Robot-assisted gait training improves motor performances and modifies Motor Unit firing in poststroke patients.

BACKGROUND: Robotics and related technologies are realizing their promise to improve the delivery of rehabilitation therapy but the mechanism by which they enhance recovery is still unknown. The electromechanical-driven gait orthosis Lokomat has demonstrated its utility for gait rehabilitation after stroke. AIM: To test the efficacy of Lokomat in gait retraining and to investigate the neurophysiological mechanisms underlying the recovery process. DESIGN: Case series study. SETTING: Unit of Neurorehabilitation of a University Hospital. POPULATION: Fifteen patients with post-stroke hemiparesis. METHODS: Patients underwent a six weeks rehabilitative treatment provided by Lokomat. The outcome measures were: Fugl-Meyer Motor Scale (FMMS), Berg Balance Scale (BBS), 10 metres Walking Test (10mWT), Timed Up and Go test (TUG), 6 Minute Walking Test (6MWT). Strength and Motor Unit firing rate of vastus medialis (VM) were analyzed during isometric knee extension through an isokinetic dynamometer and surface EMG recording. RESULTS: An increase of duration and covered distance, a decrease of body weight support and guidance force on the paretic side along the sessions were observed. The FMMS, the BBS, the TUG and the 6MWT demonstrated a significant improvement after the training. No increase of force was observed whereas a significant increase of firing rate of VM was recorded. CONCLUSION: The evidence that the improvement of walking ability observed in our study determines a significant increase of firing rate of VM not accompanied by an increase of force could suggest an effect of training on motorneuronal firing rate that thus contributes to improve motor control. CLINICAL REHABILITATION IMPACT: Given the current wide use of robotics in gait retraining after stroke, our approach can contribute to clarify the mechanisms underlying its rehabilitative impact so as to incorporate the findings of evidence-based practice into appropriate treatment plans for persons poststroke.

Intensive aerobic training improves motor performances and oxidative metabolism efficiency in chronic polymyositis: a case report.

We describe the case of a 64-year-old woman affected by chronic polymyositis with gait disturbance, fatty replacement and swelling of thigh muscles. She achieved significant clinical improvement after 5 weeks intensive aerobic training. In particular the patient improved in motor performance tests, showed an improvement in the efficiency of oxidative metabolism and quality of life. Furthermore, analysis of creatinephosphokinase levels showed a reduction of muscle damage susceptibility. In conclusion, a specific intensive exercise program can be safely used with beneficial effects on muscle function in patients with chronic polymyositis.

A surface EMG analysis of sarcolemma excitability alteration and myofibre degeneration in Steinert disease.

OBJECTIVES: To apply surface electromyography (EMG) using low and high stimulation frequencies, to establish the contribution of myotonia and/or dystrophy to muscle impairment in subjects affected by myotonic dystrophy (MyD). METHODS: A motor point stimulation protocol, at 15 and 35 Hz, was carried out on the tibialis anterior (TA) of 25 MyD patients. These were subdivided into 3 subgroups, MyD3 (9), MyD4 (10) and MyD5 (6), on the basis of their TA MRC score. The surface myoelectric signal was recorded and the average rectified value of amplitude (ARV) was evaluated. In 4 MyD5 patients we simultaneously recorded EMG and force. RESULTS: Each subgroup presented a characteristic ARV trend both at 15 and 35 Hz - increasing in MyD3 (like the controls), slightly decreasing in MyD4 and clearly decreasing in MyD5. The low frequency permitted a greater resolution of the statistical analysis. Two out of 4 patients showed an opposite trend of ARV with respect to the force, whereas the others presented a parallel decreasing trend. CONCLUSIONS: The analysis of the ARV during a stimulated contraction permits the identification and quantification of the sarcolemma excitability alteration and/or the myofibre degeneration contributing to muscle impairment in MyD. The lower frequency is more sensitive and offers better inter-experiment repeatability.

Cerebral perfusion in hypertensives with carotid artery stenosis: a comparative study of lacidipine and hydrochlorothiazide.

