Thalidomide neuropathy: a clinical electrophysiological, and histological follow-up study.

Author:

Fullerton P M,O'Sullivan D J

Publisher

BMJ

Subject

Psychiatry and Mental health,Neurology (clinical),Surgery

Reference33 articles.

1. many of the toxic neuropathies in which primary;Cavanagh, J.B.;J. Path. Bact; Peripheral nerve changes in ortho-cresyl axonal degeneration occurs, a dying back process has been demonstrated whereby the greatest damage occurs at the peripheral ends of the longest fibres. This has been demonstrated following tri-orthocresyl phosphate (Cavanagh, 1964) and acrylamide (Fullerton and Barnes, 1966) poisoning in experimental animals. When degeneration is limited to the distal ends of the fibres, regeneration with rapid functional recovery might be expected. If, on the phosphate poisoning in the cat,1964

2. The conduction velocity of regenerated peripheral nerve fibres;Cragg, B.G.; Thomas, P.K.;J. Physiol. (Lond.),1964

3. The relative excitability and conduction velocity of sensory and motor nerve fibres in man;Dawson, G.D.;J. Physiol. (Lond.),1956

4. Morphologische Veranderungen bei experimentaller Thalidomid-Neuropathie und thalidomidbedingten Extremitatenmissbildungen;Diezel, P.B.;Munch. med. Wschr,1963

5. Teratogenic activity of thalidomide and related compounds;Fabro, S.; Schumacher, H.; Smith, R.L.; Williams, R.T.;Life Sci,1964

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