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PubMed1997

[Juvenile cerebral infarction with familial hyperlipoproteinemia (a)--case report].

A 34-year-old male with a history of angina pectoris suddenly developed weakness in the right upper and lower limbs, and consulted our hospital. Computed tomography (CT) and magnetic resonance imaging (MRI) suggested cerebral infarction. Cerebral angiography revealed stenosis at the M1 portion of the left middle cerebral artery. Hypertension, diabetes, tobacco or hyperlipidemia were not considered as risk factors for cerebral infarction. The lipoprotein (a) [Lp(a)] level was high. In the present case, medication with a nicotinic acid agent, niceritrol, for hyperlipoproteinemia and low density lipoprotein (LDL) apheresis were performed. Concerning family history, the patient's mother and younger sister had hyperlipoproteinemia. Recent studies have reported that increased Lp(a) levels are an independent risk factor even in cerebral infarction and coronary artery disease. Measurement of Lp(a) levels and treatment for increased Lp (a) levels may be important.

Adult↗
PubMed1989

Prospective analysis of carotid endarterectomy and silent cerebral infarction in 97 patients.

To determine the incidence of perioperative silent cerebral infarction, 97 patients who underwent carotid endarterectomy were prospectively studied with preoperative and postoperative computed tomograms. Thirty-one of 96 patients (32%) had findings of cerebral infarction on preoperative computed tomograms. Silent cerebral infarction was found preoperatively in 17 patients (18%) (lacunar infarction in 10, cortical infarction in five, both cortical and lacunar infarctions in one, and cerebellar infarction in one). Transient ischemic attacks occurred in 10 of the 17 patients with silent cerebral infarction; however, symptoms were appropriate to the site in only five of these 10 patients. Fourteen of the 17 patients with silent cerebral infarction had a hemodynamically significant carotid stenosis, and seven patients had an ulcerated plaque on preoperative angiogram. The incidence of these lesions was similar to that found in the group of 66 patients without cerebral infarction. Endarterectomy specimens revealed a higher but not significantly different incidence of ulcerated plaque in the silent cerebral infarction group. There were no perioperative deaths. Following surgery, one patient (1%) with a preoperative silent cerebral infarction suffered a transient ischemic attack, and two patients (2%) with normal preoperative computed tomograms developed permanent neurologic deficits with new cortical infarctions on postoperative computed tomograms. No new silent cerebral infarctions were found on postoperative computed tomograms in any of the 97 patients. Our data suggest that silent cerebral infarction is a common preoperative finding with an as-yet unclear etiology and that carotid endarterectomy does not appear to be a cause.

Aged↗
PubMedDate not supplied

Importance of the hematocrit as a risk factor in cerebral infarction.

The relationship between the indicence of cerebral infarction and the hematocrit was studied using 432 consecutive autopsied patients with the average age of 77.1 years. The incidence of cerebral infraction was higher in patients with hematocrit values of more than 46%, (the average in younger adult subjects). The increase in the frequency of cerebral infarction with high hematocrit values was more conspicuous in patients with severe cerebral atherosclerosis than in those with slight cerebral atherosclerosis. High blood pressure per se did not influence the relationship between the hematocrit value and the incidence of cerebral infarction. With hematocrit values of more than 41%, cerebral infarction occurred more frequently in patients over 78 years of age than in the younger patients, but the difference was not significant statistically. High hematocrit values are associated with a higher risk of cerebral infarction in deep subcortical structures of the brain than for cartical infarctions. The pathogenetic and preventive implications of these results are discussed in the light of blood rheology.

Age Factors↗
PubMed2005

[Role of complex aortic atheroma plaques in the recurrence of unexplained cerebral infarction].

