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PubMed1982

[Dynamic pathophysiology of cerebral infarction and revascularization. I. Ischemic cerebral edema].

A natural history of ischemic cerebral edema was analyzed in 100 patients with occlusive cerebrovascular diseases admitted within one week of onset, with serial computed tomography (CT) and angiograms. Cerebral edema was defined as a low-density area with mass sign on CT. A total of 446 studies of CT were performed. In 40 patients with major completed stroke admitted 24 hours of onset, a total of 73 studies of CT were taken within 48 hours of onset, and a timing of appearance of cerebral edema was analyzed. Patients were allocated to two groups according to the findings on angiograms; 68 patients who showed occlusive lesions on sequential angiograms (the group of no-recanalization), and 32 patients who showed reopening of occluded vessels on the first or sequential angiograms (the group of no-recanalization). In the group of no-recanalization a low-density area gradually appeared between 6 and 24 hours of onset A. mass sign reached its peak on the 3rd day with a peak incidence of 56%, and midline shift was present in 30% of the cases. It was resolved within 2 weeks in most cases. In the group of recanalization, a low density area appeared after 4 hours and rapidly increase after 6 hours. All patients had a low-density area at 12 hours of onset. A mass sign progressed until the 6th day with a peak incidence of 82%, and midline shift was present in 50% of the cases. The duration of mass sign was longer than that in the group of no-recanalization. These results suggest that the permissible duration of ischemia is considered to be within 6 hours of onset in profound ischemia. After 6 hours, ischemic tissue damage may not be reversible by the revascularization, even if CT shows no change during ischemia. An abrupt revascularization may not contribute to the recovery of brain damage, but accelerate the ischemic cerebral edema.

Aged↗
PubMed1999

Transplantation of fetal kidney tissue reduces cerebral infarction induced by middle cerebral artery ligation.

The authors, and others, have recently reported that intracerebral administration of glial cell line-derived neurotrophic factor (GDNF) or osteogenic protein-1 protects against ischemia-induced injury in the cerebral cortex of adult rats. Because these trophic factors are highly expressed in the fetal, but not adult, kidney cortex, the possibility that transplantation of fetal kidney tissue could serve as a cellular reservoir for such molecules and protect against ischemic injury in cerebral cortex was examined. Fetal kidneys obtained from rat embryos at gestational day 16, and adult kidney cortex, were dissected and cut into small pieces. Adult male Sprague-Dawley rats were anesthetized with chloral hydrate and placed in a stereotactic apparatus. Kidney tissues were transplanted into three cortical areas adjacent to the right middle cerebral artery (MCA). Thirty minutes after grafting, the right MCA was transiently ligated for 90 minutes. Twenty-four hours after the onset of reperfusion, animals were evaluated behaviorally. It was found that the stroke animals that received adult kidney transplantation developed motor imbalance. However, animals that received fetal kidney grafts showed significant behavioral improvement. Animals were later sacrificed and brains were removed for triphenyltetrazolium chloride staining, Pax-2 immunostaining, and GDNF mRNA expression. It was noted that transplantation of fetal kidney but not adult kidney tissue greatly reduced the volume of infarction in the cerebral cortex. Fetal kidney grafts showed Pax-2 immunoreactivity and GDNF mRNA in the host cerebral cortex. In contrast, GDNF mRNA expression was not found in the adult kidney grafts. Taken together, our data indicate that fetal kidney transplantation reduces ischemia/reperfusion-induced cortical infarction and behavioral deficits in adult rats, and that such tissue grafts could serve as an unique cellular reservoir for trophic factor application to the brain.

Animals↗
PubMed1996

[Study on experimental parameters for diagnosing ganyang huafeng syndrome of cerebral infarction].

