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The incidence of MG ranges between 1 and 9 per million, while prevalence is estimated to be between 25 and 142 per million2 11 The incidence of MG is slightly greater in women than in men The age of onset is bimodal for both men and women Women demonstrate annual peak incidences at ages 20 24 and 70 75 years, while men have peak rates between 30 34 and 70 74 years In the early disease presentation group, a female-to-male ratio is roughly 7:3, while in the lateonset group, the gender ratio is 1:1 The mean mortality rate per million population approximates 17 (09 31) for all patients with a diagnosis of MG, while the mortality rate directly attributable to the disease itself is 08 106 (00 22) These gures differ signi cantly from a previous era where knowledge of the disease and therapeutic options were limited, and the adjective gravis was more apt than is currently the case DNMT, particularly autoimmune MG, have clinical features that distinguish them from most other neuromuscular diseases12 Many of these distinctive features, particularly the uctuating nature of a patient s strength or stamina, are derived from the unique pathophysiology of impaired NMT This pathophysiology produces, in many cases, a dynamic rather than xed disorder This behavior is in part due to the biology of NMT, which
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SECTION II
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TABLE 23 1 DISORDERS OF NEUROMUSCULAR TRANSMISSION
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Presynaptic Lambert Eaton myasthenic syndrome Botulism and botulinum toxin Tick paralysis (Australian) Congenital myasthenia gravis Choline acetyltransferase de ciency Paucity of synaptic vesicles and reduced quantal release Drugs and toxins Hypermagnesemia Envenomation black and green mamba, Australian tiger snake, Pandinus scorpion, conus marine snails, multibanded krait, Brazilian rattlesnake, and black and brown widow spider Aminoglycosides and other antibiotics Calcium channel blocking agents (minor) Aminopyridines Corticosteroids Hemicholinium-3 Synaptic Congenital myasthenic syndromes end plate acetylcholinesterase de ciency Drugs and toxins Cholinesterase inhibitors edrophonium, pyridostigmine, and neostigmine Organophosphates Postsynaptic Myasthenia gravis Transient neonatal myasthenia Drug-induced myasthenia gravis Penicillamine Alpha-interferon Congenital myasthenic syndromes Primary kinetic defects slow and fast channel syndromes Primary AChR de ciency Rapsyn de ciency Sodium channel myasthenia Plectin de ciency MuSK mutations Dok-7 Drugs and toxins D-Tubocurarine, vecuronium, and other nondepolarizing blocking agents Succinylcholine, decamethonium, and other depolarizing blocking agents Tetracyclines, lincomycin, and other antibiotics Envenomation by banded kraits, Siamese cobra, Conus marine snail
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AChR, antiacetylcholine receptor; MuSK, muscle-speci c tyrosine kinase
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includes the relative ease by which NMJs are repaired, particularly in comparison to other components of the neuromuscular system Many diseases that affect the cell bodies of either sensory or motor neurons, peripheral nerve axons or their myelin sheaths, or even muscle are more likely to have persistent if not permanent effects once established The biology of the NMJ allows the symptoms of MG, and to a lesser extent Lambert Eaton myasthenic syndrome (LEMS), to uctuate on a minute-to-minute, diurnal, or week-to-week basis This uctuation is a key diagnostic feature of the DNMT DNMT may also provide a fairly distinctive pattern(s) of weakness Many have a predilection for muscles innervated by cranial nerves The basis of this is not completely understood but, in the case of MG, may be related to the differences in the type and distribution of NMJs in at least some of the muscles that myasthenia tends to affect1 The diurnal fatiguing nature of the painless weakness of MG is a quality that may be a dominant feature of the patient s history or may be overlooked13 18 Patients may complain of various factors that exacerbate their feeling of weakness or fatigue in addition to exercise such as warm weather, systemic infections, menses, anxiety, emotional stress, and pregnancy7,19 30,30 32 Enquiries referable to speci c muscles, brought on or worsened by physical activities or simply by the rigors of the evolving day, should be made Occasionally, variation in disease severity over weeks to months unrelated to interventions or other variables may be notable in patients with MG as well The pattern as well as intensity of weakness in MG can be extremely variable It may be focal, multifocal, or diffuse Any voluntary muscle may be affected, although those controlled by cranial nerve motor bers are typically the most susceptible Visual obscuration related to ptosis, diplopia, dysarthria, dysphagia, and dif culty chewing are among the most common symptoms Approximately half of patients with MG will initially have isolated ocular symptoms17,33 35 Ptosis is the presenting symptoms in 50 90% of patients, while 15% complain of blurred vision or frank diplopia36,37 If not a presenting symptom, external ocular muscle involvement is present at some point in about 90 95% of patients Different speech patterns may be noted The voice may be hypophonic due to vocal cord or expiratory muscle weakness, either of which may be the presenting complaint38 40 The patient may be dysarthric as a result of weakness of the lips, tongue, or cheeks It may have a nasal quality due to palatal insuf ciency and air leak Palatal and pharyngeal muscle weakness eventually manifests in roughly 40% of all patients Nasal regurgitation of food and liquid, dif culty removing food from between the cheek and teeth due to tongue weakness, as well as ineffective snif ng, coughing, nose-blowing, or throat-clearing may be noted Presentations dominated
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