Limbic encephalitis (LE) is a clinical syndrome characterized by the progressive development of neuropsychiatric symptoms including personality changes, memory loss followed by seizures, autonomic dysfunction, and involvement of the medial temporal lobes.1 Limbic encephalitis most commonly presents secondary to an autoimmune aetiology which can be further subclassified into autoimmune and paraneoplastic. Autoimmune LE can be classified according to the presence of autoantibodies into two categories. The first one is associated with antibodies to intracellular neuronal antigens and the other with antibodies to cell surface antigens.2 Intracellular antigens include Hu, Ma2, Collapsin response - mediator protein 5 (CRMP - 5) and cell surface antigens like the voltage-gated potassium channel (VGKC), N - methyl - D - aspartate receptor (NMDA) and others. The autoimmune form of LE is important because it can be treated with immunotherapy if detected early. We present a case of a patient with recurrent vertigo followed by progressive cognitive dysfunction and involuntary movements. She was diagnosed with autoimmune limbic encephalitis associated with glutamic acid decarboxylase (GAD) 65 antibodies. Her symptoms showed improvement following immunomodulatory therapy.
P3-309: NEUROPSYCHIATRIC SYMPTOMS IN ANTI GLUTAMIC ACID DECARBOXYLASE (GAD) ASSOCIATED LIMBIC ENCEPHALITIS IN ADULTS: A SYSTEMATIC REVIEW