One hundred patients with cerebral infarction were observed, the results showed that Ganyang Huafeng Syndrome (GYHFS) was the major syndrome of acute cerebral infarction which was accounted for 60% and Qiyin Liangxu Syndrome (QYLXS), Qixu Xueyu Syndrome (QXXYS) were mainly observed at convalescent stage of this disease which was accounted for 37.78% and 31.11% respectively. This study chose plasma norepinephrine (NE), epinephrne (E), thromboxane B2(TXB2), 6-keto-PGF1 alpha, cortisol (F) and serum triiodothyroidoglobulin (T3) as the monitoring parameters, and the results showed that the increase of plasma NE,F,TXB2, the decrease of serum T3 could be considered as the comprehensive experimental parameters for diagnosing GYHFS of cerebral infarction.

Adult↗
PubMedDate not supplied

Functional CT perfusion imaging in predicting the extent of cerebral infarction from a 3-hour middle cerebral arterial occlusion in a primate stroke model.

BACKGROUND AND PURPOSE: Our purpose was to determine whether cerebral perfusion functional CT (fCT), performed after endovascular middle cerebral artery (MCA) occlusion, can be used to predict final cerebral infarction extent in a primate model. METHODS: fCT with bolus tracking was performed before and 30 and 150 minutes after 3-hour digital subtraction angiography (DSA)-guided endovascular MCA occlusion in five baboons. Parametric cerebral blood flow (CBF), cerebral blood volume (CBV) and mean transit time (MTT) maps were constructed by voxel-by-voxel gamma variate fitting and used to determine lesion sizes. Animals were sacrificed 48 hours after the occlusion, and ex vivo MR imaging was performed. Lesion sizes on fCT and MR images were compared. RESULTS: Hypoperfusion was clearly identified on all images obtained after MCA occlusion. Thirty and 150 minutes after occlusion onset, respectively, mean lesion sizes were 737 mm(2) +/- 33 and 737 mm(2) +/- 44 for CBF, 722 mm(2) +/- 32 and 730 mm(2) +/- 43 for CBV, and 819 mm(2) +/- 14 and 847 mm(2) +/- 11 for MTT. Mean outcome infarct size on MR images was 733 mm(2) +/- 30. Measurements based on CBV and CBF (R(2) = 0.97 and 0.96, P <.001), but not MTT (R(2) = 0.40, P >.5), were highly correlated with final lesion size. CONCLUSION: An endovascular approach to MCA occlusion provides a minimally invasive, reproducible animal model for controlled studies of cerebral ischemia and infarction. Derived cerebral perfusion maps closely predict the 48-hour infarct size after 3-hour MCA occlusion.

Angiography, Digital Subtraction↗
PubMed2000

[Antithrombotic therapy in cerebral infarction].

Antithrombotic therapy for the acute stage of cerebral infarction consists of thrombolysis, anticoagulant therapy and antiplatelet therapy, and their indications depend on the clinicopathological type of lesion, time after onset, and severity of illness. Tissue plasminogen activator has been approved in the United States for use in cerebral infarction within 3 hours after onset. The usefulness of heparin as anticoagulant therapy at the acute stage of cerebral infarction was not proved by the International Stroke Trial due to hemorrhagic complication. A selective thrombin inhibitor (argatroban) is used in Japan for atherothrombotic cerebral infarction within 48 hours after onset. A selective thromboxane A2 synthetase inhibitor (sodium ozagrel) had been approved for cerebral thrombosis within 5 days after onset. Aspirin (160-300 mg/day) is effective, but slightly, in the acute stage of cerebral infarction by the International Stroke Trial and Chinese Acute Stroke Trial. To prevent recurrence of stroke in the chronic stage of cerebral infarction, antiplatelet therapy (with aspirin or ticlopidine) is used for atherothrombotic cerebral infarction, and anticoagulant therapy with warfarin for cardioembolic cerebral infarction.

Acute-Phase Reaction↗
PubMed1989

[Cerebral hemodynamics in multiple cerebral infarction with or without dementia].

