Showing papers on "Middle cerebral artery published in 1985"

The biphasic opening of the blood-brain barrier to proteins following temporary middle cerebral artery occlusion.

Abstract: The behavior of the blood-brain barrier (BBB) was studied in cats following release after 1-h middle cerebral artery (MCA) occlusion. The regional cerebral blood flow (rCBF) was determined by hydrogen clearance method in the caudate nucleus and the cerebral cortex. The BBB was assayed with Evans blue (EB) tracer and by immunohistochemical peroxidase-antiperoxidase (PAP) method. Following release of MCA occlusion, there were two openings of the BBB, separated by a refractory period. The first opening, occurred shortly after recirculation; this was associated with rCBF below 15 ml/100 g/min during the ischemic period and a pronounced reactive hyperemia promptly following release of MCA occlusion. A refractory period of the BBB was indicated by the absence of EB leakage in cats injected with the tracer 30 min before killing at 3 h after recirculation, although the rCBF values in these animals were even lower (6 +/- 1 ml/100 g/min) during occlusion, and all of them showed a pronounced hyperemia after recirculation. The occurrence of the previous BBB opening in these animals was confirmed by the PAP staining. The second opening of the BBB was observed at 5 and 72 h after recirculation in cats which were injected with EB 30 min before killing, and which showed rCBF below 15 ml/100 g/min during occlusion, followed by a pronounced reactive hyperemia. No EB extravasations were observed at any time in cats in which the rCBF during occlusion was above 15 ml/100 g/min and which failed to show a marked reactive hyperemia.

Ischemic brain edema following occlusion of the middle cerebral artery in the rat. I: The time courses of the brain water, sodium and potassium contents and blood-brain barrier permeability to 125I-albumin.

Abstract: The present study was undertaken to analyze the roles of brain cations and of the blood-brain barrier (BBB) to albumin in the development of ischemic brain edema. Using the rat middle cerebral artery (MCA) occlusion model, changes in the brain water, sodium, and potassium contents were followed for a period of seven days. The permeability of the BBB to proteins was also followed by 125I-albumin transfer from the blood into the brain. A significant edema developed as early as three hours after MCA occlusion. This progressed rapidly to reach a maximum on the third day, gradually regressing thereafter. The increase in the brain water contents showed a parallel time course to the increase in the sodium and decrease in the potassium contents. A significant increase in the BBB permeability to albumin occurred 72 hours after MCA occlusion. However, there was no correlation between the brain water content and BBB permeability to albumin in the hemispheres studied 72 hours after MCA occlusion. The correlation between the brain water and sodium contents was not clear during the first six hours, but became highly significant thereafter. The data suggest that an increase in the BBB permeability to sodium occurred 12-48 hours after MCA occlusion, which, together with an antecedent intracellular shift of sodium, resulted in a massive influx of water and sodium into the brain. The BBB permeability change to sodium, not to proteins, seems to play a predominant role in the pathogenesis underlying ischemic brain edema.

Assessment of intracranial hemodynamics in carotid artery disease by transcranial Doppler ultrasound

Abstract: ✓ Noninvasive transcranial Doppler recordings were correlated to the angiographic findings in 77 patients with carotid artery disease. Stenoses reducing the luminal area of the internal carotid artery by 75% or more also reduced the pulsatility transmission index (PTI) of the ipsilateral middle cerebral artery (MCA). The PTI is the pulsatility index of the artery under study expressed as a percent of the pulsatility index of another intracranial artery with presumed unimpeded inflow in the same individual. For stenoses in the 75% to 89% category, PTI reduction was significantly greater in patients with bilateral carotid stenosis, indicating an impaired potential for collateral flow in these patients. The PTI reduction probably reflects both the pressure drop across the stenosis and the cerebral autoregulatory response. Two criteria proved useful in demonstrating collateral MCA supply through the circle of Willis. On the recipient side, retrograde flow in the proximal anterior cerebral artery was demonstra...

Multiple intracranial aneurysms: determining the site of rupture

Abstract: ✓ A retrospective hospital chart and radiograph review was performed of all patients with multiple intracranial aneurysms seen over a 52-month period. Sixty-nine patients with a total of 205 aneurysms were studied. Among the patients with aneurysms, the incidence of multiple aneurysms was 33.5%. Multiple aneurysms were much more common in women, with a female to male ratio of 5:1 for all patients and 11:1 for patients with three or more aneurysms. Common locations for multiple aneurysms were the posterior communicating artery (22%), middle cerebral artery (21.5%), anterior communicating artery (12%), and ophthalmic artery (11%). However, locations with the highest probability of rupture were the anterior communicating artery (62%), posterior inferior cerebellar artery (50%), and basilar artery summit (50%). The middle cerebral artery was the least likely site for rupture. In contrast to previous studies, in this series irregularity of contour was more important than size in identifying the site of rupture...

