Direct Comparison of Posterior Subthalamic Area Stimulation versus Subthalamic Nucleus Deep Brain Stimulation in Parkinson's Disease.

In this case report, we describe successful tremor capture via stimulation of the posterior subthalamic area (PSA) for a patient with tremor-predominant Parkinson's disease. In this scenario, the patient had a deep brain stimulation (DBS) lead placed in the PSA of the right hemisphere and a DBS lead placed in the subthalmic nucleus (STN) of the left hemisphere. Therefore, we were able to directly compare tremor capture in the same patient receiving stimulation in two different brain areas. We show that both placements are equally efficacious for tremor suppression, though the DBS lead placed in the PSA required slightly higher current intensity. This comparison in the same patient confirms that stimulation of the PSA can successfully suppress tremor in Parkinson's disease.

Spinal cord intramedullary pressure in thoracic scoliotic deformity: a cadaveric study.

STUDY DESIGN: In vitro cadaveric study of thoracic spinal cord intramedullary pressure (IMP) in scoliotic deformity. OBJECTIVE: To define the relationship between thoracic scoliotic deformity and spinal cord IMP. SUMMARY OF BACKGROUND DATA: Clinical studies of patients with thoracic scoliosis without other spinal pathology (spinal stenosis, etc.) have rarely reported an associated thoracic myelopathy. Previous clinical and cadaveric studies of kyphosis have reported associated myelopathy and increased spinal cord IMP. We sought to determine if IMP changes in response to main thoracic scoliotic deformity. METHODS: In 6 fresh-frozen cadavers, a progressive main thoracic scoliotic deformity was created. Cadavers were positioned sitting with physiological spinal alignment, head stabilized using a skull clamp and spine segmentally instrumented from occiput to L3. The T3-T4 ligamentum flavum was removed, dura opened, and 3 pressure sensors were advanced caudally to T4-T5, T7-T8, and T10-T11 within the cord parenchyma. A step-wise main thoracic scoliotic deformity was then induced by sequentially releasing and retightening the skull clamp while coronally bending, concavity compressing, and convexity distracting posterior segmental instrumentation, allowing closure of lateral segmental osteotomies. After each step, fluoroscopic images and pressure measurements were obtained; the T4-T11 coronal Cobb angle was measured. RESULTS: Induction of main thoracic scoliosis did not significantly increase IMP. The mean main thoracic maximal scoliotic deformity created was 77° ± 2° (range: 71°-84°). At maximal deformity, the mean ΔIMP at T4-T5, T7-T8, T10-T11 was 2.2 ± 1.9 mm Hg, 1.0 ± 0.7 mm Hg, and 1.0 ± 0.8 mm Hg, respectively. CONCLUSION: In this cadaveric study, main thoracic scoliotic deformity did not significantly increase thoracic IMP. This correlates with clinical presentation such that clinical studies of patients with thoracic scoliosis without other spinal pathology have rarely reported an associated thoracic myelopathy with the thoracic scoliosis. This study helps explain the relative absence of myelopathy in isolated main thoracic coronal plane deformity. LEVEL OF EVIDENCE: 5.

Full-band electrocorticography of spreading depolarizations in patients with aneurysmal subarachnoid hemorrhage.

Cortical spreading depolarizations (CSDs) are a pathologic mechanism occurring in patients with aneurysmal subarachnoid hemorrhage and may contribute to delayed cerebral ischemia. We conducted a pilot study to determine the durations of depolarizations as measured by the negative direct current shifts in electrocorticography. Cortical electrode strips were placed in six patients (aged 35-63 years, Fisher grade 4, World Federation of Neurosurgical Societies [WFNS] 3-4) with ruptured aneurysms treated by clip ligation. Full-band electrocorticography was performed by direct current amplification (g.USBamp, Guger Tec, Graz, Austria) with ±250-mV range, 24-bit digitization, and recording/display with a customized BCI2000 platform. We recorded 191 CSDs in 4 patients, and direct current shifts of CSD (n = 403) were measured at 20 electrodes. Amplitudes were 7.2 mV (median; quartiles 6.2, 7.9), and durations were 2 min 14 s (1:53, 2:45). Ten direct current shifts in two patients with delayed infarcts were longer than 10 min, ranging up to 28 min. Taken together with previous studies, results suggest a threshold of 3-3.5 min to distinguish a normally distributed class of short CSDs with spreading hyperemia from prolonged CSDs with initial spreading ischemia. Results further demonstrate the clinical feasibility of direct current electrocorticography to monitor CSDs and assess their role in the pathology and management of subarachnoid hemorrhage.