Explore the vast range of titles available.

Abstract BACKGROUND Estrogen deficiency is associated with cerebral aneurysm rupture, but the precise mechanism is unknown. OBJECTIVE To test the hypothesis that IL-6 is required for the increase in aneurysm rupture rate observed in estrogen-deficient mice. METHODS We analyzed IL-6 expression in human cerebral aneurysms. We induced cerebral aneurysms in estrogen-deficient female C57BL/6 mice that had undergone 4-vinylcyclohexene diepoxide (VCD) treatment or bilateral ovariectomy (OVE). Mice were blindly randomized to selective IL-6 inhibition (IL-6 receptor [IL-6R] neutralizing antibody, n = 25) or control (isotype-matched IgG, n = 28). Murine cerebral arteries at the circle of Willis were assessed for aneurysm rupture and macrophage infiltration. RESULTS IL-6 is expressed in human cerebral aneurysms, but not in control arteries. Serum IL-6 is elevated in ovariectomized female mice compared to sham control (14.3 ± 1.7 pg/mL vs 7.4 ± 1.5 pg/mL, P = .008). Selective IL-6R inhibition suppressed cerebral aneurysm rupture in estrogen-deficient mice compared with control (VCD: 31.6% vs 70.0%, P = .026; OVE: 28.6% vs 65.2%, P = .019). IL-6R inhibition had no effect on formation or rupture rate in wild-type mice. IL-6R neutralizing antibody significantly reduced macrophage infiltration at the circle of Willis (1.9 ± 0.2 vs 5.7 ± 0.6 cells/2500 μm2; n = 8 vs n = 15; P < .001). CONCLUSION IL-6 is increased in the serum of estrogen-deficient mice and appears to play a role in promoting murine estrogen deficiency-associated cerebral aneurysm rupture via enhanced macrophage infiltration at the circle of Willis. Inhibition of IL-6 signaling via IL-6 receptor neutralizing antibody inhibits aneurysm rupture in estrogen-deficient mice. IL-6 receptor inhibition had no effect on aneurysm formation or rupture in wild-type animals.

A 54-year-old man presented with gait disturbances, urinary incontinence, and headache for 6 months. Head computed tomography indicated several high-density mass lesions in the quadrigeminal cistern, causing occlusive hydrocephalus. Digital subtraction angiography confirmed tentorial dural arteriovenous fistulae (AVF). Transarterial embolization (TAE) achieved complete angiographic resolution. However, acute occlusive hydrocephalus worsened, necessitating endoscopic third ventriculostomy (ETV). The patient was discharged without new symptoms and no hydrocephalus recurrence at six-month follow-up. Hydrocephalus is rare in patients with dural AVF and mostly resolves spontaneously after treatment; however, if thrombosis and enlargement of the varix occur after treatment, acute occlusive hydrocephalus can develop.

Background: This study was performed to examine the efficacy of endoscopic transsphenoidal surgery (ETS) for Cushing's disease at a single institute and to review past reports. Material and Methods: We studied eight consecutive patients who underwent ETS for Cushing's disease. The radiological evaluation comprised a detailed examination of preoperative magnetic resonance images (MRIs), including inferior petrosal sinus sampling, for cases with normal renal function. Remission was evaluated at least three months after surgery and was defined by the presence of hypocortisolemia that required steroid replacement therapy or eucortisolemia with suppression to <1.8 μg/dL after 1mg of dexamethasone. Results: In all cases preoperative MRI was abnormal and included two macroadenomas (25 %). Pathological confirmation of an adenoma was possible in all patients. The mean follow-up period was 5.6 (2-7) years. Remission was confirmed in 75.0% of the cases and was higher in rate for microadenoma (100%) than for macroadenoma (50%). Postoperatively , no cerebrospinal fluid rhinorrhea occurred, but new endocrine deficits were noted in 25% of patients. Conclusion: Based on this study, ETS enhanced the intrasellar identification of adenomatous tissue, which led to low remission and complication rates that were comparable with those of traditional microsurgery for Cushing's disease.

