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Biomedical subjects

H Sohmer

Publications and source records attributed to H Sohmer.

At least 73 records · Page 4Linked to original sources
PubMed1990

Evoked potential changes in cats following injection of an extract from the venom sac of the oriental hornet (Vespa orientalis).

Venom sac extract from the hornet Vespa orientalis was injected (via the subclavian artery) into cats and its effects on evoked potentials in two different sensory pathways (auditory and somatosensory) was investigated. A comparison was made between the venom sac extract from adult hornets and that from young (0-24 hr of age) hornets. There was a bimodal change in blood pressure, a hypothermic effect and a decrease in amplitude of the last waves of the auditory and somato sensory pathways when venom sac extract of adult hornets was injected. Venom sac extract from young hornet workers had the same influence on the blood pressure, did not affect thermoregulation and the effect on the auditory and somato sensory pathways were less consistent. Adult venom sac extract had mainly a central effect whilst the venom sac extract from young hornets (in larger doses) affected the central and/or peripheral nervous system. The central effects could be interpreted as due to opening of the blood-brain barrier by the venom.

Animals↗
PubMed1990

Noise and hypoxia induced temporary threshold shifts in rats studied by ABR.

Rats were exposed for 2 h either to 115 dB SPL noise, to 5% oxygen in nitrogen (hypoxia) or to both hypoxia and noise. Auditory nerve-brainstem evoked responses (ABR) to 80 dB HL clicks and threshold were recorded prior to exposure, immediately (5-10 min) after the exposure, 2 h after and 2 weeks after the exposure. The findings in each experimental animal were compared to those in the control (non-exposed) group and to those in the other groups. Thresholds were elevated in each of the experimental groups, but these were temporary threshold shifts, since 2 weeks following the exposure, threshold had returned to normal. Latencies (wave I and the IV-I interpeak latency difference- (IPLD] were prolonged in the groups exposed to hypoxia (hypoxia alone and hypoxia + noise). These results are discussed in view of possible mechanisms of these noise and hypoxia induced temporary threshold shifts.

Animals↗
PubMed1990

Vestibular evoked potentials with short and middle latencies recorded in humans.

Following success in recording short latency vestibular evoked potentials in experimental animals, we have succeeded in our attempts to record such potentials in human subjects. The stimuli were repetitive, short steps of high intensity angular acceleration (10,000 degrees/sec2) with short rise times which would synchronously activate many neurons of the vestibular pathway. Stringent control procedures ensured that the recorded activity was not an artefact. Short latency vestibular evoked potentials were recorded in 10 normal subjects with peak latencies of 3.5, 6.0 and 8.4 msec and amplitudes of 0.5 microV. Middle latency potentials were also recorded with latencies of 8.8, 18.8 and 26.8 msec and amplitudes of 15 microV. These responses were absent in a cadaver and in patients with bilateral dead labyrinths. In normal subjects, these vestibular evoked potentials were not affected by white noise. In conclusion, short and middle latency vestibular evoked potentials were recorded in normal human subjects.

Adolescent↗
PubMed1990

Efficacy of self-hypnosis for tinnitus relief.

The efficacy of self-hypnosis (SH) on tinnitus relief was compared with two control procedures: 1) presentation of a brief auditory stimulus (BAS) to the ear with tinnitus; 2) waiting list (WL), i.e. patients receiving no formal treatment. The results have shown that 73% of SH subjects reported disappearance of tinnitus during treatment sessions, as compared with only 24% in the BAS group. Moreover, the short-term (1 week) and long-term (2 months) symptom profiles of only SH subjects revealed a significant improvement. Thus, SH may well be a beneficial method for the relief of tinnitus.

Adult↗
PubMed1989

ABR threshold is a function of blood oxygen level.

