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Quantitative reverse transcription-polymerase chain reaction of GABA(A) alpha1, beta1 and gamma2S subunits in epileptic rats following photothrombotic infarction of neocortex.

Photothrombotic brain infarction can result in altered expression of cortical GABA(A) receptors and in epileptic seizures. We sought to determine whether infarct size and/or epileptic seizures resulted in a differential expression of cortical GABA(A) receptor subunit mRNA in adult rats. A reverse transcription-polymerase chain reaction (RT-PCR) was used with internal standards for GABA(A) receptor subunits to quantify alpha(1), beta(1), and gamma(2S) subunit mRNA expression in cortex ipsilateral and contralateral to left cerebral infarcts in small or large infarct/nonepileptic cohorts, a large infarct/epileptic cohort, and a young adult control cohort. Unilateral hemispheric subunit mRNA was pooled for each cohort, quantified, and expressed as mean values+/-S.E.M. In general, the magnitude of mRNA expression (pg/1 microg total RNA) was different for the individual subunits: gamma(2S) (10(4)), alpha(1) (10(2)), and beta(1) (10(1)). Hemispheric subunit mRNA expression for the different cohorts was compared by ANOVA testing, which noted significant differences for the alpha(1) (P<0.001) and beta(1) (P<0.001) subunits in ipsilateral cortex. Bonferroni post-testing for alpha(1) cohorts indicated that mRNA expression for the large infarct/epilepsy cohort (624.2+/-6.8 pg) was greater than all other cohorts (P<0.001); control (162.7+/-32.2 pg). For beta(1) cohorts, there was decreased mRNA expression in the large infarct/nonepileptic cohort (9.2+/-0.8 pg; P<0.01) and the large infarct/epileptic cohort (10.5+/-2.2 pg; P<0.05) compared to control (23.2+/-2.6 pg). Additionally, paired t-tests compared subunit mRNA expression within individual animal cohorts (ipsilateral vs. contralateral) and indicated decreased mRNA expression ipsilaterally for the beta(1) subunit in the small infarct cohort (14.2+/-2.6 vs. 22.9+/-3.0 pg; P=0.0102) and the large infarct/epilepsy cohort (10.5+/-2.3 vs. 18.0+/-3.6 pg; P=0.0462). These findings suggest that large photothrombotic infarcts of the neocortex can result in a long-lasting differential expression of GABA(A) receptor subunit mRNAs in ipsilateral cortex variably associated with the epileptic state.

Analysis of Variance↗

Basal ganglia infarction mimicking glioblastoma.

Modern brain imaging techniques usually allow a very good differential diagnosis of intracerebral lesions, but in some cases the differential diagnosis is difficult. We report the case of a 52 year old male with acute brachiofacial paresis and a hyperintense lesion with mass effect and ring-enhancement in basal ganglia suspiciously to a tumor. The neurosurgeons recommend stereotactical brain biopsy for diagnosis, but the patient recovered in following time gradually and in repeated computer tomographic images contrast enhancement disappeared and a hypodense zone in the basal ganglia remains. Our case demonstrates that brain infarctions can mimick glioblastoma in taking cystic appearance and contrast enhancement. Stereotactic biopsy would have been a precipitated invasive procedure in this case.

Basal Ganglia↗

[Magnetic resonance spectroscopy of acute cerebral infarctions].

Eight patients with brain infarction were examined serially in the acute phase and one week and two to four weeks after stroke with water-suppressed proton magnetic resonance spectroscopy. Ten healthy volunteers served as controls. The time courses of N-acetylaspartate (NAA), total creatine (Cr), choline containing compounds (Cho), lactate content, and regional cerebral blood flow (rCBF) measured by SPECT were studied. A high lactate level was found in the acute phase. The lactate content decreased to barely detectable levels during the following two to four weeks, while rCBF increased during this period. The content of NAA in infarcted tissue was significantly reduced (p < 0.01) compared to healthy controls, Cr was also reduced (p < 0.02), whereas Cho content did not change. The inverse relationship between lactate level and cerebral blood flow suggests that lactate plays no substantial role in the vasodilatation underlying the hyperaemia that follows reperfusion. The amount of lactate present in the acute phase reflects the severity of ischaemia in the affected region. The content of NAA may be used as a neuronal marker, and thus perhaps as a marker of the effect of future treatment procedures.

Acute Disease↗

[Prognosis after transient ischemic attacks].