Cerebral blood flow and metabolism in 25 patients with multiple cerebral infarcts (14 with dementia) and 5 healthy age-matched controls were measured to investigate the difference in cerebral blood low (CBF) and cerebral oxygen consumption (CMRO2) between patients with dementia and patients without dementia. None of the patients had any lesions in the cortex, but all had multiple lesions in the basal ganglionic region, and in the white matter, according to CT images. CBF, CMRO2 and oxygen extraction fraction were measured by positron emission tomography (PET) using the 15O2, C15O2 steady state inhalational technique. In patients with multiple cerebral infarcts the absolute values of CBF and CMRO2 were decreased significantly from normal control values, and there was no significant difference in the absolute values of CBF and CMRO2 between patients with dementia and patients without dementia. In most patients with dementia, relative values (regional value/mean cortical value) of CBF and CMRO2 decreased in the frontal and the parietal cortex. Four patients had repeated PET studies. In two of them, decrease in CMRO2 was preceded by decrease in CBF. These results suggest that dysfunction of frontal cortex and parietal cortex, and chronic ischemia might be related to the occurrence of dementia in patients with multiple cerebral infarcts, which were in the basal ganglia and the white matter.

Aged↗
PubMed1997

Hemorheologic profiles of plasma fibrinogen and blood viscosity from silent to acute and chronic cerebral infarctions.

Hemorheologic changes from silent to acute and chronic cerebral infarction have seldom been reported. We evaluated hemorheologic profiles of the whole blood viscosity, plasma viscosity and fibrinogen level in stroke at-risk patients with silent cerebral infarction, patients with acute or chronic cerebral lacunar infarction, and subjects at low risk for stroke. Hemorheologic profiles were measured in 88 subjects: (1) 36 patients with silent cerebral infarction (mean 64.7 years), who provided no clinical history of having had definitive stroke but showing > 5 mm lesions of cerebral infarction or periventricular hyperintensity (PVH) observed in magnetic resonance imaging (MRI) T2-weighted images; (2) 12 patients with acute cerebral lacunar infarction (mean 69.1 years), measured within 3 days and repeated 1 month after onset; (3) 25 patients with chronic cerebral lacunar infarction (mean 66.2 years), measured 12.5 months after onset; and (4) 15 subjects at low risk for stroke (mean 65.8 years) without cardiovascular risk factors or lesions on MRI. Patients with silent cerebral infarction were subdivided into two groups of less advanced and more advanced grades, based on the number of infarctions or the grade of PVH. Whole blood viscosity (shear rates: 22.5-225.0 s-1), corrected blood viscosity for 45% standard hematocrit (Hct), plasma viscosity, fibrinogen, serum total protein, albumin, and Hct were measured. Plasma fibrinogen levels were lower in silent cerebral infarctions than in chronic cerebral infarctions (P < 0.01), and patients with more advanced grades of silent cerebral infarction showed higher levels of plasma fibrinogen than those with less advanced grades (P < 0.01 and P < 0.05). Whole blood viscosity, corrected blood viscosity (Hct 45%), plasma viscosity and fibrinogen levels in acute cerebral infarction within 3 days after onset were higher significantly than those in subjects at low risk for stroke. Plasma fibrinogen level persisted to be elevated up to 1 month after onset, which continued as well in patients with chronic cerebral infarction. Advanced grades of silent cerebral infarction in stroke at-risk patients are accompanied by elevations of plasma fibrinogen level, which increases further after onset of cerebral infarction; such abnormalities persist up to the chronic stage. Elevated plasma fibrinogen level might reflect progression of atherogenesis in patients with advanced grades of silent cerebral infarction, resulted in an increased probability as to be a risk factor for cerebral infarction.

Acute Disease↗
PubMed1997

The factor V Leiden mutation (R506Q) is not a major risk factor for migrainous cerebral infarction.

The etiology of migrainous cerebral infarction is unknown, but may involve prothrombotic coagulation abnormalities. Therefore, we studied resistance to activated protein C and the presence of the Arg506Gln factor V Leiden mutation in 20 patients with migrainous cerebral infarction. Only one heterozygous carrier of the mutation was found, whereas other patients did not carry the mutation. This indicates that the factor V Leiden mutation is not a major risk factor for migrainous cerebral infarction.