CBF and time thresholds for the formation of ischemic cerebral edema, and effect of reperfusion in baboons

Abstract: Ischemic cerebral edema has been studied in 41 baboons, with regional cerebral blood flow (CBF) determined by hydrogen clearance, and edema measured by microgravimetry. A threshold of ischemia has been identified for baboon cortex and subcortical white matter, which has to be crossed before edema formation begins. This threshold is 40.5% of normal CBF in cortex, and 34.4% of normal flow in subcortical white matter. A time threshold has also been determined, and the baboon brain can withstand 30 minutes of ischemia of the middle cerebral artery without significant edema formation. Reperfusion of ischemic brain has no effect on tissue water if the ischemic flow and time thresholds have not been crossed. Reperfusion of cortex, where water has begun to accumulate, exacerbates the water accumulation in proportion to the extent of the reperfusion. If these results are applicable to man, restoration of flow should not be attempted after an ischemic insult that reduces flow to less than 40% of normal unless it can be accomplished within 30 minutes of the insult. Provided CBF can be restored to above the 40% threshold within 30 minutes, reversal of the neurological deficit and prevention of ischemic edema can be expected.

Effect of pretreatment with the calcium antagonist nimodipine on local cerebral blood flow and histopathology after middle cerebral artery occlusion.

Abstract: We used the [14C]iodoantipyrine autoradiography technique to study the effect of pretreatment with the calcium antagonist nimodipine on local cerebral blood flow (lCBF) in rats that underwent middle cerebral artery (MCA) occlusion. In untreated control animals there were profound localized reductions in 1CBF 30 minutes after MCA occlusion. These were most pronounced in neocortical areas and in the caudate nucleus ipsilateral to the MCA occlusion. In animals pretreated with nimodipine (1 microgram X kg-1 X min-1 for 30 minutes before and 30 minutes after MCA occlusion), the ipsilateral decrease in 1CBF in cortical regions was significantly less than that in control animals. The drug did not appear to alter 1CBF in the ipsilateral caudate nucleus. Neuropathological quantification of the ischemic damage present 3 hours after occlusion showed that nimodipine pretreatment reduced the volume and extent of cellular damage in the periphery but not in the core of the lesion.

The International Cooperative Study of Extracranial/Intracranial Arterial Anastomosis (EC/IC Bypass Study): methodology and entry characteristics. The EC/IC Bypass Study group.

Abstract: This report summarizes the protocol of a randomized trial of superficial temporal artery-middle cerebral artery (STA-MCA) bypass procedure and presents the entry characteristics of its patients. The trial has been designed to determine whether this EC/IC bypass reduces the rate of subsequent stroke among patients with recent hemispheric or retinal strokes and/or transient ischemic attacks who have angiographically proven atherosclerotic narrowing or occlusion of the ipsilateral internal carotid or middle cerebral artery. Of the 1377 eligible patients entered from the 71 participating centers, 714 (52%) have been assigned to medical treatment alone (daily aspirin and aggressive hypertension control) while 663 (48%) have been assigned to receive STA-MCA bypass in addition to medical therapy. The two treatment groups have been well balanced for important prognostic factors. Bypass patency rates of 95% have been documented. At the end of the study in mid-1985, an average follow-up of five years and a minimum follow-up of 33 months will have been achieved. On both clinical and methodologic grounds, this study will have provided a rigorous test of the STA-MCA bypass procedure.

Occlusive disease of the middle cerebral artery.

Abstract: We studied 20 patients with severe occlusive disease of the mainstem middle cerebral artery (MCA) or its major division branches, and 25 patients with internal carotid artery (ICA) disease. MCA disease patients were more often black, female, younger, and had fewer TIAs than the ICA disease patients. Neurologic signs in patients with MCA disease evolved progressively during days to weeks, whereas ICA disease patients more often had an acute onset of nonprogressive deficits. CT commonly showed restricted subcortical or wedge-shaped infarcts in MCA disease patients. All MCA disease patients had stroke, but 40% of ICA disease patients had no infarction. MCA lesions usually affected the mainstem MCA or its major superior division. Patients with MCA disease seldom had recurrent ischemia in the same vascular territory as the stroke and had a low incidence of subsequent cardiac death.

