The syndrome of the sinking skin flap (SSSF) has been described as one of the causes of neurological deficits after decompressive craniectomy We report a case of a 57-year-old woman with SSSF. Two years earlier, this patient, with no neurological deficits, underwent removal of the bone flap during treatment of an epidural abscess due to wound infection after a clipping operation for a ruptured aneurysm. The patient, who subsequently developed a sinking skin flap, gradually presented with gait disturbance and poor activity around 1 year before she came to our facility. On admission, neurological examination showed left hemiparesis and mild confusion. Cranioplasty with titanium mesh plate was performed. The cerebral blood flow (CBF) value in CT perfusion imaging in the symptomatic hemisphere increased from 23 to 31 cm3/100 g/min, and the value in the contralateral side increased from 37 to 41 cm3/100 g/min after cranioplasty. CT perfusion imaging after cranioplasty revealed the improvement of cerebral blood flow not only on the symptomatic side but also on the contralateral side. The patient recovered well and was discharged without hemiparesis and confusion 2 weeks after cranioplasty. As far as we know, this is the first reported case of SSSF examined with CT perfusion imaging before and after cranioplasty.

The incidence of hypothalamic hamartomas (HHs) has increased since the introduction of magnetic resonance (MR) imaging. The etiology of this anomaly and the pathogenesis of its peculiar symptoms remain unclear, but recent electrophysiological, neuroimaging, and clinical studies have yielded important data. Categorizing HHs by the degree of hypothalamic involvement has contributed to the accurate prediction of their prognosis and to improved treatment strategies. Rather than undergoing corticectomy, HH patients with medically intractable seizures are now treated with surgery that targets the HH per se, e.g. HH removal, disconnection from the hypothalamus, stereotactic irradiation, and radiofrequency lesioning. Although surgical intervention carries risks, total eradication or disconnection of the lesion leads to cessation or reduction of seizures and improves the cognitive and behavioral status of these patients. Precocious puberty in HH patients is safely controlled by long-acting gonadotropin-releasing hormone agonists. The accumulation of knowledge regarding the pathogenesis of symptoms and the development of safe, effective treatment modalities may lead to earlier intervention in young HH patients and prevent the decline in their cognitive abilities and quality of life. This review of hypothalamic hamartomas presents current classifications, pathophysiologies, and treatment modalities.

Vascular endothelial growth factor (VEGF) has been found to be involved in vasculogenesis in different intracranial lesions. We investigated meningeal cellularity and VEGF expression in dura mater of patients with and without moyamoya disease. Nine dural specimens from nine cerebral hemispheres of seven patients with moyamoya disease and four control dural specimens from four non-moyamoya patients were collected during surgery and investigated. Dural specimens were immunohistochemically stained with VEGF antibody, and then meningeal cellularity and VEGF expression in dural tissue were analyzed. The mean+/-standard error (SE) of total number of meningeal cells (meningeal cellularity) in dural tissue was 21.5+/-3.0 in the moyamoya disease patients, whereas it was 2.7+/-0.7 in control patients. The mean+/-SE of VEGF expression was 51.1+/-4.9% in the moyamoya disease patients, whereas it was 13.8+/-5.9% in control patients. The meningeal cellularity and VEGF expression were statistically significantly higher in the moyamoya group in comparison to control group (p<0.0001). Meningeal cellularity and VEGF expression are significantly increased in dura mater of the patients with moyamoya disease.

BackgroundEndovascular therapy has been shown to be effective in patients with acute cerebral large‐vessel occlusion, but real‐world efficacies are unknown.Methods and ResultsWe conducted a prospective registry at 46 centers between October 2014 and January 2017. Eligible patients were those who were aged 20 years or older, with acute cerebral large‐vessel occlusion, and who were hospitalized within 24 hours of the onset. We enrolled both consecutive patients who were treated with or without endovascular therapy. Endovascular therapy included thrombectomy, balloon angioplasty, stenting, local fibrinolysis, and piercing. The primary outcome was a favorable outcome as defined by a modified Rankin Scale of 0 to 2 at 90 days after onset. Secondary outcomes were modified Rankin Scale of 0 to 1 and mortality. Safety outcomes were intracerebral hemorrhage or a recurrence of ischemic stroke. We constructed the 2242 (1121 each) propensity score–matched patients cohort based on a propensity score for endovascular therapy and estimated the adjusted odds ratio, followed by sensitivity analyses on original 2399 (1278 in endovascular therapy versus 1121 in no endovascular therapy) patients. In the propensity score–matched cohort, favorable outcomes were observed in 35.3% and 30.7% of patients in the endovascular therapy and no endovascular therapy groups, respectively (P=0.02). The adjusted odds ratio for the favorable outcome was 1.44 (95% confidence interval, 1.10–1.86, P=0.007). The efficacy of endovascular therapy in achieving favorable outcomes did not differ between our subgroups and in the sensitivity analyses.ConclusionsEndovascular therapy decreased disabilities at 90 days in real‐world patients with acute cerebral large‐vessel occlusion.Clinical Trial RegistrationURL: http://www.clinicaltrials.gov. Unique identifier: NCT02419794.

ICBi aneurysms were deviated to the side of the A1 segment of the ACA, where the artery might suffer higher hemodynamic stress.