Showing papers on "Middle cerebral artery published in 1995"
TL;DR: The histological effects of an intracranial arterial occlusion in the adult rat can be predicted on day 1 by the neurological score described in this report, and significant improvement can be obtained in these animals by reestablishing arterial flow 60 minutes or sooner after the ictus.
Abstract: Background and Purpose Occluding a large intracranial artery in rats produces a brain lesion that grows in terms of an increase in both surface area and number of necrotic neurons. The present study investigated whether reperfusing the ischemic territory 30 to 60 minutes after the arterial occlusion would have a beneficial effect on either the clinical or the histological outcome of the lesion. Methods One hundred four adult rats (including appropriate controls) were used; 97 had a middle cerebral artery occluded by inserting a nylon monofilament via the right external carotid artery. The arterial occlusion was transient in two groups and permanent in another; survival times were comparable for all groups. Control animals were subjected to a sham operation during which the artery was occluded for less than 1 minute. The outcome was evaluated by measuring the extent of the neurological deficit and the severity of the histological injury. Results Mean neurological score and mean number of necrotic neurons i...
1,274 citations
TL;DR: These data show that in normal human subjects measurement of dynamic autoregulation yields similar results as static testing of intact and pharmacologically impaired autoreGulation.
Abstract: Background and Purpose Cerebral autoregulation can be evaluated by measuring relative blood flow changes in response to a steady-state change in the blood pressure (static method) or during the response to a rapid change in blood pressure (dynamic method). The purpose of this study was to compare the results of the two methods in humans with both intact and impaired autoregulatory capacity.
Methods Using intraoperative transcranial Doppler sonography recordings from both middle cerebral arteries, we determined static and dynamic autoregulatory responses in 10 normal subjects undergoing elective surgical procedures. The changes in cerebrovascular resistance were estimated from the changes in cerebral blood flow velocity and arterial blood pressure in response to manipulations of blood pressure. Static autoregulation was determined by analyzing the response to a phenylephrine-induced rise in blood pressure, whereas rapid deflation of a blood pressure cuff around one thigh served as a stimulus for testing dynamic autoregulation. Both measurements were performed in patients with intact autoregulation during propofol anesthesia and again in the same patients after autoregulation had been impaired by administration of high-dose isoflurane.
Results There was a significant reduction in autoregulatory capacity after the administration of high-dose isoflurane, which could be demonstrated using static ( P <.0001) and dynamic ( P <.0001) methods. The correlation between static or steady-state and dynamic autoregulation measurements was highly significant ( r =.93, P <.0001).
Conclusions These data show that in normal human subjects measurement of dynamic autoregulation yields similar results as static testing of intact and pharmacologically impaired autoregulation.
819 citations
TL;DR: It appears that IL-1 beta may play an important role in ischemic brain damage after reperfusion, and its results tended to correlate with the neutrophilic infiltration into the parenchyma.
Abstract: Background and Purpose It has been suggested that interleukin-1 (IL-1) is a potent inflammatory mediator and that it is synthesized and secreted into the brain parenchyma. The aim of the present study is to evaluate the contribution of IL-1 to brain edema formation after focal brain ischemia. Methods The brain water content was measured to evaluate postischemic brain injury in rats after 60 minutes of middle cerebral artery occlusion and reperfusion. The effects of exogenous application of recombinant human interleukin-1β (rhIL-1β), anti–interleukin-1β neutralizing antibodies (anti–IL-1β), and the IL-1 blocker zinc protoporphyrin (ZnPP) on brain water content were observed, and histological technique was used to measure the infarction size and number of inflammatory cells infiltrated into the brain. Results Transient ischemia induced marked increase of brain water content, necrosis, and neutrophilic infiltration in the cortex perfused by the middle cerebral artery and the dorsal and ventral areas of the c...
585 citations
TL;DR: The presence and anatomical location of cells exhibiting DNA fragmentation after transient MCA occlusion suggest that apoptosis contributes to the development of ischemic infarct and suggests that apoptotic isChemic brain damage is a dynamic ongoing process.
