Over the ensuing years, the pathomechanism of SPS was further characterized with novel electrodiagnostic neuronal excitability studies [19–21]; GABA measurements in the CSF [18] and brain with MRS spectroscopy [22]; immunological studies including GAD epitopes and search for other antibodies affecting GABAergic neurotransmission [23–26]; performance of two controlled clinical trials [27, 28]; and defining the natural history of the disease based on the largest series of SPS patients examined by the same clinicians longitudinally over a 20 year period [29]. The gene discussed is GAD1; the disease is stiff-person syndrome.