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PubMed2005

Risk factors for early infection after an acute cerebral infarction.

BACKGROUND AND OBJECTIVE: Infection is a common complication after an acute stroke. This is important because it may cause death or delayed successful rehabilitation. Investigation of the risk factors for infection after an acute stroke is limited The objective of this study was to determine the risk factors for early infection after an acute cerebral infarction. DESIGN: Retrospective analystical study. MATERIAL AND METHOD: The medical records of patients admitted within 48 hours of onset of symptoms to Prasat Neurological Institute from 1 January 2002 to 31 December 2003, with a diagnosis of cerebral infarction, confirmed with CT or MRI of the brain were retrospectively studied. Collected data included clinical features, risk factors for stroke, comorbid conditions, infection, and results of diagnosis tests. Univariate and multiple logistic regression analyses were used to determine factors that were associated with the risk of early infection. RESULTS: During the 24-month study period, 332 cerebral infarct patients were identified. Early infection occurred in 7.6%. The most common infection was pneumonia (4.3%). In the final multiple logistic model, independent risk factors for early infections were atrial fibrillation (OR, 9.31; 95% CI, 2.18-39.75), thromboembolic infarction (large vessel disease) (OR, 6.04; 95% CI, 1.97-18.54), admission conscious level (subconscious or unconscious/coma) (OR, 4.82; 95% CI, 1.60-14.55) and previous stroke (OR, 3.20; 95% CI, 1.21-8.47) respectively. CONCLUSION: Atrial fibrillation, thromboembolic infarction (large vessel disease), admission conscious level (subconscious or unconscious/coma), and previous stroke were independent risk factors for development of early infection.

Aged↗
PubMed2003

Racial differences in survival post cerebral infarction among the elderly.

OBJECTIVE: To investigate whether there are differences in poststroke survival between African American and white patients, aged 65 and over, in the United States. METHODS: A biracial cohort of patients was selected from a random 20% national sample of Medicare patients (age 65 and over) hospitalized with cerebral infarction in 1991, and was followed up to a period of 3 years. The Cox regression model was used for covariate adjustment. RESULTS: A total of 47,045 patients (including 5,324 African Americans) were identified for our analysis. Compared to white patients, African American patients on average were 6% more likely to die post cerebral infarction. The subpopulation analyses further suggest that African Americans age 65 to 74 had much lower 3-year survival probabilities (15 to 20%) than their white counterparts. CONCLUSIONS: The authors find evidence of racial disparities in survival post cerebral infarction among the elderly, although the differences by race are not as great as reported elsewhere for stroke incidence and mortality. Future analyses, using more clinically detailed data, should focus especially on whether survival differences by race persist in the young-old (age 65 to 74) population.

Black or African American↗
PubMed1983

Mucin and fat emboli in mucinous carcinomas. Cause of hemorrhagic cerebral infarcts.

A patient with a mucin-producing carcinoma of the breast died after three weeks of progressive neurologic deterioration. At autopsy, numerous small hemorrhagic cerebral infarcts of varying ages were found. The infarcts were primarily located in arterial boundary zones of cerebral and cerebellar hemispheres. They were associated with numerous mucin and fat emboli. In any unexplained cerebral infarct in patients with mucin-producing carcinoma, mucin and fat emboli should be considered and searched for.

Adenocarcinoma, Mucinous↗
PubMed1995

Acute subdural hematoma associated with cerebral infarction in the full-term neonate.

Acute subdural hematomas in the full-term neonate are usually thought to be a manifestation of birth trauma. Most commonly, these hematomas are associated with a tentorial tear, and less frequently are secondary to damage to the occipital sinus accompanying occipital osteodiastasis, or to rupture of bridging superficial cerebral convexity veins. We report 6 cases of acute subdural hematoma associated with cerebral infarction (SDH/CI) in term neonates, an entity which has not been well-documented previously. This combination accounted for half the cases of neonatal acute subdural hematomas referred to a pediatric neurosurgical service. All children presented within 72 h of birth, usually after an uneventful delivery, and typically with seizures (5/6), apneic spells (3/6) and a full or bulging fontanel (5/6). Although the patients were referred to the neurosurgical servive for management of a convexity subdural hematoma, the CT scans showed a large associated cerebral infarct, which was hemorrhagic in 5 of the 6 cases, most commonly in the distribution of the middle cerebral artery. Craniotomy was performed in 4 patients, needle aspiration of the subdural hematoma in 1, and no surgical intervention in 1. The outcome in 3 patients, who have been followed for more than 1 year, has been good, with some mild focal neurologic deficits, but no seizure activity. The pathogenesis of this entity is unclear, but the acute subdural hematoma in these cases is probably secondary to the cerebral infarction. Recognition of SDH/CI as a specific entity in term neonates has significant management and possibly medicolegal implications.

