing the most common form of facioscapulohumeral muscular dystrophy was identified over 20 years ago, yet for many ensuing years there was little or no consensus in the scientific community regarding molecular pathophysiology of disease. Unlike other disease - causing mutations that disrupt normal function of identified gene, FSHD is caused by loss of subset of repeat units in D4Z4 macrosatellite repeat array on chromosome 4 that do not disrupt the structure of any gene. This lead to many different hypotheses regarding the mechanism of FSHD pathophysiology, and many disagreements among researchers in this field. The Absence of a generally accepted model for FSHD pathophysiology makes it difficult to get support for research in FSHD and limited interest in therapeutic development. Over the last several years, several key advances in FSHD research, many made possible by steady improvement in technology, have identified molecular and genetic causes of FSHD and clarified mechanisms of pathophysiology, leading to the discovery that FSHD is a disease of inefficient repeat - mediate epigenetic repression of DUX4 retrogene embed in D4Z4 repeat units. Here we will review line of experimental evidence that gradually led to this model of FSHD pathophysiology. As this model gains general acceptance in the field, greater attention and resources can now be devoted to therapeutic development, indicating that we have come to a pivotal moment in FSHD research.


Facioscapulohumeral Dystrophy

Facioscapulohumeral dystrophy is autosomal dominant dystrophy with distinct phenotype. A precise genetic defect in this major form of FSHD has yet to be identify. However, diagnosis of FSHD can be suspect and / or easily make clinically in most patients with this disorder. Typically, these children have prominent facial as well as scapulohumeral muscle weakness; parenthetically, striking asymmetry of muscle involvement is a typical feature of FSHD. The infantile variety of FSHD, which is often sporadic in inheritance, has very early onset and is rapidly progressive, with wheelchair confinement by age of 9 to 10 years in most cases. There is profound facial weakness, with an inability to close eyes in sleep, to smile, and to show any evidence of facial expression. Weakness rapidly involves shoulder and hip girdles with lumbar lordosis, resulting in pronounced forward pelvic tilt, and hyperextension of knees and head upon walking. Marked weakness of wrist extensors may result in wrist drop. Young children with early onset FSHD and very small number of chromosome 4q35 repeats often have epilepsy, mental retardation, and severe sensorineural hearing loss. A Commercial DNA test is now available for FSH muscular dystrophy; most patients with classic FSHD for whom detailed molecular studies have been do carry chromosomal rearrangement within the subtelomere of chromosome 4q. Tandem array of 3. 3 kb repeat DNA elements are deleted in patients with FSHD. In the general population, number of repeat units varies from 11 to more than 100; in FSHD patients, allele of 1 - 10 residual units is observed because of deletion of integral number of these units. Most infants with FSHD have only 1 - 3 copies of repeat unit. This new diagnostic test is positive in 93% of typical FSHD cases. Nonetheless, exact gene defect is not known yet and thus the sensitivity of genetic test for atypical cases remains uncertain. In typical cases, there is no value in performing muscle biopsy.

* Please keep in mind that all text is machine-generated, we do not bear any responsibility, and you should always get advice from professionals before taking any actions.

* Please keep in mind that all text is machine-generated, we do not bear any responsibility, and you should always get advice from professionals before taking any actions

