Search PubMed⌕ Search

SEARCH · Search PubMed

Results for “Cerebral Infarction”

Search indexed PubMed citations on genomics, clinical trials, systematic reviews and public health. Explore titles, authors and supplied subject terms, then open the PubMed record.

Quote a phrase for an exact phrase match. Source license links do not imply unrestricted reuse.

At least 901 records · Page 50Linked to original sources
PubMed1999

Chlamydia pneumoniae antibodies and high lipoprotein(a) levels do not predict ischemic cerebral infarctions. Results from a nested case-control study in Northern Sweden.

BACKGROUND AND PURPOSE: An association between high lipoprotein(a) [Lp(a)] levels and positive Chlamydia pneumoniae IgG titers in coronary artery disease has been described. The possibility of predicting ischemic stroke by measurements of plasma Lp(a) and C pneumoniae antibodies was investigated. METHODS: This incident case-control study included 101 case subjects (cases) who had suffered ischemic cerebral infarctions and 201 matched control subjects (controls). The study population was nested within the Västerbotten Intervention Program or the WHO MONICA project. Plasma samples were measured for C pneumoniae-specific IgG and IgA antibodies and Lp(a). RESULTS: A significantly higher mean Lp(a) level was found in female cases than in female controls. However, plasma Lp(a) was unable to predict ischemic cerebral infarctions in either women or men. The proportion of individuals with positive C pneumoniae-specific IgG or IgA titers did not differ between cases and controls. Antibody titers were unable to predict a future stroke. The proportion of individuals with a positive C pneumoniae IgG titer in combination with a high Lp(a) level did not differ significantly between cases and controls. CONCLUSIONS: These data suggest that there is no association between baseline plasma Lp(a) levels, presence of C pneumoniae antibodies, and future ischemic cerebral infarctions. Furthermore, no evidence of an interactive effect between high Lp(a) levels and C pneumoniae IgG titers was found. However, selection bias and a recent C pneumoniae epidemic may have influenced the results.

Antibodies, Bacterial↗
PubMed1993

Ticlopidine improves the enhanced erythrocyte aggregability in patients with cerebral infarction.

BACKGROUND AND PURPOSE: We examined the effect of ticlopidine hydrochloride on the enhanced erythrocyte aggregability in 14 patients with cerebral infarction during the chronic phase (over 1 month after onset). SUMMARY OF REPORT: Ticlopidine (100 mg BID) was administered for 8 weeks. We measured the rate of erythrocyte aggregation (aggregability), using the whole-blood erythrocyte aggregometer that we developed, before and at 4 and 8 weeks after the initiation of ticlopidine administration. Concomitant measurements were made of such blood factors as the hematocrit, albumin-globulin ratio, and fibrinogen concentration. The erythrocyte aggregation rates before and at 4 and 8 weeks after were 0.147 +/- 0.017/s, 0.138 +/- 0.019/s, and 0.133 +/- 0.017/s, respectively. The erythrocyte aggregation rates at 4 and 8 weeks were significantly lower (P < .05 by Bonferroni's modified t test) than those before ticlopidine administration. At 4 and 8 weeks after the initiation of ticlopidine treatment, the hematocrit value and concentration of fibrinogen were also significantly (P < .05) reduced. CONCLUSIONS: Our results suggest that ticlopidine can improve the enhanced erythrocyte aggregability in patients with cerebral infarction during the chronic phase.

Adult↗
PubMed1993

Analysis of IMP-SPECT in cerebral infarcts.

We performed single photon emission computed tomography with N-isopropyl[123I]-p-iodoamphetamine in 22 normal volunteers (mean age, 68.3 +/- 9.5 years) and 190 patients with unilateral cerebral infarcts (66.1 +/- 11.4 years). We then compared visual and semiquantitative assessment of the left/right ratio of the early images. Cerebral blood flow in the patients with cerebral infarcts was compared with data from normal volunteers. An abnormal left/right ratio was recognized in 110 of 136 (81%) patients in whom X-ray computed tomography (CT) showed an abnormality, while visual inspection revealed abnormalities in only 99 (73%). In 54 patients no abnormality on CT, an abnormal left/right ratio was found in 28 (52%), and visual abnormalities in only 9 (17%). Altogether, the left/right ratio was abnormal in 138 of 190 (73%) patients, and abnormalities were detected visually in 108 (57%). Of 95 patients, 56 (59%) showed markedly larger lesions using the left/right ratio method than with the visual method.

