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Biomedical subjects

A Guilhaume

Publications and source records attributed to A Guilhaume.

At least 37 records · Page 2Linked to original sources
PubMed1981

[Respiratory pauses in nocturnal sleep of infants].

In order to study the respiratory abnormalities during sleep that could select children with a high risk of sudden infant death syndrome (SIDS), 3 groups of children were studied: Group T: 18 control infants; Group G: 22 infants related to children who died from SIDS and group NM: 32 infants with near miss SIDS. A classic polygraphic EEG recording was performed during sleep. Apneas of 5 or more seconds and periodic respiration were analysed. Half of the infants in groups G and NM did not differ from those in group T. However, the groups G and NM differ from group T by a higher mean index of apneas during sleep and by the presence of a periodic respiration outside REM sleep in some of them. On the contrary, the mean duration of apneas and the number of apneas of more than 10 seconds did not seem to differ significantly in the 3 groups.

Female↗
PubMed1980

Acoustic responses after total destruction of the cochlear receptor: brainstem and auditory cortex.

Acoustically evoked neural activity has been recorded from the brainstem and auditory cortex of guinea pigs after complete destruction of the organ of Corti by the aminoglycosidic antibiotic amikacin. These responses to sound differ in important respects from the evoked potentials normally recorded from the auditory pathways. At the brainstem level they resemble the potentials reported by others after stimulation of the vestibular nerve.

Acoustic Stimulation↗
PubMed1979

"Neural" responses to acoustic stimulation after destruction of cochlear hair cells.

Electrophysiological and histological observations in guinea pig's cochleas after amikacin treatment (14 X 450 mg/kg) confirm the results obtained in a former experiment: clear, short-latency, click-evoked responses were recorded in cochleas with only very few hair cells remaining at the extreme apex. Detailed analysis of these responses strongly indicates a neural origin and confirms their low-frequency sensitivity. Careful histological observations confirm the extensive hair cell loss and the preservation of nerve fibers in the remnants of the organ of Corti and of the vestibular sense organs. These results suggest that the acoustical vibrations either stimulate the vestibular receptors or act directly or through some kind of mechano-electrical transduction on the remaining cochlear nerve fibers.

Amikacin↗
PubMedDate not supplied

Conflicting electrophysiological and anatomical data from drug-impaired guinea pig cochleas.

In guinea pigs that had been treated with very large doses of the aminoglycoside amikacin (14 x 450 mg/kg/day, i.m.) clear, short-latency responses to various click stimuli could be recorded at the round window. When the same cochleas were examined histologically, no outer or inner hair cells could be found along the entire length of the basilar membrane, save for a very few outer hair cells remaining at the apex. The response patterns resembled that of the compound action potential, and various characteristics suggest that they were of neural origin. Vestibular function, investigated by electronystagmography during rotation, appeared normal, as did most of the saccular and utricular hair cells. Transmission electron microscopy revealed a significant number of cochlear nerve fibres still innervating the remnants of Corti's organ. In other cochleas with similarly extensive destruction induced by another aminoglycoside (sisomycin, 14 x 125 mg/kg/day, 15 days as well as 3 months post-Rx), no responses could be recorded from the round window. Cochleas that were less affected, with the upper turns preserved, gave only small, long-latency responses. These preliminary observations are confirmed by further experiments now in progress. They suggest that unless a considerable number of inner hair cells remained undetected in the lower basal turn, a possibility that appears highly unlikely, there was either a direct mechanical excitation of cochlear nerve fibres, or an acoustical stimulation of vestibular sense organs.

Acoustic Stimulation↗
PubMedDate not supplied

Electrophysiological monitoring of the cochlea during and after total destruction of the organ of corti.

A series of acoustically evoked potentials can be recorded from the cochlea up to the auditory cortex in guinea pigs where the organ of Corti has been totally destroyed after extensive treatment with amikacin, but where some of the spiral ganglion neurons always remain and where the vestibular receptors are only slightly affected. The cochlear responses have been monitored in guinea pigs permanently implanted with a round window electrode and receiving such treatment. The normal auditory nerve compound action potential disappears within a few days, while the very typical response (diphasic, short latency (0.3 ms) small amplitude) appears. This response then remains remarkably constant in time as far as we could observe (up to almost one year). This response might be a component of the normal response, undiscernible under normal conditions but revealed by the selective impairment of the labyrinth by amikacin, in contrast to the global effect of every other known otodestructive agent. Some basic questions still remain: which fibres are effectively stimulated (cochlear or vestibular), what are their central projections, and what kind of sensation is conceivably associated with these responses?