Brain Damage, Chronic↗
PubMed2004

Cerebral infarction as a complication of nephrotic syndrome: a case report with a review of the literature.

Arterial thrombosis is relatively rare compared with venous thrombosis in nephrotic syndrome. However, the assessment of its pathogenesis and risk factors in individual patient with nephrotic syndrome is necessary to allow appropriate prophylactic management because it is a potentially serious problem. Hereby, with review of the literature, we report a case of a 53 yr-old man with cerebral infarction associated with nephrotic syndrome due to focal segmental glomerulosclerosis during the course of treatments with diuretics and steroid. It reveals that the hypercoagulable state in nephrotic syndrome can be associated with cerebral infarction in adults. Prophylactic anticoagulants can be considered to reduce the risk of serious cerebral infarction in nephrotic patients with risk factors such as severe hypoalbuminemia and on diuretics or steroid treatment, even in young patients regardless of types of underlying glomerular diseases.

Cerebral Infarction↗
PubMed2004

[Acute onset of somnolence and amnesia due to cerebral infarction of bilateral thalamus accompanied with tuberculous meningitis: a case report].

A 55-year-old man was admitted to our hospital because of somnolence and aspontaneity. He was hospitalized in the psychopathic ward under the initial diagnosis of depression. Chest X-ray showed infiltration in both upper lobe. Twelve days later, Mycobacterium tuberculosis was detected from his sputum and was confirmed by RT-PCR. Cerebrospinal fluid findings showed elevated ADA and mononuclear cells, suggesting the presence of tuberculous meningitis. However, the brain CT revealed no abnormal findings. By applying antituberculous treatment the pulmonary lesion improved but psychological symptoms remained. Three months later follow-up brain MRI was examined. Contrast enhanced granuloma was detected in the ambiens, suprasellar and quadrigeminal cisterns. A strong signal was seen in the left frontal thalamus and a weak enhanced lesion was detected in the right frontal thalamus on a T2 enhanced image. These lesions showed low intensity on a T1 enhanced image, suggesting cerebral infarction affecting the bilateral thalamus. Somnolence and memory disorder was due to cerebral infarction of the bilateral thalamus and tuberculous meningitis contributed to form the intracranial lesion. From the experience of this case, it is needed to consider cerebral infarction (especially the thalamus) due to tuberculous meningitis when we examine the patients with acute onset of psychological symptoms.

Amnesia↗
PubMed1999

[Effect of integrated Traditional Chinese and Western medicine on immune function in patient of acute cerebral infarction].

OBJECTIVE: To investigate the change of serum soluble vascular cell adhesion molecule-1 (sVCAM-1) in acute cerebral infarction patients treated with integrated traditional Chinese and western medicine (TCM-WM). METHODS: Serum sVCAM-1 level of patients treated with TCM-WM or western medicine alone was measured by ELISA, and compared with that of healthy person. RESULTS: TCM-WM could reduce the sVCAM-1 level in patients with cerebral infarction (P < 0.05). The therapeutic effect of TCM-WM was better than that of western treatment alone, P < 0.05. CONCLUSION: The therapeutic mechanism of TCM-WM may be related with the modulation on immune status of patients.

Aged↗
PubMed1997

[Cerebral infarction due to stenosis of the bilateral internal carotid artery in Turner's syndrome].

A 43-year-old woman was admitted into our hospital because of aphasia and right hemiparesis. Computed tomographic scan demonstrated border zone infarction in the anterior and middle cerebral artery. Magnetic resonance imaging scans showed the borderline area between the terminal branches of the lenticulostriate arteries and the perforating branches of the middle cerebral artery. Digital subtraction ICA angiogram showed severe narrowing of the distal portion of the right and left ICA. A pattern analysis of ambulatory blood pressure monitoring (ABPM) was carried out in this patient, and it was showed "dipper type". Laboratory data was elevated excretion of pituitary gonadotropines and low estrogen excretion. Chromosome analysis revealed the 45, X/46, XX. She was diagnosed with mosaic type of Turner's syndrome. The cerebrovascular abnormality might be due to congenital hypoplasia of arteries, and declining of blood pressure during sleep was possible significant factors in the pathogenesis of cerebral infarction in this patient.

Adult↗
PubMed1986

Effect of cilostazol on experimental cerebral infarction in rabbits.

