Showing papers on "Middle cerebral artery published in 1991"

Polymorphonuclear leukocytes occlude capillaries following middle cerebral artery occlusion and reperfusion in baboons.

Abstract: Microvascular perfusion defects may accompany sustained occlusion and subsequent reperfusion of the middle cerebral artery; however, the nature of such "no-reflow" defects remains unclear.In the absence of antithrombotic pretreatment, we documented lenticulostriatal microvascular flow integrity following 3-hour middle cerebral artery occlusion and 1-hour reperfusion in a baboon occlusion/reperfusion model by two methods identifying 1) microvascular occlusion and 2) microvascular patency.Microvascular "no-reflow" involved capillaries (vessels of 4.0-7.5 microns diameter) of the lenticulostriatal territory. Capillary reflow included 27-39% of all capaillaries in two subjects, indicating a significant reduction of perfusion from normal (2p = 0.045). In identical experimental preparations, single polymorphonuclear leukocytes completely occluded 4.7% of microvessels of capillary diameter in randomly selected fields, partially occluded 3.5% of postcapillary venules, and occluded 40% (four of 10) of capillaries ...

Polymorphonuclear leukocyte infiltration into cerebral focal ischemic tissue: myeloperoxidase activity assay and histologic verification

Abstract: Two different techniques were utilized to identify the infiltration of polymorphonuclear leukocytes (PMN) into cerebral tissue following focal ischemia: histologic analysis and a modified myeloperoxidase (MPO) activity assay. Twenty-four hours after producing permanent cortical ischemia by occluding and severing the middle cerebral artery of male spontaneously hypertensive rats, contralateral hemiparalysis and sensory-motor deficits were observed due to cerebral infarction of the frontal and parietal cortex. In hematoxylin-and-eosin-stained histologic sections, PMN, predominantly neutrophils, were identified at various stages of diapedesis from deep cerebral and meningeal vessels at the periphery of the infarct, into brain parenchyma. When MPO activity in normal brain tissue was studied initially, it could not be demonstrated in normal tissues extracted from non-washed homogenates. However, if tissue was homogenized in phosphate buffer (i.e., washed), MPO activity was expressed upon extraction. Utilizing this modified assay, MPO activity was significantly increased only in the infarcted cortex compared to other normal areas of the brain. This was observed in non-perfused animals and after perfusion with isotonic saline to remove blood constituents from the vasculature prior to brain removal. The increased PMN infiltration and MPO activity were not observed in forebrain tissue of sham-operated control rats. Also, MPO activity was not increased in the ischemic cortex of MCAO rats perfused immediately after middle cerebral artery occlusion, indicating that blood was not trapped in the ischemic area. By using a leukocyte histochemical staining assay, activity of peroxidases was identified within vascular-adhering/infiltrating PMN in the infarcted cortex 24 hr after focal ischemia. An evaluation of several blood components indicated that increased MPO activity was selective for PMN. The observed increase of approximately 0.3 U MPO/g wet weight ischemic tissue vs. nonischemic cerebral tissues probably reflects the increased vascular adherance/infiltration of approximately 600,000 PMN/g wet weight infarcted cortex 24 hr after focal ischemia. This combined biochemical and histological study strongly suggests that PMN adhere within blood vessels and infiltrate into brain tissue injured by focal ischemia and that the associated inflammatory response might contribute to delayed progressive tissue damage in focal stroke. This modified MPO assay is a useful, quantitative index of PMN that can be utilized to elucidate the potential deleterious consequences of neutrophils infiltrating into the central nervous system after cerebral ischemia, trauma, or other pro-inflammatory stimuli.

Ischemic thresholds of cerebral protein synthesis and energy state following middle cerebral artery occlusion in rat.

