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PubMed1996

Brain injury after perinatal hypoxia-ischemia is exacerbated in copper/zinc superoxide dismutase transgenic mice.

The role of superoxide radical formation in the pathogenesis of perinatal hypoxic-ischemic injury was examined using transgenic (Tg) mice expressing three times normal amounts of copper/zinc-superoxide dismutase (CuZn/SOD). Fourteen litters of postnatal d 7 strain 218/3 mice were subjected to right common carotid artery ligation followed by 90 min of hypoxia in an 8% oxygen/humidified chamber maintained at 37 degrees C. Both Tg mice (n = 32) and their nontransgenic (nTg) littermates (n = 30) survived the injury equally. Evaluation of infarcted brain areas measured by video image analysis of three coronal brain sections through the anterior hippocampus from each animal revealed that the Tg animals suffered brain infarction more frequently than did nTg mice. Blinded histologic scoring of cerebral cortex and striatum 5 d after injury revealed that Tg mice were more likely to have higher histologic severity scores than their nTg littermates (p = 0.0463, Mann-Whitney U test). These findings suggest that brain injury in perinatal hypoxia-ischemia may be mediated in part by free radical formation from excessive hydrogen peroxide or nitric oxide production.

Animals↗

PubMed1997

Carbonic anhydrase II in the cerebrospinal fluid: its value as a disease marker.

Carbonic anhydrase (CA) II is the predominant CA isoenzyme in the brain of mammals. We have recently developed a dual-label time-resolved immunofluorometric assay to quantify minute amounts of CA I and II in the cerebrospinal fluid (CSF). The present study was aimed at elucidating the clinical value of such measurements in the case of neurological disorders. Lumbar CSF samples were obtained from 111 patients suffering from various neurological diseases and from 97 control patients with no specific signs of central nervous system diseases. The highest CA II concentrations were found in patients with brain infarction (median 66.5 micrograms L-1, n = 20), whereas the control patients had markedly lower values (median 7.8 micrograms L-1, n = 97). Relative to a reference range calculated from the control material (10.2 +/- 17.2 micrograms L-1), the sensitivity of CA II measurement in differentiating brain infarction was 100%. Patients with transient ischaemic attack (median 11.2 micrograms L-1, n = 9), multiple sclerosis (median 14.7 micrograms L-1, n = 18) or epilepsy (median 20.3 micrograms L-1, n = 17) usually had CA II concentrations within the normal range, but those with central nervous system infection (n = 14), dementia (n = 19) or trigeminal neuralgia (n = 6) tended to have higher CA II levels in their CSF, the median values being 39.1 micrograms L-1, 45.5 micrograms L-1 and 44.0 micrograms L-1 respectively. The findings indicate that the concentration of CA II in the CSF marks disease activity in patients with brain damage. This finding could provide a basis for further studies estimating the value of CA II measurement as a new laboratory marker of diseases affecting the brain.

Adolescent↗

PubMedDate not supplied

[Cortisol in plasma and cerebrospinal fluid of patients with brain ischemia].

INTRODUCTION: One of the reactions to ischemia is increased release of glucocorticoid hormones, included in regulation of effects of numerous mediators/modulators that could be released in the acute phase of brain ischemia. The aim of our investigation was to define temporal dynamics of cortisol concentrations in plasma and cerebrospinal fluid of patients with different types of ischemic brain disease. MATERIAL AND METHODS: The study included 263 patients of both sexes, aged 55-68 years. History, clinical examination and cerebral computerized tomography were performed to establish the diagnosis. 97 patients had brain infarction, 66 had a reversible ischemic attack, 66 had a transient ischemic attack, and 34 patients had chronic encephalopathy. The control group included 22 age- and sex-matched patients, subjected to diagnostic lumbar radiculography, without disturbances in the cerebrospinal fluid passage. Cortisol concentrations were measured by direct radioimmunoassay. RESULTS AND DISCUSSION: Results obtained in this research showed that in acute brain ischemic period there was a significant increase of cortisol concentration in plasma and cerebrospinal fluid. The increase was highest in patients with brain infarction, somewhat lower in reversible ischemic attack, and the lowest in transient ischemic attack compared to controls (331.7 +/- 92.8 pmol/ml of plasma and 2.5 < or = 1.1 pmol/ml of cerebrospinal fluid). Maximum concentrations were found during the first two days after insult. The main potentially protective effects of increased cortisol concentrations in patients with acute stroke could be the decrease of effects of deleterious reactions induced by ischemia. This mechanism might be an attempt of organism to compensate for disturbed homeostasis. CONCLUSION: Measurement of cortisol in plasma and cerebrospinal fluid in patients with acute stroke is significant for monitoring the intensity of response of an organisam to acute brain damage.

