Search PubMed⌕ Search

SEARCH · Search PubMed

Results for “Brain 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 757 records · Page 42Linked to original sources
PubMed1994

Aberrant distribution of tyrosine hydroxylase and substance P in infants with brain-stem infarction.

The distribution of tyrosine hydroxylase (TH) and substance P (SP) was examined in the brain-stem of 4 infants with respiratory abnormalities associated with remote brain-stem or cerebellar infarction utilizing immunohistochemical methods. TH-immunoreactive cells and SP-immunoreactive fibers were found in and around the area of the infarction in the tegmentum, in amounts and sites different from that seen in controls. The aberrant localization of SP and TH may represent an altered repair process associated with resolution of the infarction and may be related to abnormal respiratory control or sudden death.

Brain Stem↗
PubMed2005

Depression-executive dysfunction syndrome in stroke patients.

OBJECTIVE: It has been suggested that executive dysfunction could be the core defect in patients with geriatric or vascular depression, and that this depression-dysexecutive syndrome (DES) might be related to frontal-subcortical circuit dysfunction. The authors tested this hypothesis in 158 poststroke patients, of whom 21 had both depression and executive dysfunction. METHODS: In this cross-sectional cohort study, a neurological, psychiatric, and neuropsychological examination was carried out 3 months after ischemic stroke, and brain infarcts, white-matter changes, and brain atrophy were recorded by MRI. RESULTS: The 21 patients with DES had significantly more brain infarcts affecting their frontal-subcortical circuit structures than the 137 patients without DES, or the 41 patients with depression but without executive dysfunction. Patients with DES also had more severe depressive symptoms and worse psychosocial functioning, and they coped less well in complex activities of daily living. CONCLUSIONS: DES is a valid concept and may define a subgroup of poststroke patients with frontal-subcortical pathology and with distinct prognosis and treatment options.

Aged↗
PubMed2005

[The value of diffusion MR imaging in judging pathological changes of brain multiple sclerosis].

OBJECTIVE: To analyze the findings of MR diffusion weighted imaging (DWI) and diffusion tensor Imaging (DTI) in patients with multiple sclerosis (MS), and to explore their role in reflecting the pathological changes of MR lesions. METHODS: DWI and DTI were performed on 41 MS cases and 25 sub-acute brain infarct cases which used as control group. The appearances of ADC maps, EADC maps and FA maps in patients of both groups were analyzed. Quantitative analysis of the values of ADC, EADC and FA in the center and periphery of the lesions of acute MS, chronic MS and sub-acute brain infarct was carried out separately. RESULT: In DWI, the small chronic lesions were iso-intensity, and the large acute MS lesions and the sub-acute-infarct lesions had a high signal intensity to various degrees. In the EADC map, only in 13 cases with acute MS around the peripheral zone of the lesions there was a high signal intensity, and all other cases, including the cases with chronic MS and brain infarct had no high signal lesions. The ADC values of chronic and infarct lesions were similar (P > 0.05), both of them had the highest ADC value which were higher than the signal intensity in the center (both P < 0.05) and the periphery (both P < 0.05) of the MS lesions. The FA values in the infarct lesions were the lowest, much more lower than that in the chronic MS lesions (P < 0.05). The FA value in the center of acute MS lesions was lower than that in the peripheral zone (P < 0.05), and higher than the FA value both in the chronic MS and infarct lesions (P < 0.05). The lowest ADC value outside the peripheral zone of acute MS lesions and the highest EADC value were found. CONCLUSION: The significance of DWI high signal in the diagnosis and differential diagnosis of MS is not reliable, so the patient's history and the findings found in the routine MRI must be conjugated when an imaging diagnosis is made. The EADC map is more accurate than ADC map for showing the diffusion restriction of water molecular in the MS lesions. The degree of increase of the ADC value and the degree of decease of the FA value are proportional to the degree of severity of the pathological changes of the MS lesions.

