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PubMed2000

Domains and determinants of quality of life after stroke caused by brain infarction.

OBJECTIVE: To evaluate the domain-specific quality of life (QOL), including physical, social and role functioning, mental health, vitality, bodily pain, and general health domains, and to assess QOL's clinical and sociodemographic correlates in patients who were disabled by ischemic stroke. DESIGN: One-year prospective study of an inception cohort of patients with first-ever brain infarction. SETTING: Stroke unit of a neurologic department of a university hospital. PATIENTS: Eighty-five consecutive patients (36 women, 49 men; mean age +/- SD, 65+/-12.5 yr) with first-ever stroke of a mild to moderate nature caused by brain infarction. MAIN OUTCOME MEASURES: Patients were examined at 3 and 12 months poststroke. QOL was measured using the RAND 36-Item Health Survey. The variables studied were lateralization of cerebral lesion, neurologic and functional status, depression, age, gender, marital status, and living conditions. Depression was evaluated according to the criteria of Diagnostic and Statistical Manual of Mental Disorders, Revised Third Edition. Neurologic impairment was assessed by Scandinavian Stroke Scale, performance in activities of daily living by the Barthel index, and the intellectual deterioration by the Mini-Mental State Examination. RESULTS: QOL was poorer for the patients with mild to moderate stroke impairments at 3 months poststroke. The test domains most prone to being affected were physical functioning, physical role limitations, vitality, and general health. Only the domains of physical functioning and physical role limitations improved during the follow-up at 1 year. Depression, although mostly minor, was the most important reason for impaired QOL. Depression, being married, and age emerged as significant independent contributors to the low score value of vitality. Depression and being married were related to the low score value of physical role limitations. CONCLUSIONS: Stroke affects QOL, impairing its physical and psychosocial domains. The most important determinants of low QOL seem to be depression and being married. These findings provide new challenges for stroke rehabilitation, calling for identification of patients and spouses in need of supportive services.

Adult↗
PubMed1979

Compartment analysis of contrast enhancement in brain infarctions.

Contrast enhancement has been studied with computed tomography in 18 patients with brain infarction. Four patients were examined on more than one occasion. A mode of contrast medium administration has been used that results in constant blood iodine concentration during the investigation. The enhancement pattern was analyzed using a compartment model. A fast and a slow component of contrast enhancement was quantified for different parts of the infarct. Correlation with the age of the infarct confirms earlier studies, indicating a maximum enhancement at 2 to 4 weeks after the incidence of the infarct.

Brain↗
PubMed1984

Limitations of tetrazolium salts in delineating infarcted brain.

Tetrazolium salts, histochemical indicators of mitochondrial respiratory enzymes, have been used by some pathologists to detect infarcts in myocardium. We explored the utility of this technique in detecting experimental brain infarcts and report our findings. Infarcts were produced in cats, gerbils, and rats by unilateral temporal and permanent cerebral vessel occlusion. After various time periods the animals were killed, and their brains were reacted with 2,3,5, triphenyl, 2H-tetrazolium chloride (TTC). The experimental and contralateral hemispheres were examined by light and electron microscopy. The TTC-stained tissue was correlated with histology. In some situations the histological condition of the tissue correlated well with the TTC staining results. Brain regions supplied by temporarily occluded vessels and judged infarcted by light and electron microscopy did not stain. In these regions less than 6% of the mitochondria were intact. In brain tissue from animals with permanent vessel occlusion (no reflow) mitochondria were intact despite the fact that other cellular organelles, such as nuclei, were destroyed. TTC stained such mitochondria and as a result could not distinguish infarcted brain in complete ischemia situations (no reflow). Another draw back to this staining procedure was 36 h after infarction macrophages with intact mitochondria would replace damage neurons and be stained. Under ideal conditions though this technique can detect irreversibly damaged brain as early as 2.5 h after artery occlusion.

Animals↗
PubMed2003

[Molecular mechanism of brain infarction].

