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79 - Myelitis and peripheral neuropathy

from Part X - Clinical syndromes: neurologic system

Published online by Cambridge University Press:  05 April 2015

Jeffrey M. Percak
Affiliation:
Tulane University
Rodrigo Hasbun
Affiliation:
University of Texas Medical School
David Schlossberg
Affiliation:
Temple University, Philadelphia
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Summary

Myelitis and peripheral neuropathy complicate many infections. This chapter discusses major infectious etiologies of myelitis (Table 79.1), peripheral neuropathy (Table 79.2), polymorphic syndromes (Table 79.3), and neuropathic syndromes seen in human immunodeficiency virus (HIV) infection (Table 79.4). Further, an algorithm (Figure 79.1) suggests an approach to the clinical and laboratory diagnosis of myelitis and peripheral neuropathy.

MYELITIS

Myelitis refers to inflammation of the spinal cord. Myelitis may be infectious or noninfectious and primary – directly attacking cord structures – or secondary – adjacent processes altering cord function. Primary myelitis can present as one of three discrete clinical patterns: (1) anterior poliomyelitis, (2) leukomyelitis, or (3) transverse myelitis. Poliomyelitis is inflammation involving gray matter; leukomyelitis is confined to white matter. Transverse myelitis, inflammation of an entire cross section of the spinal cord, can affect more than one spinal segment. A number of infectious agents are known to cause or to be associated with myelitis. Myelitis can also occur after infection or vaccination as in the acute disseminated encephalomyelitis (ADEM) syndrome.

There are five cardinal manifestations of spinal cord disease: pain; motor deficits; sensory deficits; abnormalities of reflexes and muscle tone; and bladder dysfunction. The distribution of neurologic deficits depends on the spinal segment(s) affected. Local pain occurs at the site of the lesion and can assume a radicular quality if the nerve roots are involved. Paresthesias have greater localizing value than radicular pain. Weakness is present in virtually all spinal cord disorders, and in myelitis may progress over hours, days, or weeks. Spinal shock is characterized by absent plantar reflexes, and areflexia and atonia below the level of the lesion. More slowly progressive lesions are associated with hyperreflexia and hypertonia. Bladder dysfunction is usually not an early sign of spinal cord disease, although if spinal shock develops, flaccid bladder paralysis ensues with urinary retention and overflow incontinence. Chronic myelopathies cause a spastic bladder and result in urgency, frequency, and incontinence.

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Publisher: Cambridge University Press
Print publication year: 2015

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