Recirculation model following MCA occlusion in rats. Cerebral blood flow, cerebrovascular permeability, and brain edema.

Abstract: A new model for establishing a successful and consistent arterial recirculation has been devised following middle cerebral artery (MCA) occlusion in the rat. A snare ligature was introduced at the stem of the MCA just distal to the lenticulostriate branches, and occlusion and recirculation were performed by pulling and releasing the thread. This method had an advantage over the use of a small clip which caused damage to the artery without good recirculation. Study of local cerebral blood flow using carbon-14 (14C)-iodoantipyrine, of cerebrovascular permeability using 14C-aminoisobutyric acid, and of brain-water content using the microgravimetric technique was performed upon recirculation following various periods of occlusion and compared with the results in permanent ischemia. A reactive hyperemia was noted within the previously ischemic area immediately upon recirculation following either a 30-minute or a 2-hour ischemic period. One or 2 hours later, delayed hypoperfusion developed in this region, but the circulation over the periphery of the ischemic area recovered well. Cerebrovascular permeability was not, however, altered during the time courses studied. Topographic changes in tissue specific gravity were compared between permanent and transient ischemia in the corresponding time-courses. Although there was a greater decrease in tissue specific gravity following recirculation when the ischemic period was maintained longer, edema formation was resolved by recirculation. Further study is required to determine thresholds of ischemic brain damage and edema formation at recirculation following focal cerebral ischemia.

Effects of extra-intracranial arterial bypass on cerebral blood flow and oxygen metabolism in humans.

Abstract: Twelve patients, eleven with a carotid obstruction and one with an occlusion of the middle cerebral artery, were studied before and after a successful unilateral extra-intracranial arterial by-pass, (EIAB) using PET and the 15-0 steady-state technique to measure regional cerebral blood flow (CBF), oxygen extraction fraction and oxygen metabolic rate (CMRO2). In the whole group of patients, both CBF and CMRO2 increased significantly on both cerebral hemispheres after EIAB, returning toward control levels defined in age-matched subjects. Mean oxygen extraction fraction, on the other hand, was not affected. Individually, three different effects of EIAB emerged: 1) Alleviation of a state of long standing unilateral "misery-perfusion", as reported earlier; 2) parallel increase of CBF and CMRO2 bilaterally, which appeared due to improvement of a hemodynamic depression of metabolism, the precise mechanism of which remains obscure; 3) Complex, unexpected changes in the CBF-CMRO2 couple again resulting in increases in CMRO2. This metabolic improvement afforded by EIAB in our patients has not been reported before; it suggests that long-standing hemodynamic failure may induce a metabolic depression that is still potentially reversible by surgical revascularization.

Perforating branches of the middle cerebral artery: Microsurgical anatomy of their extracerebral segments

Abstract: Perforating branches of the middle cerebral artery (MCA) were examined under magnification in 50 formalin-fixed brain hemispheres. Perforating vessels varied in number from three to 18, with an average of nine. The greater the number of vessels, the smaller was their diameter. In this study, the perforating arteries were divided into medial, middle, and lateral groupings. Those in the medial group usually arose directly from the MCA main trunk close to the carotid bifurcation. There were usually three vessels in the middle group, which originated not only from the MCA trunk, but also from the MCA collateral (cortical) branches. Common stems, when present, gave rise to individual perforating vessels and occasionally to thin olfactory and insular rami. Perforating arteries in the lateral group varied from one to nine in number. In addition to an origin from the MCA trunk, they also arose from cortical branches supplying the frontal and temporal lobes. The fact that lateral perforating vessels often originated from division sites and from terminal branches of the MCA is of clinical significance, because aneurysms are more commonly located at the MCA bifurcation. Anastomoses were not found among the perforating arteries. In two specimens, a fusion between a perforating artery and the MCA trunk was noted. Since the perforating vessels are obviously end arteries, injury to them must be avoided during operations for MCA aneurysms.

Cause of cerebral infarction in the carotid territory. Its relation to the size and the location of the infarct and to the underlying vascular lesion.