Adolescent↗
PubMed1996

Risk of stroke in a cohort of 815 patients with calcification of the aortic valve with or without stenosis.

BACKGROUND AND PURPOSE: We sought to establish the possible role of calcification of the aortic valve with or without stenosis as a risk factor for stroke. METHODS: Occurrences of stroke, stroke subtypes, and concomitant cardiovascular risk factors were prospectively analyzed in 300 patients with echocardiographic evidence of aortic valve calcification, 515 patients with calcified aortic valve stenosis, and 562 control subjects. RESULTS: Twenty-four patients with aortic valve calcification, 24 patients with calcified aortic valve stenosis, and 27 control subjects had a stroke during follow-up. Using Cox proportional hazards models, we found that strokes were not significantly associated with aortic valve calcification with or without stenosis, but hypertension and any carotid stenosis were associated. On multiple logistic regression analysis, we did not find any association between one of the two valve lesions and indirect possible indications of cardiogenic embolism such as territorial as opposed to small deep brain infarcts or the presence of silent brain infarcts. CONCLUSIONS: Aortic valve calcification with or without stenosis is not a risk factor for stroke.

Age Factors↗
PubMed2006

Isoflurane tolerance against focal cerebral ischemia is attenuated by adenosine A1 receptor antagonists.

PURPOSE: To investigate the role of the adenosine A1 receptor in the rapid tolerance to cerebral ischemia induced by isoflurane preconditioning. METHODS: Seventy-five rats were randomly assigned into five groups (n = 15 each): Control, 8-cyclopentyl-1,3-dipropulxanthine (DPCPX), Isoflurane, DPCPX+Isoflurane and Vehicle+Isoflurane groups. All animals underwent right middle cerebral artery occlusion (MCAO) for two hours. Isoflurane preconditioning was conducted one hour before MCAO in Isoflurane, DPCPX+Isoflurane and Vehicle+Isoflurane groups by exposing the animals to 1.5% isoflurane in 98% oxygen for one hour. In the Control and DPCPX groups, animals were exposed to 98% oxygen one hour before MCAO for one hour. A selective adenosine A1 receptor antagonist, DPCPX, was administered (0.1 mg x kg(-1)) 15 min before isoflurane/oxygen exposure in the DPCPX and DPCPX+Isoflurane groups to evaluate the effect of adenosine A1 receptor antagonist on isoflurane preconditioning. Dimethyl sulfoxide, the solvent of DPCPX, was administered (1 mL x kg(-1)) 15 min before isoflurane exposure in the Vehicle+Isoflurane group. Neurological deficit scores and brain infarct volumes were evaluated 24 hr after reperfusion. RESULTS: Animals in the Isoflurane and Vehicle+Isoflurane groups developed lower neurological deficit scores and smaller brain infarct volumes than the Control group (P < 0.01). Animals in the DPCPX+Isoflurane group developed higher neurological deficit scores and larger brain infarct volumes than the Isoflurane and Vehicle+Isoflurane groups (P < 0.01). CONCLUSION: The present study demonstrates that preconditioning with isoflurane reduces focal cerebral ischemic injury in rats, and the adenosine A1 receptor antagonist (DPCPX) attenuates the neuroprotection induced by isoflurane preconditioning.

Adenosine A1 Receptor Antagonists↗
PubMedDate not supplied

[The blood level of uric acid as a risk factor in transient cerebral ischemic attacks and in non-embolic acute cerebral infarct].

The serum uric acid level has been determined in 300 patients, both males and females. 125 of these suffered from transient cerebral ischaemic attacks and 175 from atherothrombotic brain infarction. The values obtained were compared with those determined, with the same technique, in a control group of patients with neurologic diseases, chosen at random, and with no clinical finding or historical data of cerebrovascular and/or cardiac disease. No significant statistical difference has been observed between the mean serum uric acid level in the patients with transient ischaemic attacks, or brain infarction, and the control group. All the patients examined were divided according to sex and age. As far as sex was concerned, males suffering from cerebral transient or completed focal ischaemia, had on average a lower serum uric acid level compared to the control group. The opposite happened with females. As far as age was concerned, significantly high serum uric acid levels, compared to the control group, were observed in women with either transient ischaemic attacks or brain infarction, but only in those whose age range was between 50 and 60. In conclusion, from this study, hyperuricemia does not appear to be a high risk factor in ischaemic cerebrovascular diseases.