Aged↗
PubMed1977

An ultrastructural study of developing cerebral infarction following bilateral carotid artery occlusion in spontaneously hypertensive rats.

An ultrastructural study of cerebral infarcts in spontaneously hypertensive rats 1--5 h after bilateral carotid artery occlusion was performed. The alteration of the neocortex consisted of shrinkage of the neurons surrounded by swollen astrocytic processes. Distension of the rough endoplasmic reticulum of the neuronal cytoplasm appeared early, while changes of the mitochondria were slight. Though there appeared slight to moderate perivascular astrocytic swelling, endothelial swelling was rare and there was no severe narrowing of the capillary lumen. There were no filling defects of colloidal carbon injected to the blood vessels of the ischemic brains. Ischemic neuronal alterations were proved to develop in the absence of severe morphological changes of the microvasculature in the developing cerebral infarcts in the present experimental model.

Animals↗
PubMed1998

[Palpebral ptosis and blepharospasm secondary to hemispheric cerebral infarction].

A case that combines cerebral eyelid ptosis and blepharospasm secondary to cerebral hemisphere infarction is shown. EMG recording from the facial and eyelid muscles revealed lack of the levator palpebrae superioris, orbicularis oculi and corrugator muscles activity. Any voluntary opening attempt lead to a simultaneous contraction of the three muscles. Blink reflex responses were normal although showed facilitation features on the right side and mild inhibition characteristics from the left side. Median nerve SEP revealed a loss of precentral components (P22-N30) as well as a delay and amplitude decrease of N20. Transcranial magnetic stimulation disclosed a complete lesion of corticospinal pathway for right upper limb. In this case, a right hemisphere lesion caused an unusual eyelid motor abnormality: cerebral eyelid ptosis and blepharospasm induced by the voluntary eyelid opening.

Aged↗
PubMed1984

Determination of regional cerebral blood flow in patients with cerebral infarction. Use of fluoromethane labeled with fluorine 18 and positron emission tomography.

Regional cerebral blood flow (rCBF) was determined using the tissue kinetic of fluoromethane labeled with fluorine 18 and positron emission tomography (PET) in 13 normal subjects and 21 patients with cerebrovascular diseases. The mean brain rCBF was 42.9 +/- 4.3 mL/100 g/min during the resting state. The highest rCBF (60 +/- 8 mL/100 g/min) was noted in the mesial occipital region corresponding to cortical area 17. All 17 cases of cerebral ischemic infarcts had depressed rCBF in the hemisphere ipsilateral to the infarct. Every area of decreased density shown in the conventional computed tomograms (CT) was detected on the PET as an area of decreased rCBF (mean rCBF of infarcted area, 14.3 +/- 6 mL/100 g/min). The PET images showed a wider area of depressed rCBF than the region of the anatomic infarct. Five types of remote effects were noted in areas without structural damage: (1) decreased flow in the thalamus and caudate ipsilateral to the infarct; (2) decreased flow in the hemisphere contralateral to the cerebral infarct; (3) decreased flow in the cerebellar hemisphere contralateral to the cerebral infarct; (4) decreased flow in the visual cortex distal to the optic radiation lesion; and (5) decreased flow in the frontal cortex ipsilateral to the infarct. The effects in the contralateral hemisphere and the cerebellum were present only in the acute postictal phase. In four cases of transient ischemic attacks, rCBF was normal. It is concluded that this technique of measuring rCBF is a reliable method of identifying cerebral ischemia and that the determination of the extent of impaired rCBF provides a more accurate assessment of the region of brain dysfunction than CTs.

Adult↗
PubMed1998

Increased expression of P-selectin on platelets is a risk factor for silent cerebral infarction in patients with atrial fibrillation: role of nitric oxide.

