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PubMed2000

Silent cerebral infarction: a potential risk for pneumonia in the elderly.

OBJECTIVE: To determine whether patients who have silent cerebral infarction are more likely to develop pneumonia than are controls without silent cerebral infarction. DESIGN: We examined 269 community-residing participants of the senior day-care centre without history of previous stroke, and then followed them over a two-year period to assess pneumonia. On the basis of computerized tomography scans, they were divided into two groups: no infarction (n = 102) and cerebral hemispheric infarction (n = 167). Cerebral infarcts were further divided into deep and superficial infarcts. RESULTS: The incidence of pneumonia was significantly higher in subjects with silent cerebral infarction (19.8%) than in controls (4. 9%) (odds ratio, 4.67 [95% CI, 1.87-11.67]; P < 0.01). Deep infarcts were more closely associated with the incidence of pneumonia (29.1%) than superficial infarcts (7.6%) (odds ratio, 5.00 [CI, 1.91-13.08]; P < 0.01). CONCLUSIONS: Elderly subjects with silent cerebral infarction were more likely to develop pneumonia than were controls without silent cerebral infarction. Amongst hemispheric silent cerebral infarcts, those located in the deep brain structures may be an important predictor of the development of pneumonia.

Aged↗
PubMed1997

Unilateral neonatal cerebral infarction in full term infants.

AIMS: To determine the prevalence of unilateral neonatal cerebral infarction in infants born at 32 weeks gestation and above; to describe the clinical course, imaging results, and outcome of neonatal cerebral infarction; and to investigate possible aetiology. METHODS: Twelve cases of unilateral neonatal cerebral infarction were identified from neonatal unit records for the years 1987-93. Each case was matched with two controls. RESULTS: All cases of neonatal cerebral infarction occurred in full term infants. The prevalence was around 1 in 4000, and neonatal cerebral infarction was found in 12% of infants presenting with neonatal seizures. Cerebral ultrasound scans failed to demonstrate lesions seen by computed tomography in nine of 12 cases. Cases were more likely than controls to require assisted ventilation for resuscitation at birth (OR 7.0, 95% confidence interval 1.04-53.5), but Apgar scores at 5 minutes were no different. One infant with neonatal cerebral infarction developed a hemiparesis, the other 11 had normal motor development when assessed at 11-60 (median 33) months. None had overt cognitive deficits or persisting seizure disorder. CONCLUSIONS: Neonatal cerebral infarction is a relatively common cause of neonatal seizures, but the aetiology remains unclear. Parents need to be made aware of possible neurological sequelae, but most cases in this series had a normal outcome.

Cerebral Infarction↗
PubMed2006

Experimental study on plasticity of proliferated neural stem cells in adult rats after cerebral infarction.

OBJECTIVE: To investigate whether there is endogenous neural stem cell proliferation and whether these proliferated neural stem cells represent neural plasticity in the adult rats after cerebral infarction. METHODS: Cerebral infarction models of rats were established and the dynamic expression of bromodeoxyuridine (BrdU), BrdU/polysialylated neural cell adhesion molecule (PSA-NCAM) were determined by immunohistochemistry and immunofluorescence staining. BrdU was used to mark dividing neural stem cells. PSA-NCAM was used to mark the plasticity of neural stem cells. RESULTS: Compared with controls, the number of BrdU-positive cells in the subventricular zone (SVZ) and hippocampus increased significantly at 1st day after cerebral infarction (P < 0.05), reached maximum at 7th day, decreased markedly at 14th day, but it was still elevated compared with that of the controls (P < 0.05). The number of BrdU-labeled with PSA-NCAM-positive cells increased significantly at 7th day (P < 0.05), reached maximum at 14th day, markedly decreased at 28th day, but it was still elevated compared with that of the controls (P < 0.05). It was equal to 60% of the number of BrdU-positive cells in the same period. CONCLUSION: Cerebral infarction may stimulate the proliferation of endogenous neural stem cells in situ and most proliferated neural stem cells represent neural plasticity.

Animals↗
PubMed1994

The effect of age on cerebral oedema, cerebral infarction and neuroprotective potential in experimental occlusive stroke.

