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The spread of human immunodeficiency virus(HIV)infection may result in an increased likelihood of surgery in patients with HIV infection. We treated a patient with intracranial malignant lymphoma associated with acquired immunodeficiency syndrome(AIDS)caused by HIV infection. The recommendations of the countermeasure manual for AIDS were followed. Only surgical staff without finger injury or inflammation were permitted to be involved in the operation. All staff were dressed in a waterproof, full-body surgical gown, and wore double gloves, double foot covers, and an N95 mask. The surgery could be performed safely with such infection control measures. Histological examination revealed a diffuse large B-cell lymphoma. The patient was referred to the Division of Infectious Diseases and Respiratory Medicine for chemotherapy.

Cotton surgical patties are essential to control vessel bleeding. However, conventional cotton surgical patties tend to adhere to vessels through capillary action, especially when used in combination with hemostats. Consequently, after the bleeding is controlled, rebleeding often tends to occur after removal of the adhered cotton patty. Polyester film－coated non－woven fabric has replaced conventional gauze for the protection of burn wounds, because this material does not tend to adhere to the wound but retains the same capacity to absorb fluid discharges from the wound. We describe our manufacture of a new type of polyurethane－coated surgical patty, which was evaluated for its bleeding control when used in conjunction with a hemostat and for undesirable vessel adherence. Our newly developed surgical patty is made of 100％ cotton, with only the contact surface coated with polyurethane. The coated side contains many holes, so aspiration through the surgical patty is possible from both sides. For our evaluation, we used a surgical patty with or without polyurethane coating together with a gelatinous sponge for bleeding control in the sagittal sinus, with fibrin glue－soaked oxidized cellulose cotton for bleeding control in the cavernous sinus, and with a collagen sheet for bleeding control in brain capillary vessels, in 5 patients for each use. We found that the newly developed surgical patty could be removed from the hemostat and vessels without difficulty and rebleeding was not observed. The new polyurethane－coated surgical patties appear to be more effective for vessel bleeding control when used with several types of hemostats in different applications and at different locations as compared to conventional non－coated surgical patties. （Received December 26, 2013；accepted February 4, 2014）

We here describe the first case of a ruptured aneurysm located at a collateral artery that extended from the proximal A2 segment to the M1 segment, which was associated with an anomalous branch of the anterior choroidal artery and middle cerebral artery (MCA) hypoplasia. The aneurysm was revealed by angiograms and intraoperative findings. No previous accounts have been published of such an extremely rare vessel anomaly. In practice, this case highlights the urgent need to preoperatively recognize such vascular anomalies, as well as to better understand the collateral blood supply in cerebral ischemia associated with these MCA anomalies. Such knowledge will be helpful for planning optimal surgical procedures.

Objective The aim of the present study was to investigate factors associated with the development of ventriculomegaly suggestive of hydrocephalus (VSOH) after decompressive craniectomy with hematoma evacuation for hemispheric hypertensive intracerebral hemorrhage. Methods This study focused on 21 patients who underwent decompressive craniectomy with hematoma evacuation for hemispheric hypertensive intracerebral hemorrhage. The patients' clinical and radiological findings were retrospectively reviewed. Results Eleven patients were male and ten were female, with an age range from 22 to 75 years (mean, 56.6 years). The preoperative Glasgow Coma Scale score ranged from 3 to 13 (mean, 6.9). Hematoma volumes ranged from 33.4 to 98.1ml (mean, 74.2ml). Hematoma locations were the basal ganglia in 10 patients and the subcortex in 11 patients. The presence of intraventricular hemorrhage was significantly associated with the development of VSOH ( P =0.023). The distance of the decompressive defect to the midline and the presence of meningitis showed a strong trend for association with VSOH ( P =0.051, P =0.090, respectively). Conclusion Careful attention should be paid to the occurrence of VSOH after decompressive craniectomy with hematoma evacuation in intracerebral hemorrhage patients with intraventricular extension, meningitis, and/or a short distance of the decompressive defect to the midline.

Objective Hydrogen selectively reduces hydroxyl radicals and peroxynitrite, and numerous experimental and clinical studies suggest that hydrogen can exert potent cellular protective effects against a wide variety of diseases. Furthermore, there is increasing evidence that antioxidants can modulate platelet activation. The aim of the present study was to investigate the relationship between hydrogen and collagen-induced platelet aggregation. Methods For human ex vivo studies, we collected blood samples from six healthy humans and added normal saline or hydrogen-rich saline to blood and platelet-rich plasma. We found that collagen (1 µg/mL)-induced platelet aggregation was significantly inhibited by hydrogen-rich saline compared with a normal saline group (p=0.044). For rat in vivo studies, animals (n=17) were exposed to either nitrogen-based mixed gas with hydrogen (H2 gas group; n=9) or without hydrogen (non-H2 gas group; n=8). Additionally, another animals (n=13) administered either normal (NS group; n=7) or hydrogen-rich saline (HS group; n=6) (5 ml/kg) via intravenous infusion. Blood samples were drawn from the vena cava before treatment and from the right ventricle after treatment. Collagen (12 µg/mL)-induced platelet aggregation was then measured. Results Collagen-induced platelet aggregation was significantly decreased in H2 gas and HS group rats (p=0.042, 0.018, respectively), while there was no difference in non-H2 gas and NS group rats before and after treatment. Conclusion In summary, these data suggest that hydrogen may inhibit collagen-induced platelet aggregation.

