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PubMed1990

Fatal or severely disabling cerebral infarction during hospitalization for stroke or transient ischemic attack.

Six (1%) of 578 patients admitted for cerebral infarction or transient ischemic attack (TIA) suffered a fatal or severely disabling in-hospital cerebral infarction following a period of stabilization or improvement lasting more than 1 day. These infarctions were characterized by the sudden onset of stupor or coma and subsequent development of transtentorial herniation due to carotid or middle cerebral artery territory infarction, or widespread brain-stem infarction due to basilar occlusion. Only one patient survived. Four patients had large-vessel disease documented by Doppler, angiography, or at autopsy. Each of these six infarcts occurred during the morning hours, 4-9 days after the initial event, 3-8 days after initiation of intravenous heparin, and within 4-8 h after intravenous heparin had been discontinued. No coagulation abnormalities were documented. We believe that these cases indicate that among patients admitted for cerebral infarction or TIA, fatal or severely disabling in-hospital cerebral infarction after a period of stabilization or improvement may occur in patients having an initially mild to moderate clinical deficit, that those suffering large artery disease may be at greater risk, and that there may be a relationship between heparin withdrawal and cerebral infarction in some patients.

Cerebral Infarction↗

PubMed2005

[A new rat model of cerebral infarction based on the injury of vascular endothelial cell].

OBJECTIVE: A new rat model of cerebral infarction was developed to elucidate the contribution of vascular endothelial cell during focal cerebral infarction formation. METHODS: Forty-eight Sprague-Dawley (SD) rats were randomly divided into the model group, sham operation group, and control group for indexes observation of triphenyltetrazolium chloride (TTC) dyeing, neurological deficit, plasma tissue-type plasminogen activator (tPA) activity, plasminogen activator inhibitor (PAI) activity, thromboxane B(2) (TXB(2)) content, and 6-keto-prostaglandin (6-keto-PGF(1alpha)) content. RESULTS: (1) The highest neurological score appeared at 6 h after operation, descending significantly at sequential time. (2) Using TTC dyeing and optical microscope technique, pathological changes in brains were observed. (3) Compared with control group and sham operation groups, there was a decrease in tPA activity of model rats at the initial 12 h after injection of sodium laurate (P < 0.05), PAI activity decreased markedly in the model group at 24 h after injection of sodium laurate. (4) In plasma TXB(2) concentration reached the highest level compared at 6 h after injection of sodium laurate, but there were not obvious differences in plasma 6-keto-PGF(1alpha) concentration among all groups (P > 0.05). CONCLUSION: Focal cerebral infarction in rats could be induced by some sodium laurate, showing ischemic cerebrum necrosis, function disorder of vascular endothelium-platelet, fibrinolysis abnormality. This model could play an important role in researching the contribution of vascular endothelial cell during cerebral infarction development, preventing and curing by traditional Chinese medicine.

Animals↗

PubMed1996

[Progressive stroke during the acute state of cerebral infarction in the territory of the internal carotid artery].

Diagnosis of deterioration of neurological deficits in the early stage after hospital admission immediately after the onset of cerebral infarction is important in establishing a treatment plan. This study investigated the clinical characteristics of progressive stroke on admission. The subjects were 309 patients admitted on the day of the onset of symptoms and showed a low density area on CT images within 5 days. There were 202 with cerebral infarction in the territory of the deep perforate arteries, 77 with cerebral infarction in the territory of the cortical branch of the middle cerebral artery (MCA), and the remaining 36 had cerebral infarction in the territory of MCA. The results were as follows: 1) Progressive stroke was observed in 71 patients (23.0%): 60 with completed stroke and 11 with reversible ischemic neurological deficits (RIND). 2) The patients with progressive stroke were clearly older than those with non progressive stroke (p < 0.05: Cochran Cox's test). 3) Progressive stroke was seen more frequently in patients with cerebral infarction of the cortical branch of the MCA and patients with occlusion of the internal carotid artery and MCA trunk than patients with cerebral infarction of the deep perforate arteries (p < 0.001: chi 2 test). 4) All patients with progressive stroke had initial evidence of deterioration of neurological deficits within 5 days after the onset, with 39 patients showing deterioration on day 2 and 13 patients showing deterioration on day 3. 5) Deterioration of neurological deficits usually stopped the day after the start of progression. The maximum period from the beginning to the end of the deterioration of neurological deficits was 7 days. 6) Progressive stroke was not seen in 11 patients who were admitted with higher cortical dysfunction and without sensory or motor disturbances, and was seen in only 8 (4%) of the 187 patients with sensory or motor disturbances without higher cortical dysfunction. 7) Progressive stroke was seen in 63 (57%) patients with sensory or motor disturbances and higher cortical dysfunction. 8) Progressive stroke was seen frequently in patients with atrial fibrillation (Af) on the ECG [P < 0.001). 9) Fifty-six of 71 patients with progressive stroke showed persistent severe motor impairment in the upper limbs. Therefore, to diagnose progressive stroke, it is useful to assess the higher cortical dysfunction and examine for Af on admission.

