Quantitative analysis of the trajectory of simulated basilar apex aneurysms through the internal carotid artery to assess the need for an orbitozygomatic approach.

BACKGROUND: The aim of this study was to identify the correlation between the location of the internal carotid artery (ICA) and the need for an orbitozygomatic approach (OZA) when approaching a basilar apex (BX) aneurysm. MATERIALS AND METHODS: By imaging the virtual trajectory to access the basilar artery (BA) through the ICA, the correlations among the height of the BX, the height and lateral breadth of the bifurcation of the ICA, and the need for removal of the orbital rim or zygomatic arch were investigated using three-dimensional computed tomography angiography (3DCTA) data of approximately 80 random samples not limited to BX aneurysms. Furthermore, the utility of 3D simulation to determine the need for the OZA was verified using data from five patients with BX aneurysms. RESULTS: The height of the bifurcation of the ICA was inversely correlated and the height of the BX was positively correlated with the need for the OZA (both p < 0.017). Among patients undergoing surgery, clipping was successfully performed without the OZA in two patients in whom the distance from the simulated skull point on the extended line from the BX through the bifurcation of the ICA was more than 4 cm from the zygoma and orbital rim. CONCLUSIONS: It is necessary to determine the spatial relationship between the basilar artery and the ICA to decide whether the OZA is needed for surgery. Correlations of the height of the ICA and BX with the need for the OZA were not very strong individually, though they were significant. Therefore, simulation using 3DCTA appears to be important for planning the surgical approach for the treatment of BX aneurysms.

Oblique Clip Technique via Anterior Temporal Approach for Blood Blister Aneurysm of Distal Portion of Internal Carotid Artery.

BACKGROUND: Blood blister aneurysms (BBAs) of the internal carotid artery (ICA) are challenging vascular lesions for neurosurgeons because they are fragile and difficult to clip. They are commonly found at the dorsal wall of the ICA. Trapping is an alternative for these lesions, accompanied by vascular reconstruction. However, they are sometimes close to the posterior communicating artery and anterior choroidal artery. CASE DESCRIPTION: A 30-year-old man presented with subarachnoid hemorrhage caused by rupture of a BBA in the right distal ICA. After construction of a high-flow bypass, the BBA was accessed via the standard pterional approach to end only in proximal clipping. Two weeks later, the remnant of the BBA showed a tendency to grow. Therefore, the anterior temporal approach was successfully used to obliterate the BBA using an oblique clip technique under direct inspection of patency of the perforators. CONCLUSIONS: The anterior temporal approach to a BBA in the distal ICA is amenable to application of the oblique clip technique, which can provide direct inspection of the perforators emanating from the posteromedial wall of the ICA as well as obliteration of the pathologic wall. Furthermore, less retraction of the frontal lobe is also reasonable for avoidance of premature rupture of a fragile BBA.

Antitumor effects of minodronate, a third-generation nitrogen-containing bisphosphonate, in synergy with γδT cells in human glioblastoma in vitro and in vivo.

