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young patients has already been mentioned; only their young age and the bilaterality of the pain in some of them raised the suspicion of MS, con rmed later by sensory loss in the face and other neurologic signs It is notable, however, that facial palsy along the lines of Bell s palsy is almost never a sign of MS Brachial, thoracic, or lumbosacral pain consisting mainly of thermal and algesic dysesthesias, was a source of puzzlement in several other patients until additional lesions developed Other types of pain in MS have been addressed earlier In two of our cases, the relatively acute occurrence of a right hemiplegia and aphasia rst raised the probability of a cerebrovascular lesion; in still others, a more slowly evolving hemiplegia had led to an initial diagnosis of a cerebral glioma The dystonic and paroxysmal symptoms are mentioned above; they do not typically bring the diagnosis of MS to mind Approximately 3 percent of patients reportedly have focal seizures, but it should be emphasized that this is usually in relation to an obvious cerebral lesion and advanced disease of many years duration Seizures at an early stage of illness are almost always attributable to previous head injury, idiopathic epilepsy, or as in a recent case, withdrawal of sleep medication Several times we have seen coma during relapse of MS, and in each instance it continued to death In one case it occurred in a 64-year-old woman who had had two previous episodes of nondisabling spinal MS at 30 and 44 years of age A confusional psychosis with drowsiness was the initial syndrome in another patient whom we saw later with a relapse involving the cerebellum and spinal cord Another unusual syndrome is one of slow intellectual decline with slight cerebellar ataxia A 10-year, slowly progressive cerebellar ataxia in an adolescent girl was perplexing until she later developed internuclear ophthalmoplegia A rapid onset of ascending paralysis of legs, bladder and bowel, and trunk with severe pain in sacral parts, are exia, and a mononuclear pleocytosis of 1600 cells per cubic millimeter occurred in another of our patients and lasted 2 years before she began to walk again; earlier she had had diplopia and retrobulbar neuritis Cases similar to these develop a necrotic myelopathy that is similar to Devic disease and there is little recovery As mentioned in the chapter on spinal cord disease, some instances of MS in late adult life take the form of a slowly progressive cervical myelopathy There is also certainly a form of spinal MS without cerebral involvement, as noted further on Seemingly more frequently in recent years, we have observed patients whose illness satis ed all the clinical criteria for the diagnosis of MS except for the onset of symptoms in the sixth or seventh decade Presumably we were witnessing the late deteriorative phase of the illness, earlier symptoms having been forgotten or having never been recognized Contrariwise, in our pathologic material (and increasingly with the ubiquitous use of MRI scans), we have several times found a few typical lesions of MS to which the clinical records make no reference.

Several variants of MS merit more extended discussion They are acute MS, neuromyelitis optica, acquired Schilder disease, and the conjunction of MS and polyneuropathy The chronic progressive variety of MS presents special problems that are addressed in a later section on Clinical Course and Prognosis Acute Multiple Sclerosis Rarely, MS takes a rapidly progressive and highly malignant form; Marburg s name has been attached to this variant A combination of cerebral, brainstem, and spinal man-

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ifestations evolves over a few weeks, rendering the patient stuporous, comatose, or decerebrate, with prominent cranial nerve and corticospinal abnormalities Death may end the illness within a few weeks to months without any remission having occurred, or there may be partial recovery, as noted below At autopsy the lesions are of macroscopic dimensions, in essence very large acute plaques of MS The only difference from the usual form of MS is that many plaques are of the same age and the con uence of many perivenous zones of demyelination is more obvious Large acute plaques may have associated mass effect and enhancement that simulates a tumor in radiographic appearance, but they tend to evolve at a more rapid pace clinically Two of our most striking examples of this rapidly fatal form were in a 6-year-old girl and a 16-year-old boy, both of whom died within 5 weeks of the onset of symptoms Another was a 30-year-old man who lived 2 months In none of them had there been a preceding exanthem or inoculation or any symptoms suggestive of demyelinative disease Mendez and Pogacar present such a case and point out the extensive contrast enhancement of the brain lesions on a CT scan Usually the CSF shows a cellular response but no oligoclonal bands Nonfatal clinical cases of similar type in children, adolescents, and young adults are admitted to our hospitals once or twice a year Some have responded to high doses of intravenous corticosteroids; others worsened while receiving this medication We have also had experience with two patients who improved rapidly after the institution of plasma exchange treatments, similar to the report by Rodriquez and coworkers However, it is clear that most patients with acute MS, especially those with myelitis, do not respond to this treatment Some have made an astonishing recovery after several months, and a few have then remained well for 25 to 30 years Others have relapsed, and the subsequent clinical course was typical of MS Most neurologists are familiar with similar episodes of acute deterioration that punctuate otherwise typical cases of MS These aggressive relapses occur most often in the rst year of illness and in middle-aged patients and take the form of an exacerbation of a pre-existing myelopathy in combination with a new brainstem syndrome After a severe episode of this sort or multiple ones, a few of the lesions are found to be cavitating on imaging studies rather than demyelinative It seems to the authors that more than one disease is being included in the clinical category of acute MS One type conforms in its temporal pro le to a rather protracted form of acute disseminated encephalomyelitis an acute monophasic illness extending over 4 to 8 weeks Others subsequently prove to be typical polyphasic MS The main considerations in differential diagnosis are a CNS vasculitis and intravascular lymphoma In all the variants of MS, diagnosis becomes secure only when there is evidence of multiple cerebral and spinal lesions, usually veri ed by MRIs taken over an interval of time A word of caution in using MRI for this purpose: small lesions may be overlooked and, as noted earlier, lesions similar to those of MS are caused by a large number of other processes Neuromyelitis Optica (Devic Disease, Necrotic Myelopathy; See also Chap 46) Here, there is a simultaneous or successive and usually severe involvement of optic nerves and spinal cord The combination was remarked upon by Clifford Albutt in 1870, and Gault (1894), stimulated by his teacher Devic, devoted his thesis to the subject Devic subsequently endeavored to crystallize medical thought about a condition that has come to be known as neu-.

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