Enhanced Neocortical Neural Sprouting, Synaptogenesis, and Behavioral Recovery With
            <scp>d</scp>
            -Amphetamine Therapy After Neocortical Infarction in Rats

Stroemer, R. Paul; Kent, Thomas A.; Hulsebosch, Claire E.

doi:10.1161/01.str.29.11.2381

Cited by 329 publications

(170 citation statements)

References 110 publications

Supporting

Mentioning

161

Contrasting

Unclassified

Order By: Relevance

“…It is possible that higher and more frequent doses are required, as tested in experimental models. 5,9,47,48 Fourth, treatment was started between 4 and 30 days after stroke onset. Similar studies have failed to address the issue of most favourable time to recruitment and the optimal therapeutic window remains to be elucidated.…”

Section: Discussionmentioning

confidence: 99%

Amphetamine increases blood pressure and heart rate but has no effect on motor recovery or cerebral haemodynamics in ischaemic stroke: a randomized controlled trial (ISRCTN 36285333)

et al. 2007

View full text Add to dashboard Cite

Amphetamine enhances recovery after experimental ischaemia and has shown promise in small clinical trials when combined with motor or sensory stimulation. Amphetamine, a sympathomimetic, might have haemodynamic effects in stroke patients, although limited data have been published. Subjects were recruited 3-30 days post-ischaemic stroke into a phase II randomized (1:1), double-blind, placebo-controlled trial. Subjects received dexamphetamine (5 mg initially, then 10 mg for 10 subsequent doses with 3-or 4-day separations) or placebo in addition to inpatient physiotherapy. Recovery was assessed by motor scales (Fugl-Meyer (FM)), and functional scales (Barthel index (BI) and modified Rankin score (mRS)). Peripheral blood pressure (BP), central haemodynamics and middle cerebral artery blood flow velocity were assessed before, and 90 min after, the first two doses. Thirty-three subjects were recruited, aged 33-88 (mean 71) years, males 52%, 4-30 (median 15) days post stroke to inclusion. Sixteen patients were randomized to placebo and seventeen to amphetamine. Amphetamine did not improve motor function at 90 days; mean (s.d.) FM 37.6 (27.6) vs control 35.2 (27.8) (P ¼ 0.81). Functional outcome (BI, mRS) did not differ between treatment groups. Peripheral and central systolic BP, and heart rate (HR), were 11.2 mm Hg (P ¼ 0.03), 9.5 mm Hg (P ¼ 0.04) and 7 beats per minute (P ¼ 0.02) higher, respectively, with amphetamine, compared with control. A nonsignificant reduction in myocardial perfusion (BUI) was seen with amphetamine. Other cardiac and cerebral haemodynamics were unaffected. Amphetamine did not improve motor impairment or function after ischaemic stroke but did significantly increase BP and HR without altering cerebral haemodynamics.

show abstract

Section: Discussionmentioning

confidence: 99%

Amphetamine increases blood pressure and heart rate but has no effect on motor recovery or cerebral haemodynamics in ischaemic stroke: a randomized controlled trial (ISRCTN 36285333)

et al. 2007

View full text Add to dashboard Cite

show abstract

“…Diffusion remote from MCA infarctsform synapses in previously empty spaces (Carmichael, 2003;Kristt, 1987;Stroemer et al, 1995Stroemer et al, , 1998). An alternative explanation would be a transient increase in axonal density related to neuronal regeneration as observed in the ipsilateral striatum and hippocampus in animal models of MCA occlusion (Nadareishvili and Hallenbeck, 2003;Nakatomi et al, 2002).…”

Section: Discussionmentioning

confidence: 99%

Longitudinal Diffusion Changes in Cerebral Hemispheres after MCA Infarcts

Buffon

Molko

Hervé

et al. 2005

J Cereb Blood Flow Metab

View full text Add to dashboard Cite

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.

show abstract

“…These proteins are amplified with successful neurorestorative treatments. 7 Angiogenesis in the ischemic border creates a hospitable microenvironment for neuronal plasticity, leading to functional recovery. 8 Greater microvessel density in the ischemic border correlates with longer survival in stroke patients.…”

Section: Biological Basics Of Neurorestorative Therapymentioning

confidence: 99%

Neurorestorative treatment of stroke: Cell and pharmacological approaches

Chen

Chopp

2006

NeuroRX

154

114

View full text Add to dashboard Cite

Summary:There is a compelling need to develop cell and pharmacological therapeutic approaches to be administered beyond the hyperacute phase of stroke. These therapies capitalize on the capacity of the brain for neuroregeneration and neuroplasticity and are designed to reduce neurological deficits after stroke. This review provides an update of bone marrowderived mesenchymal stem cells (MSCs) and select pharmacological agents in clinical use for other indications that promote the recovery process in the subacute and chronic phases after stroke. Among these agents are 3-hydroxy-3-methylglutarylcoenzyme A reductase inhibitors (statins), erythropoietin (EPO), and phosphodiesterase type 5 (PDE-5) inhibitors and nitric oxide (NO) donors. Both the MSCs and the pharmacologic agents potentiate brain plasticity and neurobehavioral recovery after stroke.

show abstract

Enhanced Neocortical Neural Sprouting, Synaptogenesis, and Behavioral Recovery With d -Amphetamine Therapy After Neocortical Infarction in Rats

Cited by 329 publications

References 110 publications

Amphetamine increases blood pressure and heart rate but has no effect on motor recovery or cerebral haemodynamics in ischaemic stroke: a randomized controlled trial (ISRCTN 36285333)

Amphetamine increases blood pressure and heart rate but has no effect on motor recovery or cerebral haemodynamics in ischaemic stroke: a randomized controlled trial (ISRCTN 36285333)

Longitudinal Diffusion Changes in Cerebral Hemispheres after MCA Infarcts

Neurorestorative treatment of stroke: Cell and pharmacological approaches

Contact Info

Product

Resources

About