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Stereotactic neurosurgery for the treatment of movement disorders focuses primarily on the treatment of Parkinson's disease (PD), essential tremor (ET), and dystonia. The surgical targets in use are the subthalamic nucleus (STN) and the globus pallidus internus (GPi) for PD, GPi for dystonia, and ventralis intermedius (Vim) nucleus of the thalamus for ET. Following target selection, procedures include the generation of lesions or the placement of deep brain stimulating electrodes in the selected target. Additionally, transplantation has been used in the treatment of PD. The indications, outcomes, and risks of the various procedures are reviewed.

Object. The subthalamic nucleus (STN) is a target in the surgical treatment of Parkinson disease (PD). Little is known about the neurons within the human STN that modulate movement. The authors' goal was to examine the distribution of movement-related neurons within the STN of humans by using microelectrode recording to identify neuronal receptive fields. Methods. Data were retrospectively collected from microelectrode recordings that had been obtained in 38 patients with PD during surgery for placement of STN deep brain stimulation electrodes. The recordings had been obtained in awake, nonsedated patients. Antiparkinsonian medications were withheld the night before surgery. Neuronal discharges were amplified, filtered, and displayed on an oscilloscope and fed to an audio monitor. The receptive fields were identified by the presence of reproducible, audible changes in the firing rate that were time-locked to the movement of specific joint(s). The median number of electrode tracks per patient was six (range two–nine). The receptive fields were identified in 278 (55%) of 510 STN neurons studied. One hundred one tracks yielded receptive field data. Fourteen percent of 64 cells tested positive for face receptive fields, 32% of 687 cells tested positive for upper-extremity receptive fields, and 21% of 242 cells tested positive for lower-extremity receptive fields. Sixty-eight cells (24%) demonstrated multiple-joint receptive fields. Ninety-three cells (65%) with movement-related receptive fields were located in the dorsal half of the STN, and 96.8% of these were located in the rostral two thirds of the STN. Analysis of receptive field locations from pooled data and along individual electrode tracks failed to reveal a consistent somatotopic organization. Conclusions. Data from this study demonstrate a regional compartmentalization of neurons with movement-related receptive fields within the STN, supporting the existence of specific motor territories within the STN in patients suffering from PD.

OBJECTIVE To determine the incidence of long-term hardware-related complications of deep brain stimulation (DBS). METHODS The study design is a retrospective chart review of a single-surgeon, single-institution experience with DBS in 84 consecutive cases from 1993 to 1999. Only patients with a minimum follow-up of 1 year were considered. Five patients were excluded because trial stimulation failed to achieve pain relief (n = 4) or because the procedure was aborted owing to hemorrhage (n = 1). Seventy-nine patients received 124 permanent DBS electrode implants. RESULTS The mean follow-up period was 33 months, and the cumulative follow-up time was 217 patient-years or 310 electrode-years. Overall, 20 patients (25.3%) had 26 hardware-related complications involving 23 (18.5%) of the electrodes. There were 4 lead fractures, 4 lead migrations, 3 short or open circuits, 12 erosions and/or infections, 2 foreign body reactions, and one cerebrospinal fluid leak. The hardware-related complication rate per electrode-year was 8.4%. The most common complications were related to the electrode connectors. A significant finding was a high number of complications involving erosions or infections, which occurred in 7 of 12 instances as a late complication (beyond 12 mo). CONCLUSION Long-term follow-up reveals that hardware-related complications occur in a significant number of patients. Factors that lead to such complications must be identified and addressed to maximize the important benefits of DBS therapy.

Treatment of acromegaly has long been recognized as necessary to relieve symptoms, halt progression of deformities, and decompress the sella turcica. More recently, treatment strategies have focused on decreasing GH levels to a point at which mortality rates normalize, thereby redefining previous concepts of a cure. No surgical series to date has investigated the long-term effect of treatment on mortality rates. We retrospectively reviewed 254 consecutive patients with acromegaly who underwent transsphenoidal microsurgery of GH-secreting adenomas between 1974–1992. Seventy-six percent of these patients had basal GH levels

Article abstract-A 51-year-old man had a 4-month history of progressive headache and gradual onset of somnolence. MRI suggested spontaneous intracranial hypotension (SIH) with diencephalic compression, but he did not improve after three epidural blood patches. He became alert following intrathecal saline infusion that normalized his CSF pressure. A CSF leak was noted on spinal MRI and confirmed with CT contrast myelography. Surgical ligation of a torn dural root sleeve isolating a ruptured Tarlov's cyst resulted in permanent cure.

Objective: To retrospectively examine renal cell carcinoma (RCC) vs. melanoma local control (LC) dose responsiveness. Methods: 88 patients (RCC=38; melanoma=50) with 235 tumors (RCC=92; melanoma=143) were treated with Gamma Knife from Dec. 2005 to Aug. 2012. LC was compared between RCC vs. melanoma and then at each margin dose (≤18 Gy, 20 Gy, 22 Gy, and 24 Gy). Patient survival and toxicity were analyzed. Median follow-ups were 9.8 months (RCC) and 5.4 months (melanoma). Results: Patient characteristics were similar between RCC and melanoma with respect to gender, age, KPS, GPA, lesions per patient, and tumor volume. For all margin doses, LC at 6 months was 98.6% (RCC) vs. 79.2% (melanoma). When broken down by margin dose, at ≤18 Gy (P 0.05). Small melanoma tumors (

