Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts:   Target Concepts:
Query: UMLS:C0022116 (ischemia)
 91,303 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Cerebral atrophy and the decrease in cerebral blood flow (CBF) progress with advancing age. Which of them takes first place, the changes in CBF or cerebral atrophy? We investigated longitudinal changes in CBF and cerebral atrophy in 14 patients with ischemic cerebrovascular disease (CVD): 11 patients with supratentorial lacunar infarction and 3 with carotid transient ischemia attack who were neurologically stable during the 1-3 years of observation. Cerebral atrophy was estimated by the brain atrophy index (BAI): one of the CT area measurement methods, and CBF was measured using the 133Xe inhalation technique. While significant progression of cerebral atrophy was observed, there was no significant change in CBF. Cerebral atrophy precedes the change in CBF and CVD.
 ...
PMID:Cerebral atrophy precedes the change in cerebral blood flow in patients with ischemic cerebrovascular disease: a short-term follow-up study. 161 56

A case of mitochondrial encephalomyopathy, lactic acidosis and stroke-like episodes, in which a pituitary growth hormone (GH) secretion deficiency of hypothalamic origin was revealed through neuro-endocrinological examinations, was described. The case was a 10-year-old girl, who had been suffering from generalized tonic seizures since age 5, four episodes of alternating hemiplegia since age 6, stunted growth since age 7, and simple partial motor seizures as well as gelastic seizures since age 8. Marked elevation of lactate and pyruvate in both serum and CSF, abundant ragged red fibers in biopsied muscle, and low density areas in the left occipital lobe and bilateral globus pallidus in addition to diffuse brain atrophy on CT scan and MRI of the head were demonstrated, although the activities of muscle enzymes complex I-IV were within normal ranges. Pituitary GH secretion was deficient under the loadings with insulin, L-DOPA, sleep, and a single growth hormone releasing factor (GRF) administration, but normal GH response was registered under the repetitive stimulation with GRF. Activities of other hormonal axes were normal. It is likely that short stature commonly observed in MELAS patients is due to hypothalamic dysfunction, which might be brought out by chronic ischemia and energy deficiency of the diencephalon based upon mitochondrial abnormality of that region. It is likely that gelastic seizure in this case is due to hypothalamic dysfunction.
 ...
PMID:[Hypothalamic GH Deficiency and gelastic seizures in a 10-year-old girl with MELAS]. 187 57

Computerized tomography in 134 patients with traumatic epilepsy allowed to reveal different changes in the brain tissue, meninges and CSF spaces. Early stages were characterized by signs of meningeal adhesions. With increased duration of the disease these changes were supplemented by signs brain atrophy in the form of dilatation of the subarachnoidal spaces, internal hydrocephalus. CSF cysts were diagnosed in 5 patients, porencephaly in 2, ischemia foci in the brain in 9 patients.
 ...
PMID:[The results of computed tomography in patients with traumatic epilepsy]. 251 89

One hypothesized cause of low-tension glaucoma is chronic or intermittent ischemia of the optic nerve. Since the optic nerve and brain are both parts of the central nervous system and share a common blood supply, the authors wondered if patients with low-tension glaucoma might also have clinical or radiographic evidence of cerebral atrophy. In this study, 27 patients with low-tension glaucoma were examined using neurobehavioral testing, electroencephalography, computerized tomographic scan, neurological history, and physical examination. In only a small number of patients were these tests abnormal. However, 12 of the 27 patients gave a history of common or classic migraine. This unexpected finding raises the possibility that migraine-related ischemia might be the pathogenic mechanism in some cases of low-tension glaucoma.
 ...
PMID:The neurologic evaluation of patients with low-tension glaucoma. 401