Transient ischemic attacks (TIAs) are reversible neurological deficits due to cerebral ischemia in a vascular territory lasting less than 24 hours, usually less than one hour. The natural course of TIAs is variable. One third of the patients suffer from a subsequent completed stroke with lasting disability, one third of the patients continues to experience TIAs and in one third no further symptoms are encountered. TIAs are a warning symptom of a generalized vascular process, myocardial infarction being the most common cause of mortality and ischemic brain infarction being the most common cause of morbidity. Clinical parameters--besides age--seem to be of minor prognostic relevance. Vascular risk factors should be evaluated in all TIA patients; especially, a cardiac work up including 2D-echocardiography and an exercise stress test should be performed. Duplex sonography of craniocervical vessels shows atherosclerotic lesions in a considerable proportion of patients with TIA; however, localization of these lesions does not always correspond to clinical symptomatology. Some angiographic features are of prognostic relevance. Computed tomography (CT) and magnetic resonance imaging (MRI) show ischemic lesions in a considerable proportion of patients, which connects TIAs directly to ischemic brain infarcts. The extent and localization of these lesions are of some prognostic relevance. Blow flow studies on single photon emission computed tomography (SPECT) and studies of brain metabolism on positron emission tomography (PET) are abnormal in many TIA patients for prolonged periods and also have some prognostic impact. TIA patients probably are a heterogeneous group with a common symptom. A detailed diagnostic work-up may have implications on a more specific and efficient therapy.

Aged↗

Magnetic resonance imaging correlates of depression after ischemic stroke.

BACKGROUND: Depression affects up to 40% of patients with ischemic stroke. The relationship between site and size of brain infarcts and poststroke depression is still not well characterized. Further possible contribution and interaction of white matter lesions and brain atrophy has not been studied previously. We conducted a magnetic resonance image-based study of the radiologic correlates of depression in a large, well-defined series of patients with ischemic stroke. METHODS: Modified DSM-III-R and DSM-IV criteria were used to diagnose depressive disorders during a comprehensive psychiatric evaluation in 275 of 486 consecutive patients aged 55 to 85 years 3 to 4 months after ischemic stroke. A standardized magnetic resonance imaging protocol detailed side, site, type, and extent of brain infarcts and extent of white matter lesions and brain atrophy. RESULTS: Depressive disorders were diagnosed in 109 patients (40%). Patients with depression had a higher number and larger volume of infarcts affecting the prefrontosubcortical circuits, especially the caudate, pallidum, and genu of internal capsule, with left-sided predominance. Extent of white matter lesions and atrophy did not differ in patients with and without depression. Independent correlates of poststroke depression in a logistic regression model were mean frequency of infarcts in the genu of internal capsule on the left side (odds ratio [OR], 3.2; 95% confidence interval [CI], 1.0-10.1), mean frequency of infarcts in the pallidum of any side (OR, 1.6; 95% CI, 1.1-2.3), and mean volume of infarcts in the right occipital lobe (OR, 0.98; 95% CI, 0.96-0.99). CONCLUSION: Lesions affecting the prefrontosubcortical circuits, especially on the left side, are correlates of depression after ischemic stroke.

Aged↗

Topography of cerebral infarction associated with carotid artery dissection.

Because the pathogenesis of cerebral ischaemia in internal carotid artery dissection (ICAD) is controversial we studied the topography of cerebral infarction that results from ICAD according to pathophysiology of embolic and haemodynamic stroke. Sixty-four patients with 67 ICADs diagnosed by angiography, Doppler duplex sonography and magnetic resonance imaging (MRI) were studied prospectively during the past decade. According to current pathophysiological concepts, cortical territorial infarcts and large subcortical lenticulostriate infarcts revealed by CT or MRI were classified as embolic, while smaller infarcts in the subcortical junctional zone and infarcts in the cortical borderzone between the middle (MCA) and anterior cerebral artery were interpreted as haemodynamic infarcts. Of the 67 dissections 37 (55%) were associated with brain infarcts, of which territorial MCA infarcts of variable size accounted for 60%. These were combined with infarcts of the anterior and posterior cerebral artery in 5%; 8% of the patients had complete MCA infarction. Large lenticulostriate infarcts were present in 11%. Haemodynamic infarcts involved the subcortical junctional zone in 16% but never the anterior cortical borderzone. Although different abnormal Doppler findings indicated haemodynamically significant carotid obstruction in all symptomatic ICADs, only the characteristic high-resistance Doppler signal was significantly associated with the occurrence of brain infarction (in 66%, P < 0.01). The angiographic features of ICAD did not correlate with the incidence or with the topography of cerebral infarction. Patterns of infarction in ICAD indicate a predominantly embolic causation probably due to thrombus formation in the dissected carotid artery in the presence of severe haemodynamic obstruction, as demonstrated by Doppler sonography.