Aged↗

PubMed1987

Demonstration of focal hyperemia in acute cerebral infarction with iodine-123 iodoamphetamine.

Focal hyperemia is known to occur in regions of acute cerebral infarction. Presented here are two cases in which SPECT images with 125I-labeled iodoamphetamine demonstrated focal areas of increased tracer concentration associated with cerebral infarction. These results may have important implications regarding the physiology of iodoamphetamine in cerebral infarction and, in particular, whether the distribution of this tracer is related to regional blood flow in this setting. In addition, interpretation of iodoamphetamine images in cerebral infarction should include consideration of this finding.

Aged↗

PubMed1999

[Five elderly patients with cerebral infarction seen during a heat wave].

Five elderly patients (> or = 65 y) with cerebral infarction induced by dehydration during a heat wave were described to clarify the relationship between dehydration and stroke in the aged. When the daily maximum temperature exceeded 30 degrees C every day for two weeks, 6 patients with acute stroke came to our hospital. Five of them were patients with cerebral infarction aged 73-89 (the elderly group) and one was a 52-year-old woman with putaminal hemorrhage. As control groups, patients with ischemic stroke during the period 4 weeks before and after, but excluding the heat wave period, which consisted of an elderly control group (n = 7) and a young control group (n = 5), were also studied retrospectively with regard to clinical findings and neuroimaging. The incidence of cerebral infarction in the elderly group was higher in the heat wave period among all three groups. Atherothrombotic, lacunar, and cardioembolic infarctions were seen in 1, 2 and 2 cases, respectively. The onset in the elderly group was characteristic as all occurred before noon and were related to exercise. Physical examination at arrival revealed decreased skin turgor and dry tongue. A high BUN/creatinine ratio (> or = 25) and elevated fibrinogen (> 400 mg/dl) was frequently noted, although high hematocrit (> or = 45) was not seen. According to clinical findings, dehydration was diagnosed and they were infused with fluid, resulting in the improvement of skin turgor and tongue moisture. These findings indicated that dehydration due to excess perspiration due to the heat wave induced cerebral infarction in the elderly. It suggests that water intake on awakening in summer is important to prevent dehydration and ischemic stroke because elderly people are especially susceptible to those conditions in the morning.

Aged↗

PubMed1987

[Changes in organic acids in plasma and cerebrospinal fluid in cerebral infarct].

Seventeen patients with recent cerebral infarction were included in the study. The general condition of the patients was evaluated within 3 days after the incidence (rating 1) and 7-9 days after the incidence (rating 2) using a clinical rating scale for internal, psychiatric and neurological findings. The statistical evaluation showed a clinical improvement of the score of 32%. The extent of the brain lesions was determined by cranial computed tomography. Routine analysis of the cerebrospinal fluid included determination of protein, cell count, cell type, glucose, lactic acid, and hemoglobin. In addition, spinal fluid and serum concentration of pyruvic acid, citric acid, fumaric acid, alpha-ketoglutaric acid and alpha-keto-beta-methylvaleric acid (3-MKV) were determined at the two rating times. CSF and serum values of fumaric acid, 3-MKV and pyruvic acid correlated at rating 1, while at rating 2 a correlation existed only for fumaric acid. A trend analysis infarction - postinfarction period showed the concentration of all metabolites to decrease significantly. This is interpreted as a reconstitution of the initially disturbed blood brain barrier function.

