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Biomedical subjects

G Cheron

Publications and source records attributed to G Cheron.

At least 55 records · Page 3Linked to original sources
PubMed1996

A dynamic neural network identification of electromyography and arm trajectory relationship during complex movements.

We propose a new approach based on dynamic recurrent neural networks (DRNN) to identify, in human, the relationship between the muscle electromyographic (EMG) activity and the arm kinematics during the drawing of the figure eight using an extended arm. After learning, the DRNN simulations showed the efficiency of the model. We demonstrated its generalization ability to draw unlearned movements. We developed a test of its physiological plausibility by computing the error velocity vectors when small artificial lesions in the EMG signals were created. These lesion experiments demonstrated that the DRNN has identified the preferential direction of the physiological action of the studied muscles. The network also identified neural constraints such as the covariation between geometrical and kinematics parameters of the movement. This suggests that the information of raw EMG signals is largely representative of the kinematics stored in the central motor pattern. Moreover, the DRNN approach will allow one to dissociate the feedforward command (central motor pattern) and the feedback effects from muscles, skin and joints.

Adult↗
PubMed1996

Discharge properties of brain stem neurons projecting to the flocculus in the alert cat. I. Medical vestibular nucleus.

1. The aim of this study was to characterize the signals transmitted by neurons of the medial vestibular nucleus (MVN) to the middle zone of the flocculus in alert cats. 2. Bipolar stimulating electrodes were implanted into the middle zone of each flocculus, because this zone is known to be involved in the control of horizontal eye movements. Correct implantation of the stimulating electrodes was ensured by 1) recording of Purkinje cells whose activity was related to horizontal eye movements and 2) elicitation of slow abduction of the ipsilateral eye upon electrical stimulation. 3. The rostral two-thirds of the MVN were investigated by microelectrodes during stimulation of both flocculi. Antidromically activated neurons were found only in the central part of the explored area. Forty-four units were activated from the contralateral, eight from the ipsilateral flocculus. Neurons could never be activated from both flocculi. 4. Neurons included in this study were MVN neurons that had 1) to be antidromically activated from one flocculus and 2) to modulate their firing rate during the horizontal vestibuloocular reflex (VOR) elicited by sinusoidal stimulation (0.1 Hz; 10, 20, 30 or 40 degrees). The 39 neurons matching both criteria were classified in 2 groups: 22 neurons changed their firing rate during spontaneous horizontal eye movements (EM-neurons), 17 modulated their activity only during head rotation and were labeled vestibular-only neurons (VO-neurons). 5. Sufficient data were obtained from 13 EM-neurons to allow a quantitative analysis. Among those, 12 were activated from the contralateral and 1 from the ipsilateral flocculus. Their sensitivity to horizontal eye position during intersaccadic fixation was 3.54 +/- 2.75 (SD) spikes.s-1/deg. Eight EM-neurons behaved as type I neurons, five as type II neurons. During the slow phases of the VOR, all of these neurons combined some head-velocity sensitivity (1.50 +/- 0.43 spikes.s-1/deg.s-1) with some horizontal eye-position sensitivity (3.61 +/- 2.45 spikes.s-1/deg). Additionally, seven of these neurons presented a sensitivity to eye velocity (1.34 +/- 0.55 spikes.s-1/deg.s-1). The phase difference between the modulation of firing rate and eye position varied substantially between neurons. The observed phase lead with respect to eye position ranged from 2 to 110 degrees (41.9 +/- 31.8 degrees). 6. Sufficient data were obtained from 10 VO-neurons to allow a quantitative analysis. Among those, nine were activated from the contralateral and one from the ipsilateral flocculus. All of these neurons behaved as type I neurons. The sensitivity to head velocity was 1.64 +/- 1.07 spikes.s-1/deg.s-1. The phase lead of the modulation of spike activity with respect to head velocity ranged from 4.5 to 30.5 degrees (16.4 +/- 8.9 degrees). 7. We conclude that the MVN provides the horizontal zone of the flocculus (with a strong contralateral preference) with information about head velocity (through VO-neurons and EM-neurons) and about eye velocity and position (through EM-neurons).

Animals↗
PubMed1996

Discharge properties of brain stem neurons projecting to the flocculus in the alert cat. II. Prepositus hypoglossal nucleus.