Nitrogen-containing bisphosphonates (N-BPs), which prevent bone resorption, exert direct and γδT cell (GDT)-mediated antitumor effects against several tumor cell types, including glioblastoma (GBM). However, limited information is available regarding the antitumor effects of N-BPs in GBM. Specifically, the antitumor effects of minodronate (MDA), a third-generation N-BP, in GBM are yet unclear. This study aimed to investigate the antitumor effects of MDA in GBM in vitro and in vivo. We performed growth inhibition and apoptosis detection assays using the GBM cell lines U87MG and U138MG. Apoptosis inhibition assays were also conducted. In vivo xenograft assays were performed in highly immunodeficient NOD.Cg-Prkdc(scid) Il2rg(tm1Sug)/Jic mice subcutaneously implanted with U87MG and U138MG cells. Growth inhibition and apoptosis detection assays demonstrated that MDA inhibited GBM cell growth via apoptosis, which was markedly enhanced by ex vivo expanded GDT. A pan-caspase inhibitor, z-VAD-fmk, inhibited MDA-induced U138MG apoptosis and MDA/GDT-induced U87MG and U138MG apoptosis. But z-VAD-fmk increased MDA-induced U87MG apoptosis. MDA/GDT-mediated apoptosis was blocked by the anti-T cell receptor (TCR) Vγ9, mevalonate pathway inhibitor, granzyme B inhibitor, and antitumor necrosis factor (TNF)-α. In vivo xenograft assays showed that combined intraperitoneal administration of MDA/GDT induced antitumor effects on unestablished U87MG-derived subcutaneous tumors. MDA exerted direct and GDT-mediated anti-GBM apoptotic effects in a caspase-dependent manner. GDT recognized MDA-exposed GBM cells via TCRVγ9 and induced apoptosis via granzyme B and TNF-α release. Because MDA elicited anti-GBM effects in synergy with GDT in vivo, a combination of MDA and ex vivo-generated GDT could be an effective treatment in patients with GBM.

Influence of Diabetes Mellitus and Cigarette Smoking on Variability of the Clopidogrel-Induced Antiplatelet Effect and Efficacy of Active Management of the Target P2Y12 Reaction Unit Range in Patients Undergoing Neurointerventional Procedures.

BACKGROUND: Optimal antiplatelet inhibition is essential in patients undergoing neurointerventional procedures; however, variability in response to clopidogrel can contribute to thromboembolic and hemorrhagic complications. The present study evaluated the influence of diabetes mellitus and cigarette smoking on clopidogrel reactivity. METHODS: Between 2011 and 2013, 71 consecutive patients underwent aneurysmal coil embolization (CE) or carotid artery stenting (CAS) and received clopidogrel (75 mg daily) and aspirin (100 mg daily) before the treatment. The patients were divided into 2 groups: CE (n = 31) and CAS (n = 40). The patients underwent prospective assessment of preoperative platelet function using VerifyNow assay and received adjunctive cilostazol (200 mg daily, triple antiplatelet therapy) in case of clopidogrel hyporesponse. Patients with clopidogrel hyper-response underwent clopidogrel dose reduction (clopidogrel, 12.5-50 mg daily). RESULTS: Clopidogrel resistance was noted in 15 patients (37.5%) in the CAS group and in 4 patients (12.9%) in the CE group (P = .031). Clopidogrel hyper-response was noted in 2 patients (5%) in the CAS group and in 11 patients (54.8%) in the CE group (P < .001). There was a significant difference in the baseline clinical characteristics between the 2 groups. In the multivariate logistic regression analysis, diabetes and age were independent predictors of clopidogrel hyporesponse, whereas current smoker was an independent predictor of clopidogrel hyper-response. CONCLUSIONS: Significant differences in baseline clinical characteristics were present when comparing patients undergoing endovascular treatment of unruptured cerebral aneurysms and carotid artery stenosis. Diabetes mellitus and current smoker status were independent factors related to reactivity to clopidogrel.

Glioblastoma Multiforme in the Pineal Region with Leptomeningeal Dissemination and Lumbar Metastasis.

We report a case of a 31-year-old woman with glioblastoma multiforme (GBM) in the pineal region with associated leptomeningeal dissemination and lumbar metastasis. The patient presented with severe headache and vomiting. Magnetic resonance imaging (MRI) of the brain showed a heterogeneously enhanced tumor in the pineal region with obstructive hydrocephalus. After an urgent ventricular-peritoneal shunt, she was treated by subtotal resection and chemotherapy concomitant with radiotherapy. Two months after surgery, MRI showed no changes in the residual tumor but leptomeningeal dissemination surrounding the brainstem. One month later, she exhibited severe lumbago and bilateral leg pain. Thoracico-lumbar MRI showed drop like metastasis in the lumbar region. Finally she died five months after the initial diagnosis. Neurosurgeons should pay attention to GBM in the pineal region, not only as an important differential diagnosis among the pineal tumors, but due to the aggressive features of leptomeningeal dissemination and spinal metastasis.

