Anterior spinal artery as a collateral channel in patients with acute bilateral vertebral artery occlusions. Two case reports.

Retrograde flow through the anterior spinal artery (ASA) from the cervical vertebral artery (VA) to the intracranial distal VA due to disrupted perfusion caused by bilateral VA occlusion is rare. We report two cases of hemodynamic vertebrobasilar circulatory insufficiency caused by bilateral VA occlusion. In these patients, the ASA filled in the retrograde direction, and provided collateral support to the ipsilateral posterior inferior cerebellar artery. The patients were treated with drip intravenous infusion of edaravone and/or argatroban. One patient had a good collateral supply from the posterior communicating artery and recovered almost completely within one month, but the other did not and lapsed into a coma, with generalized hyperreflexia, pin-point pupils, and ataxic respiration. Severe calcified lesions on three-dimensional computed tomography angiography at the occlusion site in the second patient indicated direct surgery including right superficial temporal artery to superior cerebellar artery anastomosis, rather than the endovascular approach. Retrograde flow through the ASA may be observed in this type of critical situation, and may be an important source of collateral supply to the posterior fossa territory.

Effectiveness of combining continuous cerebrospinal drainage and intermittent intrathecal urokinase injection therapy in preventing symptomatic vasospasm following aneurysmal subarachnoid haemorrhage.

The effect of cisternal drainage and intrathecal urokinase (UK) injections in preventing symptomatic vasospasm after aneurysmal subarachnoid haemorrhage was retrospectively studied in 69 patients with uniform backgrounds with regard to subarachnoid haemorrhage (SAH; WFNS grade I to IV, Fisher's group 3, undergoing surgery or coil embolization within 72 h of the onset). With regard to the selection of patients, 34 patients belonging to the control group (no UK injection group) underwent the treatment during the 3-year period from 2001 to 2003, while 35 patients belonging to the UK group underwent the treatment during the 3-year period from 2004 to 2006. The incidence of symptomatic vasospasm was 5/35 with the UK group, but 12/34 with a control group. The UK injection significantly reduced the incidence of symptomatic vasospasm (p = 0.042, Pearson chi-square test), resulting in an improvement shown by the Glasgow Outcome Scale (GOS; p = 0.030, Mann-Whitney U test; Table V). The distribution on the angiographic grading scales for cerebral vasospasm significantly shifted in a positive direction for the UK group (mild 0, moderate 5, severe 0) in comparison with the control group (mild 0, moderate 4, severe 8; p = 0.014, Mann-Whitney U test). This study suggests that combining continuous cerebrospinal drainage and intermittent intrathecal UK injection therapy is a relatively simple and effective method for symptomatic vasospasm prophylaxis in patients with aneurysmal SAH.

Venous drainage patterns in perimesencephalic nonaneurysmal subarachnoid hemorrhage.

OBJECTIVE: The precise etiology of perimesencephalic nonaneurysmal subarachnoid hemorrhage (P-SAH) has not yet been determined. We decided to compare the venograms of patients with P-SAH with those of patients with aneurysmal SAH (A-SAH) to examine the relationship between P-SAH and venous drainage patterns. METHODS: We retrospectively studied 18 patients with P-SAH during the past 10 years and 112 patients with ruptured A-SAH during the past 4 years by reevaluating their venograms for possible abnormalities in venous structures, particularly focusing on the basal vein of Rosenthal (BVR). Anatomical variants were classified into three types according to the drainage pathway. RESULTS: The location and drainage pathway of the BVR proved to be a significantly more primitive configuration in patients with P-SAH than in those with A-SAH (P<0.05). On the other hand, physical action including components of the Valsalva maneuver were the cause of nine cases of P-SAH (69.2%) in this case profile. The occurrence rate was significantly higher in the P-SAH group than in the A-SAH group (14.3%) (p<0.05). CONCLUSION: Our data suggest that failure of longitudinal anastomoses between the primary primitive veins as well as excessive strenuous exertion including components of the Valsalva maneuver plays an important predisposing role in the etiology of P-SAH.

Aneurysm arising from the cortical segment of the superior cerebellar artery: a case report and review of the literatures.