Abstract: Seventy-three patients with acute nonhemorrhagic stroke in the carotid territory were investigated for the cause of the stroke: middle cerebral artery (MCA) occlusion/stenosis or internal carotid artery (ICA) occlusion/stenosis; embolus from the heart and extra-cranial arteries or thrombosis. The study is prospective and consecutive comprising stroke patients below the age of 75 years, admitted in the acute state i.e. within 3 days after stroke onset. Excluded were patients with intracerebral hematoma, subarachnoid hemorrhage, vertebrobasilar stroke and patients in whom another severe disease was present. Cerebral angiography and CT-scan were performed in all patients within one and two days after admission. CT-scan was repeated 2 weeks and 6 months later. Forty percent had MCA occlusion, none had MCA stenosis, 12% had ICA occlusion, 14% had severe ICA stenosis (half of these were associated with MCA occlusion) and 41% were without significant MCA/ICA lesions. Twenty-seven percent had large infarcts with a diameter greater than 3 cm; 34% had medium-sized infarcts with a diameter between 3 and 1.5 cm; 21% had small infarcts with a diameter less than 1.5 cm; 18% had no identifiable infarct on CT-scan. MCA occlusion was responsible for 62% of the large or medium-sized infarcts. ICA occlusion or severe ICA stenosis were responsible for only 27% of the large or medium-sized infarcts. Only 11% of the patients with small or no infarct on CT-scan had significant MCA/ICA lesion.(ABSTRACT TRUNCATED AT 250 WORDS)

Multiparametric imaging of blood flow and metabolism after middle cerebral artery occlusion in cats.

Abstract: In anesthetized adult cats, acute stroke was produced by transorbital occlusion of the left middle cerebral artery. A battery of imaging techniques was used for simultaneous evaluation of regional blood flow, glucose utilization, protein synthesis, pH, and the regional tissue content of glucose, ATP, and potassium. The electrophysiological impact of stroke was monitored by EEG frequency analysis and recording of somatosensory evoked potentials. Two hours after vascular occlusion, a close correlation existed between the degree of electrophysiological changes and biochemical alterations, in particular with the extent of tissue acidosis, ATP depletion, decrease of tissue potassium content, and suppression of protein synthesis. However, there was only a poor correlation with blood flow and glucose utilization. Both of these exhibited a greatly inhomogeneous pattern with regions of reduced, normal, or increased rates. In areas remote from the infarct, the content of biochemical substrates was normal but blood flow was reduced globally by approximately 50% and glucose utilization by approximately 20%. An anatomically defined regional pattern of cerebral or cerebellar diaschisis was not observed. It is concluded that during the acute phase of stroke, imaging of blood flow and glucose utilization does not provide an accurate estimate of the actual functional or metabolic disturbance. For the clinical evaluation of the development or treatment of stroke, in consequence, alternative noninvasive techniques such as imaging of protein synthesis and/or pH may be more relevant.

Emergency embolectomy for acute occlusion of the middle cerebral artery

Abstract: ✓ Twenty cases treated with emergency embolectomy for acute occlusion of the middle cerebral artery were reviewed. There were 10 males and 10 females, with an average age of 55 years. The left middle cerebral artery was involved in 17 patients and the right in three. Flow was restored in 16 patients (75%). The embolus originated in the heart in seven, the carotid artery in seven, the aorta in three, an aneurysm in one, and an indeterminate source in two. It was technically most difficult to achieve patency with atheromatous emboli from the aorta. Two patients (10%) had an excellent result with no neurological deficit, five (25%) were left with a minimal deficit but were employable, seven (35%) had a fair result but were still independent and employable, four (20%) did poorly, and two (10%) died. Patients with an associated ipsilateral carotid artery occlusion did poorly. Collateral flow, as judged from preoperative angiograms, was the best predictor of outcome.

Results, complications, and follow-up of 415 bypass operations for occlusive disease of the carotid system.

Abstract: Selected patients with acute or continuing ischemic symptoms from occlusions or inaccessible stenotic lesions of the internal carotid artery or middle cerebral artery have been considered candidates for a carotid artery-middle cerebral artery bypass procedure at our institution since July 1974. We report herein an 8-year experience through June 1982 with 415 operations in 403 patients in whom a branch of the superficial temporal artery was anastomosed to a branch of the middle cerebral artery. Patients selected for operation usually had had more than one form of ischemic symptom. The primary indication for operation was transient ischemic attacks, and the most common vascular pathologic condition was internal carotid artery occlusion. Preoperatively, 183 patients were taking antiplatelet agents and 157 were taking anticoagulants. Neurologic function 6 months postoperatively was equal to or better than the function preoperatively in 95% of survivors. The bypass pedicle was patent in 99% of patients studied. The mortality and morbidity associated with the surgical procedure varied on the basis of the patient's preoperative neurologic condition but were 1% and 4%, respectively, for the entire group at 30 days postoperatively. Of the 54 deaths during the entire follow-up period, 27 were cardiogenic and 6 were from ischemic stroke. On the basis of patient-months of follow-up, stroke was 8 times more likely to occur within 6 months after operation than thereafter.

