Burst spinal cord stimulation for the treatment of cervical dystonia with intractable pain: A pilot study

Shimizu, T.; Maruo, T.; Miura, S.; Kimoto, Y.; Ushio, Y.; Goto, S.; Kishima, H. Burst Spinal Cord Stimulation for the Treatment of Cervical Dystonia with Intractable Pain: A Pilot Study. Brain Sci. 2020, 10, 827

Pathophysiology and treatment of cerebral ischemia

This article describes the pathophysiology of, and treatment strategy for, cerebral ischemia. It is useful to think of an ischemic lesion as a densely ischemic core surrounded by better perfused “penumbra” tissue that is silent electrically but remains viable. Reperfusion plays an important role in the pathophysiology of cerebral ischemia. Magnetic resonance imaging (MRI) and histological studies in rat focal ischemia models using transient middle cerebral artery (MCA) occlusion indicate that reperfusion after an ischemic episode of 2- to 3-hour duration does not result in reduction of the size of the infarct. Brief occlusion of the MCA produces a characteristic, cell-type specific injury in the striatum where medium-sized spinous projection neurons are selectively lost ; this injury is accompanied by gliosis. Transient forebrain ischemia leads to delayed death of the CA1 neurons in the hippocampus. Immunohistochemical and biochemical investigations of Ca2+/calmodulin-dependent protein kinase II(CaM kinase II) and protein phosphatase (calcineurin) after transient forebrain ischemia demonstrated that the activity of CaM kinase II was decreased in the CA1 region of the hippocampus early (6- 12 hours) after ischemia. However, calcineurin was preserved in the CA1 region until 1.5 days after the ischemic insult and then lost ; a subsequent increase in the morphological degeneration of neurons was observed. We hypothesized that an imbalance of Ca2+/calmodulin dependent protein phosphorylation-dephosphorylation may be involved in delayed neuronal death after ischemia. In the treatment of acute ischemic stroke, immediate recanalization of the occluded artery, using systemic or local thrombolysis, is optimal for restoring the blood flow and rescuing the ischemic brain from complete infarction. However, the window of therapeutic effectiveness is very narrow. The development of effective neuroprotection methods and the establishment of reliable imaging modalities for an early and accurate diagnosis of the extent and degree of the ischemia are imperative

CENP-A Phosphorylation by Aurora-A in Prophase Is Required for Enrichment of Aurora-B at Inner Centromeres and for Kinetochore Function

AbstractThe Aurora (Ipl1)-related kinases are universal regulators of mitosis. We now show that Aurora-A, in addition to Aurora-B, regulates kinetochore function in human cells. A two-hybrid screen identified the kinetochore component CENP-A as a protein that interacts with Aurora-A. Aurora-A phosphorylated CENP-A in vitro on Ser-7, a residue also known to be targeted by Aurora-B. Depletion of Aurora-A or Aurora-B by RNA interference revealed that CENP-A is initially phosphorylated in prophase in a manner dependent on Aurora-A, and that this reaction appears to be required for the subsequent Aurora-B-dependent phosphorylation of CENP-A as well as for the restriction of Aurora-B to the inner centromere in prometaphase. Prevention of CENP-A phosphorylation also led to chromosome misalignment during mitosis as a result of a defect in kinetochore attachment to microtubules. Our observations suggest that phosphorylation of CENP-A on Ser-7 by Aurora-A in prophase is essential for kinetochore function

Therapy-associated secondary tumor in patients with non-germinomatous malignant germ cell tumors

We report 3 patients with non-germinomatous malignant germ cell tumor (NGMGCT) who developed therapy-associated secondary tumors. They were diagnosed as having NGMGCT by elevated serum levels of β-fetoprotein (AFP), human chorionic gonadotropin (HCG), or β-HCG. Preoperatively, all patients received a combination of etoposide and platinum-based chemotherapy and radiotherapy; neo-adjuvant therapy (NAT) was followed by complete excision of the residual tumor. Postoperatively, all underwent maintenance chemotherapy and all remained free of NGMGCT without recurrence. However, they developed therapy-associated secondary tumors, i.e. glioblastoma, meningioma, or cavernous angioma after an interval of 10.1-, 9.8-, and 8.2 years, respectively. The patient with gliobastoma died 1 year after its detection. The other 2 patients are currently alive; the meningioma was completely removed and the cavernous angioma is being monitored without additional treatment. To our knowledge, therapy-associated secondary tumors in patients treated for NGMGCT are rare

Burr hole locations are associated with recurrence in single burr hole drainage surgery for chronic subdural hematoma

Background: Various factors have been reported as risk factors for chronic subdural hematomas (CSDH) recurrence. However, few studies have quantitatively evaluated the impact of CSDH locations and burr hole positions on recurrence. This study aimed to reveal the relation between CSDH recurrence and the locations of CSDH and burr holes. Methods: Initial single burr hole surgeries for CSDH with a drainage tube between April 2005 and October 2021 at Otemae Hospital were enrolled. Patients’ medical records, CSDH volume, and CSDH computed tomography values (CTV) were evaluated. The locations of CSDH and burr holes were assessed using Montreal Neurological Institute coordinates. Results: A total of 223 patients were enrolled, including 34 patients with bilateral CSDH, resulting in 257 surgeries investigated. The rate of CSDH recurrence requiring reoperation (RrR) was 13.5%. The RrR rate was significantly higher in patients aged ≥76 years, those with bilateral CSDH, and those with postoperative hemiplegia. In RrR, the preoperative CSDH volume was significantly larger, and CTV was significantly smaller. The locations of CSDH had no influence on recurrence. However, in RrR, the locations of burr holes were found to be more lateral and more ventral. Multivariate Cox proportional hazards regression analysis showed that bilateral CSDH, more ventral burr hole positions, and postoperative hemiplegia were risk factors for recurrence. Conclusions: The locations of burr holes are associated with CSDH recurrence. In RrR, CSDH profiles tend to show a larger volume and reduced CTV. Hemiplegia after burr hole surgery serves as a warning sign for RrR