Adolescent↗
PubMed2003

[A study on genetic epidemiology of cerebral infarction].

OBJECTIVE: To explore the genetic model of cerebral infarction and to examine the relationship between cerebral infarction and genetic factor. METHODS: A matched case-control study including 112 pairs pedigrees was carried out. Using the Li-Mantel-Gart method and the Falconer method to estimate the segregation ratio and the heritability of cerebral infarction. RESULTS: The prevalence rate of the first-degree and the second-degree relatives in cases was significantly higher than that in controls. The segregation ratio was 0.143 7 (0.113 0 - 0.174 4), significantly lower than 0.25, which showed that cerebral infarction did not possess the characteristics of monogenetic model. The results showed that the heritability of the first-degree and the second-degree relatives were 47.84% and 40.95% higher in male's than in female's. CONCLUSION: Cerebral infarction was a polygenetic disease, and the genetic factors played an important role in the occurrence of cerebral infarction, especially in males.

Aged↗
PubMed1994

[A study of 82 cerebral infarctions in the area of posterior cerebral arteries].

Of 598 consecutive non-selected cases of cerebral infarction included in a stroke registry, 82 cases (54 men and 28 women, mean age 66 +/- 14 years) of spontaneous and isolated posterior cerebral artery (PCA) territory infarction (right PCA in 36, left PCA in 35 and both in 11) were identified on the basis of CT combined with MRI in 51 cases. Infarction was superficial in 25 (group A), combined deep-superficial in 23 (group B) and deep in 34 (group C). Of 48 superficial lesions, 29 were massive while 19 were restricted to the territory of one branch. Of 57 deep lesions, 21 were located in the inferolateral thalamic territory, 10 in the paramedian thalamic territory, 12 in other midbrain or thalamic territories, and 14 in a combination of various midbrain and/or thalamic territories. Of 41 patients with unilateral superficial involvement, 39 had homonymous visual field defect. Unawareness of the visual defect and visual release hallucinations were observed with the same frequency in right and left lesions. Of 7 patients with bilateral superficial involvement, only 5 had bilateral visual field defect including incomplete cortical blindness in 3. The frequency of confusional state (n = 24) did not differ significantly in left versus right sided lesions while it was significantly higher in superficial or combined versus deep lesions (p = 0.05). Of 18 clinically evaluable patients with left PCA territory infarct, 14 had speech disorders including pure alexia in only one case. Of 15 patients with right territory infarction, 10 had spatial judgement disorders.(ABSTRACT TRUNCATED AT 250 WORDS)

Adolescent↗
PubMed1985

[Effect of KC-404 on experimental cerebral infarction in rats].

Experimental cerebral infarction accompanying altered cerebral energy metabolism and cerebral edema was produced in rats by injecting arachidonate into the left carotid artery. In the present study, the effects of 3-isobutyryl-2-isopropylpyrazolo [1,5-alpha]pyridine (KC-404) on these ischemic insults as well as on the regional cerebral blood flow (r-CBF) were studied. 1) Cerebral metabolism: On the 7th day of infarction, a significant decrease in ATP content and an increase in glucose content were observed, especially in the left hemisphere. There were no significant changes in lactate and pyruvate contents as compared with normal rat brain. Treatment with KC-404 (10 mg/kg, p.o.) once on the 7th day or twice on the 6th and 7th days of infarction caused a significant increase in ATP content and a decrease in lactate content. Increased content of glucose tended to be suppressed by KC-404. In normal rats, KC-404 (10 mg/kg, p.o.) caused slight but significant increases in cerebral ATP, glucose and pyruvate contents. 2) Cerebral edema: On the 4th day of infarction, significant increases in water content and Na+/K+ ratio and a decrease in K+ content were observed in the left hemisphere. Treatment with KC-404 (10 mg/kg, p.o.) for three preceding days showed a significant suppression of increased water content with a tendency to improve altered electrolyte levels. 3) r-CBF: KC-404 (0.05 mg/kg/min) infused i.v. for 15 min increased more markedly the r-CBF in the affected left hemisphere as compared with that in normal brain.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1994

[Clinical study of naoxin sutong in the treatment of acute cerebral infarction].