A 58-year-old woman with refractory hypertension presented with subarachnoid hemorrhage. Digital subtraction angiography and three-dimensional computed tomography (CT) angiography revealed a ruptured left vertebral artery (VA) aneurysm and an unruptured left middle cerebral artery (MCA) aneurysm. The patient successfully underwent neck clipping of the left VA aneurysm. However, CT obtained just after the operation showed an asymptomatic cerebral infarction along the distribution of medial striate arteries of the right anterior cerebral artery in the caudate nucleus. The pathogenesis of the infarction was unknown. Before clipping surgery of the left MCA aneurysm, detailed examinations to find the cause of her refractory hypertension were performed. Laboratory tests revealed plasma serum level of norepinephrine at 15,521 pg/ml (normal range 100-450 pg/ml). Abdominal magnetic resonance imaging revealed a pheochromocytoma in the right adrenal gland. After preoperative management of the pheochromocytoma, the neck of the left MCA aneurysm was successfully clipped. When the patient awakened from anesthesia, she noticed right hemiparesis and motor aphasia. CT showed cerebral infarction along the distribution of lenticulostriate arteries of the left MCA in the putamen. Her symptoms gradually improved, and the pheochromocytoma was removed by laparoscopic surgery. Sustained severe hypertension and depletion of blood volume resulting from excess catecholamine release from the pheochromocytoma may have caused the complications. Hypervolemic fluid infusion and maintenance of normotensive blood pressure during surgery may avoid such ischemic events.

Chronic subdural hematomas (SDHs) associated with non-operated moyamoya disease are extremely rare. A 68-year-old woman underwent burr-hole surgery for a right SDH, which resolved completely. On day 3, however, the patient suffered cerebral infarction in the right parietal lobe. Cerebral angiography demonstrated total occlusion of the bilateral internal carotid arteries with transdural anastomoses via branches of the right occipital artery and middle meningeal artery, feeding the left parietal cortex. A branch of the right middle meningeal artery passed near the burr hole, but was preserved. The patient was diagnosed of moyamoya disease. We thought that the main cause of chronic SDH might be the disruption of transdural anastomoses. Furthermore, we also hypothesized that we might have coagulated the small vessels of the transdural anastomoses which were undetectable by postoperative angiography, and that cerebral infarction might occur.

Hypertrophic pachymeningitis is an uncommon disorder that causes a localized or diffuse thickening of the dura mater. Recently, the possibility that IgG4-related sclerosing disease may underlie some cases of intracranial hypertrophic pachymeningitis has been suggested. We herein report the tenth case of IgG4-related intracranial hypertrophic pachymeningitis and review the previous literature. A 45-year-old male presented with left-sided focal seizures with generalization. Magnetic resonance imaging (MRI) revealed a diffuse thickening and enhancement of the right convexity dura matter and falx with focal nodularity. The surgically resected specimens exhibited the proliferation of fibroblast-like spindle cells and an infiltration of mononuclear cells, including predominantly plasma cells. The ratio of IgG4-positive plasma cells to the overall IgG-positive cells was 45% in the area containing the highest infiltration of plasma cells. On the basis of the above findings, IgG4-related sclerosing disease arising from the dura mater was suspected. IgG4-related sclerosing disease should be added to the pachymeningitis spectrum.

Objectives: It has been reported that near-infrared (NIR) laser irradiation is effective in cerebral ischemia. We examined the effect of 808 nm laser diode irradiation on CBF in mice. The potential of NIR laser irradiation in the treatment of cerebral ischemia was also investigated.Methods: Male C57BL/6J mice were used. An 808 nm CW diode laser was applied to the hemisphere transcranially. CBF was measured with a non-contact laser Doppler blood perfusion imager. We measured directly nitric oxide in the brain tissue during NIR laser irradiation. To confirm the effect of pretreatment by NIR laser irradiation, we conducted the 1.6 W/cm2 NIR laser irradiation to the hemisphere transcranially for 30 minutes before bilateral common carotid artery occlusion (BCCAO). The control mice were also subjected to BCCAO without pretreatment by NIR laser irradiation.Results: Transcranial NIR laser irradiation increased local CBF by 30% compared to control value in mice. NIR laser irradiation also provoked a significant increase in cerebral NO concentration. Pretreatment by NIR laser irradiation improved residual CBF following bilateral carotid occlusion in mice.Conclusions: Our data suggest that targeted increase of CBF is available by NIR laser irradiation and it is concerned in NOS activity and NO concentration. Besides, NIR laser irradiation may have a protective effect for transient ischemia.

