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those of olivopontocerebellar atrophy often coexist, each component expressing itself variably in any individual, Graham and Oppenheimer in 1969 proposed the term multiple system atrophy (MSA), which has gained wide acceptance Several large series of cases of this complex syndrome have now been published, providing a perspective on the frequency and nature of its components Aside perhaps from a unifying feature of glial and neuronal includions described below, the syndromes in which parkinsonism and cerebellar ataxia are prominent are quite different from each other on clinical grounds, for which reason we prefer to apply the term MSA only to cases displaying both features Others have categorized them as MSA-P and MSA-C, depending on whether they display predominantly parkinsonism or cerebellar ataxia In this nosology, cases in which autonomic failure as described above predominate might be denominated as MSA-A In the Brain Tissue Bank of the Parkinson Disease Society of Great Britain, MSA accounted for 13 percent of patients who had been identi ed during life as having idiopathic Parkinson disease All of the patients with MSA had one or more symptoms of autonomic failure (postural hypotension, urinary urgency or retention, urinary or fecal incontinence, impotence) and dysphonia or stridor Babinski signs were present in half the patients and cerebellar ataxia in one-third Tremor was rare Males were affected more often than females In a comparable series of 100 patients (67 men and 33 women) studied by Wenning and coworkers, the disease began with a striatonigral-parkinsonian syndrome in 46 percent; often it was asymmetrical to begin with Mild tremor was detected in 29 percent, but in only a few was it of the resting Parkinson type In another 41 percent the illness began with autonomic manifestations; orthostatic hypotension occurred eventually in almost all patients, but it was disabling in only a few Cerebellar features dominated the initial stages of the disease in only 5 percent, but ataxia was eventually obvious in half the group This presentation will be elaborated further in the section on the degenerative cerebellar ataxias The extrapyramidal illness, on the whole, was more severe than Parkinson disease, since more than 40 percent of patients were con ned to a wheelchair or otherwise severely disabled within 5 years These observations generally match the ndings in a group of 188 patients described by Quinn and colleagues In that series, pyramidal signs were present in 60 percent and autonomic features in 77 percent, a feature we have found helpful in diagnosis and one that certainly marks the illness as affecting multiple systems Colosimo and colleagues, who reviewed the clinical ndings in 16 pathologically veri ed cases of MSA, found that several signs namely, the relative symmetry of the signs and rapid course, the lack of response to L-dopa and absence or minimal amount of tremor, and the presence of autonomic disorders reliably distinguished this syndrome from Parkinson disease These observations are in keeping with our own, and we would add that abnormalities of eye movement are not prominent in MSA Additional odd features, especially dystonia, are remarked upon in other series; anterocollis or dystonia of the lower facial muscles, for example, are striking in a few cases It is noteworthy that levodopa has had little or no effect or has made these patients worse early in the disease, but we have seen exceptions This is probably attributable to the loss of striatal dopamine receptors The diagnosis of MSA has been aided to some extent by imaging techniques Both MRI and CT scans frequently show atrophy of the cerebellum and pons in those with cerebellar features The putamina are hypodense on T2-weighted MRI and may show an
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increased deposition of iron Studies with PET have disclosed an impairment of glucose metabolism in the striatum and to a lesser extent in the frontal cortex a re ection, no doubt, of the loss of functioning neuronal elements in these parts Finally, it should be repeated that, despite the frequent concurrence of striatonigral degeneration, olivopontocerebellar degeneration, and the Shy-Drager syndrome, each of these disorders occurs in pure or almost isolated form; we therefore prefer to retain their original designations This distinction was re ected in the ndings of Gilman et al, who followed a series of 51 patients with olivopontocerebellar atrophy for up to 10 years; only 17 of their patients acquired a parkinsonian syndrome or autonomic failure Pathology In recent years, attention has been drawn to the presence of abnormal staining material in the cytoplasm of astroglia and oligodendrocytes and in some neurons as well These cytoplasmic aggregates have been referred to as glial cytoplasmic inclusions (Papp et al) Although they bear little resemblance morphologically to other discrete inclusions that have come to be accepted as characteristic of certain degenerative CNS diseases (eg, Lewy bodies) they nonetheless contain -synuclein (which is the main component of Lewy bodies) It is not clear to us whether these glial cytoplasmic accumulations represent a histopathologic hallmark of sporadic cases of MSA (Chin and Goldman; Lantos), since their presence is not speci c; they have been identi ed in practically every degenerative disease that has been subjected to sensitive silver impregnation stains (Gallyas silver technique) By the same token, -synuclein positive inclusions have been detected in several neurodegenerative syndromes Appropriate control studies to determine whether the glial inclusions are found in nondegenerative lesions in brain (at the edge of an infarct, for example) are needed Also lacking is information about the frequency of these cytoplasmic inclusions in relation to the aging brain The fundamental question remains unanswered: Do the cytoplasmic glial aggregates play a central role in the genesis of this and the other degenerative diseases, or are they simply some form of detritus that accumulates in glia as a reaction to or a by-product of the basic abnormality namely, the wasting and loss of neurons
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In 1963 Richardson, Steele, and Olszewski crystallized medical thought about a clinicopathologic entity progressive supranuclear palsy, or PSP to which there had been only ambiguous reference in the past The condition is not rare or unusual By 1972, when Steele reviewed the subject, 73 cases (22 with postmortem examinations) had been described in the medical literature, and several examples are to be found in every large neurologic center; the present authors encounter approximately ve new cases yearly, most of them not previously diagnosed Rare familial clusters have been described in which the pattern of inheritance is compatible with autosomal dominant transmission (Brown et al; de Yebenes et al) No toxic, encephalitic, racial, or geographic factor has been incriminated Clinical Features Characteristically the disease has its onset in the sixth decade (range 45 to 75 years), with some combination of dif culty in balance, abrupt falls, visual and ocular disturbances, slurred speech, dysphagia, and vague changes in personality, sometimes with an apprehensiveness and fretfulness suggestive of an agitated depression The most common early complaint is unsteadiness of gait and unexplained falling At rst, the neurologic and
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