Adipokines as Potential Biomarkers in the Neurorehabilitation of Obese Stroke Patients.

BACKGROUND: Limited studies concern the influence of obesity-induced dysregulation of adipokines in functional recovery after stroke neurorehabilitation. OBJECTIVE: To investigate the relationship between serum leptin, resistin, and adiponectin and functional recovery before and after neurorehabilitation of obese stroke patients. The adipokine potential significance as prognostic markers of rehabilitation outcomes was also verified. METHODS: Twenty obese post-acute stroke patients before and after neurorehabilitation and thirteen obese volunteers without-stroke, as controls, were examined. Adipokines were determined by commercially available enzyme-linked immunosorbent assay (ELISA) kits. Functional deficits were assessed before and after neurorehabilitation with the Barthel Index (BI), modified Rankin Scale (mRS), and Functional Independence Measure (FIM). RESULTS: Compared to controls, higher leptin and resistin values and lower adiponectin values were observed in stroke patients before neurorehabilitation and no correlations were found between adipokines and clinical outcome measures. Neurorehabilitation was associated with improved scores of BI, mRS, and FIM. After neurorehabilitation, decreased values of Body Mass Index (BMI) and resistin together increased adiponectin were detected in stroke patients, while leptin decreased but not statistically. Comparing adipokine values assessed before neurorehabilitation with the outcome measures after neurorehabilitation, correlations were observed for leptin with BI-score, mRS-score, and FIM-score. No other adipokine levels nor BMI assessed before neurorehabilitation correlated with the clinical measures after neurorehabilitation. The forward stepwise regression analysis identified leptin as prognostic factor for BI, mRS, and FIM. CONCLUSION: Our data show the effectiveness of neurorehabilitation in modulating adipokines levels and suggest that leptin could assume the significance of biomarker of functional recovery.

Mean Platelet Volume During Ischemic Stroke is a Potential Pro-inflammatory Biomarker in the Acute Phase and During Neurorehabilitation Not Directly Linked to Clinical Outcome.

The prognostic role of increased mean platelet volume (MPV), as an indicator of platelet activation and large, more reactive platelets, in clinical and functional outcome of ischemic stroke is still conflicting. Studies are not currently available on the association between MPV and stroke recovery after neurorehabilitation. The relationship between MPV and clinical and functional outcome measures was assessed in twenty-four patients in the acute phase of first-ever ischemic stroke, and before and after 8-week intensive multifunctional neurorehabilitation. Neurorehabilitation was associated with improved scores of the National Institutes of Health Stroke Scale (NIHSS), the modified Rankin Scale (mRS), and the modified PULSES profile (mPULSES). When compared with apparently healthy subjects, higher MPV values were observed in stroke patients 24 hours after stroke and before neurorehabilitative treatment started not later than 14 days after stroke. Decreased MPV values were found after neurorehabilitation, even if the absolute values were still higher than those detected in control subjects. No correlation was observed between MPV values and scores of the NIHSS and mRS scales evaluated in stroke acute phase. No correlation was also observed before and after neurorehabilitative treatment between MPV and NIHSS, mRS and mPULSES scores. Our data provide evidence of the effectiveness of neurorehabilitation on modulating MPV values and support the hypothesis that high MPV could represent an expression of proinflammatory condition of the stroke patients, realistically pre-existent to acute ischemic event, than a marker of neurologic deficit and disability or of stroke recovery including motor performance and functional independence.

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

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.

Evaluation of oxidative status in coronary heart disease at baseline and during exercise test.

Oxidative stress has probably a role in coronary heart disease (CHD), but studies focused on the behaviour of oxidative status in patients with stable CHD have obtained controversial results. On the other hand, an increased release of leukocyte elastase is considered a marker of CHD. Exercise can induce oxidative stress and leukocyte activation, so the aim of this study was to evaluate oxidative status and plasma elastase level in a group of subjects with stable coronary heart disease (CHD), at baseline and during an exercise test. We enrolled 15 patients with previous acute myocardial infarction, all treated with statins and platelet antiaggregating agents. As parameters of oxidative status we determined the thiobarbituric acid reactive substances and total antioxidant status (TAS). The exercise test was performed according to the Bruce protocol. At baseline, elastase level was higher in CHD subjects than in normal controls and during the exercise test it increased in both groups in comparison with basal values. Regarding oxidative status, only TAS was slightly lower in CHD subjects than in normal controls. In both groups, during exercise test, no parameter of oxidative status was significantly different compared to basal values. In conclusion, CHD patients showed, at rest, an abnormal neutrophil activation and a lower antioxidant status. The exercise test further activated neutrophils but did not influence oxidative status. The absence of a marked oxidative stress in our patients may be partly due to the pharmacological treatment, which apparently did not influence the abnormal leukocyte activation.