Correlation of local cerebral blood flow, glucose utilization, and tissue pH following a middle cerebral artery occlusion in the rat.

Abstract: The use of three sets of the double-tracer autoradiographic technique to measure topographical changes of local cerebral blood flow (LCBF), glucose utilization (LCGU), and tissue pH following a 3 h middle cerebral artery (MCA) occlusion in the rat is described. In a sham-operated group of animals there was 10% reduction of LCBF and 7% reduction of LCGU in the most affected areas as compared to the contralateral homologous regions. However, the ratio of LCGU/LCBF in the affected areas remained within normal limits. In the MCA-occluded animals, LCGU showed a bimodal response to decreased LCBF. LCGU decreased with reduced LCBF until LCBF fell to 38% of normal. Below this LCBF level LCGU increased, most likely implying anerobic glycolysis. Decline of tissue pH corresponds to the mismatch of LCBF and LCGU. These results suggest that brain tissue pH change cannot be predicted on the basis of LCBF or LCGU alone.

Somatosensory evoked potentials as a measure of experimental cerebral ischemia

Abstract: Somatosensory evoked potentials (SEP's) reflect the integrity of the central neuronal pathway, and as such may be used to assess function that remains during a variety of cerebral insults. To evaluate the natural history and utility of SEP's during experimental cerebral ischemia and infarction, SEP's were measured in 17 adult cats at 24 hours and 1 hour prior to right middle cerebral artery (MCA) occlusion, and again immediately afterward and at either 6 hours (five cats) or 24 hours (six cats) post-occlusion. Before occlusion of the right MCA, the SEP's were identical in the right and left hemispheres. After occlusion, there was a significant slowing of the interpeak latency of the first positive peak (P1) in the right hemisphere (3.53 +/- 0.6 msec before compared to 3.99 +/- 0.6 msec after occlusion, p less than 0.001). Maximal slowing in right hemisphere P1 latency was seen in those animals in which the stroke extended into the thalamus (4.38 +/- 0.1 msec). This was significantly slower than left hemisphere values (3.92 +/- 0.32 msec, p less than 0.01). The ipsilateral cortical components of the SEP's, the second positive peak (P2), and the major negative deflection (MN) were slowed in all cats immediately after right MCA occlusion compared to preocclusion measurements (p less than 0.001). Severe infarcts in the mid-suprasylvian and posterior ectosylvian gyri (including the somatosensory cortex) resulted in a greater slowing of the latency of MN compared to less severe infarcts in that region (20.6 +/- 3.9 msec versus 16.4 +/- 1.1 msec, p less than 0.05). There was a precipitous decrease in the amplitude or voltage of the ipsilateral P2-MN complex immediately after occlusion (5.32 +/- 0.4 microV before compared to 0.98 +/- 0.3 microV after occlusion, p less than 0.001). Therefore, the central latencies and cortical amplitudes of the SEP's are sensitive experimental tools as indicators of the onset and extent of a cerebral ischemic insult.

Acute cerebral revascularization

Abstract: Fifteen patients evaluated for acute cerebral ischemia underwent acute cerebral revascularization between March, 1979, and May, 1983. Clinical presentation included crescendo transient ischemic attacks (TIA's) in eight cases, progressing neurological dysfunction in three cases, and completed nonfluctuating deficits in four cases. Nine patients received intravenous heparin but did not improve neurologically. The patients with crescendo TIA's were operated on within 4 hours of their last event; those with progressing deficits were operated on while the deficit was developing, and those with established deficits were operated on 4, 6, 9, and 12 hours, respectively, after the event began. The clinical picture for 10 patients had resolved within 10 hours after surgery. One patient with crescendo TIA's, two with progressing deficits, and two with established deficits had postoperative residual deficits, of which three were mild and two severe. One patient, who had a saphenous vein graft to the middle cerebral artery, developed an intracerebral hematoma. In this prospective noncontrolled nonrandomized study, acute cerebral revascularization was performed safely, had limited risks, and offered the potential to help some patients. Further controlled randomized studies are indicated.