INTRODUCTION AND OBJECTIVES: In a subgroup of patients with cerebral infarction, noninvasive diagnostic explorations fail to disclose the etiology. We studied the clinical course and the usefulness of transesophageal echocardiography to diagnose complex aortic atheroma plaques in patients with cerebral infarction of uncertain cause with recurrence of ischemia. PATIENTS AND METHOD: In a study population of 1840 consecutive patients with a first cerebral infarction evaluated with a screening protocol for transesophageal echocardiography, the etiology remained uncertain in 248 cases. These patients were followed during 1 year of treatment with antiplatelet agents, and transesophageal echocardiography was done if cerebral ischemia recurred. We compared the prevalence of complex aortic atheroma plaques in patients with recurrence and in patients with cerebral infarction of unknown etiology in the French Study of Aortic Plaques in Stroke, in whom there was no recurrence of cerebral infarction. RESULTS: Recurrent cerebral infarction was documented in 17 of our 248 patients with infarction of unknown etiology (6.9%). Transesophageal echocardiography established the etiology in 15 of these patients (88.2%) with complex aortic atheroma plaques being identified in 14 cases (82.4%). In contrast, in patients with cerebral infarction of unknown etiology in the French study without recurrent cerebral infarction during the first year of follow-up, the prevalence of complex plaques was 21.1% (P<.0001). CONCLUSIONS: During the first year of treatment with antiplatelet agents, most patients with cerebral infarction of unknown etiology had no recurrences. In the small subgroup with short-term recurrence, transesophageal echocardiography yielded the etiologic diagnosis in 88.2% of cases: the pathology most frequently involved was complex atherosclerotic disease of the aortic arch.

Aged↗
PubMed2001

MRI analysis of the changes in apparent water diffusion coefficient, T(2) relaxation time, and cerebral blood flow and volume in the temporal evolution of cerebral infarction following permanent middle cerebral artery occlusion in rats.

Detailed knowledge of similarities and differences between animal models and human stroke is decisive for selecting clinically effective drugs based on efficacy data obtained preclinically. Differences in the temporal evolution of stroke pathologies between animal models and man have been reported. In view of the importance of this issue for the development of neuroprotective treatments, the temporal evolution of stroke pathologies in the rat permanent middle cerebral artery occlusion (pMCAO) model has been evaluated with magnetic resonance imaging modalities under experimental conditions matching as close as possible those used in humans. Changes in the ipsilateral and contralateral cortex and striatum of cerebral blood flow (CBF) and volume (CBV), apparent diffusion coefficient (ADC), and spin-spin relaxation time (T(2)), as well as total cortical and striatal infarct volumes, calculated from CBF, ADC, and T(2) maps, were determined starting 1 h up to 216 h post-pMCAO. The temporal evolution of the MRI parameters in this rat model was similar to that observed in humans. In particular, the ADC values were decreased for more than 3 days and returned back to baseline between 4 to 8 days, to increase by day 9 only. Thus the stroke pathology in this rat model develops at a similar pace as in stroke patients arguing against a fundamental difference in the mechanisms involved. The infarct volumes however develop differently in this rat model as they invariably increase over the first 48 h, while in humans the evolution of infarct volume is slower and more heterogeneous.

Animals↗
PubMedDate not supplied

[Type A behaviour and life events as risk factors for cerebral infarct].

INTRODUCTION: The role of psychosocial factors in cerebral infarct has been little studied and is therefore still undefined. OBJECTIVE and methods. To evaluate the effect of a pattern of behaviour which predisposes to stress, and of life events, on the occurrence of cerebral infarct, we studied a group and control involving 88 patients with cerebral infarcts diagnosed clinically and on imaging studies, and a control group of 99 persons paired for age and sex who lived in our health district. To evaluate the behaviour pattern we used Jenkins abbreviated questionnaire and for life events the Holmes and Rahe questionnaire. RESULTS: The type A behaviour pattern had a highly statistically significant association with cerebral infarct, which was not associated with the effects of other variables. This relation was the greater the lower the age of the person. It was not seen after the age of 75 years. The behaviour pattern was not related to arterial hypertension or with the aetiopathological mechanisms of the patients. In relation to the life events questionnaire, the number of events was significantly associated in the group of patients, but not with the total score of the questionnaire. However, the latter was significantly related to hypertensive patients and persons with a type A behaviour pattern. The commonest life events in both groups were related to the death or health problems of family members, the previous illnesses of the person and to financial and work problems. CONCLUSION: The type A behaviour pattern is individually associated with cerebral infarct, whilst stressful life events were involved in the cerebral infarcts of hypertensive and type A behaviour patients.