1. The aim of this study was to characterize the signals transmitted by the neurons of the nucleus prepositus hypoglossal (NPH) to the middle zone of the flocculus of the cat. The methods, the behavioral testing, and the animals used in this study were the same as those used in the accompanying paper on medial vestibular nucleus neurons. 2. The rostral two-thirds of the NPH was explored in alert animals with microelectrodes during stimulation of the middle zone of both flocculi. Discharges of neurons were analyzed during spontaneous eye movements (head fixed) and during horizontal vestibuloocular reflex (VOR) activity elicited by sinusoidal stimulation (10, 20, 30, or 40 degrees at 0.1 Hz). Forty neurons were found to be antidromically activated from only one or the other of the two flocculi (latency: 0.99 +/- 0.17 ms, mean +/- SD): 37 from the contralateral flocculus and 3 from the ipsilateral one. None of the neurons could be activated antidromically from both flocculi. Floccular stimulation never resulted in direct inhibition of these NPH neurons. 3. Of the 37 units antidromically activated from the contralateral flocculus, 26 were recorded sufficiently long to allow full quantitative analysis. Most of these (20 neurons) were classified as burst-tonic (BT) neurons. The BT neurons exhibited during each saccade made in one direction (the ON direction) a burst of spikes, and during postsaccadic fixation a tonic activity that increased with gaze displacement in the ON direction. The mean sensitivity of the neurons to eye velocity during the "ON" saccades was 3.3 +/- 1.6 spikes.s-1.deg-1.s-1. During intersaccadic fixation, the mean sensitivity to eye position was 3.6 +/- 2.5 spikes.s-1.deg-1. During the VOR, the majority showed modulation in relation to both eye position and eye velocity. The mean sensitivity to eye position during the VOR was 3.4 +/- 2.6 spikes.s-1.deg-1 (range: 0.2-8.1 spikes.s-1.deg-1). The mean sensitivity to eye velocity during the VOR was 2.1 +/- 1.3 spikes.s-1.deg-1.s-1. The mean phase lead of with respect to eye position was 16.4 +/- 6.8 degrees (range: 6.0-28.9 degrees). Eighty percent of the BT neurons behaved as type I neurons. Forty-seven percent of the BT neurons also presented some head velocity sensitivity (1.48 +/- 0.6 spikes.s-1.deg-1.s-1, mean +/- SD). 4. Other NPH cells antidromically activated from the contralateral flocculus were classified in two groups: bidirectional burst (BB) neurons (n = 4) and burst-driving (BD) neurons (n = 2). The BB neurons were characterized by a burst discharge during every horizontal saccade or VOR quick phase, irrespective of the direction. The mean sensitivity of the BB neurons to eye velocity during saccades was 3.3 +/- 7.8 (SD) spikes.s-1.deg-1.s-1. Both BD neurons increased their firing rate during the slow VOR phases induced by an ipsilateral rotation (type I neurons) and exhibited high-frequency bursts in association with ipsilaterally directed quick phases. 5. The results indicate that the main projection of the NPH onto the middle zone of the flocculus comes from contralaterally located type I BT neurons. Signals transmitted in this path associate a high sensitivity for eye velocity with a high sensitivity for eye position. This type of input is consistent with the suggestion that the main function of the flocculus is to control the gain of downstream reflexes and to perform a fine adjustment of the gaze holding command.

Animals↗
PubMed1995

Molecular identification of viruses in sudden infant death associated with myocarditis and pericarditis.

A subset of infants dying suddenly and unexpectedly have myocarditis with or without pericarditis found at autopsy. To address whether viruses known to cause infantile myocarditis and pericarditis might be present in such infants, we examined myocardium, liver and skeletal muscle for the presence of genomic sequences from adenovirus, cytomegalovirus, enterovirus and echovirus 22/23 in infants enrolled in a comprehensive evaluation protocol. We studied eight infants who died suddenly and unexpectedly with histologic evidence of myocarditis and/or pericarditis detected at postmortem examination. One infant with myocarditis and pericarditis had adenovirus genome detected in the myocardium. In an additional infant with severe pericarditis alone, enterovirus genome was detected in the liver. Although echovirus 22/23 has been associated with myopericarditis in young infants, no previous studies have used molecular methods to search for the genomic sequences of these viruses in clinical samples. No echovirus 22/23 genome was detected in the patients reported here. The significance of enterovirus and adenovirus genome in the tissues of two patients dying suddenly and unexpectedly remains speculative but raises the possibility that pathogenic viruses may cause little or no clinical symptoms and yet be contributory to sudden death in young infants.