Visualization of vascular structure of spinal hemangioblastoma using intraoperative indocyanine green videoangiography and temporary feeder occlusion.

BACKGROUND AND PURPOSE: To more safely resect pathological lesions during spinal vascular lesion surgery, it is most important to understand local abnormal hemodynamics in detail. New devices or techniques that make out intraoperative local hemodynamics have been awaited. To introduce a resourceful method, we present a case of spinal hemangioblastoma for which temporary arterial occlusion during near-infrared intraoperative indocyanine green (ICG) videoangiography gives useful assessment of the main and minor feeders easily. METHODS: A 36-year-old female suffered progressive paresthesia of both lower extremities for 12 months and gait disturbance for 2 weeks. A neurological examination revealed T10 myelopathy. Magnetic resonance imaging (MRI) of the thoracic spine showed an intramedullary tumor at the T8 level and severe spinal cord edema with a flow void in the extended dorsal spinal veins. Spinal angiography showed a hemangioblastoma at the T8 level, with two main feeders and minor feeders. RESULTS: She underwent total resection of the tumor by a posterior approach. During the intraoperative ICG videoangiography, temporary arterial occlusion of the two main feeders and FLOW(®)800 analysis enabled clear understanding of the vasculature, especially of the two minor feeders. At the 9-month follow-up, her neurological manifestation was partially resolved, and post-operative MRI showed total removal of the tumor and disappearance of the spinal cord edema. CONCLUSIONS: Temporary clipping of the main feeders during intraoperative ICG videoangiography is very useful for easily determining the minor feeding arteries, and helpful for maintaining normal perfusion of the spinal cord in spinal hemangioblastoma surgery. Furthermore, the FLOW 800 analysis, especially the false color-coded variation, increased our understanding of the hemodynamics.

Rheumatoid arthritis-induced lateral atlantoaxial subluxation with multiple vertebrobasilar infarctions.

STUDY DESIGN: Case report. OBJECTIVE: To highlight the probability that lateral atlantoaxial subluxation (AAS) exists in patients with rheumatoid arthritis (RA) and induces vertebrobasilar infarctions that are more foregrounded than compressive myelopathy. SUMMARY OF BACKGROUND DATA: Although lateral subluxation is a well-known subtype of AAS, a case of cerebral ischemia associated with lateral AAS has not been reported before. METHODS: A 52-year-old male with a 6-year history of RA had a sudden onset of visual field defect and mild right cerebellar ataxia. Head magnetic resonance imaging revealed acute multiple infarctions in the vertebrobasilar area, and magnetic resonance angiography revealed stenosis of the left vertebral artery (VA). Lateral radiograph of the cervical spine in the neutral position revealed atlanto-occipital assimilation and anterior AAS. T2-weighted sagittal images on cervical magnetic resonance imaging revealed high signal intensity in the spinal cord at C1-C2. Cerebral angiography revealed right VA occlusion and severe stenosis of the left V3 segment of VA. Three-dimensional computed tomography angiography of the craniovertebral junction revealed lateral AAS, which was due to severe erosive changes of the facet joints, and the left V3 portion was stenosed by a bony component. During conservative therapy, the patient experienced left occulomotor nerve palsy due to a second stroke. RESULTS: Two months later, the patient underwent occipitocervical posterior fusion with an iliac bone graft. His postoperative course was uneventful, and the left VA stenosis disappeared. At the 45-month follow-up, he had no further infarctions. Bony fusion was radiologically confirmed, and 3-dimensional computed tomography angiography revealed good patency of the affected left VA. CONCLUSION: In patients with RA, the potential risk of AAS should be recognized. Lateral AAS in particular may induce cerebral ischemia by positional VA occlusion in advanced stages of the disease. LEVEL OF EVIDENCE: N/A.