Adult↗
PubMed2000

Electronystagmographic findings in patients with acute cerebral vascular disease and vertigo.

A neurootologist examined 233 successive cases of acute disabling vertigo from the Clinic of Neurology of Turku University Central Hospital. On magnetic resonance imaging (MRI), 24 patients had evidence of acute cerebral or cerebellar brain infarction. The examination scheme included a case history analysis, clinical neurootological examination and electronystagmography (ENG). The audiological examination included pure-tone thresholds and speech audiometry. The ENG analyses were done by two neurootologists who had no information about the aetiology of the diseases. A central disturbance in ENG was observed in 59% (10/17) of the patients with cerebral brain infarction and 71% (5/7) of the patients with cerebellar brain infarction. ENG is not valid as a screening method for the central aetiology of vertigo; imaging of the central nervous system is needed.

Acute Disease↗
PubMed2004

The selective Na+-Ca2+ exchange inhibitor attenuates brain edema after radiofrequency lesion in rats.

2-[4-[(2,5-Difluorophenyl)methoxy]phenoxy]-5-ethoxyaniline (SEA0400), a specific inhibitor of the Na+-Ca2+ exchanger, exerts cytoprotective action and reduces brain infarct volume after cerebral ischemia. We examined the effect of SEA0400 on vasogenic brain edema in rats. Histological observations showed that radiofrequency current caused brain infarct and extravasation of endogenous albumin in the brain. SEA0400 (3 and 10 mg/kg, i.v.) significantly suppressed the increase in brain water content with attenuation of Evans blue dye and sodium fluorescein extravasation after radiofrequency lesion. The findings suggest that the Na+-Ca2+ exchanger plays a role in vasogenic edema formation after radiofrequency lesion.

Aniline Compounds↗
PubMed2006

Exercise preconditioning upregulates cerebral integrins and enhances cerebrovascular integrity in ischemic rats.

We hypothesized that exercise preconditioning strengthens brain microvascular integrity against ischemia/reperfusion injury through the tumor necrosis factor (TNF)-integrin signaling pathway. Adult male Sprague Dawley rats (n = 24) were studied in: (1) exercise (the animals run on a treadmill 30 min each day) for 3 weeks, (2) non-exercise. Six animals from each group (n = 12) were subjected to stroke, the remaining animals served as controls (n = 6 x 2). Brain infarction and edema were determined by Nissl staining. Cerebral integrin expression was detected by immunochemistry and stereological methods. In addition, we used flow cytometry to address the causal role of TNF-alpha in inducing the expression of integrins in the human umbilical vein endothelial cells under TNF-alpha or vascular endothelial growth factor (VEGF) pretreatment. Exercise reduces brain infarction and brain edema in stroke. Expressions of integrin subunit alpha(1), alpha(6), beta(1), and beta(4) were increased after exercise. Exercise preconditioning reversed stroke-reduced integrin expression. An in vitro study revealed a causal link between the gradual upregulation of TNF-alpha (rather than VEGF) and cellular expression of integrins. These results demonstrated an increase in cerebral expression of integrins and a decrease in brain injury from stroke after exercise preconditioning. The study suggests that upregulation of integrins during exercise enhances neurovascular integrity after stroke. The changes in integrins might be altered by TNF-alpha.

Animals↗
PubMed2004

Diffusion-weighted magnetic resonance imaging in internal carotid artery dissection.