Adenoviridae↗
PubMed1995

Cerebrospinal fluid penetration of amikacin in children with community-acquired bacterial meningitis.

The penetration of amikacin into the cerebrospinal fluid (CSF) was studied with 16 children (mean age, 1 year and 9 months; range, 4 months to 8 years) with community-acquired bacterial meningitis. Amikacin was given intravenously at a dose of 7.5 mg/kg of body weight twice daily. CSF was collected on day 1, at the expected peak concentration of amikacin in CSF. The mean (standard deviation) concentration of amikacin in CSF was 1.65 (1.6) mg/liter. Concentrations of amikacin in CSF correlated significantly with CSF glucose levels on admission. The mean concentrations of amikacin in CSF were 2.9, 1.1, and 0.20 mg/liter in patients with CSF glucose levels of < 1, 1 to 2, and > 2 mmol/liter, respectively. Thus, amikacin penetrates the blood-brain barrier substantially in children with bacterial meningitis and achieves particularly high concentrations when CSF glucose level is < 1 mmol/liter on admission.

Amikacin↗
PubMed1995

Existence in the nucleus incertus of the cat of horizontal-eye-movement-related neurons projecting to the cerebellar flocculus.

1. Properties of nucleus incertus (NIC) neurons projecting to the cerebellar flocculus were studied in alert cats by using chronic unit and eye movement recording and antidromic activation. Projection of these neurons onto the flocculus was verified with retrograde transport of horseradish peroxidase after injections in the flocculus. 2. Bipolar stimulation electrodes were implanted into the "middle" zone of each flocculus because this zone is known to be involved in the control of horizontal eye movements. The dorsomedial aspect of the pontine tegmentum was explored with microelectrodes during stimulation of both flocculi. The majority of neurons antidromically activated from the flocculus were found in the caudal part of the NIC. 3. Of the 69 neurons activated from the flocculus, 44 were classified as burst-tonic (BT) neurons; 34 discharged in relation with horizontal movements of the eye, 10 in relation with vertical movements. Of the 14 remaining neurons, 6 were not related to eye movements and 8 were classified as burst neurons. The BT neurons of the NIC displayed a great sensitivity to both horizontal eye position and horizontal eye velocity. 4. This study demonstrates the presence of a new group of horizontal eye movement related BT neurons situated in the NIC. The fact that they project to the horizontal floccular zone emphasizes the importance of the functional specialization of the different Purkinje cell zones.

Animals↗
PubMed1994

Role of the vestibular commissure in gaze-holding in the cat: a pharmacological evaluation.

Recent theoretical studies have proposed that the vestibular commissure is a major component of the horizontal gaze-holding system. In order to test this hypothesis, we injected either bicuculline, a GABA receptor antagonist, or strychnine, a glycine receptor antagonist, into the medial vestibular nucleus of alert cats. The intervestibular connection is indeed inhibitory and mediated by GABA and glycine. As neither bicuculline nor strychnine caused serious deficit of the gaze-holding system, we conclude that the vestibular commissure is not essential for gaze-holding.

Animals↗
PubMed1994

NMDA receptors are involved in temporal integration in the oculomotor system of the cat.

Spontaneous eye movements were recorded before and after a microinjection (0.1-0.2 microliter) of either APV (an NMDA receptor antagonist) or NBQX (a non-NMDA receptor antagonist) into the nucleus prepositus hypoglossi (NPH) of the alert cat. A unilateral injection of APV caused bilateral failure of the horizontal gaze-holding system: in the light, each saccade was followed by a post-saccadic drift. A unilateral injection of NBQX caused no sign of gaze-holding failure; in the light, spontaneous eye movements were unaffected; in complete darkness, a nystagmus with linear slow phases directed towards the injected side was observed. We conclude that NMDA receptors of the NPH neurones are involved in the gaze-holding system.

