The patient is a 48-year-old African American woman with past medical history significant for HCV secondary to blood transfusion, SS, pernicious anemia, and obesity status postbariatric surgery. She presented to the neurology clinic with history of subacute onset gait ataxia, intermittent vertigo, diplopia, oscillopsia, dysarthria, and dysphagia. The patient was initially treated with high-dose intravenous methylprednisolone (IVMP) followed by high-dose oral prednisone with modest response as her ataxia continued to progress. Based on the assumption that her symptoms were secondary to central nervous system (CNS) involvement of SS, she was treated with rituximab with no significant clinical improvement though it stabilized the disease. The patient also did not respond to intravenous immunoglobulin (IVIG) treatment. No history of alcohol use or malnutrition. Her neurological examination revealed hypometric saccades, mild dysarthria, truncal ataxia, and gait ataxia without limb ataxia. A motor exam was unremarkable, and sensory exam was positive for decreased vibratory sensation distally. An extensive workup was initiated. Abnormal results include HCV viral load 193,000 copies per mL, HCV genotype I, liver biopsy (stage I HCV disease), antinuclear antibody (Ab) (ANA) positive, SS-A positive (1 : 230), antiparietal cell Ab positive, anti-intrinsic factor (IF) Ab positive, small M spike on serum protein electrophoresis (SPEP) with normal 24-hour urine protein electrophoresis (UPEP), cerebrospinal fluid (CSF) oligoclonal bands (OCBs) positive with normal cell count and protein, and increased uptake on the right submandibular gland on positron emission tomography (PET). Pertinent negative/normal results include vitamin B12 (on supplements), folic acid (on supplements), vitamin B1 (thiamine on supplements), vitamin B6, vitamin E, lactate, pyruvate, thyroid stimulating hormone (TSH), copper, ceruloplasmin, urine heavy metals, human immunodeficiency virus (HIV), rapid plasma regain (RPR), SS-B, rheumatoid factor (RF), antineutrophilic cytoplasmic Ab (ANCA), antiphospholipid Ab (a PL), angiotensin-converting enzyme (ACE), antiendomysial Ab, erythrocyte sedimentation rate (ESR), C-reactive protein (CRP), C3, C4, cryoglobulins, paraneoplastic panel, anti-amphiphysin antibody, brain and spine magnetic resonance imaging (MRI) with contrast, bone scan, bone marrow biopsy, mammogram, Pap smear, computerized tomography (CT) of the chest, abdomen, and pelvis. The most remarkable finding was a positive anti-GAD 65 Ab in the serum (titer 113.65 units per mL) and in the CSF (titer 29.4 nmole/L with a normal range of <0.02 nmole/L) with positive OCBs despite treatment with steroids, IVIG, and Rituximab. The patient had numerous fasting blood sugars (FBS) done to exclude late onset diabetes. All the FBS values were within normal limits (80-95 mg/dL). 
Antiviral therapy with interferon alpha (IFNalpha) and ribavirin was discussed with the hepatologist, but the patient was considered a poor candidate due to the possibility of exacerbation of a secondary autoimmune disease. Since the patient's cerebellar syndrome was stabilized by rituximab, we continued maintenance therapy with close monitoring of her neurological status.