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Hoffmann, R. A wiki for the life sciences where authorship matters. Nature Genetics (2008)
 

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Cerebral glucose metabolism in patients with spasmodic torticollis.

The pathophysiology of spasmodic torticollis is not clear. Basal ganglia dysfunction has been suggested to underlie this clinical syndrome. We studied resting cerebral glucose metabolism in 10 spasmodic torticollis patients and 10 healthy controls by using positron-emission tomography and [18F]2-fluoro-2-deoxy-D-glucose. Statistical parametric mapping (SPM95) was used to compare both groups on a pixel-by-pixel basis. Torticollis patients showed a significantly higher glucose metabolism bilaterally in the lentiform nucleus (p < 0.005). Analyses performed using normalization of regional to global glucose metabolism confirmed this finding (controls, 1.26 +/- 0.06, and patients, 1.35 +/- 0.06; p < 0.01). The torticollis score did not correlate with glucose metabolism, nor did disease duration or side of chin direction. Our results indicate that the lentiform nucleus plays a predominant role in the pathophysiology of idiopathic spasmodic torticollis.[1]

References

  1. Cerebral glucose metabolism in patients with spasmodic torticollis. Magyar-Lehmann, S., Antonini, A., Roelcke, U., Maguire, R.P., Missimer, J., Meyer, M., Leenders, K.L. Mov. Disord. (1997) [Pubmed]
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