In order to determine if there is a relation between auditory threshold and oxygen availability, cats were anesthetized, paralyzed and ventilated with room air and with hypoxic gas mixtures. Auditory nerve-brain stem evoked response (ABR) thresholds and arterial blood oxygen levels [partial pressures (PaO2) and percent saturation (SaO2)] were determined. The ABR threshold was unchanged as long as PaO2 was above 30 mm Hg (SaO2 greater than 45%). Below PaO2 20 mmHg (SaO2 less than 25%) the animal was not viable. Between these values, the hypoxia caused ABR threshold elevations which were reversible when the animal was again respirated with room air. ABR threshold was an inverse function of blood O2 level with an approximate 3.05 dB elevation for every mmHg decrease in PaO2 (2.89 dB/% SaO2). These findings are probably due to hypoxia induced depression of the endocochlear potential. Since ABR could be recorded in premature human neonates after at least 28 weeks gestation and since the human fetus in utero is also hypoxic, these results indicate that the fetus (greater than 28 weeks gestational age) has a sensorineural hearing loss in addition to a conductive loss.

Animals↗
PubMed1988

Concomitant changes in the acoustic impedance and the cochlear microphonic potentials during twitch contractions of the middle ear muscles in cats.

The effect of twitch contractions of the middle ear muscles in cats on sound transmission through the middle ear (as measured by the cochlear microphonic potential of the inner ear) was compared with the simultaneous changes in the acoustic input impedance of the middle ear at the same frequency. It was found that decreases in impedance were related to an increase in the amplitude of the cochlear microphonics and vice versa. This may imply that decreases in impedance measured during the initial phase of the acoustic reflex in man are true decreases and are not due to transient decoupling of the ossicular chain at any point.

Acoustic Impedance Tests↗
PubMed1988

Perinatal hypoxia and auditory brainstem response thresholds: no evidence of permanent hearing loss.

It has been suggested that pre-natal and or peri-natal hypoxia can cause permanent hearing loss as a result of interference with the generation of the endocochlear potential, especially if this interference occurs during the critical period of endocochlear potential development. This hypothesis was tested in 4 series of experiments: in neonatal rats exposed to pure nitrogen for several minutes; in neonatal and adult cats respirated with hypoxic gas mixture for an hour; in neonatal rats and cats breathing hypoxic gas mixture for several hours; and in neonatal rats in hypobaric chamber for several days. In each experiment, the auditory nerve-brainstem evoked response threshold was elevated during hypoxia in those animals in which it could be measured but was normal when determined several hours to days later. This is evidence for a remarkable ability of the auditory system to recover from periods of hypoxia even during the critical period of endocochlear potential development.

Animals↗
PubMed1987

Experimental analyses of the source of ABR wave II.

Recent reports based on direct recording from various locations along the auditory nerve in humans during neurosurgical procedures have suggested that the auditory nerve-brainstem response (ABR) wave II is generated by the same neurons which generate wave I. In order to analyze this possibility using a different approach, ABR was recorded in ten rats in response to several click intensities and click repetition rates. These studies were also repeated in ten human volunteers. The amplitudes and latencies of ABR waves I, II and III were analyzed in order to determine if wave I and II behaved in a parallel fashion with changes in stimulus intensity and latency, as would be expected from the physiological "all or none law" if both waves were generated by the same axons. Several types of analyses indicate that the amplitudes of ABR waves I and II do not grow in amplitude in a parallel fashion with increases in stimulus intensity and decreases in stimulus rate. This is evidence either for independent sources of waves I and II or for composite sources of wave II both from the auditory nerve and the cochlear nuclei.

Adolescent↗
PubMed1987

Neonatal auditory acuity following in utero vibratory acoustic stimulation.

The fetal heart rate response to externally applied vibratory acoustic stimulation is currently being evaluated as a test of fetal well-being. We have examined the safety of this procedure by subsequent testing of the auditory nerve and brain stem evoked responses in the neonates. The results demonstrated no differences in auditory acuity when control infants were compared with infants previously exposed to antenatal vibratory acoustic stimulation.

Acoustic Stimulation↗
PubMed1987

Auditory evoked potentials during deviations from homeostasis: theoretical and clinical implications.

Evoked responses of various modalities are being used for sensory and neurological clinical assessment. An additional application is their use in studying the functional activity of several sensory pathways and many brain regions during induced deviations from homeostasis in the intact animal. The auditory nerve-brain-stem evoked response (ABR) has been studied during hypoxia, hypercapnia, acidosis, hypoglycemia, systemic hypotension, intracranial hypertension and decreased cerebral perfusion pressure. In many such experiments the following were also recorded: EEG, cortical evoked potential (EP), somatosensory EP (including peripheral nerve, brain-stem and cortical components), visual and vestibular EP. Even though the EEG was already isoelectric, the ABR and many of the other EPs were not affected by relatively severe deviations in homeostasis, several of which have been shown to induce brain lesions and severe perturbations of energy metabolism. The ability of these brain pathways to produce electrical activity in such conditions may be due to the generation of such EP by oligosynaptic pathways and to compensatory mechanisms such as increased local cerebral blood flow. Clinically, these findings point out the usefulness of ABR recordings in the diagnosis of brain death and to the possibility that when ABR is continuously monitored in the intensive care patient, alterations in the ABR may indicate the need for immediate intervention.

