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PubMed1997

Focal cerebral ischemia enhances glial expression of ecto-5'-nucleotidase.

The effect of ischemia on the reactive expression of ecto-5'-nucleotidase in rat brain was studied 6 h and 1, 2 and 7 days after permanent middle cerebral artery occlusion (MCAO). The distribution of 5'-nucleotidase in the infarcted brain was compared to markers for astrocytes (glial fibrillary acidic protein (GFAP)) and microglia (complement receptor type 3, antibody OX42) using histological staining or immunohistochemistry. 5'-Nucleotidase could be associated with reactive astrocytes by immunohistochemistry and with reactive microglia by enzyme histochemistry. In the untreated control 5'-nucleotidase was associated with astrocytes only in the hippocampus and the submeningeal space. After ischemia the enzyme was expressed on reactive astrocytes in the tissue surrounding the volume of infarction. Individual reactive astrocytes were observed 6 h after MCAO and the astrocytic expression became continuously enhanced during the following days. An enzyme histochemical analysis of 5'-nucleotidase activity revealed a postischemic increase in reaction product around the infarcted tissue. Seven days after MCAO a discrete band (0.2-0.4 mm) of reaction product characterized the rim of the infarcted area. This band of activity of 5'-nucleotidase colocalized with a band of immunoreactivity for OX42, indicative of an intense accumulation of 5'-nucleotidase expressing microglia. Our results suggest that ischemia following permanent MCAO results in an upregulation of the capacity for the hydrolysis of nucleotides within the tissue adjacent to the infarcted volume. Nucleotides released from the damaged cells can be hydrolyzed and the adenosine eventually formed may exert neuroprotective functions limiting the extent of damage.

5'-Nucleotidase↗
PubMed1982

Cranial anatomy and detection of ischemic stroke in the cat by nuclear magnetic resonance imaging.

Proton nuclear magnetic resonance (NMR) images of cat heads were obtained using a small, experimental imaging system. As a prelude to the study of experimental ischemic brain infarction, the normal cat head was imaged for identification of anatomical features. Images of one cat which had undergone ligation of the middle cerebral artery three weeks previously showed brain changes associated with chronic ischemic stroke and compared favorably with findings on computed tomography (CT). The NMR images have millimetric spatial resolution. NMR parameters inherent in the tissues provide intensity variations and are sufficiently sensitive to yield contrast resolution surpassing that of CT.

Animals↗
PubMed1999

MR line-scan diffusion-weighted imaging of term neonates with perinatal brain ischemia.

BACKGROUND AND PURPOSE: MR diffusion-weighted imaging provides early demonstration of neonatal brain infarction. The evolution and limitations of diffusion-weighted imaging findings in newborns, however, have not been evaluated. Using line-scan diffusion imaging (LSDI), we investigated perinatal ischemic brain injury. METHODS: Nineteen term newborns (age, 9 hours to 8 days; mean age, 2.6 days) with perinatal brain ischemia were evaluated using LSDI (1520/62.5/1 [TR/TE/excitations]) (b maximum = 750 s/mm2) and T1- and T2-weighted spin-echo (conventional) MR imaging. Follow-up examinations were performed in seven patients and autopsy in one. Apparent diffusion coefficients (ADCs) were measured in deep gray matter, white matter, the cortex, and focal lesions. RESULTS: Based on conventional MR imaging or pathologic findings, patients were divided into two groups. Group 1 (n = 12) had symmetric/diffuse injury consistent with global hypoperfusion. Group 2 (n = 7) had focal/multifocal injury suggesting cerebrovascular occlusion. ADCs were abnormal at initial examination in 10 newborns in group 1 and in all newborns in group 2. The results of LSDI were abnormal before conventional MR imaging was performed in three newborns in group 1. ADCs were maximally decreased between days 1 and 3 in deep gray matter, perirolandic white matter, and focal lesions. Delayed decreases in ADCs were observed in subcortical white matter from days 4 through 10 in three patients in group 1. CONCLUSION: After global hypoperfusion, LSDI showed deep gray matter and perirolandic white matter lesions before conventional MR imaging. LSDI may underestimate the extent of injury, however, possibly because of variations in the compartmentalization of edema, selective vulnerability, and delayed cell death. Differences in LSDI of symmetric/diffuse and focal/multifocal lesions may reflect differences in pathophysiology or timing of the injury. These findings may have implications for acute interventions.

