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At least 397 records · Page 22Linked to original sources
PubMed1999

Diffusion-weighted echo planar imaging of acute brain infarction: a preliminary report.

The clinical usefulness of diffusion-weighted echo planar imaging (DW-EPI) was studied in 55 patients with acute brain ischemia. Ischemic lesions were identified on DW-EPI as hyperintense regions in all patients before changes were detected by conventional magnetic resonance imaging techniques in 12 cases studied earlier than 6 hours after onset. The earliest case was verified on DW-EPI at 50 minutes after onset. The ultra-fast imaging technique took less than 2 minutes to perform even for restless patients. Three patients had cardioembolic middle cerebral artery occlusion, and emergent percutaneous transluminal recanalization was carried out. Chronological changes in the signal of brain ischemia on DW-EPI depended on the site and size of the lesion, lacunar infarct of basal ganglia, and/or massive infarct due to major vessel occlusion, and were affected by associated hemorrhagic events. Coronal DW-EPI could more easily demarcate ischemia in the brainstem and/or cerebellum than axial scans when susceptibility artifacts were present. Coronal scans also demonstrated the site and direction of the pyramidal tract and its anatomical correlation with the lesions. DW-EPI has potential for the diagnostic and therapeutic planning of patients with acute brain ischemia.

Aged↗
PubMedDate not supplied

[Small brain infarcts in arterial hypertension and atherosclerosis (pathogenesis and criteria of morphologic diagnosis].

Small infarcts, few millimeters in size, localized in the deep regions of brain hemispheres, cerebellum and pons were found in 36 patients with arterial hypertension and atherosclerosis. These infarcts develop in the intracerebral arteries having the diameter up to 500 microns. Two types of these infarcts are distinguished: hypertensive and atherosclerotic. Arterial stenosis and obliteration are at the basis of hypertensive infarcts. Reduction of circulation due to the atherosclerotic stenosis is the cause of the atherosclerotic infarcts.

Adult↗
PubMed1997

Early-infantile galactosialidosis with multiple brain infarctions: morphological, neuropathological and neurochemical findings.

Post-mortem morphological, neuropathological and neurochemical findings are described in a girl, aged 14 months, with the early-infantile form of galactosialidosis. An elevation in non-lipid sialic acid was noted in both the grey and white matter of the brain, whereas the white matter displayed a clear reduction in all the major lipids. Multiple cortical-subcortical infarctions were found in the brain, most probably caused by compromised circulation due to endothelial luminal encroachment. Electron microscopy of cerebral blood vessels revealed major swelling of the endothelium due to prominent cytoplasmic vacuolisation. Multiple cytoplasmic vacuoles containing sparse granular or membranous matter were also seen in neurons and glial cells of the brain and spinal cord. Zebra bodies were found in the Purkinje cells, as well as in the spinal anterior horn cells. Prominent endothelial vacuolisation was noted in the liver and kidneys. The renal vascular encroachment was probably the cause of the arterial hypertension with elevated plasma renin activity in the present case. There were innumerable fine vacuoles in the renal epithelium and in the Kupffer cell of the liver, whereas coarser vacuoles were observed in the hepatocytes. The neuronal ultrastructural findings in the present case bear some resemblance to the few reported cases of late-infantile and adult cases of galactosialidosis. The prominent endothelial vacuolisation and focal cerebrovascular lesions, that have not previously been described in galactosialidosis, may be features specific to the rapidly progressive early-infantile form.

Brain↗
PubMed2005

Effects of combined oral conjugated estrogens and medroxyprogesterone acetate on brain infarction size after experimental stroke in rat.

The reason that estrogen is strongly protective in various estrogen-deficient animal models while seemingly detrimental in postmenopausal women remains unclear. It hypothesized that prolonged oral medroxyprogesterone (MPA) plus oral conjugated equine estrogens (CEE) diminishes estrogen ability to reduce stroke damage in the rodent stroke model. To test the hypothesis, we fed ovariectomized rats CEE or MPA, or a combination of CEE and MPA (CEP), before inducing 120 min of reversible focal stroke, using the intraluminal filament model. After 22 h reperfusion, the brains were harvested and infarction volumes were quantified. Treatment with CEE alone or with CEP reduced cortical infarction volume. However, CEP failed to provide ischemic protection in subcortical regions. It was concluded that CEE alone, or with CEP, is neuroprotective in the cortex, but interactive effects between the hormones may counteract CEE beneficial effects in subcortical brain regions.