Acute Disease↗

PubMed2002

A combined treatment with tacrolimus (FK506) and recombinant tissue plasminogen activator for thrombotic focal cerebral ischemia in rats: increased neuroprotective efficacy and extended therapeutic time window.

The authors evaluated the therapeutic efficacy of tacrolimus (FK506), administered alone or in combination with recombinant tissue plasminogen activator (t-PA), on brain infarction following thrombotic middle cerebral artery (MCA) occlusion. Thrombotic occlusion of the MCA was induced by a photochemical reaction between rose bengal and green light in Sprague-Dawley rats, and the volume of ischemic brain damage was determined 24 hours later. Intravenous administration of tacrolimus or t-PA dose-dependently reduced the volume of ischemic brain infarction, whether administered immediately or 1 hour after MCA occlusion. When tacrolimus or t-PA was administered 2 hours after MCA occlusion, each drug showed a tendency to reduce ischemic brain damage. However, combined treatment with both drugs resulted in a significant reduction in ischemic brain damage. On administration 3 hours after MCA occlusion, tacrolimus alone showed no effect, and t-PA tended to worsen ischemic brain damage. However, the combined treatment with both drugs not only ameliorated the worsening trend seen with t-PA alone, but also tended to reduce ischemic brain damage. In conclusion, tacrolimus, used in combination with t-PA, augmented therapeutic efficacy on brain damage associated with focal ischemia and extended the therapeutic time window compared to single-drug treatments.

Animals↗

PubMed2004

Aortic arch atherosclerotic lesions and the recurrence of ischemic stroke.

BACKGROUND AND PURPOSE: Aortic arch atherosclerotic lesions are often associated with embolic brain infarction. We investigated the relationship between stroke recurrence and the characteristics of aortic arch atherosclerotic lesions. METHODS: Among 487 stroke patients who underwent transesophageal echocardiography, 283 patients with brain embolism diagnosed without significant occlusive lesions (> or =50%) in their cerebral arteries were included in this study. We measured the intima-media thickness (IMT) and evaluated the extension and mobility of the aortic arch atherosclerotic lesions. During a mean follow-up period of 3.4 years, we investigated the relationship between stroke recurrence and the various characteristics of the aortic arch atherosclerotic lesions. RESULTS: An IMT > or =4.0 mm was found in 67 patients (25.3%). In 51 of these patients, the aortic lesions extended to the origin of the branches of the arch. Recurrences of cerebral ischemic events were found in 32 patients (recurrence group) and not in the other 251 (nonrecurrence group). Aortic atheroma > or =4.0 mm (41% versus 22%), aortic atheroma extending to the branches (63% versus 39%), and both (38% versus 16%) were more frequently seen in the recurrence group than in the nonrecurrence group (P<0.05, P<0.1, P<0.01, respectively). After adjustment for age and the presence of hypertension, an aortic atheroma that was > or =4.0 mm as well as extending to the branches was found to be an independent predictor of ischemic stroke recurrence (hazard ratio=2.42, P<0.05). CONCLUSIONS: Stroke recurrence is associated with the severity of the atheroma (IMT > or =4.0 mm) and plaque extension to the branches.

Aged↗

PubMed1999

Calcineurin inhibitors FK506 and SDZ ASM 981 alleviate the outcome of focal cerebral ischemic/reperfusion injury.

The neuroprotective properties of drugs binding to FKBP12, with and without subsequent inhibition of calcineurin, were investigated in rat models of ischemic embolic stroke. Drug effects on brain infarct volumes evoked by transient middle cerebral artery occlusion (MCAO) and by permanent MCAO were determined in vivo by T2-weighted magnetic resonance imaging and post mortem by triphenyltetrazolium chloride staining and histology. Drugs binding to FKBP12 and inhibiting calcineurin, such as FK506 and SDZ ASM 981, dose dependently reduced the infarct volumes, determined 48 h after MCAO by both magnetic resonance imaging and triphenyltetrazolium chloride staining but only in the transient MCAO model. In vivo potencies to reduce brain infarcts paralleled the in vitro potencies to inhibit calcineurin. Histological staining after 6 days of survival showed that the neuroprotective effects were permanent. Rapamycin, known to bind with similar affinity to FKBP12 but not to inhibit calcineurin, was not neuroprotective but abolished the neuroprotective effects of FK506 when coadministered. In the permanent MCAO models, FK506 showed no effect when injected before and little effect when injected after MCAO. Measurements of core temperatures after MCAO in controls and drug-treated rats do not support hypothermia being the mechanism responsible for neuroprotection. We conclude that drugs inhibiting calcineurin activity are neuroprotective in focal cerebral ischemia/reperfusion but not in permanent ischemia models, possibly by preventing reperfusion injury.