Asphyxia Neonatorum↗
PubMed1994

Cerebral hemodynamics in hypertensive patients compared with normotensive volunteers. A transcranial Doppler study.

BACKGROUND AND PURPOSE: The present study was designed to examine cerebral hemodynamics in early and chronic stages of hypertension using transcranial Doppler sonography. METHODS: Our study population consisted of 16 chronic hypertensive patients with chronic and small deep brain infarction, 10 young early-stage hypertensive subjects, and 16 young normotensive healthy volunteers. Using three-dimensional mapping techniques, we identified the M1 portion of the middle cerebral arteries and measured mean blood flow velocity, and we calculated the Gosling pulsatility index (PI), Fourier PI of the first harmonic (Fourier PI1), and cerebrovascular resistance. RESULTS: Mean blood flow velocity in the young hypertensive group was statistically higher (71.7 +/- 11.7 cm/s [mean +/- SD]) than among chronic hypertensive subjects (56.9 +/- 21.4 cm/s, P < .01) and normotensive subjects (63.2 +/- 11.8 cm/s, P < .05). Gosling PI presented a mirror image of mean blood flow velocity in both hypertensive and normotensive subjects. Chronic hypertensive subjects showed significantly higher Fourier PI1 (0.32 +/- 0.05) and cerebrovascular resistance (2.08 +/- 0.82 mm Hg/cm per second) than normotensive subjects (0.25 +/- 0.03 and 1.31 +/- 0.23 mm Hg/cm per second [P < .005], respectively) or early-stage hypertensive subjects (0.25 +/- 0.04 and 1.44 +/- 0.26 mm Hg/cm per second [P < .02], respectively). CONCLUSIONS: Early-stage hypertensive subjects demonstrated higher velocity, normal Fourier PI1, and near normal vascular resistance, whereas chronic hypertensive subjects showed near normal velocity, higher Fourier PI, and greater vascular resistance. Results may indicate different degrees of cerebral arteriopathy and arteriolopathy between early and late stages of hypertension.

Adult↗
PubMed1993

Effect of brain edema on infarct volume in a focal cerebral ischemia model in rats.

BACKGROUND AND PURPOSE: Infarct volume is one of the common indexes for assessing the extent of ischemic brain injury following focal cerebral ischemia. Accuracy in the measurement of infarct volume is compounded by postischemic brain edema that may increase brain volume in the infarcted region. We evaluated the effect of brain edema on infarct volume determined by triphenyltetrazolium chloride and hematoxylin and eosin stains in a focal cerebral ischemia model in rats. METHODS: In a middle cerebral artery occlusion model in rats, infarction is confined to the cerebral cortex. The infarct was delineated by triphenyltetrazolium chloride stain and, in selected samples, by hematoxylin and eosin stain. We determined infarct size at different times after the ischemic insult (6 hours to 7 days) in relation to the evolution of brain edema by the direct measurement of infarct volume. Indirect measurement to reduce the effect of edema on infarct volume was also conducted in the same brain samples. RESULTS: Direct measurement showed that infarct volume fluctuated with the evolution of brain edema (one-way analysis of variance, p < 0.0001). Infarct volume determined by indirect measurement was independent of the extent of brain edema and remained stable from 6 hours to 3 days after ischemia. There was a good correlation between triphenyltetrazolium chloride and hematoxylin and eosin stains in delineating infarct volume with both direct and indirect measurement. CONCLUSION: Traditional direct measurement of infarct volume is associated with an overestimation of infarct volume during the development of brain edema in the first 3 days after ischemia. This artifact can be reduced with indirect measurement, which is based on noninfarcted cortex volume.

Animals↗
PubMed2003

Post-treatment with a novel PARG inhibitor reduces infarct in cerebral ischemia in the rat.