Diagnosis

Diagnosis of facioscapulohumeral muscular dystrophy is suspect in patients who present with weakness in the face, shoulder girdle, and upper arm with relative sparing of deltoid muscles. Patients with suspected muscular dystrophy should be referred to a specialist with expertise in neuromuscular disorders for evaluation and diagnosis. Today, most reliable way to diagnose FSHD is with test for tiny missing section of DNA on chromosome 4. The commercial genetic test for FSHD detects shortening of repeat DNA elements located within the 4q35 region of chromosome 4. This diagnostic test, performed on blood cells, is positive in approximately 95% of typical FSHD cases. Test is considered highly accurate for FSHD. Genetic testing is not needed for every affected person with typical clinical presentation if family history is consistent with autosomal dominant inheritance and diagnosis has been genetically confirmed in first - degree relative. 1 In many cases, however, people with no family history are suspected of having either FSHD or some other neuromuscular disorder. In these situations, less expensive and less specific tests than FSHD DNA test may be do first. One test is creatine kinase level. This test, also performed on blood sample, measures the amount of enzyme known as creatine kinase in the blood. When muscle cells break down, as they do in muscular dystrophies and some other disorders, creatine kinase, or CK, level is elevate. Ck is often elevated up to 5 times upper limit of normal in symptomatic FSHD patients. Ck is rarely elevated in patients with no symptoms. Another type of diagnostic test is electromyogram, or EMG, which measures electrical activity in muscles, displayed in the form of waves. Emg typically displays alterations in patients with FSHD. Another diagnostic procedure sometimes undertaken is muscle biopsy. In this procedure, small piece of muscle is take, under local anesthesia, usually from the arm or leg. Biopsy samples reveal cellular and molecular abnormalities that suggest certain muscle disorders and rule out others. Muscle biopsies are less often performed today than in the past, especially when there is DNA test for a disease doctors suspect is causing symptoms, as there is for FSHD. Neither EMG nor muscle biopsy are needed when diagnosis of FSHD is confirmed by genetic testing.

* Please keep in mind that all text is machine-generated, we do not bear any responsibility, and you should always get advice from professionals before taking any actions.

* Please keep in mind that all text is machine-generated, we do not bear any responsibility, and you should always get advice from professionals before taking any actions

Management

Different variations of FSHD exist, resulting in the absence of an exact set of symptoms. Fshd is commonly presented as progressive muscle weakness which involves various muscle groups of the face, shoulder girdle, and upper arms. Muscle weakness prominent on one side of the body and scapular winging are two main characteristics of FSHD. Scapular winging results from weakness of lower trapezius muscle causing upward movement of scapula during flexion of arm, which becomes obvious when affected individual tries to raise their arms laterally. Shoulders tend to have forward slant with straight clavicles and prominent atrophy of pectoral muscles. Typical symptoms of FSHD also involve muscle groups of the face, abdomen and diaphragm. Early presentation of FSHD is often characterized by pronounced weakness of facial muscles, which is then followed by symptoms of shoulders. Early signs also include difficulty whistling due to being unable to purse their lips or sleeping with their eyes partially open due to being unable to completely close their eyelids. In most cases, extraocular muscles, eyelid and bulbar muscles are spar. Individuals with FSHD often have unaffected deltoid muscles in the early stages. Biceps and triceps muscles are asymmetrically involved, resulting in prominent atrophy of the upper arms without affecting forearm muscles. This leads to the appearance of large forearms in comparison to the upper arm. Abdominal muscle weakness may lead to abdominal protuberance and, in some cases, lumbar lordosis. Weakness of lower abdominal muscles results in upward displacement of umbilicus upon flexion of neck during supination. Muscular weakness of hip and pelvis results in difficulty climbing stairs or prolonged walking. This condition is further worsened by aggravated curvature in individuals presented with lumbar lordosis. Fshd individuals affected with progressive movement impairment then become physically dependent on mobility aids. In rare cases, weakness of the diaphragm leads to respiratory insufficiency, increasing the overall mortality of this disease. Retinal telangiectasia and macular edema mimicking Coat's disease may also arise due to failure of vascularization of vascular peripheries. Telangiectatic changes and microaneurysms can be detected by fluorescein angiography in up to 60 percent of affected individuals. Bilateral high - tone sensorineural hearing loss can be detected in up to 60 percent of affected individuals. Subclinical sensorineural hearing loss occurs in a higher proportion of individuals. In a study by Zatz et al., Fshd penetrance was found to differ according to age and gender. Penetrance by age of 30 was estimated to be at 83 percent for both genders, but significantly higher in males compared to females. They also report that de novo mutations were more common in females compared to male participants. No particular evidence of X - chromosome related recessive inheritance is see, which may be related to excess of symptomatic female individuals in their familial studies, including asymptomatic mothers.