Transduction of the suicide gene of Herpes simplex virus thymidine kinase (Hsv-tk) into glioma cells or neural stem cells combined with pro-drug ganciclovir (GCV) treatment has been effective to treat experimental glioma in the rat through the bystander effect. Bone marrow stromal cells (MSCs) in the adult bone marrow have tropism for brain tumors and act as tumor stromal cells. Whether adult MSCs expressing Hsv-tk can also act as effector cells of the bystander killing effect on murine glioma cells was investigated. In vitro study of co-culture between 9L/LacZ (9L) glioma cells and Hsv-tk-transduced MSCs (MSCs/tk(+)) followed by GCV administration in the culture medium resulted in apparent nuclear morphological changes in the 9L glioma cells surrounding the MSCs/tk(+). 9L glioma cell survival in the presence of MSCs/tk(+) and GCV treatment was quantitatively measured and showed significant decrease of 9L glioma cell proliferation with higher MSCs/tk(+) ratio and GCV concentration. Intracerebral co-inoculation experiments in Fisher rats used 9L glioma cells and either MSCs/tk(+) or Hsv-tk-non-transduced MSCs (MSCs/tk(-)) followed by intraperitoneal injection of GCV (100 mg/kg, daily for 7 days). The animals co-inoculated with 9L glioma cells and MSCs/tk(+) showed significant retardation of tumor growth and prolongation of survival time compared with the animals with 9L glioma cells and MSCs/tk(-). Quantitative findings were established of the novel effects of adult MSCs/tk(+) as effector cells of the bystander killing effect on glioma cells.

We report 2 pregnant women with intracerebral hemorrhage. Patient 1 was a 26-year-old woman who presented with headache and consciousness disturbance. She was initially diagnosed with eclampsia. A Cesarean section was performed, but she subsequently developed left hemiparesis, and the disturbance of consciousness deteriorated; she was hence transferred to our hospital. A computed tomography (CT) scan revealed massive intracerebral hemorrhage at the right cerebral hemisphere. She could not be saved. Patient 2 was a 34-year-old woman who presented with headache. A neurological examination revealed disturbed consciousness and left hemiparesis. A CT scan showed intracerebral hemorrhage in the right frontal lobe. Magnetic resonance imaging (MRI) indicated posterior reversible encephalopathy syndrome (PRES). On the day after Cesarean section, the intracerebral hematoma was evacuated. Aggregated abnormal vessels were identified at the base of the hematoma cavity. The histopathological examination revealed that the lesion was an arteriovenous malformation. The association of pregnancy and stroke is rare, and it is difficult to distinguish between eclampsia and stroke-induced consciousness disturbance in pregnant women. Intracerebral hemorrhage in a pregnant woman may lead to serious consequences for both the mother and baby. We emphasize that immediate, appropriate diagnosis and treatment of intracerebral hemorrhage in a pregnant woman are crucial to save invaluable lives.

A 74-year-old man presented with subarachnoid hemorrhage (SAH) and underwent neck clipping of a left middle cerebral artery (MCA) aneurysm 10 years ago. This patient presented with SAH again due to rupture of a de novo aneurysm of the anterior communicating artery (A-com. aneurysm). The A-com. aneurysm was clipped successfully. The “old” left MCA aneurysm was then inspected. A collapsed “old” aneurysmal dome and a previously applied clip were identified. The “old” aneurysmal dome was resected for histopathological examination. The wall of this aneurysmal dome varied in thickness and consisted of a thin layer of fibrous connective tissue. Fibroblasts were scattered in the aneurysmal wall and either the muscular layer or internal elastic lamina was absent. The aneurysmal dome collapsed to a certain degree, but the lumen of the dome was completely intact. In addition, neovascularization of microcapillaries was observed both inside and outside the aneurysmal dome. Some of these microcapillaries were filled with fresh erythrocytes. Thus the aneurysmal wall was apparently “vigorous.” The previous orifice of the aneurysm did not fuse together at all and could be opened widely with ease during preparation for histopathologic examination. We speculated that the clipped aneurysmal dome survived for 10 years for the following reasons: 1) Although the mechanism of neovascularization of the microcapillaries is unclear, the clipped aneurysmal dome may have obtained nourishment from the microcapillaries. 2) The cerebrospinal fluid may have incubated the dome and provided optimal circumstances for its survival. Considering the radical cure for ruptured cerebral aneurysms by neck clipping or coil embolization, the findings described in this report will be valuable for neurosurgeons and neurointerventionists. Regardless of the time since treatment, ruptured aneurysms treated by either neck clipping and/or coil embolization are at risk of recurrent subarachnoid hemorrhage when the blood re-enters the aneurysms in cases such as clip slip-off or coil compaction.

The vasodilatory effect of intra-cisternal infusion of magnesium sulfate solution was evaluated in 10 patients with symptomatic vasospasm after aneurysmal subarachnoid hemorrhage (SAH) who underwent early clipping surgery. Cisternal drainage was installed in the prepontine and/or sylvian fissures. Carotid angiography was performed immediately after the onset of symptomatic vasospasm, then intra-cisternal infusion of 15 mmol/l magnesium sulfate in Ringer solution was started at 20 ml/hr and continued until day 14. Irrigation was performed from the cisternal tube (inlet) to the spinal drainage (outlet). The cerebrospinal fluid magnesium ion concentration (1.2 +/- 0.2 mEq/l) significantly increased after the infusion therapy (6.0 +/- 1.7 mEq/l, p0.001). Repeat angiography showed vasodilatory effect on the spastic cerebral arteries at 3 hours after the infusion, especially in the arteries near to the site of cisternal drainage placement. The magnesium infusion also caused decreased mean arterial blood velocity in the spastic arteries in 6 of the 7 measured patients (162 +/- 38 cm/sec to 114 +/- 42 cm/sec, p0.001). Finally, 5 of the 10 patients achieved good recovery, 1 patient had moderate disability, 1 patient became severely disabled due to meningitis, and 3 patients were vegetative or dead, due to failure of magnesium irrigation in 1 patient and advanced age in the other 2 (more than 80 years old). This preliminary study indicates that intra-cisternal infusion of magnesium sulfate solution has vasodilatory effect on the spastic cerebral arteries after aneurysmal SAH.

