Response of the canine internal intercostal muscles to chest wall vibration.

Although high-frequency mechanical vibration of the rib cage reduces dyspnea, its effects on the respiratory muscles are largely unknown. We have previously shown that in anesthetized dogs, vibrating the rib cage during inspiration elicits a marked increase in the inspiratory electromyographic (EMG) activity recorded from the external intercostal muscles but does not affect tidal volume (VT). In the present studies, we have tested the hypothesis that the maintenance of VT results from the concomitant contraction of the internal interosseous (expiratory) intercostals. When the rib cage was vibrated (40 Hz) during hyperventilation-induced apnea, a prominent activity was recorded from the external intercostals but no activity was recorded from the internal intercostals, including when the muscles were lengthened by passive inflation. The internal intercostals remained also silent when vibration was applied during spontaneous inspiration, and the phasic expiratory EMG activity recorded from them was unaltered when vibration was applied during expiration. Thus, the internal interosseous intercostals in dogs are much less sensitive to vibration than the external intercostals, and they do not interfere with the action of these latter during rib cage vibration. This lack of sensitivity might be the result of a reflex inhibition of the muscle spindle afferents by afferents from external intercostal muscle spindles.

Response of the canine inspiratory intercostal muscles to chest wall vibration.

High-frequency mechanical vibration of the rib cage reduces dyspnea, but the effect of this procedure on the respiratory muscles is largely unknown. In the present studies, we have initially assessed the electrical and mechanical response to vibration (40 Hz) of the canine parasternal and external intercostal muscles (third interspace) during hyperventilation-induced apnea. When the vibrator was applied to the segment investigated, prominent external intercostal activity was recorded in the seven animals studied, whereas low-amplitude parasternal intercostal activity was recorded in only four animals. Similarly, when the vibrator was applied to more rostral and more caudal interspaces, activity was recorded commonly from the external intercostal but only occasionally from the parasternal. The two muscles, however, showed similar changes in length. We next examined the response to vibration of the muscles in seven spontaneously breathing animals. Vibrating the rib cage during inspiration (in-phase) had no effect on parasternal intercostal inspiratory activity but induced a marked increase in neural drive to the external intercostals. For the animal group, peak external intercostal activity during the control, nonvibrated breaths averaged (mean +/- SE) 43.1 +/- 3.7% of the activity recorded during the vibrated breaths (p < 0.001). External intercostal activity during vibration also occurred earlier at the onset of inspiration and commonly carried on after the cessation of parasternal intercostal activity. Yet tidal volume was unchanged. Vibrating the rib cage during expiration (out-of-phase) did not elicit any parasternal or external intercostal activity in six animals. These observations thus indicate that the external intercostals, with their larger spindle density, are much more sensitive to chest wall vibration than the parasternal intercostals. They also suggest that the impact of this procedure on the mechanical behavior of the respiratory system is relatively small.

Reflex inhibition of canine inspiratory intercostals by diaphragmatic tension receptors.

1. Electrical stimulation of phrenic afferent fibres in the dog elicits a reflex inhibition of efferent activity to the inspiratory intercostal muscles. However, electrical stimulation has a poor selectivity, so the sensory receptors responsible for this inhibition were not identified. 2. In the present studies, cranial forces were applied during spontaneous inspiration to the abdominal surface of the central, tendinous portion of the canine diaphragm to activate tension mechanoreceptors in the muscle. Vagal afferent inputs were eliminated by vagotomy. 3. The application of force to the central tendon caused a graded, reflex reduction in inspiratory intercostal activity, especially in external intercostal activity. This reduction was commonly associated with a decrease in inspiratory duration and was invariably attenuated after section of the cervical dorsal roots. 4. In contrast, no change in inspiratory intercostal activity was seen when high frequency mechanical vibration was applied to the central tendon to stimulate diaphragmatic muscle spindles. 5. These observations provide strong evidence that tension receptors in the diaphragm, but not muscle spindles, induce reflex inhibition of inspiratory intercostal activity. The expression of this reflex probably involves supraspinal structures.