Through many experimental brain ischemia studies, it has been suggested that all of the cellular elements in the central nervous system show dynamic stress responses depending on the degree of environmental changes induced by ischemia and reperfusion. In this symposium, first we reviewed the pathogenic role of microvascular stasis (i.e., secondary ischemia) caused by the primary ischemic event and demonstrated the important role of cell adhesion molecules through the experiments using ICAM-1 knock-out mouse as a model of brain ischemia/reperfusion. Next, we discussed the ischemia-induced neuronal cell responses in relation to the apoptosis-like selective neuronal death and the induction of adopted stress responses including stress protein synthesis and 'ischemic tolerance' phenomenon. A variety of stress proteins induced by ischemic stress have been reviewed in relation to their pathophysiological roles in the ischemic brain. Finally, we reviewed the important pathogenic roles of endoplasmic reticulum (ER) stress as well as adaptive responses of ubiquitin-proteasome system in ischemia-induced neuronal cell death. For the development of a novel therapeutic agent against ischemic stroke, it is quite important to clarify both the negative and positive cellular responses induced by brain ischemia/reperfusion.

Animals↗
PubMed2003

Chlamydia pneumoniae seropositivity in patients with cerebral ischemic attack with or without silent brain infarcts.

PURPOSE: We examined the seropositivity of specific antibodies IgG and IgA to Chlamydia pneumoniae in the patients with ischemic stroke and examined if it has a notability in stroke patients with or without silent brain infarcts. MATERIAL AND METHOD: The clinical, laboratory and radiological findings of 26 cases with silent brain infarcts (SBI) without acute stroke and 26 cases with acute ischemic stroke without SBI (30 male, 22 female) were prospectively gathered. Risk factors were noted in all subjects. Control group was consisted of fifty-three healthy volunteer blood donors (40 male and 13 female). The presence of C. pneumoniae specific IgG antibody in serum samples was determined by indirect micro-immunofluorescence test according to the method of Wang and Grayston (Euroimmun GmbH in Deustchland) and of specific IgA antibody in serum samples was determined by indirect micro-immunofluorescence test with the manufactured kit Orgenium-Helsinki. The results were evaluated according to the groups and to the risk factors. RESULTS: There was not any correlation between risk factors and C. pneumoniae seropositivity. Seropositivity for specific IgG antibody for C. pneumoniae was observed as 73.8% in SBI, as 61.5% in stroke and as 56.3% in control groups. Seropositivity for specific IgA antibody for C. pneumoniae was observed in 7 out of 16 SBI cases (43.8%) SBI and in 9 out of 19 stroke cases (47.3%) with positive IgG antiobodies. CONCLUSION: We could not confirm a relation of C. pneumoniae seropositivity neither with SBI nor with acute stroke.

Aged↗
PubMed2003

Hyperhomocysteinemia as an independent risk factor for silent brain infarction.

OBJECTIVE: To evaluate whether hyperhomocysteinemia is an independent risk factor for silent brain infarction (SBI), and to determine the relationship between homocysteine and folate in each type of methylenetetrahydrofolate reductase (MTHFR) polymorphism, in order to identify a way of reducing the risk for SBI. METHODS: The authors enrolled 161 patients with SBI and 126 healthy people, checked their fasting homocysteine and folate levels, and analyzed for the MTHFR C677T polymorphism. RESULTS: The mean plasma homocysteine level in patients with SBI (12.17 +/- 5.35 micro mol/L) was significantly higher than in normal healthy people (9.37 +/- 4.11 micro mol/L; p < 0.05). By subgroup analysis, based on the classification of plasma homocysteine levels as high (>or=11.77 micro mol/L), moderate (8.71 to 11.76 micro mol/L), and low (<or=8.70 micro mol/L), the adjusted OR (AOR) of the high group for SBI was significantly greater than that of the low group (AOR, 4.78; 95% CI, 2.45 to 9.33). The homocysteine level showed a significant inverse correlation with folate level only in patients with SBI with the MTHFR 677TT genotype (p < 0.05). CONCLUSIONS: This study demonstrates that hyperhomocysteinemia is an independent risk factor for SBI, and provides the possibility of reducing the risk for SBI in the MTHFR 677TT genotype by folate supplementation.

Brain Infarction↗
PubMed2006

Retinopathy as an indicator of silent brain infarction in asymptomatic hypertensive subjects.

