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PubMed1998

Intraarterial urokinase produces significant attenuation of infarction volume in an embolic focal ischemia model.

A number of models of focal ischemia have been created to mimic acute middle cerebral artery (MCA) occlusion. In the present series of experiments, we report our observations on the thrombin model of MCA occlusion and the neuroprotective effects of intraarterial thrombolysis with two doses of urokinase (2500 and 5000 units/kg). In all experiments male Wistar rats were used and the animals were allowed to recover for 48 h before assessment of neurobehavioral performance on a four-point scale. The extent of cerebral hemispheric damage was calculated as the percentage of brain infarction using TTC staining. Occlusion of the MCA was effected by the introduction of an autologous blood clot into the internal carotid artery (ICA) approximately 2 mm from the origin of the MCA. This clot was formed by the drawing of 10 microl of blood into a bovine thrombin (20 microg per animal) containing intraarterial catheter, which was inserted into the right ECA. After standing for 15 min to allow clot formation, the catheter was advanced gently through the ICA to the site of injection. MCA occlusion produced a consistent large infarction in all animals. Urokinase infusion (i.a. ) was started 2 h after arterial occlusion in the initial series. In animals treated with low dose urokinase infusion there was mild protection. Animals treated with high dose urokinase infusion showed a highly significant improvement in the motor recovery and a decrease in the extent of infarction compared to control animals. In the final group, the infusion of urokinase was delayed for 3 h. While producing protection in some animals, it also produced intracerebral hemorrhage in two of eight animals. Thus delay of infusion to 180 min increased the risk of hemorrhage. This model may in the future be used to test the protective effects of combination therapy with thrombolysis and neuroprotective medications.

Animals↗
PubMedDate not supplied

Assessment of cerebral blood volume with dynamic susceptibility contrast enhanced gradient-echo imaging.

OBJECTIVE: Dynamic susceptibility contrast (DSC) enhanced MRI was used to study relative cerebral blood volume (rCBV). MATERIALS AND METHODS: We examined 15 healthy subjects and 47 patients with vascular stenosis or occlusion, with brain infarctions, and with cerebral neoplasms. During bolus injection of Gd-diethylenetriamine pentaacetic acid, a series of rapid T2*-weighted fast low angle shot two-dimensional images were recorded from the same slice. From these images, changes in signal intensity during bolus passage were computed pixel-by-pixel and converted into contrast agent concentration curves. Applying the principles of indicator dilution theory, images of rCBV were calculated. RESULTS AND CONCLUSION: Regions of infarctions show almost zero rCBV. In patients with high-grade vascular stenosis or occlusion a bolus delay in comparison to the unaffected side and an increased mean transit time can be observed. Some of the affected areas show an increased rCBV, which is a well-known physiological mechanism that takes place to compensate for the reduced cerebral blood pressure. In brain tumors, rCBV imaging reveals focal or homogeneous areas of increased blood volume. This can even be observed in low-grade astrocytomas with unaffected blood-brain barrier. In CBV imaging, the effects of radiotherapy on tumor tissue can be monitored as a significant decrease of rCBV in tumor tissue after therapy.

Adult↗
PubMed1999

Electrophysiological transcortical diaschisis after middle cerebral artery occlusion (MCAO) in rats.

Remote changes in brain function following stroke are called diaschisis. These remote effects may contribute to the neurological deficit following brain infarction; in addition they may lead to post-stroke epilepsy and affect functional recovery. In the present study we addressed the question of whether an increase in excitability can be observed contralateral to middle cerebral artery (MCA) infarction. Permanent occlusion of the middle cerebral artery (MCAO) was induced experimentally in rats with an intraluminal silicon-coated filament. Seven days later, brain excitability was tested with extracellulare recording techniques in neocortical coronal brain slices using a paired-pulse stimulus protocol. In rats with MCAO, excitability was increased in the neocortex contralateral to the infarction compared with the control group. These alterations extended through wide parts of the contralateral neocortex. The study demonstrates that MCAO causes transcallosal electrophysiological diaschisis. Together with results obtained previously with photothrombotic cortical lesions, it can be concluded that these remote effects are not due to characteristics of the individual lesion model, but are common consequences of brain lesions.

Animals↗
PubMed2005

Hyperacute diffusion-weighted imaging abnormalities in transient ischemic attack patients signify irreversible ischemic infarction.

