Chronic subdural hematoma (CSDH) tends to occur in elderly patients with a history of mild head injury at a few months prior to the onset of symptoms. Intracranial arachnoid cyst is believed to be congenital and sometimes becomes symptomatic in pediatric patients. These two distinct clinical entities sporadically occur in the same young patient. Twelve of 541 cases of CSDH surgically treated in our institution had associated arachnoid cyst. The clinical and radiological characteristics of the cases of CSDH associated with arachnoid cyst were retrospectively analyzed and compared with those of CSDH without arachnoid cyst. Arachnoid cysts were located in the middle fossa (eight cases), convexity (two cases), and posterior fossa (two cases). Three cysts were less than 20 mm in diameter. The 12 patients with CSDH and arachnoid cyst (mean age 27.8 +/- 19.7 years) were significantly younger (p < 0.001) than the patients with CSDH without arachnoid cyst (69.5 +/- 13.7 years). Five of the 12 patients were pediatric cases (< 15 years old). The clinical symptoms were also significantly different. The most frequent symptom was headache followed by vomiting in the patients with arachnoid cyst, while gait disturbance and hemiparesis predominated in patients without arachnoid cyst. Hematoma evacuation through burr holes improved the symptoms in all patients with arachnoid cyst. We conclude that even a small arachnoid cyst can be a risk factor for CSDH after mild head injury in young patients and symptoms of increased intracranial pressure are common. Hematoma evacuation is adequate at first operation. If the preoperative symptoms persist, additional arachnoid cyst surgery should be considered. The present results also suggest that CSDH formation may be preceded by subdural hygroma caused by the rupture of arachnoid cyst.

Massive hemispheric cerebral infarction, also known as malignant infarction, is characterized by rapid clinical deterioration due to brain swelling and downward transtentorial herniation, and is associated with a mortality of 80%. Early patient selection and establishment of the optimum therapeutic modality are important to improve the outcome. Early clinical, computed tomography (CT), and angiographic characteristics were analysed to identify patients with malignant infarction and external and internal decompression was performed, with unco-parahippocampectomy if needed, and the outcomes were compared with those of conservative treatment. Thirty-four of 55 patients admitted with large cerebral infarctions due to embolism showed rapid clinical deterioration due to brain swelling and herniation. These 34 patients were treated under a diagnosis of malignant infarction by decompressive surgical treatment (19 cases) or conservative treatment (15 cases). CT showed significantly higher infarction volume in patients with malignant infarction (288 +/- 62 cm3) compared to patients with non-malignant infarction (200 + 57 cm3, P < 0.001) and angiography showed a higher incidence of recanalization of the occluded vessels in patients with malignant infarction (58%) compared to patients with non-malignant infarction (15%, P < 0.05). Discriminant analysis revealed that an infarction volume of more than 240 cm3 was predictive of malignant infarction with 76.4% accuracy. Basic clinical characteristics on admission and deterioration were not statistically different between the surgically treated and conservatively treated groups of patients with malignant infarction. The shift of midline structures was significantly improved (14 +/- 3.5 to 10 +/- 4.7 mm) after surgical treatment (P < 0.05). compared to deterioration (12 +/- 5.8 to 15 +/- 4.5 mm) after conservative treatment. The mortality was 67% in the conservative group and 16% in the surgical group. Surgical treatment significantly improved the mortality and Glasgow Outcome Scale score (P < 0.01). However, the mean Barthel Index scores of the survivors were not significantly different. An infarct volume of more than 240 cm3 on CT and angiographic recanalization of the occluded artery are predictors of fatal brain swelling after massive cerebral infarction. Decompressive surgical treatment dramatically improves the mortality of massive hemispheric infarction.