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History

Pedigree of patient in Case 8 - 1. The top line indicates the number of D4Z4 repeats on both copies of 4q and whether each has permissive or nonpermissive B polymorphism. The bottom line indicates presence of SMCHD1 mutation and percent of methylation at D4Z4 repeats. Note that the affected individual has SMCHD1 mutation and permissive allele while his father carries the same SMCHD1 mutation and is hypomethylated but is unaffected because he lacks permissive polymorphism. Clinical features of facioscapulohumeral muscular dystrophy., Facial weakness with flattened pucker; B, chest wall showing asymmetric wasting of pectoral muscles with prominent axillary fold, upper arm wasting with sparing of forearms, and protruberant abdomen; C, Popeye arm appearance; D, Both posterior and lateral winging of scapula on shoulder forward flexion; E, Beevor sign demonstrating asymmetric abdominal weakness with intact upper abdominals pulling umbilicus upwards when abdomen is tense. Panel C reprint with permission from Tawil R, Griggs RC, Butterworth - Heinemann. 14 1997 R Tawil and RC Griggs. Panel E modified with permission from Griggs RC, et al, Muscle Nerve. 15 1995 John Wiley & Sons, Inc. Onlinelibrary. Wiley. Com / doi / 10. 1002 / mus. 880181311 / full. Manual fixation of scapula in clinic., In this patient with facioscapulohumeral muscular dystrophy, abduction of shoulder is only to approximately 90 degrees. B, physician manually pulls the shoulder back while pushing against the scapula with the other hand, fixing the scapula to the chest wall, and abduction increases beyond 90 degrees. This would be a positive test and may support the notion that scapular fixation surgery could improve function for this patient. Reprint with permission from Tawil R, Van DerMaarel SM, Muscle Nerve. 9 2006 John Wiley & Sons, Inc. Onlinelibrary. Wiley. Com / doi / 10.

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Facioscapulohumeral Muscular Dystrophy (FSH, FSHD)

There is currentlyA no cure for FSHD. However, treatments that can help manage symptoms are available. Anti - inflammatory drugs are often prescribed to reduce pain and to help patients increase mobility. Regular physical activity and physical therapy are recommended to counteract the effects of muscle weakness and to maintain flexibility. Surgery to correct scapular awinginga and scoliosis associated with FSHD may also be an option for patients. Surgery to correct scapular awinginga that helps stabilize shoulder blades, and to help correctA scoliosis, or sideways curvature of the spine associated with FSHD, may also be options for patients. Muscular Dystrophy News is strictly news and information website about disease. It does not provide medical advice, diagnosis, or treatment. This content is not intended to be a substitute for professional medical advice, diagnosis, or treatment. Always seek advice of your physician or other qualified health provider with any questions you may have regarding medical condition. Never disregard professional medical advice or delay in seeking it because of something you have read on this website.

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Treatment:

Medical treatments for facioscapulohumeral muscular Dystrophy are relatively few, and none are specific to the disease. There is no treatment that can halt or reverse the effects of FSHD, but there are treatments and devices to help alleviate many of the symptoms. Anti - inflammatory drugs, know as nonsteroidal anti - inflammatories, or NSAIDs, are often prescribed to improve comfort and mobility. These are the same drugs taken by many people with arthritis and other inflammatory conditions. Antidepressants or antiepileptics are appropriate for chronic pain. Surgical procedures to stabilize shoulder blades by attaching them to ribs have helped some people with FSHD. In this procedure, scapulae are fixed to ribs so that they do not move. The patient gains some leverage with the arm on the side that had operation because scapulae no longer slide around. Although this type of surgery may actually decrease arm range of motion, ability of the arm to function may be better because the arm leverage point is now stable. It is important to go to a surgeon who fully understands FSHD and has had experience with this exact type of surgery. Physical therapists often recommend devices such as back supports, corsets, girdles, and special bras for people with FSHD. These supports help to compensate for weakening muscles in the upper and lower back. Lower leg braces, know as ankle - foot orthoses, or AFOs, can compensate for weakening muscles in the lower leg that cause tripping and falling. These may be recommended by a physician or physical therapist and can be purchased as off - shelf or custom - made models. Some people find lightweight, high - top shoes can be as helpful as AFO in supporting foot, at least in early stages of weakness. Physical therapists advise that those with FSHD should not resist using these types of devices for fear their muscles will get lazy. A Supportive corset or AFO can help with mobility and endurance, they say, and supporting muscle in a normal position can help you use your remaining strength more effectively. Massage or warm, moist heat are also good for discomfort associated with FSHD. Patients with severe early - onset forms of FSHD may benefit from physical, occupational, and speech therapy. Because the precise underlying defect that causes muscle loss in FSHD is not yet understood, it is hard to make precise recommendations about exercise. However, physical therapists who have observed people with FSHD for many years say that moderate exercise appears to do no harm and may even be helpful, at least for muscles that have not severely weaken. Therapists advise that exercise should not cause muscle cramping, significant muscle pain, or extreme fatigue. Exercise program for someone with FSHD should be directed by a professional, such as a physical or occupational therapist, who has experience with neuromuscular disorders. The program should emphasize exercising muscles that are still relatively strong and resting those that have weaken. This can be accomplished with careful positioning and adaptation of standard exercise regimens.