Poly(ADP-ribose) is synthesized from nicotinamide adenine dinucleotide (NAD(+)) by poly(ADP-ribose) polymerase (PARP) and degraded by poly(ADP-ribose) glycohydrolase (PARG). Overactivation of the poly(ADP-ribose) pathway increases nicotinamide and decreases cellular NAD(+)/ATP, which leads to cell death. Blocking poly(ADP-ribose) metabolism by inactivating PARP has been shown to reduce ischemia injury. We investigated whether disrupting the poly(ADP-ribose) cycle by PARG inhibition could achieve similar protection. We demonstrate that either pre- or post-ischemia treatment with 40 mg/kg of N-bis-(3-phenyl-propyl)9-oxo-fluorene-2,7-diamide, a novel PARG inhibitor, significantly reduces brain infarct volumes by 40-53% in a rat model of focal cerebral ischemia. Our result provides the first evidence that PARG inhibitors can ameliorate ischemic brain damage in vivo, in support of PARG as a new therapeutic target for treating ischemia injury.

Animals↗
PubMed1991

Bilateral carotid occlusion in normotensive rats: olds facts and new observations.

This work describes that prolonged mild cerebral ischemia may lead to either general or regional derangement of brain morphofunctional integrity. Normotensive adult Wistar rats were used. Under anesthesia with volatile agents or thiopental, the common carotid arteries were ligated permanently. In one group of animals local cerebral blood flow (1CBF) was measured two hours after carotid occlusion using the [14C]iodoantipyrine method. The other carotid-occluded animals were used for clinical rating and histological evaluation, which was performed two days to 4 weeks after surgical operation. The [14C]iodoantipyrine method showed widespread reduction in the cerebral circulation of carotid-occluded animals. Several hours after carotid occlusion, 40% of the animals showed dramatic neurological signs and died on the day of operation. In 35% of surviving animals, brain infarctions were observed in one and exceptionally two areas of the sensorimotor cortex, thalamus, hippocampus or cerebellum. The evolutionary sequence of the histopathological changes seems to date the induction of the infarcts to the early period of carotid occlusion. In conclusion, reduction of cerebral blood flow causes, in a high percentage of animals, various degrees of acute brain damage after an apparent symptom-free interval.

Animals↗
PubMed1997

A functional MRI study of subjects recovered from hemiparetic stroke.

BACKGROUND AND PURPOSE: Stroke recovery mechanisms remain incompletely understood, particularly for subjects with cortical stroke, in whom limited data are available. We used functional magnetic resonance imaging to compare brain activations in normal controls and subjects who recovered from hemiparetic stroke. METHODS: Functional magnetic resonance imaging was performed in ten stroke subjects with good recovery, five with deep, and five with cortical infarcts. Brain activation was achieved by index finger-tapping. Statistical parametric activation maps were obtained using a t test and a threshold of P < .001. In five bilateral motor regions, the volume of activated brain for each stroke subject was compared with the distribution of activation volumes among nine controls. RESULTS: Control subjects activated several motor regions. During recovered hand finger-tapping, stroke subjects activated the same regions as controls, often in a larger brain volume. In the unaffected hemisphere, sensorimotor cortex activation was increased in six of nine stroke subjects compared with controls. Cerebellar hemisphere contralateral and premotor cortex ipsilateral to this region, as well as supplementary motor areas, also had increased activation. In the stroke hemisphere, activation exceeding controls was uncommon, except that three of five cortical strokes showed peri-infarct activation foci. During unaffected hand finger-tapping, increased activation by stroke subjects compared with controls was uncommon; however, decreased activation was seen in unaffected sensorimotor cortex, suggesting that this region's responsiveness increased to the ipsilateral hand and decreased to contralateral hand movements. Use of a different threshold for defining activation (P < .01) did not change the overall findings (kappa = .75). CONCLUSIONS: Recovered finger-tapping by stroke subjects activated the same motor regions as controls but to a larger extent, particularly in the unaffected hemisphere. Increased reliance on these motor areas may represent an important component of motor recovery. Functional magnetic resonance imaging studies of subjects who recovered from stroke provide evidence for several processes that may be related to restoration of neurologic function.

