Compound muscle action potentials in newborn infants with spina bifida.

The aim of this study was to investigate the relationship between compound muscle action potentials (CMAPs) and neurological impairment in newborn infants with spina bifida. Thirty-one newborn infants (17 males, 14 females, mean gestational age 39 wks [SD 2]; mean birthweight 3336 g [SD 496]) with spina bifida were investigated at a median age of 2 days (range 1-18 d). Motor and sensory impairment and muscle stretch reflexes were assessed and neuroimaging was performed. CMAPs were recorded from the tibialis anterior muscle and the gastrocnemius muscle after percutaneous electrical nerve stimulation. CMAPs were obtained in almost all infants. The area under the curve of the CMAP (CMAP-area) was associated with motor and sensory impairment and with the presence of muscle stretch reflexes, but not with the morphological level of the spinal anomaly. These associations were stronger for the gastrocnemius muscle than for the tibialis anterior muscle. In conclusion, the CMAP-area correlates with neurological impairment in neonatal spina bifida and provides an estimate of residual motor neuron function in affected spinal segments. The assessment of CMAPs after percutaneous electrical nerve stimulation is recommended as an additional instrument to the clinical neurological examination and imaging studies.

Inhibition from the plantar nerve to soleus muscle during the stance phase of walking.

The purpose of this study is to investigate the effect and the circuit from the branch of tibial (plantar) nerve to soleus muscle and its modulation during walking in humans. Stimulation of the plantar nerve produced short latency inhibition of soleus EMG activity and the H-reflex in humans. The threshold of afferent fibers was lower than that of motor fibers. This inhibition did not converge to disynaptic reciprocal Ia inhibition nor did inhibition from the cutaneous nerve of the big toe, but to Ib inhibition from the medial gastrocnemius nerve. The inhibitory pathway from the plantar nerve therefore is considered to include Ib inhibitory interneurones. Modulation of the inhibition was investigated during walking. Less EMG depression after plantar nerve stimulation occurred in the stance phase of walking than for tonic or dynamic plantar flexion at similar background EMG activity level. The inhibition of the soleus H-reflex after plantar nerve stimulation was also decreased during the stance phase. For investigating the influence of load on the inhibition from the plantar nerve, more EMG depression occurred in the stance phase with body unloading. Similar findings were observed in Ib inhibition from the medial gastrocnemius nerve, but not in disynaptic reciprocal Ia inhibition to soleus muscle. It is concluded that transmission of inhibition from the plantar nerve to soleus muscle is modulated during walking. It would minimize this inhibition during the stance phase of walking and might enhance soleus muscle activity via this reflex pathway for the support of weight.

Reduction of common synaptic drive to ankle dorsiflexor motoneurons during walking in patients with spinal cord lesion.

It is possible to obtain information about the synaptic drive to motoneurons during walking by analyzing motor-unit coupling in the time and frequency domains. The purpose of the present study was to compare motor-unit coupling during walking in healthy subjects and patients with incomplete spinal cord lesion to obtain evidence of differences in the motoneuronal drive that result from the lesion. Such information is of importance for development of new strategies for gait restoration. Twenty patients with incomplete spinal cord lesion (SCL) participated in the study. Control experiments were performed in 11 healthy subjects. In all healthy subjects, short-term synchronization was evident in the discharge of tibialis anterior (TA) motor units during the swing phase of treadmill walking. This was identified from the presence of a narrow central peak in cumulant densities constructed from paired EMG recordings and from the presence of significant coherence between these signals in the 10- to 20-Hz band. Such indicators of short-term synchrony were either absent or very small in the patient group. The relationship between the amount of short-term synchrony and the magnitude of the 10- to 20-Hz coherence in the patients is discussed in relation to gait ability. It is suggested that supraspinal drive to the spinal cord is responsible for short-term synchrony and coherence in the 10- to 20-Hz frequency band during walking in healthy subjects. Absence or reduction of these features may serve as physiological markers of impaired supraspinal control of gait in SCL patients. Such markers could have diagnostic and prognostic value in relation to the recovery of locomotion in patients with central motor lesions.

Control of locomotor cycle durations.