Deep brain stimulation (DBS) in the ventral intermediate nucleus of thalamus (Vim) is known to exert a therapeutic effect on postural and kinetic tremor in patients with essential tremor. For DBS leads implanted near the caudal border of Vim, however, there is an increased likelihood that one will also induce paresthesia side-effects by stimulating neurons within the sensory pathway of the ventral caudal (Vc) nucleus of thalamus. The aim of this computational study was to 1) investigate the neuronal pathways modulated by therapeutic, sub-therapeutic, and paresthesia-inducing DBS settings in three patients with essential tremor, and 2) determine how much better of an outcome could have been achieved had these patients been implanted with a DBS lead containing directionally-segmented electrodes (dDBS). Multi-compartment neuron models of the thalamocortical, cerebellothalamic, and medial lemniscal pathways were first simulated in the context of patient-specific anatomies, lead placements, and programming parameters from three ET patients who had been implanted with Medtronic 3389 DBS leads. The models showed that in these patients, complete suppression of tremor was associated most closely with activating an average of 62% of the cerebellothalamic afferent input into Vim (n=10), while persistent paresthesias were associated with activating 35% of the medial lemniscal tract input into Vc thalamus (n=12). The dDBS lead design demonstrated superior targeting of the cerebello-thalamo-cortical pathway, especially in cases of misaligned DBS leads. Given the close proximity of Vim to Vc thalamus, the models suggest that dDBS will enable clinicians to more effectively sculpt current through and around thalamus in order to achieve a more consistent therapeutic effect without inducing side effects.

Objective Diathermy is contraindicated in patients with implanted deep brain stimulation (DBS) electrodes. As the clinical applications for diathermy and the number of patients with DBS implants continue to grow, the opportunity for diathermy-induced complications in the population with DBS electrodes increases. We report a case of reversible neurological deficit in a patient who underwent diathermy 4 years after implantation of bilateral DBS leads. Clinical presentation A 58-year-old man with well-controlled symptoms of Parkinson's disease after the placement of bilateral DBS systems went to his primary care physician for the treatment of recurrent neck pain. A course of diathermy was prescribed, and after the second treatment, the patient developed double-vision and severe right-sided motor contractions. These symptoms resolved when he turned off the implanted pulse generators. Intervention The implanted pulse generators were turned back on after several days, but the symptoms recurred within 48 hours. The voltages were therefore decreased, resulting in resolution of symptoms but suboptimal control of the Parkinson's disease. A magnetic resonance imaging scan of the brain showed a small amount of edema surrounding the contacts of the left-sided lead. A follow-up magnetic resonance imaging scan 4 weeks later disclosed interval reduction in the edema, and the patient was able to tolerate increased voltage without symptom recurrence. Conclusion This is the first reported case of reversible injury from diathermy in a patient with DBS implants. Neurosurgeons must continue to emphasize to their patients and to other practitioners treating this population that diathermy is contraindicated for those with DBS implants.

OBJECTIVE The subthalamic nucleus (STN) is a target in the surgical treatment of Parkinson's disease (PD). The mechanism by which electrical stimulation of the STN ameliorates symptoms of PD remains unknown. One consistent aspect of STN stimulation is the ability to reduce the dosage of dopaminergic medications; sometimes they can be eliminated altogether. Furthermore, nigrostriatal projection axons are apposed to the dorsal surface of the STN and are likely affected by the application of current in this region. We sought to determine whether STN stimulation could release endogenous striatal dopamine. METHODS Five patients with PD, who had previously undergone surgical implantation of bilateral STN stimulators, underwent [11C]raclopride positron emission tomographic scanning. l-dopa was withheld for 12 hours, and both stimulators were turned off 9 hours before scanning. We assayed for striatal dopamine release by measuring radioligand displacement as a consequence of turning on the right STN stimulator after 45 minutes of a 90-minute [11C]raclopride infusion. Patients were evaluated with the motor section of the Unified Parkinson's Disease Rating Scale before and after the studies. RESULTS Comparisons between the right and left striata, before and after right STN stimulation, demonstrated no significant differences in [11C]raclopride binding, despite significant improvements in Unified Parkinson's Disease Rating Scale motor scores with unilateral stimulation (mean improvement, 26.0 ± 16.4%; P < 0.05). This finding was also noted when the striatum was partitioned into dorsal and ventral caudate and putamen and the four regions were analyzed separately. CONCLUSION Our results suggest that STN stimulation does not mediate its anti-PD effects via the release of dopamine, as assessed with [11C]raclopride displacement.

We have measured and characterized three oxidant defense enzymes in early and late intraerythrocytic stages of the human malarial parasite, Plasmodium falciparum. Isolated early intraerythrocytic stages contain catalase (24.1 mumol min-1 (mg protein)-1) and superoxide dismutase (SOD; 6.3 units (mg protein)-1) but little or no glutathione peroxidase (GPX; less than 2 mumol min-1 (mg protein)-1). Isolated late intraerythrocytic stages of P. falciparum contain slightly less catalase (17.0 mumol min-1 (mg protein)-1) but significantly more GPX (7.7 mumol min-1 (mg protein)-1) and SOD (25.1 units (mg protein)-1). P. falciparum, like P. berghei, probably acquires most of its SOD from its host, since parasite-associated SOD is predominantly cyanide-sensitive, and has the same pI as host SOD. Unlike P. berghei, however, late stages of P. falciparum contain an additional SOD isozyme which is not cyanide-sensitive and may represent an endogenous enzyme. Parasites grown in red cells that have been partially depleted of SOD are more sensitive to exogenously generated superoxide, suggesting some dependence of the parasite on host SOD.