The pathologic changes in postinfectious myelitis take the form of numerous subpial and perivenular zones of demyelination, with perivascular and meningeal infiltrations of lymphocytes and other mononuclear cells, and para-adventitial pleomorphic histiocytes and microglia. Taken in isolation, these pathologic changes cannot be distinguished from those of MS.
Treatment Once symptoms begin, it is not clear if any treatment is of consistent value. One’s first impulse, assuming the mechanism to be 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.
The prognosis of this illness 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 probably multiple sclerosis.
Acute Demyelinating Myelitis of Multiple Sclerosis (Chap. 35)
The lesions of acute MS share many of the features of the postinfectious type as noted above. However, the clinical manifestations of the former tend to evolve more slowly, over a period of 1 to 3 weeks or even longer. Also, a relation to antecedent infections is not often seen in MS. 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.
The most typical of clinical expression of demyelinating 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 may show a mild lymphocytosis, as in the postinfectious variety, but it is as often normal. Oligoclonal bands may be absent with the first attack. Bakshi and colleagues have suggested that in myelitis as a result of MS, the changes seen on MRI occupy only a few adjacent spinal segments in comparison to the postinfectious lesions, 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. The differential diagnosis of demyelinating myelitis is considered more fully in Chap. 35.
Treatment Corticosteroids, as outlined for the treatment of MS in Chap. 35, 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 proportion of cases have even continued to worsen while the medication was being given. Plasma exchange and intravenous immune globulin have reportedly been beneficial in individual cases, particularly in those with an explosive onset (see later). The results in our patients have been too variable to interpret.
Neuromyelitis Optica, Acute and Subacute Necrotizing Myelitis, and Devic Disease (See Discussion in Chap. 35)