Search

Deep brain stimulation is now considered a routine treatment option for selected patients with advanced Parkinson's disease, primary segmental and generalised dystonia, and essential tremor. The neurosurgeon is responsible for the accurate and safe placement of the electrodes and the neurologist for the careful selection of patients and titration of medication against the effects of stimulation. A multidisciplinary team approach involving specialist nurses, neuropsychologists and neurophysiologists is required for a successful outcome. In this article we will summarise the key points in patient selection, provide an overview of the surgical technique, and discuss the beneficial and adverse outcomes that can occur.

We report on a patient with senile chorea, treated with deep brain stimulation of the left globus pallidus internus and subsequently the left ventralis oralis posterior nucleus of the thalamus. Deep brain field potential recordings and functional imaging using single photon emission tomography enabled us to suggest pathophysiological mechanisms for the symptoms.

In the current era of functional surgery for movement disorders, deep brain stimulation (DBS) of the globus pallidus internus (GPi) is emerging as the favoured intervention for patients with dystonia. Here we report our results in 20 patients with medically intractable dystonia treated with GPi stimulation. The series comprised 14 patients with generalized dystonia and six with spasmodic torticollis. Although comparisons were limited by differences in their respective neurological rating scales, chronic DBS clearly benefited both patient groups. Data conveying the rate of change in neurological function following intervention are also presented, demonstrating the gradual but progressive and sustained nature of improvement following stimulation of the GPi in dystonic patients.

Deep brain stimulation for the alleviation of movement disorders and pain is now an established therapy. However, very little has been published on the topic of hardware failure in the treatment of such conditions irrespective of clinical outcome. Such device-related problems lead to significant patient morbidity and increased cost of therapy in the form of prolonged antibiotics, in-patient hospitalization, repeat surgery, and device replacement. We report a prospective review of our experience at the Radcliffe Infirmary Oxford from the period of April 1998 to March 2001. Overall there is a 20% rate of hardware-related problems in this series, which falls between the 7% and 65% rates reported by other groups. The majority of these failures occurred early on in the series, and numbers declined with experience. Some of the problems may be idiosyncratic to the methodology of individual groups.

Subthalamic deep brain stimulation is now well established as a treatment for the dopaminergic motor symptoms of Parkinson's disease. It has little effect on postural instability and "on-state" gait freezing. Animal experiments and early human pilot studies suggest that Pedunculopontine nucleus stimulation may alleviate these phenomenon, consistent with the hypothesis that these disabling symptoms are secondary to degeneration in non-dopaminergic pathways.

In a patient of generalised dystonia treated with bilateral pallidal stimulation, serial surface EMGs recorded from the neck muscles during alternating head movements revealed progressive reduction in hypertonic activity and reversal of co-contraction to reciprocal contraction, which preceded clinical improvement.

Sensory nerve function was determined in 19 patients with amyotrophic lateral sclerosis (ALS), using a battery of clinical and neurophysiological tests. This assessment was repeated on 12 patients after intervals of 6-18 months. Twelve controls were also studied. In the ALS group, only 2 patients had noticed mild sensory symptoms and none had sensory signs. Between successive studies the vibration thresholds increased, but not to a significant degree. ALS patients showed a significant fall in amplitude of the sensory nerve action potentials in the median, radial, and sural nerves (P < 0.04); sensory nerve conduction velocity did not alter. The median nerve somatosensory evoked potential N19 latency showed a highly significant increase (P < 0.008). Significant subclinical deterioration in sensory nerve function occurs in ALS, and parallels the progressive motor decline. Neuronal degeneration in ALS is not restricted to motor neurons.

In 1992, Laitinen reported the benefits of posteroventral pallidotomy (PVP) for the treatment of advanced idiopathic Parkinson's disease when he re-visited a procedure first described by Leksell 30 years previously (Starr et al ., 1998). The resurgence of interest was driven by the failure of medical management to successfully treat the increasing number of patients with the all too familiar long-term levodopa failure syndrome, characterized by dopa-induced dyskinesias and motor oscillations. Since then, a further 20 reasonably well-designed series on 700 patients have been published in peer-reviewed journals, with similar impressive results. A recent randomized controlled trial has confirmed highly significant benefits (Vitek et al ., 1998). Critics of the procedure often cite the paper of Sutton et al . (1995) on five patients who did not show overall benefits apart from dyskinesia suppression. Two of the clinical descriptions given in this report, however, were not suggestive of idiopathic Parkinson's disease. The efficacy of unilateral PVP in selected patients with advanced idiopathic Parkinson's disease is therefore no longer a matter of debate, but despite this many questions remain over the optimal lesion size and site, the necessity of intra-operative microelectrode recording, and the long-term benefits of the procedure. Two papers in this journal begin …