A model of occlusive stroke in the aging brain has been developed and used to evaluate the effects of age upon cerebral infarction, cerebral oedema and neuroprotective potential. Focal ischaemia following left middle cerebral artery occlusion has been compared in aged (30 month) and adult (< 17 month) rats, with histological assessment of infarct volume and analysis of specific gravity as an index of cerebral oedema. Aging was associated with a significant increase in cerebral infarct size. The mean infarct volume in aged rats was 40.5% +/- 2.6% of the hemisphere volume, compared to 30.9% +/- 0.7% in adults (p < 0.01). Pre-treatment with the competitive N-Methyl-D-Aspartate (NMDA) receptor antagonist 3-(2-Carboxy Piperazin-4-yl)Propyl-l-Phosphonate (D-CPP-ene) reduced infarct volumes in both age groups to 33.0% +/- 1.8% and 20.7% +/- 3.2% in aged and adult animals, respectively (p < 0.05). There was significantly less oedema of the cerebral cortex in D-CPP-ene pre-treated rats; mean cortical specific gravity 4 hours post-infarction was 1.0381 +/- 0.0013 in untreated aged rats and 1.0391 +/- 0.0014 in untreated adults, compared to 1.0458 +/- 0.0031 in treated aged rats and 1.0442 +/- 0.0014 in treated adults (p < 0.05). At 24 hours post-infarction, D-CPP-ene pre-treated aged rats had a mean cortical specific gravity of 1.0403 +/- 0.0006 compared to 1.0361 +/- 0.0014 in untreated aged animals (p < 0.05). This study has demonstrated an age-related increase in cerebral infarct size, but has shown that the aging brain is amenable to neuroprotection by NMDA receptor antagonism.

Age Factors↗
PubMed2003

Relation of cerebral infarctions to dementia and cognitive function in older persons.

BACKGROUND: Cerebral infarctions are common in older persons but their relationship with dementia and cognitive function remains controversial. METHODS: Participants were 164 older Catholic nuns, priests, and brothers who underwent annual clinical evaluation and brain autopsy at death. The authors quantified number and volume of old cerebral infarctions on postmortem examination and determined the association with dementia and cognitive function proximate to death. Analyses controlled for age, sex, and education. RESULTS: A total of 58 (35.4%) subjects had cerebral infarctions: 29 had one infarction and 29 had multiple infarctions. In logistic regression analyses, infarctions increased the odds of dementia twofold (OR 2.12; 95% CI 1.06 to 4.25). The odds of dementia increased by 2.67-fold for multiple infarctions (95% CI 1.08 to 6.61), whereas the odds of dementia with single infarctions increased by 69% (95% CI 0.70 to 4.09). In linear regression analyses, there was a trend for multiple infarctions to be associated with lower global cognitive scores (-0.44 standard units, p = 0.057). Multiple infarctions were related to perceptual speed, visuospatial skills, and working memory, but not to episodic or semantic memory. The authors found similar results with infarction volume. In secondary analyses, only infarctions that were clinically evident during life were associated with dementia and cognitive function. CONCLUSION: Cerebral infarctions are associated with a twofold increase in odds of dementia. Odds are higher in persons with multiple, large, or clinically evident infarctions. In addition, cerebral infarctions do not affect all cognitive systems equally, showing the strongest association with perceptual speed and the weakest with episodic memory.

Aged↗
PubMed1995

[The effect of serum glucose level on acute cerebral infarction].

The relationship between the serum glucose level and the cerebral infarct size, neurological deficits, morbidity outcome, complications and mortality was investigated in 198 acute cerebral infarction patients confirmed by computerized tomography. The results suggested that patients with hyperglycemia had larger infarct size, more neurological deficits, worse morbidity outcome, more complications and higher mortality than their normoglycemic counterparts. Our findings indicated that the elevated blood glucose level in most of the patients with cerebral infarction may be a stress response or a marifestation of latent diabetes. We considered that the hyperglycemia was a factor aggravating cerebral infarction and enhancing the degree of neurological deficit and morphological brain damage. The authors are of the opinion that insulin administration be advised in acute cerebral infarction patients with hyperglycemia so as to prevent further deterioration and improve the outcome.

Acute Disease↗
PubMed1994

The magnetization transfer effect in cerebral infarction.