Animals↗
PubMed1991

Cogan's syndrome complicated by lacunar brain infarcts.

Cogan's syndrome, nonsyphilitic interstitial keratitis with vestibuloauditory dysfunction, is an uncommon disease of young adults, probably a manifestation of vasculitis. A 32 year old woman with this syndrome developed a thalamic syndrome with amnesia and dysphasia due to lacunar infarcts.

Adult↗
PubMed1999

[Two cases of brain infarction associated with dissection of the thoracic aorta].

Case 1: a 57-year-old woman, who suddenly developed disturbance of consciousness, left spatial neglect, and left hemiparesis, was admitted to our hospital on the day 1. Brain CT scan on the day 2 revealed broad edematous infarction in her middle cerebral artery territory. The dissection of the thoracic aorta was observed with transesophageal echocardiography and brain embolism due to mural thrombus of the dissecting thoracic aorta was suspected. Case 2: a 67-year-old woman, who developed disturbance of consciousness, left spatial neglect, and left hemiparesis, was admitted to our hospital on the day 15. Brain CT scan on the day 15 showed non-edematous infarction in her middle cerebral artery territory. Contrast thoracic CT scan on the day 31 revealed the dissection of the thoracic aorta. No clinical exacerbation was observed, but brain CT scan on the day 94 showed broad infarction in her middle and anterior cerebral artery territories. It is considered that pseudolumen of the dissected thoracic aorta caused occlusion of her right internal carotid artery. Transesophageal echocardiography, or contrast thoracic CT scan should be considered for detection of the dissection of the thoracic aorta in the cases of cryptogenic stroke.

Aged↗
PubMed2000

CADASIL: hereditary arteriopathy leading to multiple brain infarcts and dementia.

Cerebral autosomal dominant arteriopathy with subcortical infarcts and leukoencephalopathy (CADASIL) often begins with migraine with aura. Recurrent strokes usually appear between 30 and 50 years of age. The arteriopathy develops slowly, resulting in destruction of smooth muscle cells and thickening and fibrosis of the walls of small and medium-sized penetrating arteries with consequent narrowing of the lumen. This impairs cerebral blood flow, visible in PET, and produces characteristic white-matter hyperintensities in T2-weighted MRI on the basis of which CADASIL may be diagnosed well before the first stroke. Multiple lacunar infarcts, mainly in the frontal white matter and basal ganglia, lead to progressive permanent brain damage manifested as cognitive decline and finally as dementia. At present, no specific therapy is available. Infarcts result from thickening and fibrosis of the walls of small and medium-sized penetrating arteries with consequent obliteration and/or thrombosis. Although the symptoms are almost exclusively neurological, the arteriopathy is generalized and diagnosis can be made on the basis of accumulation of pathognomonic basophilic, PAS-positive and in electron microscopy osmiophilic material between degenerating smooth muscle cells in dermal arteries. CADASIL is caused by missense point mutations in the Notch3 gene, which encodes a transmembrane receptor protein with an important signaling function during development. The gene defects lead to either a gain or loss of a cysteine residue in the extracellular N-terminal part of the molecule, most probably causing a conformational and functional alteration. The function of Notch3 in adults and the definite pathogenesis of CADASIL are still unknown, but interestingly its intramembranous proteolytic cleavage may be regulated or implemented by presenilin similarly as cleavage of amyloid precursor protein in Alzheimer's disease.

Adult↗
PubMed2004

[Acute brain infarction clearly demonstrated by using the three-dimensional stereotactic surface projections (3D-SSP) of 99mTc-HMPAO SPECT].

We report a 66-year-old ambidextrous man who suddenly developed aphasia seven days after coronary artery bypass grafting surgery. CT scan performed 30 minutes after onset failed to depict acute ischemic lesion. MR imaging could not be performed because of intrathoracic wires. An emergent angiogram demonstrated filling defect in the right precentral artery territory. Transaxial images of 99mTc-HMPAO SPECT showed hypoperfusion areas in the right frontal and left temporo-parietal regions. Using the three-dimensional stereotactic surface projections (3D-SSP) of 99mTc-HMPAO SPECT, we could clearly detect a sharply demarcated ischemic area which was later confirmed to be an infracted lesion in the follow-up CT. 3D-SSP, thus, appears to be useful for identifying acute infarction in such cases that MRI is impermissible.

