TY - JOUR
T1 - Motor response to amphetamine treatment, task-specific training, and limited motor experience in a postacute animal stroke model
AU - Brown, Allen W.
AU - Bjelke, Börje
AU - Fuxe, Kjell
N1 - Funding Information:
The authors gratefully acknowledge Sanaz Sabouri for her assistance in behavioral data acquisition and J. N. Mandrekar, PhD, for assistance with statistical analysis. This work was supported by the Mayo Foundation for Education and Research, Mayo Clinic, Rochester, MN, the Svenska Läkarsällskapet, the King Gustav V:s and Queen Victorias Foundation, and the Medical Research Council (04X-715).
PY - 2004/11
Y1 - 2004/11
N2 - Despite advances in acute treatment of ischemic cerebrovascular events, the most common clinical outcome is disabling neurological impairment. Despite experimental evidence that psychostimulant treatment can positively affect recovery rate after focal brain lesions, beyond rehabilitation therapies there are no currently accepted medical treatments indicated for diminishing neurological impairment after clinically established stroke. To test the effect of amphetamine, task-specific training, limiting motor experience, and their interaction on motor recovery in a postacute animal model of stroke, animals were nonaversively trained in beam walking before a unilateral photochemical sensorimotor cortex lesion and tested for 10 days after lesion. Animals were randomized to groups receiving: a single session of motor training 24 h after lesion; a single injection of amphetamine 2 mg/kg 24 h after lesion; beam-walking experience limited to testing on days 1 and 10 after lesion; and groups that received amphetamine treatment combined with training or combined with limited experience. Motor recovery was maximally enhanced by training, delayed by amphetamine treatment, and most negatively affected by limiting beam-walking experience during the recovery period. These findings support physical training after stroke, indicating that limiting physical activity negatively affects motor recovery and raises questions about the role of stimulant treatment to enhance motor recovery in the postacute phase after stroke.
AB - Despite advances in acute treatment of ischemic cerebrovascular events, the most common clinical outcome is disabling neurological impairment. Despite experimental evidence that psychostimulant treatment can positively affect recovery rate after focal brain lesions, beyond rehabilitation therapies there are no currently accepted medical treatments indicated for diminishing neurological impairment after clinically established stroke. To test the effect of amphetamine, task-specific training, limiting motor experience, and their interaction on motor recovery in a postacute animal model of stroke, animals were nonaversively trained in beam walking before a unilateral photochemical sensorimotor cortex lesion and tested for 10 days after lesion. Animals were randomized to groups receiving: a single session of motor training 24 h after lesion; a single injection of amphetamine 2 mg/kg 24 h after lesion; beam-walking experience limited to testing on days 1 and 10 after lesion; and groups that received amphetamine treatment combined with training or combined with limited experience. Motor recovery was maximally enhanced by training, delayed by amphetamine treatment, and most negatively affected by limiting beam-walking experience during the recovery period. These findings support physical training after stroke, indicating that limiting physical activity negatively affects motor recovery and raises questions about the role of stimulant treatment to enhance motor recovery in the postacute phase after stroke.
KW - Animal models
KW - Cerebrovascular accident
KW - Recovery of function
KW - Rehabilitation
UR - http://www.scopus.com/inward/record.url?scp=5044223028&partnerID=8YFLogxK
UR - http://www.scopus.com/inward/citedby.url?scp=5044223028&partnerID=8YFLogxK
U2 - 10.1016/j.expneurol.2004.07.005
DO - 10.1016/j.expneurol.2004.07.005
M3 - Article
C2 - 15473984
AN - SCOPUS:5044223028
VL - 190
SP - 102
EP - 108
JO - Experimental Neurology
JF - Experimental Neurology
SN - 0014-4886
IS - 1
ER -