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PubMed1997

[Hypertension in the acute phase of cerebral infarction; not always to be treated].

Hypertension is observed in three-fourths of the patients in the acute phase of a cerebral infarction. Treatment of an elevated blood pressure in the acute phase of a cerebral infarction is discouraged for the following arguments: In most instances the elevated blood pressure decreases spontaneously in the first few days after the infarction and stabilisation of the blood pressure is usually seen within 4 to 7 days. The elevated blood pressure in the acute phase of the cerebral infarction may be considered a favourable adaptation mechanism aimed at maintaining cerebral perfusion in the region surrounding the infarction. As a consequence lowering of the elevated blood pressure may be harmful because it can lead to expansion of the infarction. No controlled prospective studies to determine if treatment of hypertension in the acute phase of a cerebral infarction might be of benefit have been performed. There are, however, several case reports showing that treatment of an elevated blood pressure in the acute phase of a cerebral infarction is associated with dramatic progression of the neurological deficit. Exceptions can be made for situations where diastolic blood is repeatedly higher than 130-140 mmHg or where there are concomitant cardiovascular diseases, such as myocardial infarction, heart failure or a dissecting aneurysm requiring immediate antihypertensive treatment.

Antihypertensive Agents↗
PubMed1987

[Pharmacodynamic action of cavinton on regional volume blood flow, central hemodynamics and the bioelectric activity of the brain in the acute stage of a cerebral infarct].

Forty-two patients with acute cerebral infarction were studied for the regional volumetric cerebral blood flow (rVCBF) and central hemodynamics (by integral rheography of the body) before and after the intravenous administration of 10 or 20 mg of cavinton (vinpocetine). It was found that in the absence of changes in the central hemodynamics an increase in the cerebral blood flow was the predominant characteristic, but parodoxical reactions were occasionally observed in the acute period of an extensive hemispherical infarct. The findings of quantitative frequency analysis of the EEG conducted in 40 patients correlated with the results of the study of the blood flow and indicated a more favourable prognosis in brain stem infarction or mild cortical infarction. Treatment of extensive cortical infarction was associated with cases of parodoxical deterioration of brain function which should be taken into account in prescribing cavinton to patients during the acute stage of cerebral infarction.

Acute Disease↗
PubMed1995

Silent cerebral infarction in a community-based autopsy series in Japan. The Hisayama Study.

BACKGROUND AND PURPOSE: The purpose of this study was to assess the prevalence and characteristics of silent cerebral infarction in a population-based consecutive autopsy series of residents of Hisayama, Kyushu, Japan. METHODS: Autopsy records, cerebral pathological findings, and clinical charts of 966 Hisayama residents recorded during the 26 years from 1961 to 1987 were examined (autopsy rate, 82.4%). The subjects were divided into three groups: those with both clinically apparent strokes and pathologically verified cerebral infarcts (stroke group), those having pathological evidence of cerebral infarction in the brain but without clinical stroke episodes (silent infarction group), and those with neither infarction nor stroke episode (noninfarction group). Risk factors and brain pathology in the three groups were compared. RESULTS: Silent cerebral infarction was found in 12.9% of the 966 subjects who had undergone autopsy, and its frequency increased with age. The subjects with silent infarcts were older, had higher systolic or diastolic blood pressure, and had atrial fibrillation more frequently than subjects in the noninfarction group. There were no significant differences in the locations of infarcts between the stroke and silent infarction groups, although infarcts tended to be located in the deeper area of the brain in the latter. The number and size of infarcts were smaller in the silent infarction group than in the stroke group. CONCLUSIONS: Diastolic blood pressure and atrial fibrillation appear to be strong predictors of silent cerebral infarction in the Japanese general population. Stroke becomes clinically apparent as infarct volume increases.

Adult↗
PubMed1994

[The importance of 24-hour-blood pressure monitoring in hemodynamic and thromboembolism-induced cerebral infarcts].

