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In NEUROLOGY 1995;45:753-761, a significant work followed 18 patients who underwent pallidotomy for 12 months, at 3 month intervals measuring motor functions. The motor functions of these patients was compared with 7 patients who did not have the surgery. The following is a synopsis: Stereotactic ventral pallidotomy for Parkinson's disease M. Dogali,MD;E. Fazzini,DO,PhD;E. Kolodny,MD;D. Eidelberg,MD; D. Sterio,MD,DSc;O. Devinsky,MD; and A. Beric,MD,DSc Selection: Patients with PD were selected by neurologists E. Fazzini and E. Kolodny and neurosurgeon M. Dogali. P. PD diagnosis for this selection was those with demonstrated parkinsonism with response to levodopa and had no history of known causative factors such as enchepalitus or neuro- leptic treatment. Those with (1) dementia, supranuclear gaze palsy, or ataxia;(2) Stage IV Hoehn and Yahr when "on";(3) Blood pressure drop greater than 30 mm Hg on standing;(4) medical, neurologic, or orthopedic illness that would compromise assessment, such as spinal stenosis, cerebrovascular disease, or metabolic disorder; or(5) the presence of a focal brain abnormality on MRI. Patient Assessment: The patients were assessed according to the "Core Assessment Program for Intracerebral Transplantation" (CAPIT). Surgical and non-surgical patients were tested after being off medication for 12 Hours (12 HOM) and several hours after waking up. Surgical patients were also tested while in the "on" state. Patients were maintained on a stable dose of antiparkinson medications for at least 2 weeks before surgery. Radiologic Investigations: Magnetic resonance imaging; All patients (surgical and nonsurgical) had T1- and T2-weighted MRI. Surgical patients had stereotactic pre- and postoperative MRI for confirmation of lesion placement and size. Post operative stereotactic MRIs confirmed the placement of all lesions with +- 1 mm of preoperatively planned targets. "Simplified" Surgical Procedure: All patients were deprived of medications for 12 or more hours before surgery. Under local anesthesia, a Leksell stereotactic G-frame was affixed at 4 points using fiberglass pins. Electrical stimulation was performed before lesioning to prevent injury to the internal capsule or optic tract; the effects and stimulation thresholds eliciting contralateral muscle contractions or visual symptoms were recorded. Multiple lesions were made at 80 degrees C for 60 seconds. Lesions were overlapped and created in sequence by withdrawing the electrode at 2-mm intervals, resulting in a cylindrically shaped lesion. Results: All surgical patients demonstrated improvement of rigidity and bradykinesia immediately after lesioning, while in the operating room. However, the first formal testing was obtained 1 week after surgery. The average length of hospitalization was 5 days, with all patients returning to their usual activities with 10 days. Lesion volume in all cases was calculated at between 60 and 90 cubic mm with a mean of 75 mm. Ten left and 8 right pallidotomies were done. There were only two events that could be considered complications. One patient was sexually disinhibited for 24 hours after pallidotomy, which was likely a transient effect of the surgery. The other patient suffered a MCA stroke 7 months after pallidotomy with infarction on the side opposite to the pallidotomy. He improved and became ambulatory with 2 to 3 months. As his 9- and 12-month follow-ups were confounded by signs of hemiparesis, they were excluded from the analysis; therefore, the 9- and 12-month follow-ups are reported for 17 patients. Improved reductions in test times for surgical patients were essentially consistent from follow-up to follow-up. Non surgical patients test times increased for the same tasks. At 1 year postoperatively, eight surgical patients demonstrated an increase in levodopa dosage or dopamine agonist use. Eight patients decreased levodopa usage or eliminated agonists, and one patient remained on the same medications and dosages. In contrast, five nonsurgical patients had increased dosage, one had decreased dosage, and one remained on the same dosage. The average levodopa dosage for surgical patients at the time of surgery was 1,041 mg/day and at the 12-month follow-up it was 1,002 mg/day, an insignificant 3.7% overall decrease. Pergolide dosage remained the same in the 10 patients who used it, which is an insignificant difference despite the tendency for decrease. Amantadine was eliminated in three of the four patients who used it preoperatively. Apart from one patient's stopping bromocriptine at the 12-month follow-up, no other changes were demonstrated in the three other patients who used it. Nonsurgical patients increased levodopa usage from 740 mg/day at baseline to 977 mg/day at 12-month follow-up, a statistically significant 32% increase. No correlation was found between the age of surgical patients and degree of improvement. Interestingly, one of the least improvements was seen in the youngest patient and one of the best improvements was seen in one of the oldest patients. If these two patients were excluded from the analysis, then younger age did correlate with better outcome in the remaining 15 patients. Discussion: Our impression that younger PD patients showed greater improvement was not supported by statistical analysis. We still believe that there is a real tendency for this to occur, but due to a relatively small number of observations as well as a few exceptions, which were alluded to in the Results, no correlation was found. Preliminary analysis of a larger group of postpallidotomy follow-ups, although with shorter follow-up periods, shows that younger patients have greater improvement. However, as some older patients enjoy considerable improvement, age should not be a relative contraindication for pallidotomy; our oldest patient was seventy-nine. Blinded review of all timed tests confirmed nonblinded clinical assessments; there was a significant improvement in PD symptoms and signs after pallidotomy. Patients experienced and reported improvements in overall functioning when in their "best on" and some decrease in fluctuation of their "on" and "off" periods; analysis of 12 HOM and "best on" improvements confirmed those observations. In comparing the degree of change or improvement for 12 HOM with "best on" 12 months after pallidotomy, 12 HOM showed significantly more improvement than "best on" for all observed parameters. Our patients were levodopa-responsive, and most had a good response to medication except for the presence of dyskinesias during short "on" periods. It was not expected that pallidotomy would dramatically improve a "best on" that was already good. Large improvements in 12 HOM, however, had to contribute to lesser fluctuations, as the "off" phase was better after pallidotomy and scores were lower, even approaching scores in the "on" phase. Overall, there was a minimal decrease in the mean daily dosage of antiparkinsonian medications at 12 months postoperatively as compared with baseline. Postoperatively, the "barrier" of contralateral dyskinesia was lifted, allowing patients to tolerate the same dosage of antiparkinsonian medications with inducing contralateral dyskinesia. Although pallidotomy may not be as effective as thalamotomy for tremor alleviation, tremor was reduced in all affected patients. Further, speech impairment, which is often a complication of thalamotomy, did not occur following dominant or nondominant hemisphere pallidotomy. Also, whereas balance impairment can be a complication of thalamotomy, pallidotomy improved balance and ambulation as well as bradykinesia. Postpallidotomy improvement appeared immediately after surgery and persisted for the duration of the 1-year follow-up. Some additional but not significant improvements at 1 year suggest that pallidotomy might slow the progression of PD, because nonsurgical controls deteriorated. Such PD arrest was suggested after some surgical interventions in the past; however, further follow-up is necessary to confirm this observation. It is conceivable hat the presence of dysfunction and hyperinhibition can further perpetuate the imbalance and contribute to the vicious cycle of PD progression, but removal of GPi hyperactivity may reduce the possible contribution of neuronal circuitry hyperactivity-imbalance to the progression of PD. John Cottingham [log in to unmask]