Abstract: The ischemic threshold of protein synthesis and energy state was determined 1, 6, and 12 h after middle cerebral artery (MCA) occlusion in rats. Local blood flow and amino acid incorporation were measured by double tracer autoradiography, and local ATP content by substrate-induced bioluminescence. The various images were evaluated at the striatal level in cerebral cortex by scanning with a microdensitometer with 75 microns resolution. Each 75 x 75 microns digitized image pixel was then converted into the appropriate units of either protein synthesis, ATP content, or blood flow. The ischemic threshold was defined as the flow rate at which 50% of pixels exhibited complete metabolic suppression. One hour after MCA occlusion, the threshold of protein synthesis was 55.3 +/- 12.0 ml 100 g-1 min-1 and that of energy failure was 18.5 +/- 9.8 ml 100 g-1 min-1. After 6 and 12 h of MCA occlusion, the threshold of protein synthesis did not change (52.0 +/- 9.6 and 56.0 +/- 6.5 ml 100 g-1 min-1, respectively) but the threshold of energy failure increased significantly at 12 h following MCA occlusion to 31.9 +/- 9.7 ml 100 g-1 min-1 (p less than 0.05 compared to 1 h ATP threshold value; all values are mean +/- SD). In focal cerebral ischemia, therefore, the threshold of energy failure gradually approached that of protein synthesis. Our results suggest that with increasing duration of ischemia, survival of brain tissue is determined by the high threshold of persisting inhibition of protein synthesis and not by the much lower one of acute energy failure.(ABSTRACT TRUNCATED AT 250 WORDS)

Temporal thresholds for neocortical infarction in rats subjected to reversible focal cerebral ischemia.

Abstract: We investigated the temporal threshold for focal cerebral infarction in the spontaneously hypertensive rat. The right middle cerebral artery and common carotid artery were occluded for 0, 1, 2, 3, 4, or 24 hours, and all the animals were sacrificed 24 hours after the onset of ischemia. Cortical infarct volumes and edema volumes were quantified in serial frozen sections of hematoxylin and eosin-stained tissue using image analysis. Upon occlusion, blood flow in the core of the ischemic zone, measured with laser-Doppler flowmetry, fell to a mean +/- standard deviation of 21 +/- 7% of the preocclusion baseline value (n = 26). During the first hour of ischemia, blood flow in the densely ischemic zone rose to 27 +/- 8% of baseline (n = 25). Release of the middle cerebral artery and common carotid artery occlusions rapidly restored cortical blood flow to 213 +/- 83% of baseline (n = 21). Focal ischemia of 1 hour's duration caused little or no infarction, while ischemic intervals of 2 and 3 hours produced successively larger volumes of infarcted cortex. Ischemic intervals of 3-4 hours' duration followed by approximately 20 hours of recirculation yielded infarct volumes that were not significantly different from those after 24 hours of permanent focal ischemia. The results indicate that 3-4 hours of focal cerebral ischemia in this rat model is sufficient to attain maximal infarction and suggest that recirculation or pharmacological interventions after this time will provide little benefit.

Cerebral vasoconstriction during head-upright tilt-induced vasovagal syncope. A paradoxic and unexpected response.

Abstract: BACKGROUNDTo determine the effect of vasovagally mediated syncope on the cerebral circulation, transcranial Doppler sonography was used to assess changes in cerebral blood flow velocity during head-upright tilt-induced syncope.METHODS AND RESULTSThirty patients (17 men and 13 women; mean age, 43 +/- 22 years) with recurrent unexplained syncope were evaluated by use of an upright tilt-table test for 30 minutes, with or without an infusion of intravenous isoproterenol (1-4 micrograms/min), in an attempt to provoke bradycardia, hypotension, or both. Transcranial Doppler sonography was used to assess middle cerebral artery systolic velocity (Vs), diastolic velocity (Vd), ratio of systolic to diastolic velocities, pulsatility index (PI = Vs-Vd/Vmean), and resistance index (RI = Vs-Vd/Vs) before, during, and after tilt. Syncope occurred in six patients (20%) during the baseline tilt and 14 (46%) during isoproterenol infusion (total positives, 66%). In the tilt-positive patients, concomitant with the development...

Assessment of cerebral autoregulation dynamics from simultaneous arterial and venous transcranial Doppler recordings in humans.