Night and day blood pressure profiles of 45 patients with cerebral infarction of hemodynamic or thromboembolic origin were assessed to detect subsequent changes of circadian blood pressure variability. The data were also analysed for a possible relationship between variability of circadian blood pressure, site of cerebral infarction and activation of the autonomic nervous system. Patients with a stroke of hemodynamic origin, when compared to a control group, manifested significantly greater variability of circadian blood pressure (diastolic: -25.2 +/- 4.5% vs. -13.8 +/- 6.5%; p < 0.005). Patients who showed the greatest decrease in vasomotor reactivity (< 40%) developed a prolonged disturbance of the blood-brain barrier. This disturbance regressed slowly only after the pathological 24-hour blood pressure profile had normalized. By way of contrast, patients with cerebral infarctions due to thromboembolic events, when compared to normal individuals, showed a distinctly decreased circadian blood pressure variability (diastolic: -5.2 +/- 6.9%). Initially 40% of these patients presented a pathological increase of nocturnal blood pressure. Circadian blood pressure variability was positively correlated with serum concentration of norepinephrine (r = 0.79; p < 0.01). Patients with a stroke affecting the insular cortex manifested an increase of nocturnal blood pressure significantly more often (66.7% vs. 11.8%; p < 0.005), indicating increased sympathetic activation. They had higher serum levels of norepinephrine (540 +/- 110 pg/ml vs. 290 +/- 178 pg/ml) as compared to patients without damage to the insula and also a significantly higher incidence of prolonged QT intervals and cardiac arrhythmias.(ABSTRACT TRUNCATED AT 250 WORDS)

Aged↗
PubMed1992

Cerebral infarction due to Aspergillus arteritis following glioma surgery.

Cerebral infarction due to fungal arteritis is an uncommon complication of neurosurgical operations and adjuvant immunosuppressive therapy, including long-term steroids. If unrecognized, the neurological deterioration which ensues may be mistreated by increasing the dose of steroids. A case of a 38-year-old Caucasian male who had no obvious immune deficiency or fungal infection prior to a craniotomy for cerebral tumour is described in whom perioperative aspergillus infection resulted in cerebral arteritis and extensive cerebral infarction with a fatal outcome. Long-term steroid therapy used in the management of cerebral tumours may carry an increased risk of systemic or cerebral fungal infection. The possibility of cerebral mycosis (arteritis) and dangers of its non-recognition are highlighted.

Adult↗
PubMed1995

[A case of malignant rheumatoid arthritis with lupus anticoagulant and cerebral infarction].

We reported a case of malignant rheumatoid arthritis (MRA) with cerebral infarction associated with a possible cause of lupus anticoagulant. The patient was a 68-year-old woman who had received treatment for rheumatoid arthritis (RA) from 15 to 16 years ago. She consulted to our hospital with a major complaint of right hemiplegia. Brain CT revealed a low density area in the left hemisphere. She was diagnosed as cerebral infarction and hospitalized. Since she was noted to have hypocomplementemia, interstitial pneumonia and pericarditis, she was diagnosed as MRA. Coagulation test disclosed positive lupus anticoagulant (LA). Generally, CNS disorders in MRA are uncommon. Cerebral infarction was complicated in the present case, suggesting the involvement of antiphospholipid antibodies as its pathogenesis.

Aged↗
PubMed1976

[A trial of surgical management of brain edema in cerebral infarction--a review with our own experiences in 31 cases (author's transl)].

We have analyzed the clinical course of 31 cases with cerebral infarction for 4 years. Of the 31 patients, 6 cases (19%) showed the brain edema on the cerebral angiograms as manifested by the shift of the midline arteries. The patients were divided into two groups, normotensive (15 cases) and hypertensive cerebral infarction (16 cases). The clinical and angiographic findings in the normotensive groups have been differed significantly from those of the hypertensive groups. The findings of brain edema on the angiograms were prominent in the hypertensive groups, and the clinical course was generally good and fair in the normotensive groups. We have reviewed the literatures about brain edema associated with cerebral infarction and have discussed on the mechanisms. From the study of our cases, it was concluded that systemic hypertension could be a facilitatory factor in the occurrence of brain edema in cerebral infarction. Furthermore, the management of massive cerebral infarction should be reduction of increased intracranial pressure and prevention of cerebral herniation. So, it will be necessary to perform a surgical treatment such as internal decompression; removal of the infarcted, necrotized area and excision of herniated tissue, and external decompression; removal of boneflap.

