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Curr Neurovasc Res. 2012 Nov;9(4):266-73.

Oxidative stress in post-acute ischemic stroke patients after intensive neurorehabilitation.

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Department of Internal Medicine, Public Health, Environmental and Life Sciences, University of L'Aquila, Piazzale Salvatore Tommasi, 67100, L'Aquila Italy.


We investigated in post-acute ischemic stroke patients the influence of intensive neurorehabilitation on oxidative stress balance during recovery of neurological deficits. For this purpose, fourteen patients were included in the study within 30 days of stroke onset. Outcome measures were the National Institutes of Health Stroke Scale (NIHSS), the modified Rankin Scale (mRS), the Barthel Index, and the Katz Index. Redox balance was assessed by measuring plasma peroxidative by-products, nitrite/nitrate metabolites (NOx), as an index of nitric oxide (NO), Cu/Zn Superoxide Dismutase (Cu/Zn SOD) activity, serum urate concentration, autoantibodies against ox-LDL (OLAB) serum level and plasma antioxidant capacity. Assessments were made before and after neurorehabilitation. Fifteen apparently healthy controls were investigated to compare redox markers. Intensive neurorehabilitation was associated with an improvement of all the outcome measures (P < 0.05). Decreased values of peroxidative by-products and of NOx (P < 0.05) were observed after neurorehabilitation in stroke patients even though their values were higher than in controls (P < 0.05). Changes observed before and after neurorehabilitation in NIHSS scores (Δ NIHSS scores) and in plasma NOx amount (Δ NOx) correlated positively (r=0.79; P < 0.005). No differences in EC-SOD activity, OLAB and serum urate concentrations were found between stroke patients and controls, before and after neurorehabilitation. Total plasma antioxidant capacity, lower in stroke patients than in controls before neurorehabilitation, was unchanged thereafter. Our data provide evidence of the effectiveness of neurorehabilitation on reducing redox unbalance in stroke patients and hints the role of NO as a messenger involved in post-ischemic neuronal plasticity influencing recovery of neurological deficits.

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