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- Caroline Tilikete, Alain Vighetto, Paul Trouillas, and Jérome Honnorat.
- Neuro-Ophthalmology Unit, Hôpital Neurologique, Hospices civils de Lyon, Bron, France. tilikete@lyon.inserm.fr
- Arch Neurol Chicago. 2005 Aug 1; 62 (8): 1300-3.
BackgroundAutoantibodies directed against glutamic acid decarboxylase (GAD-Ab) have recently been described in a few patients with progressive cerebellar ataxia, suggesting an autoimmune physiopathologic mechanism.ObjectiveTo determine the exact role of GAD-Ab and gamma-aminobutyric acid (GABA)-ergic neurotransmission in the pathogenesis of cerebellar ataxia.DesignCase report.SettingUniversity neurological hospital.PatientWe report the case of a patient with subacute cerebellar ataxia associated with GAD-Ab showing periodic alternating nystagmus (PAN).InterventionBaclofen, a GABAergic medication, was given to the patient.Main Outcome MeasuresEye movement recording of spontaneous nystagmus and postrotatory vestibular responses.ResultsBaclofen was effective in suppressing PAN and improving postrotatory vestibular responses but not for improving cerebellar ataxia.ConclusionThe presence of PAN and the response to baclofen provide a unique opportunity to suggest a direct role of GAD-Ab in cerebellar dysfunction in this patient.
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