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

To investigate the sequence and nature of the peripheral vascular responses during the prodromal period of heat stroke, rats were implanted with Doppler flow probes on the superior mesenteric (SMA), left iliac (LIA) or left renal (LRA), and external caudal (ECA) arteries. Studies were performed in unanesthetized rats (n = 6) exposed to 46 degrees C and in chloralose-anesthetized animals (n = 11) at 40 degrees C. Core (Tc) and tail-skin temperatures, heart rate, and mean arterial blood pressure (MAP) were also monitored. In both groups, prolonged (70-150 min) exposure progressively elevated Tc from 37.0 to 44.0 degrees C. MAP rose to a plateau then fell precipitously as Tc exceeded 41.5 degrees C. SMA resistance increased throughout the early stages of heating, with a sharp decline from this elevated level 10-15 min before the precipitous fall in MAP. ECA resistance fell initially but increased in the terminal stage of heating. In unanesthetized animals, LIA resistance progressively declined. In chloralose-anesthetized animals LRA resistance rose progressively, then increased markedly as Tc exceeded 41.5 degrees C. These data support the hypothesis that a selective loss of compensatory splanchnic vasoconstriction may trigger the cascade of events that characterize heat stroke. This differential vascular response was similar in both unanesthetized and anesthetized animals.
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PMID:Peripheral vascular responses to hyperthermia in the rat. 340 42

Repetitive passive movements are part of most rehabilitation procedures, especially in patients with stroke and motor deficit. However, little is known about the consequences of repeated proprioceptive stimulations on the intracerebral sensorimotor network in humans. Twelve healthy subjects were enrolled, and all underwent two functional magnetic resonance imaging (fMRI) sessions separated by a 1-month interval. Passive daily movement training was performed in six subjects during the time between the two fMRI sessions. The other six subjects had no training and were considered as the control group. The task used during fMRI was calibrated repetitive passive flexion-extension of the wrist similar to those performed during training. The control task was rest. The data were analyzed with SPM96 software. Images were realigned, smoothed, and put into Talairach's neuroanatomical space. The time effect from the repetition of the task was assessed in the control group by comparing activation versus rest in the second session with activation versus rest in the first session. This time effect then was used as null hypothesis to assess the training effect alone in our trained group. Passive movements compared with rest showed activation of most of the cortical areas involved in motor control (i.e., contralateral primary sensorimotor cortex, supplementary motor area [SMA], cingulum, Brodmann area 40, ipsilateral cerebellum). Time effect comparison showed a decreased activity of the primary sensorimotor cortex and SMA and an increased activity of ipsilateral cerebellar hemisphere, compatible with a habituation effect. Training brought about an increased activity of contralateral primary sensorimotor cortex and SMA. A redistribution of SMA activity was observed. The authors demonstrated that passive training with repeated proprioceptive stimulation induces a reorganization of sensorimotor representation in healthy subjects. These changes take place in cortical areas involved in motor preparation and motor execution and represent the neural basis of proprioceptive training, which might benefit patients undergoing rehabilitative procedures.
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PMID:Neural substrate for the effects of passive training on sensorimotor cortical representation: a study with functional magnetic resonance imaging in healthy subjects. 1072 12