Background: Visual evoked potential (VEP) is used as a means of intraoperative visual function monitoring. It remains unclear, however, whether intraoperative VEP monitoring is a means of real-time visual function monitoring that has satisfactory effectiveness and sensitivity. To evaluate this, the relationships between VEP waveform changes in endoscopic transsphenoidal surgery and postoperative visual function were analyzed retrospectively. Materials and Methods: Intraoperative VEP monitoring was carried out during 82 endoscopic transnasal transsphenoidal surgeries for 164 eyes at Nara Medical University Hospital, Nara, Japan under total intravenous anesthesia. Red light flash stimulation was provided to each eye independently. The VEP recording and postoperative visual function were then analyzed. Results: In 160 of 164 eyes (98%), steady VEP monitoring was performed. Stable VEP was acquired from eyes with a corrected visual acuity >0.1. VEP was not recorded in four eyes that had a corrected visual acuity under 0.05. A transient VEP decrease was observed in 26 eyes, 8 of which had improved visual acuity and 18 of which had no change in visual acuity. A permanent gradual VEP decrease occurred in eight eyes; this finding did not correspond to a change in visual function. The visual acuity of the patients who underwent the transsphenoidal operation in our study did not worsen. Conclusion: Intraoperative monitoring of VEP predicts postoperative visual function, and a reversible change in VEP indicates that visual function will be preserved. Intraoperative VEP monitoring will be mandatory for surgeries harboring a risk of visual impairment.

We evaluated the effects of cilostazol on venous infarction produced by a photothrombotic two-vein occlusion (2VO) model in diabetic and control rats. The cerebral blood flow (CBF) between the occluded veins was measured by laser Doppler flowmetry for 4 hours after 2VO. Infarct size and immunohistochemistry were evaluated 24, 48, 96, and 168 hours after 2VO. Cilostazol was administered 1 hour after 2VO, and thereafter at a continuous oral dose of 60 mg/kg per day. Cilostazol reduced the infarct size, and the number of terminal deoxynucleotidyl transferase-mediated deoxyuridine triphosphate nick-end labeling (TUNEL)-positive apoptotic and B-cell lymphoma 2-associated X protein (Bax)-positive cells, and improved the CBF in control rats. In diabetic rats, cilostazol reduced the infarct size, and the number of TUNEL-positive apoptotic and Bax-positive cells, 96 and 168 hours after 2VO, but did not improve the CBF 4 hours after 2VO. Cilostazol increased the number of B-cell lymphoma 2 (Bcl-2)-positive cells in both strains 48, 96, and 168 hours after 2VO, but did not improve vessel wall thickness or collagen deposits. Cilostazol appeared to limit venous infarcts by improving the penumbral CBF in nondiabetic rats, and inhibited pro-apoptotic changes through Bcl-2 overexpression, without improving the CBF in diabetic rats.

Metal-induced encephalopathy after stent-assisted coil embolization is extremely rare. The present report describes two patients who presented with symptomatic intracranial parenchymal edematous lesions after stent-assisted coil embolization. A 64-year-old woman underwent stent-assisted coil embolization for a left internal carotid artery aneurysm; 21 days after the procedure she presented with right hand weakness and MRI revealed multifocal white matter lesions. Another woman aged 52 years underwent stent-assisted coil embolization for right vertebral artery aneurysm; 18 days after the procedure she presented with left-sided sensory disturbance and MRI demonstrated multiple white matter lesions. Treatment in both cases resulted in improvement of these lesions after steroid pulse therapy, and the patients had no associated morbidity 4 months after the procedures. Clinicians should monitor for neurologic symptoms and postoperative delayed radiologic parenchymal edematous changes associated with the metal allergic reaction after nitinol stent-assisted coil embolization.