PURPOSE: To estimate the age of cerebral infarcts using magnetization transfer. METHODS: Twelve patients with radiographically and clinically documented cortical and subcortical cerebral infarctions underwent MR imaging on a 0.1T magnet. Magnetization transfer contrast images were generated by application of off-resonance pulses to every other repetition time on intermediate-weighted images. The magnetization transfer effect was calculated by obtaining an intensity value in the region of interest within the infarcted area. RESULTS: The data show a pattern in which the magnetization transfer effect decreases as the chronicity of the infarct increases. Infarcts less than 1 week old had an average magnetization transfer effect of 0.35. Those more than 1 week and less than 1 month old average 0.30. Infarcts more than 1 month and specifically those more than 1 year old averaged 0.16 or less. CONCLUSION: Magnetization transfer offers the potential to estimate the age of cerebral infarcts.

Acute Disease↗
PubMed1997

Patent foramen ovale in patients with cerebral infarction. A transesophageal echocardiographic study.

OBJECTIVES: To determine the frequency of patent foramen ovale (PFO) among various subtypes of cerebral infarction. To determine whether any historical or clinical characteristics predict the presence or absence of PFO in these patients. DESIGN: Comorbidity and infarct subtype study. SETTING: Referral-based study. PATIENTS: One hundred sixteen patients with cerebral infarction consecutively referred for transesophageal echocardiography during a 6-month period. MAIN OUTCOME MEASURES: Infarct subtype classification was made using a clinical and radiographic diagnostic rubric similar to that used by the Stroke Data Bank of the National Institute of Neurological Diseases and Stroke. The frequency of various risk factors and clinical characteristics in patients with and in those without PFO and the frequency of PFO in patients with various infarct subtypes were compared (chi 2 or Fisher exact tests). RESULTS: Patent foramen ovale was detected in 37 patients (32%). Mean age was similar in those with (60 years) and those without (64 years) PFO. Patent foramen ovale was more frequent among men (39%) than women (20%, P = .03). Patients with PFO had a lower frequency of atrial fibrillation, diabetes mellitus, hypertension, and peripheral vascular disease compared with those without PFO. There was no difference in frequency of the following characteristics in patients with PFO compared with those without PFO: pulmonary embolus, chronic obstructive pulmonary disease, pulmonary hypertension, peripheral embolism, prior cerebral infarction, nosocomial cerebral infarction, Valsalva maneuver at the same time of cerebral infarction, recent surgery, or hemorrhagic transformation of cerebral infarction. Patent foramen ovale was found in 22 (40%) of 55 patients with infarcts of uncertain cause and in 15 (25%) of 61 with infarcts of known cause (cardioembolic, 21%; large vessel atherostenosis, 25%; lacune, 40%) (P = .08). When the analysis was restricted to patients who underwent Valsalva maneuver, PFO with right to left or bidirectional shunt was found in 19 (50%) of 38 patients with infarcts of uncertain cause and in 6 (20%) of 30 with infarcts of known cause (P = .01). CONCLUSION: Although PFO was overrepresented in patients with infarcts of uncertain in our and other studies, it has a high frequency among patients with cerebral infarction of all types. The relation between PFO and stroke requires further study.

Aged↗
PubMed2000

ME3277, a GPIIb/IIIa antagonist reduces cerebral infarction without enhancing intracranial hemorrhage in photothrombotic occlusion of rabbit middle cerebral artery.