Cervical spinal epidural arteriovenous fistula with coexisting spinal anterior spinal artery aneurysm presenting as subarachnoid hemorrhage--case report.

Hemorrhagic presentation of spinal epidural arteriovenous fistulas (AVFs) is rare in patients with cervical spinal vascular lesions. The present report describes a patient with cervical spine epidural AVFs associated with anterior spinal artery aneurysm at the same vertebral level presenting with subarachnoid hemorrhage. A 54-year-old man presented with sudden onset of headache. Computed tomography of the head showed subarachnoid hemorrhage. Diagnostic angiography revealed an epidural AVF located at the C1-2 level that was fed mainly by the dorsal somatic branches of the segmental arteries from the radicular artery and anterior spinal artery. This AVF drained only into the epidural veins without perimedullary venous reflux. Further, there was a 4-mm anterior spinal artery aneurysm in the vicinity of the fistula that was thought to be the cause of the hemorrhage. Endovascular transarterial fistulas embolization from the right radicular artery was performed to eliminate the AVF and to reduce hemodynamic stress on the aneurysm. No new symptoms developed after the treatment and discharged without neurological deficits. The aneurysm was noted to be reduced in size after the treatment and totally disappeared by 1 year later, according to follow-up angiography. Anterior spinal artery aneurysm from a separate vascular distribution may coexist with spinal epidural AVFs. In the setting of spinal subarachnoid hemorrhage, comprehensive imaging is indicated to rule out such lesions.

Giant vertebral artery aneurysm in a child treated with endovascular parent artery occlusion and coil embolization.

BACKGROUND: Intracranial giant vertebral artery aneurysms are extremely rare in the pediatric population and are associated with significant morbidity and mortality. The present report describes a case of a pediatric patient with giant vertebral artery aneurysm who presented with intracranial mass effect. This patient was successfully treated with endovascular parent artery occlusion and coil embolization. CASE DESCRIPTION: A 7-year-old girl presented with tetraparesis, ataxia, dysphagia, and dysphonia. Cerebral angiography revealed intracranial giant aneurysm arising from the right vertebral artery. The patient underwent endovascular parent artery occlusion alone to facilitate aneurysmal thrombosis as an initial treatment. This was done to avoid a coil mass effect to the brainstem. However, incomplete thrombosis occurred in the vicinity of the vertebral artery union. Therefore, additional coil embolization for residual aneurysm was performed. Two additional coil embolization procedures were performed in response to recurrence. Mass effect and clinical symptoms gradually improved, and the patient had no associated morbidity or recurrence at 2 years after the last fourth coil embolization. CONCLUSION: Intracranial giant vertebral artery aneurysms are rare and challenging in pediatric patients. Staged endovascular strategy can be a safe and effective treatment option.

Cytotoxic human peripheral blood-derived γδT cells kill glioblastoma cell lines: implications for cell-based immunotherapy for patients with glioblastoma.

Glioblastoma (GBM) is a highly aggressive brain tumor for which novel therapeutic approaches, such as immunotherapy, are urgently needed. Zoledronate (ZOL), an inhibitor of osteoclastic activity, is known to stimulate peripheral blood-derived γδT cells and sensitize tumors to γδT cell-mediated killing. To investigate the feasibility of γδT cell-based immunotherapy for patients with GBM, we focused on the killing of GBM cell lines by γδT cells and the molecular mechanisms involved in these cell-cell interactions. Peripheral blood mononuclear cells were expanded in ZOL and interleukin (IL)-2 for 14 days, and γδT cells were enriched in the expanded cells by the immunomagnetic depletion of αßT cells. Gliomas are resistant to NK cells but susceptible to lymphokine-activated killer cells and some cytotoxic T lymphocytes. When the γδT cell-mediated killing of three GBM cell lines (U87MG, U138MG and A172 cells) and an NK-sensitive leukemia cell line (K562 cells) were tested, 32% U87MG, 15% U138MG, 1% A172, and 50% K562 cells were killed at an effector:target ratio of 5:1. The γδT cell-mediated killing of all three GBM cell lines was significantly enhanced by ZOL and this ZOL-enhanced killing was blocked by an anti-T cell receptor (TcR) antibody. These results indicated that TcR γδ is crucial for the recognition of ZOL-treated GBM cells by γδT cells. Since the low level killing of GBM cells by the γδT cells was enhanced by ZOL, γδT cell-targeting therapy in combination with ZOL treatment could be effective for patients with GBM.