2-Amino-5-phosphonovalerate↗
PubMed1994

Involvement of the N-methyl-D-aspartate receptors of the vestibular nucleus in the gaze-holding system of the cat.

Eye movements were recorded in alert cats after injections into one of the medial vestibular nuclei (MVN) either of a N-methyl-D-aspartate (NMDA) antagonist or of a non-NMDA antagonist. A gaze-holding failure was caused by the NMDA antagonist when it was injected into the central part of the MVN but not when it was injected into the rostral part of that nucleus. By contrast, injections of the non-NMDA-receptor antagonist into the MVN did not cause any sign of gaze-holding failure. We conclude that the NMDA receptors located in the central part of the MVN are involved in the gaze-holding system.

2-Amino-5-phosphonovalerate↗
PubMed1994

Somatosensory evoked potentials at rest and during movement in Parkinson's disease: evidence for a specific apomorphine effect on the frontal N30 wave.

Studies attempting to relate the abnormalities of the frontal N30 components of the somatosensory evoked potentials (SEPs) to motor symptoms in Parkinson's disease (PD) have shown contradictory results. We recorded the frontal and parietal SEPs to median nerve stimulation in 2 groups of PD patients: a group of 17 patients presenting the wearing-off phenomenon, and a group of 10 untreated PD patients. The results were compared with a group of 13 healthy volunteers of the same age and with a group of 10 non-parkinsonian patients. All parkinsonian and non-parkinsonian patients were studied before ("off" condition) and after a subcutaneous injection of apomorphine ("on" condition). The gating effects of a voluntary movement (clenching of the hand) on the SEPs were also studied for the wearing-off group of PD patients (in states off and on) in comparison with the healthy subjects. At rest and in the off condition the amplitude of the frontal N30 was significantly reduced in the 2 groups of PD patients. We demonstrate that the movement gating ability of the PD patient is preserved in spite of the reduced amplitude of the frontal N30. This result suggests that the specific change in the frontal N30 in PD is not the consequence of a continuous gating of the sensory inflow by a motor corollary discharge. Clinical motor improvement induced by apomorphine was associated with a significant enhancement of the frontal N30 wave. In contrast, the subcortical P14 and N18 waves and the cortical N20, P22, P27 and N45 were not statistically modified by the drug. Apomorphine infusion did not change the absolute reduced voltage of the N30 reached during the movement gating. While the frontal N30 component of the non-parkinsonian patients was significantly lower in comparison to healthy subjects, this wave did not change after the apomorphine administration. In the wearing-off PD patient group the frontal N30 increment was positively correlated with the number of off hours per day. This specific apomorphine sensitivity of the frontal N30 was interpreted as a physiological index of the dopaminergic modulatory control exerted on the neuronal structures implicated in the generation of the frontal N30.

Aged↗
PubMed1994

Concentrations of ceftriaxone in cerebrospinal fluid of children with meningitis receiving dexamethasone therapy.

The penetration of ceftriaxone into cerebrospinal fluid (CSF) was studied with 11 children (mean age: 2 years, 4 months; range: 4 months to 8 years) with meningitis, receiving dexamethasone (0.15 mg/kg of body weight intravenously four times daily) as adjunctive therapy. Ceftriaxone was given intravenously at doses of 50 mg/kg twice daily to patients < 18 months old and 100 mg/kg once daily to patients > or = 18 months old. CSF was collected after 1 day of treatment at the expected peak concentration of ceftriaxone in CSF. Concentrations of ceftriaxone in CSF ranged from 0.7 to 9.2 mg/liter, with a mean value of 4.0 (standard deviation [SD], 2.9) mg/liter. Values were significantly higher for patients with CSF glucose levels of < 1 mmol/liter on admission to the hospital than for patients with CSF glucose levels of > or = 1 mmol/liter (mean values of 7.1 [SD, 2.2] mg/liter versus 2.2 [SD, 1.1] mg/liter; P < 0.001). After 1 day of treatment, ceftriaxone concentrations in the CSF of children receiving dexamethasone are similar to the mean values reported for children not treated with dexamethasone.