Aged↗
PubMed2001

[A study on the risk factors of cerebral infarction as complication of type 2 diabetes mellitu patients].

OBJECTIVE: Cerebral infarction, a common acute cereovascular disease, is one of the main complications of type 2 diabetes mellitus (DM). This paper is to explore the risk factors of cerebral infarction among type 2 DM patients. METHODS: A pair-matched case-control study was carried out. Data was analyzed with conditional logistic regression. RESULTS: One hundred and ten type 2 DM patients with cerebral infarction and controls were selected respectively. Results showed that higher educational level and physical exercises lowered the risk of cerebral infarction among type 2 DM patients. Higher HDL-C and blood sugar under control could also lower the risk of developing cerebral infarction among type 2 DM patients. The above factors seemed to have protective functions. Excessive salt intake and snoring increased the risks of cerebral infarction development among type 2 DM patients. Hypertension served as an independent risk factor while atrial fibrillation and hyperinsulinemia were important risk factors. High LDL-C, Apo-A, Lp(a), Fg increased the risk of cerebral infarction among type 2 DM patients. The study did not discover the relationship of smoking, drinking, oral contraception, menstrual and obstetrical history, TC, TG, Apo-A and cerebral infarction among type 2 DM patients. CONCLUSION: To prevent cerebral infarction among type 2 DM, measures need to be taken as control of salt intake; eating more vegetables; regular physical exercises; control of blood sugar, blood pressure and Hyperinsulinemia.

Adult↗
PubMed1986

Nonhemorrhagic cerebral infarction in young adults.

We evaluated 144 patients (81 males and 63 females) aged 15 to 45 years who had nonhemorrhagic cerebral infarction. Atherosclerotic cerebral infarction was diagnosed in 38 patients. Potential cardiac causes of cerebral embolism were found in 33 patients. Only three events could be attributed to mitral valve prolapse. Hematologically related disorders were diagnosed in 21 patients, while 38 patients had nonatherosclerotic vasculopathies. Young patients with cerebral infarction are a heterogeneous group. A potential cause can be found in most patients. We found more than 40 possible etiologies among our patients. Mitral valve prolapse apparently is not a common cause of cerebral infarction among young adults. Cerebral infarction should not be ascribed to oral contraceptives or migraine until other possible causes have been eliminated.

Adolescent↗
PubMed2006

Posttraumatic cerebral infarction in patients with moderate or severe head trauma.

OBJECTIVE: To evaluate the frequency, types, and location of posttraumatic cerebral infarction, to assess if secondary cerebral insults were associated with cerebral infarction, and to determine if cerebral infarction affected patients' outcome. METHODS: We based diagnosis of cerebral infarction on review of brain CT scans. We assessed frequency of secondary cerebral insults, including intracranial hypertension, cerebral hypoperfusion, systolic hypo- and hypertension, arterial blood oxygen desaturation, hypocapnia, and hyperthermia, using clinical charts. We used the Glasgow Outcome Scale to evaluate outcome at 6 months after trauma. RESULTS: Of the 89 patients included, a total of 28 cerebral infarctions were found in 17 cases (19.1%). Infarctions were territorial in 23 (82.1%) and watershed in 5 (17.9%) cases. Territorial infarctions were localized to the middle cerebral artery (n = 9, 32.1%), lenticulostriate arteries (n = 6, 21.4%), posterior cerebral artery (n = 3, 10.7%), anterior cerebral artery (n = 3, 10.7%), thalamoperforating arteries (n = 1, 3.6%), and basilar artery (n = 1, 3.6%) territories. Watershed infarctions were in the boundary (n = 4, 14.3%) and terminal (n = 1, 3.6%) zones. Intracranial hypertension was the only independent variable predicting cerebral infarction (odds ratio [OR] 13.3; 95% CI 2.8 to 62.6). At 6 months after trauma, there was a lower proportion of patients with good outcome among patients with cerebral infarction vs patients without (23.5 and 61.1%; p = 0.005). Cerebral infarction was the only independent predictor of 6-month outcome (OR of good outcome 0.19, 95% CI 0.06 to 0.66). CONCLUSIONS: The risk of developing posttraumatic cerebral infarction may be higher in patients with intracranial hypertension than in those without. Patients with posttraumatic cerebral infarction may be at increased risk of residual disability.