Regional flow-metabolism couple following middle cerebral artery occlusion in cats.

Abstract: The regional flow-metabolism couple was studied during the recovery period after 1 h of left middle cerebral artery (MCA) occlusion in cats. Local CBF (LCBF) was assessed at the end of ischemia as well as at the end of 4 h of recirculation by the microsphere technique. Local CMRgl (LCMRgl) was measured at the end of the recirculation period with [14C]2-deoxyglucose. Histology was evaluated by light microscopy from coronal brain blocks adjacent to those used for the determination of LCBF and LCMRgl. When LCBF in the central and peripheral MCA territories during the recovery period was between 40 and 115% of the value in sham occlusion studies, LCMRgl was greater than the control level found in the sham studies, and was accompanied by slight histological damage. This finding suggests that anaerobic glycolysis may persist after transient ischemia in spite of the recovery of LCBF to a level that is normally greater than the threshold for the activation of anaerobic glycolysis (<40% of the control). Persistent...

Cellular mechanism of force development in cat middle cerebral artery by reducedPCO2

Abstract: These studies were undertaken to determine the effect of reducing aPCO2 below physiological levels on cat middle cerebral artery. Upon reduction ofPCO2 from 37 to 14 torr (pH 7.4) we observed membrane depolarization and force development. ReducingPCO2 decreased the slope of theEm vs. log [K]o curve and increased the slope of the steady-state I/V relationship suggesting that the change inEm was due to reduction of outward K+ conductance (gk). Elevation of pH from 7.37 to 7.6 had a very similar effect on these cerebral arterial muscle cells, depolarizing the muscle membrane (reducing theEm vs. log [K]o curve) and increasing the slope of the I/V relationship to statistically equivalent values as reduction ofPCO2. ReturningPCO2 from 14 to 37 torr rapidly relaxed these preparations, but only transiently. This relaxation was followed by a rebound contraction within 3 min, demonstrating a transient nature for the action of elevatingPCO2 in cerebral arteries. The response to changing pHo followed a slower time course but did not change with time. These studies demonstrate that both elevated pHo and reducedPCO2 activate cerebral arterial muscle by a mechanism which includes reduction ingk. However, it can not be determined if these similar responses and reduction, ofgk are mediated by changing pHi or mediated through different mechanisms. It is possible that pHo andPCO2 can modify cerebral arterial tone by direct mechanisms and not necesarily by their effect on pHi. It is clear, however, that reduction ofPCO2 and elevation of pHo both activate cerebral arterial muscle by a mechanism which includes reduction ofgk.