Ceftriaxone↗
PubMed1994

Effect of muscimol microinjections into the prepositus hypoglossi and the medial vestibular nuclei on cat eye movements.

1. For horizontal eye movements, previous observations led to the hypothesis that the legendary neural integrator necessary for correct gaze holding, adequate vestibuloocular reflex (VOR), and optokinetic nystagmus, was located in the region of the complex formed by the nucleus prepositus hypoglossi (NPH) and the medial vestibular nucleus (MVN). 2. The aim of the present study was to test the respective contributions of the NPH, of the rostral part of the MVN, which contains most second-order vestibular neurons, and of the central part of the MVN to the horizontal integrator. 3. An injection of muscimol was used to inactivate each of these three zones in the cat's brain. Muscimol is a gamma-aminobutyric acid (GABA) agonist. By binding to GABAA receptors, it induces a hyperpolarization of the neurons that nullifies their activity. Muscimol was injected into the brain stem of the alert cat through a micropipette by an air pressure system. 4. The search coil technique was used to record spontaneous eye movements and the VOR induced by rotating a turntable at a constant velocity. VOR was analyzed by a new method: transient analysis of vestibular nystagmus. 5. A unilateral injection of muscimol into the NPH induced a bilateral gaze-holding failure: saccades were followed by a centripetal postsaccadic drift. A vestibular imbalance was also present but it was moderate and variable. The VOR responses were distorted drastically. Through transient analysis of vestibular nystagmus, that distortion was revealed to be due more to a failure of the neural integrator than to an alteration of the vestibular input to the neural integrator. The responses to a rotation either toward the injected side or in the opposite direction were asymmetrical. The direction of that asymmetry was variable. 6. A unilateral injection of muscimol into the rostral part of the MVN caused a vestibular imbalance: in complete darkness, a nystagmus appeared, whose linear slow phases were directed toward the side of injection. 7. A unilateral injection of muscimol into the central part of the MVN induced a syndrome where a severe bilateral gaze-holding failure was combined with a vestibular imbalance. In the light, saccades were followed by a bilateral centripetal postsaccadic drift. In complete darkness, a nystagmus was observed, whose curved slow phases were directed towards the side of injection. The VOR responses were distorted drastically. Here again, that distortion was revealed by our analysis to be due more to a failure of the neural integrator than to an alteration of the vestibular input to the neural integrator.(ABSTRACT TRUNCATED AT 400 WORDS)

Animals↗
PubMed1993

The role of the vestibular commissure in the gaze holding of the cat.

Recent theoretical studies have proposed that the vestibular commissure is a major component of the horizontal gaze-holding system. In order to test this hypothesis, we disrupted the vestibular commissure of the cat by a parasagittal cut running between an abducens nucleus and the adjacent medial vestibular nucleus. Successfully lesioned cats suffered of a characteristic syndrome. In the light, gaze holding was impaired when the animal was looking toward the side of the lesion, but normal when looking toward the opposite side. We conclude (1) that the vestibular commissure is a component of the gaze-holding system, (2) that the vestibular commissure is less essential for gaze holding than other structures as the nucleus prepositus hypoglossi, and (3) that the horizontal gaze-holding system consists of two halves, each being more active in ipsilateral than in contralateral gaze.

Animals↗
PubMed1993

Testing the common neural integrator hypothesis at the level of the individual abducens motoneurones in the alert cat.