Abstract: We measured the temporal profile and anatomic distribution of cells exhibiting DNA fragmentation at various durations of reperfusion after middle cerebral artery (MCA) occlusion in the rat. Focal cerebral ischemia was induced in male Wistar rats (n = 62) using an intraluminal monofilament blockade of the MCA. After 2 h of MCA occlusion, the animals were killed at different durations of reperfusion (0.5, 3, 6, 9, and 12 h and 1, 2, 4, 7, 14, 21, and 28 days, n = 4 per time point). Sham-operated rats (n = 4) and normal rats not subjected to any surgical procedure (n = 4) were used as controls. Coronal brain sections (5 microns) were analyzed, using an in situ ApopTag kit, hematoxylin and eosin, and immunohistochemical double-staining methods. Six rats subjected to 2 h of MCA occlusion were killed at 24 h for measurement of DNA fragmentation by gel electrophoresis. Our data indicate that within a coronal section, DNA fragmentation was present in zero to three cells in each hemisphere of normal and sham-operated rats as well as in the contralateral hemisphere of ischemic rats. The number of cells exhibiting DNA fragmentation increased as early as 0.5 h (8 +/- 6), peaked at 24-48 h (213 +/- 59), and persisted for 4 weeks (10 +/- 2) after onset of reperfusion (p 95% neurons) were located primarily in the inner boundary zone of the infarct. With use of gel electrophoresis, purified DNA obtained from the ischemic tissue exhibited the characteristic nucleosome ladder pattern associated with apoptosis.(ABSTRACT TRUNCATED AT 250 WORDS)
483 citations
TL;DR: It is concluded that aminoguanidine selectively inhibits iNOS activity in the area of infarction and reduces the volume of the infarct produced by middle cerebral artery occlusion.
Abstract: We sought to determine whether expression of the inducible, calcium-independent isoform of nitric oxide synthase (iNOS) contributes to the tissue damage produced by focal cerebral ischemia. The middle cerebral artery was occluded in halothane-anesthetized spontaneously hypertensive rats. Twenty-four hours later rats received intraperitoneal injections of the iNOS inhibitor aminoguanidine (100 mg/kg twice per day; n = 10) or of aminoguanidine + L-arginine (300 mg/kg four times per day; n = 7), aminoguanidine + D-arginine (n = 7), arginine alone (n = 6), or vehicle (n = 9). Drugs were administered for 3 consecutive days. Infarct volume was determined by image analysis in thionin-stained brain sections 4 days after induction of ischemia. Administration of aminoguanidine reduced infarct volume by 33 +/- 4% (P 0.05 vs. vehicle). In separate rats (n = 10), aminoguanidine attenuated calcium-independent NOS activity in the infarct (P 0.05). Aminoguanidine did not affect resting cerebral blood flow or the cerebrovascular vasodilation elicited by hypercapnia, as determined by laser-Doppler flowmetry (n = 4). We conclude that aminoguanidine selectively inhibits iNOS activity in the area of infarction and reduces the volume of the infarct produced by middle cerebral artery occlusion.(ABSTRACT TRUNCATED AT 250 WORDS)
405 citations
TL;DR: Ischemic cell damage is promoted by postischemic inflammatory response after 2 hours of transient MCA occlusion, and ischemiccell damage is reduced by administration of an anti-ICAM-1 antibody during reperfusion.
Abstract: Background and Purpose Postischemic cerebral inflammation may contribute to ischemic cell damage. Intercellular adhesion molecule–1 (ICAM-1) is a glycoprotein expressed on endothelial cells that facilitates leukocyte adhesion. We investigated the effect of administration of an anti–ICAM-1 antibody (1A29) on ischemic cell damage after transient (2-hour) or permanent middle cerebral artery (MCA) occlusion in the Wistar rat. Methods Groups studied were as follows: (1) transient MCA occlusion: rats were subjected to 2 hours of MCA occlusion, and after 1 hour of reperfusion they were treated with 1A29 (n=11) or an isotype control antibody (n=9); and (2) permanent MCA occlusion: rats were treated with 1A29 (n=9) or an isotype control antibody (n=7) 2 hours after onset of MCA occlusion. All animals were killed 1 week after onset of ischemia. Brain sections were stained with hematoxylin and eosin for histological evaluation. Results Significant reductions (P<.05) in both volume (44%) of the ischemic lesion and we...
347 citations
TL;DR: There is a predictable progression in the development of neuronal necrosis after a permanent arterial Occlusion, and therapeutic interventions that start within the first 1 to 2 hours after the arterial occlusion may alter the histopathologic responses to this form of injury.
Abstract: Background and Purpose Most brain lesions that develop after an artery is occluded evolve from an initial stage of “ischemic injury” (probably reversible) to an infarct or an area where most neurons become necrotic. There is scant information on the time that must elapse after the arterial occlusion for neurons to undergo irreversible injury. The objective of these experiments was to chart the time course and the topographic distribution of the neuronal necrosis that follows the occlusion of a large cerebral artery.
Methods One hundred fifty-one adult rats (including 15 controls) were used in this study. One hundred forty-seven had the right middle cerebral artery occluded for variable periods ranging from 30 minutes to 7 days. After processing the brains for histology, a meticulous structural evaluation of each specimen, including quantitation of necrotic neurons, was followed by a detailed statistical analysis of the neuronal counts.
