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PubMed2004

Cerebral infarction and fluid collection due to an enlarged dissecting aneurysm of the middle cerebral artery--case report.

A 53-year-old man presented with cerebral infarction associated with a dissecting aneurysm of the left middle cerebral artery (MCA), with enlargement and fluid collection. Anticoagulant therapy was performed as the first stage treatment for cerebral infarction. Serial magnetic resonance imaging showed that the dissecting aneurysm had enlarged and fluid collection adjacent to the aneurysm had developed since the first admission. Surgery was performed to ligate the MCA proximal to the aneurysm. Intraoperative findings showed the branch of the MCA was obstructed by intramural hemorrhage of the aneurysm dome. Histological examination showed direct obstruction of the MCA branch artery by intramural hemorrhage of aneurysm dome had caused the cerebral infarction and the fluid collection surrounding the aneurysm resulted from minor leakage or exudation of intramural hemorrhage to the outer surface of the dissecting aneurysm.

Aortic Dissection↗
PubMed1983

Herpes zoster ophthalmicus and delayed ipsilateral cerebral infarction.

We studied five patients who had acute cerebral infarctions 5 weeks to 6 months after herpes zoster ophthalmicus (HZO). All had infarcts of the cerebral hemisphere ipsilateral to the HZO, and one also had a cerebellar infarct. Cerebral arteriography in one patient disclosed narrowing of the middle cerebral artery, occlusion of the anterior cerebral artery ipsilateral to the HZO and narrowing of the opposite anterior cerebral artery. In another case, arteriography revealed occlusion of the distal internal carotid artery on the side of the HZO.

Adolescent↗
PubMed1976

[Cerebrospinal fluid flow dynamics in cerebral infarction--Numerical study with RI Anger camera (author's transl)].

Although the cerebral blood flow dynamics in cerebral infarction has already been studied by many investigators, the CSF flow dynamics in cerebral infarction has not been well discussed. The purpose of this paper is to investigate CSF flow dynamics in chronic cerebral infarction by RI cisternography and our new quantitative method. In 12 patients with cerebral infarction, the flow of CSF was estimated following intrathecal injection of 169Yb-DTPA or 111In-DTPA. In this study, in addition to the conventional cisternograms, quantitative evaluation of CSF flow was performed in 6 patients by our method. Our previous work included the quantitative CSF flow dynamics in 26 various cerebral disorders using RI Anger camera. This method consisted of following procedure: 30 minutes after RI injection, RI activity was studied continuously for 30 minutes, afterwards playing back the record to calculate the changes of RI activity in the optimal regions of interest. These operations were performed with Anger camera, accessory digital ratemeter and tape-recorder. The changes of RI activity which appeared to be linear is called flow rate in our study for convenience. In this report, the region of interest was selected at Sylvian cistern. 6 patients had abnormal cisternograms consisting of reflux of tracer into the ventricle and delayed migration of tracer to the basal cisterns and diminished flow of tracer in the affected hemisphers. In 5 patients whose cisternograms could not demonstrate the laterality of RI perfsion over the cerebral hemishere, a marked difference of flow rate between right and left Sylvian cisterns was found. These findings probably indicated the correlation between cerebral blood flow dynamics and CSF flow dynamics in cerebral infarction. Moreover, it was confirmed that our method could be of clinical use to evaluate CSF flow dynamics quantitatively. The possible mechanisms of CSF flow disturbance in the affected hemisphere following cerebral infarction was discussed.

Adult↗
PubMed2006

[Consultation after cerebral infarction or intracerebral hematoma].

Hypertension is the principal risk factor for cerebral infarctions and intracerebral hematoma. The brain is the principal target of hypertension. The brain is the principal target of antihypertensive drugs. Controlling blood pressure and stopping smoking reduces the risk of cerebral infarction by 40%. Objectives of a consultation after cerebral infarction or intracerebral hematoma: validate diagnosis and cause, identify risk factors for recurrent cerebral infarction but also for myocardial infarction and lower limb arterial disease, begin treatment of the risk factors for recurrence, begin prevention of atherothrombotic complications and embolic heart disease, identify complications of cerebral infarction and intracerebral hematoma.