Cerebral salt wasting syndrome (CSWS) is defined as the renal loss of sodium associated with intracranial diseases (e.g., aneurysmal subarachnoid hemorrhage [SAH]) that leads to hyponatremia and decreased extracellular fluid volume. CSWS increases the risk of symptomatic vasospasm (SVS) in SAH patients. To prevent SVS, CSWS was managed by administering physiological saline and sodium chloride so as to maintain a positive water balance and serum sodium level of >140 mEq/l. The study population comprised 115 patients; the above-mentioned treatment was administered just after surgery, which was performed within 72 h after SAH. SVS occurred in 7 patients (6.09%): 5 (4.35%) presented with permanent deficits and 2 (1.74%) with transient deficits. Further, SVS occurred within a week in 6 of these patients. On Day 2, the accumulative water balance was significantly higher in the non-SVS group than in the SVS group; the water balance tended to decline in the SVS group for a few days. Until Day 6, the amount of sodium chloride administered to maintain the serum sodium level to >140 mEq/l was higher in the SVS group than in the non-SVS group. However, on Days 3-5, the serum sodium level was lower in the SVS group than in the non-SVS group. The use of physiological saline and sodium chloride therapy to maintain a positive accumulated water balance and control the serum sodium level in the management of CSWS, especially within the initial 7 days after SAH, can effectively prevent SVS.

Pilomyxoid astrocytomas have been identified as a variant of pilocytic astrocytoma. They are listed as a novel clinico-pathological entity in the 2007 World Health Organisation (WHO) classification of tumours of the central nervous system. This tumour corresponds to a WHO grade II neoplasm whereas pilocytic astrocytoma corresponds to WHO grade I. We have encountered an infratentorial tumour with pilomyxoid features in an adult. A 25 year old man presented with tinnitus and hyperacusis. Brain MRI revealed a mass occupying the fourth ventricle. We performed partial resection, but no adjuvant therapy was given. The staining index for the anti-Ki-67 monoclonal antibody MIB-1 was less than 1% in this patient. Pilomyxoid astrocytomas are not limited to the hypothalamic/chiasmatic region in children. Additional knowledge and recognition of this entity is necessary to improve treatment of pilomyxoid astrocytoma.

A 61-year-old male presented with a recurrent solitary fibrous tumor (SFT) arising from the falx cerebri with intraventricular extension manifesting as nausea and vomiting. Magnetic resonance imaging showed the heterogeneously enhanced tumor in the falx, which extended to the bilateral lateral ventricles and the third ventricle. Total tumor removal was performed via the bifrontal interhemispheric approach. Histological examination showed mostly spindle cells with rich intercellular fibers. Immunohistochemical examination showed strong staining for CD34 in the cytoplasm but no staining for epithelial membrane antigen. Reexamination of the two previous tumor specimens, previously identified as fibrous meningioma, found SFT. The differential diagnosis of SFT in the central nervous system from fibrous meningioma and hemangiopericytoma requires immunohistochemistry and electron microscopy.

Intravenous tissue plasminogen activator (IVtPA) is effective for the treatment of acute stroke. Although IVtPA is easily administered and is effective in many cases, the clinical condition of some patients can worsen after the initiation of thrombolytic therapy due to sustained cerebrovascular insufficiency. In such cases, several additional treatment options to re-establish cerebral perfusion are available, including superficial temporal artery to middle cerebral artery bypass. However, it is recommended that invasive procedures should be avoided soon after IVtPA administration because tPA is believed to exert prolonged fibrinolytic effects may continue for more than 24 hours. We described three cases of emergency superficial temporal artery to middle cerebral artery bypass performed within 24 hours of IVtPA administration, and discussed the safety of such procedures. We believe that superficial temporal artery to middle cerebral artery bypass can be safely performed even within 24 hours after IVtPA administration.

BACKGROUND We report a case of infratentorial arteriovenous malformation (AVM) associated with persistent primitive hypoglossal artery (PPHA). To our knowledge, this is the second reported case of these combined anomalies in the English literature. We discuss the embryological relationship between these two congenital vascular anomalies. CASE DESCRIPTION An 18-year-old girl, who suddenly developed severe headache and vomiting followed by loss of consciousness, was admitted to our hospital. A computed tomography scan showed intracerebellar hemorrhage with obstructive hydrocephalus. Digital subtraction angiography revealed an AVM in the left cerebellar hemisphere and an ipsilateral PPHA. After the intracranial pressure was stabilized, the AVM was surgically removed. AVMs develop during the 4(th) to 8(th) week of embryonic life. In contrast, carotid-basilar anastomoses (CBAs) including primitive hypoglossal arteries appear and close spontaneously by the 6(th) week of embryonic life. Thus, AVMs precede CBAs, and a large amount of blood flows into the adjoining AVM via ipsilateral CBAs. As a result, spontaneous closure of a CBA may be disturbed. CONCLUSION We speculate that coexistence of infratentorial AVMs and ipsilateral CBAs is not incidental but inevitable.