Aged↗
PubMed1993

Hemorrhagic transformation in cardioembolic cerebral infarction.

BACKGROUND AND PURPOSE: Because the frequency of hemorrhagic transformation of cerebral infarcts is still a matter of controversy, we performed a prospective magnetic resonance imaging study in a series of consecutive patients with cardioembolic stroke. SUMMARY OF REVIEW: Among 200 consecutive patients with transient ischemic attack or ischemic stroke, 41 were identified with a computed tomographically proven supratentorial infarct due to cardiogenic embolism. Magnetic resonance imaging (T1-weighted) was performed 3 weeks after the stroke in 35 of these 41 patients. Eight patients received anticoagulants. Magnetic resonance images showed hemorrhagic transformation in 68.6% (24) of the 35 infarcts, always without clinical deterioration. In a stepwise forward logistic regression analysis only the volume of infarction edema on the initial computed tomogram was linked significantly with the risk of hemorrhagic transformation (p = 0.037). Hemorrhages were a regular finding on magnetic resonance images of infarcts exceeding a volume of 10 cm3 (94.4%, 17 of 18). CONCLUSIONS: Hemorrhagic transformation is a regular finding in medium-sized and large cardioembolic infarcts. Thus, in therapeutic and preventive studies of acute stroke the severity, not the frequency, of hemorrhages into brain infarcts should be the matter of interest.

Adult↗
PubMed2000

Neuroprotective activity of tiagabine in a focal embolic model of cerebral ischemia.

Gamma aminobutyric acid (GABA) agonists have been shown to have neuroprotective effects when used after focal or global cerebral ischemia. In this study, we evaluated the neuroprotective effects of a GABA re-uptake inhibitory agent, tiagabine, on focal ischemic brain injury in an embolic model in rats. Tiagabine, injected at 1 h after embolization, significantly reduced brain infarction volume, measured with 2,3,5-triphenyltetrazolium chloride (TTC) histological assay. There were varying degrees of neuroprotective effect exhibited in the other experimental groups however this did not reach significance. These results suggest that tiagabine is neuroprotective when administrated at an early period after the ischemic brain injury.

Animals↗
PubMedDate not supplied

Quantification of cerebral infarct size by creatine kinase BB isoenzyme.

Creatine Kinase BB isoenzyme (CKBB) has been shown to rise in the serum and CSF following acute cerebral injury. To test the hypothesis that brain infarct size could be estimated from the appearance and disappearance of CKBB in the serum and CSF, strokes of varying size were produced in twelve mongrel dogs by silastic emboli. The rate of disappearance, Kd of CKBB (-.00732 +/- 0.001 min-1 mean +/- SE, N = 8) was determined by injecting purified CKBB (25 IU) intravenously then measuring its disappearance. Following the embolic stroke, serum samples were taken hourly for 24 hours and then at intervals for up to 160 hours for measurement of CKBB by radioimmunoassay until the animals were sacrificed. The brains were then removed, fixed in formalin, cut in 2 mm sections and photographed. The area of the infarct was measured using high pad digitizer interfaced with an Apple computer. The infarct size was then calculated from the area and thickness. Using a one-compartment mathematical model, the infarct size was estimated from the amount of CKBB appearing in the serum, the Kd of CKBB, and the amount of CKBB depleted from tissue. The computed infarct size correlated well (r = 0.94) with the measured infarct size. This model may have value in testing therapeutic modalities in the intact animal.

Animals↗
PubMed2004

Brain stem venous congestion due to dural arteriovenous fistulas of the cavernous sinus.

