Extracranial-intracranial arterial bypass for middle cerebral artery stenosis and occlusion

1985 ◽  
Vol 62 (6) ◽  
pp. 831-838 ◽  
Author(s):  
Brian T. Andrews ◽  
Norman L. Chater ◽  
Philip R. Weinstein
Keyword(s):  
Middle Cerebral Artery ◽  
Cerebral Artery ◽  
Slight Reduction ◽  
Content Type ◽  
Perioperative Stroke ◽  
Arterial Bypass ◽  
Mca Occlusion ◽  
Bypass Patency ◽  
Completed Stroke ◽  
Fine Print

✓ Forty-seven patients with middle cerebral artery (MCA) stenosis and 18 patients with MCA occlusion underwent extracranial-intracranial arterial bypass procedures. Patients presented with a history of transient ischemic attacks (TIA's), reversible ischemic neurological deficits, TIA's after initial stroke, stroke-in-evolution, or completed stroke. Angiography revealed that the MCA stenosis ranged from 70% to over 95%. Two patients (4.3%) in the stenosis group had a perioperative stroke (within 30 days of operation). There was no perioperative mortality. In the occlusion group, no patient had a perioperative stroke, and one patient (5.5%) died from a non-neurological disease. The TIA's resolved completely in 90% of the patients with stenosis and in 91.6% of those with occlusion. No patient with MCA stenosis had a late ipsilateral stroke, although five had a contralateral or vertebrobasilar stroke. One patient with MCA occlusion had a late ipsilateral stroke. The bypass patency rate at late follow-up review was 100%. The results of intracranial-extracranial arterial bypass procedures appear to be similar for patients with either stenosis or occlusion of the MCA. Symptomatic relief of TIA's was excellent and, in two patients with progressive stroke-in-evolution, the deficit was stabilized. The incidence of postoperative ipsilateral stroke was low in patients with TIA's alone or with TIA's after an initial stroke, but among patients with completed stroke, improvement was confined to slight reduction in the neurological deficit.

Middle meningeal to middle cerebral arterial bypass for cerebral revascularization

1979 ◽  
Vol 50 (6) ◽  
pp. 802-804 ◽  
Author(s):  
Clinton F. Miller ◽  
Robert F. Spetzler ◽  
Dennis J. Kopaniky
Keyword(s):  
Middle Cerebral Artery ◽  
Cerebral Artery ◽  
Middle Meningeal Artery ◽  
Cerebral Revascularization ◽  
Content Type ◽  
Arterial Bypass ◽  
Meningeal Artery ◽  
Fine Print

✓ A case is reported of successful anastomosis of the middle meningeal artery to a cortical branch of the middle cerebral artery. Based on the analyses of 50 random angiograms, the authors discuss the circumstances in which such an anastomosis might be practical and indicated.

Technique of catheterization and embolization of the lenticulostriate arteries

1981 ◽  
Vol 54 (6) ◽  
pp. 783-789 ◽  
Author(s):  
Alex Berenstein
Keyword(s):  
Arteriovenous Malformation ◽  
Middle Cerebral Artery ◽  
Cerebral Artery ◽  
High Probability ◽  
Content Type ◽  
Lenticulostriate Arteries ◽  
Balloon Catheters ◽  
Mca Occlusion ◽  
Proximal Middle Cerebral Artery ◽  
Fine Print

✓ The technique of catheterization and embolization of the lateral and medial lenticulostriate arteries, using one or two balloon catheters of various designs, is described. A case of a bilateral thalamic arteriovenous malformation is presented and a further instance of an aneurysm of a striate artery is briefly discussed. Because of the high probability of proximal middle cerebral artery (MCA) thrombosis, care must be taken to determine tolerance to MCA occlusion prior to embolization.

Thresholds of focal cerebral ischemia in awake monkeys

1981 ◽  
Vol 54 (6) ◽  
pp. 773-782 ◽  
Author(s):  
Thomas H. Jones ◽  
Richard B. Morawetz ◽  
Robert M. Crowell ◽  
Frank W. Marcoux ◽  
Stuart J. FitzGibbon ◽  
...  
Keyword(s):  
Blood Flow ◽  
Cerebral Ischemia ◽  
Middle Cerebral Artery ◽  
Cerebral Artery ◽  
Focal Cerebral Ischemia ◽  
Neurological Function ◽  
Local Flow ◽  
Content Type ◽  
Mca Occlusion ◽  
Fine Print