Results Few neurons in isolated sites showed morphological signs of necrosis during the initial 4 hours; the first significant increase in the percentage of necrotic neurons (15%) was observed within the territory of the occluded artery after 6 hours ( P <.05); 12 hours after the arterial occlusion most neurons (65%) had become necrotic ( P <.0001). Pannecrosis involving neurons, glial cells, and blood vessels was observed at 72 to 96 hours. However, even at this time pannecrosis involved only the preoptic area and the lateral putamen; a few intact neurons remained visible in the cortex, and scattered necrotic neurons could be identified beyond the edges of the “area of pallor,” which does not become clearly demarcated until 4 to 5 days after the arterial occlusion.
Conclusions There is a predictable progression in the development of neuronal necrosis after a permanent arterial occlusion. Irreversible changes appear first in the caudoputamen and then spread to the cortex. The causes for the progression of the lesion are not known; however, therapeutic interventions that start within the first 1 to 2 hours after the arterial occlusion may alter the histopathologic responses to this form of injury. It remains to be determined whether the extent of the neurological deficit induced by an arterial occlusion correlates with the number of necrotic neurons.
345 citations
TL;DR: In this paper, the authors used transcranial Doppler ultrasonography to detect and quantify the number of microemboli in the right middle cerebral artery of patients undergoing elective first coronary bypass operations (n = 117) and second coronary bypass operation ( n = 10).
335 citations
TL;DR: In this paper, the authors conducted a prospective investigation of 40 consecutive asymptomatic or recently symptomatic patients undergoing carotid endarterectomy for 70% to 95% internal Carotid artery stenosis.
Abstract: Background and Purpose Previous work has shown that rates of cerebral microemboli downstream of high-grade internal carotid artery stenosis are higher in recently symptomatic compared with asymptomatic patients. In addition, microembolic rates decline after carotid endarterectomy. We conducted a prospective investigation of 40 consecutive asymptomatic or recently symptomatic patients undergoing carotid endarterectomy for 70% to 95% internal carotid artery stenosis to determine the relationship between microembolic rate and pathoanatomic features of the carotid plaque. Methods Transcranial Doppler monitoring including automated emboli detection was performed preoperatively to assess the rate of cerebral microemboli of the ipsilateral middle cerebral artery. The corresponding endarterectomy specimens were evaluated histologically with respect to the occurrence of plaque fissuring, intraplaque hemorrhage, plaque ulceration, or intraluminal thrombosis. Results There were strong associations between plaque ulc...
332 citations
TL;DR: The quantification of ADC in the ischemic territory allows the distinction between a core region with total breakdown of energy metabolism and a corona with normal energy balance but severe tissue acidosis.
Abstract: Middle cerebral artery occlusion was performed in rats while the animals were inside the nuclear magnetic resonance (NMR) tomograph. Successful occlusion was confirmed by the collapse of amplitude on an electrocorticogram. The ultrafast NMR imaging technique UFLARE was used to measure the apparent diffusion coefficient (ADC) immediately after the induction of cerebral ischemia. ADC values of normal cortex and caudate-putamen were 726 ± 22 × 10−6 mm2/s and 659 ± 17 × 10−6 mm2/s, respectively. Within minutes of occlusion, a large territory with reduced ADC became visible in the ipsilateral hemisphere. Over the 2 h observation period, this area grew continuously. Quantitative analysis of the ADC reduction in this region showed a gradual ADC decrease from the periphery to the core, the lowest ADC value amounting to about 60% of control. Two hours after the onset of occlusion, the regional distribution of ATP and tissue pH were determined with bioluminescence and fluorescence techniques, respectively. There wa...
304 citations
TL;DR: Whether ICP elevation is a common cause of deterioration from LHIE by measuring the initial ICP and cerebral perfusion pressure in 19 patients deteriorating to stupor within 3 hours of deterioration is sought, after ruling out metabolic aberrations, medication side effects, infection, and seizures.
Abstract: Neurologic deterioration from large hemispheric infarction with edema (LHIE) often leads to the use of therapies directed at decreasing intracranial pressure (ICP). Many of these ICP therapies can potentially accentuate tissue shifts from unilateral mass lesions and lead to rebound ICP elevations. We sought to determine whether ICP elevation is a common cause of deterioration from LHIE by measuring the initial ICP and cerebral perfusion pressure (CPP) in 19 patients deteriorating to stupor from LHIE within 3 hours of deterioration, after ruling out metabolic aberrations, medication side effects, infection, and seizures and prior to commencement of any ICP-lowering therapies. We evaluated 19 patients aged 23 to 77 years--14 with complete middle cerebral artery and five with complete internal carotid artery territory infarctions. Stupor began 59 +/- 37 hours after the stroke onset. ICP monitoring (12 ipsilateral Camino, five contralateral ventriculostomy, and two ipsilateral epidural) demonstrated elevation of ICP (> 15 mm Hg) in only five patients (26.3%), with group mean initial ICP = 13.4 +/- 10 mm Hg. Similarly, the initial CPP was diminished (< 55 mm Hg) in only two patients (10.5%), with group mean initial CPP = 74.9 +/- 14 mm Hg. Globally elevated ICP is not a common cause of initial neurologic deterioration from LHIE mass effect.