BACKGROUND: To characterize the frequency and clinical features of diffusion-weighted imaging (DWI) abnormalities in the hyperacute phase of transient ischemic attacks (TIAs). METHODS: We performed DWI in 21 consecutive patients with TIA (mean age 64 years; 17 men and 4 women) during both the hyperacute phase (within 6 h after onset) and subacute phase (within 2-9 days after onset). RESULTS: DWI abnormalities were present in the hyperacute phase in 11 patients (positive group) and absent in the other 10 patients (negative group). These groups could not be differentiated based on the clinical characteristics. In the subacute phase, all 11 patients from the positive group had abnormalities on MRI including T2-weighted and fluid attenuation inversion recovery images as well as DWI, with lesions being located in regions similar to those observed in the hyperacute phase. Of the 10 patients in the negative group, new DWI abnormalities were noted in 2 during the subacute phase. CONCLUSIONS: Approximately half of TIA patients in whom MRI was performed in the hyperacute phase had DWI abnormalities, all of which persisted in the subacute phase. The findings suggest that essentially all hyperacute DWI abnormalities in TIA patients may indicate irreversibility and signify the presence of brain infarction.

Adult↗
PubMed2003

Effects of hyperthermia on infarct volume in focal embolic model of cerebral ischemia in rats.

Hyperthermia worsens outcome of stroke in patients and also in animal models. In the present study, we tested the effects of hyperthermia in a focal embolic model of cerebral ischemia in rats. Focal ischemic injury was induced by embolizing a preformed clot into the middle cerebral artery. Hyperthermia significantly increased the brain infarct volume as compared to the normothermic controls measured at 48 h following the ischemic insult. Neurological deficits were also significantly elevated in the animals undergoing hyperthermic treatment. In addition, hyperthermia also significantly increased mortality. Our data thus show that hyperthermia exacerbates neuronal injury in the focal embolic model of cerebral ischemia in rats.

Animals↗
PubMed2000

Neuroprotective effect of retro-inverso Prosaptide D5 on focal cerebral ischemia in rat.

Prosaposin (the precursor of saposins A-D) has been identified as a neurotrophic factor in vitro and in vivo. In this study, a novel 11-mer retro-inverso peptidomimetic, Prosaptide D5, was injected i.m. to assess its effectiveness in a rat ischemic model produced by reversible total occlusion of the left middle cerebral artery (MCA). Prosaptide (300 microg/kg, i.m.) injected 3 h after reversible occlusion reduced brain infarct area by 56% compared with a saline group (p < 0.01) at 21 h of reperfusion. A similar injection of D5 6h after occlusion produced a 32% decrease.

Amino Acid Sequence↗
PubMed1988

A new model of embolic stroke produced by photochemical injury to the carotid artery in the rat.

We report a new model of embolic stroke in the rat, based on endothelial disruption and platelet aggregation in the carotid artery, which leads to distal embolization and focal brain infarction. The common carotid artery was irradiated for 6.5 minutes with the focused beam of an argon laser operated at a wavelength of 514.5 nm with a peak power of 2 W and an average power of 400 mw. Ipsilateral cerebral infarcts, ranging in size from 0.1 to 1.7 mm, were produced by platelet emboli in 12 of 13 rats. A total of 44 infarcts were observed in the 12 rats: 29 in the cortex, 6 in the hippocampus, 5 in the thalamus, and 4 in the basal ganglia. Scanning electron microscopy identified platelet aggregates in the carotid artery and in a deep cortical arteriole 50 minutes after the photochemical lesion. Twenty-four hours after the experiment, scanning electron microscopy of the carotid artery revealed damaged endothelium but few remaining adherent platelets. More intense laser irradiation in 8 rats, leading to carotid occlusion, produced an infarct in only 1. This new model can be used to study the acute and chronic pathological changes in the brain associated with platelet embolism.

Animals↗
PubMed1990

Treatment of right hemispheric cerebral infarction by hemicraniectomy.

