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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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cytic anemia is reversed by the administration of B12, but the neurologic illness is less responsive (page 1092) Triorthocresyl phosphate and acrylamide are potent peripheral nerve poisons Both of these drugs cause a dying-back polyneuropathy with axonal degeneration and have been used experimentally to produce this effect Vacor, a phenylnitrosurea rodenticide, has been taken as a suicidal agent It gives rise to a profound sensory and autonomic neuropathy with abdominal pain and hyperglycemia due to acute pancreatitis Detailed accounts of the clinical and experimental neurotoxicology of these agents can be found in the monograph by Spencer et al Drug-Induced Neuropathies and Neuronopathies A large number of medications are sources of polyneuropathy of predominantly sensory type Most are dose-dependent and are therefore more or less predictable after large cummulative doses of the drug have been given (eg, in chemotherapy) or after prolonged administration for other reasons Often, in the latter case, the patient and physician fail to connect the sensory symptoms to drug toxicity Antineoplastic Drugs Among chemotherapeutic agents in current use, cisplatin and carboplatin are known to consistently evoke a predominantly sensory polyneuropathy, which begins several weeks after completion of therapy in at least half of the patients (page 1039) Proprioception and vibratory sensation are most severely impaired Some patients develop acrodynia and episodic color changes in the ngertips and toes, suggesting that autonomic nerves are also involved; in severe cases there is sensory ataxia and pseudoathetosis The severity of histopathologic changes in the peripheral nervous system corresponds to the concentration of platinum in these tissues, the highest concentrations being found in dorsal root ganglia There may be secondary degeneration in the posterior columns the basis for a Lhermitte symptom reported by these patients The taxanes paclitaxel (Taxol) and the more potent docetaxel (Taxotere), both cited as inhibitors of the depolymerization of neurotubules, are used mainly in the treatment of ovarian cancer They produce a sensory polyneuropathy similar to that of cisplatin The nerve lesion regresses slowly with a reduction in dosage (see also page 1040) Pathologic studies have shown a distal axonopathy affecting mainly large bers For decades it has been known that peripheral neuropathy commonly complicates the use of vincristine, an antineoplastic agent widely used in treatment of the lymphomas and leukemia (page 1039) Paresthesias are the most common early symptom, and loss of ankle jerks is an early manifestation Some degree of weakness usually precedes objective sensory loss; the extensor muscles of the ngers and wrists are affected; later the dorsi exors of the toes and feet causing foot drop, or, more often in our experience, foot drop may appear rst With the dose regimens currently used, the weakness is usually mild, but in the past some patients became quadriparetic and bedbound Adults are more severely affected than are children, as are persons with preexisting polyneuropathies The neuropathy is strictly dose-related, and reduction in dosage is followed by improvement of neuropathic symptoms although this may take several months Many patients are then able to continue the use of vincristine in low dosage, such as 1 mg every 2 weeks, for many months Antimicrobial Drugs As mentioned in Chap 43, isoniazid (INH)-induced polyneuropathy was a common occurrence in the early 1950s when this drug was rst used for the treatment of tu-.

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