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affected unless the involved muscles are very weak If the diagnosis is suspected, the local health authority should be notified and a sample of serum and contaminated food (if available) sent to be assayed for toxin Support for the diagnosis may be obtained by electrophysiologic studies; with repetitive stimulation of motor nerves at fast rates, the muscle response increases in size progressively Patients should be hospitalized in case respiratory assistance becomes necessary Treatment is with trivalent antitoxin, once it is established that the patient is not allergic to horse serum Guanidine hydrochloride (25 50 mg/kg/d in divided doses) to facilitate release of acetylcholine from nerve endings sometimes helps to increase muscle strength Anticholinesterase drugs are of no value Respiratory assistance and other supportive measures should be provided as necessary Further details are provided in 33
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MYOPATHIC DISORDERS 1 Muscular Dystrophies
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Muscle weakness, often in a characteristic distribution Age at onset and inheritance pattern depend on the specific dystrophy
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These inherited myopathic disorders are characterized by progressive muscle weakness and wasting They are subdivided by mode of inheritance, age at onset, and clinical features, as shown in Table 24 8 In the Duchenne type, pseudohypertrophy of muscles frequently occurs at some stage; intellectual retardation is common; and there may be skeletal deformities, muscle contractures, and cardiac involvement The serum creatine kinase level is increased, especially in the Duchenne and Becker varieties, and mildly increased also in limb-girdle dystrophy Electromyography may help confirm that weakness is myopathic rather than neurogenic Similarly, histopathologic examination of a muscle biopsy
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4 Disorders Associated with Use of Aminoglycosides
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Aminoglycoside antibiotics, eg, gentamicin, may produce a clinical disturbance similar to botulism by preventing the release of acetylcholine from nerve endings, but symptoms subside rapidly as the responsible drug is eliminated from the body These antibiotics are particularly dangerous in patients with preexisting disturbances of neuromuscular transmission and are therefore best avoided in patients with myasthenia gravis
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Table 24 8 The muscular dystrophies
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Disorder Duchenne type Inheritance X-linked recessive Age at Onset (years) 1 5 Distribution Pelvic, then shoulder girdle; later, limb and respiratory muscles Pelvic, then shoulder girdle Pelvic or shoulder girdle initially, with later spread to the other Face and shoulder girdle initially; later, pelvic girdle and legs Humeroperoneal or scapuloperoneal Onset distally in extremities; proximal involvement later External ocular muscles; may also be mild weakness of face, neck, and arms As in the ocular form but with dysphagia Face, neck, distal limbs Slow progression 14q112 q13 19q132q133; 3q213 Prognosis Rapid progression Death within about 15 years after onset Slow progression May have normal life span Variable severity and rate of progression Possible severe disability in middle life Slow progression Minor disability Usually normal life span Variable Slow progression Genetic Locus Xp21
Becker s Limb-girdle (Erb s) Facioscapulohumeral Emery-Dreifuss Distal Ocular
X-linked recessive Autosomal recessive, dominant or sporadic Autosomal dominant
5 25 10 30
Xp21 Multiple
Any age
4q35
X-linked recessive or autosomal dominant Autosomal dominant or recessive Autosomal dominant (may be recessive) Autosomal dominant Autosomal dominant
5 10 40 60 Any age (usually 5 30) Any age Any age (usually 20 40)
Xq28, 1q11, 1q212 2q13, 2p13
Oculopharyngeal Myotonic dystrophy
Nervous System Disorders
specimen may help confirm that weakness is due to a primary disorder of muscle and to distinguish between various muscle diseases A genetic defect on the short arm of the X chromosome has been identified in Duchenne dystrophy The affected gene codes for the protein dystrophin, which is markedly reduced or absent from the muscle of patients with the disease Dystrophin levels are generally normal in the Becker variety, but the protein is qualitatively altered Duchenne muscular dystrophy can now be recognized early in pregnancy in about 95% of women by genetic studies; in late pregnancy, DNA probes can be used on fetal tissue obtained for this purpose by amniocentesis The genes causing some of the other muscular dystrophies are listed in Table 24 8 There is no specific treatment for the muscular dystrophies, but it is important to encourage patients to lead as normal lives as possible Prednisone (075 mg/kg daily) improves muscle strength and function in boys with Duchenne dystrophy, but side effects need to be monitored Prolonged bed rest must be avoided, as inactivity often leads to worsening of the underlying muscle disease Physical therapy and orthopedic procedures may help counteract deformities or contractures
Kirschner J et al The congenital and limb-girdle muscular dystrophies Arch Neurol 2004 Feb;61(2):189 99 [PMID: 14967765] Moxley RT 3rd et al Practice Parameter: Corticosteroid treatment of Duchenne dystrophy: report of the Quality Standards Subcommittee of the American Academy of Neurology and the Practice Committee of the Child Neurology Society Neurology 2005 Jan 11;64(1):13 20 [PMID: 15642897] Tawil R et al Facioscapulohumeral muscular dystrophy Muscle Nerve 2006 Jul;34(1):1 15 [PMID: 16508966]
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