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PubMed1992

Silent cerebral infarction as a form of hypertensive target organ damage in the brain.

The incidence, number, size, and location of silent cerebral infarction on 0.1 T magnetic resonance imaging was investigated in 66 hypertensive patients (63 +/- 9 years old; mean +/- SD) and 42 age-matched normotensive subjects (61 +/- 9 years old) to determine the clinical significance of hypertension in silent cerebral infarction. Cerebrovascular risk factors and the severity of hypertensive changes in other major target organs were also investigated. The incidence of silent infarction in hypertensive patients (47%) tended to be higher than that of normotensive subjects (33%) and increased significantly with advancing age. In hypertensive patients, a significantly higher incidence of silent lesions was noted in patients with hypertensive changes in major target organs (72-73% in patients with organ involvement versus 33-39% in those without). The average number of lesions in hypertensive patients was significantly higher than that in normotensive subjects (6.0 versus 2.1), and the lesions in the hypertensive patients were more frequently detected in the brain areas supplied by perforating arteries than those in normotensive subjects (47% versus 24%). These results clearly demonstrate that silent cerebral infarction is frequently seen in older hypertensive patients, especially when moderate hypertensive changes are noted in major target organs, and suggest that hypertensive arterial changes play a crucial role in the occurrence of silent infarction.

Aged↗
PubMed2001

Silent cerebral infarcts in basal ganglia are advanced in congenital protein C-deficient heterozygotes with hypertension.

Congenital protein C deficiency is now widely recognized as a genetic risk for venous thrombosis. However, it remains uncertain whether this condition also confers risk for arterial thrombosis. We evaluated the association of congenital protein C deficiency with hypertension and silent cerebrovascular disease using brain magnetic resonance imaging (MRI) (T1- and T2-weighted and proton density images) in a large family pedigree of protein C deficiency diagnosed by gene analysis, compared with 46 non-pedigree related control subjects with normal protein C levels (> or = 75%) who were selected from among 55 asymptomatic hypertensive subjects matched for age and cardiovascular risk factors. Of the 58 living subjects in this pedigree, we measured plasma protein C levels in 45 subjects, and found 2 cerebral infarctions in the 24 heterozygotic subjects, whereas there was no stroke in the 21 normal homozygotic subjects. We performed brain MRI in 14 asymptomatic hypertensive subjects without any cardiovascular disease and in two patients with cerebral infarction, and found 28 cerebral infarcts (two corresponded to the patients' neurologic deficits and 26 were silent). All were lacunar infarcts < 10 cm in size. A total of 25 silent lacunar infarcts were found in nine heterozygotic subjects, whereas only one was found in the seven normal homozygotic subjects (2.8 v 0.14 lacunes per person, P = .002). No advanced white matter hyperintense lesions in T2-weighted images were found in either group. The prevalence of silent lacunar infarcts in the heterozygotic subjects was also significantly higher than that in normal control subjects (1.0 per person, P = .01). Concerning the distribution of silent infarcts, the number of lacunes located in the basal ganglia was higher in the heterozygotic subjects (2.3 per person, P < .001) than in the seven normal homozygotic subjects (0.14 per person) or in the control group (0.28 per person), whereas the number of lacunes in the white matter was not different among the groups. In conclusion, congenital protein C deficiency may accelerate the progression of silent cerebral infarct formation in hypertension, particularly in the basal ganglia, and may be a potential risk for stroke or vascularly induced dementia.

Aged↗
PubMed1987

[Hemodynamic disorders and means of their pharmacological correction in cerebral infarction in patients with ischemic heart disease].

The authors examined peculiarities of the central and cerebral hemodynamics before and after treatment in 108 patients with cerebral infarction and acute or chronic ischemic heart disease (IHD). When myocardial and cerebral infarctions were combined, as well as in most cases of cerebral ischemia in the post-infarction period, the heart worked in conditions of hypodynamia. Disorders of the cerebral circulation were expressed in hypo- and hyperperfusion of the cerebral vessels. Patients with acute versus chronic IHD displayed differences in changes of hemocirculatory parameters in the process of treatment.