The effects of 6-[4-(1-cyclohexyl-1H-tetrazol-5-yl)butoxy]-3, 4-dihydro-2(1H)-quinolinone (cilostazol, OPC-13013), acetylsalicylic acid (ASA) and ifenprodil on experimentally induced cerebral infarction were studied in anesthetized rabbits. Cerebral infarction was induced by injecting arachidonic acid (AA) at a dose of 0.5 mg/kg into the unilateral intracarotid artery. After the injection of AA, the brain was perfused with Indian ink, and the degree of thrombus formation was determined by calculating the percentage of perfused area in the hemispheres. The intracarotid injection of AA produced a non-perfused area amounting to 84% of the hemisphere in the injected side and 41% of the hemisphere in the non-injected side. Intravenously administered cilostazol did not produce a definite reduction in carbon-deficient area at 0.1 mg/kg, but it did produce a 49% reduction in the injected side and a 55% reduction in the entire brain at 1 mg/kg. ASA produced a 60% reduction in the carbon-deficient area in the injected side and a 62% reduction in the entire brain at 1 mg/kg. Ifenprodil at 1 mg/kg produced only a 19% reduction in the carbon-deficient area in the injected side.

Animals↗
PubMed1987

[Diagnosis of a cerebral infarct with a hemorrhagic component].

Using computerized methods the authors have analyzed formalized case histories of three variants of an acute disorder of the cerebral circulation in the matter of the cerebral hemispheres verified by pathoanatomical studies: (1) cerebral infarction with a hemorrhagic component (n = 88), (2) a gray ischemic cerebral stroke (n = 80), (3) parenchymatous hemorrhage (n = 71). The informative symptoms and symptom complexes identified can be employed for the differentiation between cerebral infarction with a hemorrhagic component and other types of strokes.

Acute Disease↗
PubMed2000

[Exploration on parameters of TCM syndrome in acute cerebral infarction through investigating active factors of vascular endothelium cells].

OBJECTIVE: To explore the multiple parameters of TCM Syndrome-types and the acute cerebral infarction (ACI) with blood stasis type. METHODS: Sixty-six acute cerebral infarction patients with blood stasis Syndrome, various vascular active factors such as tissue plasminogen activator (t-PA), the activity of plasminogen activator inhibitor (PAI), the concentration of prostaglandin F1 alpha (6-keto-PGF1 alpha) etc. were determined. RESULTS: (1) In Incidental Syndrome, those "Phlegm" and "stasis" predominant, mainly manifested as Wind-Phlegm-Blood stasis (WPBS), Qi deficiency-blood stasis (QDBS) and Phlegm-Heat-bowel excess (PHBE) Syndrome all showed t-PA activity lowered, among them, QDBS Syndrome lowered more obviously (P < 0.01); and in fundamental deficiency predominant Syndrome such as Yin-deficiency and Wind-move (YDWM) Syndrome, the active t-PA content increased (P < 0.05); in Liver Yang ascending (LYA) Syndrome and YDWM Syndrome, the 6-keto-PGF1 alpha lowered very significantly. (2) Through regression analysis, although influencing the severity of acute blood stasis was related with 3 factors (t-PA activity, nervous system defect score and age growth), but single factor linear relationship analysis indicated that did not existed positive-negative relationship. (3) Through statistical analysis, the factor influencing nervous system defect scores was positively related with blood stasis score (r = 0.70, P < 0.01). CONCLUSION: (1) The basis of WPBS, QDBS and PHBE Syndrome mainly was fibrinolytic system activity lowering, and YDWM and LYA Syndrome prostaglandin system activity lowering. Comprehensive analysis of multiple parameters would be helpful to differentiate the ACI blood stasis stage. (2) Single parameter would not help to differentiate the types of ACI blood stasis stage, its change merely denoted the existence of blood stasis, its type should be differentiated after comprehensive analysis. (3) Those influencing nervous system scoring, mainly was blood stasis score, which suggested that the importance of activating blood circulation to remove stasis in preventing and treating ACI. (4) Put forward ACI blood stasis, and the quantification for new standard of Syndrome for discussion.

6-Ketoprostaglandin F1 alpha↗
PubMed1993

Factors associated with occurrence of large vessel and lacunar cerebral infarctions.

A stroke registry was developed to determine the localizing value of various clinical data. Adequate localization was achieved in 98% of 246 patients with infarcts. Among 212 male patients with cerebral infarcts not due to cardiogenic embolism or an unusual etiology, there were 152 with large-vessel and 59 with lacunar infarcts. Logistic regression analysis of factors associated with large vessel and lacunar stroke identified myocardial infarction on ECG as the only statistically significant variable; its presence was associated with an odds ratio for lacunar infarction of 0.19 (95% confidence interval 0.06-0.66) (P = 0.009). Logistic regression analysis of factors associated with anterior and posterior circulation large vessel stroke identified pack years of smoking as the only statistically significant variable; the odds ratio for posterior circulation infarction for a 10-year increment in pack years of smoking was 0.83 (95% confidence interval 0.73-0.94) (P = 0.0035).