BACKGROUND: Platelet activation and decreased levels of nitrite and nitrate (NOx), stable end products of nitric oxide (NO), are reported in patients with atrial fibrillation (AF). We examined the time-course changes in plasma NOx levels and the expression of P-selectin on platelets after the onset of AF in a canine model and determined whether these parameters could be risk factors for silent cerebral infarction in patients with AF. METHODS AND RESULTS: AF was induced by rapid atrial pacing in the canine model of AF. Plasma NOx levels were significantly decreased and the levels of P-selectin on platelets and of neutrophil/platelet conjugates were significantly increased after the onset of AF in this model. The in vitro experiments demonstrated that the inhibition of NO synthesis increased the expression of P-selectin on platelets. Plasma NOx levels (19.7+/-2.4 versus 27.5+/-2.8 micromol/L) were significantly lower in 25 patients with AF compared with age- (+/-2 years) and sex-matched control subjects. Conversely, the levels of P-selectin on platelets (7.6+/-0.8% versus 4.8+/-0.7%) and of neutrophil/platelet conjugates (14.8+/-0.9% versus 8.1+/-0.6%) were significantly higher in patients with AF. Multiple regression analysis revealed that increased P-selectin on platelets and advanced age were associated with the number of foci of silent cerebral infarction. CONCLUSIONS: An irregular heart rate that is characteristic of AF appeared to blunt NO synthesis. The increased expression of P-selectin on platelets associated with the reduced NO levels was a risk factor for silent cerebral infarction in patients with AF.

Adult↗
PubMed1995

[Hemorrhagic cerebral infarction at the old age in a case with familial antithrombin III (ATIII) deficiency].

An old woman had stroke at age 67. Cerebral CT scan disclosed the low-density lesion with high-density area in the left temporal lobe, but no empty delta sign in the superior sagittal sinus. Thereafter, she had sometimes panic attacks. At the age of 70, she was admitted because of loss of consciousness probably caused by the same attack. On admission, Brain CT scan showed no fresh lesions. During the stay in the hospital, she had an episode of deep vein thrombosis of her left leg. The patient was found to have not only reduced biochemical activity but also low immunological level of AT III. Her nephew had also the low plasma AT III antigen concentration. Transesophageal echocardiography showed no abnormality, but atherosclerotic change at the aortic arch. We speculated that hemorrhagic cerebral infarction in the territory of the branch of middle cerebral artery could be induced by the arterial thrombus which was related to the hypercoagulable state associated with familial AT III deficiency, although the possibility of cardiogenic embolic infarction or of cerebral vein thrombosis could not be ruled out. Familial AT III deficiency is one of the causes of cerebral infarction even in the elderly.

Aged↗
PubMed1988

Cerebral infarction in sickle cell anemia: mechanism based on CT and MRI.

We studied 25 patients with sickle cell anemia and cerebral infarction. We classified lesions as to probable mechanism (large versus small vessel disease) based on the CT/MRI appearance of established infarction. Most patients had CT/MRI patterns of major cerebral vessel occlusion (41%) or border-zone (distal insufficiency) infarcts (31%) best explained by large cerebral vessel vasculopathy. Seven of 25 (28%) had either isolated subcortical (12%) or small cortical branch occlusion (16%) consistent with other mechanisms such as small vessel occlusion or embolism. These results suggest that most clinically recognized cerebral infarctions in sickle cell anemia are caused by large vessel disease, but this mechanism may not account for symptoms of cerebral ischemia in all cases.

Adolescent↗
PubMedDate not supplied

Hemorrhagic cerebral infarction--a prospective study.

In 65 cases of ischemic cerebral infarction, CT scans and quantitative assessments of the neurological disturbances were undertaken at specific intervals during the 4 week period after stroke. Forty-three patients underwent lumbar puncture to determine the serum/CSF albumin ratio. The etiology of the infarction was evaluated on the basis of angiographic, ultrasonic and cardiologic findings. A hemorrhagic transformation of the infarction occurred in 28 patients, eleven within the first week, and 15 within the second. Risks of hemorrhage were correlated with a severe neurological deficit, disturbance of consciousness, large infarction with a mass effect, enhancement of contrast medium in CT (especially if occurring early), involvement of the cortex, and distinct blood/CSF barrier disturbances. Cardiac embolism was a frequent etiology in patients with secondary hemorrhagic infarction, especially when transformation occurred within the first week after stroke. In addition to a heterogeneous pattern of hemorrhage, frank hematoma predominated in those infarcts which underwent early transformation, while those transforming late often showed less hyperdense cortical hemorrhagic changes. Deterioration evident on clinical evaluation was caused by the hemorrhagic transformation in three cases, in each instance within the first week after stroke.