Acute Disease↗
PubMed2003

[Detection of acute cerebral infarction by dual echo subtraction technique in MR imaging].

The purpose of this study was to develop an image enhancement technique to detect acute cerebral infarct regions in brain MR images. Transverse relaxation times for abnormal changes tend to be longer than those for normal tissues. In order to obtain MR images with two different echo times, we employed the fast spin echo sequence. We then employed the image subtraction technique using two T(2)-weighted images to enhance acute cerebral infarct regions. As a result, the areas of acute cerebral infarct regions were enhanced as regions of higher signal than normal regions of brain tissue. Further, high signal areas in dual echo subtraction images corresponded to cerebral infarct regions of high signal areas in diffusion weighted images (DWI). We found that the image subtraction technique is useful to enhance very subtle regions of acute cerebral infarction in MR images. Because we employ the difference between transverse relaxation times for normal and abnormal tissues, which does not depend on the strength of the magnetic field, the dual echo subtraction method can be used in many hospitals.

Aged↗
PubMed2004

Cerebral infarct in children aged zero to fifteen years.

Cerebral infarcts in children present peculiar characteristics either due to their diversity of causes or due to the unknown nature of the causes. The etiologies of cerebral infarct were reviewed in children from zero to 15 years old, attended at a tertiary hospital, in Ribeirão Preto (Brazil), from 1990 to 1997, adopting the modified Trial of ORG 10172 in Acute Stroke Treatment (TOAST) criteria of classification; 1-Atherosclerosis in large arteries; 2-Cardioembolic; 3-Occlusion of small vessels; 4-Other etiologies; 5-Undetermined cause. Thirty-nine children were included, 18 males and 21 females, aged 2 months to 15 years, mean age 5.67. The largest group, N=22 (56.4%), included children with "other etiologies", 7 of them aged under two years. The most common etiology was dehydration and septic shock leading to brain hypoperfusion and watershed infarcts. Nine (23%) children had "Undetermined etiology", 7 (17.9%) cardioembolic subtype and none had atherosclerosis. Laboratory improvement is needed for the large number of patients without a defined cause, and the high proportion of children with dehydration in the group with a determined cause emphasizes the need for preventive health actions among infants and children.

Age Distribution↗
PubMedDate not supplied

Paradoxical hyperfixation of hexamethylpropyleneamine oxime in cerebral infarction.

We describe four patients with cerebral infarction and 99mTc-hexamethylpropyleneamine oxime (HMPAO) hyperfixation in distributions corresponding to the infarctions seen at CT and/or MR imaging. Increased HMPAO extraction due to hyperpermeability across the blood-brain barrier and increased retention due to reduced back diffusion of the tracer probably accounted for the increased fractional fixation in infarcts seen in our patients.

Aged↗
PubMed1989

Effect of oral nimodipine on cerebral infarction and outcome after subarachnoid haemorrhage: British aneurysm nimodipine trial.

