In Japan, brain docking has enhanced the detection of unruptured intracranial aneurysms in healthy adults. At our institution, surgical clipping is the first-line treatment for unruptured intracranial aneurysms (UIA). In this study, the differences in neurological and radiological outcomes, as well as cognitive and psychological results, between standard clipping and keyhole clipping for these aneurysms detected via brain docking were evaluated. The study included 131 aneurysms detected via "brain dock." Of these, 65 were treated with keyhole clipping surgery (keyhole clipping group), and 66 were treated with standard clipping surgery (standard clipping group). Evaluations at 3 months included the National Institutes of Health Stroke Scale, modified Rankin Scale, Mini-Mental State Examination, Hasegawa's Dementia Scale-revised, Beck Depression Inventory, Hamilton Rating Scale for Depression, and radiological abnormalities. The mean operative time and postoperative hospitalization period were significantly shorter in the keyhole clipping group than in the standard clipping group (p < 0.001). Between the groups, no significant differences in postoperative neurological complications or radiological abnormalities were found. The keyhole clipping group demonstrated slightly but significantly better Beck Depression Inventory and Hamilton Rating Scale for Depression scores than the standard clipping group (Beck Depression Inventory, p = 0.046; Hamilton Rating Scale for Depression, p < 0.01). Both the Beck Depression Inventory and Hamilton Rating Scale for Depression scores at 3 months were significantly enhanced (p < 0.001) in the keyhole clipping group. These findings propose that keyhole clipping could be considered a new therapeutic option for small UIA detected via brain docking.

This study aims to determine the cutoff values for the compound muscle action potential (CMAP) stimulus in anatomically identified anterior (motor nerve) and posterior roots (sensory nerve) during cervical intradural extramedullary tumor surgery. The connection between CMAP data from nerve roots and postoperative neurological symptoms in thoracolumbar tumors was compared with data from cervical lesions. The participants of the study included 22 patients with intradural extramedullary spinal tumors (116 nerve roots). The lowest stimulation intensity to the nerve root at which muscle contraction occurs was defined as the minimal activation intensity (MAI) in the CMAP. In cervical tumors, the MAI was measured after differentiating between the anterior and posterior roots based on the anatomical placement of the dentate ligament and nerve roots. The MAIs for 20 anterior roots in eight cervical tumors were between 0.1 and 0.3 mA, whereas those for 19 posterior roots were between 0.4 and 2.0 mA. The cutoff was <0.4 mA for both the anterior and posterior roots, and sensitivity and specificity were both 100%. In thoracolumbar tumors, the nerve root was severed in 12 of 14 cases. All MAIs were determined to be at the dorsal roots as their scores were higher than the cutoff and did not indicate motor deficits. The MAIs of the anatomically identified anterior and posterior root CMAPs were found to have a cutoff value of <0.4 mA in the cervical lesions. Similar MAI cutoffs were also applicable to thoracolumbar lesions. Thus, CMAP may be useful in detecting anterior and posterior roots in spinal tumor surgery.

Recently, thyroid autoantibodies were found to be associated with moyamoya disease (MMD). The ring finger protein 213 (RNF213) p.R4810K variant represents the most important susceptibility genotype of this disease, but its relationship with thyroid autoantibodies remains to be elucidated. Thus, in this study, we aimed to evaluate the clinical relevance of thyroid autoantibodies in each RNF213 genotype in patients with MMD. Included in this study were patients with MMD without a thyroid disease history and in euthyroid status; they were then classified into the mutated or nonmutated based on the RNF213 p.R4810K genotype and positive or negative based on thyroid autoantibody (thyroperoxidase and thyroglobulin) levels. Clinical data of each group were thereafter evaluated. Among the 209 patients, the mutated RNF213 p.R4810K variant and positive thyroid autoantibodies were detected in 155 and 41 patients, respectively. Positive thyroid autoantibodies were found to be more common in the nonmutated patients than in the mutated patients (31.5% vs. 15.5%; P = 0.011). In the mutated patients, as compared to autoantibody-negative patients, autoantibody-positive patients were determined to be more likely to have advanced disease with posterior cerebral artery involvement (54.2% vs. 29.0%; P = 0.017), white matter infarction (58.3% vs. 37.6%; P = 0.046), and a higher modified Rankin Scale at last visit (16.7% vs. 3.1%; P = 0.021). These results suggest that thyroid autoantibodies can act as an immunity inducer in patients with MMD lacking the susceptibility gene RNF213 p.R4810K variant. Moreover, the simultaneous presence of thyroid autoantibodies and the variant seems to aggravate the disease, which indicates synergy between thyroid autoantibodies and the variant.

Angiogenesis is one of the growth mechanisms of chronic subdural hematoma (CSDH). Pericytes have been implicated in the capillary sprouting during angiogenesis and are involved in brain ischemia and diabetic retinopathy. This study examined the pericyte expressions in CSDH outer membranes obtained during trepanation surgery. Eight samples of CSDH outer membranes and 35 samples of CSDH fluid were included. NG2, N-cadherin, VE-cadherin, Tie-2, endothelial nitric oxide synthase (eNOS), platelet-derived growth factor (PDGF) receptor-β (PDGFR-β), a well-known marker of pericytes, phosphorylated PDGFR-β at Tyr⁷⁵¹, and β-actin expressions, were examined using western blot analysis. PDGFR-β, N-cadherin, and Tie-2 expression levels were also examined using immunohistochemistry. The concentrations of PDGF-BB in CSDH fluid samples were measured using enzyme-linked immunosorbent assay kits. NG2, N-cadherin, VE-cadherin, Tie-2, eNOS, PDGFR-β, and eNOS expressions in CSDH outer membranes were confirmed in all cases. Furthermore, phosphorylated PDGFR-β at Tyr⁷⁵¹ was also detected. In addition, PDGFR-β, N-cadherin, and Tie-2 expressions were localized to the endothelial cells of the vessels within CSDH outer membranes by immunohistochemistry. The concentration of PDGF-BB in CSDH fluids was significantly higher than that in cerebrospinal fluid. These findings indicate that PDGF activates pericytes in the microvessels of CSDH outer membranes and suggest that pericytes are crucial in CSDH angiogenesis through the PDGF/PDGFR-β signaling pathway.