Age Factors↗
PubMed1980

Neonatal polycythemia causing multiple cerebral infarcts.

A child had neonatal polycythemia, severe seizures beginning at 6 weeks of age, and a computerized tomography scan showing multiple cerebral infarcts. Follow-up showed substantial developmental delay with spastic quadriplegia. This case illustrates that neonatal polycythemia is a rare but preventable cause of multiple cerebral infarctions, subsequent seizures, and developmental delay.

Cerebral Infarction↗
PubMed1991

[Effect of diabetes mellitus and blood glucose on the size of cerebral infarction and causes of death. Neuropathological study of 77 cases of infarction in the sylvian artery area].

The influence of diabetes mellitus and hyperglycemia on cerebral infarction has been studied on 77 patients who died of infarcts in the territory of the middle cerebral artery. The size of the infarcts was assessed by transferring the surface of the infarcted area onto 8 schematic drawings corresponding to 8 brain slices and measuring this surface by means of a planimeter. An infarction volume index (IVI) was calculated by measuring the ratio of the infarcted area to the theoretical area of the middle cerebral artery territory on the 8 slices. The causes of death were assessed by full post-mortem examination. There was no statistically significant difference in size of infarcts and causes of death between diabetics and non-diabetics. However, the stroke-to-death interval was shorter (p = 0.05) in non-diabetic patients. It appears from this study that diabetes mellitus has no deleterious effect on cerebral infarction. Equally, there were non statistically significant differences in size of infarcts, stroke-to-death interval and causes of death between patients with and without hyperglycemia.

Aged↗
PubMed1978

An angiographic study of brain swelling in cerebral infarction.

In order to assess the characteristics of brain swelling due to infarction, 322 angiograms in patients with cerebral infarction have been reviewed. The rate of incidence of swelling related to time from onset, sequential angiographic changes, and factors contributing to the phenomenon are presented. Some clinical and differential diagnostic aspects are discussed.

Brain Edema↗
PubMed1992

[Cerebral infarction, placoid epitheliopathy and sarcoidosis].

We report a case of cerebral infarction in the basal territory of the left middle cerebral artery, associated with acute posterior multifocal placoid pigment epitheliopathy, most probably due to sarcoidosis. Neurological symptoms resolved spontaneously without sequelae. We discuss the relationship between acute posterior multifocal placoid pigment epitheliopathy, sarcoidosis and cerebral granulomatous angiitis.

Adult↗
PubMedDate not supplied

Subacute and chronic cerebral infarctions: SPECT and gadolinium-DTPA enhanced MR imaging.

Single photon emission computed tomography (SPECT) examinations of regional cerebral blood flow (rCBF) and regional cerebral blood volume (rCBV) were carried out in 23 patients with 19 subacute and 7 chronic cerebral infarctions. Corresponding magnetic resonance (MR) examinations (unenhanced and contrast enhanced scans) were done within a time interval of 2 days. Although all subacute lesions showed an increased rCBV, the rCBF could be either increased or decreased. Contrast enhancement in MR was associated with increased rCBV but not with increased rCBF. In all chronic lesions rCBV and rCBF were decreased and there was no contrast enhancement detectable in MR. The application of Gd-diethylenetriamine pentaacetic acid as contrast agent in MR demonstrates blood-brain barrier disruption as focal or gyral contrast enhancement in cerebral infarction. The SPECT examinations revealed an increased rCBV indicating a vasodilation or vasoparalysis. The rCBF was either increased or decreased depending on the collateral formation or recanalization of occluded vessels.

Adult↗
PubMed1993

Spa bathing activates fibrinolysis in patients with cerebral infarction.

The effects of spa bathing on blood coagulation and fibrinolysis were studied in 20 patients with chronic cerebral infarction. Blood was obtained before and after a 10-minute period of spa bathing at 41 degrees C. Prothrombin time, activated partial thromboplastin time, fibrinogen, factor VIII activity, von Willebrand factor activity, and antithrombin III activity did not show significant changes after bathing, but euglobulin lysis time was significantly reduced (p < 0.01) and fibrin lysis activity was increased (p < 0.05). These findings suggest that spa bathing activates fibrinolysis without markedly changing blood coagulation in patients with chronic cerebral infarction. It is thought that the activation of fibrinolysis without the activation of coagulation has a favorable effect on blood circulation. The results of fibrin-plate assays using C1 inactivator indicated that tissue-type plasminogen activator was the major contributor to the activation of fibrinolysis during spa bathing.

Aged↗