✓ An awake-primate model has been developed which permits reversible middle cerebral artery (MCA) occlusion during physiological monitoring. This method eliminates the ischemia-modifying effects of anesthesia, and permits correlation of neurological function with cerebral blood flow (CBF) and neuropathology. The model was used to assess the brain's tolerance to focal cerebral ischemia. The MCA was occluded for 15 or 30 minutes, 2 to 3 hours, or permanently. Serial monitoring evaluated neurological function, local CBF (hydrogen clearance), and other physiological parameters (blood pressure, blood gases, and intracranial pressure). After 2 weeks, neuropathological evaluation identified infarcts and their relation to blood flow recording sites. Middle cerebral artery occlusion usually caused substantial decreases in local CBF. Variable reduction in flow correlated directly with the variable severity of deficit. Release of occlusion at up to 3 hours led to clinical improvement. Pathological examination showed microscopic foci of infarction after 15 to 30 minutes of ischemia, moderate to large infarcts after 2 to 3 hours of ischemia, and in most cases large infarcts after permanent MCA occlusion. Local CBF appeared to define thresholds for paralysis and infarction. When local flow dropped below about 23 cc/100 gm/min, reversible paralysis occurred. When local flow fell below 10 to 12 cc/100 gm/min for 2 to 3 hours or below 17 to 18 cc/100 gm/min during permanent occlusion, irreversible local damage was observed. These studies imply that some cases of acute hemiplegia, with blood flow in the paralysis range, might be improved by surgical revascularization. Studies of local CBF might help identify suitable cases for emergency revascularization.

High-dose ibuprofen for reduction of striatal infarcts during middle cerebral artery occlusion in rats

2003 ◽  
Vol 98 (4) ◽  
pp. 860-866 ◽  
Author(s):  
David F. Antezana ◽  
Richard E. Clatterbuck ◽  
Nabil J. Alkayed ◽  
Stephanie J. Murphy ◽  
Lauren G. Anderson ◽  
...  
Keyword(s):  
Middle Cerebral Artery ◽  
Cerebral Artery ◽  
Focal Cerebral Ischemia ◽  
Intercellular Adhesion Molecule ◽  
High Dose ◽  
Neurosurgical Procedures ◽  
Intercellular Adhesion Molecule 1 ◽  
Content Type ◽  
Mca Occlusion ◽  
Fine Print

Object. Ibuprofen is an antiinflammatory drug that disrupts leukocyte—endothelial cell interactions by limiting expression of endothelial adhesion molecules such as intercellular adhesion molecule-1 (ICAM-1), also known as CD54. The authors hypothesized that ibuprofen could reduce the size of the infarct associated with transient focal ischemia by inhibition of ICAM-1 expression, and they evaluated its effects in rats treated with middle cerebral artery (MCA) occlusion. Ibuprofen treatment was compared with mild systemic hypothermia, which is known to be neuroprotective and is commonly used during neurosurgical procedures. Methods. The maximum ibuprofen dose (240 mg/kg/day) that could be tolerated with no systemic toxicity was established in the initial experiments. In the efficacy experiment, rats were pretreated with vehicle, ibuprofen, or hypothermia (33°C) prior to 2 hours of MCA occlusion; then their brains were harvested at 24 hours of reperfusion for histological studies. End-ischemic cerebral blood flow (CBF) was evaluated using [14C]iodoantipyrine autoradiography in additional cohorts. Expression of ICAM-1 within ischemic compared with nonischemic caudate nucleus and putamen (striatum) or cortex was evaluated using immunohistochemical studies. Compared with vehicle treatment, ibuprofen produced a 46.2% reduction (p = 0.01) in striatal infarcts, which was comparable to hypothermia (48.7% reduction, p = 0.02). Ibuprofen did not alter end-ischemic CBF in any region studied, and the ibuprofen treatment group had the lowest proportion of animals with marked ICAM-1 staining. Conclusions. Ibuprofen given in maximum tolerated doses reduces the striatal infarct size after focal cerebral ischemia. The neuroprotective mechanism does not work through preservation of intraischemic CBF and is consistent with inhibition of ICAM-1 expression; however, at the doses used in this study, other effects of ibuprofen on platelet and endothelial function are possible.

