Lesson of the month 2: Autoimmune sequelae of anti-GAD antibodies – thinking outside the box

Abstract

A 52 year-old female with no signifi cant medical problems presented with left-sided weakness, unsteady gait and speech disturbance. It was thought that she had neuro-infl ammation and she remained clinically stable. Several years later, she was diagnosed with latent autoimmune diabetes of adulthood. Her neurological symptoms deteriorated and she was admitted into hospital. The cerebrospinal fl uid was normal, as were an array of blood tests. Imaging tests, including magnetic resonance imaging, computerised tomography and positron emission tomography scans were normal. However, her anti-glutamic acid decarboxylase antibody serum level, which had been taken in the diabetes outpatient clinic, returned at 2,000,000 IU/mL (normal range 0-10). This led to the diagnosis of glutamic acid decarboxylase (GAD) positive cerebellar ataxia. She was treated with plasma exchange and intravenous immunoglobulins and over next 12 weeks her symptoms improved. Our case highlights the need for appropriate treatment of patients with GAD positive cerebellar ataxia to achieve good outcomes.

Thalamic Lesions in a Toddler with Glutamic Acid Decarboxylase Autoimmune Encephalitis

“…3 GAD autoantibodies have been linked to several neurological conditions such as limbic encephalitis, autoimmune cerebellar ataxia, stiff person syndrome (SPS), and intractable epilepsy. 5 We discuss a 21-month-old normally developing girl who presented with superrefractory SE and a fever. She subsequently developed dyskinetic movements and was found to have GAD autoantibodies.…”