Biomedical subjects

H Sohmer

Publications and source records attributed to H Sohmer.

At least 55 records · Page 3Linked to original sources

PubMed1995

ABR interpeak latencies in rats are shorter at low click intensities.

There are conflicting findings concerning whether auditory nerve-brainstem evoked response (ABR) interpeak latencies (e.g. brainstem transmission time - BTT) are constant in response to different stimulus intensities. In order to study the effects of click intensity on the BTT, and to try to determine the mechanism of such an effect, ABR was recorded from 10 adult white Sabra rats in response to different click intensities. The stimulus intensity was reduced from the highest intensity generated by the equipment until no responses could be obtained. Band-reject (notched) noise was presented simultaneously with the clicks in order to restrict the region of basilar membrane activation. BTT decreased with decreasing click intensity and this was accompanied by a prolongation of the latency of wave I to a greater extent than that of wave IV. At high and intermediate intensities, wave I appeared as two split peaks. These effects were not abolished by the restricting notched noise. Possible mechanisms of these latency changes are considered.

Acoustic Stimulation↗

PubMed1995

Functional development of auditory sensitivity in the fetus and neonate.

The human fetus responds to sound stimuli while still in utero. The rat and cat begin to hear only after birth. Therefore neonatal rat and cat are used as models of the development of auditory sensitivity in the human fetus. The inner ear of rat responds to stimuli delivered directly to it (bone conduction) before the middle ear can conduct sounds to the inner ear. During this period, middle ear development involves mesenchyme resorption, ossicular hardening and opening of the external canal. The latter stages of inner ear development involve increased magnitude of the endocochlear potential which augments cochlear transduction and the active cochlear amplifier. These developmental stages are probably controlled by thyroid hormone which activates several genes leading to the synthesis of proteins and enzymes required for the structural and functional maturation of the ear. This likely includes the Na+,K(+)-ATPase of the stria vascularis which generates the endocochlear potential. The magnitude of the endocochlear potential is dependent on oxygen supply so that the human fetus in utero whose blood carries less oxygen than the newborn has a hypoxia-induced sensorineural hearing loss. Upon birth and transition from placental to pulmonary oxygenation, the oxygen content of blood is increased, the magnitude of the endocochlear potential is elevated and auditory sensitivity is enhanced.

Acoustic Stimulation↗

PubMed1995

The contribution of cranial-nerve nuclei to the short latency vestibular evoked potentials in cat.

The object of this study was to assess the contributions of various cranial nerve nuclei to the short latency vestibular evoked potentials (VsEPs) in cat. The following nuclei were investigated: vestibular nuclei, and 3rd, 6th and 10th cranial nerve nuclei. In unilateral labyrinthectomized cats, suboccipital craniectomy and partial cerebellectomy were carried out in order to place bipolar electrodes into the neural structures under investigation. The surface recorded VsEPs (far-field) were compared with the potentials recorded intracranially in response to the same acceleration impulses. The exact locations were later confirmed histologically. Reversible lesions also were induced by injecting of lignocaine 2%. The results indicate that the 2nd wave (P2) is mainly generated in the superior and medial vestibular nuclei. The 3rd, 6th and 10th cranial nerve nuclei apparently contribute to the later waves of the VsEPs, particularly P3 and P4.

Animals↗

PubMed1995

Psychological profile of help-seeking and non-help-seeking tinnitus patients.

The psychological profile of tinnitus patients who sought treatment (Help-Seeking, HS) was compared with that of patients who did not seek help (non-help-seeking, NHS) and with normal control subjects. Psychological evaluations as well as hearing, tinnitus loudness, and tinnitus pitch were measured. Overall, the psychiatric symptomatology of HS (n = 50) was more severe with poorer effective coping abilities and externalization of locus of control than NHS (n - 50). However, the psychiatric symptomatology of the NHS was remarkably more severe than that in the normals (n = 73) and more like that in the HS even though they did not turn to treatment. Tinnitus loudness was significantly lower in HS than in NHS subjects. The lower the tinnitus loudness, the higher the psychiatric symptomatology. The trend towards subclinical abnormalities in NHS indicates their vulnerability to pathology and this requires the attention of the therapist in order to increase the patient's self-awareness and to suggest preventive coping strategies or relaxation techniques.