A previously healthy 34-year-old woman and a previously healthy 35-year-old woman with spontaneous intracranial hypotension (SIH) presented within 1 week of the onset of symptoms. Brain magnetic resonance (MR) imaging with gadolinium demonstrated no abnormality, whereas spinal MR imaging revealed extradural fluid collection in both patients. Both patients were treated conservatively with bed rest and intravenous hydration. Their symptoms almost completely resolved. We suggest that spinal MR imaging findings of extradural fluid collection can help to establish the early diagnosis of SIH.

We herein describe a patient with symptomatic common carotid artery occlusion who underwent a reverse superficial temporal artery (STA)-middle cerebral artery (MCA) single bypass using a naturally formed "bonnet" STA. The surgical procedure was performed without difficulty, and no further neurological deterioration was observed after surgery. In practice, this case highlights that the reverse STA-MCA bypass can be achieved safely and less invasively using a naturally formed "bonnet" STA.

A metastatic brain tumor originating from esophageal carcinoma is very rare, accounting for only about 2% of all intracranial metastatic tumors. We review three cases of metastatic brain tumor from esophageal carcinoma and present one interesting case. A 60-year-old man was referred to our hospital with aphasia, 3 years after surgery for esophageal carcinoma. Magnetic resonance imaging demonstrated a 7-cm mass lesion with a cystic component in the left temporal lobe. Tumor resection was performed and an Ommaya reservoir system was placed. Histological analysis indicated squamous cell carcinoma, and metastatic brain tumor from esophageal carcinoma was diagnosed. After surgery, the cystic component was collapsed by drainage through the Ommaya reservoir, and cyberknife therapy was performed as an adjunctive therapy. Regrowth of the cystic component and exacerbation of cognitive dysfunction were identified 2 months later, so aspiration of cyst fluid through the Ommaya reservoir was continued. However, the cystic component regrew 5 months after the operation, and the patient died 1 month later. Metastatic brain tumors from primary esophageal carcinoma often have a cystic component, which makes treatment difficult. Control of cyst growth by aspiration using the Ommaya reservoir is effective for improvement of functional prognosis in such patients.

Symptomatic cervical carotid artery stenosis is one of the common causes of ischemic stroke in octogenarians. The records for 90 consecutive patients with symptomatic cervical carotid artery stenosis treated by carotid endarterectomy(CEA)were analyzed retrospectively. The patients were divided into two groups:21 patients aged 80 years or over and 69 patients aged less than 80 years. CT angiography revealed that ulcer formation was significantly more common and the length of carotid artery stenosis was significantly greater in the octogenarians. Histological examination of the plaque revealed no significant difference between the two groups in terms of ulcer formation, lipid content, and intraplaque hemorrhage. However, all three of these pathological findings were present in a significantly higher number of octogenarians. No significant difference was observed for new ischemic lesions on diffusion-weighted MR imaging, neurological complications, or cardiac and pulmonary complications. However, treatment with an albumin preparation and loop diuretics was significantly more common in octogenarians after CEA. The present study suggests that with careful postoperative management CEA can be safely performed in symptomatic patients aged 80 years or over with almost the same risk as that for patients aged less than 80 years.

Several animal subarachnoid hemorrhage (SAH) models have been proposed for the investigation of cerebral vasospasm. We describe the experimental procedures of a canine double-SAH model and also examine the model based on the canine physiological parameters and occurrence of angiographic delayed cerebral vasospasm using magnetic resonance (MR) imaging and digital subtraction angiography. Autologous blood was injected twice on days 1 and 3 in 36 beagles. All animals showed delayed angiographic vasospasm in the vertebrobasilar arteries on day 7. The degree of vasospasm was 29-42 % of the arterial caliber. MR imaging did not show any ischemic change. This animal model can produce definite delayed vasospasm without detectable cerebral infarction on MR imaging. The canine SAH model is suitable for the quantitative and chronological study of delayed angiographic vasospasm, but not for investigating early brain injury and delayed cerebral ischemia.

An 81-year-old man presented with poor visual acuity of the left eye, swelling of the left eyelid, and elevation of the left intraocular pressure after contusion of the left palpebral portion. CT revealed left ocular proptosis and left intraorbital hematoma. Traumatic optic neuropathy was suspected, and emergent optic nerve decompression was performed through extradural anterior clinoidectomy followed by optic canal release. Postoperatively, his left visual acuity was markedly improved and the elevated intraocular pressure decreased. Postoperative CT demonstrated improvement of the left ocular proptosis and decompression of the optic nerve. Emergent optic canal release has been recommended in patients who have suffered visual dysfunction caused by optic canal fracture or intraorbital hematoma. The advantages of extradural anterior clinoidectomy followed by optic canal release include a shorter surgical route and easy identification of the optic nerve, resulting in fewer surgical complications. In addition, this procedure can achieve intraorbital decompression. We recommend extradural anterior clinoidectomy followed by optic canal release as a safe and reliable procedure for optic nerve decompression in patients with traumatic optic neuropathy.