Abstract: We investigated the validity of transcranial Doppler recordings for the analysis of dynamic responses of cerebral autoregulation. We found no significant differences in percentage changes among maximal (centerline) blood flow velocity, cross-sectional mean blood flow velocity, and signal power-estimated blood flow during 24-mm Hg stepwise changes in arterial blood pressure. We investigated blood flow propagation delays in the cerebral circulation with simultaneous Doppler recordings from the middle cerebral artery and the straight sinus. The time for a stepwise decrease in blood flow to propagate through the cerebral circulation was only 200 msec. Brief (1.37-second) carotid artery compression tests also demonstrated that the volume compliance effects of the cerebral vascular bed were small, only about 2.2% of normal blood flow in 1 second. Furthermore, transients associated with inertial and volume compliance died out after 108 msec. We also investigated the hypothesis that autoregulatory responses are influenced by hyperventilation using the same brief carotid artery compressions. One second after release, the flow index increased by 17% during normocapnia and 36% during hypocapnia. After 5 seconds, the flow index demonstrated a clear oscillatory response during hypocapnia that was not seen during normocapnia. These results suggest that the intact human cerebral circulation in the absence of pharmacological influences does not function as predicted from pial vessel observations in animals.

Cardiac sources of embolism and cerebral infarction—clinical consequences and vascular concomitants The Lausanne Stroke Registry

Abstract: We studied clinical characteristics and coexisting causes of stroke in 305 patients admitted to a population-based primary care center with an initial ischemic stroke and a potential cardiac source of embolism (PCSE). Using systematic standardized cardiac, arterial, and cerebral investigations and the logistics of the prospective Lausanne Stroke Registry, we found that nonprogressive onset, hemianopia without hemiparesis or hemisensory disturbances, Wernicke9s aphasia, ideomotor apraxia, involvement of specific territories (posterior division of middle cerebral artery, anterior cerebral artery, cerebellum, multiple territories), and a hemorrhagic component were associated with the presence of a PCSE, as compared with 1,006 initial ischemic stroke patients without PCSE. Although age and sex did not differ, the frequency of hypertension, diabetes, cigarette smoking, elevated blood cholesterol, and deep hemispheric or brainstem infarcts was higher in the patients without a PCSE. Nearly one-fourth of the patients with a PCSE had a coexisting potential arterial cause of stroke (large artery ≥ 50% stenosis or small-vessel disease). In the majority of patients with a PCSE (76.7%), cardioembolism was the most likely cause of stroke, although a direct source of embolism was uncommon (4.3%) and intracranial embolie occlusions were present in less than one-half of the patients who were angiographed.

Temporal evolution of ischemic damage in rat brain measured by proton nuclear magnetic resonance imaging.

Abstract: We studied the effect of focal cerebral ischemia on the "state" of brain water using proton nuclear magnetic resonance imaging. Focal cerebral ischemia was induced in five halothane-anesthetized rats via tandem occlusion of the left common carotid artery and the left middle cerebral artery. The proton transverse relaxation time, the proton density, and the water diffusion coefficient were measured at various times from the same region of brain tissue from 1.5 to 168 hours after occlusion. Early measurements indicated significant changes in the transverse relaxation time (p = 0.004) and water diffusion coefficient (p = 0.002) of ischemic brain tissue compared with a homologous region from the contralateral hemisphere. However, the transverse relaxation time, proton density, and water diffusion coefficient in ischemic brain tissue showed different temporal evolutions over the study period. Diffusion coefficient weighting was superior to relaxation time and proton density weighting for the visualization of early cerebral ischemia. Our data suggest that nuclear magnetic resonance imaging is sensitive in detecting changes in proton-associated parameters during early cerebral ischemia and confirm significant changes (p less than or equal to 0.01) in the temporal evolution of transverse relaxation times, proton densities, and diffusion coefficients following middle cerebral artery occlusion.

