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PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
6
pubmed:dateCreated
1981-3-24
pubmed:abstractText
Sixteen patients presenting with trophic changes associated with a peripheral neuropathy were investigated. Muscle power was normal in all patients, but neurogenic muscle atrophy was demonstrated in 4 of the 7 patients who had a muscle biopsy. Alcoholism was responsible for the neuropathy in 11 patients. In the other patients, one had primary hemochromatosis without diabetes and another a dominantly inherited primary hypertrophic neuropathy. Qualitative and quantitative light and electron microscopic studies, including teased nerve fiber preparations, showed axonal loss as the most salient feature. In the alcoholic patients, the large myelinated fibers were primarily involved, followed by small myelinated and unmyelinated fibers. The lesions were predominant distally as shown in patients who had a sural nerve biopsy at both calf and ankle levels. A mechanism of dying-back degeneration of the longest sensory fibers is the most plausible explanation for neurological and pathological abnormalities. In alcoholic neuropathy with trophic changes, loss of sensory fibers is more important than in alcoholic neuropathy without trophic changes. In familial and sporadic cases, axonal loss is more severe and unmyelinated fibers are more severely affected than in alcoholic acrodystrophic neuropathy. Patients with peripheral neuropathies who present with loss of pain sensation but have preserved muscle power are especially exposed to the development of trophic changes induced by usual trauma in insensitive tissues.
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:status
MEDLINE
pubmed:issn
0148-639X
pubmed:author
pubmed:issnType
Print
pubmed:volume
3
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
491-501
pubmed:dateRevised
2004-11-17
pubmed:meshHeading
pubmed:articleTitle
A clinicopathologic study of acrodystrophic neuropathies.
pubmed:publicationType
Journal Article