Intracranial meningioma as initial clinical manifestation of occult lung carcinoma: case report.

Intracranial meningioma with intratumor metastasis have been occasionally reported. However, to our knowledge, there are almost no reports of malignant tumors initially discovered due to metastasis to meningioma. A 74-year-old woman presented with amnesia. Magnetic resonance imaging showed a well-defined mass arising from falcotentorial junction and homogeneous enhancement. Histopathologic findings showed that the mass was a meningothelial meningioma, with the majority of the tumor cells propagating in sheets, however, a single area in the tumor tissue showed the different histology. Immunohistologically, cytokeratin 7 (CK7), thyroid transcription factor-1 (TTF-1), and Napsin were positive, which led to lung adenocarcinoma metastasis. Furthermore, E-cadherin staining showed a 70% positive rate in lung adenocarcinoma and 30% in meningothelial meningioma. We report our experiences regarding a case of lung cancer that metastasized to intracranial meningioma and its clinical presentation and pathology.

Surgical management of minimally invasive anterior lumbar interbody fusion with stand-alone interbody cage for L4-5 degenerative disorders: clinical and radiographic findings.

Surgical treatment for degenerative spinal disorders is controversial, although lumbar fusion is considered an acceptable option for disabling lower back pain. Patients underwent instrumented minimally invasive anterior lumbar interbody fusion (mini-ALIF) using a retroperitoneal approach except for requiring multilevel fusions, severe spinal canal stenosis, high-grade spondylolisthesis, and a adjacent segments disorders. We retrospectively reviewed the clinical records and radiographs of 142 patients who received mini-ALIF for L4-5 degenerative lumbar disorders between 1998 and 2010. We compared preoperative and postoperative clinical data and radiographic measurements, including the modified Japanese Orthopaedic Association (JOA) score, visual analog scale (VAS) score for back and leg pain, disc height (DH), whole lumbar lordosis (WL), and vertebral wedge angle (WA). The mean follow-up period was 76 months. The solid fusion rate was 90.1% (128/142 patients). The average length of hospital stay was 6.9 days (range, 3-21 days). The mean blood loss was 63.7 ml (range, 10-456 ml). The mean operation time was 155.5 min (range, 96-280 min). The postoperative JOA and VAS scores for back and leg pain were improved compared with the preoperative scores. Radiological analysis showed significant postoperative improvements in DH, WL, and WA, and the functional and radiographical outcomes improved significantly after 2 years. The 2.8% complication rate included cases of wound infection, liquorrhea, vertebral body fractures, and a misplaced cage that required revision. Mini-ALIF was found to be associated with improved clinical results and radiographic findings for L4-5 disorders. A retroperitoneal approach might therefore be a valuable treatment option.

Unilateral oculomotor nerve palsy as an initial presentation of bilateral chronic subdural hematoma: case report.