Aged↗

PubMedDate not supplied

"Fogging effect" in MR of cerebral infarct.

In a case of cerebral infarction the lesions were isointense to slightly hyperintense in the T2-weighted MR images obtained approximately 2 weeks after the onset. Earlier (1 week after onset), they had been markedly hyperintense. The probably mechanisms behind this phenomenon, referred to as "MR fogging" are discussed.

Aged↗

PubMed1984

Protective effect of FR35447 on experimental cerebral infarction.

The protective effect of 2-(5-chloro-2-phenoxyanilino)-2-imidazoline [FR35447] on cerebral infarction was examined in animal models. FR35447 in p.o. doses of 1 mg/kg or more caused a marked reduction of arachidonate-induced cerebral infarction in rats. Since FR35447 (10(-6) M) inhibited platelet aggregation induced by adrenaline plus the divalent cation ionophore A23187, as did yohimbine (10(-6) M), the protective effect of FR35447 is presumed to be due to its blocking activity on the alpha 2 adrenoceptors of platelets. However, additional mechanisms appear to participate in the protective effect of FR35447 on cerebral infarction. A ten-day treatment with FR35447 in p.o. doses of 1 to 10 mg/kg/day decreased serum lipid peroxide levels in vitamin E deficient rats, suggesting that FR35447 may have free radical scavenging activity. Moreover, FR35447 (greater than or equal to 10(-5) M) increased red cell deformability. These effects of FR35447 suggest that it may be useful in preventing or treating cerebral infarction.

Animals↗

PubMed1991

[Effect of lisuride on experimental cerebral infarction in rats].

Lisuride is an ergot derivative with central dopaminergic (D2 agonistic) and serotonergic (5-HT1A agonistic) activity. The effect of lisuride on experimental cerebral infarction in rats was investigated. Cerebral infarction was induced by intracarotid infusion of a 50-microliters mixture in which deformed and rigid red blood cells treated with hypertonic solution were contained. Lisuride or 0.9% NaCl was administered subcutaneously 30 min before induction of cerebral infarction. Lisuride (0.01 mg/kg) not only prolonged the survival time of the animals but also suppressed cerebral edema, increase in the electrolytes content and histological damage in the brain. These results suggest that lisuride has a protective effect against cerebral infarction.

Animals↗

PubMed1989

[Specific cell-mediated cytotoxicity in patients with cerebral infarct].

The purpose of the work was to assess changes in the activity of cytotoxic lymphocates in patients with cerebral infarction. The material comprised 27 patients with the diagnosis of cerebral infarction and 18 controls. The authors analyzed the activity of cytotoxic lymphocytes, against the cerebral antigen-encephalitogenic peptide (EP). As target cells they used syngenic lymphocytes coated with EP and labelled with 51Cr, the activity of which released during reaction with supernatan is proportional to the amount of cells disrupted by cytotoxic lymphocytes. The reaction is specific for the encephalitogenic peptide. The activity of specific cytotoxic lymphocytes was in patients with cerebral infarction almost four times higher than in controls. The percentage activity was higher in "seriously affected patients" and two weeks after the onset of the disease. Then the activity declined. Investigation of the activity of cytotoxic lymphocytes could prove important in patients with cerebral infarction with symptoms of sensitization against cerebral antigen.

Adult↗

PubMed1994

[Increased plasma endothelin-1 concentration in acute cerebral infarction and its clinical significance].

In acute cerebral ischemia there are severe damages of endothelium recognized as the stimuli for secretion of endothelin-1, that is a endothelium-derived peptide and seems to be the most potent vasoconstrictor known. The goal of this study is to measure plasma endothelin-1 level in patients with cerebral infarction and determine the relationship between endothelin-1 and ischemic stroke. Plasma level of endothelin-1 was measured in 21 consecutive patients. The measurement was performed 3 times at different stages of stroke. There was a marked increase in plasma endothelin-1 level in the patients and the elevation lasted the entire acute and subacute stage of stroke. There was a correlation between the peptide concentration and infarct volume (r = 0.665, P < 0.01). The result suggests that endothelin-1 plays an important role in the regulation of brain circulation. Apparent and lasting increase in plasma level of endothelin-1 is associated with cerebral ischemia and infarction. The peptide seems to be involved in the pathophysiology of acute cerebral ischemia and have a deleterious effect in the evolution of cerebral infarction.

