Paroxysmal Kinesigenic Dyskinesia and Cervical Disc Prolapse With Cord Compression: More Than a Coincidence?

To the Editor: Paroxysmal kinesigenic dyskinesia (PKD) is a relatively rare neurological condition which is characterized by sudden, brief (seconds to 5 minute) attacks of involuntary movements which are precipitated by sudden voluntary movement. 1 Although often inherited in an autosomal dominant pattern, the pathophysiology of the disease remains largely unknown. 2 Besides evidence supporting the paroxysmal kinesigenic dyskinesia as a form of epilepsy or basal ganglia disorder, many patients with symptomatic movement disorders have also been associated with a focal lesion. 1 These reported lesions are distributed widely from the cerebral cortex to the spinal cord and make the pathophysiological correlation difficult.

A 43-year-old male was admitted because of paroxysmal abnormal movements. There was no family history of paroxysmal movement disorders, seizures, or epilepsy. Ictal electroencephalograms of his attacks without loss of consciousness or a seizure were normal. The neurologic examination demonstrated choreiform movements of proximal and distal parts of the right arm and fingers, especially when he moved his right arm suddenly. But interestingly, the same dyskinetic movements did not appear when the patient was asked to get up from the sitting position and walk or when the patient was resting quietly or moved his other limbs. These movements appeared suddenly and lasted for 15–30 seconds. His face and the other upper limbs were not affected. Motor examination showed mild right monoparesis (grade 4/5) and minimally increased tone and hyperreflexia with no clonus on the right upper extremity. Systemic and blood examination was otherwise unremarkable. Magnetic resonance imaging (MRI) of cervical spine revealed multiple prolapsed discs at the C3-4, C4-5, C5-6 and C6-7 levels; severe cord compression was more prominent at the C5-6 level ( Figure 1 and Figure 2 ). Brain MRI scan did not show any abnormalities. Interictal electroencephalograms were normal. Electroneuromyography suggested mild C7-8 radix involvement but the electrophysiologic evidence of posterior column abnormality on somatosensory evoked potential examination was not shown. The patient was treated with carbamazepine, 100 mg twice daily, which was remarkably effective in stopping the attacks.