TL;DR: Whether Doppler measurement of the fetal middle cerebral artery peak systolic velocity can be used to detect fetal anemia in pregnancies complicated by maternal blood group immunization is investigated.
Abstract: We investigated whether Doppler measurement of the fetal middle cerebral artery peak systolic velocity can be used to detect fetal anemia in pregnancies complicated by maternal blood group immunization. We first studied normal values for the middle cerebral artery peak systolic velocity in 135 fetuses (Group A), and also in 23 fetuses at risk for anemia who underwent 56 cordocenteses to assess the fetal hematocrit (Group B). A test to detect fetal anemia, based on the middle cerebral artery peak systolic velocity, was developed by using the data of the fetuses of Group A and Group B. Successively, the middle cerebral artery peak systolic velocity was prospectively determined in 16 fetuses at risk for anemia who underwent 42 cordocenteses (Group C) to assess the test developed, in a multicenter prospective fashion, by using the data of Group A and Group B. In the normal fetuses an exponential model expressed the increase of the middle cerebral artery peak systolic velocity values with advancing gestation. By using the data of the fetuses of Group A and Group B, four zones of anemia risk were identified. In Group C, none of the anemic fetuses had the middle cerebral artery peak velocity below the normal mean value, whereas all of the anemic fetuses had the peak velocity above the normal mean. The middle cerebral artery blood velocity increases with advancing gestation and is a non-invasive method of detecting anemia in pregnancies complicated by maternal blood group immunization.
TL;DR: This study demonstrates that diffusion-weighted imaging detects both the core and the penumbra of the evolving infarction but is not able to differentiate between the two parts.
TL;DR: A comparison of the major cerebral arteries between humans and rats shows many similarities, including anomalies in their general organization, the structure of these vessels at the light and electron microscope levels and their morphological changes associated with cerebral vascular diseases.
Journal Article•
TL;DR: Results suggest that inhibiting the proinflammatory effects of IL-1 with a receptor antagonist is an effective way of influencing the leukocyte responses elicited by an arterial occlusion, and seemingly attenuates the number of necrotic neurons resulting from the occlusions of a large brain artery.
Abstract: Marked increases in the brain expression of interleukin (IL)-1 have been reported in rats after permanent occlusion of a large cerebral artery. Interactions between endothelial cells and leukocytes have been implicated in the pathogenesis of several types of ischemic injury to the myocardium and other organs. In this study we asked whether inhibiting the effects of IL-1 would affect the outcome of an experimental brain infarct. Adult male Wistar rats (n = 13) with permanent occlusion of the middle cerebral artery were given IL-1 receptor antagonist. A second group (n = 13) with the same type of brain injury was given a placebo. A third group, subjected to a sham operation, was given either IL-1 receptor antagonist (n = 2) or a placebo (n = 2). Experiments were terminated after either 24 hours or 7 days. Compared with the control group, animals treated with IL-1 receptor antagonist improved their neurological score (P < 0.05), experienced less pronounced changes in body weight (P < 0.05), and had fewer necrotic neurons (P < 0.001) and fewer leukocytes in the ischemic hemisphere (P < 0.001) as well as a smaller area of pallor (P < 0.05) in the ischemis hemisphere. The results suggest that inhibiting the proinflammatory effects of IL-1 with a receptor antagonist is an effective way of influencing the leukocyte responses elicited by an arterial occlusion. Such leukocyte inhibition seemingly attenuates the number of necrotic neurons resulting from the occlusion of a large brain artery.
TL;DR: Even if delayed, arterial recanalization may improve clinical outcome in a subgroup of patients with middle cerebral artery occlusion.
Abstract: Background and Purpose We sought to determine whether early (<8 hours) or delayed (8 to 24 hours) recanalization after stroke may be an independent variable in the improvement of clinical outcome in patients with occlusion of the middle cerebral artery. Methods We prospectively studied 77 patients by combined Scandinavian Stroke Scale score at admission, repeated computed tomography and angiography before and after thrombolytic treatment at <8 hours after stroke onset, and transcranial Doppler ultrasound 24 hours later. We tested an association between clinical and neuroradiological baseline characteristics, recanalization, and outcome as assessed by the modified Rankin Scale 4 weeks after stroke and determined the effect of recanalization on mortality and good outcome (Rankin Scale grades 0 to 3) by multiple logistic regression analyses. Results Recanalization rates at 8 and 24 hours after stroke correlated with sites of occlusion (middle cerebral artery branch, 73% and 73%; trunk, 27% and 38%, respectiv...
