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Not only finger tapping speed, but also tapping regularity can be impaired after stroke, contributing to reduced dexterity. The neural substrates of impaired tapping regularity after stroke are unknown. Previous work suggests damage to the dorsal premotor cortex (PMd) and prefrontal cortex (PFCx) affects externally-cued hand movement. We tested the hypothesis that these two areas are involved in impaired post-stroke tapping regularity. In 19 right-handed patients (15 men/4 women; age 45-80 years; purely subcortical in 16) partially to fully recovered from hemiparetic stroke, tri-axial accelerometric quantitative assessment of tapping regularity and BOLD fMRI were obtained during fixed-rate auditory-cued index-thumb tapping, in a single session 10-230 days after stroke. A strong random-effect correlation between tapping regularity index and fMRI signal was found in contralesional PMd such that the worse the regularity the stronger the activation. A significant correlation in the opposite direction was also present within contralesional PFCx. Both correlations were maintained if maximal index tapping speed, degree of paresis and time since stroke were added as potential confounds. Thus, the contralesional PMd and PFCx appear to be involved in the impaired ability of stroke patients to fingertap in pace with external cues. The findings for PMd are consistent with repetitive TMS investigations in stroke suggesting a role for this area in affected-hand movement timing. The inverse relationship with tapping regularity observed for the PFCx and the PMd suggests these two anatomically-connected areas negatively co-operate. These findings have implications for understanding the disruption and reorganization of the motor systems after stroke., (Copyright (c) 2009 Elsevier Inc. All rights reserved.)

Although everyone knows fatigue personally, it is a difficult concept to define. For muscular fatigue, one must know the aspect of performance affected. The most obvious demonstrations are decreased maximal force and slowed muscular answer. Fatigue can have a central origin, by reducing cognitive performance or lowering excitation of motoneurons. Various mediators are in question (serotonin, moduline, dopamine). The fatiguing muscular contractions are accompanied by reduced discharges of motoneurons. The neuromuscular junction does not seem to be in question. Cold reduces muscular power, whereas a hot environment limits exercise by a central mechanism, which starts the normal behavioural response to stop the exercise. Fatigue can also be the consequence of overtraining. In the periphery, the electric activity of the membrane's surface is the first possible sign of failure, which explains high-frequency fatigue: the accumulation of potassium outside the cell blocks the sodic channels to block the potentials of action or slow down their propagation. With fatigue, less calcium is released and limits the number of attached actin-myosin bridges connections of actin-myosin. The slowing down of the muscular answer represents a deterioration of the function of actin-myosin bridges. On the metabolic level, the most-often evoked changes are reduced pH and increased intracellular lactate level. However, these variations cannot all describe fatigue, since patients with Mc Ardle disease do not exhibit these variations but very quickly experience tiredness. In fact, an association of small metabolic intracellular variations could explain tiredness. The fast fibres are larger than slow fibres; their metabolic needs are higher and they are thus more sensitive to tiredness. The half time of recovery is within approximately 1 min: normal values of force and power are recovered after 5 to 10 min. During endurance activities, the limiting factors are glycogen reserves and levels of oxidative enzymes. On the whole, mechanisms of fatigue must be explored to completely understand the governing phenomena.

Five patients with left striatocapsular infarction were studied twice with PET during auditory-cued right thumb-index tapping, around 2 months after stroke and again around 8 months after stroke. At PET1 and PET2, the ipsilesional primary sensorimotor (SM1) activation peak Talairach coordinates were compared to those from seven aged-matched healthy controls. At PET1, there was a significant posterior displacement of SM1 activation peak, which confirms a previous report and may represent unmasking/disinhibition of motor representations. Over time, there was no significant change in the coordinates, and no significant correlation between coordinate changes from PET1 to PET2 and concomitant motor recovery. The implications of posterior displacement of SM1 activation peak for recovery therefore remain elusive.

We prospectively studied 5 patients while they were recovering from left-sided subcortical stroke affecting the cortico-spinal tract, and examined them twice with H(2)(15)O-PET over several months while performing an identical task with the affected hand. Concomitant motor recovery was assessed by measuring the number of thumb-to-index tappings performed in 15 s at each PET session. Across patients, the hemispheric activation balance tended to shift over time toward the unaffected hemisphere, but the magnitude of this shift was highly variable from patient to patient and significantly correlated with recovery. Thus, in subcortical stroke, a shift of activation balance towards the unaffected hemisphere appears associated with lesser initial recovery and, conversely, the more this physiological balance is maintained over time the better the recovery.