Adult↗
PubMed2006

Impact of diffusion-weighted MRI-measured initial cerebral infarction volume on clinical outcome in acute stroke patients with middle cerebral artery occlusion treated by thrombolysis.

INTRODUCTION: Magnetic resonance imaging (MRI) may help identify acute stroke patients with a higher potential benefit from thrombolytic therapy. The aim of our study was to assess the correlation between initial cerebral infarct (CI) volume (quantified on diffusion-weighted MRI) and the resulting clinical outcome in acute stroke patients with middle cerebral artery (MCA) (M(1-2) segment) occlusion detected on MRI angiography treated by intravenous/intraarterial thrombolysis. METHODS: Initial infarct volume (V(DWI-I) ) was retrospectively compared with neurological deficit evaluated using the NIH stroke scale on admission and 24 h later, and with the 90-day clinical outcome assessed using the modified Rankin scale in a series of 25 consecutive CI patients. The relationship between infarct volume and neurological deficit severity was assessed and, following the establishment of the maximum V(DWI-I) still associated with a good clinical outcome, the patients were divided into two groups (V(DWI-I) < or =70 ml and >70 ml). RESULTS: V(DWI-I) ranged from 0.7 to 321 ml. The 24-h clinical outcome improved significantly (P=0.0001) in 87% of patients with a V(DWI-I) < or =70 ml (group 1) and deteriorated significantly (P=0.0018) in all patients with a V(DWI-I) >70 ml (group 2). The 90-day mortality was 0% in group 1 and 71.5% in group 2. The 90-day clinical outcome was significantly better in group 1 than in group 2 (P=0.026). CONCLUSION: Clinical outcome could be predicted from initial infarct volume quantified by MRI-DWI in acute CI patients with MCA occlusion treated by intravenous/intraarterial thrombolysis. Patients with a V(DWI-I) < or =70 ml had a significantly better outcome.

Diffusion Magnetic Resonance Imaging↗
PubMed1991

[Cerebral infarction after coronary artery bypass surgery--its cause, management and prevention].

Among 535 cases of simple CABG, cerebral infarction was complicated in 5 cases (0.9%). Their mean age (65.2 years old) was high, and 80% of them had the history of hypertension or diabetes mellitus or both. The causes of the cerebral infarction were considered to be the embolism of atheromatous debris from the ascending aorta (3 cases), the cerebral hypoperfusion due to cerebral arterial disease and hypotension during cardiopulmonary bypass (1 cases), and the embolism of the left atrial thrombus formed during repeated supraventricular tachyarrhythmias (1 case). Both cases of the multiple infarctions were lost in-hospital 10 months and 21 months postoperatively. Two of the three cases of single infarction suffered from the permanent neurological deficits. To prevent cerebral infarction which might totally deprive of the efficacy of the CABG, it is important to check and properly manage the atheromatous change of the ascending aorta, the cerebral arterial disease, and also postoperative supraventricular tachyarrhythmias.

Adolescent↗
PubMed2006

A multidisciplinary health care team's efforts to improve educational attainment in children with sickle-cell anemia and cerebral infarcts.

The primary objective of this study was to improve the educational success of children with sickle-cell disease (SCD) and cerebral infarcts. A prospective intervention trial was conducted; a multidisciplinary team was created to maximize educational resources for children with SCD and cerebral infarcts. Students were evaluated systematically before and after the intervention. A baseline evaluation was completed assessing the presence of an Individualized Education Plan (IEP), grade retention in school, and days absent from school in the year preceding the intervention. A postintervention assessment occurred 2 years later for these same measurements. At baseline, 74% (17 of 23) of the students were receiving IEPs. Two years later, 87% (20 of 23) students received IEPs (p = .34). Despite the intervention, the rate of children retained in their school grade increased from 0.6 per 100 years in school at baseline to 1.7 per 100 years, 95% CI (-3.86, 1.49). The school absenteeism rate did not significantly change after the intervention; the average days absent per student rose from 15.5 to 22.5, (p = .05). The multidisciplinary team effort alone was insufficient to decrease grade retention and absenteeism rate. Further support, from either the parents or school administration, is needed to increase education attainment of students with cerebral infarcts.