BACKGROUND: Acute multiple brain infarction pattern on diffusion-weighted imaging is associated with arterial or cardiac sources of embolism. OBJECTIVES: To review the diffusion-weighted imaging characteristics of patients with strokes secondary to internal carotid artery (ICA) dissection and to gain further insights into the mechanisms of cerebral ischemia. DESIGN: Patients with ICA dissection and ischemic stroke were identified by review of an angiographic database and hospital discharge codes. Patients were included if the diagnosis of ICA dissection was confirmed and diffusion-weighted imaging was obtained within 10 days of symptom onset. Infarct patterns were analyzed according to established templates of vascular territories. RESULTS: Inclusion criteria were met by 14 patients. Internal carotid artery occlusion was present in 10. Acute multiple brain infarction was found in 10 (71%) of the 14 patients. Cortical involvement was found in 8 patients, while the infarct was restricted to the subcortical region in 6. In 9 (64%) of the 14 patients, ischemic lesions were located in 1 of the 3 border zones. CONCLUSIONS: Acute multiple brain infarction pattern with border zone involvement is frequently found in ICA dissection-related strokes. This finding may further support an interaction of hemodynamic and embolic mechanisms as a cause of cerebral ischemia in this condition.

Acute Disease↗
PubMed2001

Expression of P-selectin and intercellular adhesion molecule-1 in human brain after focal infarction or cardiac arrest.

Data from experimental studies indicate that acute inflammation contributes to ischaemic brain damage. Tethering of neutrophils to brain endothelium is mediated by selectins, and subsequent adhesion and migration by endothelial intercellular adhesion molecule-1 (ICAM-1) and neutrophil CD18. In experimental studies of ischaemia-reperfusion injury, brain damage has been ameliorated by administration of antibodies to these adhesion molecules. We studied the expression of P-selectin and ICAM-1 in sections of brain from patients who had experienced cardiac arrest or focal brain infarction, and who died 3.5 h to 9 days later. Endothelial immunopositivity for both adhesion molecules was maximal at about 2-3 days then declined. Between 1 day and 3 days, P-selectin was also detected on platelets in blood vessels within infarcted tissue. Within infarcts, but not sections of brain from cardiac arrest patients, P-selectin and ICAM-1 were again detectable at 1 week, when hyperplastic endothelial cells were labelled in capillaries in and immediately adjacent to the infarcted tissue. The finding that P-selectin and ICAM-1 are upregulated within focally infarcted brain tissue supports the concept that blocking neutrophil adhesion may be of benefit in treating atherothrombotic strokes in man.

Adult↗
PubMedDate not supplied

Survival and recurrence following stroke. The Framingham study.

Survival and recurrences after stroke were assessed prospectively in a general population sample of 5184 subjects followed biennially for 26 years. Initial strokes occurred in 198 men and 196 women. There were 84 second and 27 third strokes and 223 deaths reported. Thirty day case-fatality rates for initial strokes were: 15% (33/222) for brain infarction, 16% (10/63) for cerebral embolus, 46% (18/39) for subarachnoid hemorrhage, and 82% (14/17) for intracerebral hemorrhage. Cumulative, age-adjusted 5 year survival rates for brain infarction were reduced by pre-stroke cardiac disease (coronary heart disease and/or congestive heart failure) and hypertension prior to initial stroke from .85 to .35 in men and .70 and .56 in women. Hypertension alone reduced survival from .85 to .51 in men, but not in women. Recurrences were primarily of the same type as the initial stroke. Cumulative 5 year recurrence rate for brain infarction was .42 for men, almost double that for women. Rates were reduced by excluding hypertensives and those with combined cardiac comorbidity and hypertension. Thus, risk of death or recurrence after stroke is substantial and profoundly influenced by sex and by cardiac comorbidity and hypertension present prior to the initial event.

Adult↗
PubMed2005

Measures of brain morphology and infarction in the framingham heart study: establishing what is normal.