Adolescent↗

[Etiology of cerebral infarcts caused by emboli--subacute bacterial endocarditis].

Bacterial endocarditis is a rare cause of brain infarction. Prediposing factors are frequently valvular defects secondary to rheumatic conditions. A slowly progressive course and atypical symptoms of the disease can mask the condition to such an extent that the correct diagnosis is obtained only through the work up of secondary embolic complications. Modern antibiotic combinations therapy yields a cure in 98% of the cases. The problems obtaining the diagnosis and the course of the disease with antibiotic therapy will be demonstrated in a case of embolic brain infarction secondary to bacterial endocarditis.

Adult↗

Distribution of brain oedema in the contralateral hemisphere after cerebral infarction: repeated MRI measurement in the rat.

The appearance of local cerebral dysfunction at remote regions from the focus in the acute stage of stroke (diaschisis) is well known, but its mechanism has not been established. We have analysed serial MR images of the infarcted brain of rats to evaluate the distribution of oedema. Forty-seven Sprague-Dawley rats were anaesthetized with halothane, and the right middle cerebral artery (MCA) was permanently occluded via the intraluminal approach using a nylon 2-0 suture. At 3, 6, 9 and 24 hours after the occlusion, coronal T(2)-weighted MR images were taken and the signal intensity (SI) was computed at each region of the brain. After occlusion of the right MCA, SI increased diachronically up to 24 hours on the occluded side of the cortex (52.9+/-3.2 to 104.8+/-22.4) and striatum, which are within the perfusion territory of the MCA. SI increment was also observed at the hippocampus, alveus hippocampi and pyriform lobe, which are not within the territory of the MCA, and at some regions of the contralateral side (52.5+/-4.8 to 69.4+/-14.8 at the cortex). These changes were prominent in ischaemia-vulnerable portions, mild in the cortex, and minimal in the striatum. This contralateral side SI increment indicates remote oedema, which corresponds to diaschisis. We suggest that the mechanism of this remote contralateral oedema is the movement of extravasated protein from the lesion.

Animals↗

[The role of vascular reconstructive surgery in the treatment of cerebrovascular insufficiency].

BACKGROUND: Management of cerebrovascular insufficiency (CVI) is one of the greatest medical challenges in our country. Retardation in this field has been causing serious medical and socioeconomic consequences. MAIN PURPOSE AND STARTING POINTS (OBJECTIVES): In spite of existing unfavourable conditions the authors of this paper have managed to standardize their own policy in diagnosis, surgical indications and techniques. This caused substantial improvement of their results, as well as cooperation with the neurologic clinics. In connection with the increasing numbers of operations and improved results, the authors report their recent experience in this field and compare them with the results from previous years. METHODS: The authors compare two series of patients. The first series of 65 consecutive patients surgically treated from 1st Jan. 1987 to 31st Dec. 1990 (69 operations altogether). The 2nd series of 169 consecutive patients surgically treated from January 1st 1993 to December 31st 1994 (191 operations altogether), 149 due of them were subjected to carotid endarterectomy (CEA). Mean age of the first series was 55.3 (35-73), 2nd series 59.7 years (42-86). The authors have studied participation of neurologically and angiographically unstable patients. In the first series the ratio of neurologically stable and unstable patients was 63.4:36.6%, while in the 2nd series it was 75.4:24.6%. The ratio of angiographically stable and unstable patients was in the 1st series 60.2:39.8%, while in the 2nd series it was 50.3:49.7%. In the 2nd series the authors observed also the percent age of ulcerated lesions in the carotid bifurcation and found a surprisingly high number-59.2%. RESULTS: The combined mortality-morbidity index of the first series was 11.6%, of the 2nd series 3.1%. In the first series there were two deaths (2.9%) and 6 brain infarctions. In the 2nd series four patients died from acute myocardial infarction (2.1%) and there were two cases of a perioperative brain infarction, respectively. The necessity of wound revision due to of bleeding was found in two patients (2.9%) in the first series, and in two cases (1%) in the 2nd series. CONCLUSIONS: The authors emphasize the complicated nature of these problems, the necessity to recognize the surgical indications and techniques, and protective measures to prevent serious complications. There is, in their opinion, inevitable to increase bringing the patients in need of surgical reconstruction under control. On the other hand, there is the necessity to increase the accessibility of qualified surgery in the CVI. That means in the first place to increase the number of centers able to accomplish these operations with minimal combined mortality-morbidity index. (Tab. 10, Ref. 37.).