BACKGROUND AND PURPOSE: Silent brain infarction (SBI), which is cerebral target organ damage of hypertensive microangiopathies, is frequently seen in hypertensive patients. The purpose of this study is to investigate the relation between hypertensive retinopathy (HTR) and SBI in subjects without a history of stroke or transient ischemic attack. METHODS: Five hundred-fifty hypertensive subjects without history of stroke or transient ischemic attack had brain MRI and retinal photographs taken. The presence of SBI was assessed from the MRI scans, which was defined as a lesion of at least 3 mm in diameter with typical imaging characteristics. The presence HTR was defined from digitized retinal photographs. RESULTS: Seventy-seven subjects (14%) showed HTR (grade 1 in 46, grade 2 in 31 persons). A multivariate analysis showed that age (OR, 1.07; 95% CI, 1.03 to 1.10) and HTR (OR, 2.01 for grade 1; OR, 3.03 for grade 2) were the independent indicators for the presence of SBI. The higher the grade of HTR, the more prevalent SBI than persons with normal retina (by linear by linear association test, p=0.001). CONCLUSION: HTR is associated with the presence of SBI. This finding suggests that retinal photography may be useful for identifying hypertensive subjects at increased risk of having SBI regardless of current blood pressure status.

Aged↗
PubMedDate not supplied

Michaelis-Gutmann bodies in a healing brain infarct.

A case of Michaelis-Gutmann bodies in a healing brain infarct is described. Morphologically this was consistent with cerebral malacoplakia. There are only 6 previously reported cases of cerebral malacoplakia, and only 1 of them was a consequence of postpartum stroke. The histologic and ultrastructural features of the malacoplakia lesion are reported and compared with the previously reported cases.

Aged↗
PubMed1978

[Survived brain infarction in old age - clinical and morphological findings. part I: extracranial stenoses of carotis arteries (author's transl)].

By clinical and post mortem findings we searched for the risk factors, important for brain infarctions in people of nearly 80 years. We were especially interested in the conditions of the extracranial vessels such as the carotid arteries and the murmurs at this point. The number of arterial stenoses in this region, ascertained in younger people is similar in old age. Besides of others factors, caused by old age, the many cases of multiple extracranial stenoses are probably responsible for the overproportional big brain infarctions in this series. In nearly 50% of all stenoses we heard vascular murmurs, mostly in both of the carotid arteries. Despite of some uncertainly of the clinical importance - just in old age many cardiac murmurs of the ejection type with tendency to transmission have been heard - they should give rise to investigate carefully the region of the neck in symptomatic patients.

Age Factors↗
PubMed2006

[Research on association between atherosclerotic brain infarction and human leukocyte antigen DR gene].

OBJECTIVE: To evaluate the relationship between atherosclerotic brain infarction (ABI) and human leukocyte antigen DR (HLA-DR) gene at molecular level. METHODS: By using polymerase chain reaction sequence specific probe (PCR-SSP), gene special position of the HLA-II DR alleles were determined in 31 patients and 30 healthy individuals as controls, all of them were inhabitants of Northeastern China. RESULTS: The HLA-DR B1*0301 gene frequency in the group of ABI was obviously higher than that of control group (RR=5.6842, P<0.05). CONCLUSION: The HLA-DR B1*0301 gene may be the susceptible gene of ABI in Northeastern China, or it may associate with other genes to produce the disease.

Adult↗
PubMed1988

Brain infarction in sickle cell anemia: magnetic resonance imaging correlates.

Brain infarction is a well-known but poorly understood complication of sickle cell disease. Seventy-three sickle cell disease patients underwent neurological examinations and high-field, heavily T2-weighted axial cranial magnetic resonance image (MRI) scanning. Eighteen of the 73 had a history of stroke, defined as an acute, focal neurological sign lasting longer than 1 hour; in the event of a convulsive onset, an MRI abnormality as a correlate was necessary. Sixteen of the 18 stroke patients demonstrated focal MRI abnormalities consistent with arterial borderzone infarctions. Fifty-five of the 73 patients had no history of stroke. Six of the 55 (11%) had focal MRI abnormalities suggesting previous subclinical stroke. Five of these lesions were in borderzone regions. The distinguishing feature in 21 of the 22 patients with MRI abnormalities was the predilection for lesions in the high cortical convexity, in the general regions of arterial borderzones between the major cerebral arteries and adjacent deep white matter. The pattern of MRI lesions suggests two pathogenetic mechanisms: (1) proximal large-vessel disease with inadequate cerebral perfusion (distal field insufficiency syndrome) and (2) distal small-vessel disease (sludging syndrome).

Adolescent↗
PubMed1990

[Two cases of brain infarction associated with hypertriglyceridemia].

We reported two cases of brain infarction. They were cousins. Case 1 was a 12-year-old girl, who complained of aphasia, dyscalculia, right-left disorientation and right homonymous hemianopsia. CT showed low density areas in left superior and middle temporal gyri. Case 2 was a 15-year-old boy, who had left hemiplegia and hypesthesia to pain, temperature and touch on the left side of the body. CT showed low density areas from the genu of the internal capsule to the corona radiata, and from the posterior portion of putamen to the posterior limb of the internal capsule on the right side. Both cases had hypertriglyceridemia which might be associated with the etiology of infarction.

