Long term outcome of unilateral pallidotomy: follow up of 15 patients for 3 years.

OBJECTIVES: With the advent of new antiparkinsonian drug therapy and promising results from subthalamic and pallidal stimulation, this study evaluated the long term efficacy of unilateral pallidotomy, a technique which has gained popularity over the past decade for the management of advanced Parkinson's disease. METHODS: The 15 patients reported here are part of the original cohort of 24 patients who underwent posteroventral pallidotomy for motor fluctuations and disabling dyskinesias 3 years ago as part of a prospective study. Evaluation scales included the unified Parkinson's disease rating scale, the Goetz dyskinesia scale, and the Purdue pegboard test. RESULTS: When compared with the prepallidotomy scores, the reduction in the limb dyskinesias and off state tremor scores persisted on the side contralateral to pallidotomy at the end of 3 years (dyskinesias were reduced by 64% (p<0.01) and tremor by 63% (p<0.05). Other measures tended to deteriorate. The dosage of antiparkinsonian medications did not change significantly from 3 months prepallidotomy to 3 years postpallidotomy. CONCLUSIONS: Although unilateral pallidotomy is useful in controlling the contralateral dyskinesias and tremor 3 years after surgery, all other early benefits disappear and activities of daily living continue to worsen.

Reassessment of unilateral pallidotomy in Parkinson's disease. A 2-year follow-up study.

Unilateral pallidotomy has gained popularity in treating the motor symptoms of Parkinson's disease. We present the results of a 2-year post-pallidotomy follow-up study. Using the Unified Parkinson's Disease Rating Scale (UPDRS), the Goetz dyskinesia scale and the Purdue Pegboard Test (PPBT), we evaluated 20 patients at regular intervals both off and on medications for 2 years post-pallidotomy. There were no significant changes in the dosages of antiparkinsonian medications from 3 months pre-pallidotomy to 2 years post-pallidotomy. On the side contralateral to the operation, the improvements were preserved in 'on'-state dyskinesia (83% reduction from pre-pallidotomy to 2 years post-pallidotomy, P < 0.001) and 'off'-state tremor (90% reduction from pre-pallidotomy to 2 years post-pallidotomy, P = 0.005). There were no statistically significant differences between pre-pallidotomy scores and those at 2 years post-pallidotomy in ipsilateral dyskinesia, axial dyskinesia, 'off'- or 'on'-state PPBT, 'off'-state Activities of Daily Living (ADL) and 'off'-state gait and postural stability. After 2 years, the 'on'-state ADL scores worsened by 75%, compared with pre-pallidotomy (P = 0.005). We conclude that 2 years after pallidotomy, the improvements in dyskinesia and tremor on the side contralateral to pallidotomy are preserved, while the initial improvements in most other deficits disappear, either because of progression of pathology or loss of the early efficacy achieved by surgery.

Efficacy, stability and predictors of outcome of pallidotomy for Parkinson's disease. Six-month follow-up with additional 1-year observations.

We tested the efficacy, stability and predictors of outcome of unilateral pallidotomy used to treat patients with Parkinson's disease inadequately controlled with pharmacotherapy (IP). The surgical procedure was as simple as possible; we used CT rather than MRI, and we omitted microelectrode recording. We studied 24 patients with IP; 22 of these patients had drug-induced dyskinesias. There was a significant and stable improvement in all the major parkinsonian motor signs in the OFF (medication) state on the contralateral side. In the ON (medication) state peak-dose dyskinesias were alleviated on the contralateral side. The only significant and stable change on the ipsilateral side was improvement in dyskinesias less marked than on the contralateral side. The improvement in Unified Parkinson's Disease Rating Scale motor scores in the OFF state increased with age. The improvement in total dyskinesia scores occurred irrespective of age, but increased with duration of disease, duration of dyskinesias and baseline severity of dyskinesias. Five patients had transient neurological complications while facial paresis was permanent in one subject. Our results are similar to those obtained by others who used the time consuming microelectrode recording technique for localization. By simplifying the procedure in the way that we describe, the operation could become available to a greater number of patients.

A case of self-inflicted leucotomy.