Adolescent↗
PubMed1988

Magnetic resonance imaging in young adults with cerebral infarction due to moyamoya.

The number, size, and location of cerebral infarctions, and blood flow in the middle cerebral artery as seen on proton magnetic resonance imaging were assessed in six white adults with angiographically documented moyamoya. Findings were correlated with clinical presentation, computed tomography, and angiography. Large hemispheric infarctions were found in five hemispheres, predominantly in watershed regions. Subcortical infarctions (n = 56) were found in all hemispheres. They were predominantly located in the centrum semiovale, in the distal beds of supply of the penetrating branches of the anterior and middle cerebral arteries. Infarction of the putamen was found in three hemispheres, caudate nucleus in four, globus pallidus in two, and anterior limb of the internal capsule in two. There were none in the posterior limb of the internal capsule, thalamus, brain stem, or cerebellum. Middle cerebral artery flow was visualized as a signal-void flow sign in only three hemispheres. Cerebral infarctions due to moyamoya are bilateral, multiple, often small, and asymptomatic, affecting predominantly the carotid circulation in watershed regions. Subcortical infarctions in the centrum semiovale and large hemispheric infarctions in hemodynamically compromised areas are the predominant findings.

Adolescent↗
PubMed1980

Correlation between CT findings and subsequent development of cerebral infarction due to vasospasm in subarachnoid haemorrhage.

We have studied the correlations between computed tomograms (CT), clinical severity at the time of onset, and subsequent development of cerebral infarction due to vasospasm in 32 cases with subarachnoid haemorrhage secondary to rupture of cerebral aneurysms. It was found that the clinical severity could be judged by CT as shown by the amount of blood in subarachnoid space. Furthermore, it was possible to predict the subsequent occurrence of cerebral infarction by sequential findings of CT. A Hounsfield number of the high density area over 60 showed good correlation with the development of cerebral infarction.

Adult↗
PubMed1990

[Risk factors in atherothrombotic cerebral infarct. Are there differential risk profiles in extensive cortical infarct and lacunar infarct? A case-control study].

A study of cases and controls was performed to define the factors associated with nonembolic cerebral infarction and to compare the risk profiles of extensive cortical infarction (ECI) to those of lacunar infarction (LI). One hundred and four patients with ECI were matched with 71 patients with LI and with 90 controls. Although the initial analysis disclosed multiple factors associated with cerebral infarction, the analysis with control of the factors revealed that the only factors related with the occurrence of atherothrombotic infarction were: arterial hypertension [odds ratio (OR) = 6.8], diabetes mellitus (OR = 5.6), ischemic cardiac disease (OR = 5.5), increased hematocrit value (OR = 3.0), and atherogenic lipids in patients without arterial hypertension nor diabetes. Diabetes appeared as the only factor specifically associated with LI when compared with ECI (OR = 2.1). This study supports the following conclusions: 1) the risk profile of nonembolic cerebral infarction is concise and intelligible, 2) the possible role of arterial hypertension in the genesis of LI was not confirmed, and 3) diabetic microangiopathy may be implicated in the genesis of most of LI. Conclusions from this retrospective study should be taken as an interpretation of the results since some restriction in the sensitivity of the data analysis was deliberately introduced.

Aged↗
PubMed1999

[Mechanisms of progression of cerebral infarction].

The progression of neurologic symptomatology in the first 48 hours after cerebral infarction appears in more than one third of the patients causing greater morbidity and mortality. Early detection of neurologic deterioration, identification of the predictive factors of worsening and knowledge of the pathogenic mechanisms responsible and their correction make up the basis of the most effective therapy in cerebral infarction. Different hemodynamic alterations (progressive occlusion and growth of the thrombus, insufficiency of colateral circulation, arterial hypotension, etc.) influence, although to different degrees in each patient, in all progressive infarctions. These mechanisms sequentially and progressively condition the necrosis of the areas of ischemic shadow and how new peripheral areas of healthy cerebral tissue are included in the ischemic region, progressively increasing the intensity or the extension of the neurologic manifestations.