Surgical treatment of paraclinoid tumors adjacent to important anatomical structures, such as the optic nerve, optic chiasm, pituitary stalk, and internal carotid artery, should emphasize maximum resection and preservation of visual function. Thus, early localization and exposure of the optic nerve, and complete mobilization and decompression of the optic nerve and internal carotid artery, are necessary in order to prevent intraoperative neurovascular injuries. However, this technique requires wide exposure of the optic-carotid space through the interpeduncular cistern. We have developed an extradural temporopolar approach for resection of paraclinoid tumors, which can also allow early devascularization of arteries that feed the tumors. We evaluated the surgical outcomes of this approach, paying special attention to clinical and visual outcomes.Thirteen patients(4 men, 9 women;24-78 years, mean age 54 years), underwent tumor removal using an extradural temporopolar approach between March 2000 and April 2013. We retrospectively reviewed medical charts, radiological findings, intensive care unit flow sheets, and surgical records.Histological diagnoses included craniopharyngioma(4 cases), pituitary adenoma(3 cases), medial sphenoid ridge meningioma(2 cases), tuberculum sellae meningioma(2 cases), trigeminal neurinoma(1 case), and malignant epidermoid(1 case). Tumors were 1.5-6.0cm in length(mean 3.2cm). Tumors were cystic in all 4 craniopharyngiomas and solid in the other 9 cases. Preoperative neurological deficits included visual disturbance in 10 patients, double vision caused by oculomotor nerve palsy in 2 patients, and vertigo in 1 patient. Additional orbitozygomatic craniotomies were performed in 8 patients. Total tumor removal was performed in 7 patients and subtotal removal performed in 6. The pituitary stalk was microscopically preserved in all patients. Postoperative complications included transient diabetes insipidus in 2 patients, chronic subdural hematoma in 1 patient, and abducens palsy in 1 patient. All complications were completely resolved. Surgical outcomes on discharge were recorded as follows:good recovery(11 patients), moderate disability(1 patient), and severe disability(1 patient, who suffered preoperative consciousness disturbance). Visual outcomes were improved in 7 patients, unchanged in 5, and worsened in 1, with recurrence.The present extradural temporopolar approach, which allows early decompression of the optic nerve, and early devascularization and detachment of the tumor, may lead to greater tumor resection and improved visual outcomes in patients with paraclinoid tumors.

Background The failures of recent studies intended to prevent cerebral vasospasm have moved the focus of research into delayed cerebral ischemia away from cerebral artery constriction towards other mechanisms. Recent accumulating evidence has suggested that early brain injury is also involved in the development of delayed cerebral ischemia, and that hydrogen can prevent early brain injury. Therefore, we have established a combination therapy of intravenous hydrogen infusion and intra-cisternal magnesium sulfate infusion for the treatment of both early brain injury and cerebral vasospasm. The present randomized controlled clinical trial is designed to investigate the effects of this novel therapeutic strategy on the occurrence of cerebral vasospasm, delayed cerebral ischemia, and clinical outcomes after high-grade subarachnoid hemorrhage. Methods This study is a randomized, double-blind, placebo-controlled design to be conducted in two hospitals. A total of 450 patients with high-grade subarachnoid hemorrhage will be randomized to one of three arms: (i) Mg + H2 group, (ii) Mg group, and (iii) control group. Patients who are assigned to the Mg + H2 group will receive intra-cisternal magnesium sulfate infusion (2.5 mmol/L) at 20 mL/h for 14 days and intravenous hydrogen-rich fluid infusion (200 mL) twice a day for 14 days. Patients who are assigned to the Mg group will receive intra-cisternal magnesium sulfate infusion (2.5 mmol/L) at 20 mL/h for 14 days and intravenous normal glucose-electrolyte solution (200 mL) without added hydrogen twice a day for 14 days. Patients who are assigned to the control group will receive intra-cisternal Ringer solution without magnesium sulfate at 20 mL/h for 14 days and intravenous normal glucose-electrolyte solution (200 mL) without added hydrogen twice a day for 14 days. Primary outcome measures will be occurrence of delayed cerebral ischemia and cerebral vasospasm. Secondary outcome measures will be modified Rankin scale score at 3, 6, and 12 months and biochemical markers. Discussion The present protocol for a randomized, placebo-controlled study of intravenous hydrogen therapy with intra-cisternal magnesium infusion is expected to establish the efficacy and safety of this therapeutic strategy. Trial registration UMIN-CTR: UMIN000014696

Several animal subarachnoid hemorrhage (SAH) models have been proposed for the investigation of cerebral vasospasm. We describe the experimental procedures of a canine double-SAH model and also examine the model based on the canine physiological parameters and occurrence of angiographic delayed cerebral vasospasm using magnetic resonance (MR) imaging and digital subtraction angiography. Autologous blood was injected twice on days 1 and 3 in 36 beagles. All animals showed delayed angiographic vasospasm in the vertebrobasilar arteries on day 7. The degree of vasospasm was 29–42 % of the arterial caliber. MR imaging did not show any ischemic change. This animal model can produce definite delayed vasospasm without detectable cerebral infarction on MR imaging. The canine SAH model is suitable for the quantitative and chronological study of delayed angiographic vasospasm, but not for investigating early brain injury and delayed cerebral ischemia.

A 53-year-old man presented with a choroid plexus carcinoma in the body of the right lateral ventricle manifesting as gait disturbance due to left mild hemiparesis and papilledema. Subtotal removal of the tumor was performed. Histological examination revealed well-differentiated papillary adenocarcinoma. Immunohistochemical examination showed intense reactivity for carbohydrate antigen 19-9 (CA19-9). The serum level of CA19-9 was significantly high, but decreased rapidly after radiation therapy. Systemic examinations found no malignancy in other organs. This second case of choroid plexus carcinoma producing CA19-9 indicates that CA19-9 may be a useful marker of choroid plexus carcinoma.

