Effect of Dexmedetomidine on Perception of Paresthesia during Subthalamic Nucleus Deep Brain Stimulation Surgery for Parkinson's Disease.

Background: Deep brain stimulation (DBS) has become a well-established treatment for the management of Parkinson's disease (PD). The most common method of lead targeting utilizes microelectrode recording (MER) and intraoperative macrostimulation to confirm accurate placement of the lead. This has been significantly aided by the use of dexmedetomidine (DEX) sedation during the procedure. Despite the frequent use of DEX, it has been theorized that DEX may have some effects on the MER during intraoperative testing. The effect on the perception of sensory thresholds during macrostimulation in the form of paresthesia is still unreported. Objectives: To investigate the effect of the sedative DEX on sensory perception thresholds observed in the intraoperative versus postoperative settings for patients undergoing subthalamic nucleus (STN) DBS surgery for PD. Materials and Methods: Adult patients (n = 8) with a diagnosis of PD underwent placement of DBS leads (n = 14) in the STN. Patients were subjected to intraoperative macrostimulation for capsular and sensory thresholds prior to placement of each DBS lead. These were compared to sensory thresholds observed in the postoperative setting during outpatient programming at three depths on each lead (n = 42). Results: In most contacts (22/42) (P = 0.19), sensory thresholds for paresthesia perception were either perceived at a higher voltage or absent during intraoperative testing in comparison to those observed in the postoperative setting. Conclusions: DEX appears to have measurable (though not statistically significant) effect on the perception of paresthesia observed during intraoperative testing.

Inherited genetic syndromes and meningiomas.

Meningiomas arising with inherited genetic syndromes occur nearly exclusively in the context of neurofibromatosis type 2 (NF2). NF2 is an autosomal dominant familial neoplasia syndrome that results from a mutation in the NF2 tumor suppressor gene located on the long arm of chromosome 22. The NF2 gene encodes for the protein merlin (moesin-ezrin-radixin-like protein), which has tumor suppressive effects that are reduced/inactivated in NF2-associated tumors. NF2-associated neoplasms affect the nervous system (schwannomas, meningiomas, ependymomas, astrocytomas, and neurofibromas) and skin. Other NF2 findings include ophthalmological lesions and peripheral neuropathy. Meningiomas are the second most frequent NF2-associated tumors (occurring in approximately half of all NF2 patients). They are often multiple and have unpredictable growth patterns. NF2-associated meningiomas can cause significant morbidity and mortality due to their location and a mass effect. Because of the multiplicity, frequent development of new tumors, and their protean nature, defined treatment strategies with serial surveillance is critical for optimal management of NF2-associated meningiomas. While surgical resection is the primary treatment for NF2-associated meningiomas, radiation plays an important adjunctive role in the management of recurrent and inoperable meningiomas.

Validation of the Surgical Intervention for Traumatic Injury scale in the pediatric population.

OBJECTIVE: While the Glasgow Coma Scale (GCS) has been effective in describing severity in traumatic brain injury (TBI), there is no current method for communicating the possible need for surgical intervention. This study utilizes a recently developed scoring system, the Surgical Intervention for Traumatic Injury (SITI) scale, which was developed to efficiently communicate the potential need for surgical decompression in adult patients with TBI. The objective of this study was to apply the SITI scale to a pediatric population to provide a tool to increase communication of possible surgical urgency. METHODS: The SITI scale uses both radiographic and clinical findings, including the GCS score on presentation, pupillary examination, and CT findings. To examine the scale in pediatric TBI, a neurotrauma database at a level 1 pediatric trauma center was retrospectively evaluated, and the SITI score for all patients with an admission diagnosis of TBI between 2010 and 2015 was calculated. The primary endpoint was operative intervention, defined as a craniotomy or craniectomy for decompression, performed within the first 24 hours of admission. RESULTS: A total of 1524 patients met inclusion criteria for the study during the 5-year span: 1469 (96.4%) were managed nonoperatively and 55 (3.6%) patients underwent emergent operative intervention. The mean SITI score was 4.98 ± 0.31 for patients undergoing surgical intervention and 0.41 ± 0.02 for patients treated nonoperatively (p < 0.0001). The area under the receiver operating characteristic (AUROC) curve was used to examine the diagnostic accuracy of the SITI scale in this pediatric population and was found to be 0.98. Further evaluation of patients presenting with moderate to severe TBI revealed a mean SITI score of 5.51 ± 0.31 in 40 (15.3%) operative patients and 1.55 ± 0.02 in 221 (84.7%) nonoperative patients, with an AUROC curve of 0.95. CONCLUSIONS: The SITI scale was designed to be a simple, objective communication tool regarding the potential need for surgical decompression after TBI. Application of this scale to a pediatric population reveals that the score correlated with the perceived need for emergent surgical intervention, further suggesting its potential utility in clinical practice.

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.