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Biomedical subjects

G Cheron

Publications and source records attributed to G Cheron.

105 records · Page 6Linked to original sources
PubMed1981

Non-cephalic reference recording of early somatosensory potentials to finger stimulation in adult or aging normal man: differentiation of widespread N18 and contralateral N20 from the prerolandic P22 and N30 components.

Prerolandic and parietal SEPs to electrical stimulation of fingers or median nerve were studied with non-cephalic reference in 40 normal young adults and in 35 healthy octogenarians. Limb temperatures were 36-37 degrees C. Intersubject variations of SEP components were analysed. A new widespread component N18 was identified and shown to be generated below the cortex. This N18 is about the only early component recorded at the parietal ipsilateral region after the positive far-field potentials P9, P11 and P13-P14. Transit times along the central somatosensory pathway were replicated and discussed as well as other evidence about the sequential activation of the various neural structures involved. The N20 potential representing the earliest cortical response is recorded from the contralateral parietal region, but is absent ipsilaterally. The prerolandic potential is related to distinct generators and is elicited by a separate thalamocortical pathway rather than by corticocortical connections from areas 2 and 5 in parietal cortex. The changes associated with normal aging have been confirmed and extended.

Adult↗
PubMed1980

Central somatosensory conduction in man: neural generators and interpeak latencies of the far-field components recorded from neck and right or left scalp and earlobes.

Early somatosensory evoked potential (SEP) components to median nerve or finger stimulation were recorded with non-cephalic references in normal young adults. Detailed topographic data over scalp and neck were related to anatomical observations on the actual conduction distances in dorsal column, medial lemniscus and thalamo-cortical parts of the somatosensory pathway. The extrapolation of afferent conduction velocity (CV) measured from sensory nerve potentials along the peripheral nerve to the C6-C7 spinal segments identified the spinal entry time with the onset of the neck N11 or scalp P11 (far field 2 or FF2). The first far field (FF1) is generated in the nerve proximal to axilla. The definite latency shift of the spinal negativity along the neck indicates a CV of 58 m/sec. Data about the maximal diameter of lemniscal axons in man were used to calculate a CV of 40.5 m/sec. Consideration of transit times from spinal entry to cortex and of synaptic delays clarified the arrival times of the afferent volley at various relay nuclei, and also suggested a thalamo-cortical CV of about 33 m/sec. Interpeak and onset-to-peak measures on scalp far fields suggest that FF3-FF4 are generated in medial lemniscus rather than above the thalamus. Consistent differences in amplitude, but not in wave form, were recorded at right and left earlobes for FF2 (larger ipsilaterally) and FF3-FF4 (larger contralaterally). The scalp topography of far fields was analysed in detail.

Adult↗
PubMedDate not supplied

Gating of the early components of the frontal and parietal somatosensory evoked potentials in different sensory-motor interference modalities.

Three different interfering conditions were studied during the recording of pre- and postcentral somatosensory evoked potentials (SEPs) following median nerve stimulation at the wrist in 16 normal subjects: active finger movement (MVT), light superficial massage (LSM) and deep muscular massage (DMM) of the hand. Special attention was focused on selective effects on individual SEP components. The frontal N30 component showed the most significant amplitude reduction during the three interfering conditions (76.4% of reduction in MVT, 36.4% in DMM and 32.9% in LSM). In contrast the frontal N23 was not significantly changed and the preceding P22 component was only reduced in the MVT condition. Postcentral N20 was unchanged by the three conditions while P27 was clearly gated by movement but not significantly by LSM and DMM. The three interfering conditions enhanced the parietal N32 and had no significant effect on the parietal P45. An important point was the interindividual variability of these effects and it appeared that group average wave forms would therefore be confusing. The peak latency of some SEP components was changed during the interfering conditions. The most important effect was an increase of postcentral P45 latency which was found to be related to the amplitude enhancement of N32.

Adult↗
PubMedDate not supplied

Mental movement simulation affects the N30 frontal component of the somatosensory evoked potential.

It is known that somatosensory evoked potentials can be influenced by several centripetal and centrifugal factors which modify their amplitude. The present study shows for the first time that the frontal waves N30 and to a lesser extent N23 are specifically attenuated during mental movement simulation (MMS) activity. This gating phenomenon, tested on 16 normal subjects, occurred when repeated fast finger movements on the stimulated side are mentally simulated. In contrast, no significant modification appeared when the subject performed the MMS activity with the hand contralateral to that receiving electrical stimuli or when the subject performed a mental operation unrelated to the MMS. The MMS was shown by Roland et al. (1980) to increase the regional blood flow exclusively in the supplementary motor area (SMA). Our experimental data therefore indicate that the SMA could play an important role in the generation of the frontal N30.

Adult↗
PubMedDate not supplied

[Peripheral and central somatosensory pathways and evoked cerebral potentials during aging (author's transl)].

This study used electrical stimulation of the fingers and hands and evoked potentials to determine the functional state of the peripheral and central somatosensitive pathway in octogenarian subjects after very strict selection to exclude associated disease. The nerve fibers of the digital nerves were studied by recording the antidromic potential. Despite a marked reduction in the amplitude of this potential and an increase in latent period and duration, absolute and functional refractory periods were not increased with aging. Slowing in the rate of orthodromic conduction was demonstrated by the recording of nerve potentials and the spinal evoked potential. The amplitude of this evoked activity in the neck is significantly reduced in octogenarians. By contrast, the central transit of the somatosensory afferent impulses from the spinal cord to the cortex is remarkably well preserved. In addition, the amplitude of the parietal components of S.E.P. are significantly increased in the octogenarian.