BACKGROUND: Aneurysms arising from the distal portion of the SCA are relatively rare. A case is presented of an aneurysm arising from the cortical segment of the SCA. CASE DESCRIPTION: A 45-year-old woman was admitted to our institution because of severe headache. Radiological examination revealed SAH caused by rupture of the aneurysm located in the cortical segment of the SCA and was treated successfully with coil embolization. CONCLUSIONS: This type of aneurysms may be difficult to treat surgically because of its inaccessibility and of the common difficulty in preserving the involved parent artery. In view of the previously reported cases, these peripheral aneurysms of the SCA often have undefinable necks, as is shown in our case, which makes a reconstructive endovascular and/or surgical technique more or less difficult. However, the overall outcome is almost always favorable, even if surgical treatment results in proximal parent artery occlusion or trapping with surgical clips. These results imply that an equivalent endovascular approach to these rare lesions can be an effective alternative method of management.

Computer-aided diagnosis scheme for detection of lacunar infarcts on MR images.

RATIONALE AND OBJECTIVES: The detection and management of asymptomatic lacunar infarcts on magnetic resonance (MR) images are important tasks for radiologists to ensure the prevention of severe cerebral infarctions. However, accurate identification of the lacunar infarcts on MR images is a difficult task for the radiologists. Therefore the purpose of this study was to develop a computer-aided diagnosis scheme for the detection of lacunar infarcts to assist radiologists' interpretation as a "second opinion." MATERIALS AND METHODS: Our database comprised 1,143 T1- and 1,143 T2-weighted images obtained from 132 patients. The locations of the lacunar infarcts were determined by experienced neuroradiologists. We first segmented the cerebral region in a T1-weighted image by using a region growing technique for restricting the search area of lacunar infarcts. For identifying the initial lacunar infarcts candidates, a top-hat transform and multiple-phase binarization were then applied to the T2-weighted image within the segmented cerebral region. For eliminating the false positives (FPs), we determined 12 features--the locations x and y, signal intensity differences in the T1- and T2-weighted images, nodular components from a scale of 1 to 4, and nodular and linear components from a scale of 1 to 4. The nodular components and the linear components were obtained using a filter bank technique. The rule-based schemes and a support vector machine with 12 features were applied to the regions of the initial candidates for distinguishing between lacunar infarcts and FPs. RESULTS: Our computerized scheme was evaluated by using a holdout method. The sensitivity of the detection of lacunar infarcts was 96.8% (90/93) with 0.76 FP per image. CONCLUSIONS: Our computerized scheme would be useful in assisting radiologists for identifying lacunar infarcts in MR images.

Improvement of automated detection method of lacunar infarcts in brain MR images.

The detection of asymptomatic lacunar infarcts on magnetic resonance (MR) images are important tasks for radiologists to ensure the prevention of sever cerebral infarction. However, their accurate identification is often difficult task. Therefore, the purpose of this study is to develop a computer-aided diagnosis scheme for the detection of lacunar infarcts. Our database consisted of 1,143 T1- and 1,143 T2-weighted images obtained from 132 patients. We first segmented the cerebral region in the T1- weighted image by using a region growing technique. For identifying the initial lacunar infarcts candidates, white top-hat transform and multiple-phase binarization were then applied to the T2- weighted image. For eliminating false positives (FPs), we determined 12 features, i.e., the locations x and y, density differences in the T1- and T2- weighted images, nodular components (NC), and nodular & linear components (NLC) from a scale 1 to 4. The NCs and NLCs were obtained using filter bank technique. The rule-based scheme and a neural network with 12 features were employed as the first step for eliminating FPs. The modular classifier was then used for eliminating three typical sources of FPs. As a result, the sensitivity of the detection of lacunar infarcts was 96.8% with 0.30 FP per image. Our computerized scheme would assist radiologists in identifying lacunar infarcts on MR images.

Two cases of dissecting aneurysm of the distal posterior inferior cerebellar artery: possible involvement of segmental mediolytic arteriopathy in the pathogenesis.

BACKGROUND: Dissecting aneurysm of the posterior inferior cerebellar artery (PICA) uninvolved with the vertebral artery is rare. The exact pathohistological diagnosis might result in 'unknown' because the underlying pathoanatomical features are, for a variety of reasons, not always identified. CASE DESCRIPTION: We report herein two cases of dissecting aneurysm harbored in different segments of the distal posterior inferior cerebellar artery. In our cases, after trapping the PICA at both just proximal and distal to the aneurysm, the abnormal portion was successfully resected with/without an end-to-end anastomosis. The first patient made a good recovery, while the other died 2 days after the surgery. Although its pathogenetic etiology was unidentified in the second case, the formation of dissecting aneurysm had resulted from a segmental mediolytic arteriopathy in the first case. CONCLUSION: This is the first report of a segmental mediolytic arteriopathy possibly being identified as causing an isolated dissecting aneurysm at this site.