Adult↗
PubMed2001

Silent cerebral infarction: risk factor for stroke complicating carotid endarterectomy.

"Silent" cerebral infarction is found in 20% to 30% of patients with significant internal carotid artery (ICA) disease. Our purpose was to determine whether such "silent" cerebral infarction in the operated carotid territory represents a risk factor for stroke during and immediately after carotid endarterectomy. Over 5 years we followed a cohort of 663 patients with symptomatic and asymptomatic ICA stenosis who were consecutively scheduled for surgery. The stenosis was more than 70% in patients with transient ischemic attacks and more than 95% in asymptomatic stenosis patients. All patients underwent preoperative computed tomography to determine the frequency, extent, and location of any "silent" cerebral infarction. Patients were grouped by the absence or presence of infarction in the operated carotid territory. Among the entire cohort, 20 patients had a major perioperative stroke (3.0%). All deaths were stroke-related. No intracranial bleeding occurred. Major stroke occurred in four (0.8%) patients without appropriate "silent" cerebral infarction, compared with 16 (8.8%) with an appropriate "silent" cerebral infarct (p < 0.001). After adjustment for confounding co-variables (e.g., gender, presence of preoperative symptoms, and age), "silent" cerebral infarction was found to be the only independent predictor of perioperative major stroke for symptomatic and asymptomatic stenosis (overall adjusted relative risk 11.5, 95% confidence interval 3.8-34.9, p < 0.0001). Patients with "silent" cerebral infarction seem to be at increased risk of perioperative stroke. Consequently, preoperative cerebral imaging is important for risk classification.

Aged↗
PubMed2004

Predictors of cerebral infarction in aneurysmal subarachnoid hemorrhage.

BACKGROUND: Clinical and radiologic predictors of cerebral infarction occurrence and location after aneurysmal subarachnoid hemorrhage have been seldom studied. METHODS: We evaluated all patients admitted to our hospital with aneurysmal subarachnoid hemorrhage between 1998 and 2000. Cerebral infarction was defined as a new hypodensity located in a vascular distribution on computed tomography (CT) scan. RESULTS: Fifty-seven of 143 patients (40%) developed a cerebral infarction. On univariate analysis, occurrence of cerebral infarction was associated with a worse World Federation of Neurological Surgeons grade (P=0.01), use of ventriculostomy catheter (P=0.01), preoperative vasospasm (P=0.03), surgical clipping (P=0.02), symptomatic vasospasm (P<0.01), and vasospasm on transcranial Doppler ultrasonography (TCD) or repeat angiogram (P<0.01). On multivariable analysis, only presence of symptoms ascribed to vasospasm (P<0.01) and evidence of vasospasm on TCD or angiogram predicted cerebral infarction (P<0.01). TCD and angiogram agreed on the diagnosis of vasospasm in 73% of cases (95% CI, 63% to 81%), but the diagnostic accuracy of this combination of tests was suboptimal for the prediction of cerebral infarction occurrence (sensitivity, 0.72; specificity, 0.68; positive predictive value, 0.67; negative predictive value, 0.72). Location of the cerebral infarction on delayed CT was predicted by neurological symptoms in 74%, by aneurysm location in 77%, and by angiographic vasospasm in 67%. CONCLUSIONS: Evidence of vasospasm on TCD and angiogram is predictive of cerebral infarction on CT scan but sensitivity and specificity are suboptimal. Cerebral infarction location cannot be predicted in one quarter to one third of patients by any of the studied clinical or radiological variables.

