Tourette’s syndrome is a movement disorder that involves basal ganglia dysfunction. Since glutamatergic mechanisms have been implicated in the etiology and treatment of schizophrenia, we proposed that nitric oxide (NO), acting on the NMDA receptor as a neurotransmitter, is involved in the pathogenesis of basal ganglia in Tourette’s syndrome. Twelve drug-free Tourette’s syndrome subjects without a history of pediatric autoimmune disorders associated with streptococcal infection (PANDAS) or asthma were recruited. Expiration NO levels were measured and compared to 12 matched control subjects. Peak expiration fl ow rate was also monitored. We also measured NO levels from fathers, mothers and siblings of each of the subjects with Tourette’s syndrome. There was no signifi cant difference between the level of NO between the Tourette’s syndrome subjects and the control group. However, the subjects with Tourette’s syndrome had signifi cantly higher peak expiratory fl ow rate than the control group. A signifi cant correlation between NO levels in subjects with Tourette’s syndrome and their mothers, but not their fathers or siblings, was also observed. Future studies are warranted to investigate the role of NO in the different phenotypes of Tourette’s syndrome. The higher peak expiratory fl ow might be one of the pathophysiological effects with regard to the neuroanatomy of Tourette’s syndrome.