An anecdotal series of nine patients (three men and six women with an average age of 57 years) presented with progressive neurologic deterioration while on medical therapy for large right hemispheric cerebral infarction. Clinical signs of uncal herniation (anisocoria or fixed and dilated pupils, and/or left hemiplegia with right decerebrate posturing) were present in seven of these nine patients. Computerized tomography of the head confirmed mass effect from cerebral edema. It was the clinical judgment of the treating neurologists and neurosurgeons that each of these nine patients would perish unless surgical decompression of the infarcted brain was performed. Accordingly, each was treated with right hemicraniectomy and dural augmentation. Six patients demonstrated neurologic improvement on the first postoperative day. One patient, with a postoperative diagnosis of lung cancer, died 1 month after surgery. The remaining eight patients are currently living with their families with a follow-up period ranging from 5 to 25 months. Patient outcome as evaluated by the Barthel Index indicates that three individuals are functioning with minimal assistance and that the remaining six patients are functionally dependent. After rehabilitative therapy, four patients returned for elective cranioplasty. These results suggest that hemicraniectomy can be an effective lifesaving procedure for malignant cerebral edema after large hemispheric infarction.

Activities of Daily Living↗
PubMedDate not supplied

The arterial patterns associated with internal carotid disease and cerebral infarcts.

In 20 necropsies with 15 stenosed and 17 thrombotic occluded internal carotid arteries there were 46 cerebral infarcts larger than 1 cm diameter. Using portmortem arteriographic and pathological techniques the patterns of the neck and brain artery systems were correlated with the situation and extent of the brain infarcts. Massive infarcts involving two major cerebral artery territories were associated with distal internal carotid artery occlusion and grossly ineffective cervical and circle of Willis anastomoses. Isolated middle cerebral artery territory infarcts were associated with internal carotid occlusion or stenosis and impairment of the circle of Willis anastomoses, perhaps with middle cerebral artery stenosis. The pattern of adequate size arteries determined if these infarcts were total, deep central, anterior, medium or posterior partial territory infarcts. Boundary zone infarcts were associated with internal carotid artery disease and limitation of anterior or posterior circle of Willis anastomoses. These limitations determined which boundary zones were affected. Isolated anterior cerebral artery territory infarcts were associated with bilateral internal carotid disease and an anterior cerebral artery stenosis or small caliber anterior communicating artery. Isolated posterior cerebral artery territory infarcts were associated with internal carotid disease and a direct impairment of the ipsilateral posterior cerebral artery capability.

Adult↗
PubMed2004

Intima-media thickness of common carotid artery, carotid atherosclerosis and subtypes of ischemic cerebral disease.

It has been shown that common carotid intima-media thickness (CCA-IMT) is a useful outcome measure in clinical studies and intervention trials reflecting early stage of atherosclerosis and cardiovascular risk. The present study examined the association between CCA-IMT and incident ischemic stroke and its subtypes in 75 cases and 21 controls. Cases with ischemic brain infarctions (IBI) were consecutively recruited and classified into subtypes by CT and Bamford's classification (the size and site of infarct) like total anterior circulation infarcts (TACIs), partial anterior circulation infarcts (PACIs), posterior circulation infarcts (POCIs) or lacunar infarcts (LACIs). Controls were recruited among individuals hospitalized at the same institutions and matched for age and sex. Patients and control subjects underwent B-mode ultrasonographic measurements of IMT of the distal wall of both common carotid arteries. Of 75 patients with an acute ischemic stroke, 10 (14%) were classified as TACIs, 34 (45%) with PACIs, 12 (16%) with POCIs and 19 (25%) with LACIs. Mean CCA-IMT was higher in cases (1.03+/-0.18 mm) than in controls (0.85+/-0.18 mm; p<0.0001). The difference in CCA-IMT between cases and controls was significant and the relation between CCA-IMT and IBI remained after adjustment for main cardiovascular risk factors. Regarding the subtypes of IBI, IMT values were significantly higher in patients with TACIs and PACIs versus those with LACIs and POCIs. An increased CCA-IMT was associated with the all subtypes IBI and was significantly higher in those with anterior circulation infarcts versus posterior circulation and lacunar infarcts.

Analysis of Variance↗
PubMed1995

[Spectroscopic imaging of the brain. Examination technique and clinical applications].