Background: Adiponectin is a hormone secreted exclusively by adipose tissue, and is important in the regulation of tissue inflammation and insulin sensitivity. Adiponectin exerts its effects through two cell-surface receptors: Adiponectin receptor 1 (ADR1) and ADR2. However, the relationship between ADR1/2 expression and progression of atherosclerosis or plaque vulnerability remains unclear. Aims: To investigate the relationship between ADR1/2 expression and plaque characteristics in patients with carotid artery atherosclerosis. Materials and Methods: Forty-three patients who underwent carotid endarterectomy for treatment of carotid artery stenosis were reviewed. Immunohistochemical staining for ADR1 and ADR2 was performed in the specimens of carotid plaque. The relationships between ADR1/2 expression and clinical characteristics were analyzed statistically. Results: Plaque was stable in 7 patients and vulnerable in 36 patients. ADR1 expression was considered weak in 29 patients and strong in 14 patients. The formation of vulnerable plaques was significantly correlated with weak ADR1 expression (P < 0.003). ADR2 expression was considered weak in 14 patients and strong in 29 patients. Rates of formation of vulnerable plaque did not differ between patients with weak and strong ADR2 expression. Conclusions: Based on previous and the present results, ADR1 may be strongly related to the stabilization of established atherosclerotic plaques via inactivating macrophages. Enhancement of ADR1 expression could serve as a therapeutic target for the prevention of the formation of vulnerable plaque.

Cerebral developmental venous anomalies (DVAs) very rarely cause massive haematoma, but should be included in the differential diagnosis of atypical massive intracerebral haematoma (ICH). We describe a case of massive ICH caused only by a DVA and successfully treated by haematoma evacuation with surgical resection of the DVA.

Adiponectin affects nitric oxide production, and low plasma adiponectin levels are associated with impaired endothelium-dependent vasorelaxation. However, adiponectin pathophysiology in the acute phase after stroke, especially subarachnoid hemorrhage, is not well understood. The present study evaluated the changes in plasma adiponectin concentrations in patients with subarachnoid hemorrhage and investigated the relationship between plasma adiponectin and delayed cerebral ischemia. Serial plasma samples from 27 patients with subarachnoid hemorrhage were obtained on day 0 or 1 after hemorrhage, and days 3, 7, 10, 14, and 21. As a control, plasma samples were obtained from 26 healthy volunteers. Differences between patients with and without delayed cerebral ischemia were assessed to investigate the relationship between plasma adiponectin concentrations and the occurrence of delayed cerebral ischemia. There were no significant differences in the clinical characteristics of patients with and without delayed cerebral ischemia. The plasma adiponectin concentrations were significantly lower in patients on days 3 and 7 compared with controls. Plasma adiponectin concentrations in patients with delayed cerebral ischemia were significantly lower than in those without delayed cerebral ischemia on days 3, 7, 10, and 14. The present results indicate that low plasma adiponectin concentrations from day 3 to day 14 might be associated with the development of delayed cerebral ischemia.

The primary pathology associated with mild -traumatic brain injury (TBI) is selective axonal injury, which may characterize the vast majority of blast-induced TBIs. Axonal injuries in cases of mild TBI have been considered to be the main factors responsible for the long-lasting memory or attentional impairment in affected subjects. Among these axonal injuries, recent attention has been focused on the cingulum bundle (CB). Furthermore, recent studies with diffusion tensor MR imaging have shown the presence of injuries of the CB in cases of mild TBI in humans. This study aimed to provide a better laboratory model of mild TBI.Sprague-Dawley rats were subjected to mild TBI using laser-induced shock waves (LISW) (sham, 0.5 J/cm(2), or 1.0 J/cm(2); n = 4 per group). Bodian-stained brain sections 14 days after LISW at 0.5 J/cm(2) or 1.0 J/cm(2) showed a decrease in the CB axonal density compared with the sham group, whereas there were no differences in the axonal density of the corpus callosum.The present study shows that this model is capable of reproducing the histological changes associated with mild TBI.

Decompressive craniectomy (DC) is an established therapeutic option following severe traumatic brain injury (TBI). However, several delayed complications of DC have been reported, including ventriculomegaly, which can lead to poor patient outcomes. Nevertheless, ventriculomegaly can occur after TBI even without DC. The aim of the present study was to investigate the influence of DC on ventriculomegaly.Adult male Sprague-Dawley rats (300-400 g) were subjected to lateral fluid percussion injury using a fluid percussion device. Rats were randomly divided into four groups: sham, craniectomized without trauma (D group), traumatized without DC (FPI group), and craniectomized immediately after trauma (FPI + D group). On day 28 of recovery, ventricular volumes were measured by image analysis.There was no significant difference in ventricular size between the sham group and the D group animals or between the FPI group and the FPI + D group animals.These data suggest that DC may not be a risk factor for ventriculomegaly after TBI.

Adiponectin, a circulating adipose-derived hormone regulating inflammation and energy metabolism, has beneficial actions on cardiovascular disorders. Recent studies have suggested that adiponectin might be a potential molecular target for ischemic stroke therapy; however, little is known about the effects of adiponectin on traumatic brain injury. The present study examined the immunoactivity of adiponectin.Adult male Sprague-Dawley rats were subjected to lateral fluid percussion injury using the Dragonfly device. Immuno-histochemical studies showed that the adiponectin expression was increased in the cerebral cortex at 24 h after injury and in the hippocampus at 72 h after injury. Our findings suggest that adiponectin might participate in the pathophysiological process occurring after traumatic brain injury.

