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November 1994

Pseudochoreoathetosis: Movements Associated With Loss of Proprioception

Author Affiliations

From the Department of Neurology (V127), University of California, and the Department of Veterans Affairs Medical Center, San Francisco, Calif (Drs Sharp, Rando, Greenberg, and Sagar); and the Department of Neurology, Albert Einstein School of Medicine, Bronx, NY (Dr Brown).

Arch Neurol. 1994;51(11):1103-1109. doi:10.1001/archneur.1994.00540230041010

Objective:  To describe seven patients with proprioceptive sensory loss and choreoathetoid movements.

Design:  Case series.

Setting:  Outpatient and inpatient university referral.

Patients:  Patients with sensory loss and abnormal movements.

Intervention:  None.

Main Outcome Measure:  None.

Results:  One patient had a parietal cortex injury, one had a thalamic infarction, two had spinal cord lesions, two had dorsal root ganglion neuronopathies, and one had an ulnar neuropathy. In each case, the duration of abnormal movements correlated with the duration of proprioceptive sensory loss, and the abnormal movements were restricted to body parts with proprioceptive sensory loss. The movements varied from chorea and athetosis to dystonia.

Conclusions:  These cases suggest that proprioceptive sensory loss can lead to a movement disorder, termed pseudochoreoathetosis, which occurs following the appearance of lesions anywhere along proprioceptive sensory pathways, from peripheral nerves to the cerebral cortex. It is hypothesized that pseudochoreoathetosis occurs because of the failure to process limb proprioceptive information in the striatum. Therefore, both choreoathetosis and pseudochoreoathetosis may be manifestations of the failure of the striatum to properly integrate cortical motor and sensory inputs.