Amikacin↗
PubMedDate not supplied

Spiral ganglion changes after massive aminoglycoside treatment in the guinea pig. Counts and ultrastructure.

Morphological changes of the eighth nerve were observed in the guinea pig between 1 month and 1 year after treatment with large doses of the antibiotic amikacin which resulted in complete cochlear hair cell destruction. The neural retrograde degeneration was found to be relatively fast, with a considerable loss (30 to 55%) of ganglion cells one month after treatment, continuously increasing (up to 85) after one year. Gross changes in the habenula perforata and in the spiral ganglion are described, together with ultrastructural alterations of organelles important for the cell metabolism and axonal transport. The rapid degeneration and the morphological findings suggest a direct influence of toxic substances on the ganglion cells.

Amikacin↗
PubMedDate not supplied

Vestibular acoustic reception in the guinea pig: a saccular function?

After complete destruction of cochlear but preservation of vestibular hair cells in the guinea pig acoustically evoked responses can still be recorded from the round window up to the auditory cortex. At all levels these responses differ from those observed in normal animals but their frequency sensitivity and selectivity make them akin to responses from auditory organs. In a series of experiments a complete cochlear destruction was combined with a total or partial destruction of the vestibule. After complete cochlear and vestibular hair cell destruction no acoustic response could be recorded. But in cases of total cochlear and drastic ampullar and utricular destruction together with an almost undamaged saccular sensory epithelium the same peculiar acoustic responses could be observed. These results support the hypothesis of a functional acoustic reception by the saccule in a mammal.

Aminoglycosides↗
PubMedDate not supplied

Dynamic changes following combined treatment with gentamicin and ethacrynic acid with and without acoustic stimulation. Cellular uptake and functional correlates.

Regional selectivity of gentamicin (GM) ototoxicity was studied in guinea pigs (GPs) using electrophysiological, morphological, autoradiographic and immunohistological observations following combined treatment with GM (150 mg/kg i.m.) and ethacrynic acid (EA) (30 mg/kg i.c. or i.v., 1.5 h after GM injection). The GPs were either continuously stimulated every 5 min with a series of 256 clicks (70 dB peSPL, 10/s) during 3 h for monitoring fast changes in VIII nerve compound action potential (CAP) after the EA injection, and thereafter kept in the animal quarters (background noise of 60 dB SPL) (group I), or similarly monitored for only 10 min after the EA injection and thereafter kept in a soundproof room (around 0 dB SPL) (group II). Whenever GM labelling was observed it was localized only in the sensory hair cells. From 3 h after EA injection, the GPs in group I presented threshold elevations in the high-frequency region, which progressed to 60-80 dB at all frequencies at and after 48 h. Parallel to the threshold pattern, GM uptake in outer hair cells (OHCs) was seen with an increasing concentration from apex toward base from 3 to 24 h, while after 48 h almost all OHCs were destroyed and inner hair cells (IHCs) were marked by GM. In group II no changes in CAP thresholds were observed until more than 24 h, although GM was detected in the hair cells from 6 h on. At this early stage, the distribution of GM lacked a clear pattern, particularly without a clear apex-base gradient, and GM deposits were found only around the basal body. However in both groups, in late stage (greater than 24 h), the base-apex gradient was more pronounced and GM was found throughout the cell body, with a marked concentration below the cuticular plate. These results suggest that GM may penetrate hair cells around the basal body and that activating the cells by sound potentiates both GM uptake and its intracellular toxicity.

Acoustic Stimulation↗
PubMedDate not supplied

[Sudden death in new-born babies (author's transl)].

This sudden death of a new-born baby, which had been thriving up to then, is a dramatic but not exceptional event. A systematic search for the etiology must be made, and this should include an autopsy in order that the diagnosis of "sudden and unexplained death" is confirmed only after eliminating all other possible causes. Knowledge of this syndrome has benefited from epidemiological surveys which have defined the previous clinical condition, but none of the many etiollotical hypotheses envisaged can take into account the total number of cases reported. One of the most recent cases developed apnoea during sleep, which could explain some unexpected deaths in new-born babies. This was discovered by polygraphic sleep recordings and confirmed by pathological examinations. These demonstrated indirect signs of chronic hypoxia which could have been related to the sudden death of the baby. Though there does not appear to be any relationship between the apnoea syndrome during sleep and these sudden and unexpected deaths, this hypothesis has opened up a new promising line of research which could help to identify new-born babies at risk from "sudden death", and to propose preventative measures.

Apnea↗