The brain's response to ischemia, which helps determine clinical outcome after stroke, is regulated partly by competing genetic programs that respectively promote cell survival and delayed cell death. Many genes involved in this response have been identified individually or systematically, providing insights into the molecular basis of ischemic injury and potential targets for therapy. The development of microarray systems for gene expression profiling permits screening of large numbers of genes for possible involvement in biological or pathological processes. Therefore, we used an oligodeoxynucleotide-based microarray consisting of 374 human genes, most implicated previously in apoptosis or related events, to detect alterations in gene expression in the hippocampus of rats subjected to 15 minutes of global cerebral ischemia followed by up to 72 hours of reperfusion. We found 1.7-fold or greater increases in the expression of 57 genes and 1.7-fold or greater decreases in the expression of 34 genes at 4, 24, or 72 hours after ischemia. The number of induced genes increased from 4 to 72 hours, whereas the number of repressed genes decreased. The induced genes included genes involved in protein synthesis, genes mutated in hereditary human diseases, proapoptotic genes, antiapoptotic genes, injury-response genes, receptors, ion channels, and enzymes. We detected transcriptional induction of several genes implicated previously in cerebral ischemia, including ALG2, APP, CASP3, CLU, ERCC3, GADD34, GADD153, IGFBP2, TIAR, VEGF, and VIM, as well as other genes not so implicated. We also found coinduction of several groups of related genes that might represent functional modules within the ischemic neuronal transcriptome, including VEGF and its receptor, NRP1; the IGF1 receptor and the IGF1-binding protein IGFBP2; Rb, the Rb-binding protein E2F1, and the E2F-related transcription factor, TFDP1; the CACNB3 and CACNB4 beta-subunits of the voltage-gated calcium channel; and caspase-3 and its substrates, ACINUS, FEM1, and GSN. To test the hypothesis that genes identified through this approach might have roles in the pathophysiology of cerebral ischemia, we measured expression of the products of two induced genes not heretofore implicated in cerebral ischemia-GRB2, an adapter protein involved in growth-factor signaling pathways, and SMN1, which participates in RNA processing and is deleted in most cases of spinal muscular atrophy. Western analysis showed enhanced expression of both proteins in hippocampus at 24 to 72 hours after ischemia, and SMN1 was localized by immunohistochemistry to hippocampal neurons. These results suggest that microarray analysis of gene expression may be useful for elucidating novel molecular mediators of cell death and survival in the ischemic brain.
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PMID:Microarray analysis of hippocampal gene expression in global cerebral ischemia. 1145 15

Thy-1 nephritis was induced in stroke-prone spontaneously hypertensive rats (SHR-SP) with unilateral nephrectomy (UNX) and normotensive same genetic strain Wistar-Kyoto (WKY) rats with UNX to evaluate whether the tubulointerstitial injury in Thy-1 nephritis is accelerated by long-term systemic and intraglomerular hypertension. SHR-SP that underwent UNX at twelve weeks of age were randomly assigned to receive monoclonal anti-thy 1.1 antibody (group SP), and normal saline (group SC). Age-matched normotensive WKY rats served as controls and were given the same dose of monoclonal anti-thy 1.1 antibody after UNX (group WK). In all groups, the blood pressure and renal function were assessed, and morphologic changes of tubulointerstitium were examined by using immunohistochemistry and light microscopy twelve weeks after Thy-1 nephritis induction (in groups SP and WK) and UNX alone (in group SC). In all groups, histological findings, the degree of monocyte/macrophage infiltration, interstitial expression of alpha-smooth muscle actin (alpha-SMA), which is a marker for myofibroblasts, and the degree of tubular cell proliferation were examined. In addition, assessments of blood pressure, serum creatinine and BUN levels, and the degree of proteinuria were made. In parallel to glomerular structural damage, interstitial fibrosis with predominant monocyte/macrophage influx, increased interstitial expression of alpha-SMA and tubular cell proliferation were observed in group SP. A significant increase in serum creatinine and proteinuria were also present in this group. In contrast, the changes observed in group SC were not so evident or extensive as in group SP. The level of proteinuria was lower than that in group SP. No evident tubulointerstitial changes were found in group WK. The results showed that tubulointerstitial injury was prominently progressed in the hypertensive model with Thy-1 nephritis. This suggests that sustained systemic and glomerular hypertension is not only ultimately responsible for the progression of immunologically mediated glomerular injury, but is also responsible for subsequent tubulointerstitial changes. Migration and proliferation of myofibroblasts and intense influx of monocytes/macrophages may contribute to the development of tubulointerstitial fibrosis.
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PMID:Tubulointerstitial injury of Thy-1 nephritis in uninephrectomized stroke-prone spontaneously hypertensive rats. 1150 77