It was shown that the cerebral ischemia-reperfusion produced free radicals are the main factor that causes irreversible cerebral injury. The mechanism of Naoxin Sutong (NXST) treated acute cerebral infarction was elucidated. It is compared with Ligustrazine (LT), which has been proved to be an effective drug for cerebral infarction. The curative effect and the changes of serum malondialdehyde (MDA) levels, blood rheology, blood lipid, etc. of 41 patients with acute cerebral infarction within 3 days, who were confirmed by CT. The therapeutic result showed that after 4 weeks of treatment the points of progress for central nervous system deficit scoring of NXST and LT group were 10.67 +/- 5.02 and 6.85 +/- 4.49 respectively. The difference between these two groups was significant. MDA levels of the patients and the healthy subjects were 6.46 +/- 1.70 and 3.87 +/- 0.67 nmol/ml respectively, the difference was also significant (P < 0.01). After 2 weeks of treatment, MDA content of NXST was less than before (P < 0.05). However the level of LT group did not reduce, while after 3 weeks of treatment, MDA content of NXST group was 4.34 nmol/ml. It was much less than that of LT group and approached that of healthy subjects. Results also showed that blood rheology improved, blood lipid reduced after NXST treatment. All these indicated that the effect of NXST in treating acute cerebral infarction was good, and the mechanism as that NXST could scavenge free radicals, ameliorate cerebral ischemia-reperfusion injury, improve blood rheology and reduce blood lipid.

Acute Disease↗
PubMed1989

Risk factors for the complication of cerebral infarction in Japanese patients with acute myocardial infarction.

The incidence and risk factors for cerebral infarction in Japanese patients with acute myocardial infarction were evaluated. Seven (5.0%) of 140 patients with acute myocardial infarction suffered from cerebral infarction during their initial hospitalization. The incidence was slightly higher than those reported in Western countries. Anterior wall myocardial infarction and a past history of cerebrovascular disease were considered to be probable risk factors for the complication. A beneficial effect of anticoagulant therapy in preventing cerebral infarction in cases of acute myocardial infarction with those risk factors is suggested.

Aged↗
PubMed2003

Cerebral infarction in perinatal and childhood bacterial meningitis.

BACKGROUND: Cerebral infarction is an important neurological complication of childhood bacterial meningitis, but little is known about its epidemiology and outcomes. AIM: To determine the predictive factors, clinical features, causative pathogens, and outcomes of cerebral infarction secondary to perinatal and childhood bacterial meningitis. DESIGN: Retrospective analysis METHODS: Over the period 1986-2001, 166 perinatal and childhood patients were identified as having culture-proven bacterial meningitis, of whom 14 had cerebral infarction at admission. The clinical and CSF data of patients with and without cerebral infarctions on admission were compared. RESULTS: Cerebral infarction patients accounted for 10% (14/166) of bacterial meningitis cases, mostly in the first year of life (11/14, 79%). Salmonella species (n = 4) and Streptococcus pneumoniae (n = 4) were the most frequent causative pathogens, accounting for 57% (8/14) of episodes. Single infarctions were found in four patients and multiple infarctions in 10. At 1 year follow-up, outcome was good in three, but poor in 11. Significant differences between the two patient groups at admission included age bands, presence of seizures, hydrocephalus, disturbed consciousness on admission, and CSF lactate concentration. DISCUSSION: There was a high prevalence of cerebral infarctions when the disease was caused by S. pneumoniae and Salmonella species. Occurrence was highest in the first year of life, and the prognosis in this patient group is poor. Risk factors associated with cerebral infarction in our patients included age 28-365 days, seizures, hydrocephalus, disturbed consciousness on admission, and high CSF lactate concentrations.