Abstract BACKGROUND: The increasing number of neurosurgical procedures for elderly patients and the development of skull base neurosurgery have increased interest in cerebral venous injury that might occur in a neurosurgical setting. Brain-derived neurotrophic factor (BDNF) may have neuroprotective effects against cerebral venous ischemia. OBJECTIVE: To investigate the intraventricular effects of BDNF infusion on infarct size, suppression of apoptosis, and regional cerebral blood flow (rCBF) in cerebral venous ischemic lesions in a rat 2-vein occlusion model. METHODS: Thirty-three male Wistar rats were randomly divided into BDNF-treated and vehicle control groups; each group was further randomly divided into 2-day and 7-day postocclusion groups. BDNF (2.1 μg/day) or vehicle was delivered continuously via intraventricular infusion pumps. Two adjacent contralateral cortical veins were then photochemically occluded. Two and 7 days after occlusion, we histologically measured ratios of infarct volume to contralateral hemisphere volume and counted (2-day group) terminal deoxynucleotidyl transferase-mediated deoxyuridine triphosphate nick-end labeling (TUNEL)-positive apoptotic cells in the penumbra. rCBF was measured via full-field laser perfusion imaging. RESULTS: The mean infarct volume after venous occlusion was significantly smaller in BDNF-treated rats than in controls at 2 days (1.49 ± 1.44% vs 3.66 ± 1.51%; P < .05) and 7 days (0.93 ± 0.47% vs 1.69 ± 0.58%; P < .05). Two days after occlusion, there were significantly fewer TUNEL-positive apoptotic cells in the BDNF-treated rats (17.0 ± 15.1) than in the controls (39.0 ± 19.6; P < .05). There were no differences in rCBF. CONCLUSION: After 2-vein occlusion, continuous intraventricular administration of BDNF protected the cerebral cortex against apoptosis and reduced infarct size without affecting rCBF.

Metal-induced encephalopathy after stent-assisted coil embolization is extremely rare. The present report describes two patients who presented with symptomatic intracranial parenchymal edematous lesions after stent-assisted coil embolization. A 64-year-old woman underwent stent-assisted coil embolization for a left internal carotid artery aneurysm; 21 days after the procedure she presented with right hand weakness and MRI revealed multifocal white matter lesions. Another woman aged 52 years underwent stent-assisted coil embolization for right vertebral artery aneurysm; 18 days after the procedure she presented with left-sided sensory disturbance and MRI demonstrated multiple white matter lesions. Treatment in both cases resulted in improvement of these lesions after steroid pulse therapy, and the patients had no associated morbidity 4 months after the procedures. Clinicians should monitor for neurologic symptoms and postoperative delayed radiologic parenchymal edematous changes associated with the metal allergic reaction after nitinol stent-assisted coil embolization.

A 14-year-old boy experienced sudden headache in the left parietal region, without any history of head trauma. Approximately 40 ml of hematoma was aspirated using a 22-gauge needle, and scalp swelling immediately disappeared. However, the swelling recurred bilaterally 2 weeks later. Left external carotid angiography revealed a reticular shadow consistent with subgaleal hematoma from a branch of bilateral superficial temporal arteries, without any arteriovenous shunts. The patient was successfully treated using the combination of hematoma aspiration and embolization of the superficial temporal artery. The combination of aspiration of hematoma and embolization may be effective for refractory non-traumatic subgaleal hematoma.

Metal-induced encephalopathy after stent-assisted coil embolization is extremely rare. The present report describes two patients who presented with symptomatic intracranial parenchymal edematous lesions after stent-assisted coil embolization. A 64-year-old woman underwent stent-assisted coil embolization for a left internal carotid artery aneurysm; 21 days after the procedure she presented with right hand weakness and MRI revealed multifocal white matter lesions. Another woman aged 52 years underwent stent-assisted coil embolization for right vertebral artery aneurysm; 18 days after the procedure she presented with left-sided sensory disturbance and MRI demonstrated multiple white matter lesions. Treatment in both cases resulted in improvement of these lesions after steroid pulse therapy, and the patients had no associated morbidity 4 months after the procedures. Clinicians should monitor for neurologic symptoms and postoperative delayed radiologic parenchymal edematous changes associated with the metal allergic reaction after nitinol stent-assisted coil embolization.