Adolescent↗
PubMed1995

Brain infarction developed in hypertensive and normotensive patients during hospitalization--hemodynamic factors.

To determine the effects of changes in blood pressure (BP) on the development of ischemic stroke, 17 patients who developed acute brain infarction during hospitalization were analyzed in relation to the vascular risk factors such as hypertension, previous stroke, diabetes mellitus, and hyperlipidemia. Their BPs were retrospectively referred to the onset of stroke. The average values of mean arterial blood pressure (MABP) on admission were 137 mmHg in hypertensive patients (HT; n = 9) and 101 mmHg in normotensives (NT; n = 8). HT patients received antihypertensive treatment after admission and MABP decreased by 22 mmHg (14%) prior to the ictus (three to sixty-five days after admission). MABP in NT patients remained constant before the attack (-1.4 mmHg, four to one hundred ten days after admission). Similarly, MABP decreased by 17 mmHg (four to ninety-three days) before the ictus in patients with previous stroke (n = 9), whereas it changed only a little in patients without history of stroke (n = 8). BP in each group elevated immediately after the stroke and gradually decreased to 90% of the resting level after two weeks. An excessive reduction of BP may induce brain infarction in HT or chronic stroke patients or cause it to recur.

Acute Disease↗
PubMed2003

Reduced brain infarct volume and improved neurological outcome by inhibition of the NR2B subunit of NMDA receptors by using CP101,606-27 alone and in combination with rt-PA in a thromboembolic stroke model in rats.

OBJECT: A novel postsynaptic antagonist of N-methyl-D-aspartate (NMDA) receptors, CP-101,606-27 may attenuate the effects of focal ischemia. In current experiments, the authors investigated its neuroprotective effect alone and in combination with recombinant tissue plasminogen activator (rt-PA) in thromboembolic focal cerebral ischemia in rats. METHODS: Forty-eight male Wistar rats underwent embolization of the right middle cerebral artery to produce focal cerebral ischemia. After random division into six groups (eight rats in each group), animals received: vehicle; low-dose (LD) CP-101, 606-27, 14.4 mg/kg; high-dose (HD) CP- 101,606-27, 28.8 mg/kg; rt-PA, 10 mg/kg; low-dose combination (LDC) CP- 101,606-27, 14.4 mg/kg plus rt-PA, 10 mg/kg; or high-dose combination (HDC) CP- 101,606-27, 28.8 mg/kg plus rt-PA, 10 mg/kg) 2 hours after induction of embolic stroke. Animals were killed 48 hours after the onset of focal ischemia. Brain infarction volume, neurobehavioral outcome, poststroke seizure activity, poststroke mortality, and intracranial hemorrhage incidence were observed and evaluated. Compared with vehicle-treated animals (39.4 +/- 8.6%) 2 hours posttreatment with CP-101,606-27 or rt-PA or in combination a significant reduction in the percentage of brain infarct volume was seen (LD CP-101,606-27: 20.8 +/- 14.3%, p < 0.05; HD CP-101,606-27: 10.9 +/- 3.2%, p < 0.001; rt-PA: 21.1 +/- 7.3%, p < 0.05; LDC, 18.6 +/- 11.5%, p < 0.05; and HDC: 15.2 +/- 10.1%, p < 0.05; compared with control: 39.4 +/- 8.6%). Combination of CP-101,606-27 with rt-PA did not show a significantly enhanced neuroprotective effect. Except for the control and LDC treatment groups, neurobehavioral outcome was significantly improved 24 hours after embolic stroke in animals in all other active therapeutic groups receiving CP-101,606-27 or rt-PA or in combination. The authors also observed that treatment with HD CP-101,606-27 decreased poststroke seizure activity. CONCLUSIONS: The data in this study suggested that postischemia treatment with CP-101,606-27 is neuroprotective in the current stroke model; however, the authors also note that although rt-PA may offer modest protection when used alone, combination with CP-101,606-27 did not appear to enhance its effects.

Animals↗
PubMed1997

Embolic brain infarction in nonrheumatic atrial fibrillation: a clinicopathologic study in the elderly.

