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Included under this title is a group of diseases affecting the neuromuscular junction, the most important of which is myasthenia gravis As a group, these disorders exhibit several characteristic and striking features, the essential one being a uctuating weakness and fatigability of muscle Some degree of weakness is usually present at all times, but it is made worse by activity The weakness and fatigability re ect physiologic abnormalities of the neuromuscular junction that are demonstrated by clinical signs and by special electrophysiologic testing As an aid to understanding the diseases discussed in this chapter, the reader should consult the discussion of the structure and function of the neuromuscular synapse given in Chap 48
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The main feature of myasthenia gravis, referred to simply as myasthenia, is a uctuating weakness of certain voluntary muscles, particularly those innervated by motor nuclei of the brainstem, ie, ocular, masticatory, facial, deglutitional, and lingual Manifest weakening during continued activity, quick restoration of power with rest, and dramatic improvement in strength following the administration of anticholinesterase drugs such as neostigmine are the other notable characteristics of the weakness Historical Note Several students of medical history af rm that Willis, in 1672, gave an account of a disease that could be none other than myasthenia gravis Others give credit to Wilks (1877) for the rst description and for having noted that the medulla was free of disease, in distinction to other types of bulbar paralysis The rst reasonably complete accounts were those of Erb (1878), who characterized the disease as a bulbar palsy without an anatomic lesion, and of Gold am (1893); for many years thereafter, the disorder was referred to as the Erb-Gold am syndrome Jolly (1895) was the rst to use the name myasthenia gravis, to which he added the term pseudoparalytica to indicate the lack of structural changes at autopsy Also it was Jolly who demonstrated that myasthenic weakness could be reproduced in affected patients by repeated faradic stimulation of the relevant motor nerve and that the fatigued muscle would still respond to direct galvanic stimulation of its membrane Interestingly, he suggested the use of physostigmine as a form of treatment, but there the matter rested until Reman, in 1932, and Walker, in 1934, demonstrated the therapeutic value of the drug Campbell and Bramwell (1900) and Oppenheim (1901) each analyzed over 60 cases and crystallized the clinical concept of the disease The relationship between myasthenia gravis and tumors of the thymus gland was rst noted by Laquer and Weigert in 1901, and in 1949 Castleman and Norris gave the rst detailed account of the pathologic changes in the gland In 1905 Buzzard published a careful clinicopathologic analysis of the disease, commenting on both the thymic abnormalities and the in ltrations of lymphocytes (called lymphorrhages) in muscle He postulated that an autotoxic agent caused the muscle 1250
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weakness, the lymphorrhages, and the thymic lesions He also commented on the close relation of myasthenia gravis to Graves disease and Addison disease, which are all now considered to have an autoimmune basis In 1960, Simpson and, independently, Nastuk and coworkers theorized that an autoimmune mechanism must be operative in myasthenia gravis Finally, in 1973 and subsequently, the autoimmune nature of myasthenia gravis was established through a series of investigations by Patrick and Lindstrom, Fambrough, Lennon, and A G Engel and their colleagues (see further on, under Etiology and Pathogenesis ) These and other references to the early historical features of the disease are to be found in the reviews by Viets and by Kakulas and Adams; A G Engel s monograph (1999) is an excellent modern reference
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Clinical Manifestations
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Myasthenia gravis, as the name implies, is a muscular weakness formerly with a grave prognosis Repeated or persistent activity of a muscle group exhausts its contractile power, leading to a progressive paresis, and rest restores strength, at least partially These are the identifying attributes of the disease; their demonstration, assuming that the patient cooperates fully, is sometimes enough to establish the diagnosis The special vulnerability of certain muscles gives myasthenia a characteristic stamp Usually the eyelids and the muscles of the eyes and somewhat less often of the face, jaws, throat, and neck are the rst to be affected Infrequently the initial complaint is referable to the limbs More speci cally, the weakness of the levator palpebrae or extraocular muscles is the initial manifestation of the disease in about half the cases, and these muscles are involved eventually in more than 90 percent Ocular palsies and ptosis (weakness of eyelid opening) are usually accompanied by weakness of eye closure, a combination that is virtually always myopathic and not neuropathic in origin, eg, observed in myasthenia and muscular dystrophy Diplopia in myasthenia does not correspond to the innervatory pattern of a nerve but is the result instead of asymmetric weakness of several muscles in both eyes As the disease advances, it often spreads from the cranial to the limb and axial muscles The onset of weakness is usually insidious, but there are instances of fairly rapid development, sometimes apparently initiated by an emotional upset or infection (usually respiratory) In most patients, however, a precipitating event cannot be identi ed Symptoms may rst appear during pregnancy or, more commonly, in the puerperium or in response to drugs used during anesthesia Thymic abnormalities of several types are closely connected with the disease, as elaborated further on, and weakness may begin months or years after removal of a thymoma Certain ocular signs are highly characteristic of myasthenia Sustained upgaze for 30 or more seconds will usually induce or exaggerate ptosis and may uncover a myasthenic ocular motor
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