OBJECTIVE: To determine the efficacy of oral nimodipine in reducing cerebral infarction and poor outcomes (death and severe disability) after subarachnoid haemorrhage. DESIGN: Double blind, placebo controlled, randomised trial with three months of follow up and intention to treat analysis. To have an 80% chance with a significance level of 0.05 of detecting a 50% reduction in an incidence of cerebral infarction of 15% a minimum of 540 patients was required. SETTING: Four regional neurosurgical units in the United Kingdom. PATIENTS: In all 554 patients were recruited between June 1985 and September 1987 out of a population of 1115 patients admitted with subarachnoid haemorrhage proved by the results of lumbar puncture or computed tomography, or both. The main exclusion criterion was admission to the neurosurgical units more than 96 hours after subarachnoid haemorrhage. There were four breaks of code and no exclusions after entry. One patient was withdrawn and in 130 treatment was discontinued early. All patients were followed up for three months and were included in the analysis, except the patient who had been withdrawn. INTERVENTIONS: Placebo or nimodipine 60 mg was given orally every four hours for 21 days to 276 and 278 patients, respectively. Treatment was started within 96 hours after subarachnoid haemorrhage. END POINTS: Incidence of cerebral infarction and ischaemic neurological deficits and outcome three months after entry. MEASUREMENTS: Demographic and clinical data, including age, sex, history of hypertension and subarachnoid haemorrhage, severity of haemorrhage according to an adaptation of the Glasgow coma scale, number and site of aneurysms on angiography, and initial findings on computed tomography were measured at entry. Deterioration, defined as development of a focal sign or fall of more than one point on the Glasgow coma scale for more than six hours, was investigated by using clinical criteria and by computed tomography, by lumbar puncture, or at necropsy when appropriate. All episodes of deterioration and all patients with a three month outcome other than a good recovery were assessed by a review committee. MAIN RESULTS: Demographic and clinical data at entry were similar in the two groups. In patients given nimodipine the incidence of cerebral infarction was 22% (61/278) compared with 33% (92/276) in those given placebo, a significant reduction of 34% (95% confidence interval 13 to 50%). Poor outcomes were also significantly reduced by 40% (95% confidence interval 20 to 55%) with nimodipine (20% (55/278) in patients given nimodipine v 33% (91/278) in those given placebo). CONCLUSIONS: Oral nimodipine 60 mg four hourly is well tolerated and reduces cerebral infarction snd improves outcome after subarachnoid haemorrhage.

Administration, Oral↗
PubMed1993

Blood lipids, the risk factor of cerebral infarction.

A hospital-based case-control study was undertaken at Prasat Neurological Hospital and Institute, Bangkok, in 1990 to determine the association between blood lipid variables (i.e., total cholesterol and triglycerides) and cerebral infarction. To alleviate the unwanted effects of sample selection a number of inclusion and exclusion criteria were also made. A total of 193 newly diagnosed cerebral infarction patients together with an equal number of age-sex-matched controls, male and female 45 to 84 years of age, were studied. The association was assessed by logistic regression analysis. Other potential risk factors for cerebral infarction were entered in the logistic models as covariates to be adjusted. The results showed that, total cholesterol and triglycerides were statistically significant related to cerebral infarction (p < 0.0001) in univariated analysis. After adjusting for the covariates through multivariate logistic regression analyses, total cholesterol remained significantly related to cerebral infarction (p = 0.0430) but triglycerides was not significant (p = 0.3953). Other factors, namely, hypertension, cardiac impairment, diabetes mellitus and hemoglobin concentration were strongly related to cerebral infarction in both the univariate and multivariate analyses. The interaction between blood lipids variables and potential risk factors was also assessed. The finding showed significant multiplicative interaction between triglyceride levels and diabetes mellitus status (p = 0.0026). Other interaction terms did not approach statistical significance.

Aged↗
PubMed2000

Cerebral infarction in adult AIDS patients: observations from the Edinburgh HIV Autopsy Cohort.

BACKGROUND AND PURPOSE: Autopsy series of patients with AIDS have found a 4% to 29% prevalence of cerebral infarction. Little is known of the prevalence of cerebral infarction when not associated with non-HIV central nervous system (CNS) infection, lymphoma, or cardioembolic sources. Clinical correlation has seldom been available. We describe the pathological and clinical features of patients from the Edinburgh HIV Cohort Study found to have had cerebral infarcts without evidence of non-HIV CNS infection, CNS lymphoma, or cardioembolic sources at autopsy. METHODS: From 183 autopsy cases, 26 without evidence of opportunistic cerebral infection or lymphoma were selected. These 26 cases went through a second selection process in which the presence of cerebral infarction, in the absence of the conditions mentioned, was verified. Histology and clinical records for the remaining patients were reviewed. RESULTS: Ten (5.5%) cases fulfilled the inclusion criteria and demonstrated similar hypoxic-ischemic lesions. Small-vessel thickening was seen in all cases, and perivascular space dilatation, rarefaction, and pigment deposition, with vessel wall mineralization and perivascular inflammatory cell infiltrates, were seen in some cases. Vasculitis was not found. One patient had had a transient ischemic attack, and no patient had had a stroke. CONCLUSIONS: Cerebral infarcts in HIV-infected patients are not common in the absence of cerebral non-HIV infection, lymphoma, or embolic sources. We found an HIV-associated vasculopathy with similar features in all risk groups. In AIDS patients presenting with stroke or transient ischemic attack, potentially treatable causes, such as cerebral coinfection or tumor, should be sought.

