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| Predicate | Object |
|---|---|
| rdf:type | |
| lifeskim:mentions | |
| pubmed:issue |
34
|
| pubmed:dateCreated |
1979-7-16
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| pubmed:abstractText |
Some conclusions are drawn from findings in 167 consecutive patients with the ordinary "garden variety" of polyneuropathy; the aetiology was unknown in 15%. Histological findings in sural nerves were related to clinical and electrophysiological abnormalities. In some patients with discrete clinical abnormalities, sensory and motor conduction and amplitudes of evoked sensory and muscle action potentials were normal, whereas the nerve biopsy showed slight but definite abnormalities. The reverse, abnormal nerve conduction and normal histological findings, did not occur. Histological findings were rarely, and electrophysiological findings were not, specific for the aetiology or type of a neuropathy. Thus, neither conduction studies nor conventional or single fibre electromyography can identify the underlying pathology: loss of large myelinated fibres (greater than 7 micrometers) was equally prominent in nerves with de- and re-myelination as in those without them. Paranodal and segmental demyelination in less than 20% of the teased fibres occurred as often in nerves with as in those without disproportionate slowing in conduction. When the recorded conduction velocity was equal to that to be expected from the fibres with the largest diameter, slowing in conduction could be explained by axonal degeneration ("proportionate" slowing, 79% of the nerves). When the recorded velocity was disproportionately slower than that expected from fibre diameter (21% of the nerves), causes other than loss of the largest fibres must be assumed to explain the slowing in conduction. Myelin abnormalities in more than 50% of the teased fibres were found only in nerves from patients with the hypertrophic type of peroneal muscular atrophy and in postgastrectomy neuropathy and can probably explain the marked disproportionate slowing in conduction. The material contained, however, only one patient with acute idiopathic polyradiculoneuropahy. In diabetic neuropathy, segmental demyelination was present in only 8 of 502 teased fibres (9 nerves), remyelination was present in 135 fibres, and could not explain the disproportionate slowing in conduction. The mechanism of disproportionate slowing, when it is not due to demyelination, is still obscure.
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| pubmed:language |
eng
|
| pubmed:journal | |
| pubmed:citationSubset |
IM
|
| pubmed:status |
MEDLINE
|
| pubmed:issn |
0424-8155
|
| pubmed:author | |
| pubmed:issnType |
Print
|
| pubmed:owner |
NLM
|
| pubmed:authorsComplete |
Y
|
| pubmed:pagination |
373-83
|
| pubmed:dateRevised |
2007-10-8
|
| pubmed:meshHeading |
pubmed-meshheading:220006-Alcoholism,
pubmed-meshheading:220006-Axons,
pubmed-meshheading:220006-Biopsy,
pubmed-meshheading:220006-Demyelinating Diseases,
pubmed-meshheading:220006-Electromyography,
pubmed-meshheading:220006-Humans,
pubmed-meshheading:220006-Neural Conduction,
pubmed-meshheading:220006-Peripheral Nervous System Diseases,
pubmed-meshheading:220006-Sural Nerve
|
| pubmed:year |
1978
|
| pubmed:articleTitle |
Polyneuropathy. Facts and fancies.
|
| pubmed:publicationType |
Journal Article
|