Brain↗
PubMed1994

[Cerebral infarction in patients aged 16 to 35 years. Prospective study of 52 cases].

OBJECTIVES: Aetiologies of cerebral ischemic events in young adults are various and often contraversial: atherosclerosis plays a role after age 35 years, cardioembolism is often recognized as the major cause, and numerous new predisposing conditions have been described. To evaluate very premature cerebral infarction, we studied prospectively 52 consecutive patients (34 women and 18 men) aged 16-35 years (mean 28.6 +/- 5.6 years) admitted over a 6-year period for an arterial cerebral infarct identified on CT, on MRI or both. METHODS: All patients were investigated using a standard protocol including cerebral angiography, transthoracic echocardiography, 24-hour Holter ECG monitoring, coagulation inhibitors levels, lupus anticoagulant testing, HIV and syphilitic serologies. Additional investigations were performed in a majority of patients: transesophageal echocardiography in 33, contrast echocardiography in 50, and anticardiolipin antibodies levels in 38. RESULTS: The arterial distribution of infarction did not differ from that of overall stroke patients. Sixteen cases were classified as certain aetiologies, including cardiac diseases with high embolic risk (n = 9), spontaneous arterial dissection (n = 4), moya-moya disease (n = 1), atherosclerosis (n = 1), and inherited antithrombine III deficiency (n = 1). Eighteen cases were classified as possible aetiologies including cardiac diseases with low embolic risk (n = 11) such as mitral valve prolapse or atrial septal aneurysm, miscellaneaous arteriopathies (n = 3) such as arterial dysplasia, antiphospholipid antibodies syndrome (n = 1) and migrainous stroke (n = 3). The 18 last cases were classified as unknown aetiologies, despite all patients but one had at least one vascular risk factor: this group significantly differed from the formers in that the patients were more frequently women using oral contraceptive associated with tobacco consumption, hypercholesterolemia, or both. Two patients died acutely and the survivors were followed 31 +/- 18 months. Three patients experienced recurrent stroke. Functional outcome was assessed using the Rankin scale on admission and 6 to 12 months after the onset of stroke: patients evaluated < or = 2 (no to mild handicap) were 31% on admission and 82% after recovery. Twenty six p. cent remained unable to resume a work. CONCLUSION: Despite extensive evaluation, identification and classification of aetiologies of cerebral infarction in young adults should be cautious because the risk as well as the pathogenesis of many potential causes still need to be defined.

Adolescent↗
PubMed1999

Moyamoya disease presenting as cerebral infarction after cesarean.

BACKGROUND: Moyamoya disease with pregnancy is rare and might present with cerebral hemorrhage. CASE: A 22-year-old primigravida suddenly developed muscular weakness in the right arm and facial discomfort 3 days after cesarean. Computed tomography and cerebrovascular angiography found cerebral infarction attributable to moyamoya disease. Bilateral anastomosis of superficial temporal and middle cerebral arteries was done. CONCLUSION: Moyamoya disease with pregnancy might present as cerebral infarction after cesarean.

Adult↗
PubMed1999

Effects of nifedipine on bladder overactivity in rats with cerebral infarction.