Acquired Immunodeficiency Syndrome↗
PubMed1986

High dose steroid treatment in cerebral infarction.

Steroid treatment is widely used in acute cerebral infarction yet its value is controversial. High dose dexamethasone (480 mg over 12 days) was given in a double blind, randomised controlled trial to 113 consecutive eligible patients with acute cerebral infarction admitted to an acute stroke unit. Those with stroke for more than 48 hours, known embolic sources, diabetes, and infection were excluded. Death and quality of survival were recorded over 21 days. The active drug group (54 patients) matched the placebo group (59 patients) for age, initial stroke score, delay in beginning treatment, and other relevant variables. The two groups did not differ significantly in death rate or quality of survivorship. The small difference in mortality between the two groups may have represented a marginal therapeutic effect, which might reach significance in a larger sample. The widespread use of steroids in response to such a marginal therapeutic gain would expose large numbers of patients with stroke to more serious hazards of steroid treatment and convert patients who would otherwise have died into neurovegetative survivors. High dose steroid treatment was ineffective in ischaemic stroke, and the data suggest that further evaluation by a larger multicentre trial is not justified.

Aged↗
PubMed2005

Reassessment of defibrase in treatment of acute cerebral infarction: a multicenter, randomized, double-blind, placebo-controlled trial.

OBJECTIVE: To evaluate the efficacy and safety of defibrase in patients with acute cerebral infarction by a large sample, multicenter, randomized, double-blind, placebo-controlled clinical trial. METHODS: Patients with acute cerebral infarction within 12 hours of stroke onset were randomly assigned to receive either an initial intravenous infusion of defibrase 15 U plus normal saline 250 mL or 250 mL of normal saline only. Subsequent infusions of defibrase 5 U or placebo (normal saline) were given on the 3rd, 5th, 7th, and 9th day, respectively. Both groups received standard care of acute cerebral infarction. The primary efficacy outcome was functional status (Barthel Index) at 3 months after treatment. Safety outcome were bleeding events and mortality rate. Secondary outcome included Chinese Stroke Scale (CSS) score at 14 days and recurrence rate of stroke at 1 year. RESULTS: A total of 1053 patients were enrolled at 46 centers from September 2001 to July 2003, and 527 patients were randomly assigned to receive defibrase and 526 to receive placebo. A similar proportion of patients in both groups completed a full course of treatment. There was a significantly greater proportion of favorable functional status (Barthel Index > or = 95) in defibrase group than in placebo group at 3 months (52.2% vs. 42.8%, P < 0.01), and the proportion of dependent functional status (Barthel Index < or = 60) was a little lower in defibrase group compared with placebo group (27.7% vs. 32.4%). These differences were more obvious among patients who were treated within 6 hours of stroke onset. Patients in defibrase group had better improvement with respect to CSS score than those in placebo group at 14 days (P < 0.05). Recurrence rate of stroke at 1 year was lower in the defibrase group compared with placebo group (6.2% vs. 10.1%, P = 0.053). Patients in defibrase group had higher risk of extracranial bleeding events (4.7% vs. 1.5%, P < 0.01) and a tendency of higher risk of symptomatic intracranial hemorrhage. The hemorrhage incidence was higher in patients with fibrinogen level < 130 mg/dL than > or = 130 mg/dL (10.6% vs. 3.8%, P < 0.05). Mortality rate at 3 months were slightly higher in defibrase group than placebo group (5.9% vs. 4.2%). CONCLUSIONS: The defibrase is effective to improve neurological function and function of daily living for patients with acute cerebral infarction within 12 hours of symptom onset. The efficacy was even better for acute cerebral infarction within 6 hours of onset. The increased risks of intra- and extracranial hemorrhage during defibrase administration were related to the plasma fibrinogen level.

