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DISORDERS OF NEUROMUSCULAR TRANSMISSION
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nicotinic AChR desensitizes or blocks receptors leading to increased weakness This type of crisis needs to be distinguished from the myasthenic crisis due to the underlying disease710 These two types of crises may be distinguished by performing an edrophonium test on the patient as described above If IV edrophonium results in clinical worsening, the increased weakness in the patient is most likely the result of overdosing the anticholinesterase medication If weakness improves following edrophonium, the weakness is due to the underlying MG Pyridostigmine is typically delivered orally but exists in a parenteral preparation as well It should be noted that the IV dose is 1/30th to 1/60th that of the oral preparation Neostigmine can be used in lieu of pyridostigmine but the latter is typically preferred, as it is longer acting and may have better activity on bulbar muscles Physostigmine should not be used as a treatment for MG, as, unlike the other two agents, it crosses the blood brain barrier and leads to unwanted CNS cholinergic effects Patients with MuSK antibody MG are frequently insensitive to the bene cial effects of anticholinesterases88,90 These patients commonly respond to the other immunomodulating drugs described in subsequent paragraphs that have been traditionally used in patients who are anti-AChR seropositive and negative73,85,88,90
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The most commonly used immunosuppressive agents are corticosteroids Various trials have demonstrated the ef cacy of corticosteroids in the treatment of MG129,711 717 Corticosteroid treatment results in marked improvement (45%) or remission (30%) in the majority of patients with myasthenia Prednisone, at least initially, is the drug of choice for the majority of patients with moderate to severe generalized MG Patients with diabetes or signi cant osteopenia represent two groups where alternative rst-line treatments may be considered There are two treatment strategies generally employed when using prednisone in patient with MG: (1) aggressive high-dose daily steroids at the onset of treatment approach and (2) a start low and go slow approach A more rapid improvement is likely to occur from a high-dose regimen Prednisone is initiated at a dose of 15 mg/kg/d (up to 100 mg) for 2 4 weeks Typically, the patient is transitioned to an alternate-day regimen This can be done by maintaining the high dose on odd days and going immediately to zero on the even days Alternatively, weaning can be accomplished by lowering the dose on the alternate day, eg, 100 mg on odd days and 80 mg on the even Higher doses are maintained until strength has normalized or the improvement plateaus Subsequently, prednisone is tapered slowly, eg, by reducing 5 mg every 2 3 weeks until 20 mg qod is reached Past 20 mg
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qod, tapering generally progresses more slowly, with incremental drops of 1 25 mg being recommended It is usually at these lower doses that patients may relapse Most patients will require some amount of immunosuppressive medication The goal is to nd the lowest dose necessary to maintain their strength Understandable fears regarding the adverse effects of longterm corticosteroids may lead the inexperienced clinician to wean steroids too rapidly, a frequent observation made in experienced neuromuscular clinics The addition of other immunosuppressive agents may have a prednisone sparing effect and allow for lower doses of the corticosteroid It is an entirely reasonable and often effective strategy to begin corticosteroids and another immunomodulating agent simultaneously As the second-line drugs typically have signi cantly slower onsets of action, the strategy is to get the patient under control with corticosteroids and then maintain that control with a second-line agent with a more delayed onset effect, as the steroids are being weaned over the ensuing months Importantly, as many as 30% of patients experience a varying degree of initial worsening (within the rst 1 3 weeks) lasting about 1 week after they are started on high doses of steroids129,707,718 Signi cant weakness is estimated to occur in <10% of patients Nevertheless, it is prudent to hospitalize patients for the 1 week after initiating treatment with high-dose corticosteroids The mechanism of the exacerbation of myasthenic symptoms is not clear It would appear to be related to NMT as opposed to nerve or muscle as it corresponds with worsening of the decremental response to repetitive stimulation719 It has been hypothesized that corticosteroids have mild neuromuscular blocking properties that precede the bene cial effects of immunomodulation It is possible that the worsening may have a mechanism similar to weakness in patients with acute quadriplegic myopathy who most frequently develop generalized weakness in the setting of high-dose corticosteroid combined with neuromuscular blocking agents The AChR antibodies in myasthenics in combination with corticosteroids may have the same synergistic role that corticosteroids have with nondepolarizing neuromuscular blocking agents in critical illness myopathy In view of the transient myasthenic worsening associated with corticosteroid introduction, some have advocated the start low and go slow approach 18 Patients are started at a dose of 15 20 mg/d and the dose is slowly increased by 5 mg every 2 4 days or so until de nite improvement is noted Alternatively, based on results of the recent mycophenolate trials, patients may be maintained on and experience a bene cial effect without escalating the prednisone dose past 20 mg/day Unfortunately, improvement takes much longer with this approach and is therefore unsatisfactory in patients with severe weakness This approach may be preferable in patients with
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