Neuronal network disturbance after focal ischemia in rats.

Diffusion tensor imaging can be used in vivo to assess the longitudinal and regional microstructural changes occurring after middle cerebral artery (MCA) infarcts in humans. Nine patients were investigated 1 week (D7), 1 (M1), 3 (M3), and 6 months (M6) after the occurrence of an isolated MCA infarction. First, an overall analysis was performed using histograms of mean diffusivity (MD) and fractional anisotropy (FA) in each hemisphere. Thereafter, the regional pattern of diffusion changes was investigated voxel by voxel with statistical parametric mapping 99. In the hemisphere ipsilateral to the infarction, histogram analysis revealed a significant decrease in FA between D7 and M6 associated with a progressive increase in MD from D7 to M3. Remote from the MCA territory, the voxel by voxel analyses detected a significant increase in MD within the thalamus at M3 and M6 and a reduction in FA along the pyramidal tract at M6. In the contralateral hemisphere, between D7 and M6, a significant hemispheric atrophy was observed in association with a global reduction in anisotropy, in the absence of distinctive regional diffusion changes. These results suggest that micro-and macrostructural tissue modifications can be detected with diffusion tensor imaging in regions remote from the ischemic area in both hemispheres.

Section: Introductionsupporting

confidence: 59%

Longitudinal Diffusion Changes in Cerebral Hemispheres after MCA Infarcts

Buffon

Molko

Hervé

et al. 2005

“…The disturbance of somatosensory transmis sion observed 1 day after occlusion is attributable to acute ischemic elimination of corticofugal facilita tive activities upon the thalamic relay neurons. This has been suggested by our previous deoxyglucose study (Kataoka et al, 1989). Transient recovery of somatosensory transmission occurred 4-7 days af ter infarct and preceded subsequent depression ob served on the 14th postocclusion day.…”

Section: ----------------------------------------------supporting

confidence: 69%

“…The Fink-Heimer silver impregnation method revealed massive terminal degeneration in the ipsi lateral thalamus 4 days after MCA occlusion (Kataoka et al, 1989). In the present study, TTC staining decreased in the ipsilateral thalamus 4 days after MCA occlusion.…”

Section: ----------------------------------------------supporting

confidence: 58%

“…It has been suggested that these pro cesses are attributable to neurotrophic mechanisms (Yamada et aI., 1991). However, there is a lack of knowledge concerning neurofunctional changes during these processes except for a deoxyglucose autoradiographic study, which showed decreases in ipsilateral thalamic glucose utilization in the acute stage (Kataoka et al, 1989). We investigated the sequential changes in the direct function of the tha lamic neurons during degeneration after cortical in farct by recording the thalamic unit activity follow ing middle cerebral artery (MCA) occlusion in rats.…”

mentioning

confidence: 99%

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Functional Changes in Thalamic Relay Neurons after Focal Cerebral Infarct: A Study of Unit Recordings from VPL Neurons after MCA Occlusion in Rats

Tokuno

Kataoka

Asai

et al. 1992

Summary:We evaluated neuronal and histological changes of thalamic neurons 1, 4, 7, and 14 days after middle cerebral artery (MCA) occlusion in rats. After the somatosensory evoked potentials (SEPs) were measured from the cerebral cortex, the thalamic relay neuronal ac tivities were recorded with a glass microelectrode follow ing repetitive electrical stimulation of the contralateral forepaw at frequencies ranging from 1 to 50 Hz. In -95% of the occluded rats, the ipsilateral somatosensory cortex and/or the subcortical somatosensory pathway developed infarct, resulting in SEP loss. We evaluated unit data from rats with abolished SEPs. The average firing rate of the nucleus ventralis posterolateralis (VPL) neurons in response to 25 stimulations at 30 Hz was significantly reduced to 0.1 spike/stimulus 1 day after MCA occlusion.After the occurrence of a localized brain lesion, neuronal structures remote from the primary lesion develop functional and/or histological changes through the neuronal pathway. The thalamocortical and the corticothalamic pathway closely connects the cerebral cortex and the ipsilateral thalamus. Cortical infarct results in progressive degeneration in the ipsilateral thalamus in humans and rats

“…Numerous afferent and efferent cortical projections pass through or end in the infarcted zone, which included part of the somatosensory cortex and lateral striatum. After unilateral middle cerebral artery occlusion in rats, prominent axonal and terminal degeneration has been shown in cortical, striatal, thalamic, and nigral areas adjacent to the infarct (Iizuka et al, 1989;Kataoka et al, 1989). Furthermore, Yam et al (1998) have reported breakdown of axonal cytoskeleton and disruption of axonal transport inside and around the infarct after cerebral ischemia in rats.…”

Section: Restoration Of Ipsilateral Connectivitymentioning

confidence: 99%

Manganese-Enhanced MRI of Brain Plasticity in Relation to Functional Recovery after Experimental Stroke

Zijden

Bouts

et al. 2007

Restoration of function after stroke may be associated with structural remodeling of neuronal connections outside the infarcted area. However, the spatiotemporal profile of poststroke alterations in neuroanatomical connectivity in relation to functional recovery is still largely unknown. We performed in vivo magnetic resonance imaging (MRI)-based neuronal tract tracing with manganese in combination with immunohistochemical detection of the neuronal tracer wheatgerm agglutinin horseradish peroxidase (WGA-HRP), to assess changes in intra-and interhemispheric sensorimotor network connections from 2 to 10 weeks after unilateral stroke in rats. In addition, functional recovery was measured by repetitive behavioral testing. Four days after tracer injection in perilesional sensorimotor cortex, manganese enhancement and WGA-HRP staining were decreased in subcortical areas of the ipsilateral sensorimotor network at 2 weeks after stroke, which was restored at later time points. At 4 to 10 weeks after stroke, we detected significantly increased manganese enhancement in the contralateral hemisphere. Behaviorally, sensorimotor functions were initially disturbed but subsequently recovered and plateaued 17 days after stroke. This study shows that manganese-enhanced MRI can provide unique in vivo information on the spatiotemporal pattern of neuroanatomical plasticity after stroke. Our data suggest that the plateau stage of functional recovery is associated with restoration of ipsilateral sensorimotor pathways and enhanced interhemispheric connectivity.