Acute Disease↗

PubMed1978

Sequential changes of regional circulation in cerebral infarction.

Sequential changes of regional cerebral circulation and effects of spontaneous recanalization of occluded artery on cerebral circulation were observed in 50 patients with cerebral infarction. 1) Luxury perfusion was predominantly recognized in the recanalized patients within 16 days after onset. 2) Impairment of vasomotor responses was almost the same in the recanalized patients and the occluded patients. 3) CO2 response tended to recover about 3-4 weeks after onset, but disautoregulation to induced hypertension persisted up to 2 months after onset. Some clinical problems are discussed.

Adult↗

PubMed2006

Paeonol reduced cerebral infarction involving the superoxide anion and microglia activation in ischemia-reperfusion injured rats.

Both Moutan cortex of Paeonia suffruticosa Andrews (MC) and the root of Paeonia lactiflora Pall (PL) are important Traditional Chinese herbs used commonly to treat inflammatory and pyretic disorders. Paeonol, a common component of MC causes anti-platelet aggregation and scavenges free radicals. Therefore, the aim of the present study is to investigate the effects of Paeonol on cerebral infarct. A total of 60 male Sprague-Dawley (SD) rats were studied. An animal model of cerebral infarct was established by occluding both common carotid arteries and the right middle cerebral artery for 90 min, followed by a 24 h period of reperfusion. The percentage of cerebral infarction area to total brain area in each piece of brain tissue, and neuro-deficit score were measured. Superoxide anion was determined by the number of lucigenin-chemiluminescence (CL) counts. ED1 (mouse anti rat CD68) and interleukin-1beta (IL-1beta) immunostaining in the cerebral infarction region were also investigated for activation of microglia. The results indicated that Paeonol 15 and 20 mg/kg pretreatment and 20 mg posttreatment reduced the cerebral infarction area; Paeonol 15 and 20 mg/kg pretreatment reduced the neuro-deficit score. In addition, Paeonol 20 mg/kg pretreatment reduced the lucigenin-CL counts at 2 h period of reperfusion. The number of ED1 and IL-1beta immunoreactive cells also reduced in the cerebral infarction region; there were no significant changes in blood sugar levels. The results show that Paeonol reduced cerebral infarct and neuro-deficit in rat, suggesting Paeonol might play a similar role in reducing cerebral infarction in humans. Paeonol suppresses and scavenges superoxide anion, and inhibit microglia activation and IL-1beta in ischemia-reperfusion injured rats.

Acetophenones↗

PubMed1985

[Relation between long loop reflex findings and the topography of cerebral infarcts].

27 patients with demarcated cerebral infarctions were examined in the computed tomograms. The long loop-reflexes were elicited by electrical stimulation of the median nerves. The localization of substance defects was clearly related to the loss of the late M2-potentials. This result points out a transcortical reflex loop through medial lemniscus, ventral posterolateral nucleus of the thalamus, dorsal limb of the internal capsule, corona radiata and somatosensory cortex.

Adolescent↗

PubMed1999

Echocardiography in patients with cerebral infarction.

Fifty consecutive patients of cerebral infarction underwent a detailed evaluation for the presence of cardiac disease, by means of a standard questionnaire, clinical examination, a 12 lead electrocardiogram, and a 2-D echo and colour Doppler examination. Only 9 patients had a normal echocardiogram, while as many as 27 (54%) demonstrated potential cardio-embolic abnormalities. Clinical and ECG evidence of pre-existent cardiac disease had been demonstrable in only 13 (26%) patients.

Adult↗

PubMedDate not supplied

[Hyperhomocysteinemia in acute cerebral infarction].