GPIIb/IIIa antagonists are expected to have a beneficial effect on acute cerebral infarction, however, the occurrence of intracranial hemorrhage has not been as widely investigated. A rabbit focal thrombotic occlusion model of the middle cerebral artery was established by creating a photochemical reaction between green light and Rose Bengal. Hemorrhagic transformation was common in the area of cerebral infarction. Using this model, the effect of a GPIIb/IIIa antagonist, ME3277 (low dose, (L); 0.15 mg/kg + 0.125 mg/kg x h, middle dose, (M); 0.3 mg/kg + 0.25 mg/kg x h and high dose, (H); 0.6 mg/kg + 0.5 mg/kg x h), aspirin (20 mg/kg) and sodium ozagrel (thromboxane A2 synthase inhibitor, 1 mg/kg + 2 mg/ kg x h) were evaluated. Drugs were intravenously administrated 30 minutes after the photochemical reaction for 24 hours. Aspirin inhibited the ex vivo platelet aggregation induced by arachidonic acid and collagen but not by adenosine diphosphate (ADP), while sodium ozagrel only inhibited the arachidonic acid-induced aggregation. ME3277 dose-dependently inhibited the platelet aggregation induced by all the inducers (approximately 60% in L, 80% in M, and 90% in H). At 24 hours of middle cerebral artery (MCA) occlusion, infarct volume was significantly reduced by aspirin and each dose of ME3277. These agents improved neurologic deficits, with ME3277 being more potent than aspirin. Sodium ozagrel did not alter the infarct volume nor neurologic deficits. No drug was found to worsen hemorrhage volume despite increasing bleeding time (2-3 fold) in the skin. In this model, the occluded artery was spontaneously recanalized and re-thrombosed frequently. One mechanism by which antiplatelet agents reduced infarct volume was inhibition of rethrombosis of the MCA. These results suggest that treatment with a GPIIb/IIIa antagonist is a useful intervention for acute cerebral infarction prolonging dose bleeding time to 3 times the basal value.

Amides↗
PubMed1993

[Temporal lobectomy in cerebral infarction with mass effect].

Cerebral edema secondary to ischemia can threaten life, mainly due to frequent failure of medical management. Imminent herniation of the temporal lobe can be timely detected by clinical signs and CT-scan. Eight patients (4M, 4F; 48-74 years, mean 62) with ischemic stroke and imminent herniation, were surgically decompressed by a standard temporal lobectomy as described by Olivier for temporal lobe epilepsy. Six patients survived, two died and were considered failure of the procedure, probably due to late surgical indication. In conclusion, temporal lobectomy is life-saving for patients with large ischemic cerebral infarction with mass effect and deteriorating signs of brain stem compression.

Aged↗
PubMed1992

Fetal cortical cells survive in focal cerebral infarct after permanent occlusion of the middle cerebral artery in adult rats.

Fetal rat cortical cells have been shown previously to survive at the periphery of cerebral infarction. The present study was designed to examine the ability of fetal cells to survive at the edge of the central core of ischemia. In three groups of 8 adult Sprague-Dawley rats, fetal cortical cells from ED 16 were stereotactically transplanted at 3 h, 24 h, and 7 days after unilateral middle cerebral artery occlusion. In 6 rats, fetal cells were transplanted by using the same coordinates, without arterial occlusion, for control. In the ischemic groups, overall graft survival was 85%, and in the control group, all grafts survived. Graft survival was determined by light microscopy. No significant difference was found in the survival of grafts transplanted at different intervals after middle cerebral artery occlusion. It is concluded that fetal cortical cells can survive in cerebral tissue undergoing severe ischemic change.

Animals↗
PubMed2000

Possible existence of platelet activation before the onset of cerebral infarction.

To study the existence of platelet activation before the onset of cerebral infarction, the ultrastructural features of platelets (7-day survival) and coagulation-fibrinolytic markers (70-100-min life span) were measured 2-12 h (acute phase), 7 days (subacute phase) and 6 months (chronic phase) after onset in 18 patients with cerebral infarction. Seven patients with atherosclerosis but without cerebral infarction and eight healthy subjects were studied as controls. Ultrastructural study included folds, pseudopods, vacuoles and centralization in addition to immunochemical staining such as platelet peroxidase and fibrinogen. Furthermore, beta-thromboglobulin, platelet factor-4, thrombin antithrombin complex and alpha(2)-plasmin inhibitor plasmin complex were examined as coagulation-fibrinolytic markers. Ultrastructural study of circulating platelets demonstrated no difference between acute and chronic phases and little difference between cerebral infarction and atherosclerosis, although plasma coagulation-fibrinolytic markers showed an increase in cerebral infarction at the acute phase but no difference among the chronic phase of cerebral infarction, atherosclerosis and normal healthy subjects. It is considered that shape change in circulating platelets was caused by pre-existed atherosclerosis rather than the thrombotic event itself though coagulation-fibrinolytic markers were derived from the thrombotic event.

Aged↗
PubMed1999

[Current techniques in MR imaging of cerebral infarction].