Animals↗

PubMed2000

Enhanced neuroprotection and reduced hemorrhagic incidence in focal cerebral ischemia of rat by low dose combination therapy of urokinase and topiramate.

Thrombolysis is increasingly being used in treating acute ischemic stroke but it is also accompanied with a serious complication of cerebral hemorrhage in a dose-dependent fashion. As a lower dose may result in decreased effectiveness, we tested the efficacy of combining a neuroprotective agent, topiramate (TPM), with lower doses of intra-arterial urokinase in an embolic stroke model. Focal ischemia was produced by introduction of an autogenous thrombus into the right middle cerebral artery. Urokinase was infused via the ipsilateral internal carotid artery and neuroprotective agent, TPM, was administrated intra-peritoneally 2 h following ischemic insult. The animals were assigned to five groups: (1) control group (n=6); (2) urokinase 5000 units/kg (n=8); (3) urokinase at 2500 units/kg (n=8); (4) topiramate at 20 mg/kg (n=8); (5) urokinase at 2500 units/kg and topiramate at 20 mg/kg (n=8). Neurobehavioral outcome and the degree of brain infarct volume were assessed at 24 h. Three animals in the group treated by high dose urokinase developed intracranial hemorrhage but none in other groups. Animals in all medication-groups showed significant improvement in neurobehavioral score. Post-ischemia treatment with urokinase or TPM alone significantly attenuated brain infarct volume (low-dose urokinase, 39.1+/-13.0%, p<0.05; high-dose, 18.4+/-8.5%, p<0.001; TPM, 20. 1+/-11.2%, p<0.001) when compared to the control (54.2+/-9.04%). Addition of TPM to low dose urokinase achieved better neuroprotection (8.2+/-6.0%) than any single-drug-treated groups. Our data suggests that combination of low dose urokinase with a neuroprotective agent may benefit ischemic stroke treatment by improving neurologic recovery, attenuating infarction size, and reducing the risk of cerebral hemorrhage.

Animals↗

PubMed1992

Functional 3D localization of cerebrovascular accidents by magnetoencephalography (MEG).

Spontaneous magnetic slow wave brain activity can be used to locate the underlying sources with sufficient accuracy by using the single current dipole model. To locate focal sources from spontaneous activity a tool had to be developed to extract focal densities of dipoles across time-the dipole density plot. The first version works on discrete volume units and is used for screening. The second version avoids a possible localization error and works continuously and this even is done on individual slices. The DDP seems to be a valuable tool for extracting and separating different focal sources from the background activity. Not only brain infarctions and haemorrhages (and cysts and angiomas) could be located, but also functional sources associated with TIAs even one week after the symptoms. First results let us assume that clinically silent TIAs also (in analogy to clinically silent brain infarctions) could be detected and located.

Brain↗

PubMed1993

Gene polymorphism of apolipoprotein AI, the major protein of high density lipoprotein in predicting stroke risk among white and black subjects.

BACKGROUND AND PURPOSE: Restriction fragment length polymorphism of the apolipoprotein AI gene, which encodes the most prominent apoproteins in high density lipoprotein (HDL), were investigated using the restriction enzymes Sac I and Pst I in white and black subjects to determine the potential role of genetic variations as stroke risks as determined by carotid stenosis and an atherogenic serum profile, such as elevated total cholesterol and low density lipoprotein (LDL) levels or reduced HDL levels. METHODS: Ninety-eight subjects, including normal control subjects with no carotid stenosis and subjects with carotid stenosis, who were believed to be at stroke risk, were the study subjects and included 70 white and 28 black subjects. RESULTS: Sac I polymorphic S2 allele frequency was higher in stroke-risk groups. Significantly higher levels of serum cholesterol, triglycerides, and LDL (P < .05) and significantly lower levels of HDL (P < .05) were present in the stroke-risk group with carotid stenosis. Our study showed the following: Sac I polymorphism frequency was significantly higher in black than white subjects (chi 2 = 3.92, P < .05). Triglyceride level was significantly higher in white subjects compared with black subjects (P < .05). In white subjects, carotid artery stenosis was associated with significantly elevated total cholesterol and LDL levels (P < .01) but not with Sac I polymorphism. In black subjects, the reverse was seen with the Sac I polymorphic S2 allele associated with carotid bifurcation stenosis but did not reach statistical significance because of the small number of subjects. In addition, Sac I polymorphism did not correlate with any lipid profile. Pst I polymorphism was not associated with an abnormal atherogenic lipid profile or carotid artery stenosis abnormalities. CONCLUSIONS: Our study shows that carotid artery stenosis in white subjects is associated with increased plasma total cholesterol and LDL levels and an atherogenic profile but not with Sac I polymorphism for apoprotein AI. In black subjects, Sac I polymorphism appears to identify individuals with significant carotid stenosis, a necessary precursor to atherothrombotic brain infarction, but not those with elevated total cholesterol or LDL and/or reduced HDL levels. These results suggest that Sac I polymorphism may identify black subjects at increased risk for atherothrombotic brain infarctions.