Cerebral blood flow (CBF) rises when the glucose supply to the brain is limited by hypoglycemia or glucose metabolism is inhibited by pharmacological doses of 2-deoxyglucose (DG). The present studies in unanesthetized rats with insulin-induced hypoglycemia show that the increases in CBF, measured with the [14C]iodoantipyrine method, are relatively small until arterial plasma glucose levels fall to 2.5 to 3.0 mM, at which point CBF rises sharply. A direct effect of insulin on CBF was excluded; insulin administered under euglycemic conditions maintained by glucose injections had no effects on CBF. Insulin administration raised plasma lactate levels and decreased plasma K+ and HCO3- concentrations and arterial pH. These could not, however, be related to the increased CBF because insulin under euglycemic conditions had similar effects without affecting CBF; furthermore, the inhibition of brain glucose metabolism with pharmacological doses (200 mg/kg intravenously) of DG increased CBF, just like insulin hypoglycemia, without altering plasma lactate and K+ levels and arterial blood gas tensions and pH. Nitric oxide also does not appear to mediate the increases in CBF. Chronic blockade of nitric oxide synthase activity by twice daily i.p. injections of NG-nitro-L-arginine methyl ester for 4 days or acutely by a single i.v. injection raised arterial blood pressure and lowered CBF in normoglycemic, hypoglycemic, and DG-treated rats but did not significantly reduce the increases in CBF due to insulin-induced hypoglycemia (arterial plasma glucose levels, 2.5-3 mM) or pharmacological doses of deoxyglucose.

The possibility that adenosine and ATP-sensitive potassium channels (KATP) might be involved in the mechanisms of the increases in cerebral blood flow (CBF) that occur in insulin-induced hypoglycemia was examined. Cerebral blood flow was measured by the [14C]iodoantipyrine method in conscious rats during insulin-induced, moderate hypoglycemia (2 to 3 mmol/L glucose in arterial plasma) after intravenous injections of 10 to 20 mg/kg of caffeine, an adenosine receptor antagonist, or intracisternal infusion of 1 to 2 mumol/L glibenclamide, a KATP channel inhibitor. Cerebral blood flow was also measured in corresponding normoglycemic and drug-free control groups. Cerebral blood flow was 51% higher in untreated hypoglycemic than in untreated normoglycemic rats (P < 0.01). Caffeine had a small, statistically insignificant effect on CBF in normoglycemic rats, but reduced the CBF response to hypoglycemia in a dose-dependent manner, i.e., 27% increase with 10 mg/kg and complete elimination with 20 mg/kg. Chemical determinations by HPLC in extracts of freeze-blown brains showed significant increases in the levels of adenosine and its degradation products, inosine and hypoxanthine, during hypoglycemia (P < 0.05). Intracisternal glibenclamide had little effect on CBF in normoglycemia, but, like caffeine, produced dose-dependent reductions in the magnitude of the increases in CBF during hypoglycemia, i.e., +66% with glibenclamide-free artificial CSF administration, +25% with 1 mumol/L glibenclamide, and almost complete blockade (+5%) with 2 mumol/L glibenclamide. These results suggest that adenosine and KATP channels may play a role in the increases in CBF during hypoglycemia.

Middle cerebral artery (MCA) aneurysms often have unfavorable anatomical characteristics preventing successful endovascular occlusion. We reviewed the outcomes of our series of endosaccular embolization of MCA aneurysms using bare platinum coils, angiographic images, and medical records. Immediate and follow-up angiographic results were categorized as complete occlusion, residual neck, and residual flow. Follow-up angiographic changes were categorized as unchanged, minor or major recurrence, and progressive thrombosis. Between December 2001 and August 2007, 112 patients with 113 MCA aneurysms underwent endovascular treatment, of whom 60 presented with subarachnoid hemorrhage (SAH) due to MCA aneurysm rupture. Immediate angiographic outcomes for 103 aneurysms revealed complete occlusion in 64, residual neck in 21, residual flow in 18, and failed embolization in 10. Follow-up angiography of 70 aneurysms demonstrated 41 unchanged, 10 minor recurrences, 12 major recurrences, 7 progressive thromboses, and no bleeding of coil embolized aneurysms. Outcomes of 58 SAH patients treated endovascularly revealed 45 good recovery and moderate disability, 10 severe disability or persistent vegetative state, and 3 deaths. Forty-four of the 45 patients with unruptured aneurysms treated endovascularly had no changes in their neurological status. One of 5 patients with complications had permanent morbidity. For patients with MCA aneurysms suitable for endovascular surgery, bare platinum coil embolization can be performed with acceptable low morbidity and mortality rates, with a lower risk of postprocedural aneurysmal bleeding.