Reduction by delayed hypothermia of cerebral infarction following middle cerebral artery occlusion in the rat: a time-course study

1992 ◽  
Vol 77 (3) ◽  
pp. 438-444 ◽  
Author(s):  
Christopher J. Baker ◽  
Stephen T. Onesti ◽  
Robert A. Solomon
Keyword(s):  
Body Temperature ◽  
Middle Cerebral Artery ◽  
Cerebral Artery ◽  
Time Course ◽  
Right Hemisphere ◽  
Infarct Volume ◽  
Moderate Hypothermia ◽  
Content Type ◽  
Mca Occlusion ◽  
Fine Print

✓ The effect of hypothermia on neuronal injury following permanent middle cerebral artery (MCA) occlusion in the rat was examined. Moderate hypothermia (body temperature 24°C) was induced before MCA occlusion (0-minute delay group) in six rats, at 30 minutes in eight rats, and at 1 (seven rats), 2 (seven rats), and 3 (nine rats) hours after occlusion. The rats were kept at a 24°C body temperature for 1 hour, then allowed to rewarm over 90 minutes. The animals were sacrificed 24 hours after MCA occlusion, and infarction was visualized by staining of coronal sections with 2,3,5-triphenyltetrazolium chloride. Infarct volumes were compared to matched normothermic control rats (body temperature 36°C). Additional groups of 0-minute delay hypothermic (10 rats) and control animals (nine rats) were sacrificed 72 hours after MCA occlusion to examine the effects of prolonged survival. A significant reduction in the percentage of infarcted right hemisphere was seen in the animals sacrificed after 24 hours with 0-minute, 30-minute, and 1-hour delays in inducing hypothermia (mean ± standard error of the mean: 2.2% ± 0.7%, 4.4% ± 0.9%, and 3.6% ± 1.1%, respectively) as compared to normothermic control rats (10.8% ± 1.5%, p < 0.01 by Student's t-test). In the 2- and 3-hour delay groups, the percentage of infarcted right hemisphere was 17.1% ± 2.4% and 12.0% ± 2.7%, respectively, and no decrease in infarct volume was observed. The 0-minute delay hypothermia group sacrificed after 72 hours also displayed a significant reduction in right hemisphere infarct compared to their respective controls (4.8% vs. 11.7%, p < 0.05). These findings indicate that, in the setting of permanent MCA occlusion, hypothermia markedly decreases brain injury even when its induction is delayed for up to 1 hour after the onset of ischemia. Ischemic damage does not appear to be merely retarded but permanently averted.

Effect of delayed albumin hemodilution on infarction volume and brain edema after transient middle cerebral artery occlusion in rats

1997 ◽  
Vol 87 (4) ◽  
pp. 595-601 ◽  
Author(s):  
Ludmila Belayev ◽  
Raul Busto ◽  
Weizhao Zhao ◽  
James A. Clemens ◽  
Myron D. Ginsberg
Keyword(s):  
Carotid Artery ◽  
Middle Cerebral Artery ◽  
Brain Edema ◽  
Cerebral Artery ◽  
Infarct Volume ◽  
Content Type ◽  
Mca Occlusion ◽  
Neurological Score ◽  
Albumin Therapy ◽  
Fine Print

✓ The authors examined the effect of delayed high-concentration albumin therapy on ischemic injury in a highly reproducible model of middle cerebral artery (MCA) occlusion in rats. Male Sprague—Dawley rats weighing 270 to 320 g were anesthetized with halothane and subjected to 120 minutes of temporary MCA occlusion induced by means of a poly-l-lysine—coated intraluminal nylon suture inserted retrograde via the external carotid artery into the internal carotid artery and MCA. The agent (20% human serum albumin [HSA]) or control solution (sodium chloride 0.9%) was administered intravenously at a dosage of 1% of body weight immediately after suture removal following a 2-hour period of MCA occlusion. The animals' neurological status was evaluated during MCA occlusion (at 60 minutes) and daily for 3 days thereafter. The brains were perfusion-fixed, and infarct volumes and brain edema were determined. The HSA significantly improved the neurological score compared with saline at 24 hours after MCA occlusion. The rats treated with HSA also had significantly reduced total infarct volume (by 34%) and brain edema (by 81%) compared with saline-treated rats. There was a strong correlation between hematocrit level and brain edema (p < 0.01), and between total infarct volume or brain edema and neurological score at 24, 48, and 72 hours postinjury (p < 0.0002). These results strongly support the beneficial effect of delayed albumin therapy in transient focal ischemia and indicate its possible usefulness in treating patients with acute ischemic stroke.

Posttraumatic bilateral middle cerebral artery occlusion

1975 ◽  
Vol 42 (2) ◽  
pp. 217-221 ◽  
Author(s):  
Skip Jacques ◽  
C. Hunter Shelden ◽  
D. Thomas Rogers ◽  
Anthony C. Trippi
Keyword(s):  
Middle Cerebral Artery ◽  
Middle Cerebral Artery Occlusion ◽  
Cerebral Artery ◽  
Artery Occlusion ◽  
Content Type ◽  
Pathophysiological Mechanisms ◽  
Cerebral Artery Occlusion ◽  
Fine Print

✓ The authors report a case of bilateral posttraumatic middle cerebral artery occlusion. Previously reported unilateral cases are reviewed and possible pathophysiological mechanisms disscussed.

