Retrospective Analysis of the French National Cohort of Patients With GAD Antibodies and Cerebellar Ataxia

Retrospective Analysis of the French National Cohort of Patients With GAD Antibodies and Cerebellar Ataxia

Glutamic acid decarboxylase (GAD) is an enzyme whose function in the body is to decarboxylate glutamate to GABA. GAD65 antibodies (GAD65Ab) have been associated with type-1 diabetes (80% of new-onset patients) and various neurological conditions, mainly stiff-person syndrome (SPS/PERM), cerebellar ataxia (CA), limbic encephalitis (LE) and temporal lobe epilepsy. These syndromes all seem to result from a reduced transmission of GABA. These neurological conditions are rare and can cause symptoms like confusion, memory loss, muscle stiffness, muscle spasms, behavioural disorders, and pharmacoresistant epilepsy. When finding high levels of GAD65-Ab in the serum, a cerebrospinal fluid (CSF) sample should be taken to look for oligoclonal IgG bands and intrathecal GAD-Ab production to prove an auto-immune cause for the various neurological symptoms.

Inclusion Criteria:

• neurological symptoms with GAD antibody
• GAD antibody in sera and/or CSF
• patient with cerebellar ataxia

Exclusion Criteria:

• tested positive to another antibody.
• no data
• any test in paraneoplastic neurological syndrome and autoimmune encephalitis center