MRI findings and risk factors for vascular dementia were evaluated with multi-variate analysis in 96 multi-infarct patients without dementia and 40 multi-infarct patients with dementia (MID). Only subjects with small infarcts in the territory of the perforator artery or deep white matter were studied. The diagnosis of MID was diagnosed according to DMS-III criteria and Hachinski's ischemia score. Location and area of patchy high-intensity areas including small infarcts, the degree of periventricular high intensity (PVH), and the degree of brain atrophy were examined with MR images. Independent variables were: history of hypertension, diabetes mellitus, other complications; systolic and diastolic blood pressure, atherosclerotic index, hematocrit, history of smoking, level of education, and activities of daily life (ADL). Hayashi's quantification method II was used to analyze the data. The most significant correlation was found between history of hypertension and dementia (partial correlation coefficient: 0.39). Significant correlations were also found between ADL and dementia (0.32), between thalamic infarction and dementia (0.31), and between PVH and dementia (0.27). Age, brain atrophy index, and history of diabetes mellitus contributed little to dementia. The contribution to dementia did not differ significantly between right and left patchy high-intensity areas on MR images. Location of infarcts, except for bilateral thalamic infarcts and large PVH, contributed little to dementia. Thus it would be difficult to base a prediction of the prevalence of vascular dementia on MRI findings. However, both hypertension and ADL contribute to vascular dementia and both are treatable, which may be significant for the prevention of dementia.
 ...
PMID:[Difference in MRI findings and risk factors between multiple infarction without dementia and multi-infarct dementia]. 749 60

We investigated the effect of beraprost sodium (BPS), a new prostacyclin analog, and dizocilpine (MK-801) on repeated ischemia-induced cerebral atrophy and chronic cortical neuronal loss in gerbils. The left common carotid artery of gerbils was repeatedly occluded (for 10, 7, 7, and 7 min) at intervals of 24 h. The thickness of the cerebral cortex of the ischemic hemisphere diminished with increasing time of reperfusion after an ischemic insult. The animals were given BPS (1-100 micrograms/kg, po) or MK-801 (3-300 micrograms/kg, sc) after the first ischemic insult, and then twice daily for 4 wk. Increases in the amount of neuronal loss and acidophilic neurons, and progressive atrophy were observed with increasing time of reperfusion in the cerebral cortex of the ischemic hemisphere. Cortical sections revealed no astrocytes positive for glial fibrillary acidic protein (GFAP), whereas the hippocampal CA1 area showed neuronal loss accompanied by GFAP-positive astrocytes. In control animals at 4 wk survival, the area ratio (area of ischemic cortex/area of opposite cortex) and the cortical neurons ratio (number of neurons in ischemic cortex/number of neurons in opposite cortex) were 89.8 +/- 3.0% and 74.6 +/- 3.4%, respectively. BPS was found to inhibit atrophy and chronic cortical neuronal loss in the ischemic hemisphere in a dose-dependent manner, whereas MK-801 showed no inhibitory effects at any dose tested. These results may suggest that the nature of neuronal degeneration differs between the cortical and hippocampal areas, that cortical neuronal degeneration might not involve glutamate pathways with NMDA receptors in this model, and that prostacyclin could play an essential role in prevention of ischemia-induced progressive neuronal loss.
 ...
PMID:Effect of beraprost sodium (BPS), a prostacyclin analog, and dizocilpine (MK-801) on repeated ischemia-induced chronic cortical atrophy in gerbils. 770 5

Pattern of neurosonographic (NSG) abnormalities in 150 term newborn infants with hypoxic ischemic encephalopathy (HIE) was studied. Sonographic abnormalities, presumably indicating cerebral edema and or ischemia, were observed in 86% (n = 129) cases. Obliteration of the ventricles occurred as the sole abnormality in 30 (20%) cases. Eighty (53%) patients had diffusely increased echogenicity of the brain parenchyma (DPE) in addition to the compression of the ventricles, sulci and the interhemispheric fissure. Focal parenchymal echodense (FPE) lesions occurred in nine (6%) neonates with HIE. Ten (6.6%) patients, however, had increased periventricular echogenicity (PVE). Two patients, one with focal parenchymal lesions and the other with PVE had obliterated ventricles in addition. Regarding temporal sequence earliest NSG abnormalities were DPE or slit like ventricles that were observed on day-1 itself. Focal or periventricular echogenic lesions, however, made their first appearance on day-3 of life. Twenty one patients had normal scans. Fifty patients with abnormal scans died. None of the infants with normal scans, however, died (p < 0.001). At 4 weeks of age, scans performed in 100 survivors revealed no abnormality in 51 cases. Others showed development of cerebral atrophy (n = 21), multicystic encephalomalacia (n = 2), porencephalic cyst (n = 1), or persistence of PVE without cystic changes (n = 4). The results of this study highlight the diagnostic efficacy of neurosonography in cases of HIE. We suggest that it should be incorporated in the routine evaluation of patients with hypoxic brain injury.
 ...
PMID:Neurosonographic abnormalities in neonates with hypoxic ischemic encephalopathy. 789 Mar 38