BACKGROUND: Venous congestion of the brain stem due to dural arteriovenous fistulas (DAVFs) in the cavernous sinus is rare and presents therapeutic challenges. To assess the prognosis of patients with symptomatic DAVFs and brain stem dysfunction, we evaluated the degree of venous ischemia by examining pre- and post-treatment magnetic resonance images (MRI) in 2 patients presenting with venous congestion of the brain stem. METHODS: A 56-year-old woman with left hemiparesis and a 70-year-old woman with gait disturbance attributable to right cavernous sinus DAVFs were referred to our hospital. In both cases, T2-weighted magnetic resonance imaging (MRI) disclosed a hyperintensity lesion in the brainstem due to venous congestion. FINDINGS: Both patients underwent open surgery for direct embolization of the cavernous sinus because there were no approach routes for transvenous embolization. The patient whose pretreatment MRI demonstrated Gd enhancement continued to manifest neurological deficits and persistence of the abnormal hyperintensity on post-treatment T2-weighted MRI. In the other patient whose pretreatment MRI showed no Gd enhancement, treatment produced a complete response of her neurological deficit and disappearance of the abnormal hyperintensity area. CONCLUSIONS: We tentatively conclude that lesions corresponding to hyperintensity areas on non-Gd-enhanced, T2-weighted MRI may reflect a reversible condition whereas lesions identified as hyperintense areas on GD-enhanced T2-weighted MRI may be indicative of irreversibility.

Aged↗
PubMed1996

Phenytoin pretreatment prevents hypoxic-ischemic brain damage in neonatal rats.

This study was performed to investigate whether the anticonvulsant phenytoin has neuroprotective effect in a model of hypoxia-ischemia with neonatal rats. The left carotid artery of each rat was ligated, followed by 3 h of hypoxic exposure (8% O2) in a temperature-regulated environment (36 degrees C). Two weeks later, brain damage was assessed by measuring loss of brain hemisphere weight. Phenytoin had no effect on body temperature or plasma glucose, but attenuated brain damage in a dose-dependent manner (3, 10, and 30 mg/kg i.p.) when administered before the hypoxic episode. Phenytoin administered during or after hypoxia did not alter hypoxic brain damage significantly. A parallel experiment using histological examination of frozen brain sections demonstrated less brain infarction after phenytoin treatment (30 mg/kg i.p.). In an additional experiment measuring breakdown of an endogenous brain calpain substrate, spectrin, phenytoin treatment reduced this measure of early cellular damage. Our results indicate that pretreatment with phenytoin is neuroprotective at a plasma phenytoin concentration of approximately 12 micrograms/ml. These results are consistent with the hypothesis that blockade of voltage-dependent sodium channels reduces brain damage following ischemia.

Animals↗
PubMed1988

Cerebral infarction does not occur typically at night.

In a hospital-based series of 66 consecutive patients with non-progressive cerebral infarction, the time of onset and the type of infarction on computed tomography were studied retrospectively. Forty-six (78%) patients suffered cerebral infarction between 6 am and 6 pm. Only five patients (8%) had their infarct between midnight and 6 am. Only three patients had a watershed-infarct, and these occurred during the daytime. Our results do not support the belief that atherothrombotic brain infarction is largely determined by haemodynamic factors.

Cerebral Arteries↗
PubMed2004

Basilar artery vasospasm and delayed posterior circulation ischemia after aneurysmal subarachnoid hemorrhage.

BACKGROUND AND PURPOSE: The clinical and hemodynamic impacts of basilar artery (BA) vasospasm (VS) after aneurysmal subarachnoid hemorrhage (SAH) are ill-defined. The purpose of the present study was to evaluate the relationship between BA-VS and regional cerebral blood flow (rCBF) with posterior circulation after aneurysmal SAH. METHODS: Daily transcranial Doppler (TCD) measurements of posterior and anterior circulation arteries were conducted in 162 patients with aneurysmal SAH. rCBF to the brain stem (BS) and other brain territories was assessed by multiple single-photon emission computed tomography with (99m)Tc ethyl cysteinate dimer single-photon emission computed tomography (ECD-SPECT) imaging during the course of VS. RESULTS: SPECT imaging showed delayed BS hypoperfusion in 29 patients (17.9%). Of them, 23 patients (79.3%) were found to have BA-VS. Patients with very high BA flow velocities (FVs; >115 cm/s) had a 50% chance of developing delayed BS ischemia. BA-VS was found at a higher rate in patients who experienced reduced rCBF in the cerebellum (56.3%), thalamic nuclei (68.4%), and occipital lobe (81.8%). Although patients with delayed BS hypoperfusion did not present with a higher clinical grade, their clinical outcome was significantly worse (Glasgow Outcome Score after 30 days 2.48+/-1.16 versus 3.3+/-1.27; P=0.001). CONCLUSIONS: These findings suggest for the first time that BA-VS after aneurysmal SAH is associated with hypoperfusion to BS and other posterior circulation territories. The risk for delayed BS ischemia increased significantly when TCD BA-FVs were >115 cm/s.