1. As far as horizontal eye movements are concerned, the well-known hypothesis of a common neural integrator states that the eye-position signal is generated by a common network, regardless of the type of versional movement. The aim of this study was to evaluate the validity of this hypothesis by analysing the behaviour of the abducens motoneurones, the system into which the horizontal neural integrator(s) project(s). If there were a common neural integrator, the different motoneurones would receive the eye position signal through the same pathway and the sensitivity to eye position would be the same regardless of the type of versional movement. If there were multiple integrators, the sensitivity to eye position in one type of versional movement might be different from the sensitivity to eye position in another type of versional movement, at least for occasional motoneurones. 2. The discharge of thirty-one antidromically identified abducens motoneurones was recorded in the alert cat during spontaneous eye movements made in the light and in response to sinusoidal rotations of the head in complete darkness. 3. All of the abducens motoneurones exhibited a burst of action potentials for lateral saccades. During fixation between saccades, they maintained a steady firing rate that increased as the cat fixated increasingly lateral eye positions. 4. For each abducens motoneurone, the sensitivity to eye position (Kf) was determined from measurements carried out during intersaccadic fixations. Kf was calculated from the slope of the firing rate-eye position linear regression line. 5. The discharge rate of the identified motoneurones was observed during four sinusoidal vestibular stimulations (+/- 10 deg, 0.10 Hz; +/- 20 deg, 0.10 Hz; +/- 30 deg, 0.10 Hz; +/- 40 deg, 0.10 Hz). The motoneurones exhibited a burst of activity during fast phases in the lateral direction and paused during fast phases in the opposite direction. During slow phases, motoneurones modulated their activity as a function of the vestibularly induced eye movements except for slow phases that occurred in position ranges below their recruitment threshold. In these cases their activity was cut off. 6. A new method was developed to measure the sensitivity to eye position of neurones during vestibular slow phases. The difficulty came from the fact that, during slow phases, eye velocity and eye position changed simultaneously and that each of those two variables could influence neuronal activity.(ABSTRACT TRUNCATED AT 400 WORDS)

Action Potentials↗
PubMed1993

Differential effect of injections of kainic acid into the prepositus and the vestibular nuclei of the cat.

1. In order adequately to control eye movements, oculomotoneurones have to be supplied with both an eye-velocity signal and an eye-position signal. However, all the command signals of the oculomotor system are velocity signals. Nowadays, there is general agreement about the existence of a brainstem network that would convert velocity command-signals into an eye-position signal. This circuit, because of its function, is called the oculomotor neural integrator. The most obvious symptom of its eventual failure is a gaze-holding deficit: in this case, saccades are followed by a centripetal post-saccadic drift. Although the oculomotor neural integrator is central in oculomotor theory, its precise location is still a matter for debate. 2. Previously, microinjections of kainic acid (KA) into the region of the nucleus prepositus hypoglossi (NPH) and of the medial vestibular nucleus (MVN) were found to induce a horizontal gaze-holding failure both in the cat and in the monkey. However, the relatively large volumes (1-3 microliters) and concentrations (2-4 micrograms microliters-1) used in these injections made it difficult to know if the observed deficit was due to a disturbance of the NPH or of the nearby MVN. These considerations led us to inject very small amounts of kainic acid (50 nl, 0.1 microgram microliter-1) either into the rostral part of the MVN or into different sites along the NPH of the cat. 3. The search coil technique was used to record (1) spontaneous eye movements (2) the vestibulo-ocular reflex (VOR) induced by a constant-velocity rotation (50 deg s-1 for 40 s) and the optokinetic nystagmus (OKN) elicited by rotating an optokinetic drum at 30 deg s-1 for 40 s. 4. In each injection experiment, the location of the abducens nucleus of the alert cat was mapped out by recording the antidromic field potentials evoked by the stimulation of the abducens nerve. Two micropipettes were then glued together in such a way that when the tip of the recording micropipette was in the centre of the abducens nucleus the tip of the injection micropipette was in a target area. The twin pipettes were then lowered in the brainstem until the recording micropipette reached the centre of the abducens nucleus. Kainic acid was then injected into the brainstem of the alert cat through the injection micropipette by an air pressure system. 5. Carried out according to such a protocol, KA injections into the NPH or the rostral part of the MVN consistently led to specific eye-movement changes.(ABSTRACT TRUNCATED AT 400 WORDS)

Animals↗
PubMed1992

Gaze holding defect induced by injections of ketamine in the cat brainstem.

The signal responsible for horizontal gaze holding is known to be generated, at least in part, by the prepositus hypoglossi (PH) nucleus, whereas that responsible for vertical gaze holding is known to be generated by the interstitial nucleus of Cajal (INC). An intramuscular injection of ketamine was recently demonstrated to induce a gaze holding failure. The aim of the present study was to analyse if ketamine produced this effect by acting, at least in part, on the PH nucleus. We found that a unilateral injection of a small amount of ketamine in the PH nucleus could cause either bilateral horizontal gaze holding failure or a vertical gaze holding failure or both an horizontal and a vertical gaze holding failure.

Animals↗