Adult↗
PubMedDate not supplied

Evaluation of plasma endothelin-1 levels in patients with cerebral infarction.

Endothelin-1 (ET-1) is a vasoconstrictor peptide derived from endothelium. Many authors have shown that ischemic stroke is associated with elevated plasma ET-1 levels. Also, the present findings related to plasma ET-1 levels with clinical status, size of the infarction, location of the infarction, and prognosis of the cerebral infarction were contradictory. In this study, plasma ET-1 levels in 30 patients with cerebral infarction within 72 hours after the onset of focal neurologic deficit and at their seventh day postinfarction were measured by a microplate enzyme immunoassay. Thirty sex- and age-matched healthy subjects were accepted as a control group. The mean plasma ET-1 concentrations in patients on admission, in patients at day 7, and in control subjects were 1.93 +/- 1.79, 1.03 +/- 1.02, and 0.65 +/- 0.32 fmol/mL, respectively. The mean plasma ET-1 level of patients on admission was found to be significantly higher than in patients at day 7 and in control subjects (p < 0.05). No significant difference in ET-1 levels was observed between the patients at day 7 and control subjects. Furthermore, there was no correlation between plasma ET-1 concentration and size of infarction, location of infarction, degree of clinical neurologic deficit, or prognosis of cerebral infarction. It was concluded that plasma ET-1 levels shortly after ischemic stroke were increased, which may be associated with the acute-phase reaction of cerebral infarction and may have deleterious effects on development of neuronal injury.

Adult↗
PubMed1991

Transcranial Doppler evaluation of cerebral infarction in the neonate.

We recorded cerebral artery flow velocities (CAFV) in two neonates with cerebral infarction, using transcranial Doppler sonography (TCD). Cerebral infarction was diagnosed by brain imaging. The arteries investigated were the middle cerebral artery (MCA), the internal carotid artery (ICA) and the anterior cerebral artery (ACA). The whole territory of right MCA was involved. A decrease in CAFV was noted in MCA and ICA of the affected side. Furthermore, early recordings of CAFV allowed us to distinguish perinatal infarction from antenatal infarction: in the former, Doppler signal was completely absent during the first days of life whereas in the latter, Doppler signal was reduced but present. The process of recanalization could be followed. The asymmetry of CAFV recorded in the neonatal period seems to persist definitively at least in MCA. These Doppler data correlate well with the evolutive stages of cerebral infarction shown by brain imaging. Beside US, CT and MRI scans, TCD may be a useful adjunct for identifying and following infants with suspected occlusion of major cerebral vessels.

Blood Flow Velocity↗
PubMed2006

High-cholesterol feeding aggravates cerebral infarction via decreasing the CB1 receptor.

We examined how feeding conditions affect the CB1 receptor and cerebral infarction caused by cerebral ischemia. Mice were divided into the following three groups: normal diet (ND), caloric restriction (CR) and high-cholesterol-enriched diet (HCD), and were kept for 6 weeks. After 6 weeks, we measured both serum and brain cholesterol and the expression level of cannabinoid CB1 receptor within the brain in intact mice. In addition, middle cerebral artery (MCA) was occluded for 2 h following reperfusion. Serum cholesterol significantly increased in the HCD group in comparison with both the ND and CR groups. However, brain cholesterol decreased in the HCD group. Then, the expression level of CB1 receptor significantly decreased in the HCD group, while that of the CR group clearly increased in comparison with the ND group in intact mice. In MCA-occluded mice, The HCD group produced the most severe cerebral infarction, while cerebral infarction was significantly decreased in the CR group. These results suggest that CR prevents infarction by increasing CB1 receptor expression, while high-cholesterol feeding aggravates cerebral infarction both by hypercholesterolemia in serum and by decreasing CB1 receptor expression modulated by hypocholesterolemia within the brain.