TL;DR: Ultrasound performed within the first weeks can corroborate a clinically suspected carotid dissection in up to 95% of patients.
Abstract: Article abstract-Background and purpose: To analyze the value of ultrasound for early diagnosis and follow-up of internal carotid artery dissection. Methods: The carotid arteries were evaluated in 43 consecutive patients using extracranial and transcranial pulsed-wave Doppler and duplex sonography. Results: Ultrasound examination was performed, on average, 7.7 days after the first symptoms. The dissections subsequently were verified by MRI (16 patients), angiography (13 patients), or both (14 patients) on average 4.4 days later. The overall sensitivity of the combined examination was 95% (93% for extracranial Doppler, 86% for transcranial Doppler, and 79% for duplex sonography). All three methods detected occlusions or high-grade stenoses in 100% of patients and moderate- or low-grade stenoses in 80% (combined methods), 70% (extracranial Doppler), 40% (transcranial Doppler), and 20% (duplex) of the patients. The findings in 33 patients with an occlusion or high-grade stenosis according to neuroradiology were as follows: absent flow signal in the internal carotid artery (100%) and biphasic (stump) flow in its bulb (86%), high-resistance flow pattern of the ipsilateral common carotid artery (91%), signs of collateral flow across the circle of Willis (97%), and low flow in the middle cerebral artery (79%) on transcranial insonation. In seven patients, a moderate stenosis of the high cervical carotid segment was found because of a retromandibular high-velocity signal. In five of them this was the only abnormal finding. Duplex examination was helpful because it confirmed absent internal carotid artery flow or stump flow in the case of occlusion or high-grade stenosis (100%) and excluded an atherosclerotic origin by demonstrating a patent bulb (100%) and the absence of plaques (95%). Follow-up studies showed recanalization in 63% of patients, occurring at variable intervals. Occlusion persisted in 37%. Conclusions: Ultrasound performed within the first weeks can corroborate a clinically suspected carotid dissection in up to 95% of patients. Repetitive follow-up studies in most cases are sufficient to monitor evolution. NEUROLOGY 1995;45: 691-698
TL;DR: This prospective pilot study suggests that cerebral microembolism detected with transcranial Doppler sonography may define a high-risk subgroup among patients with asymptomatic high-grade internal carotid artery stenosis.
Abstract: Background and Purpose Previous work has shown that cerebral microembolism detected with transcranial Doppler sonography distal to internal carotid artery stenosis occurs more frequently in recently symptomatic compared with asymptomatic patients. It has remained unclear whether cerebral microembolism also indicates a higher risk of future cerebral or retinal ischemia.
Summary of Report Sixty-four asymptomatic patients with unilateral 70% to 90% internal carotid artery stenosis were investigated prospectively (mean follow-up, 72 weeks). Five patients developed ischemic symptoms attributable to the stenosis (transient ischemic attack, 2 patients; stroke, 3 patients). A microembolic rate of ≥2 per hour in the ipsilateral middle cerebral artery was associated with a substantially increased risk of developing ischemia of the corresponding carotid territory (odds ratio, 31; 95% confidence interval, 3 to 302; P =.005).
Conclusions This prospective pilot study suggests that cerebral microembolism detected with transcranial Doppler sonography may define a high-risk subgroup among patients with asymptomatic high-grade internal carotid artery stenosis.
TL;DR: Basic fibroblast growth factor was infused intravenously for 3 h, beginning at 30 min after permanent middle cerebral artery occlusion by intraluminal suture in mature Sprague–Dawley rats and showed that labeled bFGF crossed the damaged blood–brain barrier to enter the ischemic hemisphere.
Abstract: Basic fibroblast growth factor (bFGF) is a polypeptide that supports the survival of brain cells (including neurons, glia, and endothelia) and protects neurons against a number of toxins and insults in vitro. This factor is also a potent dilator of cerebral pial arterioles in vivo. In previous studies, we found that intraventricularly administered bFGF reduced infarct volume in a model of focal cerebral ischemia in rats. In the current study, bFGF (45 μg/kg/h) in vehicle, or vehicle alone, was infused intravenously for 3 h, beginning at 30 min after permanent middle cerebral artery occlusion by intraluminal suture in mature Sprague–Dawley rats. After 24 h, neurological deficit (as assessed by a 0- to 5-point scale, with 5 = most severe) was 2.6 ± 1.0 in vehicle-treated and 1.5 ± 1.3 in bFGF-treated rats (mean ± SD; TV = 12 vs. 11; p = 0.009). Infarct volume was 297 ± 65 mm3 in vehicle- and 143 ± 135 mm3 in bFGF-treated animals (p = 0.002). During infusion, there was a modest decrease in mean arterial bloo...
