Unilateral thalamic deep brain stimulation for disabling kinetic tremor in multiple sclerosis.

BACKGROUND: Surgical options of multiple sclerosis (MS) tremor treatment are limited and narrowed to thalamotomy or deep brain stimulation of the thalamic nucleus ventralis intermedius. Lack of qualification protocol frequently results in poor outcome. OBJECTIVE: To determine prospectively the efficacy and safety of unilateral ventralis intermedius deep brain stimulation as a tool to control disabling kinetic arm tremor related to MS. METHODS: Neurological and neuropsychological evaluations were performed 1 month and 1 day before surgery and 1, 3, and 6 months after surgery. The evaluation included measurement of tremor and dexterity, Extended Disability Status Scale, Mini Mental State Examination, and quality-of-life assessment. Nine consecutive patients were enrolled in the group. Mean age at the time of surgery was 38.9 ± 9 years; median Extended Disability Status Scale at baseline was 7.1. Mean MS duration was 11.7 years, and mean tremor duration was 6.11 years. Mean postural and kinetic scores and hand capacity were measured. RESULTS: One month after surgery, median scores off and on stimulation were 12 and 6 for postural tremor, 12 and 10.5 for kinetic tremor score, 12 and 7.5 for manual capacity, and 22 and 20 for functional handicap, respectively. Similar results were 10 and 4, respectively, at the 3-month follow-up. Six months after surgery, median scores off and on stimulation were 10.4 and 4 for postural tremor and 12 and 7.8 for kinetic tremor, respectively. CONCLUSION: This prospective study confirms the value and safety of ventralis intermedius deep brain stimulation for treatment of kinetic tremor related to MS. Accurate and precise presurgical qualification plays a key role in successful treatment.

Behavioral and morphological comparison of two nonhuman primate models of Huntington's disease.

OBJECTIVE: Huntington's disease is a progressive neurodegenerative disease characterized by movement disorder, cognitive deterioration, and selective striatal degeneration. No effective treatment exists, and thus stable primate models could aid in the development of novel therapies. METHODS: Two primate models of Huntington's disease were analyzed: bilateral stereotactic intrastriatal injections of quinolinic acid (QA), and daily systemic intramuscular administration of 3-nitropropionic acid (3-NP) for up to 8 weeks in male Cebus apella monkeys. The animals' behavior was evaluated before, during, and 3 months after administration of the neurotoxin. Magnetic resonance imaging scans of the brain were obtained before and after treatment. RESULTS: Frontal cognitive function as evaluated by object retrieval-detour task test demonstrated a marked deterioration in successful responses, with an increase in barrier reaches in both groups. No significant change in performance of fine motor tasks was observed. QA-treated animals displayed hyperactivity at night. Animals in both groups demonstrated abnormal posture, and the 3-NP-treated group showed spontaneous and apomorphine-induced dystonia and dyskinesia. The QA-treated group displayed large areas of increased signal on T2-weighted images in the caudate and putamen bilaterally. Treatment with 3-NP resulted in smaller lesions. Immunohistochemistry and morphometric analyses revealed that both groups had lesions in the striatum. A large area of neuronal loss with glial sparing was observed in the QA-treated group, including the caudate and putamen bilaterally. The 3-NP-treated group displayed smaller lesions restricted to the dorsolateral putamen. CONCLUSION: These results suggest that both QA and 3-NP induce behavioral and morphological features that resemble the juvenile and akinetic-rigid variants of Huntington's disease, with the group with 3-NP-induced lesions displaying smaller lesions and spontaneous dyskinesia.