Animals↗
PubMed2004

Proliferation and differentiation of neural stem cells in adult rats after cerebral infarction.

OBJECTIVE: To investigate proliferation and differentiation of neural stem cells in adult rats after cerebral infarction. METHODS: Models of cerebral infarction in rats were made and the time-course expression of bromodeoxyuridine (BrdU), Musashi1, glial fibrillary acidic protein (GFAP), and neuronal nuclear antigen (NeuN) were determined by immunohistochemistry and immunofluorescence staining. BrdU and Musashi1 were used to mark dividing neural stem cells. GFAP and NeuN were used to mark differentiating neural stem cells. RESULTS: Compared with controls, the number of BrdU-labeled and BrdU-labeled with Musashi 1-positive cells increased strikingly 1 day after cerebral infarction; approximately 6 fold with a peak 7 days later; markedly decreased 14 days later, but was still elevated compared with that of controls; decling to the control level 28 days later. The number of BrdU-labeled with GFAP-positive cells nearly remained unchanged in the hippocampus after cerebral infarction. The number of BrdU-labeled with NeuN-positive cells increased strikingly 14 days after cerebral infarction, reached maximum peak in the hippocampus 28 days after cerebral infarction in rats. CONCLUSION: Cerebral infarction stimulate proliferation of inherent neural stem cells and most proliferated neural stem cells differentiate into neurons.

Animals↗
PubMed2004

[Changes of plasma CD62p levels in patients with acute cerebral infarction].

OBJECTIVE: To explore the function of CD62p in cerebral infarction and the relation between the changes of its level and the severity and recovery of cerebral infarction, MPV, PDW and PLT by studying the changes of the levels of plasma CD62p in patients with acute cerebral infarction. METHODS: The levels of plasma CD62p were measured by ELISA in 60 patients at 48 hours, 6 - 8 days and 15 days after ischemia, and at the same time, we evaluated neurological function deficiency score and measured MPV, PDW and PLT. The levels of 30 healthy persons mating cerebral infarction group in both sex and ages were measured. RESULTS: The levels of plasma CD62p in the patients with acute cerebral infarction were obviously higher than the levels of the healthy controls (P < 0.001). The levels of plasma CD62 p in CI group at 48 hours postischemia were higher than the levels at 6 - 8 days and at 15 days with obvious difference (P <0.01). The levels of plasma CD62p in the medium and the severe SSS patients were higher than the levels of the lights (P <0.001). The levels of plasma CD62p were positively correlated with SSS, MPV and PDW (r = 0.61, 0.51, 0.47, P < 0.01), and negatively correlated with PLT (r = -0.32, P < 0.01). CONCLUSION: CD62p may participate in acute cerebral infarction and play a crucial role, and the change of its levels correlates with SSS, MPV, PDW and Plt.

Adult↗
PubMedDate not supplied

Cerebral infarction after envenomation by viper.

A case of cerebral infarction after viper bite is described; the patient also had features of diffuse encephalopathy. Findings on MRI were suggestive of subacute hemorrhagic infarcts. Possible mechanisms for cerebral infarction in these circumstances were discussed. The mechanism of cerebral infarction in this case seemed to be vasospasm due to the action of the toxin, hemorrhagin, present in the venom.

Adolescent↗
PubMed1994

Cerebral infarction in pediatric acquired immunodeficiency syndrome.

Cerebral infarction is an uncommon complication of AIDS in pediatric patients. We have seen three HIV-infected children who developed acute neurological deficits due to stroke. Cerebral infarction must be considered in the work-up of a child with AIDS who presents with focal neurological deficit, seizure or mental status change. Stroke is a complication of HIV infection that occurs in approximately 1% of affected children [1]. At autopsy, evidence of cerebral infarction was documented in 10-30% of children with HIV infection [2]. We have seen three children with focal infarction who are HIV positive.

Acquired Immunodeficiency Syndrome↗