A bedside test for cerebral autoregulation using transcranial Doppler ultrasound

Abstract: Although disorders of cerebral autoregulation are commonly seen in neurosurgical disease, there is currently no test of autoregulation in widespread use that may be performed safely at the bedside. The presence of autoregulation, however, can be seen in the brief hyperemic response in the middle cerebral artery distribution following a transient manual carotid artery compression in the neck. This transient hyperemic response (THR) is readily measured with transcranial Doppler techniques, and therefore might serve as a qualitative marker of cerebral autoregulation. To evaluate the THR as a clinical tool, carotid compressions were performed during 172 TCD studies on 79 patients with neurosurgical disorders and on 10 patients without cerebral disease. The results were correlated with clinical status (e.g., Hunt-Hess Grade for subarachnoid hemorrhage and Glasgow Coma Score for trauma). There were no complications arising from the compressions. A separate assessment of autoregulation was made from TCD recordings obtained intraoperatively during 16 procedures and correlated to the pre-operative THRs. Autoregulation was further assessed in 4 patients during a hypotensive challenge, and again compared to the THRs. A strong correlation was seen between the THR results and clinical status. The THR was also strongly correlated with the intraoperative assessments, and all 4 patients receiving hypotensive challenges had abnormal THRs and demonstrated evidence of poor autoregulation during the challenge. None of the control patients had abnormal THRs. The THR arising from transient artery compression is readily detected with TCD techniques and correlates well with clinical status and other indicators of autoregulatory ability.(ABSTRACT TRUNCATED AT 250 WORDS)

Reduction of infarct volume by magnesium after middle cerebral artery occlusion in rats.

Abstract: The effects of magnesium, an endogenous inhibitor of calcium entry into neurons, upon ischemic brain damage were investigated using a well-characterized model of focal cerebral ischemia in rats. Infarct volumes were determined by 2,3,5-triphenyltetrazolium chloride transcardiac perfusion 48 h after middle cerebral artery (MCA) occlusion. The area of ischemic damage was quantified by image analysis in coronal sections taken every 0.5 mm. MgCl2 (1 mmol/kg) was injected intraperitoneally just after MCA occlusion and again 1 h later. Posttreatment with MgCl2 (16 control and 16 treated rats) significantly reduced the cortical infarct volume. Compensation for the hyperglycemic effect of MgCl2 with insulin (17 rats) further reduced the infarct volume in the neocortex. No systemic effects of either treatment could account for the observed neuroprotection.

Effect of mild hyperthermia on the ischemic infarct volume after middle cerebral artery occlusion in the rat

Abstract: We investigated the effect of mild whole-body hyperthermia (40 °C) on a permanent middle cerebral artery occlusion (MCAo) model in Fisher rats by subjecting them to MCAo under the following conditions: (1) normothermia (n = 20); (2) hyperthermia (n = 14) before (1 hour), during, and after (1 hour) MCAo; and (3) post-MCAo hyperthermia (n = 14) for 1 hour. We measured brain and body temperatures during the experiment using micro-thermocouples and blood-brain-barrier (BBB) permeability using Evans blue staining of the brain. We measured the volume of the infarcted brain tissue 4 days after MCAo. We detected no differences in BBB permeability among three groups. The volume of infarcted tissue was significantly greater ( p

Diffusion/perfusion MR imaging of acute cerebral ischemia.

Abstract: In vivo echo-planar MR imaging was used to measure apparent diffusion coefficients (ADC) of cerebral tissues in a comprehensive noninvasive evaluation of early ischemic brain damage induced by occlusion of the middle cerebral artery (MCA) in a cat model of acute regional stroke. Within 10 min after arterial occlusion, ADC was significantly lower in tissues within the vascular territory of the occluded MCA than in normally perfused tissues in the contralateral hemisphere. Sequential echo-planar imaging was then used in conjunction with bolus injections of the magnetic susceptibility contrast agent, dysprosium DTPA-BMA, to characterize the underlying cerebrovascular perfusion deficits. Normally perfused regions of brain were identified by a dose-dependent 35–70% loss of signal intensity within 6–8 s of contrast administration, whereas ischemic regions appeared relatively hyperintense. These data indicate that sequential diffusion/perfusion imaging may be diagnostically useful in differentiating permanently damaged from reversibly ischemic brain tissue. © 1991 Academic Press, Inc.

Hyperdense middle cerebral artery CT sign. Comparison with angiography in the acute phase of ischemic supratentorial infarction.

Abstract: The early CT finding of an hyperdensity of a portion of the middle cerebral artery Hyperdense Middle Cerebral Artery Sign (HMCAS), in patients with supratentorial stroke, is often indicative of an embolic occlusion. Aim of this study was to verify the incidence and reliability of the HMCAS and its possible correlation with early CT findings and with the extent of late brain damage. We studied 36 patients presenting with symptoms of stroke in the MCA territory, by means of CT and angiography performed respectively within 4 and 6 hours. Follow-up CT scans were then obtained after one week and three months from the ischemic event. The HMCAS was present in 50% of our patients and in this group it always correlated positively with the angiographic finding of occlusion. The same group presented a high incidence of erly CT hypodensity (88%). Finally the presence of HMCAS might be considered a negative prognostic sign for the development of extensive brain damage.

