Larger anastomoses in angiotensinogen-knockout mice attenuate early metabolic disturbances after middle cerebral artery occlusion.
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Abnormalities in the homeostasis of the renin-angiotensin system have been implicated in the pathogenesis of vascular disorders, including stroke. The authors investigated whether angiotensinogen (AGN) knockout mice exhibit differences in brain susceptibility to focal ischemia, and whether such differences can be related to special features of the collateral circulation. Wild-type and AGN-knockout mice were submitted to permanent suture occlusion of the middle cerebral artery (MCA). The collateral vascular system was visualized by systemic latex infusion, and the ischemic lesions were identified by cresyl-violet staining. The core and penumbra of the evolving infarct were differentiated by bioluminescence and autoradiographic imaging of ATP and protein biosynthesis, respectively. In wild-type mice, mean arterial blood pressure was 95.0 +/- 8.6 mm Hg, and the diameter of fully relaxed anastomotic vessels between the peripheral branches of the anterior and middle cerebral arteries 26.6 +/- 4.0 microm. In AGN knockouts, mean arterial blood pressure was significantly lower, 71.5 +/- 8.5 mm Hg (P < .01), and the anastomotic vessels were significantly larger, 29.4 +/- 4.6 microm (P < .01). One hour after MCA occlusion, AGN-knockout mice exhibited a smaller ischemic core (defined as the region of ATP depletion) but a larger penumbra (the area of disturbed protein synthesis with preserved ATP). At 24 hours after MCA occlusion, this difference disappeared, and histologically visible lesions were of similar size in both strains. The observations show that in AGN-knockout mice the more efficient collateral blood supply delays ischemic injury despite the lower blood pressure. Pharmacologic suppression of angiotensin formation may prolong the therapeutic window for treatment of infarcts. (+info)
Flow dynamics in a lethal anterior communicating artery aneurysm.
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We describe and analyze the flow dynamics in replicas of a human anterior communicating artery aneurysm. The replicas were placed in a circuit of pulsating non-Newtonian fluid, and flows were adjusted to replicate human physiologic parameters. Individual slipstreams were opacified with isobaric dyes, and images were recorded on film and by CT/MR angiography. When flow in the afferent (internal carotid) and efferent (anterior and middle cerebral) arteries was bilaterally equal, slipstreams rarely entered the aneurysm. When flow in either the afferent or efferent vessels was not symmetrical, however, slipstreams entered the aneurysm neck, impinged upon the aneurysm dome, and swirled within the aneurysm. Unequal flow in carotid or cerebral systems may be necessary to direct pathologic, fluid slipstreams into an aneurysm. (+info)
Hemodynamic changes around cerebral arteriovenous malformation before and after embolization measured with PET.
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To estimate the changes in regional cerebral blood flow (rCBF) around cerebral arteriovenous malformation (AVM) before and after embolization, 6 patients with AVM were sequentially examined with positron emission tomography (PET). PET depicted the remodeling of rCBF in the ipsilateral hemisphere of AVM after embolization. Decrease of rCBF in the ipsilateral hemisphere was also detected in patients with focal symptoms before embolization, and improvement of clinical symptoms after embolization corresponded to disappearance of rCBF decrease. PET can detect hemodynamic changes after embolization, and has a possibility to estimate the effect of embolization in patients with AVM. (+info)
Neuropsychological changes after surgery for anterior communicating artery aneurysm.
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Neuropsychological disturbances following surgery for anterior communicating artery aneurysms were analyzed in 26 patients (11 males, 15 females) using the Hasegawa dementia scale-revised (HDS-R) over a 3-year period. The patients were aged from 34 to 76 years (mean 54.1 years). Lesions in the frontal lobe were evaluated using computed tomography (CT). Twenty-three patients had symptoms over the course. Four patients had basal forebrain lesion, five had ventral frontal lesion, and 12 had no lesion. Patients with basal forebrain lesion and no lesion tended to show disorientation. The mean HDS-R score was 10.2 points in the patients with ventral frontal lesion, and 13.5 points in the patients with no lesion. These scores are within the range for dementia. The mean HDS-R score in patients with basal forebrain and striate lesions was over 25 points and beyond the range for dementia. Significant differences were observed in the HDS-R score between patients with ventral frontal lesion and basal forebrain lesion, and between patients with no lesion and basal forebrain lesion (p < 0.05). Recovery from neuropsychological disturbances was poorer in patients with ventral frontal lesion and no lesion compared to those with basal forebrain and striate lesions, and their symptoms tended to persist. (+info)
Prolapsing gyrus rectus as a cause of progressive optic neuropathy.