PURPOSE: MR spectroscopy allows the acquisition of a two-dimensional array of spatially resolved proton spectra of the human brain, known as MR spectroscopic imaging. Here the examination protocol and clinical applications in focal brain lesions are presented. METHOD: An array of data is acquired from a tissue slice positioned in the brain. These data can be presented as a set of spectra, in which each spectrum is allocated to a specific position in the sample, or as a set of images or "metabolite maps". RESULTS: The NAA signal typical for neuronal tissue is decreased in the centre of brain tumours as well as in brain infarcts. The intensity of the choline signal is increased in solid tumour tissue, whereas it is reduced in infarcts. CONCLUSION: Spectroscopic imaging reveals metabolite alterations in and around focal lesions. The spatial resolution of spectroscopic imaging enables matching with other macro-morphological or functional imaging methods like positron emission tomography.

Adult↗
PubMed2000

Activation of caspase-3 in permanent and transient brain ischaemia in man.

Animal studies have shown brain ischaemia to cause oxidative damage to DNA and activation of caspase-3, leading to apoptosis. These changes may be exacerbated by reperfusion. To assess caspase-3 activation after transient and permanent brain ischaemia in man, we examined brain tissue from patients who had experienced a cardiac arrest with resuscitation or an atherothrombotic brain infarct, and died 12 h to 9 days later. Sections were immunostained for activated caspase-3 or the 89 kDa caspase-3-mediated cleavage product of poly(ADP-ribose) polymerase. Brain ischaemia caused activation of caspase-3 in macrophages/microglia. Some neurons showed delayed activation of caspase-3 after cardiac arrest, but very few in atherothrombotic infarcts. In man, activation of caspase-3 plays little part in neuronal death in atherothrombotic infarcts but may contribute to delayed death of neurons after cardiac arrest.

Adult↗
PubMed2003

Honokiol protects rat brain from focal cerebral ischemia-reperfusion injury by inhibiting neutrophil infiltration and reactive oxygen species production.

We have previously shown that honokiol, an active component of Magnolia officinalis, displayed protective effect against focal cerebral ischemia-reperfusion (FCI/R) injury in rats. Production of reactive oxygen species (ROS) and infiltration of neutrophils to injured tissue play deleterious roles during cerebral ischemia. To study the mechanism(s) in mediating neuroprotective effect of honokiol, FCI/R-induced neutrophil infiltration and lipid peroxidation in brain tissue, and activation of neutrophils in-vitro were examined. Intravenous administration of honokiol (0.01-1.0 microg/kg) 15 min before (pretreatment) or 60 min after (post-treatment) middle cerebral artery occlusion reduced the total infarcted volume by 20-70% in dose-dependent manner. Pretreatment or post-treatment of honokiol at concentration of 0.1 and 1.0 microg/kg significantly decreased the neutrophil infiltration in the infarcted brain. Time course of neutrophil infiltration was performed in parallel with the lipid peroxidation in infracted brain tissue during FCI/R injury. The results indicate that honokiol can protect brain tissue against lipid peroxidation and neutrophil infiltration during FCI/R injury and cerebral infarction induced by FCI/R is accompanied with a prominent neutrophil infiltration to the infarcted area during FCI/R course. In-vitro, honokiol (0.1-10 microM) significantly diminished fMLP (N-formyl-methionyl-leucyl-phenylalanine)- or PMA (phorbol-12-myristate-13-acetate)-induced neutrophil firm adhesion, a prerequisite step behind neutrophil infiltration, and ROS production in neutrophils. Intracellular calcium overloading activates calcium-stimulated enzymes and further exaggerates FCI/R injury. Honokiol (0.1-10 microM) impeded the calcium influx induced by fMLP (a receptor agonist), AlF(4)(-) (a G-protein activator) or thapsigargin (an intracellular calcium pool releaser). Therefore, we conclude that the amelioration of FCI/R injury by honokiol can be attributed to its anti-oxidative and anti-inflammatory actions through, at least in part, limiting lipid peroxidation and reducing neutrophil activation/infiltration by interfering firm adhesion, ROS production, and calcium overloading that may be primed/activated during FCI/R injury.

Animals↗
PubMed1999

Etiology of cerebral vasospasm.

Cerebral vasospasm is a gradual onset and prolonged constriction of the cerebral arteries in the subarachnoid space after subarachnoid hemorrhage. The principal cause is the surrounding blood clot. The significance of vasospasm is that flow through the constricted arteries may be reduced sufficiently to cause cerebral infarction. Subarachnoid blood clot is sufficient to cause vasospasm; it does not require additional arterial injury, intracranial hypertension or brain infarction, although these elements are often coexistent. The blood released at the time of aneurysmal rupture into the alien subarachnoid environment is an extraordinarily complex mix of cellular and extracellular elements that evolves as clotting occurs; cells disintegrate; local inflammation, phagocytosis and repair take place; severe constriction alters the metabolism and structure of the arterial wall as well as the balance of vasoconstrictor and dilator substances produced by its endothelium, neurogenic network and perhaps smooth muscle cells.