The stroke syndrome of striatocapsular infarction.

Abstract: Striatocapsular infarction has recently been described as a distinct stroke entity and forms an important subgroup of subcortical infarctions. In a prospective study of 50 consecutive patients over a 10 yr period with this syndrome, clinical and neuropsychological features, pathogenesis and outcome were studied to provide information concerning management and prognosis. The most common clinical presentation was that of a stroke affecting mainly the upper limb with cortical signs such as dysphasia, neglect or dyspraxia. Evidence from EEG, angiographic and neuropsychological data supported a vascular/haemodynamic basis for the presence of the acute neuropsychological changes, while the chronic changes were more likely to be due to diaschisis. A study of risk factors and cerebral angiography enabled 4 pathophysiological subgroups to be identified: (1) cardiac emboli to the origin of the middle cerebral artery; (2) severe extracranial carotid artery occlusive disease with presumed embolism to the same site and/or involvement of haemodynamic factors; (3) proximal middle cerebral artery abnormalities causing occlusion of multiple lateral striate arteries at their origins; (4) normal angiography where pathogenesis was uncertain. The risk factors of cardiac disease and smoking were significantly increased as compared with age and sex-matched controls with other forms of ischaemic stroke. Stroke or vascular death rate was 2.7% per yr during a mean follow-up period of 2.25 yrs. Predictors of an excellent recovery with return to normal lifestyle were younger age, only brachial or brachiofacial weakness with absence of cortical signs at presentation and minimal change on angiography. This stroke entity deserves particular recognition in the spectrum of subcortical infarctions because of its specific pathogenesis, distinct neuropsychological features and reasonable prognosis.

Thalamic atrophy following cerebral infarction in the territory of the middle cerebral artery

Abstract: We investigated shrinkage of the ipsilateral thalamus following infarction in the territory of the middle cerebral artery in 33 patients who were admitted less than or equal to 2 days after the stroke and who were followed by computed tomography for greater than 1 year with no recurrences. The thalamic area was measured on the computed tomograms, and the ratio of the ipsilateral area to the contralateral area was calculated. All values were compared with values from the initial computed tomogram taken less than or equal to 2 days after the stroke. The values of the ratio on follow-up computed tomograms decreased gradually in 15 patients. In these cases, the area of the ipsilateral thalamus was significantly reduced after 1 year (p less than 0.01) and marked atrophy was observed. These results demonstrate the significance of remote changes over a long period of time after focal cerebral infarction.

The neuroprotective action of dizocilpine (mk-801) in the rat middle cerebral artery occlusion model of focal ischaemia

Abstract: 1. An acute model of focal ischaemia, which involves permanent occlusion of the middle cerebral artery of the rat with 4 h survival, was used to find the minimum effective plasma concentration of dizocilpine (MK-801) and to determine its dose-effect relationship. 2. MK-801 was administered at the time of occlusion and was given as an i.v. bolus followed by an infusion for 4 h to maintain a steady state plasma concentration of the drug throughout the study. MK-801 was given at 3 dose levels; 0.04 mg kg-1 i.v. bolus + 0.6 micrograms kg-1 min-1 infusion; 0.12 mg kg-1 i.v. bolus + 1.8 micrograms kg-1 min-1 infusion; 0.4 mg kg-1 i.v. bolus + 6 micrograms kg-1 min-1 infusion, which gave mean plasma levels over the 4 h of 8.0 ng ml-1, 18.9 ng ml-1 and 113.2 ng ml-1 respectively. 3. MK-801 at 8.0 ng ml-1 gave 10% reduction in the volume of ischaemic brain damage in the cerebral cortex which just reached significance. The middle dose of MK-801 (18.9 ng ml-1) gave a highly significant reduction in the volume of ischaemic brain damage in the cerebral cortex and hemisphere, volumes of ischaemic tissue being reduced by 60% and 50% compared to saline-treated animals, respectively. The highest plasma concentration of MK-801 (113.2 ng ml-1) resulted in a 35% reduction in the volume of hemispheric damage and a 40% reduction in the volume of cortical damage, which were significant.4. The reduction in the amount of protection afforded by the highest dose of MK-801 may be due to the hypotensive effect of this dose. There was no protection against the volume of damage in the caudate nucleus for any of the doses of MK-801 tested.5. Therefore the minimum effective plasma concentration of MK-801 was 8.0 ngml1, although the greatest protection was seen with a plasma level of 18.9 ng ml- 1. This correlates well with the concentration of MK-801 required to block N-methyl-D-aspartate (NMDA) receptors and prevent NMDA receptor mediated neurotoxicity in vitro.