A suicide attempt with a gun resulted in left frontal lobe damage in a 19-year-old obsessive man. While intelligence did not suffer and no frontal lobe syndrome emerged, the patient's obsessive rituals were significantly reduced.

Stimulation of the basal nucleus of Meynert in senile dementia of Alzheimer's type. A preliminary report.

The basal nuclei of Meynert are the principal sources of cholinergic innervation of the cerebral cortex. It has been hypothesized that the depressed cortical glucose metabolic activity in senile dementia of Alzheimer's type (SDAT) may result primarily from diminished activity and loss of these cells. The present study was designed to test the hypothesis that electrical stimulation of the basal nuclei would bring about clinical improvement and increase cortical glucose metabolic activity in SDAT. An electrode was implanted in September 1984 into the left basal nucleus of a 74-year-old man with SDAT. Repetitive cycles of stimulation for 9 months since have had no definite effect clinically but a follow-up positron emission tomography scan shows that cortical glucose metabolic activity was preserved in the ipsilateral temporal and parietal lobes while it declined elsewhere in the cortex.

Percutaneous lumbar rhizotomy for spasms in paraplegia.

Twenty-one patients with myelopathy causing uncontrollable spasms of the legs underwent percutaneous lumbar rhizotomy. There were two groups: active, otherwise healthy people with spinal lesions whose rehabilitation was hampered by spasms of flexion or extension of the hips and knees; and a second group of hospitalised, debilitated paraplegic patients with unhealing decubitus ulcers. Fourteen of the 16 active patients had excellent results initially, as did all five of the patients with pressure sores. Six have undergone repeat procedures in 7 to 18 months for recurrences of some component of the spasms. All have had at least minor recurrences. Of six patients with significant sensory preservation pre-operatively, four found the resulting numbness disturbing and two did not achieve good relief from the spasms. The procedure is recommended when uncontrollable spasms interfere with rehabilitation or healing of pressure sores in patients with spinal lesions with complete motor and sensory loss.

Thalamic stimulation for neuropathic pain.

Eighteen patients with neuropathic pain underwent thalamic electrode implantation. Satisfactory initial pain relief ensued in 14, and their electrode systems were internalized for long-term use. Twelve of the 14 continue to obtain either complete or partial pain relief by regular stimulation. One of the other two patients has had a complete remission of pain, apparently spontaneously, and the other had to have the electrodes removed after it retracted from his thalamus on two occasions. The electrodes have been placed in the sensory nucleus of the thalamus where stimulation evokes paresthesias in the painful part of the body. Technical problems consisting of our inability to locate the target in two patients and our failure to fix the electrode adequately in one prevented us from employing the treatment in three patients. The fourth patient had temperature dysesthesia which was not altered during 2 weeks of stimulation.

Microangiographic study of experimental spinal cord injuries.

The pathology of spinal cord injury has been studied in 34 rabbits and 5 dogs with attention focused on the condition of the microvasculature during the evolution of neuronal and axonal degeneration and necrosis. The animals were killed and perfused arterially with colloidal barium from 10 min to 14 days after a controlled spinal injury. Microradiographs of the injured tissues were obtained and compared with corresponding histological sections. Microangiography at 7 to 14 days defines two zones in the injured spinal cord. Zone 1 is located in the posterocentral part of the cord. Capillaries in this region progressively lose their ability to conduct blood and perfusate over the first 4 hours. Degenerative changes in neurons are visible by 1 hour after injury. Necrosis of all elements including capillaries ensues. Zone 2 surrounds Zone 1. Microvascular patterns are normal in Zone 2 although neuronal and axonal degeneration is severe. Pericapillary hemorrhages which occur as early as 10 min after injury in Zone 1 and become progressively larger over the first 4 hours seldom are seen in Zone 2. The evidence indicates that at all times in the pathogenesis of spinal cord injury the microvasculature in Zone 2 is capable of perfusion. Degeneration of neural structures either precedes microvascular breakdown (Zone 1) or occurs in the absence of microvascular disruption (Zone 2). Recovery of damaged neurons and axons depends upon a preserved microcirculation.