The Cerebral Infarct Pathology, Pathogenesis, and Computed Tomography

Abstract: I Cerebral Infarcts and Computed Tomograms.- 1 Introduction.- 2 Incidence of Cerebral Infarcts in a Series of Unselected Computed Cranial Tomograms.- 3 Concept of Cerebral Infarction.- 3.1 General Semiology of Infarction.- 3.2 The Hemorrhagic Type of Infarction.- 4 Technical Aspects of Interpreting Computed Tomograms.- 4.1 Time Course of the Changes in Density of the Tissue.- 4.2 Contrast Enhancement.- 4.3 The Fogging Effect.- 4.4 Increased Volume of the Tissue.- 4.5 Protein-Rich Edema.- 4.6 Improper Prognosis.- 4.7 Relating a Focal Lesion to a Transient Ischemic Attack.- 4.8 Flow Measurements.- II Correlations of CT Scan Patterns with Pathoanatomical Specimens.- III The Systematic Classification of Brain Infarcts.- 1 Carotid Territory.- 1.1 Superficial Infarcts in the Territory of the Middle Cerebral Artery.- 1.1.1 Infarcts of the Middle Cerebral Artery.- 1.1.1.1 Complete Infarct of the Middle Cerebral Artery Including the Striate and Anterior Choroidal Arteries.- 1.1.1.2 Infarct of the Middle Cerebral Artery Excluding the Striate Arteries.- 1.1.1.3 Infarct of the Middle Cerebral Artery, Anterior Third.- 1.1.1.4 Infarct of the Middle Cerebral Artery, Middle Third.- 1.1.1.5 Infarct of the Middle Cerebral Artery, Posterior Third.- 1.1.1.6 Four Special Types of Infarct Within the Territory of the Middle Cerebral Artery.- 1.1.1.7 Spotty Infarcts of the Territory of the Middle Cerebral Artery.- 1.1.1.8 Bilateral Infarcts of the Middle Cerebral Artery.- 1.1.1.9 Subcortical Infarct in the Territory of the Middle Cerebral Artery.- 1.1.2 Infarcts in the Anterior Cerebral Artery Territory.- 1.1.2.1 Infarcts of the Anterior Cerebral Artery, Anterior Division.- 1.1.2.2 Infarcts of the Anterior Cerebral Artery, Posterior Division.- 1.1.2.3 Total Infarction of the Anterior Cerebral Artery Territory.- 1.1.2.4 Spotty Infarcts in the Anterior Cerebral Artery Territory.- 1.1.2.5 Infarcts in the Territory of the Long Central Artery (Recurrent Artery of Heubner).- 1.1.3 Combined Infarcts.- 1.1.3.1 Combined Infarcts of the Anterior and Middle Cerebral Artery Territories.- 1.1.3.2 Combined Infarcts of the Middle and Posterior Cerebral Arteries.- 1.1.4 Total Infarcts of the Internal Carotid Artery Territory.- 1.2 Deep Infarcts in the Area of the Middle Cerebral Artery.- 1.2.1 Infarcts in Putamen and Head of Caudate Nucleus (Borderline Pattern).- 1.2.2 Total Infarcts of the Striatum.- 1.2.3 Terminal Infarcts in Putamen and/or Caudate Nucleus (Most Distant Field).- 1.2.4 Lacunar Infarcts.- 1.2.4.1 Lacunar Infarct in the Semioval Center.- 1.2.4.2 Lacunar Infarct in Thalamus.- 1.2.4.3 Lacunar Infarct in Putamen.- 1.2.4.4 Lacunar Infarct in Pons.- 1.2.4.5 Lacunar Infarct in Cerebellum.- 1.2.4.6 Lacunar Infarcts in the Territory of the Anterior Choroidal Artery.- 2 The Vertebrobasilar Circulation - Infarcts in the Territory of the Vertebral and Basilar Arteries 58.- 2.1 Infarcts in the Territory of the Posterior Cerebral Artery.- 2.1.1 Infarcts of the Calcarine Artery (Medial Occipital Infarct).- 2.1.2 Infarcts of the Occipitotemporal Artery (Lateral Occipital Infarct).- 2.1.3 Cortical Infarcts Within the Area of the Posterior Cerebral Artery.- 2.1.4 Total Infarct of the Posterior Cerebral Artery.- Bilateral Infarcts of the Posterior Cerebral Arteries.- 2.1.6 Infarcts in the Center of the Territory of the Posterior Cerebral Artery.- 2.2 Infarcts in Thalamus (Thalamogeniculate and Thalamoperforate Arteries).- 2.3 Infarcts in Cerebellum.- 2.3.1 Dorsal Cerebellar Infarct (Superior Cerebellar Artery).- 2.3.2 Ventral Cerebellar Infarcts (Anterior Inferior Cerebellar Artery).- 2.3.3 Infarcts at the Watersheds (Border Zone) of the Cerebellar Arteries.- 2.3.4 Infarcts in the Pedunculi (Perforating Arteries, Unilateral or Bilateral).- 2.3.5 Infarcts of Pons (Paramedian Pontine Artery, Short and Long Circumflex Arteries).- 2.3.5.1 Infarct of the Paramedian Pontine Artery.- 2.3.5.2 Infarct of the Long Circumflex Pontine Artery.- 2.3.5.3 Infarcts of the Posterior Inferior Cerebellar Artery (Wallenberg's Artery).- 3 The Watershed (Border Zone) Infarcts.- 3.1 Annular Infarcts.- 3.1.1 Annular Infarct of the Watersheds, Anterior Part.- 3.1.2 Annular Infarct of the Watersheds, Posterior Part.- 3.1.3 Three-Territory Border Infarct (Dreilandereck-Infarkt).- 4 The Multiinfarct Brain.- 5 Atrophic Processes: Ischemic Atrophies.- Addendum.- References.- Name Index.

Cerebral revascularization to a main limb of the middle cerebral artery in the Sylvian fissure. An alternative approach to conventional anastomosis.

