Ipsilateral motor response - is it an artefact?

The lack of information about the ipsilateral motor response to cortical stimulation prompted the present study. Motor evoked potentials (MEPs) in 60 patients with acute stroke were recorded bilaterally. The patients' ages ranged between 24 and 83 years; 45 were males. Intracerebral haemorrhage was present in 23 and infarction in 37 patients. In none of these patients was an ipsilateral response recorded from the hemiplegic side when a contralateral response was absent. One the non-hemiplegic side in all these patients an MEP was recorded on both contralateral and ipsilateral cortical stimulation. Unrecordable MEPs became recordable in 6 patients after 1-15 months of stroke. In these patients MEP latencies on ipsilateral cortical stimulation were either identical to that on contralateral stimulation(2 patients) or within the range of normal intraindividual variation. On the basis of these results, it is concluded that the ipsilaterl motor response in our study may be due to cross stimulation of the normal hemisphere and not through the uncrossed motor pathways. Our results should be interpreted in the context of the stimulation conditions employed. Further studies are recommended using more focal stimulation to minimise the spread of current.     

Is the human primary motor cortex involved in motor imagery?

Participation of the primary motor cortex (M1) in motor imagery was addressed using functional magnetic resonance imaging at 2.0 T and 2 x 2 x 4 mm3 resolution in six right-handed subjects. Paradigms comprised visually cued execution and imagination of a sequential finger-to-thumb opposition task (12 s) contrasted with motor rest and visual imagery (18 s), respectively. Motor execution activated M1 as well as other parts of the motor system including supplementary motor area (SMA) and premotor areas (PM). In contrast, motor imagery did not lead to activations in M1 except for 1/6 subjects but involved SMA and PM bilaterally as well as the anterior intraparietal cortex. Moreover, a region-of-interest analysis revealed a weak initial MRI signal increase in M1 in 4/6 subjects. This novel finding of a transient response reflecting the onset of imagination which does not lead to sustained M1 activation may explain previous contradictory reports.     

Tonic and kinetic motor units revisited: does motor unit firing behavior differentiate motor units?

OBJECTIVE: We tried to differentiate motor unit into two distinct populations, tonic and kinetic, on the basis of the relationship between the mean inter-spike interval and its variability. METHODS: During voluntary isometric contraction myoelectric activity was recorded with a special quadrifilar electrode from first dorsal interosseous, biceps brachii, soleus, and tibialis anterior muscle. Motor unit action potentials (MUAP) were decomposed into individual MUAP trains, by electromyography (EMG) signal decomposition. The variability in the instantaneous firing rate was assessed at two or more levels of contraction in each muscle. RESULTS: We found each muscle tested had a homogeneous population. There were no tonic and kinetic motor units. But there were differences in the variability in the instantaneous firing rate in the 4 muscles tested. CONCLUSION: Motor unit firing behavior in a muscle may be fitted for its function.     

Do the motor manifestations of parkinson disease alter motor axon excitability?

Background: Axonal excitability is altered in common medical conditions such as stroke, multiple sclerosis, and spinal cord injury. Given the motor neuron changes in the presence of rigidity and tremor in Parkinson disease, we examine whether there are also changes in motor axon excitability. Methods: Axonal excitability studies were performed in 15 Parkinson subjects and 12 age‐matched control subjects. Results: There was no significant difference in excitability indices between Parkinson subjects and control subjects. Conclusions: It is unlikely that the lack of change in the excitability indices reflects a balance between the effects of bradykinesia (“underactivity”) and the effects of rigidity and tremor (“overactivity”) on the motoneuron and its axon. It is more likely that plastic changes in motoneuron properties do not occur symmetrically with decreases and increases in activity, being more profound when activity levels are interrupted and less obvious when they are enhanced. Muscle Nerve 45: 43–47, 2012     

Survival motor neuron: motor neuron insurance for a whole lifespan?

The SMN (survival motor neuron) gene plays an important role in ontogenesis and its dysfunction leads to immatu-rity of skeletal muscles and motor neurons in the spinal cord. As a result of SMN mutations the affected cells die and clinical symptoms of spinal muscular atrophy (SMA) develop. Physiologically, SMN together with gemins is part of a multiprotein complex of particular importance to motor neuron development. Since the SMN gene is necessary for normal motor neuron maturity, a question arises whether its expression is preserved in postnatal life or finishes with the end of ontogenesis. To answer this question we examined expression of SMN and gemins 2, 3 and 4 in spinal cords of Wistar rats at age 1-350 days using immunofluorescence and immunohistochemical methods. In the examined animals expression of SMN appeared in neurons in 20-day old rats and increased with animal age. In rats aged 30-350 days SMN immunoreactivity was similar in all the examined animals. The same phenomenon was observed in assessment of gemin expression. Our study revealed that in rat spinal cord expression of SMN and gemins 2, 3 and 4 is present through a whole animal lifespan and not only in motor but also in sensory and autonomic neurons.     

Does diabetes mellitus target motor neurons?