Angiographic extravasation of contrast medium in acute traumatic subdural hematoma from arterial rupture

1972 ◽  
Vol 37 (2) ◽  
pp. 226-228 ◽  
Author(s):  
Jusuke Ito ◽  
Komei Ueki ◽  
Hisayuki Ishikawa
Keyword(s):  
Contrast Medium ◽  
Middle Cerebral Artery ◽  
Cerebral Artery ◽  
Subdural Hematoma ◽  
Carotid Angiography ◽  
Content Type ◽  
Arterial Rupture ◽  
Visual Evidence ◽  
Subpial Hemorrhage ◽  
Fine Print

✓ Carotid angiography of a patient with suspected subdural hematoma showed extravasation of the contrast medium from an ascending branch of the middle cerebral artery. The leak was verified at operation. There was no visual evidence of an aneurysm, angioma, subarachnoid or subpial hemorrhage.

Delayed breaking of a Heifetz aneurysm clip

1977 ◽  
Vol 47 (3) ◽  
pp. 463-465 ◽  
Author(s):  
Antti Servo ◽  
Matti Puranen
Keyword(s):  
Middle Cerebral Artery ◽  
Cerebral Artery ◽  
Left Middle Cerebral Artery ◽  
Carotid Angiography ◽  
Content Type ◽  
Aneurysm Clip ◽  
Correct Placement ◽  
Left Middle ◽  
Fine Print

✓ An aneurysm of the left middle cerebral artery was treated by clipping with a Heifetz clip. The correct placement was confirmed angiographically immediately after the operation. At carotid angiography 1 year later the clip was found to have broken, and the aneurysm had increased in size.

The perforating branches of the middle cerebral artery

1985 ◽  
Vol 62 (2) ◽  
pp. 261-268 ◽  
Author(s):  
Felix Umansky ◽  
Francisco B. Gomes ◽  
Manuel Dujovny ◽  
Fernando G. Diaz ◽  
James I. Ausman ◽  
...  
Keyword(s):  
Middle Cerebral Artery ◽  
Cerebral Artery ◽  
Interventional Neuroradiology ◽  
Great Majority ◽  
Outer Diameter ◽  
Main Trunk ◽  
Content Type ◽  
Brain Hemispheres ◽  
Medial Group ◽  
Fine Print

✓ The perforating branches (PFB's) of the middle cerebral artery (MCA) were studied in 34 unfixed brain hemispheres which were injected with a polyester resin and dissected under the operating microscope. Five hundred and eight vessels were identified and their site of origin, branching pattern, outer diameter (OD), and length recorded. Four hundred and two PFB's (79%) originated from the main trunk of the MCA before its division; the remaining 106 vessels (21%) had their origin from branches of the MCA as follows: superior trunk, 43 vessels (8.5%); inferior trunk, 30 vessels (6%); middle trunk, four vessels (0.8%); early temporal branch, 27 vessels (5.3%); and early frontal branch, two vessels (0.4%). The number of PFB's in each hemisphere varied from five to 29 (mean 14.9 ± 0.7 vessels). The great majority of PFB's (96%) originated along the proximal 17 mm of the MCA. The PFB's arising in the first 10 mm had a mean OD of 0.35 ± 0.01 mm and a mean length of 9.25 ± 0.19 mm, and those arising from the second 10 mm had a mean OD of 0.47 ± 0.02 mm and a mean length of 16.67 ± 1.4 mm. A clear distinction between a medial and lateral group of PFB's was present in only 14 hemispheres (41%). In nine hemispheres (26%), perforating vessels from the anterior cerebral artery (A1 segment) and from the recurrent artery of Heubner replaced the medial group of PFB's of the MCA. In one case this group originated in an accessory MCA. In three hemispheres (9%) a small anastomosis (OD 0.2 mm) was seen between a PFB of the recurrent artery of Heubner and one of the MCA. From a total of 508 PFB's, 255 vessels (50%) originated as single vessels, while 253 vessels (50%) originated as branches of common stems. The OD of the single vessels ranged from 0.1 mm to 1.1 mm (mean 0.39 ± 0.02 mm), and the length from 3 to 20 mm (mean 10.8 ± 0.2 mm). The common stems ranged in OD from 0.6 to 1.8 mm (mean 0.87 ± 0.04 mm), and in length from 1 to 15 mm (mean 4.1 ± 0.4 mm). The clinical application of these anatomical data to the management of aneurysms and arteriovenous malformations of the MCA, and in the field of interventional neuroradiology is described. The most frequent pathological entities involving the perforating vessels are also discussed.

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