Acute Disease↗
PubMed1991

Sensorimotor performance and rotation correlate to lesion size in right but not left hemisphere brain infarcts in the spontaneously hypertensive rat.

In order to correlate behavioural deficits to lesion size and to reveal possible functional asymmetries in the rat brain, locomotor activity, rotation and sensorimotor integration to touch were studied in spontaneously hypertensive rats (SHR) subjected to right or left middle cerebral artery occlusion. Control and infarcted rats showed no difference in locomotor activity. Infarcted rats tended to rotate towards the side of the lesion. A large sensorimotor deficit was found contralateral to the infarcted hemisphere. The absolute values of the side-biases for the rotation and sensorimotor tests were of the same degree irrespective of lesion side. Whereas the left hemisphere lesion size did not correlate to the behavioural outcome, the size of the right hemisphere lesion was highly correlated to the total sensorimotor deficit. Furthermore, the sensorimotor deficit of specific body parts was found to correlate to the damage of certain brain regions in a rostrocaudal fashion, reminiscent of a somatotopical organization. The extent of ipsilateral rotation correlated to brain tissue loss at the level of the posterior caudate-putamen. The present results indicate an asymmetrical organization for brain functions involved in the performance of the rotation and sensorimotor tests.

Animals↗
PubMed1991

Dynamics of interstitial and intracellular pH in evolving brain infarct.

We examined the relationships between intracellular pH (pHi) and interstitial pH (pHe) in a rat model of focal ischemia. Interstitial pH was measured with pH-sensitive microelectrodes, and the average tissue pH was measured with the [14C]dimethadione method in rats subjected to occlusion of the right middle cerebral and common carotid arteries (MCA-CCAO). In normal cortex, pHe and pHi were 7.24 +/- 0.97 and 7.01 +/- 0.13 (means +/- SD, n = 6), respectively. In the ischemic cortex, pHe fell to 6.43 +/- 0.13, whereas pHi decreased only to 6.86 +/- 0.11 (n = 5) 1 h after MCA-CCAO. After 4 h of ischemia, the pHe was 6.61 +/- 0.09 and pHi was 6.62 +/- 0.20 (n = 4). Treatment with glucose before ischemia markedly lowered the pHe (5.88 +/- 0.17) but not pHi (6.83 +/- 0.03, n = 4) measured 1 h after ischemia. In the ischemic cortex of animals made hypoglycemic by pretreatment with insulin, neither pHe (7.25 +/- 0.06) nor pHi (6.99 +/- 0.13, n = 4) decreased. The demonstrated difference in pHi and pHe indicates that some cells remained sufficiently functional to maintain a plasma membrane gradient of protons within the evolving infarct. If the calculated pHi values accurately reflect the true pHi of cells within zones of severe focal ischemia, then cerebral infarction can proceed at pHi levels not greatly altered from normal.

Animals↗
PubMed1995

[Clinical application of magnetoencephalography for brain infarction].

Magnetoencephalography (MEG) is a noninvasive functional imaging technique that provides information regarding neuronal activity with high spatial resolution. Analyses of spikes and slow waves in various brain disorder have performed using spontaneous magnetic field, and functional mapping studies have performed using evoked magnetic field. The goal of this study was to determine the characteristics of MEG findings in these two magnetic fields for ischemic stroke patients. In the first examination, we recorded the spontaneous magnetic activity with a 37-channel neuromagnetometer and counted the number of equivalent current dipoles (neuromagnetic sources) which were divided into 6 groups with different frequencies of every 4 Hz. There were much more dipoles below 8 Hz in stroke patients than in normal controls, which tended to distribute in the hypoperfusion area near the infarct. In the second examination, we recorded auditory evoked responses for tone burst stimuli and analyzed the localization of dipoles for the 100-m.sec. component after the onset of the stimuli. The dipoles lay near the Heschl gyrus in most of control group. On the contrary, they often distributed apart from the Heschl gyrus in stroke patients with severely damaged regional oxygen metabolism measured by positron emission tomography, indicating an inappropriate response for auditory stimuli. In conclusion, MEG brought interesting informations for the brain function of stroke patients.

Brain↗