Effects of vigabatrin on motor potentials evoked with magnetic stimulation.

We studied the effect of an acute loading dose of vigabatrin on threshold of motor responses and duration of silent period elicited with cortical magnetic stimulation in normal subjects. In contrast to phenytoin, vigabatrin does not increase the motor threshold of first dorsal interosseus muscle. We also show that, although vigabatrin increases GABA concentrations in the central nervous system, duration of silent period studied at various stimulus intensities is not modified after vigabatrin administration.

Abnormal motor evoked responses to transcranial magnetic stimulation in focal dystonia.

We evaluated motor responses evoked after magnetic cortical stimulation in dystonia, emphasizing the relationship between resting and facilitation state. We studied 15 normal controls (mean age, 37.9 years; range, 23 to 63) and 13 dystonic patients (mean age, 43.4 years; range, 20 to 56). Surface electrodes were placed over the right first dorsal interosseous muscle to measure motor evoked potentials and inhibitory silent periods obtained with magnetic stimulation. The amplitude ratio of motor evoked potentials measured during facilitation and at rest with low-intensity magnetic stimulation was significantly higher in dystonic patients (15.09) when compared with normal subjects (5.43; p = 0.04). The ratio of duration of silent periods evoked with 120% motor threshold (MT) and MT + 25% magnetic stimulus intensity was significantly higher in dystonic patients (78.4%) when compared with normal subjects (69.7%; p = 0.04). We conclude that with low-intensity magnetic stimulation the relationship between amplitudes of motor potentials evoked at rest and during facilitation, as well as the responses of pathways that mediate silent periods, are disturbed in focal dystonia.

Effects of diphenylhydantoin on motor potentials evoked with magnetic stimulation.

We studied the effect of an acute loading dose of diphenylhydantoin (DPH) on motor responses elicited with cortical magnetic stimulation in normal subjects. DPH increased significantly the motor threshold activation of ADM, APB, FDI and biceps. The motor threshold increase was of greater magnitude for the proximal muscle. Spinal soleus alpha-motoneuron pool excitability assessed by H-reflex was increased significantly suggesting that the motor threshold increase is related to a supraspinal effect of the drug. Our study demonstrates that the motor threshold increase observed after DPH administration occurs not only in epileptic patients but also in normal subjects.

Somatosensory central conduction time after sural and tibial nerve stimulation.

We recorded spinal and cortical somatosensory evoked potentials (SEPs) after sural and tibial nerve stimulation at the ankle in 34 normal subjects. Spinal SEPs were reproducible with sural nerve stimulation in only 65% of normal subjects. The spinal amplitudes were significantly smaller after sural nerve stimulation. Central conduction time (CCT) was significantly shorter when measured from onset instead of peak latencies. There was a significant difference between CCT with tibial nerve and sural nerve stimulation. Our results are consistent with the idea that CCT measures from onset and peak latencies do reflect the travel of the afferent volley in different spinal fiber populations.

Spinal and brain-stem SEPs and H reflex during enflurane anesthesia.

Whereas cortical SEPs are altered by halogenated anesthetics, spinal and subcortical SEPs are thought to be hardly affected. In this study the spinal N13 potential (recorded with anterior neck reference) showed a significant delay with enflurane anesthesia. The P13 and P14 far-field potentials, however, remained unchanged. Our results indicate that oligosynaptic as well as polysynaptic pathways are influenced by halogenated anesthetics and that enflurane has different effects on spinal gray matter and cuneate synapses. Our data also demonstrate that earlobe reference recordings are not adequate to measure pharmacologic effects on subcortical SEPs.

Dissociation of P13-P14 far-field potentials: clinical and MRI correlation.

P13 and P14 far-field potentials are recorded over the scalp with median nerve stimulation when non-cephalic reference is used to measure somatosensory evoked potentials. The dissociation of these 2 potentials is exceptional. Only 2 cases subsequent to pontine lesions have been described hitherto. We report the case of a 31-year-old woman with a low grade glioma located at the spino-medullary junction who presented a P13-P14 far-field dissociation. This case fully supports the independent nature of the P13 and P14 potential generators.

