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Query: UMLS:C0038454 (stroke)
 147,016 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

In order to compare the sensitivity of multichannel derived median nerve SEP with EEG in vascular cerebral lesions we examined 22 normals and 23 patients. SEP components within the first 50 ms could be divided into main waveform patterns: (1) a W-shaped parietal pattern consisting of N20, P25, N35 and P45 in most cases. (2) a frontal pattern with P20 and N30 as well as possibly detectible N24, P28, P33, N40 and P50. (3) a central P22. Two younger normals showed a V-shaped parietal pattern with N20 and P35, a frontal pattern with P20 and N36, and central P22 with a remarkably long latency. All components could be analysed sufficiently by means of three representative electrode positions (stimulation right/left): P3/P4, C3/C4, and F3/F4, which reduces the expense of recording and analysing considerably. 21 patients (91.3%) showed abnormal results in SEP, whereas 14 patients (60.9%) in EEG. A three channel electrode array can increase the usefulness of SEP and detect cerebral dysfunctions in cerebral lesions in spite of normal EEG under routine examination conditions. Analysis of multichannel derived SEPs during treatment and recovery after stroke and search for the prognostic value in the acute stage of the disease should be done in future.
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PMID:Multichannel derived median nerve SEP compared to EEG in patients with vascular cerebral lesions. 1144 39

Stroke in term neonates remains a significant cause of long-term neurological morbidity. This study was designed to assess the relationships between ischemic stroke induced by permanent unilateral carotid ligation in P12 CD1 mice and the structural and functional outcomes in the young mice as a consequence. After P12 ischemic strokes, mice were behaviorally tested using accelerated rotorod, spontaneous alternation on a T-maze, open-field, and cylinder tests between P33 and P39. Brain injury was scored by histology at P40 with cresyl violet-stained coronal sections and computerized quantification of the ischemic injury. The ligation-injured mice were not different from controls on cylinder testing for asymmetric use of their forelimb, or on rotorod measures. In the spontaneous alternation task, however, injured mice demonstrated significantly lower rates of alternation indicating a deficit in working memory. Open-field testing repeated on two consecutive days revealed that the ligated mice were less active than the controls and that they failed to habituate to the open field environment between sessions indicating a learning deficit. Overall, our results demonstrate that ischemia induced by our neonatal stroke model produces behavioral deficits that are consistent with the brain injury.
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PMID:Chronic brain injury and behavioral impairments in a mouse model of term neonatal strokes. 1876 Oct 39

Stroke in the neonatal brain is an understudied cause of neurologic morbidity. Recently we have characterized a new immature mouse model of stroke utilizing unilateral carotid ligation alone to produce infarcts and acute seizures in postnatal day 12 (P12) CD-1 mice. In this study, the amount of poststroke neural progenitor proliferation was examined in the subgranular (SGZ) of the dentate gyrus and the subventricular zone (SVZ) 7, 14, and 21days after ischemia (DAI). A single IP injection (50 mg/kg) of bromodeoxyuridine (BrdU) given 2 hr before perfusion fixation labeled newborn cells. Early cell phenotypes were quantified by colabeling with GFAP, nestin, and DCX. Control mice revealed an age-dependent decrease in neural proliferation, with an approximately 50% drop in BrdU-labeled cell counts at P33 compared with P19 both in the SGZ and in the SVZ. Significant reduction in the amount of neural proliferation in the ipsilateral injured SGZ of ligated mice correlated with both the severity of the stroke-injury and the acute seizure scores. Similar correlations were not detected contralaterally. Contralateral SGZ neural proliferation was initially lowered at 7 DAI but normalized by 21 DAI. In both injured and control brains, approximately 90% of newborn SGZ cells colabeled with nestin, approximately 30% colabeled with GFAP, and a few colabeled with DCX. In contrast, poststroke SVZ cell proliferation was enhanced ipsi- more than contralaterally at 7 DAI. In the SVZ, the enhanced neural proliferation normalized to control levels by P33. In conclusion, the neural cell proliferation was differentially altered in the SGZ vs. SVZ after neonatal stroke.
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PMID:Poststroke subgranular and rostral subventricular zone proliferation in a mouse model of neonatal stroke. 1939 74