Acidosis↗
PubMed1986

Multi-modality evoked potentials in hypoxaemia.

The auditory nerve-brain-stem evoked response (ABR) has been shown to be insensitive to hypoxic inspiratory gas mixtures which severely depress the EEG. In order to determine the relative sensitivities of additional brain regions and pathways to hypoxaemia, anaesthetized paralysed cats were ventilated with various gas mixtures while recording the evoked responses of the auditory, somatosensory (including peripheral nerve, brain-stem and primary cortical components), visual and vestibular systems. Arterial blood pressure was maintained by dopamine infusion and pH was corrected with bicarbonate. Hypoxic gas mixtures (6-7% O2) presented for 60 min, causing severe hypoxaemia (paO2 20-30 mm Hg; O2 saturation 25-50%), were without effect on the somatosensory, vestibular and visual EPs while the auditory evoked potentials (ABR and cortical components) were depressed. However, if arterial blood pressure was allowed to fall, all of the evoked potentials became severely depressed and isoelectric. These results and others indicate that the cortical components are qualitatively similar to the more peripheral evoked potentials. The resistance of these evoked potentials to controlled hypoxaemia is probably due to their generation by oligosynaptic pathways and to a compensatory switch to anaerobic metabolism and to an elevation of cerebral blood flow.

Animals↗
PubMed1986

The depression of the auditory nerve-brain-stem evoked response in hypoxaemia--mechanism and site of effect.

During severe hypoxaemia in the cat the ABR was depressed in 2 different patterns: if mean arterial blood pressure (MAP) was maintained then all other evoked potentials (EPs--somatosensory and visual) remained. If MAP was not maintained, all of these EPs were depressed. This study sought to document these different patterns of ABR depression and to ascertain their mechanisms. When MAP fell, the ABR loss began with the later waves and progressed to the earlier waves. These are signs of a central brain lesion. The hypoxaemia, detrimental to normal function of the cardiovascular system, leads to depression of MAP, to a fall in cerebral perfusion pressure and blood flow, to cerebral ischaemia and ABR loss. On the other hand, when MAP was maintained, severe hypoxaemia was accompanied by a depression of all of the ABR waves at the same time. The cochlear microphonic potential was also simultaneously depressed. These are signs of a peripheral, cochlear effect similar to the demonstrated depression of the positive endocochlear resting potential of the scala media and of the cochlear microphonic potential during hypoxaemia. This leads to interference with the cochlear transduction mechanism so that all of the auditory evoked potentials, including the ABR, are simultaneously depressed. These results lead to the suggestion that the ABR abnormalities seen in patients who suffered a hypoxic (anoxic) insult or an ischaemic episode (prolonged interpeak latencies, loss of later waves and finally all waves absent or only the first wave remaining) is always due to ischaemia even when the initial insult was hypoxic.

Animals↗
PubMed1985

Effects of body temperature elevation on auditory nerve-brain-stem evoked responses and EEGs in rats.

ABRs and EEGs were recorded in anaesthetized rats during whole body hyperthermia. ABR amplitudes were decreased during warming, with little recovery as body temperature was lowered. The latencies of the ABR waves decreased with warming and increased with subsequent cooling. The major latency changes were in the later ABR waves. Warming was accompanied by suppression of the EEG. These results point out that ABR evaluation of patients must take into account elevated body temperatures. Since it has been shown that the rat can serve as a model of the effects of heat on man, an attempt is made to relate these ABR and EEG findings in rats to studies of human psychomotor performance during heat exposure.

Animals↗
PubMed1985

The persistence of somatosensory and auditory pathway evoked potentials in severe hypoglycemia in the cat.