Adult↗
PubMed2005

[The relationship between the five beta-fibrinogen gene polymorphisms and cerebral infarction].

OBJECTIVE: To investigate the relationship among beta-fibrinogen (Fg) concentration, related gene polymorphisms (including -148C/T, -249C/T, -455G/A, 448G/A, 1689T/G) and cerebral infarction. METHODS: Fg level and its five gene polymorphisms were analyzed with by polymerase chain reaction-restriction fragment length polymorphism in 132 patients with cerebral infarction, 79 patients with other neurological diseases and 92 healthy elders. RESULTS: The plasma Fg level in cerebral infarction patients was significantly higher than that in the patients with other neurological diseases or healthy elders (P < 0.05). In the three groups, the plasma Fg levels in individuals with T-148 and A-455 alleles were higher than those in individuals without T-148 and A-455 alleles (P < 0.05). However, there were no statistically significant differences in the genotype and allele frequencies in the five mutation gene polymorphisms among the three groups (P > 0.05). CONCLUSIONS: Cerebral infarction is a multifactorial disease and an increased Fg level is a risk factor for cerebral infarction. T-148 and A-455 allele can lead to elevated Fg concentration.

Aged↗
PubMed2004

[Effect of Baisuifang Granule on cognitive malfunction after cerebral infarction].

OBJECTIVE: To explore the mechanism of Baisuifang Granule in treating cognitive malfunction after cerebral infarction. METHODS: One hundred and sixty patients with cerebral infarction were divided randomly into two groups. Eighty patients were treated with Baisuifang Granule and 80 with nimodipine for two months. Clinical observation and laboratory examinations were performed for Mini-Mental State Examination (MMSE), clinical symptoms, Chinese Stroke Scale (CSS), hemorrheological indexes and fibrinogen before and after the treatment. RESULTS: Baisuifang Granule could improve MMSE, reduce the scores of clinical symptoms and CSS, and meliorate the blood rheology. The total effective rate for clinical symptoms in the Baisuifang treated group accounted to 76.25%, with statistical difference comparing to 58.75% of nimodipine treated group (P<0.05). There was significant difference in symptom integral, CSS and whole blood viscosity at the high shear rate, respectively (P<0.01). CONCLUSION: Baisuifang Granule is an effective Chinese medicine for treating cognitive malfunction after cerebral infarction.

Aged↗
PubMed1988

Verbal memory and learning in unilateral posterior cerebral infarction. A report on 30 cases.

Unilateral posterior cerebral infarction, sparing memory-related structures in the diencephalon, may represent a means of investigating the role of hippocampal afferents and the parahippocampal areas in memory processing. Among 30 patients with unilateral posterior cerebral infarction a group of 12 subjects with left-sided lesions suffered from marked verbal memory and learning dysfunction, whereas the remaining subjects with left or right-sided lesions showed no obvious memory deficit. The impairment was most prominent for verbal learning tasks, while recall of isolated and complex verbal information appeared to be less affected. In some cases the memory disturbance could be detected up to one year after the causative event. Analysis by CT scanning revealed a coincidence of mnestic disturbances with lesions around the left collateral sulcus affecting the posterior parahippocampal gyrus and the collateral isthmus. The latter term refers to the fibre stem of the medial temporal lobe limited by the floor of the lateral ventricle and the depth of the collateral sulcus. Through this bottle-neck, bidirectional fibres run between the posterior parahippocampal gyrus and different sensory-specific and multimodal association areas. A lesion within the collateral isthmus or, more particularly, a combined lesion of the collateral isthmus and the posterior parahippocampal gyrus, deprives the hippocampus itself of its main afferent projection source and, on the other hand, prevents dissemination of the hippocampal output to widespread neocortical areas. It cannot be excluded, at least in some cases, that small lesions in the fimbria-fornix route, in the retrosplenial cortex or in the hippocampal formation itself also contribute to the memory and learning dysfunction. However, these small lesions, so far as they could be detected by CT scanning, were present in patients with and without memory disturbances.

Adult↗