Adult↗
PubMed1979

[Histopathological study on experimental cerebral infarction in rat (author's transl)].

An experimental model of cerebral infarction in rat brain was successfully established by means of the unilateral internal carotid injection of carbon microspheres. A histopathological investigation of the infarcted brain was performed. The results were as follow: 1. No cerebral infarction was made by the unilateral internal carotid ligation alone. 2. Focal cerebral edema was most marked at the white matter of the embolized hemisphere. 3. The edema was also conspicuous in the deep cerebral gray matter, especially in hippocampus. Degeneration and pyknosis of the neurons were observed at the same area. 4. Transudative hemorrhage in the focal cerebral edema was usually observed in the thalamus. 5. Edematous change in the cortical gray matter was not so marked as compared with the hippocampus and thalamus. 6. Carbon microsphere was not found in the capillaries of ipsilateral choroid plexus. The present experimental model of cerebral infarction will be useful in elucidating the pathological mechanisms of the cerebral infarction.

Animals↗
PubMedDate not supplied

Migrainous cerebral infarction: a tomographic study of cerebral blood flow and oxygen extraction fraction with the oxygen-15 inhalation technique.

A patient with migraine who had a permanent visual field defect was studied by angiography and CT scan. He also had a tomographic study of cerebral blood flow (CBF) and oxygen extraction fraction (EO2) using the non-invasive continuous oxygen-15 (15O) inhalation technique. Angiography was normal. CT scan revealed an area of decreased density with contrast enhancement suggestive of a recent infarct in the left occipital lobe. The 15O inhalation technique showed a decrease in CBF and EO2, typical of recent infarcts, in the corresponding area, an increase in CBF with normal EO2 in the left temporal lobe, and a decrease in CBF with increased EO2 in the right occipital cortex. These findings illustrate the unusual nature and extent of the ischemic process underlying migrainous cerebral infarction.

Cerebral Angiography↗
PubMed2004

Association of apolipoprotein E 4 polymorphism with cerebral infarction in Chinese Han population.

AIM: To study the association between APOE polymorphisms and cerebral infarction through a case-control study among the Chinese Han population. METHODS: First-ever cerebral infarction patients (n=226) whose ages ranged from 40 to 60 years old were recruited from Department of Neurology, Zhongshan Hospital, Shanghai, and Zhejiang Chinese Traditional Medicine Hospital, Zhejiang, China. Unrelated healthy controls (n=201) were selected from the general population in the same area with similar age and sex distribution. APOE was amplified by one-stage PCR using the forward primer: 5'-GGC ACG GCT GTC CAA GGA GCT-3' and reverse primer: 5'-GAT GGC GCT GAG GCC GCG CT-3'. The PCR product was digested directly with 5 U of CfoI and separated by a 20 % polyacrylamide (acrylamide: bis-acrylamide=29:1) nondenaturing gel. RESULTS: Both cerebral infarction patient and control groups were in Hardy-Weinberg equilibrium. The allele frequency of APOE*2, APOE*3, and APOE*4 was 4.6 %, 81.9 %, and 13.5 % respectively in the patients with cerebral infarction; 5.7 %, 87.3 %, and 7.0 % respectively in the healthy control group. Compared with APOE3/3 subjects, APOE4/4 carriers had a 2.1-fold risk of cerebral infarction (odds ratio 2.1, 95 % confidence limits 1.3 to 3.4). The allele frequency of APOE*4 in the cerebral infarction patient group was significantly higher than that in the control group (13.5 % vs 7.0 %; P=0.002). CONCLUSION: APOE 4 is a risk factor for cerebral infarction among the Chinese Han population.

Adult↗
PubMedDate not supplied

Experimental cerebral infarction. Part 1: Production of thalamic infarction in dogs.