The imaging of cerebral infarction is a current topic now that the usefulness of both thrombolysis for hyperacute infarction and carotid endarterectomy has been established. Diffusion-weighted imaging (DWI) by EPI is a highly sensitive method of detecting hyperacute infarction. Further, the combination of DWI and perfusion MR makes it possible to detect hyperacute infarction as well as predict the final size of infarction. Contrast-enhanced MRA can demonstrate carotid bifurcation without flow-related signal loss within 30 seconds and can visualize major cervical arteries from the aortic arch to the circle of Willis.

Adult↗
PubMedDate not supplied

Hematocrit and clinical outcome in acute cerebral infarction.

Hematocrits of 131 cerebral infarction cases were correlated with the outcome at 2 weeks. Bivariate analysis showed that cases with more intense admission deficit had lower admission hematocrit and that cases with poorer outcome had lower Day 2 and 4 hematocrits. However, multivariate analysis of several prognostic factors (including hematocrit, glycemia, blood pressure, age, and sex) showed that hematocrit was not independently related to outcome. Higher hematocrit thus is not indicative of less favorable short-term outcome.

Cerebral Infarction↗
PubMedDate not supplied

CT demonstration of calcification within old cerebral infarcts.

Calcifications within old cerebral infarcts were demonstrated by CT in three patients who had suffered strokes probably due to emboli from a carotid or cardiac source. In two of them, calcifications were not shown on CT at onset but were first noted on follow-up CT approximately 2 years later in one, and 5 years later in the other. In the third case a large solitary calcification was found on the first CT carried out 13 years after onset. To our knowledge, these findings have not been described previously.

Brain Diseases↗
PubMed2005

Cerebral infarcts complicating tuberculous meningitis.

Cerebral infarction (CI) is a serious complication of tuberculous meningitis (TBM). It can be asymptomatic or symptomatic, causing stroke. We studied 40 TBM patients. All had initial CT brain scan, CT/MRI brain scan 3 months later and urgent CT brain scan for deterioration. CI was classified into lacunar infarction (LI) or large artery infarction (LAI). Twelve (30%) had CI, in 9 (23%) it was symptomatic and in 3 (8%) silent. Seven (58%) had LAI +/- LI. Eight (67%) had multiple CI. Two died from brainstem CI and 6 were dependent at 1 year. Patients with LAI might develop posterior circulation CI more frequently than those with LI only. CI is a common complication of TBM locally, with LAI and multiple CI being common. Two thirds of TBM patients complicated by CI had poor prognosis despite adjunctive dexamethasone treatment.

Adolescent↗
PubMed1988

Neurofibrillary tangle formation in the nucleus basalis of Meynert ipsilateral to a massive cerebral infarct.

Two cases of massive cerebral infarct in the territory of the middle cerebral artery on one side of the brain are presented, in which many (Patient 1) or several (Patient 2) neurofibrillary tangle-bearing neurons were observed in the nucleus basalis of Meynert (nbM), ipsilateral to the infarcts. Tangles were absent or rare in the opposite nbM or in other areas of the brain. Considering the widespread projection of nbM axons to the ipsilateral cerebral cortex, this suggests that formation of neurofibrillary tangles can occur as a retrograde reaction in nbM neurons secondary to massive, old cerebral infarction.

Aged↗
PubMed2006

[Prevention of vascular events after transient ischemic attack or cerebral infarct].

After a first cerebral ischemic event, secondary prevention should be started as soon as possible, especially in transient ischemic attacks where the risk of recurrence is the highest, especially during the first week, needing a diagnostic workup in a short period of time, secondary prevention measures depending on the presumed cause of the event. Secondary prevention of vascular events after transient ischemic attack or cerebral infarct consists of 3 types of strategies: 1. treatment of risk factors for stroke, especially high blood pressure, high cholesterol and smoking cessation; 2. aspirin (50 to 325 mg), or clopidogrel, or association aspirine-dipyridamole in high-risk subjects, or warfarin in patients with high-risk cardiopathies; and 3. carotid surgery in patients selected by clinical and imaging criteria. Other strategies are currently partly under evaluation: statins in normocholesterolemic ischemic stroke patients without coronary event, angioplasty with stenting. Audits of practice are necessary to determine whether patients are actually treated according to scientific evidence. This is a crucial issue if we want the results of trials to be translated in the true life, and really improve health at the community level.

Angioplasty, Balloon↗