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Biomedical subjects

Jonathan S Katz

Publications and source records attributed to Jonathan S Katz.

4 recordsLinked to original sources
PubMed2005

Toxic neuropathies.

Many substances, organic and manufactured, may induce peripheral nerve damage when exposed to them. The expected clinical phenotype is of a distal, sensory or sensorimotor polyneuropathy, often painful, with axonal characteristics on electrodiagnostic and histopathologic analysis. Treatment is limited; often, the only effective management is supportive care and avoidance from or removal of the offending toxin. Fortunately, the majority of toxic neuropathies are self-limited and improves gradually after toxin elimination.

Animals↗
PubMed2003

Post-irradiation polyradiculopathy mimics leptomeningeal tumor on MRI.

Three patients with a remote history of Hodgkin's disease treated with total or subtotal lymphoid radiation 17 to 24 years earlier developed lumbosacral polyradiculopathy associated with nodular meningeal enhancement of the conus medullaris and cauda equina on MRI. None had evidence of recurrent Hodgkin's disease or second malignancy, and the MRI findings may be sequelae of radiation therapy.

Adult↗
PubMed2003

Late-onset distal muscular dystrophy affecting the posterior calves.

Miyoshi myopathy, caused by mutations in the membrane protein dysferlin, is the most common muscular dystrophy that presents in the posterior calves. Its onset is before the age of 30 years and it is associated with marked elevations of serum creatine kinase (CK). In contrast, little is known about calf myopathies with onset after the age of 30, and it is not clear whether such patients have a dysferlinopathy. We describe five patients with a myopathy predominantly affecting the calf muscles, with onset after the age of 30. Muscle tissue was analyzed by immunoblot for dystrophin and dysferlin. All five had normal dysferlin but one had a dystrophinopathy. Serum CK levels ranged from 3 to 15 times the upper limit of normal. In contrast, all of 13 patients presenting before age 30 with calf weakness had a dysferlinopathy. Thus, isolated calf atrophy and weakness with onset after age 30, and associated with serum CK levels that are only moderately elevated, represents a distinct myopathy phenotype. Most of these cases are sporadic, although the overall phenotype appears genetically heterogeneous and dysferlinopathy is uncommon.

Adult↗