Premium
Potential Role of Anti‐GAD Antibodies in Abnormal Eye Movements
Author(s) -
TILIKETE CAROLINE,
VIGHETTO ALAIN,
TROUILLAS PAUL,
HONNORAT JÉROME
Publication year - 2005
Publication title -
annals of the new york academy of sciences
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.712
H-Index - 248
eISSN - 1749-6632
pISSN - 0077-8923
DOI - 10.1196/annals.1325.042
Subject(s) - glutamate decarboxylase , cerebellar ataxia , autoantibody , ataxia , gabaergic , neuroscience , nystagmus , eye movement , pathophysiology , medicine , neurotransmission , stiff person syndrome , pathogenesis , endocrinology , antibody , psychology , immunology , chemistry , audiology , receptor , biochemistry , enzyme
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.