TL;DR: The results suggest that decompressive craniectomy for cerebral ischemia not only reduces mortality but also significantly improves outcome and reduces infarction size, probably because of increased perfusion pressure through leptomeningeal collaterals.
Abstract: Background and Purpose Acute ischemia in the territory of the carotid artery can lead to massive cerebral edema with raised intracranial pressure and progression to coma and death due to uncal, cingulate, or tonsillar herniation. Thus far, only anecdotal experience with supratentorial ischemia treated by decompressive craniectomy has been reported, and there are no published experimental data dealing with this kind of therapy in acute supratentorial stroke. In this study, we present our results on the effect of decompressive craniectomy in an endovascular model of cerebral infarction in rats. Methods Focal cerebral ischemia was induced in 50 rats using an endovascular occlusion technique of the middle cerebral artery. Decompressive craniectomy was performed in 30 animals: in 15 animals after 1 hour and in the remaining 15 animals 24 hours after vessel occlusion. Twenty animals were not treated by decompressive craniectomy (control group). Results Mortality in the nontreated group was 35%, whereas none of ...
TL;DR: Transcranial color-coded duplex sonography is a noninvasive bedside method that provides rapid and reliable data regarding stroke subtype and mechanism immediately after onset and window failure is a serious limitation of this method.
Abstract: Background and Purpose Transcranial color-coded duplex sonography (TCCS) enables visualization of the intracranial parenchymal structures and measurement of blood flow velocity in the basal cerebral arteries. The present study aims to evaluate prospectively the clinical usefulness of TCCS in patients with acute stroke.
Methods Eighty-four consecutive patients with central nervous symptoms suggesting acute stroke were investigated within the first 48 hours after clinical onset. TCCS was performed with a 2.5-MHz sector transducer through the temporal bone window. CT was available in all patients.
Results Forty-eight patients suffered from an infarction or a transient ischemic attack (TIA) in the territory of the middle cerebral artery (MCA). Fifteen of them showed an MCA occlusion, and 12 of the 15 developed recanalization during follow-up. Twelve revealed an increased, decreased, or oscillating flow pattern in the MCA main stem, and 21 patients had no ultrasonic abnormalities. The positive and negative predictive values of a pathological flow pattern in patients with MCA infarctions or TIA were .92 and .48, respectively. Fifteen patients suffered from an intracerebral hematoma, which could be diagnosed by TCCS in 14 cases. The positive and negative predictive values of a pathological parenchymal echo pattern were .88 and .96, respectively. Three patients suffered from an infarction and one from a TIA in the posterior cerebral artery territory. One female patient with an acute deterioration of a hemiparesis showed a glioma. The dropout rate due to an insufficient acoustic temporal bone window was 20% (17/84).
Conclusions TCCS is a noninvasive bedside method that provides rapid and reliable data regarding stroke subtype and mechanism immediately after onset. Window failure is a serious limitation of this method.
TL;DR: During CEA the presence of microembolism (> 10 microemboli) during dissection shows a statistically significant relationship with perioperative cerebral complications and with new ischemic lesions on magnetic resonance images of the brain.
TL;DR: These studies suggest asymptomatic embolic signals correlate with clinical risk and whether embolic signal detection may allow prediction of stroke risk and monitoring of the effectiveness of therapy.
Abstract: Transcranial Doppler ultrasound of middle cerebral arteries (MCAs) was used to detect asymptomatic embolic signals in a prospective study in patients with symptomatic and asymptomatic carotid stenosis. Recording from each artery for 20 min, embolic signals were more common ipsilateral to symptomatic arteries (eight of 38) than ipsilateral to asymptomatic arteries (one of 28, P = 0.04), or than in the MCAs of age-matched normal controls (none of 52, P < 0.005). Recording a subgroup of patients revealed that previously embolic-signal negative symptomatic stenoses frequently became embolic-signal positive when recording was repeated on another day. Including all recording periods (mean time: symptomatic 36.2 min, asymptomatic 46.2 min) embolic signals were detected ipsilateral to 13 of 38 symptomatic stenoses but only one of 28 asymptomatic stenoses (P = 0.003). In symptomatic subjects with embolic signals, median number of signals per hour was three (mean 26). One month following carotid endarterectomy embolic signals were not detected except in one patient who continued to experience frequent amaurosis fugax; in this patient following aspirin both symptoms and embolic signals were abolished. These studies suggest asymptomatic embolic signals correlate with clinical risk. Outcome studies are required to determine whether embolic signal detection may allow prediction of stroke risk and monitoring of the effectiveness of therapy. The technique may also prove useful in studying the pathophysiology of cerebral embolism.