Background and Purpose: Although excessive brain activation during affected hand motion after stroke is well documented, its time course has been rarely studied, and when studied, this has either been with passive movement or with active but cognitively complex task and uncontrolled performance over time, complicating interpretation., Methods: According to a prospective and longitudinal design, we studied 5 right-handed patients with right-sided hemiparesis due to first-ever left striatocapsular infarction. Three-dimensional PET H(2)O(15) studies were performed twice ( approximately 7 and approximately 31 weeks after stroke [PET1 and PET2, respectively]) during right thumb-to-index tapping executed at the same rate in both studies (1.26 Hz, auditory cued). With SPM96 software, significant group and individual overactivations (P<0.05, corrected for multiple comparisons) were computed by comparison with a group of 7 healthy age-matched right-handed control subjects performing the same task., Results: Motor recovery was significant from PET1 to PET2. Both the group and individual analyses revealed striking overactivations at PET1, affecting notably the cortical hand area and the whole motor network bilaterally. These overactivations were less prominent at PET2 over both hemispheres, not only in terms of Z score but also in terms of spatial extent (almost reaching statistical significance in the affected hemisphere for the latter, P=0.09). However, new overactivations were found at PET2 in the left prefrontal areas, the putamen, and the premotor cortex., Conclusions: This study is the first to document that to perform the same simple movement of the paretic fingers, the brain with subcortical infarction shows less overactivations at the late than at the early timepoint, especially on the affected side, suggesting reduced recruitment of affected-hemisphere motor networks. However, unaffected-hemisphere prefrontal, premotor, and putaminal overactivations, observed at PET2 only, may suggest late-appearing compensatory reorganization.

Young high-level athletes are frequently exposed to deficiencies, the most frequent origin of which is dietary. Supervision must be clinical, biological and dietary. Recommendations should be made individually, based on the nature and intensity of the exercise, and are calculated from the recommended supplements for the paediatric population. Protein, glucid and lipid supplements must represent approximately 12, 60 and 28% of the daily energetic intake respectively, the glucid ratio reaching 70% under certain conditions of prolonged exercise. Liquids must be controlled when exercise takes place in a warm atmosphere because young athletes are rapidly exposed to dehydration, the osmolarity of the selected drink being below 250 mosm/l. Mineral and vitamin supplementations are recommended. For minerals, perspiration losses may be associated with dietary deficiency. Possible vitamin deficiencies concern B1, B2, B6, B9, B12, C and D vitamins. The daily mineral supplements are estimated at 10 mg for iron, 5 mg for zinc and 1 mg for copper, and have to be prescribed in regular treatment after biological control.

The purpose of our study was to evaluate the interest of passive motion rehabilitation with an automatic device. Our protocol has been made of 120 TKA performed in the same surgical department between february 1987 to June 1990. We draw lots, a group "RC" with usual rehabilitation program and a second group "AM" with the same program added with passive motion two hours per day. The passive motion device was Toronto Mobilimb. Passive range of motion (ROM) of flexion and extension, pain level, deep venous thrombosis existence, volume of blood postop drainage, mobilisation under anaesthesia, device tolerance were studied. The results showed a flexion ROM average of 86.7 degrees in the RC group at discharge and 90 degrees in the AM group. This difference is statistically significant and evokes the efficacy of passive motion. At the term of one year postop, the flexion averages reaches 108 degrees in both groups. The extension lag falls from 8.2 degrees and 9.2 degrees average in AM and RC group at discharge to 3 degrees and 3.7 degrees in the same groups at one year. The mean of blood postop drainage by suction was very different in the RC group than AM group (1149ml-968ml). In conclusion, we can say that passive motion device is useful to reach enough flexion in the first days after surgical day and may give some comfort. In our experience the classical rehabilitation program with physiotherapist must be continued.

Serum levels of selenium and vitamin E were prospectively studied in children with Duchenne de Boulogne muscular dystrophy of variable age and muscular status. In contrast with previous studies, we found no differences with controls. However, we believe that selenium and vitamin E, two natural antioxydants, may contribute to the pathophysiology of pseudohypertrophic muscular dystrophy. A study of the effects of supplementation is on-going.