Adult↗

High-cervical spinal cord electrical stimulation in brain low perfusion syndromes: experimental basis and preliminary clinical report.

Previous studies of our group showed that C1-C2 spinal cord stimulation increases carotid and brain blood flow in normal conditions in the goat and dog and it has a beneficial vasomotor effect in a model of vasospasm in the rat. For further clinical application it seemed rational to investigate the possible vascular changes mediated by this technique in experimental brain infarction. To this aim, 45 New Zealand rabbits were used. Brain infarction was produced by bilateral carotid ligation in 15, unilateral microcoagulation of the middle cerebral artery in 15 and by microcoagulation of the vertebral artery at the craniocervical junction in the other 15. One week later, following daily clinical scoring and cortical and posterior fossa blood flow readings by laser Doppler, a period of 120 min of right C1-C2 spinal cord electric stimulation was performed. A mean of 27% increase in previous blood flow recordings was obtained at the right hemisphere and a mean of 32% in the posterior fossa. This procedure was used in 10 patients presenting with various cerebral low perfusion syndromes. Though not constant, an increase in alertness, retention, speech, emotional lability and performance in skilled acts was achieved. No MR changes were observed, though SPECT readings showed an increase in blood flow in the penumbral perilesional area.

Adult↗

MRI for the management of neonatal cerebral infarctions: importance of timing.

PURPOSE: Focal ischemic stroke in neonates is a rare occurrence. Diagnosis with most imaging modalities is difficult, but necessary for initiating an anticoagulatory treatment. The purpose of this study was to evaluate the sensitivity of MRI sequences within the first 14 days of birth. PATIENTS AND METHODS: Four patients with neonatal stroke presenting as seizures were examined using a standard MRI protocol including diffusion-weighted images (DWI) and magnetic resonance angiography (MRA) within 72 h of birth. The time between the onset of symptoms and MRI ranged from 6 h to 48 h. Follow-up examinations were performed on days 5 ( n=1), 7 ( n=2), and 14 ( n=1) for the control of a treatment with low-molecular heparin. RESULTS: Eight infarctions were detected in the four patients, 5 in the middle cerebral artery (MCA), three in the posterior cerebral artery (PCA) territory. All lesions were visible using DWI, four on T2-weighted images. Whereas in two patients small lesions contralateral to a large stroke were missed on T2-weighted images, the diagnosis would have been missed altogether without DWI in one patient. On follow-up, the visibility of the infarctions had declined using DWI after 5 days and the lesions were invisible after 1 week. Fourteen days after the stroke, an increased diffusion was detected in the infarcted brain tissue. By this time, all lesions were visible on T2-weighted images. CONCLUSION: In neonates, infarcted brain tissue can be detected using DWI with high sensitivity during the first 2 days after stroke and before other sequences are diagnostic. However, the diffusion restriction does not persist beyond 1 week. After 5 days, diagnosis has to rest mainly on T2-weighted images.

Brain Mapping↗

Evidence for disordered cyclic amp metabolism in patients with cerebral infarction.

Systemic blood cyclic AMP levels were elevated but urinary excretion was unaltered in patients with recent cerebral infarction. Cerebral venous levels for cyclic AMP were significantly higher than arterial levels. CSF cyclic AMP levels were also elevated. After intravenous 10% glycerol, CSF cyclic AMP levels decreased and cerebral A-V differences were reduced. Elevation of cyclic AMP levels in plasma may be due to alteration of neuroendocrinal function after cerebral infraction and contributed to in part by release from infarcted brain. Cyclic AMP release into cerebral venous blood and CSF suggests (1) blood brain barrier damage and (2) extracellular cyclic AMP accumulation in infarcted brain secondary to abnormal neurotransmitter release and/or impaired cellular function which appears to be partially reversed by glycerol.

Cyclic AMP↗

Hyperacute infarction: early CT findings.