Topographic analysis of the effects of isoflurane anesthesia on SEP.

Isoflurane anesthesia induces a striking increase in the P22 potential recorded over the precentral scalp whereas the amplitude of the N20 is reduced. It is not known whether the increased "P22" enhanced by isoflurane arises from the same generator as the small precentral P22 potential recorded in the normal awake subject. Multi-channel recordings of SEP before and during isoflurane anesthesia were performed in 13 normal subjects. Isopotential topographic maps showed that isoflurane did not change the distribution of the precentral "P22" despite its clear amplitude increase. Our data confirm that isoflurane enhances the precentral P22 and that the enhanced "P22" arises from the same generator as the P22 recorded before isoflurane anesthesia.

Inhibitory effects of ATP and other nucleotides on atrial natriuretic peptide (ANP) binding to R1-type ANP receptors in human neuroblastoma NB-OK-1 cell membranes.

ATP dose-dependently inhibited rat 125I-ANP-(99-126) binding to membranes from the human neuroblastoma cell line NB-OK-1 by increasing the KD value for the hormone without altering the Bmax value. After a 20 min preincubation with 37.5 pM 125I-ANP-(99-126) and 0.5 mM ATP, followed by the addition of 0.3 microM unlabelled ANP-(99-126), the proportion of rapidly dissociating receptors was 4-times higher than in the absence of ATP. The other nucleotides ADP, AMP, AMP-PNP, ATP gamma S, GTP, GDP, GMP, GMP-PNP and GTP gamma S were also inhibitory but with a lower potency and/or efficacy. Binding equilibrium data were satisfactorily simulated by a computer program based on partially competitive binding of ANP-(99-126) and the nucleotides, and this, together with the data on dissociation kinetics, strongly suggests that several nucleotides, when added at concentrations up to 1 mM, form a ternary ANP-receptor-nucleotide complex.

Synaptic effects of halogenated anesthetics on short-latency SEP.

We evaluated the effects of different stable end-tidal concentrations of isoflurane, enflurane, or halothane on short-latency somatosensory evoked potentials recorded during general anesthesia. Isoflurane and enflurane significantly enhanced the P22 over the pre-central scalp, whereas the parietal N20 amplitude did not increase. The P22 increase did not occur with halothane, which indicates that the P22 changes are a specific effect of certain anesthetics, probably related to their influence on synaptic events. At the subcortical level, isoflurane and enflurane increased significantly the N13 peak latency and decreased the interval between the N13 peak and P14 peak, which implicates interference with synaptic transmission at the spinal level. Halothane had no effect at the spinal level. All three anesthetics significantly increased the central conduction time.

Acute effects of diphenylhydantoin on peripheral and central somatosensory conduction.

We studied the acute effects of an intravenous loading dose of DPH (16 mg/kg body weight) on peripheral and central somatosensory conduction in 10 normal volunteers. Somatosensory evoked potentials were recorded before and at regular intervals after DPH infusion. There was no effect on peripheral conduction. DPH significantly delayed N13 peak latency without changing conduction in the posterior spinal columns. Although the N13-N20 interpeak interval remained stable because of the parallel shift of the 2 peaks, the central conduction time measured from onset latencies of N11 and N20 significantly increased. We conclude that acute administration of DPH at serum levels below 30 micrograms/ml induces a reversible delay of synaptic transmission in spinal and central somatosensory structures.

[Course of central somatosensory conduction in a case of vitamin B12 deficiency]. / Etude évolutive de la conduction somesthésique centrale dans un cas d'avitaminose B12.