Focal cerebral hypoperfusion is a common finding in uncomplicated hypertensives even in the absence of large vessel atherosclerosis, and neuropsychological deficits correlate with cerebral hypoperfusion in hypertensive patients with cerebral microangiopathy. We investigated the effects on cerebral perfusion of the dihydropiridine calcium antagonist lacidipine and of hydrochlorothiazide (HCTZ) in asymptomatic hypertensive patients with concomitant atherosclerosis of the carotid arteries. Fifteen essential hypertensives (including 13 males, aged 55-75 years) with at least one 30-60% stenosis of the internal carotid artery at echo-color Doppler examination were treated in a double-blind, randomized, parallel study with lacidipine (4-6 mg od) or HCTZ (25-50 mg od) for 3 months after a 4-week single-blind placebo period. Regional cerebral perfusion was assessed at baseline and at the end of the treatment period with HMPAO-SPECT. Relative perfusion of cortical and subcortical areas was calculated as the ratio between their tracer activity and that of the cerebellum. At baseline, mean relative perfusion (MRP) of the cortical and subcortical areas was similar in the stenotic and the contralateral side. Despite the fall in pressure, lacidipine increased MRP both in the cortical and in the subcortical areas, whereas HCTZ increased MRP only in the cortical areas. The mean change in local vascular resistance, adjusted for initial perfusion value, was -20 A.U. (arbitrary unit) with lacidipine and -12 A.U. with HCTZ (p < 0.001). These differential effects of antihypertensive drugs on subcortical perfusion may be of benefit in the long-term prevention of vascular dementia in hypertensive patients.

Cerebral perfusion in hypertensive patients: effects of lacidipine and hydrochlorothiazide.

Previous studies have shown areas of cerebral hypoperfusion in the frontal and parietal lobes of asymptomatic hypertensives, in the absence of extracranial carotid artery stenosis. The aims of the present study were: (a) to correlate the presence of focal cortical hypoperfusion with the presence of white matter lesions (WML), lacunae and extracranial carotid artery stenosis; and (b) to compare the effects on cerebral perfusion of the dihydropyridine calcium entry blocker lacidipine and of hydrochlorothiazide (HCTZ) in hypertensive patients with carotid artery stenosis. Forty-one patients (30 males, aged 40-75) with mild to moderate essential hypertension and with negative history for cerebrovascular diseases were investigated. Twenty-four had normal extracranial carotid arteries at echo-colourDoppler examination, while 17 had at least one 50-70% stenosis of the internal carotid artery (ICA). At computed tomography (CT) scan, five patients had one or more lacunar infarctions, four WML, three lacunar infarctions and WML, and 26 a normal CT scan. Three, with old cortical infarctions, were excluded from further analysis. The prevalence of lesions was significantly higher among the patients with carotid artery stenosis (44% vs. 29%; p < 0.05). Distribution of mean relative cortical perfusion (MRCP) of regions of interest [hexamethyl-propileneamine oxime-single photon emission tomography (SPET)] was not normal, with a negative skewness in patients with lacunae. MRCP was slightly but significantly reduced in patients with lacunae in comparison with hypertensives with normal CT scan and with WML. The asymmetry index of tracer distribution was significantly greater in the patients with lacunar infarctions and WML than in the hypertensive patients with normal CT scan, irrespective of the presence of internal carotid artery stenosis. Fifteen hypertensives (13 males, aged 55-75 years) with at least one moderate stenosis of ICA at duplex scanning were treated in a double-blind, randomised, parallel study with lacidipine (4-6 mg o.d.) or HCTZ (25-50 mg o.d.) for 3 months after a 4-week single-blind placebo period. At baseline, perfusion of the cortical and basal areas was similar in the stenotic and the contralateral side. Despite the fall in pressure, both treatments increased MRCP in the stenotic side and in the contralateral side. The lower the baseline perfusion, the larger its increase with treatment. The decrease of local cerebral vascular resistance was significantly greater with lacidipine than with HCTZ. We conclude that in hypertensive patients, the distribution of cerebral flow is uneven, mostly in the presence of small asymptomatic subcortical lesions and independently from internal carotid artery stenosis. Antihypertensive treatment with lacidipine and HCTZ reduces local cerebral resistance and corrects focal hypoperfusion without inducing steal effects in patients with ICA stenosis.

Effects of canrenoate on red cell sodium transport and calf flow in essential hypertension.

The effects of potassium canrenoate (100 mg/day, orally for 1 month) on blood pressure, calf blood flow at rest and after ouabain (0.5 mg intravenous bolus), and red cell Na homeostasis were investigated in 15 patients (7 men, 8 women, aged 18 to 63) with essential hypertension and without peripheral vascular diseases. On placebo, acute intravenous ouabain administration significantly and transiently reduced calf flow and increased calf vascular resistance without affecting blood pressure. Canrenoate significantly decreased blood pressure (from 159 +/- 21/105 +/- 9 mm Hg to 141 +/- 14/94 +/- 10, P < .05) and the rise of calf resistance after intravenous ouabain bolus. The latter effect was variable, since it was inhibited almost completely in 8 patients and unaffected in the others. In the patients in whom exogenously administered ouabain was antagonized, canrenoate diminished blood pressure through vasodilation and heightened the red cell Na/K pump. None of these parameters changed significantly in the other patients. Thus these data suggest that the fall in vascular resistance induced by canrenoate is mediated, in part, by the antagonism of endogenous ouabain-like factors.