Abstract: ✓ Thirteen patients underwent an anastomosis of the superficial temporal artery (STA) or a saphenous vein graft to one of the secondary trunks of the middle cerebral artery (MCA). They included five patients with giant MCA trifurcation aneurysms, four patients in whom an earlier conventional STA-MCA anastomosis had become occluded, two patients who had stenosis of one of the secondary limbs of the MCA, and one patient who had a carotid-cavernous fistula. One patient had a saphenous vein graft from the common carotid artery to a secondary trunk of the MCA to bypass an occluded internal carotid artery and severely stenosed external carotid artery. The primary advantages of this procedure are that a large-caliber anastomosis to one of the secondary limbs of the MCA immediately restores flow into the MCA tree with a larger amount of vessel filling than with a standard cortical bypass, and large vessels can be used for the anastomosis. The disadvantages are that one of the secondary branches of the MCA must be...

Polyamine and prostaglandin markers in focal cerebral ischemia.

Abstract: This study examines the pathophysiology of stroke secondary to focal cerebral ischemia. The interaction of arachidonic acid metabolites and polyamines, a class of ubiquitous ornithine-derived molecules with important membrane effects on edema, Ca++-dependent endocytosis, platelet function, and prostaglandin (PG) formation, are correlated with regional changes in H2 clearance, cerebral blood flow (rCBF), ischemic edema, and somatosensory evoked responses (SSERs) after middle cerebral artery (MCA) occlusion. Thirty cats were studied up to 3 hours before and 6 hours after right MCA occlusion. Four areas of brain showing different levels of perfusion after MCA occlusion were sampled for tissue levels of PGs: 6-keto-PGF1 alpha, PGE2, and as well as thromboxane B2 (TXB2), ornithine decarboxylase activity (ODC) (a measure of polyamine activity) and gravimetric determination of cerebral edema. After right MCA occlusion, right hemisphere SSER amplitude decreased and interpeak latency increased markedly. rCBF was distributed into zones of dense, partial, and no ischemia ranging from 12.6 to 59.4 ml/100 g/minute. Ischemic edema was distributed inversely to rCBF and was increased in areas of dense ischemia (85.2 +/- 0.5%) and ischemia (82.7 +/- 0.7%), but not in partially ischemic or control areas. 6-Keto-PGF1 alpha (1257.3 pg/mg), PGE2 (1628.5 pg/mg), and TXB2 (1572.8 pg/mg) were all significantly (P less than 0.05) increased in areas of partial ischemia that had not yet developed edema. ODC levels were significantly elevated (3812 pmole/g/hour, P less than 0.05) and increased with time in areas of slightly denser ischemia that showed an intermediate increase in edema, but not the presence of infarction. This is the first demonstration that ODC, the rate-limiting enzyme for polyamine synthesis, is stimulated by cerebral ischemia.(ABSTRACT TRUNCATED AT 250 WORDS)

Modification of cerebral ischemia with Fluosol.

Abstract: Fluosol-DA (Perfluorochemical Blood Substitute) was investigated in a previous study and found to provide some protection from ischemia and possible usefulness in limiting the size of infarction. In the present study, larger doses over longer periods of acute focal cerebral ischemia were used. Twenty four cats had transorbital ligation of the middle cerebral artery (MCA). The 12 experimental animals were given 20% Fluosol-DA. The control group of 12 received isotonic saline solution. Twenty-four hours after the MCA occlusion, the cats were perfused with saline and phosphate-buffered formalin. The brains were removed and immersed in 10% formalin for 2 weeks. The results of macroscopic and histological examination suggested that, although Fluosol-DA did not provide complete protection from ischemic injury to the brains of the cats treated, it may have helped to slow the development of the pathological changes.

Rupture of previously unruptured giant carotid aneurysm after superficial temporal-middle cerebral artery bypass and internal carotid occlusion.

Abstract: A 51-year-old woman with an unruptured giant aneurysm of the internal carotid artery was treated by gradual occlusion of the internal carotid artery in the neck combined with a superficial temporal artery to middle cerebral artery bypass graft. Visual field defects improved after the operation, and thrombosis of the aneurysm was confirmed by angiography and computed tomography. Nevertheless, a fatal hemorrhage occurred 34 days after the final turn of the Selverstone clamp. The possible mechanism of rupture of the apparently thrombosed aneurysm is discussed. There is a risk of rupture of the aneurysm as long as the aneurysmal lumen remains after proximal ligation, no matter how small it may be.