Although CT studies have addressed symptomatic and asymptomatic cerebral infarctions in nonrheumatic atrial fibrillation (NRAF), pathologic verification of the results is lacking. The purpose of this study was to assess the frequency, location, and extent of symptomatic and asymptomatic brain infarction in autopsy specimens from elderly patients with NRAF. We examined autopsy specimens from 136 consecutive NRAF patients 70 years of age or older who received no anticoagulant therapy during their lifetime and compared them with 231 age-matched control subjects with similar health histories except for the absence of NRAF. Symptomatic cerebral infarctions were present in 82 (60.3%) NRAF patients and in 55 (23.8%) control subjects (p < 0.0001). Of symptomatic cerebral infarctions, cardioembolic infarction was present in 53 (64.6%) NRAF patients and in two (3.6%) of the control subjects (p < 0.0001), atherothrombotic infarction in 13 (15.9%) NRAF patients versus 36 (65.5%) control subjects (p < 0.0001), and lacunar infarction in four (4.9%) NRAF patients versus 12 (21.8%) control subjects (p < 0.01). Stroke-related death occurred in 34 (25.0%) NRAF patients and in 18 (7.8%) control subjects (p < 0.0002). Symptomatic cerebral infarction was generally accompanied by asymptomatic infarctions in both NRAF patients and control subjects. Asymptomatic cortical infarctions were more common in NRAF patients, but asymptomatic infarctions in the white matter or deep structures were more common in control subjects. In this autopsy series of individuals over 70 years of age, symptomatic brain infarction was 2.5 times more common in NRAF patients than in NRAF-free control subjects; two-thirds of the infarctions in the NRAF cases were judged to be cardioembolic in origin. Most asymptomatic cerebral infarctions in the NRAF patients were located in the cortices.

Aged↗
PubMed2005

Mechanisms of bihemispheric brain infarctions in the anterior circulation on diffusion-weighted images.

BACKGROUND AND PURPOSE: Multiple acute brain infarctions in both cerebral hemispheres usually suggest an embolic mechanism, particularly one of aortic or cardiac origin. The purpose of this study was to clarify the etiologic mechanisms and topographic features of bihemispheric infarctions depicted on diffusion-weighted imaging (DWI). METHODS: Among 411 consecutive patients with ischemic stroke who underwent MR imaging in the acute phase, DWI showed bilateral infarctions in 19 (4.6%). In these patients, we analyzed the presence of carotid, aortic or cardiac embolic sources by using ultrasonography, cerebral angiography, and/or transesophageal echocardiography and evaluated the size and topographic distribution of the lesions. We assessed intracranial cross-flow through the anterior communicating artery, mainly on the basis of the anatomic information obtained from angiography or MR angiography. RESULTS: Bilateral lesions were derived from cardiac and/or aortic embolic sources in 16 (84%) of 19 patients and appeared to originate from unilateral carotid diseases in three (16%). In nine (82%) of 11 patients with cardiac embolic sources, at least one large territorial or subcortical lesion was found in either hemisphere, whereas in all eight patients without a cardiac embolic source, the lesions were small and disseminated bilaterally. CONCLUSION: Unilateral carotid lesions can cause bihemispheric infarctions through cross-flow in the anterior communicating artery. On DWI, small bihemispheric, disseminated lesions strongly suggest an artery-to-artery embolism. In such cases, aortic and carotid lesions should be assessed as potential embolic sources.

Aged↗
PubMed1996

The size of territorial brain infarction on CT relates to the degree of internal carotid artery obstruction.

We studied the relationship between infarct size and degree of internal carotid artery stenosis in 227 stroke patients without a source of embolism in the heart, who had a CT-verified territorial brain infarct. We used logistic regression analysis adjusting for differences between groups in co-associated variables such as age, sex, hypertension, diabetes mellitus, and a history of ischaemic heart disease. Ipsilateral carotid stenosis greater than 50% was more strongly associated with large than small infarcts; adjusted odds ration [(a)OR]: 4.56; 95% confidence interval (CI): 1.21-17.2; P = 0.02. For ipsilateral carotid occlusion the association was even stronger--(a)OR: 36.80; 95% CI: 2.54-533; P = 0.007. When large infarcts were compared with infarcts of small and moderate size together the ORs were 2.29, 95% CI 1.14-4.58 and 2.57, 95% CI 1.17-5.67 for carotid stenosis or occlusion, respectively. Our data show a relationship between greater than 50% carotid stenosis or occlusion and large brain infarcts. We suggest that haemodynamic impairment may contribute to infarct size in territorial infarcts of non-cardiac origin.

Adult↗