TL;DR: The potential application of NIRS in adults and the importance of using multiple parameter recording systems in the interpretation of cerebral events are discussed.
Abstract: A multimodality recording system was used in 14 ventilated patients with closed head injury to assess the potential use of near-infrared spectroscopy (NIRS) in the neurointensive care unit. Signals of intracranial pressure, cerebral perfusion pressure, peripheral oxygen saturation, jugular venous saturation, and NIRS-derived changes in the chromophores of oxy- and deoxyhemoglobin were digitized and recorded. After a review of 886 hours of continuous monitoring, 376 hours were considered free from artifact and were entered for final analysis. In nine of the patients 38 events were recorded that demonstrated clear changes in cerebral perfusion pressure accompanied by hemodynamic changes in middle cerebral artery flow velocity (transcranial Doppler) and cortical perfusion (laser Doppler flowmetry). Near-infrared spectroscopy showed correlated changes in 37 events (97%) whereas jugular venous saturation monitoring registered only 20 (53%). There was associated peripheral oxygen desaturation in eight cases (21%), intracranial hypertension in 10 (26%), and cerebral hyperemia in eight (21%). The remaining 12 events (32%) appeared to be complex changes of uncertain origin. Iatrogenic factors were identified as causative in 14 cases (37%). The potential application of NIRS in adults and the importance of using multiple parameter recording systems in the interpretation of cerebral events are discussed.
TL;DR: A significant neuroprotective effect of rNIF with continuous treatment for 48 hours following 2 hours of MCAO is demonstrated, correlated with a reduced number of neutrophils within the ischemic tissue.
Abstract: We tested the neuroprotective potential of neutrophil inhibitory factor (rNIF), a novel 41-kd recombinant glycoprotein derived from a hookworm, in a model of focal cerebral ischemia in the rat. Male Wistar rats were assigned to treatment with rNIF and vehicle. Middle cerebral artery occlusion (MCAO) for 2 hours was induced by insertion of an intraluminal suture. Infusion of the drug was initiated at the onset of reperfusion. Infarct volume was determined 48 hours after reperfusion. Neutrophils were measured within the ischemic tissue by myeloperoxidase (MPO) staining. Treatment with rNIF resulted in a 48% reduction in cerebral infarction compared with control animals (p < 0.01). Neutrophil accumulation in the ischemic brains of rNIF-treated rats was reduced significantly (p < 0.01) compared with control animals. The number of neutrophils within the infarcted tissue correlated positively with the size of the area of infarction (p < 0.001, r = 0.6) within representative cerebral coronal sections. We demonstrated a significant neuroprotective effect of rNIF with continuous treatment for 48 hours following 2 hours of MCAO. The neuroprotective effect was correlated with a reduced number of neutrophils within the ischemic tissue. These results demonstrate potential therapeutic properties of rNIF in the management of stroke.
TL;DR: The demonstration of the continuing loss of cerebral metabolites within an infarct region suggests that further cell loss occurs up to 10 days after infarction, which may represent continued ischemic damage after middle cerebral arteryInfarction.
Abstract: Background and Purpose Proton MR spectroscopy is a noninvasive method of monitoring in vivo metabolite concentration changes over time. The aim of this work was to study the ischemic penumbra in humans by measuring the metabolic changes that occur after a middle cerebral artery territory infarction.
Methods Diagnostic MRI and short–echo time MR spectroscopy were performed on a 1.5-T system. Localized proton MR spectroscopy was performed within the area of cerebral infarction and in a homologous area of the contralateral hemisphere. The residual water resonance in the spectra was removed with the use of the Hankel Lanczos singular value decomposition method, after which peak area estimates were obtained by means of the variable projection time domain fitting analysis. The unsuppressed water signal was used as an internal concentration standard. Ten patients with acute middle cerebral artery infarction were studied within 28 hours of stroke onset and followed up for a period of up to 3 months.
Results Significant changes were seen in the initial spectra from the infarct compared with the contralateral spectra. Lactate, a marker of anaerobic metabolism, was present within the infarct but not detected in the contralateral hemisphere. N -Acetyl aspartate, a neuronal marker, and total creatine were significantly reduced. The initial choline signal, arising from choline-containing compounds within the cell and cell membrane, remained unchanged in the infarct core compared with the contralateral hemisphere. Further reductions in N -acetyl aspartate and total creatine concentrations occurred within the first week. A fall in the lactate concentration was seen within the infarct core during the first 7 to 10 days. Similar reductions in the choline concentration were observed during this period.
Conclusions The demonstration of the continuing loss of cerebral metabolites within an infarct region suggests that further cell loss occurs up to 10 days after infarction. The continuing loss of neurons may represent continued ischemic damage after middle cerebral artery infarction.
