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Dear Editor, Neurologic processes associated with anti-glutamic acid decarboxylase antibodies (anti-GAD) are rare and difficult to diagnose. This disease group may be associated with other autoimmune diseases such as insulin-dependent diabetes mellitus (DM) and includes ‘stiff person syndrome’ (SPS), cerebellar ataxia, gluten ataxia, progressive encephalomyelitis with rigiditymyoclonus, refractory epilepsy-limbic encephalitis, and palatal myoclonus subheadings (1). A woman aged 25 years was evaluated during a consultation while she was hospitalized at the psychiatry clinic. Following an emotional trauma one week before, she reported anorexia, nauseavomiting, dizziness, double vision, speech and gait disturbance that were added within days. The patient, who was unable to sit without support and kept her eyes closed, had dysarthria, chaotic eye movements, fixation difficulty, and distinct truncal ataxia. Complete blood count, blood biochemistry, thyroid function tests, and beta-human chorionic gonadotropin were within normal limits. Thiamine replacement treatment was initiated, and there were no abnormalities in electroencephalography and neuroimaging studies (brain computed tomography, unenhanced and enhanced brain magnetic resonance (MR) imaging, extracranial and intracranial MR angiography). A cerebrospinal fluid (CSF) investigation revealed 35 leukocytes/mm3, no atypical cells, normal biochemistry, an immunoglobulin (Ig) G index of 0.47, and positive oligoclonal bands (OCB). Antiviral therapy was initiated due to CSF pleocytosis. The patient’s serum immunoelectrophoresis was normal, and anti-thyroperoxidase, anti-thyroglobulin antibodies, vasculitic and infectious markers, malignancy screening and paraneoplastic antibodies (anti-Hu, anti-Yo, anti-Ri, anti-amphiphysin, anti-Tr, anti-parietal cell antibodies-2, anti-Ma, anti-CV2.1, anti-ANNA-3) were negative. Electromyography of the patient showed increased input activity, consecutive positive spike series, fibrillation potentials and rare neuromyotonia-like discharges. With these findings interpreted in favor of "membrane hyperexcitability", intravenous Ig (IVIG) therapy was initiated with a diagnosis of "nonneoplastic immune-mediated cerebellar ataxia" due to non-clinical improvement. The serum anti-GAD antibody level was found high (54.2 IU/mL, N<10 IU/mL, enzyme immunoassay) on day 6. serum anti-gliadin and anti-tissue transaminase antibodies were negative. The patient benefited from IVIG treatment and was able to walk without support at the end of the first week. Antibodies against GAD were first described against major antigen of islet cells in patients with type 1 DM. Today, antiGAD antibody positivity is close to 80% in patients with type 1 DM (2). The detection of anti-GAD antibodies in neurologic diseases in the absence of type 1 DM suggests that this antibody can be used as a marker in some neurologic diseases. Anti-GAD

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The Importance of Consultation Neurology: A Patient with Anti-Glutamic Acid Decarboxylase Antibody-Associated Cerebellar Ataxia Recognized in the Psychiatry Inpatient Clinic