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Widespread abnormality of the ?-aminobutyric acid-ergic system in Tourette syndrome.

ABSTRACT: Dysfunction of the ?-aminobutyric acid-ergic system in Tourette syndrome may conceivably underlie the symptoms of motor disinhibition presenting as tics and psychiatric manifestations, such as attention deficit hyperactivity disorder and obsessive-compulsive disorder. The purpose of this study was to identify a possible dysfunction of the ?-aminobutyric acid-ergic system in Tourette patients, especially involving the basal ganglia-thalamo-cortical circuits and the cerebellum. We studied 11 patients with Tourette syndrome and 11 healthy controls. Positron emission tomography procedure: after injection of 20?mCi of [(11)C]flumazenil, dynamic emission images of the brain were acquired. Structural magnetic resonance imaging scans were obtained to provide an anatomical framework for the positron emission tomography data analysis. Images of binding potential were created using the two-step version of the simplified reference tissue model. The binding potential images then were spatially normalized, smoothed and compared between groups using statistical parametric mapping. We found decreased binding of GABA(A) receptors in Tourette patients bilaterally in the ventral striatum, globus pallidus, thalamus, amygdala and right insula. In addition, the GABA(A) receptor binding was increased in the bilateral substantia nigra, left periaqueductal grey, right posterior cingulate cortex and bilateral cerebellum. These results are consistent with the longstanding hypothesis that circuits involving the basal ganglia and thalamus are disinhibited in Tourette syndrome patients. In addition, the abnormalities in GABA(A) receptor binding in the insula and cerebellum appear particularly noteworthy based upon recent evidence implicating these structures in the generation of tics.

SUBMITTER: Lerner A

PROVIDER: S-EPMC3359755 | biostudies-literature | 2012 Jun

REPOSITORIES: biostudies-literature

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Widespread abnormality of the γ-aminobutyric acid-ergic system in Tourette syndrome.

Lerner Alicja A Bagic Anto A Simmons Janine M JM Mari Zoltan Z Bonne Omer O Xu Ben B Kazuba Diane D Herscovitch Peter P Carson Richard E RE Murphy Dennis L DL Drevets Wayne C WC Hallett Mark M

Brain : a journal of neurology 20120510 Pt 6

Dysfunction of the γ-aminobutyric acid-ergic system in Tourette syndrome may conceivably underlie the symptoms of motor disinhibition presenting as tics and psychiatric manifestations, such as attention deficit hyperactivity disorder and obsessive-compulsive disorder. The purpose of this study was to identify a possible dysfunction of the γ-aminobutyric acid-ergic system in Tourette patients, especially involving the basal ganglia-thalamo-cortical circuits and the cerebellum. We studied 11 patie ...[more]

PMID: 22577221

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Project description:Objective: Tourette syndrome (TS) is a complicated sensorimotor disorder. Some patients with TS relieve their involuntary premonitory urges via tics. However, the effect of the motor system on the sensory system has not yet been elucidated. The purpose of the present study was to investigate changes in the excitability of the sensory cortex following repetitive transcranial magnetic stimulation (rTMS) of the motor cortex in patients with TS. Methods: Twenty-nine patients with TS and 20 healthy, age-matched controls were enrolled in this study. All subjects were divided into four groups: patients with rTMS, patients with sham-rTMS, controls with rTMS, and controls with sham-rTMS. The clinical severity of tics was evaluated using the Yale Global Tic Severity Scale. Single somatosensory evoked potentials (SEPs) and paired SEPs were recorded by stimulating the median nerve at the wrist of all subjects. The resting motor threshold (RMT) was tested in each subject in the rTMS group. Afterwards, all four groups were administered rTMS (1 Hz, 90% RMT) or sham-rTMS for 200 s, followed by a 15-min rest. Finally, single SEPs and paired SEPs were repeated for each subject. Results: No significant differences in RMT, the amplitudes of single SEPs, or the suppression of paired SEPs were observed between patients with TS and controls at baseline. After rTMS, a significant suppression of the peak-to-peak amplitude of the N20-P25 responses of single SEPs was observed in both controls (p = 0.049) and patients (p < 0.0001). The suppression of the N20-P25 peak-to-peak amplitude was more significant in patients than in controls (p = 0.039). A significant difference in the suppression of paired SEPs after rTMS was not observed between groups. Conclusions: The more significant suppression of N20-P25 components of single SEPs with normal suppressed paired SEPs in patients with TS after 1-Hz rTMS of the motor cortex suggests that the suppressive effect of the motor system on the sensory system might originate from the motor-sensory cortical circuits rather than the sensory system itself.

Dataset Information

Widespread abnormality of the ?-aminobutyric acid-ergic system in Tourette syndrome.

Publications

Widespread abnormality of the γ-aminobutyric acid-ergic system in Tourette syndrome.

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