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The pathogenesis of optic neuropathy caused by neurovascular compression or by similar mechanisms is unclear. Thin-slice magnetic resonance (MR) imaging was performed in 69 patients with optic neuropathy without demonstrable ophthalmological lesions (57.0 +/- 17.1 years of age) and 102 normal subjects (57.7 +/- 13.9 years of age). The MR imaging features were classified into "no compression" by the internal carotid artery (ICA), "compression" by the ICA, "no contact" with the anterior cerebral artery (ACA) or the gyrus rectus, "contact" with either or both, "compression" by the ACA, and "compression" by the gyrus rectus. The Spearman correlation coefficients were calculated between patients or controls, the MR classification, and the age, and the number of patients in each MR classification were evaluated by the chi 2 test. Five of the 69 patients with rapidly progressive symptoms were operated on via the frontotemporal approach. The MR imaging feature of "compression" by the gyrus rectus was the best predictor of optic neuropathy (Spearman correlation coefficients rho = -0.23646, p < 0.0018). This MR imaging feature was observed in 38 of 69 patients and in 32 of 102 controls (p = 0.002). Compression of the nerve by the gyrus rectus or the ACA was confirmed in all five operated cases. Decompression of the nerve was fully achieved in four of the five patients, and their symptoms have not progressed since then. Optic neuropathies due to compression by the prolapsing gyrus rectus are not well understood. Such neuropathies may be detected by MR imaging. (+info)
Ruptured aneurysm at the origin of the median artery of the corpus callosum associated with accessory middle cerebral artery--case report.
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A 62-year-old male presented with ruptured anterior communicating artery (ACoA) aneurysm manifesting as severe headache associated with the rare combination of median artery of the corpus callosum (MACC) and accessory middle cerebral artery (MCA). Computed tomography demonstrated diffuse subarachnoid hemorrhage. Left carotid angiography demonstrated an anomalous vessel originating from the ACoA complex and passing forward in the interhemispheric fissure between the two companion A2 segments. This vessel was identified as the MACC. Another anomalous vessel originated from the left A1-A2 segment and passed into the sylvian fissure. This vessel was identified as the accessory MCA. Left frontotemporal craniotomy was performed to clip the neck of the aneurysm. After identifying both A1 and A2 segments, accessory MCA, and the MACC, the aneurysm neck was occluded successfully. The ACoA complex is one of the most frequent sites of vascular anomalies. Preoperative and intraoperative care is required to identify the presence of anomalies of the ACoA complex prior to clip placement, to avoid accidental damage or clipping, which may result in severe neurological deficits. (+info)
Histomorphometrical study of the elastic fiber system in the anterior cerebral artery of man.
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The aim of the present study was to quantify the distribution of the elastic fiber system within the wall of the anterior cerebral artery. The study is based on the works of Glynn (1940) and Stehbens (1989) concerning the incidence and origin of brain aneurysms and recent studies of the elastic fibers. The anterior cerebral artery was divided into three segments, S1, S2 and S3: S1 corresponds to the origin of the anterior cerebral artery, S2 is located at the junction of the anterior cerebral artery with the anterior communicating artery, and S3 at the junction of the rostrum and genu of the corpus callosum,which were submitted to routine histological procedures. A histomorphometrical study was undertaken using an estimation of the linear density (Ld) of the components of the fibrous elastic system which evaluates their full length in each segment. Data were analyzed using first order linear regression methods. The results show a decreasing quantity of elastic fibers in the three segments (S1>S2>S3). Study of the elastic fiber system may originate new concepts regarding the genesis of cerebral artery aneurysm. (+info)
A modified transorbital baboon model of reperfused stroke.
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BACKGROUND AND PURPOSE: Although pathophysiological studies of focal cerebral ischemia in nonhuman primates can provide important information not obtainable in rodent models, primate experimentation is limited by considerations of cost, availability, effort, and ethics. A reproducible and quantitative model that minimizes the number of animals necessary to detect differences between treatment groups is therefore crucial. METHODS: Eight male baboons (weight, 22+/-2 kg) underwent left transorbital craniectomy followed by 1 hour of temporary ipsilateral internal carotid artery occlusion at the level of the anterior choroidal artery together with bilateral temporary occlusion of both anterior cerebral arteries (A1) proximal to the anterior communicating artery. A tightly controlled nitrous oxide-narcotic anesthetic allowed for intraoperative motor evoked potential confirmation of middle cerebral artery (MCA) territory ischemia. Animals survived to 72 hours or 10 days if successfully self-caring. Outcomes were assessed with a 100-point neurological grading system, and infarct volume was quantified by planimetric analysis of both MRI and triphenyltetrazolium chloride-stained sections. RESULTS: Infarction volumes (on T2-weighted images) were 32+/-7% (mean+/-SEM) of the ipsilateral hemisphere, and neurological scores averaged 29+/-9. All animals demonstrated evidence of hemispheric infarction, with damage evident in both cortical and subcortical regions in the MCA vascular territory. Histologically determined infarction volumes differed by <3% and correlated with absolute neurological scores (r=0.9, P:=0.003). CONCLUSIONS: Transorbital temporary occlusion of the entire anterior cerebral circulation with strict control of physiological parameters can reliably produce reperfused MCA territory infarction. The magnitude of the resultant infarct with little interanimal variability diminishes the potential number of animals required to distinguish between 2 treatment regimens. The anatomic distribution of the infarct and associated functional deficits offer comparability to human hemispheric strokes. (+info)