Isolated oculomotor nerve palsy is well known as a symptom of microvascular infarction and intracranial aneurysm, but unilateral oculomotor nerve palsy as an initial manifestation of chronic subdural hematoma (CSDH) is a rare clinical condition. We report a rare case of an 84-year-old woman with bilateral CSDH who presented with unilateral oculomotor nerve palsy as the initial symptom. The patient, who had a medical history of minor head injury 3 weeks prior, presented with left ptosis, diplopia, and vomiting. She had taken an antiplatelet drug for lacunar cerebral infarction. Computed tomography (CT) of the head showed bilateral CSDH with a slight midline shift to the left side. She underwent an urgent evacuation through bilateral frontal burr holes. Magnetic resonance angiography (MRA) after evacuation revealed no intracranial aneurysms, but constructive interference in steady-state (CISS) magnetic resonance imaging (MRI) revealed that the left posterior cerebral artery (PCA) ran much more anteriorly and inferiorly compared with the right PCA and the left oculomotor nerve passed very closely between the left PCA and the left superior cerebellar artery (SCA). There is the possibility that the strong compression to the left uncus, the left PCA, and the left SCA due to the bilateral CSDH resulted in left oculomotor nerve palsy with an initial manifestation without unconsciousness. Unilateral oculomotor nerve palsy as an initial presentation caused by bilateral CSDH without unconsciousness is a rare clinical condition, but this situation is very important as a differential diagnosis of unilateral oculomotor nerve palsy.

Early inhibition of natriuresis suppresses symptomatic cerebral vasospasm in patients with aneurysmal subarachnoid hemorrhage.

BACKGROUND: Hyponatremia is a common complication occurring in one third of patients after subarachnoid hemorrhage (SAH). One mechanism that likely mediates the development of hyponatremia in SAH is cerebral salt wasting syndrome (CSWS), which induces natriuresis and reduces total blood volume, resulting in a risk of symptomatic vasospasm (SVS). The mineral corticoid fludrocortisone acetate enhances sodium reabsorption in the renal distal tubules and may help prevent post-SAH hyponatremia. However, management with fludrocortisone acetate is ineffective if hyponatremia is advanced, because CSWS and subsequent SVS develop rapidly. Therefore, an additional earlier marker is required to predict the development of hyponatremia for the initiation of immediate treatment in select patients. However, no conclusive evidence exists showing that hyponatremia influences the risk of SVS, and no standard treatment protocol exists for treating hyponatremia in patients with SAH. This study was undertaken to evaluate whether selective early treatment of hyponatremia prevents SVS in patients with increased urinary sodium excretion in the early phase following SAH. METHODS: A total of 103 patients with aneurysmal SAH were managed for a postoperative electrolyte disorder after aneurysmal clipping or coil embolization. Between 2004 and 2007 (period 1), 54 patients started treatment to correct the electrolyte disorder after hyponatremia had occurred. Between 2007 and 2011 (period 2), 49 patients were prospectively subjected to sodium replacement treatment according to their daily sodium balance, and inhibition of natriuresis with fludrocortisone acetate was initiated just after an increase in urinary sodium excretion >300 mEq/day. The occurrence of hyponatremia, SVS, and outcomes were compared between the two periods. RESULTS: Hyponatremia was observed in 14 patients (26%) in period 1 and 7 patients (14%) in period 2. The incidence of fludrocortisone acetate administration was significantly higher, and initiation of electrolyte correction was significantly earlier, in period 2 patients. We observed a significant difference in the frequency of SVS, which occurred in 10 patients (18.5%) in period 1 and 3 patients (6.1%) in period 2. Both urinary sodium excretion and urine volume at day 7 were significantly different between the two periods. However, no significant difference was observed in overall outcome between the two periods. CONCLUSIONS: Early inhibition of natriuresis with fludrocortisone acetate before the occurrence of hyponatremia prevented SVS after aneurysmal SAH. Increased urinary sodium excretion in the early phase of SAH is a good indicator for the initiation of electrolyte correction with fludrocortisone acetate.

The use of susceptibility-weighted imaging as an indicator of retrograde leptomeningeal venous drainage and venous congestion with dural arteriovenous fistula: diagnosis and follow-up after treatment.