It is well known that patients with poor-grade aneurysmal subarachnoid hemorrhage (SAH) have poor outcomes owing to significant mass effect and brain stem compression. On the other hand, decompressive craniectomy (DC) has shown efficacy in reducing morbidity and mortality in patients with intracranial hypertension. Here, we study the efficacy of DC in poor-grade SAH with attention to surgical outcome. A total of 38 consecutive patients with poor-grade SAH was treated in our hospital between 1 August 2005 and 30 July 2010. Among these 38 patients, we involved 15 patients with DC in the present study. We retrospectively reviewed medical charts and radiological findings. Glasgow Outcome Scale score on discharge showed good response in 1 (6.7 %), moderate disability in 6 (40.0 %), severe disability in 4 (28.1 %), vegetative state in 2 (1.3 %), and death in 2 (13.3 %). In particular, 3 grade IV patients (50.0 %) had a favorable outcome. Recent several experimental studies also indicated that DC significantly improves outcome owing to increased perfusion pressure or reduced intracranial pressure. We suggest that the DC provided the efficacy in reducing mortality in poor-grade SAH patients.

Recent attention has been paid to the -cerebrospinal fluid (CSF) dynamics between the intracranial subarachnoid space (SAS) and the SAS around the optic nerve (ON-SAS). We experienced three patients who had an expanded ON-SAS associated with mass lesions extending into the optic canal, and studied their MRI findings after decompressive surgery. In all three patients, decompressive surgery of the optic canal resulted not only in the disappearance of the expanded ON-SAS, but also in improvement of the visual function. The present study may indicate that normalization of the ON-SAS can be considered to be the achievement of "effective" decompression. Therefore, we suggest that, in patients with an expanded ON-SAS associated with mass lesions, the state of the ON-SAS should be evaluated by pre- and postoperative MRI, in addition to the degree of tumor resection.

Intracerebral hemorrhage (ICH) is a common and often fatal subtype of stroke. Estimation of the stage of hemorrhage allows clinicians to know when the hemorrhage occurred, even in unconscious patients, enabling decisions to be made about the optimal management and treatment strategy. After ICH, oxidative denaturation of the hemoglobin progresses, and deoxyhemoglobin is gradually converted to methemoglobin. MRI has been used to estimate the stage of hemorrhage by evaluating the status of hemoglobin. However, there is currently no bedside device that can be used for the measurement of hemoglobin derivatives in patients with hematomas. The aim of the present study was to investigate the validity of using optical diffuse reflectance spectroscopy (ODRS) for bedside evaluation of the stage of hemorrhage. An ICH model was generated in adult Sprague-Dawley male rats by stereotactically injecting 50 μl of autologous blood into the right caudate nucleus. To analyze the hemoglobin derivatives in the hematomas, ODRS measurement was performed for the rats in vivo. In all rats, we found increased absorption at around 630 nm, which indicated the formation of methemoglobin. In conclusion, the results of the present study suggest that ODRS allows clinicians to more easily evaluate the stage of hemorrhage at the patient's bedside.

The primary pathology associated with mild ­traumatic brain injury (TBI) is selective axonal injury, which may characterize the vast majority of blast-induced TBIs. Axonal injuries in cases of mild TBI have been considered to be the main factors responsible for the long-lasting memory or attentional impairment in affected subjects. Among these axonal injuries, recent attention has been focused on the cingulum bundle (CB). Furthermore, recent studies with diffusion tensor MR imaging have shown the presence of injuries of the CB in cases of mild TBI in humans. This study aimed to provide a better laboratory model of mild TBI.

Objective: Decompressive craniectomy (DC) is an established therapeutic option following severe traumatic brain injury (TBI). However, several delayed complications of DC have been reported, including ventriculomegaly, which can lead to poor patient outcomes. Nevertheless, ventriculomegaly can occur after TBI even without DC. The aim of the present study was to investigate the influence of DC on ventriculomegaly.

Decompressive craniectomy (DC) improves the survivability and functional outcome in patients with malignant hemispheric infarction (MHI). The decompressive effect of DC depends on the decompressive volume (DV). The value of the formulas for estimating DV has not been reported to date. We have investigated the value of the formulas to estimate DV in patients with MHI. We analyzed the head CTs of six patients who underwent DC for MHI. We examined 1/2ABC, 1/3ABC, π/6ABC, and 2/3Sh formulas to determine the formula that gives the closest estimation of DV compared with computer-assisted volumetric analysis (gold standard). The mean volume values of the gold standard, 1/2ABC, 1/3ABC, π/6ABC, and 2/3Sh formulas were 100.2, 102.4, 68.3, 105.2, and 109.2 mL respectively. Spearman's correlation coefficient was assessed for DV obtained by each of the four different formulas relative to the gold standard. These were as follows: 1/2ABC = 0.8095 (p 0.05). In conclusion, the 1/2ABC formula is the most useful and the closest estimation of DV in patients with MHI after DC.

Adiponectin, a circulating adipose-derived hormone regulating inflammation and energy metabolism, has beneficial actions on cardiovascular disorders. Recent studies have suggested that adiponectin might be a potential molecular target for ischemic stroke therapy; however, little is known about the effects of adiponectin on traumatic brain injury. The present study examined the immunoactivity of adiponectin.