Intracanalicular aneurysm at the meatal loop of the distal anterior inferior cerebellar artery: a case report and review of the literature.

BACKGROUND: Distal aneurysms of the anterior inferior cerebellar artery (AICA) are rare. Most of the reported cases have been located near the internal auditory meatus. Among these cases, only six located in the internal auditory meatus have been reported in the literature. METHODS: A 64-year-old female presented with sudden onset of severe headache. Computed tomography (CT) revealed moderate subarachnoid hemorrhage and Gd-DTPA enhanced magnetic resonance imaging (MRI) showed a small high-intensity mass at the right cerebellopontine angle. Although initial digital subtraction angiography (DSA) showed no vascular abnormalities, repeated DSA disclosed a saccular aneurysm at the top of the meatal loop of the right AICA. The patient underwent a suboccipital craniectomy on the 18th day after the hemorrhage RESULTS: . In this case, the aneurysm was completely buried in the internal auditory meatus. After unroofing the meatus, the aneurysm was successfully clipped. After 3 months of hospitalization, the patient was discharged with right-sided deafness, partial facial palsy, and no other complications. CONCLUSIONS: We discuss some of the clinical features and pitfalls in the surgical management of intracanalicular AICA aneurysms and review previous reports of similar cases.

Normalization of endothelial and inducible nitric oxide synthase expression in brain microvessels of spontaneously hypertensive rats by angiotensin II AT1 receptor inhibition.

Inhibition of angiotensin II AT1 receptors protects against stroke, reducing the cerebral blood flow decrease in the periphery of the ischemic lesion. To clarify the mechanism, spontaneously hypertensive rats (SHR) and normotensive control Wistar Kyoto (WKY) rats were pretreated with the AT1 receptor antagonist candesartan (0.3 mg. kg.(-1) d(-1)) for 28 days, a treatment identical to that which protected SHR from brain ischemia, and the authors studied middle cerebral artery (MCA) and common carotid morphology, endothelial nitric oxide synthase (eNOS) and inducible nitric oxide synthase (iNOS) messenger RNA (mRNA), and protein expression in cerebral microvessels, principal arteries of the Willis polygon, and common carotid artery. The MCA and common carotid artery of SHR exhibited inward eutrophic remodeling, with decreased lumen diameter and increased media thickness when compared with WKY rats. In addition, there was decreased eNOS and increased iNOS protein and mRNA in common carotid artery, circle of Willis, and brain microvessels of SHR when compared with WKY rats. Both remodeling and alterations in eNOS and iNOS expression in SHR were completely reversed by long-term AT1 receptor inhibition. The hemodynamic, morphologic, and biochemical alterations in hypertension associated with increased vulnerability to brain ischemia are fully reversed by AT1 receptor blockade, indicating that AT1 receptor activation is crucial for the maintenance of the pathologic alterations in cerebrovascular circulation during hypertension, and that their blockade may be of therapeutic advantage.

Intracisternal administration of Angiotensin II AT1 receptor antisense oligodeoxynucleotides protects against cerebral ischemia in spontaneously hypertensive rats.

Pharmacological blockade of peripheral and brain Angiotensin II (Ang II) AT(1) receptors protects against brain ischemia. To clarify the protective role of brain AT(1) receptors, we examined the effects of specific antisense oligodeoxynucleotides (AS-ODN) targeted to AT(1) receptor mRNA administered intracisternally to spontaneously hypertensive rats (SHRs), 4 and 7 days before middle cerebral artery (MCA) occlusion, and we determined the infarct size and tissue swelling 24 h after surgery. A single intracisternal injection of AT(1) mRNA receptor antisense oligodeoxynucleotides reduced systemic blood pressure for 5 days and AT(1) receptor binding for at least 4 days in the area postrema and the nucleus of the solitary tract. A similar injection of scrambled oligodeoxynucleotides (SC-ODN) was without effect. Both blood pressure and AT(1) receptor binding returned to normal 7 days after antisense receptor mRNA administration. Both the infarction size and the tissue swelling after middle cerebral artery occlusion were reduced when the antisense oligodeoxynucleotide was administered 7 days, but not 4 days, before the operation. We conclude that 4 to 5 days of decrease in brain AT(1) receptor binding by a single administration of an AT(1) receptor mRNA oligodeoxynucleotide are sufficient to significantly protect the brain against ischemia resulting from total occlusion of a major cerebral vessel.

Cell permeable ROS scavengers, Tiron and Tempol, rescue PC12 cell death caused by pyrogallol or hypoxia/reoxygenation.