We studied the development of brain atrophy after transient focal ischemia in rats. The animals were subjected to cerebral ischemia induced by embolization of the right middle cerebral artery (MCA) for 60 min. The brains were studied morphologically 7 days, 1 month, 3 months and 9 months after recirculation. In addition, the effects of a new calcium antagonist, KB-2796, and a glutamate receptor antagonist, 6,7-dinitroquinoxaline-2,3-dione (DNQX); were evaluated in this model 1 month after ischemia. The hemispheric volume of the ipsilateral ischemic side, expressed as a percentage of that on the contralateral non-ischemic side, was 99% in the sham operation group, 94% at 7 days, 87% at 1 month, 68% at 3 months and 65% at 9 months. Atrophy of the striatum and cortex, but not the hippocampus, was observed 1 month after ischemia. Atrophy of the ipsilateral substantia nigra and the thalamus, which are remote from the ischemic region, was observed 7 days and 1 month, respectively, after ischemia. Correlations between the extent of the atrophy in the striatum and that in the substantia nigra and between the extent of the atrophy in the cortex and in the thalamus were statistically significant. Treatment with KB-2796 or DNQX administered intraperitoneally at a dose of 10 mg/kg twice 30 min before ischemia and immediately after ischemia was effective in reducing the extent of atrophy in both the ipsilateral ischemic and non-ischemic regions. These results suggest that brain atrophy on the ipsilateral ischemic side develops time-sequentially after transient focal ischemia and that ischemia affects not only the primary ischemic focus but also remote regions through transsynaptic connections, and that KB-2796 and DNQX have beneficial effects on atrophy in the chronic phase after ischemia.
 ...
PMID:Chronological atrophy after transient middle cerebral artery occlusion in rats. 837 56

Ninety-six patients with transient ischemia attacks were examined by transcranial Doppler (TCD), carotid color-coded ultrasonic imagine, brain computed tomographic scan (CT), compared with digital subtract angiography (DSA), MRI and MRA were done in some cases. The abnormality of CT and MRI was 30.2% and 74.1%, respectively. The most common findings were lacunar infarction or cerebral atrophy. Sixty-two cases fulfilled the TCD criteria of definitive arterial stenosis (64.5%) and three cases of arteriovenous malformation, among whom 27 patients (43.5%) carried out the examination of DSA. There was an excellent coincidence between the DSA and TCD findings, although DSA showed more vessels involved in some patients. Of the 96 cases, the intracranial arterial stenosis or occlusion was in 48.5% and the extracranial in 17.8%. The younger patients (age < 60 years) were subject to involvement of unilateral intracranial artery, but the older had predominantly the bilateral intracranial arterial and extracranial carotid or subclavian arterial lesions.
 ...
PMID:[Intra- and extra-cranial arterial lesions in TIA patients]. 857 51

Perinatal ischemia and/or hypoxia in humans are major risk factors for neurologic injury that often manifest as sensorimotor and locomotor deficits throughout development and into maturity. In these studies, we utilized an established model of neonatal ischemic-hypoxia that creates unilateral striatal, cortical, and hippocampal damage (Rice III, J.E., Vanucci, R.C. and Brierley, J.B., Ann. Neurol., 9 (1981) 131-141) to investigate sensorimotor and locomotor deficits in these animals during development and as adults. Sensorimotor deficits were examined by measuring the amount of time that the animals were able to remain on a rotating treadmill. Locomotor abnormalities were assessed by measuring apomorphine-induced rotational asymmetry. Following the neonatal ischemic-hypoxic episode, at 3-9 weeks of age, animals were not able to remain on the treadmill as long as their normal littermate controls. In addition, these animals demonstrated an abnormal, ipsiversive rotational asymmetry in response to systemic administration of apomorphine. When these animals reached adulthood, the degree of atrophy in specific regions of the damaged hemisphere was quantified using measurements of cross-sectional area. The mean cross-sectional area of the striatum was decreased by 29%, the sensorimotor cortex area by 26%, and the dorsal hippocampus cross-sectional area was approximately 6% of its normal size. These data suggest that this rodent model of neonatal ischemic-hypoxic brain injury results in cerebral atrophy and long-lasting sensorimotor and locomotor deficits. These particular behavioral tasks may be used in future studies to assess locomotor and sensorimotor deficits following neonatal ischemic-hypoxic brain injury.
 ...
PMID:Long-term effects of neonatal ischemic-hypoxic brain injury on sensorimotor and locomotor tasks in rats. 886 51


1 2 3 4 5 6 7 8 9 Next >>