In intact animals and humans, increases in locomotor speed are usually associated with decreases in step cycle duration. Most data indicate that the locomotor central pattern generator (CPG) shortens cycle duration mainly by shortening the durations of extensor rather than flexor phases of the step cycle. Here we report that in fictive locomotion elicited by electrical stimulation of the midbrain locomotor region (MLR) in the cat, spontaneous variations in cycle duration were due more to changes in flexor rather than extensor phase durations in 22 of 31 experiments. The locomotor CPG is therefore not inherently extensor- or flexor-biased. We coined the term "dominant" to designate the phase (flexion or extension) showing the larger variation. In a simple half-center oscillator model, experimental phase duration plots were fitted well by adjusting two parameters that corresponded to background drive ("bias") and sensitivity ("gain") of the oscillator's timing elements. By analogy we argue that variations in background drive to the neural timing elements of the CPG could produce larger variations in phase duration in the half-center receiving the lower background drive, i.e., background drive may determine which half-center is dominant. The fact that data from normal cats were also fitted well by the model indicates that sensory input and central drive combine to determine locomotor phase durations. We conclude that there is a considerable flexibility in the control of phase durations in MLR-induced fictive locomotion. We posit that this may be explained by changes in background excitation of neural timing elements in the locomotor CPG.

A sound-evoked vestibulomasseteric reflex in healthy humans.

Averaged responses to loud clicks were recorded in the unrectified and rectified masseter electromyogram (EMG) of 18 healthy subjects. Unilateral clicks (0.1 ms, 3 Hz, 70-100 dB NHL), delivered during a steady masseter contraction, evoked bilateral responses that appeared to consist of 2 components on the basis of threshold, latency, and their appearance in rectified EMG. The lowest threshold response appeared as a p16 wave (onset 11-13 ms) in the unrectified EMG and corresponded with a 10- to 12-ms period of inhibition in the rectified EMG. Higher-intensity clicks recruited an earlier p11 response in the unrectified EMG (onset 7.0-9.2 ms) that sometimes appeared as an initial increase in the rectified EMG before suppression. The amplitude of the p11 wave scaled with background EMG level and was asymmetrically modulated by 30 degrees tilt of the whole body. The threshold of the early p11/n15 wave in masseter was the same as the threshold for click-induced vestibulocollic reflexes. Single motor unit recordings demonstrated that responses in masseters corresponded to a silent period in unit firing that began earlier and lasted longer at 100 dB than at 80 dB. We propose that loud clicks induce 2 partially overlapping short-latency reflexes in masseter muscle EMG: a p11/n15 response, which we suggest is of vestibular origin, and a p16/n21 response, which we suggest is equivalent to the previously described jaw-acoustic reflex.

Nerve lesions after therapy for childhood acute lymphoblastic leukemia.

BACKGROUND: The objective of the current study was to use somatosensory evoked potentials (SEP) to detect signs of nerve lesions in the peripheral nerve and in the central nervous system (CNS) after 3 years of treatment for childhood acute lymphoblastic leukemia (ALL). METHODS: The somatosensory potentials evoked by stimulation of the median nerve and posterior tibial nerve were recorded in 31 children with ALL after 3 years of therapy. All patients were examined clinically. The 14 standard risk patients had been treated with chemotherapy according to the Nordic regimen, and the 17 intermediate risk or high risk patients had been treated with chemotherapy and cranial irradiation according to the ALL BFM-83 protocol. RESULTS: A decrease in amplitudes was observed at the brachial plexus and spinal cord (C7) in the median SEP, and at the knee, spinal cord (Th12), and cortex in the tibial SEP, indicating axonal injury within the entire CNS in the patients with ALL compared with healthy age-, gender-, and height-matched controls. Prolongation of the SEP latencies was found within the spinal cord, indicating demyelination. These SEP changes had persisted for 2 years since the last injection/infusion of vincristine or methotrexate, which are the principal neurotoxic drugs used in chemotherapy for ALL. Clinical signs of nerve injury such as depressed deep tendon reflexes and gross or fine motor difficulties were found in approximately 33% of the patients and dysdiadochokinesia in 50%. CONCLUSIONS: Treatment of ALL in children principally with vincristine and methotrexate causes long-standing axonal injury throughout the nervous system and demyelination within the spinal cord. These changes are associated with clinical neurologic findings.