Multiple point electrical stimulation of ulnar and median nerves.
A computer-assisted method of isolating single motor units (MUs) by multiple point stimulation (MPS) of peripheral nerves is described. MPS was used to isolate 10-30 single MUs from thenar and hypothenar muscles of normal subjects and patients with entrapment neuropathies, with the original purpose of obtaining a more representative mean motor unit potential for estimating the number of MUs in a muscle. The two important results that evolved from MPS however, were: (1) in the absence of 'alternation' MUs were recruited in an orderly pattern from small to large, and from longer to shorter latencies by graded electrical stimulation in both normal and pathological cases, (2) a comparison of the sizes of MUs recruited by stimulation proximal and distal to the elbow suggested that axonal branching can occur in the forearm 200 mm or more proximal to the motor point in intrinsic hand muscles. (+info)
The Thr124Met mutation in the peripheral myelin protein zero (MPZ) gene is associated with a clinically distinct Charcot-Marie-Tooth phenotype.
We observed a missense mutation in the peripheral myelin protein zero gene (MPZ, Thr124Met) in seven Charcot-Marie-Tooth (CMT) families and in two isolated CMT patients of Belgian ancestry. Allele-sharing analysis of markers flanking the MPZ gene indicated that all patients with the Thr124Met mutation have one common ancestor. The mutation is associated with a clinically distinct phenotype characterized by late onset, marked sensory abnormalities and, in some families, deafness and pupillary abnormalities. Nerve conduction velocities of the motor median nerve vary from <38 m/s to normal values in these patients. Clusters of remyelinating axons in a sural nerve biopsy demonstrate an axonal involvement, with axonal regeneration. Phenotype-genotype correlations in 30 patients with the Thr124Met MPZ mutation indicate that, based on nerve conduction velocity criteria, these patients are difficult to classify as CMT1 or CMT2. We therefore conclude that CMT patients with slightly reduced or nearly normal nerve conduction velocity should be screened for MPZ mutations, particularly when additional clinical features such as marked sensory disturbances, pupillary abnormalities or deafness are also present. (+info)
Relationships between lead absorption and peripheral nerve conduction velocities in lead workers.
The motor sensory, and mixed nerve conduction velocities of median and posterior tibial nerves were measured in 39 lead workers whose blood lead (PbB) concentrations ranged from 2 to 73 mug/100 g with anaverage of 29 mug/100 g. The PbB concentrations significantly correlated with the maximal motor nerve conduction velocities (MCV) and mixed nerve conduction velocities (MNCV) of the median nerve in the forearm and with the MCV of the posterior tibial nerve. Erythrocyte delta-aminolevulinic acid dehydratase (ALAD) activity correlated similarly with the MCV and MNCV of the median nerve in the forearm, and the 24-hour urinary lead excretion following the intravenous administration of CaEDTA (20 mg/kg) (lead mobilization test) correlated with the MNCV. But no parameter correlated with the sensory nerve conduction velocities. By multiple regression analysis, a combination of the three parameters of lead absorption was found to correlate significantly with the MCV and MNCV of the median nerve in the forearm. The MCVs of the median and posterior tibial nerves in lead workers were significantly delayed in the PbB range of 29-73 mug/100 g (mean 45), in the lead mobilization test range from 173 to 3,540 mug/day (mean 973), and the ALAD activity range from 4.4 to 19.4 u. (mean 14.0), respectively. (+info)
Simultaneous early processing of sensory input in human primary (SI) and secondary (SII) somatosensory cortices.
Simultaneous early processing of sensory input in human primary (SI) and secondary (SII) somatosensory cortices. The anatomic connectivity of the somatosensory system supports the simultaneous participation of widely separated cortical areas in the early processing of sensory input. We recorded evoked neuromagnetic responses noninvasively from human primary (SI) and secondary (SII) somatosensory cortices to unilateral median nerve stimulation. Brief current pulses were applied repetitively to the median nerve at the wrist at 2 Hz for 800-1,500 trials. A single pulse was omitted from the train at random intervals (15% of omissions). We observed synchronized neuronal population activity in contralateral SII area 20-30 ms after stimulation, coincident in time with the first responses generated in SI. Both contra- and ipsilateral SII areas showed prominent activity at 50-60 ms with an average delay of 13 ms for ipsilateral compared with contralateral responses. The refractory behavior of the early SII responses to the omissions differed from those observed at approximately 100 ms, indicative of distinct neuronal assemblies responding at each latency. These results indicate that SII and/or associated cortices in parietal operculum, often viewed as higher-order processing areas for somatosensory perception, are coactivated with SI during the early processing of intermittent somatosensory input. (+info)
Evidence for brainstem and supra-brainstem contributions to rapid cortical plasticity in adult monkeys.
