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DISEASES OF SPINAL CORD, PERIPHERAL NERVE, AND MUSCLE
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Table 53-2 Major disorders of the neuromuscular junction
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CAUSAL AGENT MYASTHENIC SYNDROMES OR GENE DEFECT ONSET DECADE TREATMENT CLINICAL FEATURES
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Acquired Myasthenic Syndromes Presynaptic Botulism (Chap 43) Peptide toxin from Clostridium botulinum Lambert-Eaton Autoimmune reduction in calciummyasthenic mediated quantal release syndrome Synaptic Insecticides Organophosphates (Chap 43) (inhibits ACLE)
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Any Mid-life
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Supportive; ventilation 3,4-DAP Possibly IVIG
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Blurred vision, dysphagia, limb weakness Truncal weakness, dysautonomic features Two-thirds have cancer Miosis, diarrhea, cramps, weakness Delayed sensorimotor neuropathy Diplopia, ptosis Limb weakness with exertion Acute weakness
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Postsynaptic Myasthenia gravis
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Autoimmune attack on postsynaptic membrane Antibodies to AChR or MuSK protein
Adult
Multiple peptide toxins that lyse muscle, bind Na channels, K channels (acting both post- and presynaptically) Hereditary and Congenital Myasthenic Syndromes Presynaptic Episodic apnea Choline acetyltransferase
Snake venom toxins (Chap 43)
AChE inhibitors, IVIG Other immunosuppressants Supportive Possibly AChE inhibitors
AChE inhibitors Apnea monitor AChE inhibitors
Paucity of synaptic vesicles Synaptic AChE de ciency
Unknown
Mild episodes of weakness; recurrent apnea Ptosis common Recurrent, sometimes pronounced weakness Diffuse weakness, ptosis
AChE Collagen tail for AChE
None Avoid AChE inhibitors Quinidine, AChE inhibitors Avoid 3,4-DAP 3,4-DAP AChE inhibitors, 3,4-DAP AChE inhibitors, 3,4-DAP 3,4-DAP
Postsynaptic Slow channel syndrome
AChR subunits
1st 6th
Fast channel syndrome Primary AChR de ciency Rapsyn de ciency Plectin de ciency
AChR subunits AChR subunits Rapsyn Plectin
1st 1st 1st 1st
Ptosis, diffuse weakness, delayed motor milestones Often show atrophy of dorsal forearms Ptosis, recurrent weakness, motor development delays Ptosis, recurrent weakness, motor development delays Ptosis, recurrent weakness Myasthenic features, epidermolysis bullosa
AChE, acetylcholine esterase; AChR, acetylcholine receptor; MuSK, muscle-speci c kinase; IVIG, intravenous immune globulin; DAP, diaminopyridine
dren, usually with no relation to tumor In the tumor cases, death usually occurs in a few months or years from the effect of the tumor itself; the idiopathic ones uctuate over years As mentioned above, the response to neostigmine and pyridostigmine is poor or at least unpredictable In contrast, d-tubocurarine, suxamethonium chloride, gallamine, and other muscle relaxants have a deleterious effect Just as in myasthenia gravis, when given during anesthesia, they increase the weakness and even lead to fatality Conventional electrodiagnostic studies have shown no abnor-
mality in the peripheral nerves A single stimulus of nerve may evoke a low-amplitude muscle action potential (in contrast to myasthenia gravis, in which it is normal or nearly so), whereas at fast rates of stimulation (50 per second as shown in Fig 45-5B) or with strong voluntary contraction (for 15 s or longer), there is a marked increase in the amplitude of action potentials (incrementing response) Single- ber recordings show an increase in jitter, as in myasthenia gravis (page 1106) In the Lambert-Eaton syndrome, there is an increased representation of HLA-B8 and -DR3 haplotypes, as occurs in other au-
MYASTHENIA GRAVIS AND RELATED DISORDERS OF THE NEUROMUSCULAR JUNCTION
toimmune diseases Elmquist and Lambert, from a series of studies of excised muscle, deduced that there is a defect in the release of ACh quanta from the presynaptic nerve terminals, akin to the effects of botulinum toxin, magnesium excess, and neomycin (see further on) The presynaptic vesicles themselves appear to be normal in electron micrographs Also in contrast to myasthenia gravis, the extent of the receptor surface in this syndrome is actually increased (A G Engel) The physiologic mechanism in Lambert-Eaton myasthenic syndrome is not fully delineated; however, a fundamental defect is a loss of voltage-sensitive calcium channels on the presynaptic motor nerve terminal The calcium channels become cross-linked and aggregated by IgG autoantibodies, ultimately reducing the number of functioning channels (Fukunaga et al) In other words there are antibodies against a speci c component of the presynaptic membrane that have the effect of reducing the presynaptic release of ACh, virtually the opposite of myasthenia gravis A serologic test for these antibodies is available and is performed to con rm the diagnosis Even in patients without detectable antibodies against voltage-gated calcium channels, passive transfer indicates the presence of a circulating factor with similar activity Muscle biopsy is normal or shows only the same slight, nonspeci c changes as in myasthenia gravis The thymus is, of course, normal Recognition of the Lambert-Eaton syndrome should lead to a search for an occult tumor, particularly of the lung A PET scan of the body may be useful in this regard, although CT of the lungs is usually adequate If found, it should of course be treated; this alone may result in improvement in the neurologic syndrome If none is found, the search should be repeated at regular intervals, since the tumors at rst are small and may be inapparent even at autopsy Treatment Most patients with this disease bene t from administration of 3,4-diaminopyridine (3,4-DAP), an agent that blocks potassium channels in the distal motor terminal, thus prolonging depolarizations and enhancing the release of ACh vesicles The drug is given as 20 mg, up to 5 times a day either alone or in conjunction with pyridostigmine (Lundh et al) This has largely replaced the use of guanidine hydrochloride (20 to 30 mg/kg/day in divided doses), which had proved to be more effective in increasing strength than neostigmine or pyridostigmine but had signi cant hematologic and renal toxicity with long-term use With regard to more long-term relief, numerous regimens have been tried and favored by different groups Streib and Rothner were able to achieve long-term improvement with prednisone Dau and Denys have claimed the best results in nontumor cases with repeated courses of plasmapheresis in combination with prednisone and azathioprine Intravenous immune globulin has also been effective in a few reported cases Bain and coworkers indicate that the bene t is due to reduction in calcium channel autoantibodies, but the precise mechanism whereby intravenous immune globulin produces this effect could not be established Because of the unpredictable side effects of these drugs, many clinicians prefer alternate-day administration of prednisone and azathioprine prednisone 25 to 60 mg/day, and azathioprine 2 to 3 mg/kg body weight daily supplemented intermittently as needed by intravenous immune globulin The response to treatment tends to be slow, over a period of months and sometimes up to a year Some patients recover fully; in others, restoration of power is incomplete Diagnosis A syndrome of symmetrical weakness and fatigability of proximal muscles coupled with dry mouth, sphincter distur-
bances, aching muscles, and diminished re exes should be diagnostic The illnesses with which it might be confused are myasthenia gravis, inclusion body myopathy, and polymyositis There is a super cial resemblance to hysterical paralysis, where the patient may do better with encouragement on making a succession of voluntary contractions, and arthritis, where pain hampers the rst movements more than the successive ones Then the electrodiagnostic and speci c serologic tests are of value
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