The aim of our study is to determine how early and reliably ischemic brain infarcts can be detected on CT scanning. We report two cases of an early CT finding of acute ischemic infarcts where CT examination was obtained within the first 3 hours of onset of neurological symptoms. CT examination showed blurred outlines and decreased attenuation of the left lentiform nucleus, loss of the white-gray matter interface in the left insular cortex and left cortical global hypoattenuation with obliteration of left cortical sulci in one patient. In second patient CT showed the following: hyperdense left middle cerebral artery, loss of clear margins of left lentiform nucleus, subtle focal cortical hypodensity in the left fronto-parietal area with signs of mass effect in the form of ventricular compression. CT is still the first choice in the deferential diagnosis of acute stroke. Although older literature positions have suggested that CT was negative during the first 48 hours, modern CT technology can demonstrate positive findings even in the first 3 hours of onset. This is important in patients with acute stroke, as thrombolytic therapy when elected, has to be given within the first 3-6 hours after onset of symptoms. To determine how early and reliably ischemic brain infarcts can be detected on CT scanning, we report two cases of an early CT finding of acute ischemic infarcts where CT examination was obtained within the first 3 hours of onset of neurological symptoms.

Acute Disease↗

Cerebellar infarction: natural history, prognosis, and pathology.

Using clinical and computed tomography (CT) criteria, an analysis of 2,000 consecutive stroke unit patients from 1977 to 1984 revealed 30 patients with cerebellar infarction. The case fatality rate was 23%, higher than for any other location of brain infarction studied over the same period. Death was most often due to concomitant brainstem infarction. Obstructive hydrocephalus occurred in 4 patients (13%), and in 2 cases diagnosis, facilitated by urgent CT scanning, allowed early surgical intervention that was life saving. Patients who survived the acute phase were followed for an average of 21 months, and over that time 22% sustained further brainstem infarction, representing a 13% stroke rate per year. Over the latter 3 years of the clinical study, an autopsy survey revealed 11 cases of cerebellar infarction that had been clinically unrecognized. None of these died as a direct result of their infarction. Mechanisms of infarction inferred from autopsy included in situ thrombosis, embolism, watershed, and lacunar infarction, with in situ thrombosis being the most common. We conclude that the case fatality rate of cerebellar infarction is greater than of any other form of brain infarction, but it may be reduced by prompt recognition of those patients who will benefit from surgical decompression. In survivors, a high risk of subsequent hindbrain stroke exists. More attention needs to be paid to this entity in terms of early diagnosis and prevention of subsequent stroke.

Aged↗

[Experimental and clinical study of the efficacy of intracarotid administration of curantil in the treatment of cerebral ischemia].

Curantil intracarotid injection resulted in brain blood supply and in brain oxygen consumption increase as well as in redox processes normalization in 75 cats with main brain arteries occlusion and heart insufficiency induced by chemical necrosis of the myocardium. A single intravenous injection of a higher curantil dose resulted in a significantly less effect. Long-term (3-72 hours) curantil infusion led to the improvement of the functions disturbed (limb movements, speech, vision) in 32 of 42 patients with brain ischemic insult. The greatest therapeutic efficacy was observed in patients with nonobturated brain infarction induced by brain vascular spasm or cardiocerebral vascular insufficiency.

Adult↗

[Urinary incontinence in elderly patients in the chronic stage of stroke].

One hundred and six elderly patients with chronic stroke who were admitted to Seiai Rehabilitation Hospital were studied regarding urinary incontinence. The average age of the subjects was 74 +/- 8 years old, ranging from 60 to 94 years. Seventy three of the 106 patients (69%) had urinary incontinence which was found in 72% of brain infarction, 61% of brain hemorrhage and 67% of subarachnoid hemorrhage. The prevalence of urinary incontinence in cases of brain stem, thalamic, and putaminal hemorrhage was 80%, 67% and 46%, while that in cases of cortical infarction and infarct of perforating arteries was 84% and 68%, respectively. The rate of urinary incontinence was significantly higher in those aged 75 years or over (p < 0.05), those with poor activities of daily living (ADL, p < 0.005), or with dementia (p < 0.001). Dementia was a complicating factor more frequently in aged patients (p < 0.05) and in those with poor ADL (p < 0.001), although no correlation was seen between age and ADL (p = 0.08). These results indicated the high prevalence of urinary incontinence in elderly inpatients with chronic stroke, which is significantly related to impairment of mental and physical activities.

Activities of Daily Living↗