Computed tomographic-angiographic findings within the first five hours of cerebral infarction.

Abstract: Modern management of acute stroke necessitates early diagnosis. To this end, we sought to delineate the radiographic features of focal hemispheric infarction within 5 hours of ictus. Fifty patients, ages 54-79, with ischemic strokes productive of at least hemiparesis underwent computed tomographic scanning and cerebral angiography (n = 38) or carotid ultrasound (n = 12). Radiographic lesions were characterized for location, size, and pathophysiology. Acute abnormalities, hypodensity, and mass effect were seen in 56% of scans and confirmed on a second scan 5-7 days later. Intracranial angiographic abnormalities occurred in 61% of patients: arterial occlusions in 45% and delayed arterial filling in 16%. Hemorrhagic infarctions occurred in 26% of second scans and were associated with mass effect (100%) and arterial occlusions (89%). Infarcts with hemorrhagic transformation were larger on both scans than those without (p = 0.001). Of four patients with infarctions in watershed territories on the scans, two had middle cerebral artery occlusions on angiography, thereby questioning the specificity of such scan lesions to low-flow states. We conclude that cerebral infarctions are often visible on early scans, but their locations may not be etiologically determinative. The infarcts associated with intracranial arterial occlusions (45%) were of thromboembolic origin, but, given current controversies as to the pathophysiology of lacunar and watershed infarctions, we cannot ascertain the etiology in the remainder. These findings are relevant to the new stroke therapies that require administration in the first hours after infarction.

Cerebral blood flow velocity changes after rapid administration of surfactant.

Abstract: A computer linked Doppler system was used to make continuous measurements of cerebral blood flow velocity (CBFV) from the middle cerebral artery, mean arterial blood pressure (MAP) from the umbilical artery, and heart rate before, during, and for 20 minutes after the endotracheal administration of 200 mg/kg of porcine surfactant in 10 preterm infants with respiratory distress syndrome. Within two minutes of surfactant administration, there was a median fall of 6 mm Hg (15%) fall in MAP and 36% in CBFV. There was a change in the Doppler spectra with almost complete loss of diastolic velocities. A rapid reduction in pulmonary vascular resistance with consequent left to right ductal shunting is one possible cause. These acute changes in MAP and CBFV after bolus surfactant administration may increase the risk of intraventricular haemorrhage.

Parasympathetic denervation of rat pial vessels significantly increases infarction volume following middle cerebral artery occlusion.

Abstract: Studies were undertaken in Long Evans rats to examine the hypothesis that chronic unilateral sectioning of vasodilating nerve fibers (parasympathetic and/or sensory) innervating the circle of Willis increases infarction volume following unilateral branch occlusion of the middle cerebral artery (MCA) combined with temporary (45 min) bilateral common carotid occlusion. Infarct size was measured 24 h after surgical occlusion from seven coronal slices. Infarction volume (mean +/- SD) in sham animals (group A) and surgically naive animals (group B) measured 153 +/- 43 and 131 +/- 38 mm3, respectively. After lesions of both sensory (nasociliary nerve) and parasympathetic efferents at the ethmoidal foramen (group C, combined lesion) or selective lesions of parasympathetic efferents (group D), infarction volume increased [214 +/- 47 mm3 (p less than 0.01) and 209 +/- 46 mm3 (p less than 0.05), respectively]. No increases were detected after cutting the nasociliary nerve alone (group E) or occluding the external ethmoidal artery (group F) [145 +/- 39 mm3 (p greater than 0.05) and 124 +/- 63 mm3 (p greater than 0.05), respectively]. The infarct was predominantly located within cortical gray matter and became enlarged on its superior and inferior aspects after parasympathectomy. Large infarcts were noted whether animals breathed spontaneously (all of the above) or were artificially respired or whether animals were anesthetized with xylazine and ketamine or chloral hydrate. Taken together, these studies suggest a previously unrecognized protective role for autonomic parasympathetic fibers in the pathophysiology of focal cerebral ischemia that is not shared by sensory fibers. The importance of autonomic vasodilating fibers to blood flow in ischemic brain merits further study.