Journal Article•
TL;DR: Papaverine was effective in dilating narrowed arteries in most patients with symptomatic vasospasm caused by subarachnoid hemorrhage with encouraging clinical results with no recurrence of neurologic deterioration in those patients who responded well to papaverine.
Abstract: PURPOSE To evaluate the techniques and efficacy of intracranial intraarterial papaverine infusion for symptomatic vasospasm after subarachnoid hemorrhage caused by aneurysm rupture. METHODS Papaverine was infused on 19 occasions in 14 patients, 6 hours to 2 days after spasm became apparent clinically. Sixty vascular territories were treated. Infusion was made into the supraclinoid internal carotid artery 20 times, cavernous internal carotid artery once, selective A1 anterior cerebral artery 8 times, M1 middle cerebral artery 7 times, and basilar artery 3 times. Papaverine doses ranged from 150 to 600 mg and exceeded 400 mg on 8 occasions. RESULTS Angiographic improvement occurred in 18 (95%) of the 19 treatment sessions: results were excellent in 3 sessions, moderate in 8, and mild in 7. The best angiographic results often were obtained with superselective infusion, although angiographic results did not always correlate with clinical response. Seven (50%) of the 14 treated patients showed dramatic acute clinical improvement within 24 hours of papaverine therapy, and there was no clinical evidence of recurrent vasospasm in these patients. Recurrence of angiographic vasoconstriction was demonstrated in three patients; one showed marked clinical improvement after a second treatment. There were no episodes of systemic hypotension in any of the cases. Monocular blindness developed in one patient because of papaverine infusion near the ophthalmic artery. CONCLUSIONS Papaverine was effective in dilating narrowed arteries in most patients with symptomatic vasospasm caused by subarachnoid hemorrhage. This series showed encouraging clinical results with no recurrence of neurologic deterioration in those patients who responded well to papaverine. Superselective infusion appears to be indicated in some cases for adequate papaverine delivery.
TL;DR: It is suggested that ketamine can be used in anesthetized, mechanically ventilated patients with mildly increased ICP without adversely altering cerebral hemodynamics.
Abstract: Ketamine's effect on cerebral hemodynamics is controversial. We hypothesized that ketamine would not increase intracranial pressure (ICP) and cerebral blood flow (CBF) velocity in anesthetized, ventilated patients. Twenty patients requiring craniotomy for brain tumor or cerebral aneurysm were studied. After induction with thiopental, anesthesia was maintained with isoflurane and nitrous oxide in oxygen. During controlled ventilation (PaCO2 34 +/- 1 mm Hg); middle cerebral artery blood flow velocity (VMCA), mean arterial blood pressure (MAP), bilateral frontooccipital processed electroencephalogram (EEG), and ICP were measured before and for 10 min after intravenous ketamine 1.0 mg/kg. Cerebral arteriovenous oxygen content difference (AVDO2) and cerebral perfusion pressure (CPP) were calculated. After ketamine, MAP, CPP, PaCO2, and AVDO2 were unchanged. ICP decreased from 16 +/- 1 mm Hg to 14 +/- 1 mm Hg (mean +/- SE; P < 0.001) and VMCA decreased from 44 +/- 4 cm/s to 39 +/- 4 cm/s (P < 0.001). Total EEG power decreased (P < 0.02). These results suggest that ketamine can be used in anesthetized, mechanically ventilated patients with mildly increased ICP without adversely altering cerebral hemodynamics.
TL;DR: The data indicate that NO is released in the brain after the onset of ischemia and NO levels can be modulated by administration of NO substrate and NO antagonists.
TL;DR: The results demonstrate that measurement of the size of middle cerebral artery infarction with MRI is a useful tool in assessing prognosis and will have a valuable role in assessing new therapeutic agents.
Abstract: Background and Purpose An accurate measure of the severity of ischemic insult and the resulting prognosis is needed to assess the effectiveness of new treatments for acute stroke. We studied the reproducibility and accuracy of measurements of infarct volume with MRI and correlated the measurements with outcome. Methods Infarct volume was measured on T2-weighted images with the Analyze image analysis software. This technique was found to be highly accurate and reproducible. Results Measurements of infarct volume were found to be highly accurate and reproducible. Twenty-one patients (mean age, 66.5 years; range, 28 to 90 years) with cortical middle cerebral artery territory infarcts in whom adequate data could be obtained were studied within 72 hours from onset (mean delay to MRI, 27.5 hours; range, 5 to 72 hours). The Scandinavian Stroke Scale was used to calculate a prognostic score, and clinical outcome was assessed at 3 months. Infarct volume was found to significantly predict outcome. Mean infarct volu...