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PubMed1989

Hereditary ataxia.

The hereditary ataxias, also referred to as the spinocerebellar degenerations, comprise a series of clinical manifestations that include ataxia and dysmetria, resulting from the predominant involvement of the cerebellum and its afferent and efferent pathways. These disorders are system degenerations; many of them are specific entities clearly inherited as autosomal dominant or autosomal recessive traits. Although the clinical manifestations and neuropathologic findings of cerebellar disease dominate the spinocerebellar degenerations, there may also be characteristic changes in the basal ganglia, optic atrophy, retinitis pigmentosa, or peripheral nerve disease. There are many gradations from pure cerebellar manifestations to mixed cerebellar and brain-stem disorders, cerebellar and basal ganglia syndromes, and spinal syndromes or peripheral nerve disease. The clinical picture may be consistent in one family, but sometimes there is a characteristic syndrome in the majority of family members and an entirely different disorder in one or several members.

Chromosome Mapping↗
PubMed1998

Antiganglioside GM1 antibodies and their complement activating capacity in central and peripheral nervous system disorders and in controls.

So far, the pathogenic significance and use for diagnosis of antiganglioside GM1 antibodies (anti-GM1) are unclear. We therefore compared serum IgM and IgG antimonosialo ganglioside GM1 levels of 33 patients with presumed immune-mediated neuropathies, 100 patients with various other central or peripheral neurological disorders, and 110 controls by ELISA. We also measured the complement-activating capacity of anti-GM1 by C5b-9-GM1-ELISA to evaluate its value to distinguish between pathogenic and nonpathogenic autoantibodies. Low levels of anti-GM1 were observed in all disease categories and in controls (healthy blood donors). Twenty-four of the controls including the 10 with the highest serum IgM or IgG anti-GM1 were examined for neurological disorders in a double-blind checkup study. In the patients, elevated IgM anti-GM1 levels were predominantly found in those with neuropathies (NP), but barely in patients with central nervous system disease (CNSD). We found elevated IgG anti-GM1 levels predominantly in patients with NP of inflammatory origin (multifocal motor neuropathy, chronic inflammatory demyelinating polyneuropathy or Guillain-Barré syndrome), rarely in patients with NP of noninflammatory origin or CNSD, but not in the control disease group myasthenia gravis (MG). Median levels of IgM-, IgG-, (IgM+IgG)-, and C5b-9-binding anti-GM1 were significantly higher in patients with inflammatory NP as compared to the controls (p < 0.025). In addition, median levels of IgG- and (IgM+IgG)-anti-GM1 were significantly higher in inflammatory NP versus CNSD. Elevated complement-binding activity was associated with low or elevated IgM and/or IgG anti-GM1. Nevertheless, there was a significant correlation between anti-GM1 level (IgM+IgG) and the respective complement-activating capacity (r = 0.758; n = 243). Estimation of anti-GM1 and their respective complement-activating capacity may be helpful in the diagnosis of inflammatory neuropathies. However, neither an elevated anti-GM1 level nor an increased C5b-9 binding seems specific for a given disease category (e.g. peripheral nerve disease) nor a disease process (e.g. demyelination or inflammation).

Adolescent↗
PubMedDate not supplied

NERVE INJURIES.

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Neurosurgery↗