A pattern of peripheral neurodegeneration occurs in chronic diabetes mellitus in which an early, but selective retraction of distal axons may occur prior to any irretrievable neuronal loss. Clinical observations suggest that sensory systems undergo damage before those of motor neurons. In this work, we examined the fate of the spinal motor neuron in a long-term chronic model of experimental (streptozotocin-induced) diabetes already known to be associated with substantial loss of sensory neurons. The integrity, physiological function, and critical forms of protein expression of the full motor neuron tree was examined in mice exposed to 8 months of diabetes. Motor neurons developed progressive features of distal loss of axonal terminals but without perikaryal dropout, indicating distal axon retraction. While numbers and caliber of motor neuron perikarya and their nerve trunk axons were preserved, axons developed conduction velocity slowing, loss of motor units and neuromuscular junctions, and compensatory single motor unit action potential enlargement. Four critical proteins directly linked to diabetic complications were altered in motor neurons of diabetic mice: an elevated perikaryal expression of RAGE and PARP, molecules associated with cellular stress, along with concurrent rises in HSP-27 and pAKT, molecules alternatively identified with neuroprotective survival. Moreover, Akt mRNA was increased in diabetic lumbar spinal cords. Overall these findings indicate that although motor neurons are resistant to irretrievable dropout, they are targeted nonetheless by diabetes and gradually withdraw their terminals from distal innervation.     

Entrapment of motor nerves in motor neuron disease: does double crush occur?

OBJECTIVE: To investigate whether "diseased nerves" are more prone to entrapment neuropathy than normal nerves. Nerve conduction studies of human neuropathies have shown that electrophysiological abnormalities are often most prominent at potential sites of nerve entrapment, and entrapments are more common in patients with radiculopathies--a concept designated as "double crush". As entrapment neuropathies commonly occur in otherwise healthy subjects, it is unclear whether this relation is coincidental or whether peripheral nerves affected by disease are rendered more susceptible to effects of repeated minor trauma, traction, or mechanical compression. METHODS: Sequential ulnar nerve conduction studies were prospectively performed at baseline and at four, eight, and 12 month intervals in 16 patients with amyotrophic lateral sclerosis. Ulnar nerve entrapment was defined as a focal reduction (> 10 m/s) in conduction velocity in the across-elbow segment. RESULTS: Ulnar sensory and motor nerve fibres showed similar findings of ulnar nerve entrapment at baseline and at follow up over the period of the study. Nerves with ulnar nerve entrapment showed a significantly greater reduction in distal motor amplitudes than nerves without entrapment, even though distal ulnar sensory amplitudes remained unchanged. CONCLUSIONS: Motor nerves in motor neuron disease do not seem to be more susceptible to entrapment at the elbow than do healthy sensory nerves, thus casting doubt on the double crush hypothesis. Nerves with double pathology (amyotrophic lateral sclerosis and ulnar nerve entrapment), however, seem to undergo more rapid axonal loss than do nerves with single pathology (amyotrophic lateral sclerosis or ulnar nerve entrapment alone).     

Is it only neurogenesis?

For a long time, the occurrence of neurogenesis in the adult mammalian brain was deemed non-existent or, at best, restricted to phylogenetically old brain regions. The pendulum of current opinion has now swung in the opposite direction with growing awareness that incorporation of labeled precursors into neuronal DNA occurs widely in the brain, and undergoes significant modulation with learning, different kinds of experiential inputs, and a number of physiological manipulations. A thorough review of the literature indicates that unscheduled DNA synthesis may significantly contribute to available evidence. Notably, data interpreted in terms of nerve cell turnover are more likely to reflect turnover of neuronal DNA, as suggested by earlier investigations.     

Is one motor cortex enough for two hands?

We report on a patient with mirror movements sustained by a mono‐hemispheric fast control of bilateral hand muscles and normal hand function. Transcranial magnetic stimulation of the right motor cortex evoked contractions of muscles in both hands while no responses were observed from the left hemisphere. Somatosensory‐evoked potentials, functional magnetic resonance, and diffusion tractography showed evidence of sensorimotor dissociation and asymmetry of corticospinal projections, suggestive of reorganization after early unilateral left brain lesion. This is the first evidence that, in certain rare conditions, good hand function is possible with ipsilateral corticospinal reorganization, supporting the role of unexplored mechanisms of motor recovery.     

The moving phantom: Motor execution or motor imagery?

Amputees who have a phantom limb often report the ability to move this phantom voluntarily. In the literature, phantom limb movements are generally considered to reflect motor imagery rather than motor execution. The aim of this study was to investigate whether amputees distinguish between executing a movement of the phantom limb and imagining moving the missing limb. We examined the capacity of 19 upper-limb amputees to execute and imagine movements of both their phantom and intact limbs. Their behaviour was compared with that of 18 age-matched normal controls. A global questionnaire-based assessment of imagery ability and timed tests showed that amputees can indeed distinguish between motor execution and motor imagery with the phantom limb, and that the former is associated with activity in stump muscles while the latter is not. Amputation reduced the speed of voluntary movements with the phantom limb but did not change the speed of imagined movements, suggesting that the absence of the limb specifically affects the ability to voluntarily move the phantom but does not change the ability to imagine moving the missing limb. These results suggest that under some conditions, for example amputation, the predicted sensory consequences of a motor command are sufficient to evoke the sensation of voluntary movement. They also suggest that the distinction between imagined and executed movements should be taken into consideration when designing research protocols to investigate the analgesic effects of sensorimotor feedback.