Numerous anatomical and brain imaging studies find substantial differences in brain structure between men and women across the span of human aging. The ability to extend the results of many of these studies to the general population is limited, however, due to the generally small sample size and restrictive health criteria of these studies. Moreover, little attention has been paid to the possible impact of brain infarction on age-related differences in regional brain volumes. Given the current lack of normative data on gender and aging related differences in regional brain morphology, particularly with regard to the impact of brain infarctions, we chose to quantify brain MRIs from more than 2200 male and female participants of the Framingham Heart Study who ranged in age from 34 to 97 years. We believe that MRI analysis of the Framingham Heart Study more closely represents the general population enabling more accurate estimates of regional brain changes that occur as the consequence of normal aging. As predicted, men had significantly larger brain volumes than women, but these differences were generally not significant after correcting for gender related differences in head size. Age explained approximately 50% of total cerebral brain volume differences, but age-related differences were generally small prior to age 50, declining substantially thereafter. Frontal lobe volumes showed the greatest decline with age (approximately 12%), whereas smaller differences were found for the temporal lobes (approximately 9%). Age-related differences in occipital and parietal lobe were modest. Age-related gender differences were generally small, except for the frontal lobe where men had significantly smaller lobar brain volumes throughout the age range studied. The prevalence of MRI infarction was common after age 50, increased linearly with age and was associated with significantly larger white matter hyperintensity (WMH) volumes beyond that associated with age-related differences in these measures. Amongst men, the presence of MRI infarction was associated with significant age-related reductions in total brain volume. Finally, statistically significant associations were found between the volume of MRI infarcts in cubic centimeters and all brain measures with the exception of parietal lobe volume for individuals where the volume of MRI infarctions was measured. These data serve to define age and gender differences in brain morphology for the Framingham Heart Study. To the degree participants of the Framingham Heart Study are representative the general population, these data can serve as norms for comparison with morphological brain changes associated with aging and disease. In this regard, these cross-sectional quantitative estimates suggest that age-related tissue loss differs quantitatively and qualitatively across brain regions with only minor differences between men and women. In addition, MRI evidence of cerebrovascular disease is common to the aging process and associated with smaller regional brain volumes for a given age, particularly for men. We believe quantitative MRI studies of the Framingham community enables exploration of numerous issues ranging from understanding normal neurobiology of brain aging to assessing the impact of various health factors, particularly those related to cerebrovascular disease, that appear important to maintaining brain health for the general population.

Adult↗
PubMed1999

Transient mutism resolving into cerebellar speech after brain stem infarction following a traumatic injury of the vertebral artery in a child.

A 3.7-year-old girl presented with an anterior neck injury followed by progressive subcutaneous emphysema and loss of consciousness. After resuscitation, a laceration on the first tracheal cartilage was closed surgically. As she was extubated one week later, she was found to have right hemiplegia and muteness. MRI showed a T2-bright lesion on the tegmentum of the left midbrain down to the upper pons. Right vertebral angiography disclosed an intimal flap with stenosis at the C3 vertebral level presumably caused by a fracture of the right C3 transverse process later confirmed in a cervical 3D-CT scan. Her muteness lasted for 10 days, after which she began to utter some comprehensible words in a dysarthric fashion. Her neurological deficits showed improvement within 3 months of her admission. Transient mutism after brain stem infarction has not been reported previously. We discuss the anatomical bases for this unusual reversible disorder in the light of previous observations and conclude that bilateral damage to the dentatothalamocortical fibers at the decussation of the superior cerebellar peduncle may have been responsible for her transient mutism.

Brain Mapping↗
PubMed2000

How well does the Oxfordshire community stroke project classification predict the site and size of the infarct on brain imaging?