Difficulties in achieving focal temporary cerebral ischemia in experimental animals have delayed study of the prevention and treatment of cerebral infarction. We have succeeded in producing focal cerebral infarction by temporary occlusion of brain arteries. Infarction confined to the anterior portion of the thalamus was obtained by simultaneous occlusion of the 4 cerebral arteries: internal carotid, anterior cerebral, middle cerebral and posterior communicating arteries for 60-120 minutes. This experimental model in dogs is unique, since thalamic infarction can be produced with high frequency, and the dogs can be kept alive and managed for sufficient periods after temporary artery clipping. With this model it is possible to investigate cerebral infarction not only from the pathophysiological viewpoint, but also from the viewpoint of prevention and treatment of cerebral infarction in man.

Animals↗
PubMed1998

Cognitive screening examinations for silent cerebral infarcts in sickle cell disease.

OBJECTIVE: In children with sickle cell disease (SCD), silent cerebral infarcts are the most frequent cause of neurologic injury. We determined the sensitivity and specificity of selective neurocognitive measures when separating children with silent cerebral infarcts and SCD from sibling controls. Additionally, we tested the validity of the same cognitive measures to identify patients with overt strokes. METHODS: We examined performance on a neuropsychologic battery containing measures of attention/executive, spatial, language, memory, and motor functioning for seven children with SCD and silent cerebral infarct, 21 children with SCD and overt stroke, and 17 normal siblings. Diagnosis of cerebral infarct was based on results of MRI. RESULTS: Measures from the attention and executive domains were the most useful for identifying children with silent cerebral infarct. The Test of Variables of Attention was the most robust measure and yielded a sensitivity rate of 86% and a specificity rate of 81%. This measure also showed a sensitivity rate of 95% in identifying overt stroke. CONCLUSIONS: Brief cognitive screening measures, if properly constructed, may be an effective means of identifying children with silent cerebral infarct. Future prospective studies should be pursued to assess the utility of cognitive screening for silent cerebral infarcts in SCD.

Adolescent↗
PubMed2002

The administration of complement component C9 augments post-ischemic cerebral infarction volume in neonatal rats.

To determine whether ischemic cerebral infarction is mediated in part by complement component C9, C9-deficient neonatal rats were subjected to unilateral cerebral ischemia. Brains were harvested 24 h later, stained with 2,3,5-triphenyl tetrazolium chloride, and cerebral infarct volumes were quantified by computer-based planimetry. Compared with buffer, prophylactic intraperitoneal (i.p.) administration of the complement inhibitors soluble complement receptor type 1 (sCR1), a molecular hybrid of sCR1 and the selectin inhibitor sialyl Lewis x (sCR1-sLex), or cobra venom factor did not affect the cerebral infarct volume. In contrast, i.p. human C9 (75 microg/g body weight) significantly increased the volume of infarct located 6 through 10 mm posterior to the frontal pole. Therefore, in the post-ischemic brain, C9 was neurotoxic and augmented the focal cerebral infarct volume.

Animals↗
PubMed1996

[Cerebral infarction associated with meningitis].

Among 43 adult patients with meningitis, 8 (18.6%) had cerebral infarction associated with meningitis during their clinical course. The total number of cerebral infarctions was 18. In 4 patients of good outcome (ambulatory in 3 cases and wheelchair in 1 case) with a mean age of 39 years, the number of cerebral infarctions was 1 per patient, and did not increase. In 4 patients of poor outcome (vegetative in 2 cases and died in 2 cases) with a mean age of 68 years, the number of cerebral infarctions was 1 in two cases and 2 in two cases, and later increased in 3 of the cases. Locations of cerebral infarctions were 3 in the striatocapsular lesion, 1 in the posterior limb of internal capsule, 1 in the middle cerebral artery territory, 5 in the tuberothalamic artery territory, 5 in the capsular genu, 1 in the posterior choroidal artery territory, and 2 in the medial striate artery territory. Patients of poor outcome had capsular genu infarction. It was concluded that multiplicity and multiplication of cerebral infarction were markers of the severity of the meningitis.