BACKGROUND: Retrograde leptomeningeal venous drainage (RLVD) in dural arteriovenous fistulas (DAVFs) is associated with intracerebral hemorrhage and nonhemorrhagic neurological deficits or death. Angiographic evidence of RLVD is a definite indication for treatment, but less invasive methods of identifying RLVD are required. OBJECTIVE: To evaluate the efficacy of susceptibility-weighted magnetic resonance imaging (SWI) in detecting RLVD in DAVFs. METHODS: We retrospectively identified 17 DAVF patients who had angiographic evidence of RLVD and received treatment. Conventional angiography and SWI were assessed at pretreatment and posttreatment time points. The presence of RLVD on SWI was defined as cortical venous hyperintensity, and the presence of venous congestion on SWI venograms was defined as increased caliber of cortical or medullary veins. RESULTS: Cortical venous hyperintensity was identified in pretreatment SWI of 15 patients. Cortical venous hyperintensity was absent in early posttreatment SWI, consistent with the absence of RLVD in posttreatment angiography, in all but one of these patients. In 2 patients, cortical venous hyperintensity was identified during follow-up, indicating the recurrence of RLVD. Cortical venous hyperintensity was not identified in the pretreatment SWI of 2 patients despite angiographic evidence of RLVD. Venous congestion was identified in pretreatment SWI venograms of 11 patients and had an appearance similar to that identified from angiography. Venous congestive signs improved over the follow-up period. CONCLUSION: The presence of SWI hyperintensity within the venous structure could be a useful indicator of RLVD in DAVF patients. Thus, SWI offers a noninvasive alternative to angiography for the identification of RLVD in pretreated and posttreated DAVF patients.

Pupil-sparing oculomotor nerve palsy caused by upward compression of a large posterior communicating artery aneurysm. Case report.

A 69-year-old woman without diabetes or hypertension presented with a large posterior communicating artery aneurysm projecting beneath the oculomotor nerve manifesting as a 2-week history of progressive diplopia. Neurological examination revealed external ophthalmoplegia and blepharoptosis without pupil involvement. Neuroimaging showed a large aneurysm in the left internal carotid artery projecting postero-inferiorly. Craniotomy and neck clipping of the aneurysm revealed the origin at the junction of the internal carotid artery and posterior communicating artery, and elevation of the oculomotor nerve. Pupil-sparing oculomotor nerve palsy is often assumed to be caused by ischemic injury such as hypertension and diabetes mellitus. Sometimes compressive lesion can cause pupil-sparing oculomotor nerve palsy with a short interval from the onset of symptoms to diagnosis. Despite the 2-week interval from the onset of symptoms, this patient presented with pupil-sparing oculomotor nerve palsy caused by compressive lesion. Involvement or sparing of the pupil is often considered to be the most important criterion in the diagnosis of isolated oculomotor nerve palsy. This unique case demonstrated that unusual compressive lesions must be taken into consideration in the diagnosis of pupil-sparing oculomotor nerve palsy.

Subarachnoid hemorrhage in a case of segmental arterial mediolysis with coexisting intracranial and intraabdominal aneurysms.

The authors report the rare case of a 58-year-old man with segmental arterial mediolysis (SAM) with associated intracranial and intraabdominal aneurysms, who suffered subarachnoid hemorrhage (SAH) due to rupture of an intracranial aneurysm. This disease primarily involves the intraabdominal arterial system, resulting in intraabdominal and retroperitoneal hemorrhage in most cases. The patient presented with severe headache and vomiting. The CT scans of the head revealed SAH. Cerebral angiography revealed 3 aneurysms: 1 in the right distal anterior cerebral artery (ACA), 1 in the distal portion of the A(1) segment of the right ACA, and 1 in the left vertebral artery. The patient had a history of multiple intraabdominal aneurysms involving the splenic, gastroepiploic, gastroduodenal, and bilateral renal arteries. He underwent a right frontotemporal craniotomy and fibrin coating of the dissecting aneurysm in the distal portion of the A(1) segment of the right ACA, which was the cause of the hemorrhage. Follow-up revealed no significant changes in the residual intracranial and intraabdominal aneurysms. An SAH due to SAM with associated multiple intraabdominal aneurysms is extremely rare. The authors describe their particular case and review the literature pertaining to SAM with associated intracranial and intraabdominal aneurysms.