* Please keep in mind that all text is machine-generated, we do not bear any responsibility, and you should always get advice from professionals before taking any actions.

* Please keep in mind that all text is machine-generated, we do not bear any responsibility, and you should always get advice from professionals before taking any actions

Clinical description

Facioscapulohumeral muscular dystrophy is a disorder characterized by muscle weakness and wasting. This condition gets its name from muscles that are affected most often: those of the face, around shoulder blades, and in the upper arms. Signs and symptoms of facioscapulohumeral muscular dystrophy usually appear in adolescence. However, onset and severity of condition vary widely. Milder cases may not become noticeable until later in life, whereas rare severe cases become apparent in infancy or early childhood. Weakness involving facial muscles or shoulders is usually the first symptom of this condition. Facial muscle weakness often makes it difficult to drink from straw, whistle, or turn up corners of mouth when smiling. Weakness in muscles around the eyes can prevent eyes from closing fully while a person is asleep, which can lead to dry eyes and other eye problems. For reasons that are unclear, weakness may be more severe on one side of the face than other. Weak shoulder muscles tend to make shoulder blades protrude from the back, common sign know as scapular winging. Weakness in the muscles of the shoulders and upper arms can make it difficult to raise arms over head or throw a ball. Muscle weakness associated with facioscapulohumeral muscular dystrophy worsens slowly over decades and may spread to other parts of the body. Weakness in muscles of the lower legs can lead to a condition called foot drop, which affects walking and increases the risk of falls. Muscular weakness in the hips and pelvis can make it difficult to climb stairs or walk long distances. Additionally, affected individuals may have exaggerated curvature of lower back due to weak abdominal muscles. About 20 percent of affected individuals eventually require use of a wheelchair. Additional signs and symptoms of facioscapulohumeral muscular dystrophy can include mild high - tone hearing loss and abnormalities involving light - sensitive tissue in the back of the eye. These signs are often not noticeable and may be discovered only during medical testing. Rarely, facioscapulohumeral muscular dystrophy affects heart muscle or muscles needed for breathing. Researchers have described two types of facioscapulohumeral muscular dystrophy: type 1 and type 2. Two types have the same signs and symptoms and are distinguished by their genetic cause. Facioscapulohumeral muscular dystrophy is caused by genetic changes involving the long arm of chromosome 4. Both types of disease result from changes in region of DNA near the end of the chromosome known as D4Z4. This region consists of 11 to more than 100 repeated segments, each of which is about 3 300 DNA base pairs long. The entire D4Z4 region is normally hypermethylated, which means that it has large number of methyl groups attached to DNA. The addition of methyl groups turns off genes, so hypermethylated regions of DNA tend to have fewer genes that are turned on. Facioscapulohumeral muscular dystrophy results when the D4Z4 region is hypomethylated, with a shortage of attached methyl groups.

* Please keep in mind that all text is machine-generated, we do not bear any responsibility, and you should always get advice from professionals before taking any actions.

* Please keep in mind that all text is machine-generated, we do not bear any responsibility, and you should always get advice from professionals before taking any actions

Sources

* Please keep in mind that all text is machine-generated, we do not bear any responsibility, and you should always get advice from professionals before taking any actions.

* Please keep in mind that all text is machine-generated, we do not bear any responsibility, and you should always get advice from professionals before taking any actions

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