Aged↗

PubMed1987

Migraine-related strokes. Clinical profile and prognosis in 20 patients.

We reviewed the records of 4874 patients, aged 50 years and younger, who were seen at the Mayo Clinic, Rochester, Minn, from 1976 to 1980, and had received a diagnosis of migraine, migraine equivalent, or vascular headache. Twenty patients (16 females and four males) who had migraine-associated brain infarctions are described. The areas of infarction and corresponding angiographic abnormalities were most frequently in the distribution of the posterior cerebral artery. During a mean follow-up period of seven years, two patients had a second brain infarction. At last follow-up examination, 18 of the 20 patients had minimal or no functional impairment. For the period 1976 to 1979, we reviewed the available data on cerebral infarction for the Rochester, Minn, population aged 50 years or younger; 25% of all incidence cases of cerebral infarction were migraine associated.

Adolescent↗

PubMed2005

Diffusion-weighted magnetic resonance imaging in symptomatic vertebrobasilar atherosclerosis and dissection.

BACKGROUND: Acute multiple brain infarction (AMBI) pattern on diffusion-weighted imaging (DWI) is associated with arterial and cardiac sources of embolism. The DWI characteristics of patients with stroke due to vertebrobasilar arterial dissection and atherosclerotic disease have not been reported in detail. OBJECTIVE: To describe the DWI stroke patterns in patients with posterior circulation occlusive disease to determine mechanisms of ischemia. DESIGN: Retrospective analysis of infarct patterns in patients with symptomatic vertebrobasilar disease. SETTING: Large community-based teaching hospital. PATIENTS: Patients admitted with stroke due to vertebrobasilar disease were identified retrospectively. Patients were included if DWI was obtained within 7 days of symptom onset. MAIN OUTCOME MEASURE: Infarct patterns were analyzed according to established templates of vascular territories. RESULTS: Eleven patients with vertebral dissection and 39 patients with atherothrombosis were identified. An AMBI pattern was present in 8 (72%) of 11 patients with arterial dissections and 25 (64%) of 39 patients with atherosclerotic disease (P = .48). Distal embolism to the terminal branches of the basilar artery occurred with equal frequency in both groups and was found in half of all cases. Isolated thalamic infarction did not occur. Pontine infarction was noted in 2 (18%) of 11 patients with dissections and 18 (46%) of 39 patients with atherosclerosis (P = .09). Cerebellar border zone involvement was found in 14 (36%) of 39 patients with atherosclerosis and 4 (37%) of 11 patients with dissections (P = .6). CONCLUSIONS: Large arterial disease is frequently associated with AMBI in the posterior circulation. The incidence of AMBI was comparable to that reported in the anterior circulation. This DWI study supports the importance of embolism as the main mechanism of infarction in patients with vertebrobasilar occlusive disease. On the basis of our experience, large-vessel vertebrobasilar disease rarely causes isolated small-vessel thalamic infarction.

Adult↗

PubMed2005

A patient with cerebral Whipple's disease and a stroke-like syndrome.