OBJECTIVES: The Oxfordshire Community Stroke Project (OCSP) classification is a simple clinical scheme for subdividing first ever acute stroke. Several small studies have shown that when an infarct is visible on CT or MRI, the classification predicts its site in about three quarters of patients. The aim was to further investigate this relation in a much larger cohort of patients in hospital with ischaemic stroke. METHODS: Between 1994 and 1997, inpatients and outpatients with ischaemic stroke were assessed by one of several stroke physicians who noted the OCSP classification. A neuroradiologist classified the site and extent of recent infarction on CT or MRI. RESULTS: Of 1012 patients with ischaemic stroke, 655 (65%) had recent visible infarcts. These radiological lesions were appropriate to the clinical classification in 69/87 (79%) patients with a total anterior circulation syndrome, 213/298 (71%) with a partial anterior circulation syndrome, 105/144 (73%) with a lacunar syndrome, and 105/126 (83%) with a posterior circulation syndrome. Overall, 75% of patients with visible infarcts were correctly classified clinically. If patients without a visible infarct did have an appropriate lesion in the brain (best case), the classification would have correctly predicted its site and size in 849/1012 (84%) patients, compared with only 492/1012 (49%) in the worst case scenario. CONCLUSION: The OCSP classification predicted the site of infarct in three quarters of patients. When an infarct is visible on brain imaging, the site of the infarct should guide the use of further investigations, but if an infarct is not seen, the OCSP classification could be used to predict its likely size and site.

Aged↗
PubMed2004

Apotransferrin, C1-esterase inhibitor, and alpha 1-acid glycoprotein for cerebral protection during experimental hypothermic circulatory arrest.

BACKGROUND: Because of current limitations in improving metabolic support to the brain during hypothermic circulatory arrest (HCA), attenuation of ischemia-reperfusion injury remains an area of therapeutic intervention of relevance. Apotransferrin (Apo-Tf), alpha 1-acid glycoprotein (AGP), and C1-esterase inhibitor (C1-INH) have been herein evaluated as potential beneficial agents in reducing the ischemia-reperfusion injury in a surviving model of HCA. METHODS: Apo-Tf 100 mg/kg (n = 6), C1-INH 50 IU/kg (n = 6), AGP 100 mg/kg (n = 6), or NaCl 0.9% 2 ml/kg (n = 6) were randomly administered to 24 juvenile pigs after a 75-min period HCA at a brain temperature of 18 degrees C. RESULTS: Animals in the Apo-Tf group had a slightly better 7-day survival (66.7%) compared with the other study groups (50%), but such a difference was not statistically significant. Some favorable changes in the brain glucose metabolism parameters were observed in the AGP, C1-INH, and Apo-Tf groups, but these did not reach statistical significance. Semiquantitative analysis of the histopathological findings did not show any significant difference between the study groups. However, only two out of four surviving animals in the Apo-Tf group developed brain infarction, whereas all three survivors of the remaining study groups developed brain infarction. CONCLUSIONS: Although the small size of the study groups may affect the present findings, none of the metabolic and hemodynamic parameters as well as outcome endpoints indicate a substantial therapeutic efficacy of Apo-Tf, AGP, and C1-INH as neuroprotective agents after experimental HCA.

Animal Experimentation↗
PubMed1980

[Immunologic reactivity in the acute phase of a stroke].

Examinations of the clinical and immunological state of 68 patients with the acute stage of cerebral stroke were carried out, and so were immunomorphological examinations of the spleen and the subclavicular lymph nodes in 36 of them whose disease ended in death. An analysis of the results obtained has shown that the immunological reactivity increases from the very first day of the disease. The authors believe that the early immunological response, especially in cases of brain infarction, is due to development of the cerebral stroke in a sensitized body. A rise of selective antibody titres depending on the character of the cerebrovascular disorder was noted: there were: anti-encephalic antibodies targeted at the malacia focus in cases of brain infarction, and antivascular, and to a lesser extent anti-encephalic antibodies in cases of a hemorrhagic stroke. The informative value of the complement fixation test was found to be greater than that of the hemagglutination inhibition test. High degrees of plasmatization of the splenic tissue and the presence of the anti-encephalic immune complexes in it, mainly in cases of brain infarction, also point to the activity of the immunogenesis in the acute stage of the cerebral stroke.

Acute Disease↗