A rare brainstem hemorrhage during transvenous embolization of a cavernous dural arteriovenous fistula.

Intravascular treatment of cavernous dural arteriovenous fistula (dAVF) is usually safe and effective. However, we describe a patient with a rare brainstem hemorrhage during transvenous embolization (TVE). A 79-year-old woman suffered from left chemosis and diplopia. Cerebral angiography revealed a left cavernous dAVF with cortical venous drainage. The patient underwent TVE of the cavernous sinus (CS) via the left inferior petrosal sinus. Superior petrosal sinus (SPS) outflow occlusion was performed to avoid venous congestion, followed by superficial middle cerebral vein outflow occlusion, selective shunt occlusion of the middle meningeal artery, and superior orbital vein outflow occlusion. The patient's condition suddenly deteriorated during CS packing. A CT scan revealed a massive brainstem hemorrhage. Cerebral angiography did not show SPS reopening or redistributed drainage to the posterior fossa. Thus, TVE for cavernous dAVF can result in life-threatening vascular complications. Well-planned treatment strategies could avert this rare complication.

Evaluation of combined use of transcranial and direct cortical motor evoked potential monitoring during unruptured aneurysm surgery.

The feasibility and reliability of combined use of transcranial and direct cortical motor evoked potential (MEP) monitoring during unruptured aneurysm surgery were evaluated. Forty-eight patients with unruptured cerebral aneurysms underwent craniotomy and neck clipping accompanied by muscle MEP monitoring. MEPs were elicited successfully by transcranial electrical stimulation in all patients. Direct cortical stimulation elicited MEPs in 44 patients. Reduction in MEP amplitude to less than 50% of baseline was considered significant. No postoperative motor paresis occurred in 39 patients in whom transcranial and direct MEPs remained unchanged. Four patients in whom direct MEPs could not be recorded had no intraoperative abnormality in transcranial MEPs and no postoperative motor dysfunction. Four of the other 5 patients manifested significant transient direct MEP changes without transcranial MEP changes. The transient MEP changes were observed in 3 patients during temporary clipping of the parent artery and in one patient with inadequate clipping of an middle cerebral artery aneurysm, and were considered due to insufficiency of blood flow. Decrease or disappearance of direct MEP waves recovered immediately after re-application of the clip and release of the temporary clip. Direct MEP waves disappeared and did not recover until the end of microsurgical procedures in one patient, although transcranial MEP amplitude remained at less than 50% of baseline. She developed hemiparesis postoperatively, which recovered within 6 hours. The duration of temporary occlusion in patients with direct MEP changes was significantly longer than that in patients without (p < 0.05). Direct MEP was sensitive in detecting ischemic stress to descending motor pathways during aneurysm surgery. Transcranial MEPs could be elicited in patients in whom direct MEPs could not be obtained, and during periods such as craniotomy or after dural closure, in which direct MEPs could not be recorded. These findings suggest that combined transcranial and direct cortical MEP recording may improve the feasibility and reliability of MEP monitoring during unruptured aneurysm surgery.

Orbital schwannoma extending to the lateral wall of the cavernous sinus through the superior orbital fissure--case report.

A 58-year-old man presented with a rare orbitocavernous sinus schwannoma that originated from the orbital opthalmic nerve, and manifested as slowly progressive hypesthesia of the right side of the forehead, proptosis, and ocular pain with rapidly worsening visual acuity. Magnetic resonance imaging revealed a huge orbital tumor extending to the lateral wall of the cavernous sinus through the superior orbital fissure. Microsurgical total resection of the tumor was achieved using an epidural orbitofrontal approach with orbito-fronto-zygomatic craniotomy. The histological diagnosis was schwannoma with Antoni type A formation. The postoperative course was uneventful except for the hypesthesia on the right side of the forehead and transient oculomotor paralysis. Surgery was effective to relieve the symptoms and improve the activities of daily living.