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Primary kinetic defect +/ AChR de ciency The slow (to close) channel disorders refer to dominantly inherited kinetic defects that prolong the duration of AChR channel opening as a result of different mutations of the AChR -, -, or subunits168,174,560 This, in turn, leads to an increased half-life of MEPP and EPP decay The mechanisms may involve an accelerated rate of channel opening, a delay in channel closing, or an enhanced af nity of ACh for the AChR Again, increased cationic migration through these prolonged channel openings leads to degeneration of junctional folds, decreased AChR synthesis, a resultant reduction in AChR numbers, as well as depolarization block The latter is a result of sequential stimuli arriving at a time of a refractory period that also has a prolonged duration Fast (to close) channel disorders due to subunit mutations of the AChR are recessively in-
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DISORDERS OF NEUROMUSCULAR TRANSMISSION
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simpli ed junctional folds diminish both MEPP and EPP amplitude
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LAMBERT EATON MYASTHENIC SYNDROME
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LEMS is an acquired, autoimmune disorder caused by antibodies directed against P/Q type voltagegated calcium channels and to a lesser extent the N-type voltage-gated calcium channels and synaptotagmin on and in the presynaptic motor nerve terminals200,202,207,209,210,228,431,432,564,565 Passive transfer of IgG from patients with paraneoplastic and nonparaneoplastic LEMS to animals induces all of the morphologic and electrophysiologic features of the disease201 In addition, passive transfer experiments in seronegative LEMS suggest that this is an autoimmune disorder in which the culprit antibody has yet to be identi ed The trigger for initiating the afferent limb of the autoimmune response is unknown In patients with cancer, it is speculated that the tumor cells express an embryonic-type calcium channel or calcium channel protein subcomponent that provokes the production of autoantibodies capable of cross-reacting with presynaptic neuronal calcium channels in persons genetically predisposed566 The antigenic substrate located on the tumorous calcium channels is believed to be the same, or share a similar antigenic signature, as the neuronal calcium channels165 167,430,431,432 A common antigenic relationship between small cell carcinoma and calcium channels is supported by observations of the polypeptide neurotoxin -conotoxin secreted by the marine snail Conus geographus These effects will be subsequently described in the last paragraphs of this chapter, which discuss drug and toxin effects on NMT By whatever mechanism, the immune system is activated to produce antibodies directed against these nerve terminal calcium channels200,228,270,567 The antibodies bind to the voltage-gated calcium channels and inhibit the entry of calcium into the nerve terminal Additionally, the antibodies may cross-link neighboring calcium channels, thus precipitating the process of internalization and degradation of the calcium channels Complement does not appear to be involved in this process because the nerve terminal maintains a grossly normal appearance without evidence of lytic destruction419 Antibody binding with the calcium channels act to reduce the amount of calcium entry during an action potential The reduced nerve terminal calcium concentration limits vesicular release from the nerve terminal s internal cytoskeletal bridgework There is some indication that calcium serves to cleave the bonds holding the vesicles to this intraneural framework The net result is less availability of vesicles to fuse with the membrane Cross-
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linking and internalization of calcium channels have the same net result of reduced calcium entry and hence hinder the vesicle s ability to attach or dock with recognition proteins at the active zones568 In patients with LEMS, intracellular microelectrode recordings reveal potentially paradoxical ndings The MEPP s magnitude in LEMS is quite similar to that recorded in normal muscle, implying that the amount of ACh per vesicle is normal The frequency of MEPP production, however, may be normal or somewhat greater than that of normal muscle, ie, 057 vs 024/s, respectively192,204,569 This increased frequency of quantal release appears to be incompatible with the concept of antibody binding to the synaptic vesicle and fusion hindrance If this mechanism were true, it would be anticipated that the frequency of MEPPs should decline and should not increase The reason for the increased MEPP frequency is unknown, although it could be postulated that the spontaneous synaptic release is not calcium dependent to the extent that vesicle release prompted by a nerve action potential is The nerve terminal response to depolarization is of interest The mean quantal content in LEMS is roughly 8 (33 15), while a normal terminal releases approximately 56 (24 106) quanta This nding of diminished quantal release is quite similar to what is observed when the extracellular uid bathing the nerve terminal is deprived of calcium, and/or the magnesium concentration is dramatically elevated, ie, reduced quantal release to neural depolarization The hypothesis of reduced calcium entry secondary to immune-mediated channel dysfunction, disorganization, or destruction is compatible with the physiologic ndings of reduced quantal release Decreasing calcium entry serves to decrease the probability of ACh release, thereby decreasing the amount of ACh released per nerve terminal depolarization and decreasing the muscle EPP The histologic and physiologic ndings appear to be concordant In LEMS, normal-appearing vesicles contain normal amounts of ACh If suf cient amounts of ACh are released, the postsynaptic membrane responds normally, as evidenced by EPPs more than capable of reaching threshold The reduced quantal content is evidenced by subthreshold EPPs, which reach threshold following rapid rates of stimulation, which were described in the laboratory evaluation setting This effect is most likely due to the residual calcium overwhelming the binding/sequestering mechanism, thereby increasing the probability of vesicle release The increased amounts of residual nerve terminal calcium compensates for the diminished amount of calcium entering the terminal in response to each nerve stimulus The cumulative effect of calcium is necessary for the appropriate amounts of ACh to be released and generate suprathreshold EPPs All of these physiologic effects directly impact on what
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