Functional neurosurgery for Parkinson's diseaseBMJ 1998; 316 doi: https://doi.org/10.1136/bmj.316.7140.1259 (Published 25 April 1998) Cite this as: BMJ 1998;316:1259
Has come a long way, though much remains experimental
- Niall Quinn, Professor of clinical neurology,
- Kailash Bhatia, Senior lecturer in clinical neurology
Acquired brain lesions have long been known to modify the symptoms and signs of Parkinson's disease. After many false starts, in which various surgical lesions abolished tremor only at the expense of a hemiplegia, and with the advent of stereotactic techniques, neurosurgeons found that discrete lesions of the globus pallidus or thalamus could improve features of parkinsonism without (usually) causing a hemiplegia. Tremor appeared most responsive to thalamotomy, so this procedure became widely applied in the 1950s and 60s. Despite often permanent relief of tremor and rigidity, thalamotomy had no effect on akinesia, the core disabling feature of Parkinson's disease. Also, although unilateral surgery in this disease, which classically presents unilaterally or asymmetrically, was associated with low morbidity, as the disease progressed a second, contralateral, lesion was often made but with an unacceptably high (25%) incidence of pseudobulbar speech and swallowing difficulties. After the introduction of levodopa in 1967, the first treatment that dramatically alleviated akinesia, surgery took a dive until the mid-1980s, since when surgical approaches to treating Parkinson's disease have experienced a renaissance.
While using a stimulating electrode to guide lesion placement for Vim thalamotomy, Benabid's group in Grenoble found that high frequency discharges could abolish tremor.1 Why not, therefore, simply insert a chronic stimulating electrode without making a destructive lesion? This technique of deep brain stimulation provided excellent control of …
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