Brain Magnetic Resonance Spectroscopy in Tourette Syndrome and ADHD

Grant Type
Grant Year
Institution Location
Institution Organization Name
University of Western Ontario Canada
Investigators Name
Nicolson, Rob, MD

Although the neurobiological abnormalities underlying Tourette syndrome (TS) are unknown, various brain imaging studies suggest abnormalities of circuits connecting the frontal lobes, the basal ganglia, and the thalamus. While abnormalities of the brain cells within these cortico- striatal-thalamic-cortical (CSTC) circuits are unknown, proton magnetic resonance spectroscopic imaging (MRSI) provides a unique opportunity for investigating cellular neurochemistry. In the only MRSI study of TS to date, we found evidence of reduced neuronal integrity and abnormalities of membrane metabolism within these circuits. Further, using transverse relaxation time (T2) imaging, we also found evidence of increased tissue water content in components of the CSTC circuits. However, these results were limited by the incidence of Attention-Deficit/Hyperactivity Disorder (ADHD) among the TS patients thus making it difficult to confidently attribute the findings to TS as opposed to ADHD. The purpose of this study will be to use MRSI to assess the impact of co-morbid ADHD on the neurobiological abnormalities tentatively ascribed to TS. Children and adolescents with TS without ADHD, patients with ADHD who do not have a tic disorder and a control group of children without any major psychiatric illness will undergo magnetic resonance scanning on a 3 Tesla magnetic resonance scanner. The concentration of metabolites such as NAA (a marker of neuronal integrity), choline (a marker of membrane metabolism), and glutamate (the most abundant excitatory amino acid) will be measured in the components of the CSTC circuits using MRSI. We hypothesize that patients with TS (without ADHD) will have reductions in NAA (suggesting reduced neuronal integrity) in the basal ganglia (caudate nucleus and putamen) and motor areas of the frontal lobes, while those with ADHD (without tics) will have NAA reductions only in parts of the basal ganglia (the caudate but not the putamen). Further, we hypothesize that patients with TS will show increased glutamatergic activity in the thalamus, while patients with ADHD will not. If our hypotheses are confirmed, we will have evidence that the aberrant neurodevelopment underlying TS and ADHD includes CSTC circuits, with different circuits being involved in each. These results will provide important information regarding the pathophysiology of TS which could lead to a greater understanding of the aberrant neurodevelopment involved in the disorder and could suggest novel treatments for the disorder. Rob Nicolson, M.D. University of Western Ontario, London, Ontario, Canada Award: $58,752 Tourette Association of America Inc. – Research Grant Award 2005-2006