Endovascular occlusion of intracranial vessels for curative treatment of unclippable aneurysms: report of 16 cases.

Abstract: ✓ Among 121 intracerebral aneurysms presenting at one institution between 1984 and 1989, 16 were treated by endovascular means. All 16 lesions were intradural and intracranial, and had failed either surgical or endovascular attempts at selective exclusion with parent vessel preservation. The lesions included four giant middle cerebral artery (MCA) aneurysms, one giant anterior communicating artery aneurysm, six giant posterior cerebral artery aneurysms, one posterior inferior cerebellar artery aneurysm, one giant mid-basilar artery aneurysm, two giant fusiform basilar artery aneurysms, and one dissecting vertebral artery aneurysm. One of the 16 patients failed an MCA test occlusion and was approached surgically after attempted endovascular selective occlusion. Treatment involved pretreatment evaluation of cerebral blood flow followed by a preliminary parent vessel test occlusion under neuroleptic analgesia with vigilant neurological monitoring. If the test occlusion was tolerated, it was immediately follo...

Monitoring of somatosensory evoked potentials during surgery for middle cerebral artery aneurysms.

Abstract: Somatosensory evoked potentials (SEPs) were monitored during 53 procedures for aneurysms of the middle cerebral artery (MCA). "Significant" changes were reported to the surgeon, who took corrective action when possible. Changes in the SEPs were categorized as follows: Type I, no change; Type II, significant change with complete return to baseline; Type III, significant change with incomplete return to baseline; Type IV, complete loss with no return; and Type V, no response at baseline. Only 1 of 37 patients with a Type I SEP had a new neurological deficit, and this was a patient who could not be examined for several days after surgery because he was in a pentobarbital coma. All 4 patients with Type III and IV changes had new postoperative neurological deficits. Perhaps of greater importance, 4 of 5 patients with Type II changes had no new deficit. These patients all had changes in SEPs that were completely reversible by clip adjustment (2), prompt removal of temporary clips (1), and inducing hypertension after aneurysm trapping (1). These cases may, therefore, represent instances in which SEP monitoring allowed the clinicians to prevent a neurological deficit. The MCA supplies the area of the somatosensory cortex that controls the hand. Median nerve SEPs are, therefore, a theoretically ideal monitor during surgery for MCA aneurysms. This study suggests that the results of MCA aneurysm surgery may be accurately predicted and improved with SEP monitoring.

Cerebral vasospasm evaluated by transcranial Doppler ultrasonography at different intracranial pressures.

Abstract: The present study evaluates the interdependence of clinical stage, cerebral vasospasm, intracranial pressure (ICP), and transcranial Doppler ultrasonographic parameters. The mean flow velocity of blood in the middle cerebral artery and the index of cerebral circulatory resistance as a measure of the peripheral vascular flow resistance were determined in 76 patients with spontaneous subarachnoid hemorrhage. The ICP was measured using an epidural transducer in 41 patients. There was no case in which both high ICP and a high mean flow velocity were observed simultaneously. The investigations led to the following conclusions. 1) In patients with a resistance index of less than 0.5, changes in the mean flow velocity seem to reflect sufficiently the actual severity and time course of vasospasm. 2) During the time course of vasospasm, an increase in the resistance index above values of 0.6 with a simultaneously decreased mean flow velocity indicates a rise in ICP rather than a reduction in vasospasm. 3) With a pronounced increase in ICP, evaluation of the severity and time course of vasospasm by transcranial Doppler ultrasonography based solely upon the mean flow velocity can lead to false-negative results.

Transient hypothermia reduces focal ischemic brain injury in the rat.