Age Factors↗
PubMed2006

[Monitoring in acute cerebral infarction].

BACKGROUND: Cerebral ischaemia is potentially reversible during the first few hours. Monitoring of physiological variables such as temperature, blood pressure, heart rhythm, oxygen saturation and cerebral blood flow may be important for efficient treatment and reduction of the infarct volume. MATERIAL AND METHODS: This article is based on a review of relevant articles in international journals over the last 15 years on the pathophysiology of acute ischaemic stroke and treatment in intensive stroke units compared with conventional stroke units. RESULTS AND DISCUSSION: Two pilot studies indicate that continuous monitoring in intensive stroke units improves outcome compared with conventional stroke units. Future studies must draw the balance between continuous monitoring and mobilization in the early phase of ischaemic stroke.

Acute Disease↗
PubMed2002

Contribution of cerebral nitric oxide to bladder overactivity after cerebral infarction in rats.

PURPOSE: We investigated the contribution of cerebral nitric oxide to neurogenic voiding dysfunction after cerebral infarction. MATERIALS AND METHODS: The left mid cerebral artery in female Sprague-Dawley rats was occluded with 4-zero monofilament nylon thread. Bladder activity was monitored during infusion cystometrography. Time or dose dependent effects of intracerebral ventricular administration of the nonselective nitric oxide synthase inhibitor NG-nitro-L-arginine methyl ester (L-NAME), were investigated in conscious, sham operated and cerebral infarcted rats. The selective neuronal nitric oxide synthase inhibitor 1-(2-trifluoromethylphenyl) imidazole was also administered to determine the participation of nitric oxide synthase subtypes. Cross-sectional infarct area was measured and infarct volume was calculated 12 hours after mid cerebral artery occlusion. RESULTS: Bladder capacity was reduced by 54% 30 minutes after mid cerebral artery occlusion. L-NAME significantly increased bladder capacity in a dose and time dependent manner in cerebral infarcted rats but had no effect on sham operated rats. L-NAME (50 microg./kg.) administered 3 or 5 hours after occlusion significantly increased bladder capacity. This effect of L-NAME was reversed by injecting 250 microg. L-arginine per rat, which alone did not produce any significant change in bladder capacity in cerebral infarcted rats. Administration of 1-(2-trifluoromethylphenyl) imidazole also significantly increased bladder capacity in these rats. On the other hand, 5 microg. of the nitric oxide donor FK-409 per rat reduced bladder capacity for 10 to 15 minutes. None of the drugs affected infarct volume. CONCLUSIONS: These results indicate that supraspinal nitric oxide has an important role in bladder overactivity after cerebral infarction but it does not affect normal micturition in rats. This finding suggests a central mechanism sensitive to nitric oxide for bladder overactivity after cerebral infarction.

Animals↗
PubMed1996

Sensorimotor impairments in Wistar Kyoto rats with cerebral infarction, induced by unilateral occlusion of the middle cerebral artery: recovery of function.

Wistar Kyoto (WKY) rats with cerebral infarction induced by permanent unilateral occlusion of the middle cerebral artery (MCA) and sham-operated rats were tested in a series of simple behavioral test 2, 16 and 37 days after surgery. In addition, the motility of the animals was measured over a period of 62 h, after the third test series. A subset of the tests appeared to be suitable to assess the effects of cerebral infarction, namely, grasping reflex of contralateral hindpaw, circling behavior, forelimb flexion, hindlimb flexion, and latency to fall off a square bridge. Except for the impaired grasping reflex of the contralateral hindpaw, there was spontaneous complete recovery of function by the third test session, 37 days after surgery. Some of the other tests might not have been sensitive enough to detect the effects of the unilateral MCA-occlusion (MCA-O) on behavior. Moreover, the WKY rats were very inactive in some of the tests, so that reliable scoring of the effects was not always possible. A rat strain other than the WKY strain might be more suitable to study the behavioral consequences of MCA-O.

Animals↗