The role of superoxide anion (O(2)*-) in neuronal cell injury induced by reactive oxygen species (ROS) was examined in PC12 cells using pyrogallol (1,2,3-benzenetrior), a donor to release O(2)*-. Pyrogallol induced PC12 cell death at concentrations, which evidently increased intracellular O(2)*-, as assessed by O(2)(*-)-sensitive fluorescent precursor hydroethidine (HEt). Caspase inhibitors, Z-VAD-FMK and Z-Asp-CH(2)-DCB, failed to protect cells from injury caused by elevation of intracellular O(2)*-, although these inhibitors had effects on hypoxia- or hydrogen peroxide (H(2)O(2))-induced PC12 cell death. Two known O(2)*- scavengers, Tiron (4,5-dihydroxy-1,3-benzenedisulfonic acid) and Tempol (4-hydroxy-2,2,6,6-tetramethylpiperydine-1-oxyl) rescued PC12 cells from pyrogallol-induced cell death. Hypoxia/reoxygenation injury of PC12 cells was also blocked by Tiron and Tempol. Further understanding of the underlying mechanism of the protective effects of these radical scavengers reducing intracellular O(2)*- on neuronal cell death may lead to development of new therapeutic treatments for hypoxic/ischemic brain injury.

Ruptured infectious aneurysm of the distal middle cerebral artery manifesting as intracerebral hemorrhage and acute subdural hematoma--case report.

A 21-year-old woman with severe mitral valve regurgitation due to infectious endocarditis was transferred to our institute in a deep coma with intracerebral hemorrhage and acute subdural hematoma. She had no history of head injury. Brain computed tomography revealed left frontoparietal intracerebral hematoma and adjacent acute subdural hematoma that were evacuated on the day of admission, but the distal middle cerebral artery (MCA) aneurysm remained undetected. Follow-up cerebral angiography demonstrated the distal MCA aneurysm, which had enlarged by 25% at 2 weeks following the first operation. The aneurysm originated from a branch of the angular artery and was successfully resected on Day 22. Histological examination of the aneurysm section showed no infectious nature, but the final diagnosis was infectious intracranial aneurysm based on the presence of infectious endocarditis.

Protection against ischemia and improvement of cerebral blood flow in genetically hypertensive rats by chronic pretreatment with an angiotensin II AT1 antagonist.

BACKGROUND AND PURPOSE: Pretreatment with angiotensin II AT(1) receptor antagonists protects against cerebral ischemia. We studied whether modulation of cerebral blood flow (CBF) and morphometric changes in brain arteries participated in this protective mechanism. METHODS: We pretreated adult spontaneously hypertensive rats with equally antihypertensive doses of candesartan (0.1 or 0.3 mg/kg per day), nicardipine (0.1 mg/kg per day), or captopril (3.0 mg/kg per day) for 3 or 28 days via subcutaneous osmotic minipumps followed by permanent left middle cerebral artery (MCA) occlusion distal to the origin of the lenticulostriate arteries. We measured CBF by autoradiography with 4-iodo-[N-methyl-(14)C]antipyrine 3 hours after operation and the areas of infarct and tissue swelling 24 hours after operation. Morphometric changes in the MCA were studied after antihypertensive treatment. RESULTS: Twenty-eight days of candesartan pretreatment decreased the infarct area by 31%; reduced the CBF decrease at the peripheral area of ischemia and the cortical volume of severe ischemic lesion, where CBF was <0.50 mL/g per minute; increased the MCA external diameter by 16%; and reduced the media thickness of the MCA by 23%. Captopril pretreatment for 28 days decreased the infarct area by 25%. Pretreatment with candesartan for 3 days or nicardipine for 28 days was ineffective. CONCLUSIONS: Angiotensin II system inhibition protects against neuronal injury more effectively than calcium channel blockade. Protection after AT(1) receptor blockade is not directly correlated with blood pressure reduction but with normalization of MCA media thickness, leading to increased arterial compliance and reduced CBF decrease during ischemia at the periphery of the lesion.

Dissecting aneurysm of the middle cerebral artery manifesting as subarachnoid hemorrhage and hemorrhagic infarctions--case report.

A 46-year-old woman presented with a dissecting aneurysm of the right middle cerebral artery manifesting as subarachnoid hemorrhage followed by hemorrhagic infarctions. The aneurysm was clipped and wrapped. However, serial angiography showed progression of the lesion, which was probably responsible for the clinical course of this patient. Intracranial dissecting aneurysms are less common, and the natural history of these lesions is unclear. Conservative management might be preferable in this patient.