Adult↗
PubMed1990

Distribution of cerebral infarcts on computed tomography.

Locations of cerebral infarcts on computed tomography were analyzed on all patients admitted for ischemic stroke or status lacunaris in 1984. Patients who had only one symptomatic infarct, without histories of strokes or transient ischemic attacks, were allocated to group A, the rest made up group B. Group A showed that 47.6% of symptomatic infarcts were lacunes with similar percentages in the following areas: lenticular nucleus (12.7%), internal capsule (12.7%), and subcortical white matter (11.1%). In group A, the cortex (49.2%) was the most common site of infarction, while in group B, it was the subcortical white matter (31.7%). However, if the structures supplied by the basal perforating arteries (basal ganglia, thalami, and internal capsules) were considered as a whole, this area (41.8%) was the most common site for infarcts in group B. Thus, asymptomatic infarcts and those of status lacunaris contributed greatly to the overall distribution of cerebral infarcts.

Adult↗
PubMed1998

Mitochondrial susceptibility to oxidative stress exacerbates cerebral infarction that follows permanent focal cerebral ischemia in mutant mice with manganese superoxide dismutase deficiency.

Mitochondrial injury has been implicated in ischemic neuronal injury. Mitochondria, producing adenosine triphosphate by virtue of electron flow, have been shown to be both the sites of superoxide anion (O2-) production and the target of free radical attacks. We evaluated these mechanisms in an in vivo cerebral ischemia model, using mutant mice with a heterozygous knock-out gene (Sod2 -/+) encoding mitochondrial manganese superoxide dismutase (Mn-SOD). Sod2 -/+ mice demonstrated a prominent increase in O2- production under normal physiological conditions and in ischemia, as evidenced by specific oxidation of a fluorescent probe, hydroethidine, reflecting decreased activity of Mn-SOD. A mitochondrial viability assay that used rhodamine 123, which is accumulated by transmembrane potential of viable mitochondria, demonstrated accelerated development of mitochondrial injury. This rapid progress of ischemic injury resulted in exacerbation of infarct size and hemisphere enlargement, causing advanced neurological deficits but without altering DNA fragmentation induction. The present study suggests that O2- overproduced in a mitochondrial compartment, when uncoupled from antioxidant defenses, induces impairment of mitochondrial function and causes exacerbation of cerebral infarction after ischemia.

Animals↗
PubMed1998

Brain SPECT imaging using three different tracers in subacute cerebral infarction.

Two patients with subacute cerebral infarction underwent benzodiazepine receptor imaging using I-123-iomazenil and cerebral perfusion imaging with Tc-99m HMPAO and Tc-99m ECD. Iomazenil early images resembled HMPAO images, which demonstrated increased uptake in a part of the infarcted site. Iomazenil delayed images and ECD images showed reduced accumulation in the same area. Crossed cerebellar diaschisis was observed in HMPAO, ECD, and iomazenil early images, but it was not remarkable in iomazenil delayed images. These cases suggest that sequential iomazenil images visualized increased uptake with relatively impaired viability in the infarcted site and hypoperfusion with preserved viability in the contralateral cerebellar hemisphere, which could not be recognized without using both HMPAO and ECD in the subacute phase of cerebral infarction.

Adult↗
PubMedDate not supplied

[Prognostic factors of cognitive deterioration in patients with cerebral infarcts].

