This method, in which both sulcal and functional mapping are used for surgery planning and neuronavigation, provides helpful information. It is a promising procedure for the treatment of patients who harbor lesions in areas around the eloquent cortex.
The facilitation of the tendon reflex of quadriceps, induced by voluntary contraction of a muscle group in the upper limb, evolves in the three phases and depends on several factos. These include the strength and type (ballistic or ramp) of the contraction. In the absence of any electromyographic activity in the conditioning muscle (from a lesion of its nerve trunk or by blockage of conduction by injection of xylocaine), a voluntary attempt to contract it causes only a moderate facilitation of the quadriceps motor nucleus; while reflex activation of the conditioning muscles, by vibration or sudden stretching. causes a more marked facilitation. Thus, it is concluded that at least two distinct mechanisms act sequentially. First, a general motor facilitation of supraspinal origin induces the first moderate phase of facilitations (phase I). This early facilitation precedes the onset of electromyographic activity in the conditioning muscle. Secondly, the more marked facilitation (phase II) is related to the stimulation of afferents originating from the conditioning muscles, either by fusimotor excitation in voluntary contraction or by manoeuvres which stimulate the spindle receptors mechanically. To investigate the transmission pathways of these facilitations, the latencies of these two phases were compared at two distant motor nuclei, the trigeminal motor nucleus and the quadriceps nucleus, following voluntary contractions of the tibialis anterior. Since the facilitations of the trigeminal motor nucleus precede those of the quadriceps motor nucleus, a slowly-travelling rostro-caudal facilitation is postulated during phase II when the facilitation is related to afferents coming from the contracting muscle. A long loop, therefore, is postulated to interpret the second phase of the facilitation curves.
Recovery after stroke is closely linked to cerebral plasticity. Magnetoencephalography (MEG) is a non-invasive technique, which allows location of cerebral cells activities. In the present work, a cohort of patients has been studied with MEG. Twelve patients with a recent ischemic or hemorragic stroke were included as soon as possible after onset of stroke. Neurologic assessment, including standard neurologic examination, functional independence measure (FIM) and Orgogozo's scale was performed for 1 year in addition to a study of the somatosensory evoked field (SEF) using a 37-channel Biomagnetometer system. No response could be recorded in five patients at the first SEF exploration. In three cases, no response was ever recorded during the study. All these patients had a bad recovery. The location of the SEF sources was always in the normal non-infarcted cortex of the postcentral gyrus. Sensory recovery seemed to be linked to the reorganization of the persistent functional cortex, which was a limiting factor for recovery. These observations confirm the experimental results obtained in animal models. After stroke it can be assumed that in the case of incomplete lesion, an intensive sensory peripheral stimulation could maximize the use of residual sensory function and then contribute to improve the sensory deficit. In case of total sensory loss other techniques have to be used, such as visual monitoring of hand activity in order to improve hand function.
Metabolic events were followed by 31-P NMR spectroscopy during mechanical exhaustion of directly stimulated rat gastrocnemius. During mechanical fatigue, phosphocreatine (PCr) and pH first declined but although stimulation continued high values were recovered without mechanical recovery. Total recovery was only observed after cessation of stimulation. Partial mechanical recovery was elicited by lowering stimulation rhythm; it was accompanied by decrease in PCr to a steady-state level without pH alteration. When exhaustive exercise was induced immediately after nonexhaustive exercise, failure of mechanical function occurred without decrease in pH. Major findings were: first, during exhaustive stimulations, the greater the muscle fatigue, and the higher the PCr level at the end of stimulation. Secondly, PCr and force levels did not depend on preceding levels of PCr and pH. Thirdly, acidosis was observed transiently during the first minutes of the first exercise period. These findings strongly suggested that electrical events and/or excitation-contraction (EC) coupling play a crucial role in this type of fatigue.
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