Adult↗
PubMed2004

[Alarming symptoms in vertebrobasilar circulatory disorders. Part I].

Dizziness and vertigo--like headache--are the most common complaints which leads patients to visit the doctor. In spite of the headache--which may be primary (e.g. migraine) or symptomatic--dizziness and vertigo do not appear to be a separate nosologic entity but rather the symptoms of several neurological disorders. For differential diagnosis, interdisciplinary thinking and activity is needed because the vestibular, neurological and psychiatric disorders might have a common role in the development of symptoms and further overlapping can also occur. The vascular disorders of the vertebrobasilar system are discussed in detail in this review. The importance, occurrence and causes of vertigo as a warning symptom is in the focus. The author draws attention to life-threatening conditions with acute onset in cases of the posterior scale ischemia and emphasizes the importance of the correct and early diagnosis. The author tries to clear up the nihilistic aspect in treating of stroke and stresses the necessity of thrombolysis and interventional radiological procedures which may be the only chance for the recovery of the patients. The pharmacological prevention of recurrent vascular events is also important and obligatory for the clinicians.

Algorithms↗
PubMed1984

[Experimental study of cerebral protective effect on cerebral ischemia of various antioxidants and other agents. With special reference to the combined treatment of mannitol, vitamin E, dexamethasone and perfluorochemicals].

We have previously reported that the combined administration of mannitol and perfluorochemical blood substitutes is evidently effective in protecting the brain from cerebral ischemia. This experimental study was designed to develop more effective method in suppressing brain infarction than the combined treatment of mannitol and PFC. Using the "Canine model of complete ischemic brain regulated with a perfusion method" in which it is possible to control the degree of blood flow to a cerebral hemisphere via a perfusion pump, the effect of eight agents including six kinds as the free radical scavenger on cerebral ischemia was investigated. Eight agents were mannitol, vitamin E (Vit. E), dimethyl sulfoxide (DMSO), vitamin C, glycerol, nizofenone (Y-9179), dexamethasone (Dexa.) and suloctidil (MY-103). After pretreatment with each agent, blood flow was reduced via the pump to 1/10 of the normal state and 1 hour later, return to the normal state was allowed. Subsequent changes in EEG were observed and the effects of the drugs evaluated. In the control group, no recovery of electrical activity was seen, but in six groups among eight treated groups, i.e., treated with mannitol, Vit. E, DMSO, MY-103, Y-9179 and Dexa, gradual emergence of slow waves was observed. And more favorable effects were found when the combined administration of mannitol, Vit. E and Dexa was made in the same experimental schedule as compared with the single administration of each of these drugs. Furthermore in the animals administered with PFC in combination with mannitol, Vit. E and Dexa, flattening of electrical activity could not be seen throughout the period of severe ischemia. Moreover, the power of electrical activity recovered nearly to the preischemic state immediately after recirculation. Although the possible mechanisms are not yet completely clarified, the present results are thought to indicate that this new combination therapy utilizing PFC with mannitol, Vit. E and Dexa may be useful in the treatment of cerebral ischemia.

Animals↗
PubMed1996

Cerebrovascular disease.

Cerebrovascular disease may be secondary to various disorders including hypothyroidism, sepsis, neoplasia, hypertension, vascular malformation, and coagulopathy. Brain infarction or hemorrhage should be suspected in an animal with a sudden onset of a focal brain lesion. The recent availability of CT and MRI has improved our ability to diagnose cerebrovascular disease in animals. Treatment is directed at maintaining adequate oxygenation of the brain, controlling elevations of ICP, treating seizures, and identifying and treating any underlying disease. With appropriate care, many animals can recover.

Animals↗