Abstract: The effect of transient hypothermia on focal cerebral ischemia was evaluated using a rat model of permanent middle cerebral artery (MCA) occlusion. MCA occlusion was performed on 10 rats at a temporalis muscle temperature of 24 degrees C (hypothermic group) and on 10 rats at 36 degrees C (normothermic group). Rats in the hypothermic group were maintained at 24 degrees C for 1 hour after MCA occlusion and then allowed to rewarm to 36 degrees C over the next 2 hours. Animals in both groups were killed 24 hours after MCA occlusion. Cerebral infarcts were visualized by staining of coronal brain sections with 2,3,5-triphenyltetrazolium chloride. Normothermic rats displayed an average infarct volume of 233.1 +/- 13.2 mm3 (standard error of the mean), whereas hypothermic rats had an average infarct volume of 166.2 +/- 22.8 mm3 (P less than 0.01). Expressed as a percentage of the volume of the right hemisphere, the normothermic group had an infarct volume of 22.1 +/- 1.5% and the hypothermic group an infarct volume of 16.0 +/- 2.2% (P less than 0.05). These results demonstrate that transient hypothermia to a temporalis muscle temperature of 24 degrees C significantly reduces subsequent infarct size in an experimental model of permanent arterial occlusion.

Development of collaterals in the cerebral circulation.

Abstract: Sudden occlusion of the middle cerebral artery (MCA) in normotensive rats increases blood flow through anastomosing branches into the territory of the occluded artery. Three weeks after MCA occlusion,

Intracarotid infusion of leukotriene C4 selectively increases blood-brain barrier permeability after focal ischemia in rats

Abstract: Intracarotid infusions of leukotriene C4 (LTC4) were used to open selectively the blood–brain barrier (BBB) in ischemic tissue after middle cerebral artery (MCA) occlusion in rats. BBB permeability was determined by quantitative autoradiography using [14C]aminoisobutyric acid. Seventy-two hours after MCA occlusion, LTC4 (4 μg total dose) infused into the carotid artery ipsilateral to the MCA occlusion selectively increased the unidirectional transfer constant for permeability K1 approximately threefold within core ischemic tissue and tissue adjacent to the ischemic core. No effect on BBB permeability was seen within nonischemic brain tissue or in ischemic tissue after only 24 h after MCA occlusion. γ-Glutamyl transpeptidase (γ-GTP) activity was decreased in capillaries in ischemic tissue at 48 and 72 h after infarction, compared to high γ-GTP in normal brain capillaries and moderate γ-GTP in capillaries in the ischemic tissue at 24 h after infarction. These findings suggest that normal brain capillaries r...

Ischemic brain damage: reduction by sodium-calcium ion channel modulator RS-87476.

Abstract: A novel sodium-calcium ion channel modulator, RS-87476, reduced cerebral infarct size in cats subjected to permanent unilateral occlusion of the middle cerebral artery Cerebral injury was assessed in vivo with a combination of magnetic resonance (MR) imaging and spectroscopy for 5-12 hours after occlusion and was compared with the area of histochemically ischemic brain tissue Compared with infarcts in placebo-treated animals, infarcts in cats given RS-87476 were reduced by an average of 70% at the lowest dose, 75% at the intermediate dose, and 88% at the highest dose Tissue edema, observed as areas of signal hyperintensity on diffusion- and T2-weighted spin-echo images, was confined to small regions of the parietal cortex and basal ganglia in drug-treated animals Mean plasma levels of RS-87476 at the lowest dose were 13 ng/mL initially, falling to maintenance levels of 3-5 ng/mL; at the intermediate and highest doses, plasma levels of drug were approximately five- and 20-fold greater The drug was onl

Sex and side differences of cerebral arterial caliber

Abstract: The diameter of 261 middle cerebral and 225 anterior cerebral arteries was measured on half axial antero-posterior (ap) view, and the diameter of 217 internal carotid arteries on side view angiograms. Mean diameter was significantly larger by 9.3%, 8.8% and 9.7% respectively in males than in females. In the females the vessels of the left hemisphere were wider but not significantly so than those of the right hemisphere, and the contrary was true for the males. In both sexes the side difference was reversed in the eighth decennium. There was no correlation of vessel diameter with age except for a statistically significant increase by 7.8% of right middle cerebral artery diameter in males from the fifth to the sixth decennium.