In:
Annals of the New York Academy of Sciences, Wiley, Vol. 1039, No. 1 ( 2005-04), p. 446-454
Abstract:
A bstract : Glutamic acid decarboxylase (GAD) catalyzes the conversion of glutamic acid to γ‐aminobutyric acid (GABA). Autoantibodies directed against GAD (antiGAD‐Ab) have been described in patients with insulin‐dependent diabetes mellitus, stiff‐man syndrome, and in a few patients with progressive cerebellar ataxia. The presence of these autoantibodies suggests an autoimmune pathophysiological mechanism for the neurological manifestations in these disorders. However, the exact role of antiGAD‐Ab and GABAergic neurotransmission in the pathogenesis of the neurological manifestations, particularly in progressive cerebellar ataxia, is not fully understood. The cases of two patients with subacute cerebellar ataxia associated with antiGAD‐Ab presenting with abnormal eye movements are reported. One patient presented a periodic alternating nystagmus (PAN), whereas the other presented a downbeat nystagmus (DBN) and slow vertical saccades. The potential role of antiGAD‐Ab and the resultant GABAergic neurotransmission deficit in oculomotor manifestations is discussed.
Type of Medium:
Online Resource
ISSN:
0077-8923
,
1749-6632
DOI:
10.1196/annals.1325.042
Language:
English
Publisher:
Wiley
Publication Date:
2005
detail.hit.zdb_id:
2834079-6
detail.hit.zdb_id:
211003-9
detail.hit.zdb_id:
2071584-5
SSG:
11
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