Brain↗
PubMed1991

Circadian variations of platelet aggregability and fibrinolytic activity in patients with ischemic stroke.

The purpose of this study was to determine circadian dynamics of platelet aggregability and fibrinolytic activity in patients with ischemic stroke. The study was carried out in 21 male patients, aged from 51 to 65 years in acute phase of severe hemispheric brain infarction diagnosed clinically and radiologically. The examinations showed that circadian variations of platelet aggregability and fibrinolytic activity were persistent, but the intervals and the degree of oscillation differed from those in healthy persons. The significance of these disorders for clinical purposes was discussed.

Aged↗
PubMed1991

[Cerebral creatine kinase isoenzyme in the cerebrospinal fluid: importance of its measuring for prognosis of the disease outcome in cerebral ischemic disorders].

The concentration of cerebral isoenzyme of creatine kinase was measured repeatedly in the cerebrospinal fluid (CSF) in 84 patients with ischemic disorders of brain circulation. Of these, 14 patients presented with transitory ischemic attacks, 20 patients with regressing deficit, and 50 with brain infarction. The patients' health status and functional capacities were estimated on discharge from the hospital. It was discovered that in each patient, the maximum level of cerebral isoenzyme in the CSF was in a good agreement with the clinical course of the disease and neurological status in the survived patients. It may be concluded that measurements of the concentration of the enzyme in the CSF makes it possible to draw more valid prognostic conclusions in patients with ischemic disorders of brain circulation.

Adult↗
PubMedDate not supplied

[Prognostic factors of supratentorial cerebrovascular accidents].

Our aim was to delimit prognostic factors in supratentorial stroke based on data obtained upon hospitalization. We studied two series of patients, the first being 150 with brain infarct and the second 135 having intracerebral haemorrhage. We analyzed: age, Glasgow and Canadian scales, glucose and urgence haemogram and the size of the lesion across its greatest diameter using computerized tomography (CT). Follow-up time was until death or one year after the stroke. Those who lived longer than one year after were subclassified according to the Rankin scale as < 3 and > or = 3. There was a significant difference between those who survived for less than one month and those surviving more than one year: their age (p < 0.01), average score on the scale (p < 0.001) and size of infarct (p < 0.05) or haematoma (p < 0.001). The Rankin subgroups < 3 and > or = 3 also differed significantly with regard to age. Noteworthy were the unfavourable data: Glasgow < 10 points and Canadian < 5 points, in infarcts > 6 cm and haematomas > 4 cm in diameter. We comment on other evolutionary variables which may influence prognostic assessment such as clinical deterioration or CT sensitivity of the infarct depending on the carry-out time.

Adolescent↗
PubMed2002

'Footprints' of transient ischemic attacks: a diffusion-weighted MRI study.

OBJECTIVE: Diffusion-weighted imaging (DWI) conveys temporal as well as anatomic information about brain infarction, and is therefore well suited to identify ischemic injury that has occurred simultaneously, or closely linked in time, with a transient ischemic attack (TIA). We aimed to determine the proportion and clinical characteristics of patients with TIA who harbor infarction(s) on DWI. METHODS: Using T(2)-weighted imaging (T(2)-WI), fast fluid attenuated inversion recovery (FLAIR), and DWI, we studied 57 consecutive patients presenting with acute focal neurologic symptoms lasting less than 24 h. RESULTS: A hyperintense DWI lesion was identified in a vascular territory appropriate to the symptoms in 27 patients (47%). Lesions judged to be clinically appropriate on T(2)-WI and FLAIR overlapped with a DWI lesion in 41 and 48% of patients, respectively. Independent predictors of infarction on DWI were previous nonstereotypic TIAs, presentation with motor symptoms, and identified stroke mechanism. CONCLUSION: DWI establishes that recent infarction occurs in almost half of patients with the clinical syndrome of TIA and this subgroup is more likely to harbor an underlying cardiac or cerebrovascular abnormality.

Aged↗