MISCELLANEOUS DNMT Organophosphate Poisoning
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The electrophysiologic presentation of acute organophosphate intoxication is rather unique230 232,408,409 414 Motor and sensory nerve conduction velocities are essentially normal within the rst 24 48 hours Mild conduction slowing may develop subsequently CMAP amplitudes are decreased in severe intoxication with limited effects in milder exposures In about 60% or more of patients, an afterdischarge(s) as described above may be seen (Fig 23 4) This is believed to be the most sensitive EDX indicator of early toxicity230 232 A rather unique feature of organophosphate toxicity is a decrement increment pattern to repetitive stimulation observed either early in the course of the disorder or in later stages of recovery Speci cally, there is an
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DISORDERS OF NEUROMUSCULAR TRANSMISSION
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initial decrement to repetitive stimulation, with a subsequent increment to the baseline CMAP at high rates of stimulation During repetitive stimulation, the afterdischarges evoked during single stimulation are absorbed into the subsequent CMAPs and are no longer observed Patients with signi cant intoxication reveal a decrement to repetitive stimulation at low rates of stimulation, while those with moderate-to-mild intoxication only reveal a decrement at rates >10 Hz With slow repetitive stimulation, edrophonium chloride administration, in contrast to MG, results in a marked worsening of the decremental response, which returns to the resting level within about 30 seconds229 Application of d-tubocurarine, an AChR-blocking agent, repairs the decrement by decreasing the number of AChRs available to the excess ACh Needle electromyographic examination does not reveal positive sharp waves or brillation potentials during the initial stages of the disease The only abnormality is a reduction in the number of voluntary MUAPs In patients who develop an axonal neuropathy as a result of delayed or chronic organophosphate exposure, a typical length-dependent EDX neuropathy pattern eventually develops In patients given nondepolarizing neuromuscular blocking agents, there is a reduced CMAP that is expected to decrement with slow repetitive stimulation The results are similar to those observed in MG The MUAP can be seen to decline in magnitude as single muscle bers belonging to a particular motor unit serially block with increasing dosages of curare415 As might be expected with SFEMG analysis, doses of curare that do not produce weakness may nevertheless produce an increase in jitter values416
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pletely normal To date, there have been no convincing morphological changes of the NMJ attributed to MuSK antibodies Muscle biopsies in these latter patients have demonstrated minor simpli cation of some end plates The density and distribution of AChR in patients with MuSK are essentially normal in the studies reported to date Complement deposition or other markers of an immune-mediated disease has not been identi ed423,424
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CONGENITAL MYASTHENIC SYNDROMES1
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The histologic changes of the CMS are, in large part, limited to those detectable by ultrastructural analysis This evaluation is a very specialized undertaking done at a limited number of centers Light microscopic analysis of muscle is not routinely performed in patients with suspected CMS In most of these disorders, routine muscle biopsy ndings are normal or nonspeci c in nature
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Histopathology is not part of the routine evaluation in the majority of patients with MG Routine light microscopy may reveal mild, nonspeci c abnormalities on muscle biopsy including type 1 ber predominance, mild ber type grouping, or type 2 ber atrophy233 Focal interstitial in ammatory in ltrates, so-called lymphorrhages, are not uncommon, particularly at the end plates230 232,417 Ultrastructural abnormalities are more evident Immunoelectron microscopy of the postsynaptic membrane region in patients with myasthenia demonstrates IgG and complement precipitation on the membrane, an increased synaptic space, reduced postsynaptic membrane complexity with fewer postjunctional folds, and decreased numbers of AChRs Many of the remaining AChRs are bound with IgG181,182,233,418 422 In contrast, the presynaptic portion of the NMJ appears com-
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Choline acetyltransferase de ciency has limited morphological change Synaptic vesicles are smaller than normal Postsynaptic structure is normal Light microscopic analysis from patients with end-plate AChE de ciency demonstrates normalappearing muscle tissue or type 1 ber predominance172,173,180 184 Electron microscopic analysis reveals a reduction in the size of the nerve terminals that do not cover the entire endplate region and an AChR number that varies from muscle to muscle There is an atrophy of presynaptic terminals in an apparent compensatory attempt to limit quantal release and prevent AChR overstimulation Despite this, there is degeneration of synaptic folds with a reduced number of secondary synaptic clefts and diminished postsynaptic area Immunocytochemistry studies reveal the presence of fetal AChR that contain the -subunit instead of the -subunit Paucity of synaptic vesicles and reduced quantal release is associated with a decreased density of synaptic vesicles in the immediate release zone of the presynaptic terminal Slow channel syndrome reveals light microscopic changes unlike most CMS These include type I ber predominance with associated isolated grouping of atrophic type I or type II bers, ber size variation, tubular aggregates, ber splitting, endomysial brosis, and vacuolization near the NMJ165 167,172,173,185,425,426 Ultrastructural examination reveals degeneration of the junctional folds of the end plate Apoptotic nuclei and degenerating organelles may also be observed