Adult↗
PubMed2004

Serial urinary 11-dehydrothromboxane B2, aspirin dose, and vascular events in blacks after recent cerebral infarction.

BACKGROUND AND PURPOSE: Incomplete platelet inhibition by aspirin (aspirin resistance) may be a reason for stroke recurrence in some patients. 11-dehydrothromboxane B2 (11-DTB2) is a stable thromboxane A2 metabolite that reflects in vivo platelet activation. This pilot study was intended to evaluate the reproducibility of urinary 11-DTB2 over time and to look for evidence of aspirin resistance. METHODS: All subjects were screened for the African American Antiplatelet Stroke Prevention Study (AAASPS) 7 to 90 days after noncardioembolic cerebral infarction. Of 83 subjects with at least 1 urine sample, 52 were enrolled in AAASPS (randomized to blinded treatment with aspirin 650 mg/d or ticlopidine 500 mg/d), and 31 were enrolled in an open-label antiplatelet therapy cohort. Subjects were followed up for 2 years, with 11-DTB2 measurements scheduled at baseline and 6, 12, and 24 months. Vascular events were cerebral infarction, myocardial infarction, or vascular death. RESULTS: Despite considerable individual up or down fluctuations, the median 11-DTB2 change did not significantly differ from zero in any of the subgroups. However, in 6 subjects with a 4-fold decrease in aspirin dose from 1300 to 325 or 81 mg/d, the 11-DTB2 level increased from 611 to 1881 pg/mg creatinine (P=0.06). Vascular events occurred in 7 of 61 aspirin-treated subjects, and 11-DTB2 levels did not correlate with the events. CONCLUSIONS: Fluctuations in urinary 11-DTB2 after cerebral infarction in blacks do not correlate with changes in aspirin doses, except perhaps when the dose changes by a factor of 4 or more. A larger study is needed to look further for aspirin resistance.

Anti-Inflammatory Agents, Non-Steroidal↗
PubMed1991

[Pathological and etiological studies on cerebral infarction in the vertebrobasilar arterial system].

25 cases of cerebral infarcts in vertebrobasilar arterial system are reported. Those were divided into 4 groups: 1. Embolism (10), the causes were NBTE, pulmonary infarct, rheumatic or congenital heart disease, coronary artery disease, respectively, and 2 unknown. 2. Thrombosis (5), the causes were arteriosclerosis, vascular malformations in the basal part of cerebrum. 3. Inflammatory infarcts (3), those were verified from tuberculosis, syphilis and aspergillosis respectively. 4. Lacunar infarcts (7), the causes were considered from hypertension. Pathologically, it was noticed that the location of embolism often situated at the terminal of basilar artery, and that if the embolism was completely obliterated, often a hemorrhagic infarction would follow. But the thrombosis in basilar artery, even the lumen was completely obliterated, any infarct would not follow, if the related collateral circulation was satisfactory. Clinically, the embolism in basilar artery often showed sudden onset, and that the symptoms of brain stem would aggravate quickly, but the thrombosis in basilar artery, if the collateral circulation was satisfactory, and symptom of brain stem might not follow.

Adult↗
PubMed1991

Risks factors for cerebral infarction in good-grade patients after aneurysmal subarachnoid hemorrhage and surgery: a prospective study.

A prospective series of 265 patients with aneurysmal subarachnoid hemorrhage (SAH) of Grades I to III (Hunt and Hess classification) upon admission were evaluated as to neurological outcome and computerized tomography (CT) findings 1 to 3 years (mean 1.4 years) after the SAH and surgery. A total of 73 patients underwent acute surgery (within 72 hours after the bleed: Days 0 to 3), 86 were operated on subacutely (between Days 4 and 7), and 91 had late surgery (on Day 8 or later). Fifteen patients died before surgery was undertaken and another 20 patients died during the follow-up period. A total of 104 patients received nimodipine and the rest of the patients received either placebo (109 patients) or no medication (52 patients). A logistical regression analysis revealed the following prognostic factors for cerebral infarction, in order of importance: the amount of blood on the primary CT scan; postoperative angiographic vasospasm; the timing of the operation; and a history of hypertension. The use of nimodipine was associated with a significant reduction of cerebral infarcts visualized by CT scanning in patients who received intermediate or late surgery. In patients who underwent acute surgery no significant difference between the incidence of cerebral infarcts was observed.