The central nervous system (CNS) may be affected in up to 50% of patients with Whipple's disease and this can occur even with little or no gastrointestinal involvement. We describe a 63-year-old patient in whom CNS involvement with Whipple's disease had the clinical and imaging features of a brain infarction. Treatment with aspirin and ceftriaxone followed by trimethoprim-sulfamethoxazole resulted in a good neurological recovery and complete remission of the malabsorption syndrome. Cerebral Whipple's disease resembling a stroke syndrome has so far been reported in only two other patients and in both cases it represented the first presentation of the disease. Arterial or arteriolar fibrosis, thrombosis and thickening associated with the inflammation of adjacent brain parenchyma and leptomeninges, and cerebral vasculitis caused by the hematogenous spread of Tropheryma whippelii to the brain may all be important triggers of brain infarction in patients with Whipple's disease. Our case report highlights the important point that cerebral Whipple's disease with the features of a stroke syndrome, if recognized early and treated aggressively with antibiotics, could have a favorable course with no long-term disability sequelae.

Anti-Infective Agents↗

PubMed1998

Epidermal growth factor receptor in proliferating reactive glia following transient focal ischemia in the rat brain.

Severe transient focal cerebral ischemia causes brain infarction with a strong glial reaction. We have studied whether postischemic reactive glial cells express epidermal growth factor receptor (EGFR) following middle cerebral artery occlusion in the rat. We have also looked for signs of proliferating activity, as EGFR is known to be involved in cell growth and proliferation in certain non-neural cells. EGFR was studied using three different antibodies which were found to stain for a tyrosine-phosphorylated protein (p170) corresponding to the membrane-anchored EGFR. Neurons of the control brain were strongly immunoreactive to EGFR, but a decrease of EGFR-immunoreactivity was seen in the ipsilateral brain side from 24 h postischemia due to neuronal loss. However, the presence of abundant glial cells strongly immunoreactive to EGFR became apparent in this area from 4 days postischemia onward. The use of microglial (lectin or OX-42) and astroglial (GFAP) markers showed that these postischemic EGFR-stained cells were reactive microglia/macrophages and astroglia. The subcellular localization of EGFR in reactive microglia/macrophages was compatible with the network of the Golgi apparatus, as revealed with an antibody against a peripheral membrane-bound protein of the Golgi. The presence of abundant proliferating cells in the ischemic brain was detected from 4 days postischemia with an antibody against proliferating cell nuclear antigen. Proliferating reactive microglia/macrophages were abundant within the infarcted brain side, whereas proliferating astrocytes were found mainly in the immediate periphery of the infarct limiting the necrotic area from the undamaged tissue. These proliferating cells were immunoreactive to EGFR. The results show the presence of EGFR in postischemic reactive glial cells and suggest that EGFR-dependent pathways mediate signal transduction in reactive glia following transient focal cerebral ischemia.

Animals↗

PubMed1992

Restriction fragment length polymorphism of the apoprotein A-I-C-III gene cluster in control and stroke-prone white and black subjects: racial differences.

BACKGROUND AND PURPOSE: The presence of known restriction fragment length polymorphisms in the apoprotein A-I-C-III gene cluster, which encodes their respective apoproteins, was investigated using the restriction enzymes Sac I and Pst I to determine the potential role of genetic variations for stroke risk in an American population. METHODS: Ninety-eight subjects (70 white, 28 black subjects), both normal controls with no carotid stenosis and those with carotid stenosis believed at risk for stroke, defined as showing stenosis focally or diffusely at that site, composed the study population. RESULTS: Sac I polymorphic S2 allele frequency was higher in stroke-risk groups, whereas Pst I polymorphic P2 allele frequency was similar in control and stroke-risk groups. Significantly higher levels of serum cholesterol, triglycerides, and low density lipoprotein (p less than 0.05) and significantly lower levels of high density lipoprotein (p less than 0.05) were observed in stroke-risk groups with diffuse stenosis. Results of our study with the two racial groups show the following: the frequency of Sac I polymorphism was significantly higher in American black compared with American white subjects (chi 2 = 3.92, p less than 0.05). Among serum lipids, triglycerides were significantly higher in white compared with black subjects (p less than 0.05). In white subjects, carotid artery stenosis was associated with significantly elevated total cholesterol and low density lipoprotein (p less than 0.01) but not with Sac I polymorphism. In black subjects the converse was observed, namely, the Sac I polymorphic S2 allele seemed to be associated with carotid bifurcation stenosis but did not reach statistical significance because of the small number of subjects. In addition, Sac I polymorphism did not correlate with any lipid profile. Pst I polymorphism was not associated with any lipid profile or carotid artery stenosis abnormalities. CONCLUSIONS: Our results indicate that carotid artery stenosis identifies white subjects with increased plasma total cholesterol and low density lipoprotein, an atherogenic profile, but not with Sac I polymorphism. These findings suggest that carotid bifurcation stenosis in white subjects is associated with an atherogenic lipid profile but not with apoprotein A-I-C-III restriction fragment length polymorphisms. In black subjects, Sac I polymorphism seems to identify those individuals with significant carotid stenosis, a necessary precursor to atherothrombotic brain infarction, but not those with elevated total cholesterol, elevated low density lipoprotein, and/or reduced high density lipoprotein. These results suggest that Sac I polymorphism may identify black subjects at increased risk for atherothrombotic brain infarctions.