INTRODUCTION: Cognitive deterioration is a frequent finding in patients who have had a cerebral infarct which affected their quality of life. The prognostic factors associated with this are still not completely clear. OBJECTIVES: To determine the frequency of cognitive deterioration following cerebral infarct and the prognostic factors associated with its appearance. PATIENTS AND METHODS: We made a study of a prospective pohort in the Hospital Clínico Quirúrgico Hermanos Ameijeiras de Ciudad de La Habana, Cuba, in 401 patients with the confirmed diagnosis of cerebral infarct during the period March 1997 February 2000. A questionnaire was completed for all patients. This contained the possible variables for prognosis. The neuropsychological tests were done 3 and 6 months after the cerebral infarct occurred to determine the appearance of cognitive deterioration. Statistical analysis included the c2 test, relative risk estimation, and multiple logistic regression analysis. RESULTS: The frequency of cognitive deterioration 3 and 6 months after the cerebral infarct occurred was 22.2% and 6.9% respectively. Multiple logistic regression analysis showed prognostic variables of cognitive deterioration to be arterial hypertension (p=0.001, RR:2.0) and the number of current cerebral infarcts shown on computerized axial tomography (p=0.000, RR:5.2). CONCLUSIONS: Cognitive deterioration was a frequent complication after a cerebral infarct and several prognostic factors were associated with its appearance.

Aged↗
PubMed1996

[Favorable prognosis in a case of recurrent cerebral infarctions caused by chronic disseminated intravascular coagulation due to ovarian carcinoma].

We report a 53-year-old woman who developed a cerebral infarction in the left middle cerebral artery area. Although she did not have a hemorrhagic tendency, the results of her examination showed a chronic disseminated intravascular coagulation (DIC) and a left ovarian carcinoma. Gabexate mesilate (FOY) and nafamostat mesilate (FUT) were not effective for her DIC. One month after admission, she had another cerebral infarction in the right posterior cerebral artery area. She was treated by heparin sodium and her chronic DIC improved. Then, she was operated on for ovarian carcinoma; the histologic finding was clear cell adenocarcinoma. No recurrence of DIC nor cerebral infarction was observed postoperatively. Patients with cerebral infarctions caused by chronic DIC due to ovarian carcinoma have been reported in the literature, but few patients had a favorable prognosis such as the present case. Heparin therapy appears to be the treatment of choice for chronic DIC rather than FOY or FUT, if there is no hemorrhagic tendency. When a patient with DIC develops cerebral infarction, one should always investigate for possible malignant tumors.

Adenocarcinoma, Clear Cell↗
PubMed2004

Growth arrest and DNA damage-inducible gene 153 increases transiently in the thalamus following focal cerebral infarction.

The thalamus degenerates following cerebral infarction in the territory supplied by the middle cerebral artery (MCA), and apoptosis is suspected to be the mechanism of this phenomenon. The author studied the role of the growth arrest and DNA damage-inducible gene (GADD) 153 in this thalamic degeneration. The MCA was occluded in stroke-prone spontaneously hypertensive rats. The expression of GADD 153 and Bcl-2, and the release of cytochrome c from the mitochondria to cytosol, were examined in the thalamus until 7 days after ischemia using in situ hybridization, immunoblot, immunohistochemistry and RT-PCR analyses. Gadd153 mRNA expression and GADD153 protein increased transiently at 2, 3, 5 and 7 days, and at 3 and 5 days after ischemia. Bcl-2 mRNA expression and Bcl-2 protein decreased at 3 and 5 days. The release of cytochrome c from the mitochondria was detected at 5 days. These results suggest that increased GADD 153 suppresses Bcl-2 expression, which causes the release of cytochrome c from the mitochondria and leads to thalamic degeneration.

Animals↗
PubMedDate not supplied

[Effect of low-molecular dextran on leukergy and thrombergy in cases of cerebral infarct].

In cases of thrombotic cerebral infarction the leucergic and thrombergic tests were done on the 2nd and 3d days of the disease and after 48 hours from the first dextran loading. Fleck's test tube method was used in the leucergy test. The proportion of agglutinated platelets was calculated from a smear stained by Papanicolau method. The results were processed statistically. An inhibitory effect of dextran on aggregation of white blood cells and platelets was observed in the blood of patients with cerebral infarction. The inhibitory effects of dextran was greater in relation to aggregation of platelets than white blood cells. However, in our investigations the effect of this agent on both processes was transient.

Aged↗