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of myelitis, including autopsy proven ones, in which the disease develops without an apparent antecedent infection There is understandable uncertainty in such cases as to whether the illness is the opening phase of MS of the type described below under Demyelinative Myelitis In the numerous cases of transverse myelitis under our care, fewer than half have shown other signs of MS after 10 to 20 years (this is a far lower incidence than following a bout of optic neuritis) Also, there is an isolated form of relapsing myelitis, sometimes but not always triggered by an infection that does not manifest lesions elsewhere in the neuraxis and therefore has an ambiguous relationship to MS Further discussion of acute transverse myelitis in relation to other demyelinating diseases can be found below and on pages 778 and 791 The pathologic changes take the form of numerous subpial and perivenular zones of demyelination, with perivascular and meningeal in ltrations of lymphocytes and other mononuclear cells, and para-adventitial pleomorphic histiocytes and microglia (page 772) Taken in isolation, these changes cannot be clearly distinguished from those of MS Treatment Once symptoms begin, it is doubtful if any treatment is of consistent value One s rst impulse, assuming the mechanism to be an autoimmune, is to administer high doses of corticosteroids a practice we have followed but without conviction Perhaps it is advisable to do so, but there is as yet no evidence that this alters the course of the illness We have also used plasma exchange or intravenous immune globulin in several patients, with uncertain results, although this approach was seemingly helpful in a few patients who had an explosive clinical onset In general, the prognosis is better than the initial symptoms might suggest Invariably, the myelitic disease improves, sometimes to a surprising degree, but there are examples in which the sequelae have been severe and permanent Pain in the midthoracic region or an abrupt, severe onset usually indicates a poor prognosis (Ropper and Poskanzer) The authors have several times given a good prognosis for long-term recovery and assurance that no relapse will occur, only to witness a recrudescence of other symptoms at a later date, indicating that the original illness was MS Demyelinative Myelitis (Acute Multiple Sclerosis) The lesions of acute MS presenting as a myelitis share many of the features of the postinfectious type except that the clinical manifestations of the former tend to evolve more slowly, over a period of 1 to 3 weeks or even longer Also, their relation to antecedent infections is less certain, and in most recorded examples such provocative events were lacking Only the occurrence of subsequent attacks or additional lesions revealed by MRI or evoked potentials indicates that the basic illness is one of chronic recurrent demyelination, indistinguishable from the usual type of MS The most typical mode of clinical expression of demyelinative myelitis is with numbness that spreads over one or both sides of the body from the sacral segments to the feet, anterior thighs, and up over the trunk, with coincident but variable and usually asymmetric weakness and then paralysis of the legs As this process becomes complete, the bladder is also affected The sensorimotor disturbance may extend to involve the arms, and a sensory level can be demonstrated on the upper parts of the trunk The CSF usually shows a mild lymphocytosis, as in the postinfectious variety, but it is as often normal Oligoclonal bands may be absent with the rst attack Bakshi and colleagues have suggested that in myelitis due to MS, the changes seen on MRI occupy only a few adjacent spinal segments in comparison to the postinfectious le-
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sions which have a longer vertical extent, but this has not been a consistent distinction in our experience As a general rule, acute spinal MS is relatively painless and without fever, and the patient usually improves, with variable residual signs Those cases with a necrotic element, Devic disease and the closely related subacute necrotic myelopathy, may stabilize but then worsen (see below) The differential diagnosis of demyelinative myelitis is considered more fully in Chap 36 Treatment Corticosteroids, as outlined for the treatment of MS (page 787), may lead to a regression of symptoms, sometimes with relapse when the medication is discontinued (after 1 to 2 weeks) Other patients, however, show no apparent response, and a a proportion of cases have even continued to worsen while the medication was being given Plasma exchange and intravenous immune globulin have reportedly been bene cial in individual cases, particularly in those with an explosive onset (see later) The results in our patients have been too variable to interpret Acute and Subacute Necrotizing Myelitis and Devic Disease (see page 781) In every large medical center, occasional examples of this disorder are found among the many patients who present with a subacute paraplegia or quadriplegia, sensory loss, and sphincter paralysis The neurologic signs may erupt so precipitously that a vascular lesion is assumed In most other cases, the disease evolves at a slower and usually stepwise pace, over several months or years (Katz and Ropper) It is the saltatory progression that we have found most characteristic of the disease and, when present, that distinguishes it best from other processes such as a tumor within the cord Necrotizing myelopathy is distinguished from the more common types of transverse myelitis by a persistent and profound accidity of the legs (or arms if the lesion is cervical), are exia, and atonicity of the bladder all re ecting a widespread necrosis that involves both the gray and white matter of the spinal cord over a considerable vertical extent This picture is unexpected for a spinal cord lesion and, therefore, is often mistakenly attributed to spinal shock or to a completely different process such as Guillain-Barre syndrome This combination of spinal cord necrosis and optic neuritis corresponds to the syndrome described by Devic in 1894 and named by him neuromyelitis optica (Devic disease, page 781) Nearly all neurologists agree that a similar clinical syndrome involving the optic nerve and spinal cord (usually without necrosis) may also be caused by postinfectious encephalomyelitis and probably more often, by MS However, a case has been made for considering Devic disease as an entity apart from MS, as discussed in Chap 36 It follows that subacute necrotic myelopathy without optic neuritis might also be the result of MS or even a postinfectious process; the relationship between all of these entities is ambiguous, as discussed in Chap 36 In both the isolated necrotic myelopathy and in Devic disease, a few or up to several hundred mononuclear cells per cubic millimeter and increased protein may be found in the CSF but oligoclonal banding is usually absent Some cases show only an elevated protein concentration More so than with postinfectious transverse myelitis, the MRI reveals extensive signal changes and gadolinium enhancement, usually extending over several spinal segments (Fig 44-5) Highly characteristic on imaging studies performed weeks or more later is severe atrophy of the involved segments of cord Persistent swelling of the affected region is more suggestive of spinal cord tumor or another type of in ammation, but the permissible duration of cord swelling in cases of necrotic myelopathy is
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