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jitter (>80 100 microseconds), the increased quantal content results in an EPP of larger magnitude This subsequently results in a faster rise time approaching, but not reaching, normalcy with less inherent variability and an increased safety factor This leads to a reduction in the jitter With abnormal NMJs, the increased ACh release offsets the prolongation effect of temperature on rise time and variability The above-discussed processes are equally applicable in pre- as well as postsynaptic disorders In a presynaptic disease process where fewer quanta are released per nerve impulse at slow rates of stimulation, a reduction in temperature leads to more quanta being released in addition to more ACh reaching the postsynaptic membrane secondary to the reduced hydrolytic action of AChE This effect is likely suf cient to correct the reduced quantal content problem in effect at warmer muscle temperatures Larger EPPs occur in presynaptic disorders not only because of enhanced quantal release in response to cooler temperatures but due to prolonged opening of AChRs as well The net effect is an improvement in the safety factor, thus reducing the amount of neuromuscular block and hence an improvement in both clinical strength and fatigue A cogent explanation as to why circulating antibodies in MG may produce weakness that is asymmetric and in which certain muscle groups are selectively vulnerable is hard to provide The preferential involvement of the external ocular muscles may be related to the elevated temperature of the head compared to limbs, speci c anatomic and physiologic aspects of these muscles, different antigenic AChR subtypes, ring rates, and/or other poorly understood factors511,512

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In this exercise, you ll learn how to create an MMC You ll also create a desktop icon that you can use to access this customized software toolkit whenever you need it At the end of this lab, you ll be able to

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Despite multiple insights into the pathogenesis of MG, the actual cause(s) remains unknown There are suggestions that a genetic predisposition exists, at least in some patients513,514 Studies of asymptomatic relatives of patients with MG who undergo SFEMG demonstrate that a third will have abnormal jitter values269,514 A role has been suggested for infectious agents as a precipitating cause as well515 The thymus has always played a central role in MG disease theories As many as 40 70% of patients with autoimmune MG have thymic hyperplasia and about 10 15% of patients have a documented thymoma516 519 The observation that some patients with MG apparently respond clinically to the removal of the thymus gland lends further support to this hypothesis One potential explanation involves the recognition that the thymus contains myoid cells and other types of stem cells that may serve as autoantigens by the expression of AChRs or AChR antigens on their surface520 There are also AChR-speci c B lymphocytes within the thymus

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