Scientific publications 

The subthalamic nucleus, hemiballismus and Parkinson's disease: reappraisal of a neurosurgical dogma

Jorge Guridi (1) and José A. Obeso (2)
(1) Service of Neurosurgery, Hospital de Navarra
(2) Movement Disorders and Basal Ganglia Unit, Department of Neurology and Neurosurgery, Neuroscience Program, Clinica Universitaria and Medical School, Universidad de Navarra, 31008 Pamplona, Spain

Magazine: Brain

Date: Jan 1, 2001

Neurology [SP] Neurosurgery Department

The subthalamic nucleus (STN) currently is considered to play a key role in the pathophysiological origin of the parkinsonian state and is therefore the main target for surgical treatment of Parkinson's disease.

The authors review the incidence of hemichorea/ballism (HCB) as a complication of thalamotomy, pallidotomy or campotomy procedures before the introduction of levodopa therapy, including the few reported cases accompanied by a neuropathological study. The literature shows that only a small number of parkinsonian patients with HCB had a lesion of the STN.

Preliminary data in Parkinson's disease patients submitted to a subthalamotomy with current functional stereotaxy also indicate that HCB is a very rare complication. To explain this observation, we suggest that the parkinsonian state is characterized by an increased threshold for the induction of dyskinesia following STN lesioning.

This arises as a consequence of reduced activity in the 'direct' GABA projection to the globus pallidus medialis (GPm) which accompanies dopamine depletion. Lesioning of the STN reduces excitation of the GPm, and theoretically this should induce dyskinesias. However, an STN lesion also, simultaneously, further reduces the hypoactivity in the globus pallidus lateralis (GPl) that is a feature of Parkinson's disease, and hence may compensate for GPm hypoactivity, thus self-stabilizing basal ganglia output activity and reducing the risk of HCB.

We conclude that lesioning of the STN in Parkinson's disease is a feasible approach in some circumstances.

CITATION  Brain. 2001 Jan;124(Pt 1):5-19

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