ANTECEDENTS: Hyperhomocysteinemia has recently been recognized as contributing directly or associatively to the arteriosclerotic process in cerebral infarction. OBJECTIVE: To determine plasmatic homocysteine levels in with patients with acute cerebral infarction and to seek an association between clinical sub-types of cerebral lesion and homocysteine levels and risk factors present. MATERIALS AND METHODS: A descriptive study was carried out on patients diagnosed with acute cerebral infarction. The study included 22 patients of both sexes between the ages of 40 and 85 years. Samples were collected on the second day of hospitalization after 12 h of fasting. RESULTS: In 13 of 22 patients, elevated levels of serum homocysteine were found. The homocysteine average was 20-68 mumol/l +/- 9.6 SD. No association between degree of cerebral lesion and risk factors was found (p > 0.05). CONCLUSION: An increase in homocysteine was found in 59% of cerebral infarction patients. No correlation between hyperhomocysteinemia and known risk factors such as smoking, alcoholism, high blood pressure, and diabetes was found. It is necessary to continue this line of investigation to identify conditioning factors that elevate homocysteine and to implement measures to lower levels of hyperhomocysteinemia, thus helping reduce the incidence of cerebrovascular disease.

Acute Disease↗

PubMedDate not supplied

[Association between cerebral infarction and malignant glioma].

INTRODUCTION: It is very rare for cerebral infarction to be the first symptom of an intracranial tumour. Only three cases have been reported in which cerebral infarction is thought to have been caused by the arterial compromise triggered by incipient high grade gliomas that are not yet visible in radiological tests. CASE REPORT: A 46-year-old male with no relevant medical history or cardiovascular risk factors who presented with acute hemiplegia on the right-hand side of the body and a significantly impaired level of consciousness. Computerised axial tomography of the brain showed a left frontal malignant ischemic infarct that exerted an important mass effect. The patient was submitted to a left-side frontoparietal decompressive craniectomy. Post-operative progress was good and the patient even recovered his normal level of consciousness, although he was left with right hemiparesis and conduction dysphasia. Seven months after the craniectomy the patient experienced a progressive deterioration with symptoms of endocranial hypertension. Magnetic resonance imaging of the brain revealed the presence of a highly malignant tumour in the previously infarcted territory. A histological study of the excised lesion showed it to be a glioblastoma multiforme. CONCLUSIONS: The proximity in time, as well as the identical location of the two lesions, led us to think that the glioblastoma, although not yet visible in radiological explorations, affected a branch of the middle cerebral artery and gave rise to the infarct. Therefore, in the presence of a cerebral infarct in patients with no risk factors for suffering a brain vascular pathology, it is advisable to carry out a radiological follow-up so as to be able to diagnose a possible lesion due to a tumour.

Cerebral Infarction↗

PubMedDate not supplied

Efficacy of combination antiplatelet therapy and nicardipine for chronic cerebral infarction.

To prevent recurrence of cerebral infarction (CI), the efficacy of antiplatelet therapy, when used in combination with a calcium antagonist, was examined. The study subjects were 57 chronic CI patients (40 men, 17 women; mean age, 68.5 years) who experienced either CI or its recurrence more than 3 months before the start of the study. They were randomly allocated into one of the following four groups for the 8-week study; group A--ticlopidine hydrochloride 200 mg once daily and nicardipine hydrochloride 20 mg three times daily (TID); group B--ticlopidine hydrochloride 200 mg once daily; group C--aspirin 81 mg once daily and nicardipine hydrochloride 20 mg TID; or group D--aspirin 81 mg once daily. Platelet aggregation was measured before treatment and 4 and 8 weeks after the initiation of each therapy by using adenosine diphosphate (ADP) (2 microM and 0.5 microM) and collagen (2 micrograms/mL), and evaluated in terms of percent maximum platelet aggregation. Results showed significant suppression of 2.0 microM ADP platelet aggregation in groups A, B, and C. At 0.5-microM ADP, only groups A and B showed significant platelet aggregation suppression. All groups showed significant suppression of collagen platelet aggregation. In comparing single therapy with combination therapy, groups A and B were not significantly different from one another after 4 or 8 weeks in 2-microM ADP or collagen platelet aggregation suppression. In contrast, group C had significantly greater suppression of both 2-microM ADP and collagen aggregations compared with group D. In conclusion, nicardipine hydrochloride administration with aspirin may be a useful alternative therapy for the prevention of CI recurrence.

Adenosine Diphosphate↗