Limbic and motor circuits involved in symmetry behavior in Tourette's syndrome

CNS Spectrums ◽  
2012 ◽  
Vol 18 (1) ◽  
pp. 34-42 ◽  
Author(s):  
Froukje E. de Vries ◽  
Odile A. van den Heuvel ◽  
Danielle C. Cath ◽  
Henk J. Groenewegen ◽  
Anton J. L. M. van Balkom ◽  
...  

ObjectiveThe need for symmetry and ordering objects related to a “just right”-feeling is a common symptom in Tourette's syndrome (TS) and resembles symmetry behavior in obsessive-compulsive disorder, but its pathophysiology is unknown. We used a symptom provocation paradigm to investigate the neural correlates of symmetry behavior in TS and hypothesized the involvement of frontal-striatal and limbic brain areas.MethodsPictures of asymmetrically and symmetrically arranged objects were presented in randomized blocks (4 blocks of each condition) to 14 patients with TS and 10 matched healthy controls (HC). A H215O positron emission tomography scan was acquired during each stimulus block, resulting in 8 scans per subject. After each scan, state anxiety and symmetry behavior (the urge to rearrange objects) were measured using a visual analogue scale.ResultsDuring the asymmetry condition, TS patients showed increased regional cerebral blood flow (rCBF) in the anterior cingulate cortex, supplementary motor area, and inferior frontal cortex, whereas HC showed increased rCBF in the visual cortex, primary motor cortex, and dorsal prefrontal cortex. Symmetry ratings during provocation correlated positively with orbitofrontal activation in the TS group and sensorimotor activation in the HC group, and negatively with dorsal prefrontal activity in HC.ConclusionsResults suggest that both motor and limbic circuits are involved in symmetry behavior in TS. Motor activity may relate to an urge to move or perform tics, and limbic activation may indicate that asymmetry stimuli are salient for TS patients. In contrast, symmetry provocation in HC resulted in activation of brain regions implicated in sensorimotor function and cognitive control.

1994 ◽  
Vol 164 (6) ◽  
pp. 839-841 ◽  
Author(s):  
S. Fennig ◽  
S. Naisberg Fennig ◽  
M. Pato ◽  
A. Weitzman

A 14-year-old boy with obsessive–compulsive disorder (OCD) developed, under fluvoxamine treatment, acute symptoms of Tourette's syndrome (TS) with aggravation of the OCD. The TS symptoms did not respond to dopamine blockers and disappeared only after withdrawal of fluvoxamine. Readministration of fluvoxamine caused a re-emergence of the same symptoms.


1998 ◽  
Vol 10 (1) ◽  
pp. 116-117 ◽  
Author(s):  
Philip R. Saba ◽  
Khurshed Dastur ◽  
M. Reza Raji ◽  
Matcheri S. Keshavan ◽  
M. Ammar Katerji

2000 ◽  
Vol 2 (2) ◽  
pp. 125-139 ◽  
Author(s):  
Randall D. Buzan ◽  
Jay H. Shore ◽  
Christopher O’Brien ◽  
Christopher Schneck

Author(s):  
Brian P. Brennan ◽  
Scott L. Rauch

Studies using functional neuroimaging have played a critical role in the current understanding of the neurobiology of obsessive-compulsive disorder (OCD). Early studies using positron emission tomography (PET) identified a core cortico-striatal-thalamo-cortical circuit that is dysfunctional in OCD. Subsequent studies using behavioral paradigms in conjunction with functional magnetic resonance imaging (fMRI) have provided additional information about the neural substrates underlying specific psychological processes relevant to OCD. More recently, studies utilizing resting state fMRI have identified abnormal functional connectivity within intrinsic brain networks including the default mode and frontoparietal networks in OCD patients. Although these studies, as a whole, clearly substantiate the model of cortico-striatal-thalamo-cortical circuit dysfunction in OCD and support the continued investigation of neuromodulatory treatments targeting these brain regions, there is also growing evidence that brain regions outside this core circuit, particularly frontoparietal regions involved in cognitive control processes, may also play a significant role in the pathophysiology of OCD.


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