In a previous study it was shown that during severe insulin-induced hypoglycemia in rats and cats (0.38 mmol/l, i.e., 6.8 mg% and 0.8 mmol/l, i.e., 14 mg% respectively) with isoelectric EEG, the latency and amplitude of the auditory nerve-brain-stem evoked responses were not affected. In the present study on cats, the above evoked responses were complemented by recording in addition the cortical auditory evoked potential and the peripheral, brain-stem and cortical components of the somatosensory evoked potentials. Each of these evoked potentials remained in the presence of 0.75 mmol/l glucose in plasma. The persistence of the somatosensory cortical evoked potential was unexpected since two other groups have reported the disappearance of this potential during hypoglycemia. The types of neuronal activity which can still be recorded in severe hypoglycemia are probably generated by neuronal structures with lower metabolic demands such as axons and oligosynaptic pathways, surviving on the consumption of endogenous substrates with compensatory elevation of local cerebral blood flow.

Animals↗
PubMed1984

Persistence of auditory nerve response and absence of brain-stem response in severe cerebral ischaemia.

Cerebral ischaemia, in which the brain-stem components of the ABP were isoelectric, was accompanied by the paradoxical persistence of the compound action potential of the auditory nerve (wave 1). This ischaemia was induced in cats by reducing mean arterial blood pressure and elevating intracranial pressure, resulting in decreased cerebral perfusion pressure (CPP). This is unexpected since the inner ear is supplied by a branch of an intracranial artery. To study this phenomenon, CPP was manipulated and when average CPP was 13.5 mm Hg, only wave 1 remained. In 7 of 9 experiments, clamping of both common carotid arteries did not abolish wave 1. Experiments with radioactive tracers demonstrated a remaining residual blood flow through the inner ear. This remaining auditory nerve response is probably not due to a very low metabolism of the inner ear or to the cochlea being supplied by anastomoses from the middle ear, supplied by the external carotid artery. The residual cochlear blood flow and the persistent wave 1 can probably be explained in the following way: at low CPPs the smaller intracranial blood vessels collapse so that the brain tissue is not perfused, leading to loss of the brain-stem components of the ABP. However, flow still persists in the larger intracranial arteries. This blood preferentially flows to the cochlea since the intracochlear pressure is slightly below the intracranial pressure due to the presence of the oval and round windows. Thus a sufficient blood flow to the cochlea is maintained, with sparing of wave 1.

Animals↗
PubMed1984

Mathematical expression of relationship between auditory brainstem transmission time and age.

Brainstem transmission time (BTT) was studied in 71 subjects ranging in age from one day to 29 years in order to find a mathematical expression to best describe the relationship between BTT and age. The mathematical function which relates BTT to age is exponential. Using this data, the BTT confidence limit was calculated for subjects from birth through to eight years. Repeated recordings of auditory brainstem responses were performed in several children as they grew older and these verified the normal maturational processes of the brainstem structures in the developing infant and young child.

Age Factors↗
PubMed1984

Considerations in the differentiation between brainstem lesions and sensori-neural hearing loss using auditory nerve-brainstem evoked responses.

When auditory nerve-brainstem evoked responses are used in neurological diagnosis, an important response parameter to be evaluated is brainstem transmission time - the time interval between the auditory nerve response (wave 1) and the response from the rostal brainstem (wave P4). Occasionally the only response wave present is wave P4 and its latency is prolonged. This can be compatible with a conductive or a sensorineural hearing loss (SNHL), or a neurological (brain stem) lesion such as a retrocochlear hearing loss (RCHL). A conductive hearing loss can be excluded by otoscopic, audiometric and tympanometric examination. In order to differentiate between SNHL and RCHL, several techniques have been suggested in order to enhance the visibility of wave 1, but these are not always applicable or successful. In this study, P4 latency was plotted as a function of the audiometric hearing loss at 4 kHz for 26 ears with SNHL only. From this, the correlation coefficient (r = 0.71) was calculated along with the linear regression equation and the standard error of the prediction. This gave an estimation of the range of P4 latency to be expected for a given SNHL for comparison with the actual latency obtained in patients with neurological complaints. An actual latency greater than the expected latency range would be considered corroboratory of a RCHL. Several clinical examples are presented. These considerations also point out the need to bear in mind the otological context of these evoked responses even when used in neurological diagnosis.

Audiometry↗