Peripheral neuropathy triggered by therapeutic drugs, workplace chemicals and environmental pollutants continues to be one of the most common pathological responses of the human nervous system to chemical attack. While some agents seem to damage the nerve cell directly, and a few induce primary demyelination, the large majority produces distal axonal degeneration simultaneously in long peripheral nerves and spinal tracts. Glove-and-stocking sensory loss typically precedes the development of a similar distribution of motor weakness. Clinical signs usually appear weeks after exposure has commenced; the condition continues to evolve after chemical exposure has ceased, and recovery spans a period of months or years. Careful clinical and laboratory assessment is needed to identify environmental agents responsible for human neuropathy, and reports of cases that claim a chemical causation require verification from experimental animal studies of suspect agents. Treatment of peripheral neuropathy continues to be limited, although a new therapeutic approach to patients with neuropathy-producing heavy metal intoxication is promising. Novel methods to limit nerve degeneration and promote regeneration are under study, but none has produced a convincing therapeutic effect. These are urgently needed to prevent and control the neuropathies that limit the therapeutic usefulness of drugs used in cancer chemotherapy and AIDS treatment.
|Original language||English (US)|
|Number of pages||23|
|Journal||Bailliere's Clinical Neurology|
|State||Published - Dec 5 1995|
ASJC Scopus subject areas
- Clinical Neurology