We report clinical and neurophysiological data of a 58 year-old man with vitamin B12 deficiency and a 6 years follow-up. The initial clinical disorders did not permit a clear distinction between peripheral and central nervous system disease. Detailed analysis of the somatosensory central conduction time (measured from onset latencies of N11 and N20) showed clear evidence of slowed down conduction at spinal cervical level (reflected by the N11-P14 interval) whereas supraspinal conduction (as shown by the P14-N20 interval) was normal. The patient's condition improved under treatment, and the somatosensory central conduction time was progressively shortened. After 6 years of treatment, the neurological examination and the somatosensory central conduction interval were normal. However, analysis of the spinal conduction still showed slowed down conduction.

The effect of stimulus frequency on post- and pre-central short-latency somatosensory evoked potentials (SEPs).

We assessed the influence of the stimulus frequency on short-latency SEPs recorded over the parietal and frontal scalp of 26 subjects to median nerve stimulation and 16 subjects to digital nerve stimulation. When the stimulus frequency is increased from 1.6 Hz to 5.7 Hz, the amplitude of the N13 potential decreases whereas the P14 remains stable. The amplitude of the N20 is not changed significantly whereas the P22, the P27 and the N30 decrease significantly. In 50% of the subjects 2 components can be seen within the frontal negativity that follows the P22: an early 'N24' component, which is not affected by the stimulus rate, and the later N30, which is highly sensitive to the stimulus frequency. The distinct amplitude changes of the N20 and P22 with increasing stimulus frequency is one among other arguments to show that these potentials arise from separate generators.

Differential effects of isoflurane on SEP recorded over parietal and frontal scalp.

We evaluated the effects of different concentrations of isoflurane on short-latency somatosensory evoked potentials recorded over the parietal and frontal scalp in 14 patients during general anesthesia at stable end-tidal concentrations between 0% and 2.5%. At concentrations between 0% and 1%, there was a marked discrepancy between the amplitude of the parietal N20, which remained stable, and the striking increase of the frontal P22. At concentrations above 1.5%, the parietal N20 disappeared in 6 patients whereas the P22 was clearly identified in 12. The central conduction time increased significantly whereas the spinal conduction was not delayed by increasing levels of isoflurane. These results show that isoflurane anesthesia is a useful pharmacologic model to demonstrate the independence of the N20 recorded over the parietal scalp and the P22 recorded over the frontal scalp.

The effect of acute hemiplegia on intercostal muscle activity.

We recorded the EMG of parasternal intercostal muscles in 25 patients with flaccid hemiplegia during quiet spontaneous breathing, voluntary hyperventilation, and CO2-induced hyperventilation. The respiratory drive was abnormal on the hemiplegic side and the function of the intercostal muscles was affected specifically during voluntary hyperventilation.

Selective unilateral absence or attenuation of wave V of brain-stem auditory evoked potentials with intrinsic brain-stem lesions.

The contribution of ipsilateral and contralateral auditory brain-stem structures to the generation of wave V of brain-stem auditory evoked potentials is a controversial subject. We describe two cases with an intrinsic brain-stem lesion that involved the lateral lemniscus unilaterally in the middle and upper pons. The focal nature of the auditory structures was confirmed by detailed neuropathologic data in one case and by magnetic resonance scans in the other one. In both cases, brain-stem auditory evoked potentials revealed the unilateral absence (case 1) or marked attenuation (case 2) of wave V on stimulation of the ear contralateral to the intrinsic pontine lesion. Findings in both cases strongly suggest that wave V is predominantly generated by pontine structures contralateral to the stimulated ear and that the integrity of the contralateral lateral lemniscus is essential.

Somatosensory conduction in vitamin B12 deficiency.

We tested the hypothesis that the somatosensory central conduction time (CCT) can reveal central nervous system involvement in vitamin B12-deficient patients when this cannot be established on clinical grounds alone. Three patients with pernicious anemia and without clinical signs of upper motor neuron lesion had a striking increase of CCT. This increase was shown to be reversible in 1 patient who improved over 3 years of treatment. Detailed analysis of the CCT showed that the decrease of conduction velocity occurred in the posterior columns, whereas the conduction was normal at the thalamo-cortical level. We conclude that CCT is a useful parameter to localize and quantify central nervous system disease in vitamin B12 deficiency.