Adolescent↗
PubMedDate not supplied

Correlation of tibial nerve SEPs with the development of seizures in patients with supratentorial cerebral infarcts.

In 40 patients with supratentorial non-haemorrhagic cerebral infarct, the findings in the tibial nerve SEPs recorded during the acute stage correlated significantly with the development of seizures during a 1 year follow-up period. Abnormality in the side-to-side difference of the P40-N48 amplitude was the finding with the highest correlation with the development of seizures: 87.5% of the patients were classified correctly as to the risk of seizures.

Adult↗
PubMed1999

Neonatal cerebral infarction: an under recognised/unreconised cause of neonatal seizures?

Neonatal cerebral infarction or neonatal stroke is a well recognised cause of neonatal seizures. The awareness of its existence among healthcare workers is low and it is not even mentioned as a cause of neonatal seizures in most books. Many of the affected neonates are well, without any evidence of neurological disturbances between seizures. Awareness of its existence among healthcare workers is critical for the diagnosis of this problem. Early diagnosis can lead to early intervention, which may mean a better prognosis for these children.

Cerebral Infarction↗
PubMedDate not supplied

Cerebral infarction following bilateral carotid artery ligation in normotensive and spontaneously hypertensive rats: a pathological study.

A pathological examination was performed on normotensive rats (NTR) and spontaneously hypertensive rats (SHR) following bilateral common carotid artery ligation. After ligation, diffuse and extensive cerebral infarcts in the carotid artery territory occurred frequently in SHR, while NTR occasionally had well-circumscribed small infarcts. The posterior communicating arteries, which are the major anastomotic channels connecting the carotid and vertebrobasilar systems, did not show any anomalies and were well developed in SHR and NTR. Vascular changes secondary to hypertension, such as fibrinoid necrosis or thickening of the wall, were not observed in SHR. Because of the paucity of structural difference of the blood vessels, the more diffuse and extensive cerebral infarcts in SHR after carotid occlusion were attributed to the hemodynamic difference rather than the morphological difference between the two groups. The results of the present experiment suggest that hypertension per se, i.e., hemodynamic factors, may be operative for the development of cerebral infarction.

Animals↗
PubMedDate not supplied

[Hematocrit value and hemoglobin concentration as possible risk factors in non-embolic acute cerebral infarcts].

The hematocrit and the concentration of hemoglobin have been studied in 197 patients (125 men and 72 women) suffering from acute cerebral infarction not due to embolism. The results have been analysed statistically and compared to those of a control group formed by 123 neurologic patients (68 men and 55 women) chosen at random, belonging to the same age range and with no cerebrovascular disease. The hematocrit was significantly higher in the patients who had a cerebral stroke of a non-embolic origin, both males and females, than in the control group, although it was within normal limits. As far as the concentration of hemoglobin is concerned, there is a significant statistical difference between patients with and without cerebral infarction, but only for the female patients.

Adult↗
PubMed2003

[Usefulness of CT-perfusion in acute cerebral infarction].

CT-perfusion (CTP) examination was performed in 30 cases of acute cerebral infarction (ACI) caused by middle cerebral artery (MCA) occlusion. Data were analyzed using cerebral blood flow (CBF), cerebral blood volume (CBV), and mean transit time (MTT). The results of the affected side were compared with those of the other side in terms of relative value and difference. A high correlation in relative value was found between CBF and CBV (r=0.81) and in both the relative (r=0.76) and difference (r=0.77) value between CBF and MTT. No correlation was seen between CBV and MTT. The time-density curve, along with CBF, CBV, and MTT, was classified into three patterns of ischemic brain damage: collateral, delayed, and flat patterns. In conclusion, CT-perfusion examination is useful for determining a treatment plan in ACI.

Acute Disease↗