Aged↗
PubMedDate not supplied

Effect of incisions in the brainstem commissural network on the short-term vestibulo-ocular adaptation of the cat.

This study was intended to test the adaptive plasticity of the vestibulo-ocular reflex before and after either a midsagittal or parasagittal incision in the brainstem. Eye movements were measured with the electromagnetic search coil technique during the vestibulo-ocular reflex (VORD) in the dark, the optokinetic reflex (OKN), and the visuo-vestibular adaptive training procedure. Two types of visual-vestibular combined stimulation were applied by means of low frequency stimuli (0.05 to 0.10 Hz). In order to increase or decrease the VORD gain, the optokinetic drum was oscillated either 180 degrees out-of-phase or in-phase with the vestibular stimulus turntable. This "training" procedure was applied for 4 hours. Initial measurements of the VORD were normal with a mean gain value of 0.92 +/- 0.08. After 4 hours of "training" with the out-of-phase condition (180 degrees), VORD gain reached mean values of 1.33 +/- 0.11 (n = 6 cats). In the in-phase combination, the mean VORD gain decreased from 1.0 to 0.63 +/- 0.02 (n = 2 cats). No significant change of VORD phase was found in any of the cats. Midsagittal or parasagittal pontomedullary brainstem incisions were performed in 4 cats. Recovery of the VOR was tested on the 2nd, 7th, and 30th day after operation. After the 30th day, recovery of the VORD gain stabilized at about 66% of the initial preoperative value. At this stage of the recovery, the optokinetic response (OKN) of the midsagittal-lesioned cats was practically normal: in the parasagittal-lesioned cats, the postoperative OKN responses were asymmetric. After stabilization of recovery, lesioned cats were trained with the same adaptation procedure. Although the direct effect of the visuo-vestibular combined stimulation during the training was still operative in all lesioned cats, the adaptive plasticity was completely abolished by the lesions. These results suggest that the commissural brainstem network may play a crucial role in the acquisition of the forced VOR adaptation.

Adaptation, Ocular↗
PubMedDate not supplied

Effects of ketamine on ocular movements of the cat.

We studied the effects of ketamine, an antagonist of the N-methyl-D-aspartate receptors, on (1) the spontaneous saccades, (2) the vestibulo-ocular reflex (VOR), and (3) the optokinetic nystagmus (OKN) in 8 cats. Ketamine was given intramuscularly at four dosages (1, 2, 8, and 16 mg/kg). Eye movements were measured using the magnetic field-search coil technique. Ketamine did not prevent the occurrence of saccades, but each of them was followed by a centripetal postsaccadic drift. The time-constant of the drift induced by ketamine was 1.0 s when the given dosage was 1 mg/kg and 0.35 s when the given dosage was 16 mg/kg. Post-saccadic drift caused by a low dosage of ketamine may reflect only a mismatch between the pulse and the step commands that create saccades. The highest used dosages of ketamine aggravated the post-saccadic drift probably by disturbing the oculomotor neural integrator. To elicit the horizontal VOR, the head was submitted either to sinusoidal rotations (+/- 20 degrees; 0.05 to 1 Hz) or to a rotation at a constant velocity (100 degrees/s during 40 s). In darkness, the VOR step gain was reduced by ketamine in a dosage-dependent manner. VOR phase lead at 0.10 Hz oscillation in darkness increased from 4.0 degrees +/- 2.4 degrees to 51.6 degrees +/- 7.5 degrees after administration of ketamine at 16 mg/kg. This suggests that ketamine, at least at higher dosages, induces a failure of the neural integrator. Chemical blockade of the vestibular commissure by ketamine may also be responsible for the reduction of the VOR gain. Horizontal OKN was tested using a step stimulus (30 degrees/s during 40 s). When ketamine was given at 1 mg/kg, the average steady-state gain of the OKN diminished from 0.6 +/- 0.2 to 0.3 +/- 0.1. After administration of ketamine at 2 mg/kg, the OKN was abolished. The sensitivity of OKN to ketamine is explained at least partly by the fact that ketamine acts against the visual pathways in the retina, in the geniculate nucleus, and in the visual cortex. The time course of the optokinetic afternstagmus (OKAN) and that of the decrease of the prerotatory and postrotatory VOR were not reduced by ketamine administered at 1 or 2 mg/kg. This shows that ketamine does not affect the velocity-storage mechanism at these dosages.

Animals↗
PubMedDate not supplied

[Development of the heart rate in the first year of life and infant ill health].

Heart rate during the 1st year of life decreases from 149 to 117/min (mean) and 227 to 186 (upper range), as determined by Holter monitoring. There is little change in those at the lower frequencies. A decrease in nocturnal rhythm becomes evident by 3 months of age. In comparison to these controls, near-miss infants or their sibs and infants with "spells" demonstrate a lower basal rate with longer pauses and wider range of instantaneous variability from the 1st days of life. Near-miss infants and sibs of sudden infant death syndrome infants are harder to differentiate. However, the "sibs" + "spells" groups show prolonged pauses over 1 second in the first weeks of life and become even more prominent at 3 months. This vagal hyperreactivity may be due to immature or poorly regulated cholinergic bulbar centers.

Apnea↗
PubMedDate not supplied

[Neonatal primary hyperparathyroidism caused by clear cell hyperplasia].

Neonatal primary hyperparathyroidism is rare but must be evoke during respiratory distress with thoracic deformity and hypercalcemia. The plasma immunoreactive parathyroid hormone level allows the diagnostic. This case, with diffuse hyperplasia of water-clear cells type, develops rickets of vitamin D deficiency before surgery. A large parathyroidectomy (7/8) was performed and the child is normo-calcemic 2 years after. The time of surgery is function of calcium level.

Female↗