Aged↗

PubMed1995

[Detection of cortical infarcts in brain MR imaging: feasibility of short-TR-T2-weighted imaging using a fast spin echo sequence].

MRI of the brain using a fast SE sequence is often performed with a TR above 5000 msec, so there is a tendency for the signal of CSF to become too high. However, when cerebral atrophy is marked, small lesions of the brain parenchyma can be hard to detect. Therefore, we examined short-TR-T2-weighted images using a fast spin echo sequence. The 58 subjects included 33 men and 25 women, and cortical infarction was detected in five of them. On the short-TR-T2WI sequences, the infarct lesions were imaged as areas of higher signal intensity than cerebrospinal fluid, the signal of which was reduced. In cortical infarction cases, fluid-attenuated inversion recovery (FLAIR) images can detect the lesion more easily, but FLAIR sequences cannot be obtained with all MR equipment. Short-TR-T2WI, which readily yields images comparable to those of FLAIR, is an useful method.

Cerebral Cortex↗

PubMedDate not supplied

[Tryptophan and tyrosine in blood and cerebrospinal fluid in patients with recent cerebral infarct].

The determinations were carried out in the blood and cerebrospinal fluid of 40 patients with recent cerebral infarction and 30 controls. Tryptophan concentration was determined by the fluorimetric method of Denckla and Dewey, and tyrosine concentration by the method of Waalkes and Udenfried. A statistically significant rise of free tryptophan concentration in the plasma and tryptophan concentration in the cerebrospinal fluid was found which seemed to depend on the stress reaction following brain infarction. No statistically significant changes were observed in the concentration of tyrosine in the cerebrospinal fluid and plasma in patients with brain infarction.

Adult↗

PubMed1989

[Evolution of venous cerebral infarction and brain edema--an experimental study of sagittal sinus obstruction].

Superior sagittal sinus with/without neighboring venous system of 36 mongrel cats were occluded by cyanoacrylate polymer after i.v. administration of Evans-blue (EB). Thereafter, the cats were sacrificed 1, 3, 6, 12, 24, 72 or 120 hours after sinus-vein occlusion. According to the degree of occluded region, the cats were divided into two groups; group A (GA) and B (GB). GA showed only superior sagittal sinus occlusion, while many cortical veins were also occluded in GB. No EB nor histological changes were found in 13 cats of GA and 4 sham operated cats, while EB distribution was observed in all 20 cats of GB. The other 3 cats of GA showed a little EB in gyrus lateralis. EB distribution of GB were divided into two types. Type 1 showed EB mainly in the cortical gray matter, while type 2 showed massive EB extravasation in the white matter as well. Edematous changes with gliosis in its resolution phase, were observed in type 1. In addition, EB free zone was formed along with U-fiber zone (cortico-medullary junction) in the cats of later phase (72 hours after occlusion). The findings of EB extension in the type 1 means the existence of blockage against edema evolution from cortex toward subcortical white matter. The cats of type 2 showed fulminant hemorrhagic changes which appeared depend on time interval. Although occurrence of pathological changes were rather earlier than that of cases of clinical cerebral sinus thrombosis, this pathological findings demonstrated the typical character of venous hemorrhagic infarction. In this paper, the similarity and difference between this model and clinical case of sinus-vein thrombosis were discussed. And the possible function of the U-fiber zone in the corticomedullary junction against edema evolution was suggested.

Animals↗

PubMed1978

[Rheologic properties of the blood and lipid metabolism in patients with hemorrhagic infarct of the brain].

The clinical development, changes of the rheological blood properties and lipid metabolism were analysed in 70 patients with acute and subacute hemorrhagical infarctions into the hemispheres. Two clinical types in the development of hemorrhagical brain infarctions are described. The rheological blood properties and lipid metabolism had certain differences in comparison to patients with hemispheric hemorrhagical and ischemic strokes. They were also changed depending upon the age and duration of the illness. The pathogenesis of the changes detected is substantiated and their significance for microhemocirculation in patients with hemorrhagical brain infarctions is discussed.

Adult↗