Cortical maps can undergo amazingly rapid changes after injury of the body. These changes involve functional alterations in normal substrates, but the cortical and/or subcortical location(s) of these alterations, and the relationships of alterations in different substrates, remain controversial. The present study used neurophysiological approaches in adult monkeys to evaluate how brainstem organization of tactile inputs in the cuneate nucleus (CN) changes after acute injury of hand nerves. These data were then compared with analogous data from our earlier cortical area 3b studies, which used the same approaches and acute injury, to assess relationships of cuneate and cortical changes. The results indicate that cuneate tactile responsiveness, receptive field locations, somatotopic organization, and spatial properties of representations (i.e., location, continuity, size) change during the first minutes to hours after injury. The comparisons of cuneate and area 3b organization further show that some cuneate changes are preserved in area 3b, whereas other cuneate changes are transformed before being expressed in area 3b. The findings provide evidence that rapid reorganization in area 3b, in part, reflects mechanisms that operate from a distance in the cuneate nucleus and, in part, reflects supracuneate mechanisms that modify brainstem changes. (+info)
Modified activation of somatosensory cortical network in patients with right-hemisphere stroke.
To study the effects of parietal lesions on activation of the human somatosensory cortical network, we measured somatosensory evoked fields to electric median nerve stimuli, using a whole-scalp 122-channel neuromagnetometer, from six patients with cortical right-hemisphere stroke and from seven healthy control subjects. In the control subjects, unilateral stimuli elicited responses which were satisfactorily accounted for by modelled sources in the contralateral primary (SI) and bilateral secondary (SII) somatosensory cortices. In all patients, stimulation of the right median nerve also activated the SI and SII cortices of the healthy left hemisphere. However, the activation pattern was altered, suggesting diminished interhemispheric inhibition via callosal connections after right-sided stroke. Responses to left median nerve stimuli showed large interindividual variability due to the different extents of the lesions. The strength of the 20-ms response, originating in the SI cortex, roughly reflected the severity of the tactile impairment. Right SII responses were absent in patients with abnormal right SI responses, whereas the left SII was active in all patients, regardless of the responsiveness of the right SI and/or SII. Our results suggest that the human SI and SII cortices may be sequentially activated within one hemisphere, whereas SII ipsilateral to the stimulation may receive direct input from the periphery, at least when normal input from SI is interrupted. (+info)
Factors contributing to preferential motor reinnervation in the primate peripheral nervous system.
Functional recovery after nerve lesions in the peripheral nervous system requires the accurate regeneration of axons to their original target end organs. This paper examines axonal regeneration of the primate median nerve lesioned at the wrist over nerve gap distances of up to 50 mm. Nerve gaps were bridged by either a sural nerve graft or a biodegradable collagen nerve guide tube, and recovery was followed for up to 1100 d. Nondestructive physiological methods were used to serially examine the number of regenerated motor units, and binomial statistics were used to compare the observed number of regenerated motor units with that expected if axonal regeneration of motor neurons were random. We found up to twice the number of motor units expected by random regeneration in direct suture and sural cable graft groups but not in nerve guide repairs of 20 or 50 mm. In all repaired nerves, aberrant motor axon collaterals were detected in digital sensory nerve territory. The results support the contention that the aberrant fibers represent collaterals of an alpha-motor axon, which also innervates muscle. Although the aberrant motor axon collaterals remained in digital sensory nerve territory for long periods, they remained relatively immature compared with their sibling collateral projecting to muscle, or sensory axons within the digital nerve. The number of such aberrant motor axon collaterals decreased over time in some repair groups, suggesting a selective pruning of the inappropriate collateral under certain conditions. (+info)
Abnormal central integration of a dual somatosensory input in dystonia. Evidence for sensory overflow.
Several observations suggest impaired central sensory integration in dystonia. We studied median and ulnar nerve somatosensory evoked potentials (SEPs) in 10 patients who had dystonia involving at least one upper limb (six had generalized, two had segmental and two had focal dystonia) and in 10 normal subjects. We compared the amplitude of spinal N13, brainstem P14, parietal N20 and P27 and frontal N30 SEPs obtained by stimulating the median and ulnar nerves simultaneously (MU), the amplitude value being obtained from the arithmetic sum of the SEPs elicited by stimulating the same nerves separately (M + U). Throughout the somatosensory system, the MU : (M + U) ratio indicates the interaction between afferent inputs from the two peripheral nerves. No significant difference was found between SEP amplitudes and latencies for individually stimulated median and ulnar nerves in dystonic patients and normal subjects, but recordings in patients yielded a significantly higher percentage ratio [MU : (M + U)x100] for spinal N13 brainstem P14 and cortical N20, P27 and N30 components. The SEP ratio of central components obtained in response to stimulation of the digital nerves of the third and fifth fingers was also higher in patients than in controls but the difference did not reach a significant level. The possible contribution of subliminal activation was ruled out by recording the ratio of SEPs in six normal subjects during voluntary contraction. This voluntary contraction did not change the ratio of SEP suppression. These findings suggest that the inhibitory integration of afferent inputs, mainly proprioceptive inputs, coming from adjacent body parts is abnormal in dystonia. This inefficient integration, which is probably due to altered surrounding inhibition, could give rise to an abnormal motor output and might therefore contribute to the motor impairment present in dystonia. (+info)