Since serotonin (5-HT) stimulates motor function, pharmacological potentiation of 5-HT neurotransmission may improve motor function in healthy subjects and, possibly, recovery in post-stroke patients. Indeed, fluoxetine, a selective serotonin reuptake inhibitor (SSRI), increased activation in executive motor areas of healthy subjects as fenozolone, a releaser of monoamines (including noradrenaline, dopamine, and serotonin) from intracellular stores. This study is intended to test the hypothesis that paroxetine can likewise modulate brain motor activity in a dose-dependent manner in healthy subjects. In a double-blind counterbalanced study, six subjects underwent functional MRI examinations on three sessions 1 week apart (E1, E2, and E3) at the time of peak plasma concentrations (5 h after drug intake, i.e., either 20 or 60 mg of paroxetine or placebo) with a complex sequential opposition task. Rest and activation alternated in a block design. During activation, subjects performed, with the right hand, a 1-Hz-paced task that alternated two fist closings with a sequential opposition task. Paroxetine elicited effects similar to those reported for fluoxetine; notable changes were hyperactivation in the contralateral S1/M1, and posterior SMA and widespread hypoactivation of basal ganglia and cerebellum. There was an inverse correlation between dose and effect: significantly greater effects were observed with the 20-mg dose compared with 60 mg. Paroxetine dose-dependently modulates activation of the entire motor pathway in a way that favors motor output. Thus, a single dose of the SSRI paroxetine reorganized motor processing.
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PMID:A single dose of the serotonin neurotransmission agonist paroxetine enhances motor output: double-blind, placebo-controlled, fMRI study in healthy subjects. 1177 71

Under normal circumstances, information from a number of sources is combined to compute a unitary percept of the body. However, after pathology these influences may be perceived simultaneously, resulting in multiple dissociated conscious representations. In a recent paper, we described subject E.P., a right-handed female stroke patient with a right frontomesial lesion who sporadically experiences a supernumerary 'ghost' left arm that occupies the previous position of the real left arm after a delay of 60-90 s. We used a delayed response paradigm with functional MRI to examine the haemodynamic correlates of E.P.'s illusion. Comparison of periods of time during scanning when the ghost arm was present against when it was not revealed a single cluster (9 voxels, t = 5.11, P < 0.012 corrected for multiple comparisons) located on the right medial wall in the supplementary motor area ('SMA proper'). Our results suggest that areas traditionally classified as part of the motor system can influence the conscious perception of the body. We propose that, as a consequence of her injury, E.P. is aware of the position of the phantom limb in this 'action space' while also continuing to be aware of the true position of her real limb on the basis of afferent somatosensory information.
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PMID:Whose arm is it anyway? An fMRI case study of supernumerary phantom limb. 1202 15

Identification of novel modulators of ischemic neuronal death helps in developing new strategies to prevent the stroke-induced neurological dysfunction. Hence, the present study evaluated the gene expression changes in rat cerebral cortex at 6 and 24 h of reperfusion following transient middle cerebral artery occlusion (MCAO) by GeneChip analysis. Transient MCAO resulted in selective increased mRNA levels of genes involved in stress, inflammation, transcription and plasticity, and decreased mRNA levels of genes which control neurotransmitter function and ionic balance. In addition to a number of established ischemia-related genes, many genes not previously implicated in transient focal ischemia-induced brain damage [suppressor of cytokine signaling (SOCS)-3, cAMP responsive element modulator (CREM), cytosolic retinol binding protein (CRBP), silencer factor-B, survival motor neuron (SMN), interferon-gamma regulatory factor-1 (IRF-1), galanin, neurotrimin, proteasome subunit RC8, synaptosomal-associated protein (SNAP)-25 A and B, synapsin 1a, neurexin 1-beta, ras-related rab3, vesicular GABA transporter (VGAT), digoxin carrier protein, neuronal calcium sensor-1 and neurodap] were observed to be altered in the ischemic cortex. Real-time PCR confirmed the GeneChip results for several of these transcripts. SOCS-3 is a gene up-regulated after ischemia which modulates inflammation by controlling cytokine levels. Antisense knockdown of ischemia-induced SOCS-3 protein expression exacerbated transient MCAO-induced infarct volume assigning a neuroprotective role to SOCS-3, a gene not heretofore implicated in ischemic neuronal damage.
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PMID:Gene expression analysis of spontaneously hypertensive rat cerebral cortex following transient focal cerebral ischemia. 1243 78

