Volume 11 Issue 96
Published - 14:00 UTC 08:00 EST 14-Apr-2009 
Next Update - 14:00 UC 08:00 EST 15-Apr-2009

Editor: Susan K. Boyer, RN
© Vidyya.
All rights reserved.



Imaging reveals abnormalities in pathways connecting brain areas in those with writer's cramp

(14 Apr 2008: VIDYYA MEDICAL NEWS SERVICE) -- Abnormalities in the fibers connecting different brain areas may contribute to muscle disorders such as writer's cramp, according to a report in the April issue of Archives of Neurology, one of the JAMA/Archives journals.

Previous studies of individuals with writer's cramp have identified changes in the gray matter of several brain areas, according to background information in the article. These include the basal ganglia (structures that help control and start movement), sensorimotor cortex (controls sensory and motor functions), thalamus (coordinates multiple impulses including some related to the senses) and cerebellum (controls voluntary movements, posture and balance).

In the new study, Christine Delmaire, M.D., of Centre Hospitalier Régional Universitaire Roger Salengro, Lille, France, and Institut National de la Santé et de la Récherche Médicale, Paris, studied 26 right-handed patients with writer's cramp and 26 right-handed control participants who were the same sex and age but did not have writer's cramp. All participants underwent diffusion-tensor magnetic resonance imaging (DTI), which has been shown to assess the status of white matter (coated nerve fibers that allow impulses to travel through the brain).

The DTI scans of patients with writer's cramp revealed areas of abnormalities in the white matter of nerve pathways connecting the main sensorimotor cortex to brain areas below the cortex, such as the thalamus. The same abnormalities were not observed in healthy controls.

"In conclusion, this study suggests that writer's cramp is associated with microstructural changes involving fibers that carry afferents [information from senses to the brain] and efferents [motor information from the brain to the muscles] to the primary sensorimotor cortex," the authors write. "However, it is unknown how these changes relate to the physiopathology of the disease."

Arch Neurol. 2009;66[4]:502-508.

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