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A Rare Case of Cerebellar Ataxia Due to Voltage-Gated Calcium Channel and Glutamic Acid Decarboxylase Autoantibodies

Patient: Female, 55 Final Diagnosis: Cerebellar ataxia due to voltage-gated calcium channel and glutamic acid decarboxylase autoantibodies Symptoms: Ataxia Medication: — Clinical Procedure: — Specialty: Neurology OBJECTIVE: Rare disease BACKGROUND: Autoimmune cerebellar ataxia can be paraneoplastic...

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Detalles Bibliográficos
Autores principales: Annunziata, Giuseppe, Lobo, Pamela, Carbuccia, Cristian
Formato: Online Artículo Texto
Lenguaje:English
Publicado: International Scientific Literature, Inc. 2017
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5715982/
https://www.ncbi.nlm.nih.gov/pubmed/29176543
http://dx.doi.org/10.12659/AJCR.905476
Descripción
Sumario:Patient: Female, 55 Final Diagnosis: Cerebellar ataxia due to voltage-gated calcium channel and glutamic acid decarboxylase autoantibodies Symptoms: Ataxia Medication: — Clinical Procedure: — Specialty: Neurology OBJECTIVE: Rare disease BACKGROUND: Autoimmune cerebellar ataxia can be paraneoplastic in nature or can occasionally present without evidence of an ongoing malignancy. The detection of specific autoantibodies has been statistically linked to different etiologies. CASE REPORT: A 55-year-old African-American woman with hypertension and a past history of morbid obesity and uncontrolled diabetes status post gastric bypass four years prior to the visit (with significantly improved body mass index and hemoglobin A1c controlled at the time of the clinical encounter) presented to the office complaining of gradual onset of unsteadiness and recurrent falls for the past three years, as well as difficulties coordinating routine daily activities. The neurologic exam showed moderate dysarthria and ataxic gait with bilateral dysmetria and positive Romberg test. Routine laboratory test results were only remarkable for a mild elevation of erythrocyte sedimentation rate, and most laboratory and imaging tests for common causes of ataxia failed to demonstrate an etiology. Upon further workup, evidence of anti-voltage-gated calcium channel and anti-glutamic acid decarboxylase antibody was demonstrated. She was then treated with intravenous immunoglobulins with remarkable clinical improvement. CONCLUSIONS: We present a case of antibody-mediated ataxia not associated with malignancy. While ataxia is rarely related to autoantibodies, in such cases it is critical to understand the etiology of this disabling condition in order to treat it correctly. Clinicians should be aware of the possible association with specific autoantibodies and the necessity to rule out an occult malignancy in such cases.