Recovery of motor function after stroke is associated with reorganization in central motor networks. Functional imaging has demonstrated recovery-dependent alterations in brain activation patterns when compared to healthy controls. These alterations are variable across stroke subjects. Factors identified as contributing to this variability are the degree of functional impairment, the time interval since stroke, and rehabilitative therapies. Here, the hypothesis is tested that lesion location influences the activation patterns. Using functional magnetic resonance imaging, the objective was to characterize similarities or differences in movement-related activation patterns in patients chronically disabled by cortical plus subcortical or subcortical lesions only. Brain activation was mapped during paretic and non-paretic movement in 11 patients with subcortical stroke, in nine patients with stroke involving sensorimotor cortex, and in eight healthy volunteers. Patient groups had similar average motor deficit as measured by a battery of scores and strength measures. Substantial differences between patients groups were found in activation patterns associated with paretic limb movement: whereas contralateral motor cortex, ipsilateral cerebellum (relative to moving limb), bilateral mesial (cingulate, SMA), and perisylvian regions were active in subcortical stroke, cortical patients recruited only ipsilateral postcentral mesial hemisphere regions, and areas at the rim of the stroke cavity. For both groups, activation in ipsilateral postcentral cortex correlated with motor function; in subcortical stroke, the same was found for mesial and perisylvian regions. Overall, brain activation in cortical stroke was less, while in subcortical patients, more than in healthy controls. For non-paretic movement, activation patterns were similar to control in cortical patients. In subcortical patients, however, activation patterns differed: the activation of non-paretic movement was similar to that of paretic movement (corrected for side). The data demonstrate more differences than similarities in the central control of paretic and non-paretic limb movement in patients chronically disabled by subcortical versus cortical stroke. Whereas standard motor circuitry is utilized in subcortical stroke, alternative networks are recruited after cortical stroke. This finding proposes lesion-specific mechanisms of reorganization. Optimal activation of these distinct networks may require different rehabilitative strategies.
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PMID:Lesion location alters brain activation in chronically impaired stroke survivors. 1500 59

The aim of this 1-year longitudinal fMRI study was to compare hand motor activation patterns between cerebrovascular paretic patients with a subcortical infarction and healthy elderly subjects and to evaluate the changes between the subacute phase and the chronic phase of recovery. We studied eight right-handed patients with pure motor hemiparesis due to a single ischemic infarct of the corticospinal tract. Each patient underwent a first fMRI (E1) 20 +/- 9 days after stroke, a second (E2) after 4 months and a third (E3) 12 months after stroke. During each fMRI session, the patients performed an active motor task consisting of audio-paced (1 Hz) finger flexion-extension of the paretic hand and underwent a passive motor task consisting of flexion-extension of the paretic hand performed by an examiner. Data were analyzed with SPM99 (random effect analyses). Patients had recovered at E2, were stable between E2 and E3, but still experienced a hand weakness. Displacement of activation maxima coordinates in patients compared to healthy subjects suggested an early reorganization within the SMA and a secondary reorganization within the ipsilesional S1M1 at E2. The main differences between patients and healthy subjects were (1) recruitment of the posterior part of the cingulate cortex and SMA, (2) a general hyperactivation (except in the deefferented primary motor cortex) and (3) an evolution in the S1M1 activation from an early (20 days after stroke) contralesional hyperactivation to a later (4 months after stroke) ipsilesional hyperactivation concomitant to recovery. Changes in activation were confirmed by the passive task that involved no effort and little attention. Despite clinical stability, changes in brain processing seemed to occur between E2 and E3 corresponding to a normalization of ipsilesional S1M1 activation, a decrease of bilateral cerebellar activation, and a progressive increase in SII-BA 40 activity suggesting evolving compensatory networks to sustain recovery.
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PMID:A longitudinal fMRI study: in recovering and then in clinically stable sub-cortical stroke patients. 1552 83

In this paper, a new approach aimed at improving the performance of intraneural longitudinal interfaces (tf-LIFEs) with the peripheral nervous system (PNS) is presented. Our goal is to develop a movable interface by embedding microactuators into the flexible tf-LIFEs structure. In this way, the optimal position of the electrical contacts can be searched inside the PNS and lost connections with neural cells could be replaced. For this purpose a thin film of shape memory alloy (tf-SMA) was selected. A multisegmented SMA was realized and embedded between two polyimide thin films in order to simulate the tf-LIFE structure. Thermal evaluation, fabrication procedure, the first characterization and preliminary experimental results of the new movable interface are described in the manuscript. A total controllable stroke of about 10 microm was obtained for the presented prototype.
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PMID:Shape memory alloy microactuation of tf-lIFes: preliminary results. 1755 30


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