PURPOSE: Our objective was to evaluate the effect of the calcium (Ca2+) channel blocking agent nifedipine on bladder overactivity induced by middle cerebral artery (MCA) occlusion and determine its site of action. MATERIALS AND METHODS: Seven days after implantation of a bladder catheter, a cannula for intracerebroventricular and intrathecal administration was implanted and the left MCA was occluded with 4-0 monofilament nylon thread in male SD rats. Twenty-four hours after the induction of cerebral ischemia, saline was infused into the bladder at a constant rate (200 microL/min.) and cystometrogram was measured in conscious state. Nifedipine was administered intracerebroventricularly (5 microL) or intrathecally (20 microL) at graded doses (0.15 ng.-0.15 microg., 0.15 microg. -1.5 microg., respectively). RESULTS: Bladder capacity in conscious rats was significantly reduced after the left MCA occlusion. Intracerebroventricular administration of nifedipine significantly increased bladder capacity in cerebral infarcted rats but not in sham operated rats. Furthermore there was no significant difference in bladder capacity between before and after intrathecal administration of nifedipine in cerebral infarcted rats. CONCLUSION: These results show that Ca2+ channel blocking agents can operate especially on the supraspinal central nervous system rather than on the spinal system in rats with neurogenic bladder overactivity following cerebral infarction.

Animals↗
PubMed1999

The effects of mannitol on cerebral edema after large hemispheric cerebral infarct.

OBJECTIVE: To evaluate the effect of a single large dose of mannitol on midline tissue shifts after a large cerebral infarction. BACKGROUND: Theoretically, mannitol use in the largest cerebral infarctions may preferentially shrink noninfarcted cerebral tissue, thereby aggravating midline tissue shifts and worsening neurologic status. To test this theory, we studied patients with hemispheric infarctions using continuous and sequential MRI during administration of a single dose of mannitol. METHODS: Patients with neurologic deterioration from complete middle cerebral artery (MCA) infarctions and CT evidence of at least 3 mm of midline shift were studied using T1-weighted three-dimensional multiplanar rapid acquisition gradient echo image data sets acquired at 5- to 10-minute intervals before, during, and after a 1.5 gm/kg bolus infusion of mannitol. Horizontal and vertical displacements were calculated by previously described methods. Glasgow Coma Scale (GCS) and MCA Stroke Scale (MCASS) were measured before and after mannitol administration. Mean changes in tissue shifts were compared using repeated measures analysis of variance. Clinical variables were compared using paired t-tests. RESULTS: Seven patients were enrolled. The final average change in midline shift compared with the initial displacement was 0.0 +/- 1 mm for horizontal (F = 0.06, p = 0.99) and 0.25 +/- 1.3 mm for vertical displacement (F = 0.06, p = 0.99). Whereas average scores for the group did not change, MCASS improved in two, GCS improved in three, and pupillary light reactivity returned in two patients. No patient worsened. CONCLUSIONS: Acute mannitol used in patients with cerebral edema after a large hemispheric infarction does not alter midline tissue shifts or worsen neurologic status.

Adult↗
PubMed2004

[Clinical characteristics of cerebral infarction in China and Japan].

In order to elucidate the clinical characteristics of cerebral infarction in a northeastern district of China, 1,353 patients with first-ever cerebral infarction in Shenyang, China, were compared with 2,929 patients registered in Japan. Using the identical database (Japan Standard Stroke Registry Study), we prospectively collected clinical data on acute ischemic stroke patients who were admitted to two main hospitals in Shenyang, China, and 50 hospitals in Japan. The mean age was 67.3 years in China and 71.3 years in Japan. Of the patients in China, 78% were classified as atherothrombotic infarction, 18% as lacunae, and 1% as cardioembolism. By contrast, 30% of the patients in Japan were classified as atherothrombotic infarction, 32% as lacunae, and 31% as cardioembolism. Regarding the risk factors, the incidence of hypertension was 76% in China and 62% in Japan. Diabetes mellitus was 10% in China and 26% in Japan. Hyperlipidemia was 10% in China and 22% in Japan. Atrial fibrillation was 3% in China and 21% in Japan. As the diagnostic criteria for hyperlipidemia differed, we could not compare this risk factor between the two countries statistically; however, cardioembolism, lacunae, and atrial fibrillation were significantly less common in China than in Japan. Our data suggest that hypertension is an important risk factor for ischemic stroke, and the incidence of cardioembolism and atrial fibrillation is very low in Shenyang, China.

Age Factors↗
PubMedDate not supplied

Hematocrit as a risk factor of cerebral infarction: long-term prospective population survey in a Japanese rural community.

To elucidate the relation of hematocrit (Hct) to the incidence of cerebral infarction, a prospective follow-up study of 16 years (1965-81) was performed in a general population sample of 1220 Hisayama residents aged 44 and over, of both sexes. Most of the subjects who died during the follow-up period were autopsied, the rate being 89.0%. Hct decreased with advancing age in men, but not in women. The average value for Hct was significantly lower in women than in men. According to the mean value +/- 1 SD of Hct, the subjects were grouped into 3, in each sex as follows: low (less than 35%), normal (35-45%) and high (greater than or equal to 45%) for men, and, low (less than 30%), normal (30-40%) and high (greater than or equal to 40%) for women. During the follow-up period, cerebral infarction occurred in 117 patients. The cumulative incidence of cerebral infarction in the low Hct group for men was the lowest, even after adjustments for age and blood pressure. Conversely, the incidence in the low Hct group of women was significantly higher than that in the normal Hct group and was consistently increased with time during 2-5 years of the follow-up. After the 6th year or later, however, the incidence was gradually but significantly increased in the high Hct group, compared with the normal Hct group. Since Hct levels were related with other variables such as serum total cholesterol, serum total protein, Quetelet index and prevalence of hypertension in both sexes, heavy alcohol consumption in men, and glucose intolerance in women, such variables were taken into account using Cox's proportional hazards regression model.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
PubMed2004

Neonatal cerebral infarction and neuromotor outcome at school age.

OBJECTIVE: The aim of this study was to assess neuromotor function at school age in children who had cerebral infarction on neonatal magnetic resonance imaging (MRI). DESIGN: Twenty-two children with evidence of cerebral infarction on neonatal brain MRI (18 with arterial infarction and 4 with border-zone lesions) were assessed at school age with a structured neurologic examination and the Movement Assessment Battery for Children, a battery of tests designed to assess motor function. RESULTS: Of the 22 children, 6 (30%) had hemiplegia and a further 7 (30%) showed some neuromotor abnormality such as asymmetry on the neurologic examination (n = 4) or poor scores on the neuromotor test without any sign of asymmetry (n = 3). The remaining 9 children had a normal motor outcome. Hemiplegia was found only in children who had concomitant involvement of hemisphere, internal capsule, and basal ganglia on brain MRI. Children with involvement of the internal capsule, associated either with basal ganglia or hemispheric lesions, did not show hemiplegia but still had motor difficulties. CONCLUSIONS: Our results suggest that although hemiplegia occurs in a relatively small proportion of children with neonatal cerebral infarction, other signs of neuromotor impairment can be present, and these become more obvious at school age when a more specific assessment can be performed. These results also suggest that the involvement of the internal capsule on neonatal MRI can predict the presence of these abnormalities.

Brain↗
PubMed2004

Electrocardiographic Q-waves as a predictor of mortality in patients with cerebral infarction.

OBJECTIVE: To determine whether abnormal EKG findings could be predictive factors for death after a stroke event. METHODS: Patients with acute cerebral infarction who were 35 to 98 years old during April 1996 through November 2000 were analyzed (n = 216). A standard 12-lead EKG was recorded for each patient after acute cerebral infarction. The authors prospectively investigated the association between abnormal EKG findings and the risk for death after stroke over a 1-year period. RESULTS: Using multivariate Cox proportional hazards models, the authors found age (hazard ratio of mortality per year 1.10, 95% CI 1.06 to 1.15, p < 0.001), sex (female; hazard ratio of mortality 3.42, 95% CI 1.43 to 8.19, p = 0.006), and the presence of Q-waves in more than two leads (hazard ratio of mortality 2.75, 95% CI 1.23 to 6.14, p = 0.013) were independently associated with death after stroke. CONCLUSION: The presence of Q-waves in more than two leads could be a predictive factor for death after acute cerebral infarction.

Adult↗