Adaptation, Psychological↗

PubMed1995

Contribution of asphyxia to the induction of hearing impairment in jaundiced Gunn rats.

OBJECTIVES: This study was designed to determine whether asphyxia contributes to the induction of hearing impairment during neonatal jaundice. METHODS: Asphyxia was induced in jaundiced and nonjaundiced Gunn rats on postnatal days 1 (low bilirubin levels) and 10 (elevated bilirubin levels). Auditory nerve-brainstem evoked response thresholds were assessed in 21- and 28-day and 3-month-old rats. RESULTS: Asphyxia by itself or jaundice by itself did not lead to any type of hearing impairment. However, the combination of both high plasma bilirubin levels and asphyxia in 10-day-old rats but not in 1-day-old rats was accompanied by a progressive hearing loss in these rats. CONCLUSIONS: The contributory effect of asphyxia on neonatal jaundice may have important clinical relevance if asphyxia, for example, respiratory distress, accompanies neonatal jaundice.

Animals↗

PubMed1994

Human fetal auditory threshold improvement during maternal oxygen respiration.

It has been suggested that the near full-term fetus in-utero has a sensori-neural hearing loss compared to the neonate due to the relative hypoxia resulting from placental oxygenation compared to pulmonary oxygenation. This hypothesis was tested by estimating the threshold of the fetus to vibrio-acoustic stimulation applied to the maternal abdomen while the mother was breathing room air and again when breathing oxygen. Fetal response was assessed by maternal perception of fetal movement and by objective demonstration of movement by ultrasound. It has been shown that the fetal responses are to the acoustic component of the stimulus, that the acoustic stimulus is not overly attenuated or masked, and that maternal oxygen inhalation enhances fetal oxygenation. The results showed that the threshold was lower and/or the response was stronger when the mother was breathing oxygen compared to when she was breathing room air. Thus it is confirmed that in-utero the fetus has an hypoxia-induced sensori-neural hearing loss. At birth, with the shift to more efficient pulmonary oxygenation, there is an improvement in auditory threshold.

Acoustic Stimulation↗

PubMed1994

Improvement in sensorineural auditory threshold of the guinea-pig fetus following delivery.

The human fetus in utero is hypoxic relative to the neonate due to differences between placental and pulmonary oxygenation. Comparable degrees of hypoxia induced in young and adult animals caused an elevation in hearing threshold of a sensorineural nature. It was hypothesised therefore that the human fetus may also have such an elevation of threshold. This was tested in this study by recording ABR thresholds to bone conducted stimuli in fetal guinea-pigs that were near full term and again in the same animals, after delivery and consequent pulmonary oxygenation. In every animal studied (n = 9), the neonatal threshold was better than that in the fetus. In those fetuses in which a response could be recorded (n = 5), the neonatal threshold was on average 20 dB better than in the fetus. These findings are probably due to a depression of the endocochlear potential induced by the relatively hypoxic state of the fetus. The hypoxic state would lead to a reduced transduction current in the hair cells in response to a stimulus and an elevated hearing threshold. At birth, with the shift to pulmonary oxygenation, the neonate becomes normoxic, the endocochlear potential rapidly reaches near maximal levels and threshold is improved.

Animals↗

PubMed1994

Single P100 visual evoked potential analyses in man.

Standards evoked potential averaging leads to a loss of information inherent in the moment to moment variability of the amplitude and latency of single evoked potentials. In order to extract this information, attempts were made to develop procedures which would allow recording of single visual evoked potentials in at least a selected group of subjects. In 11 out of 25 non-selected subjects, 43% to 86% of all stimuli (reversal checkerboard pattern elicited single visual evoked potentials (VEP) which were recognized as such by a group of independent observers. The mean amplitude and latency obtained by directly measuring the peak to peak amplitudes and peak latencies of these single VEPs (arithmetic averaging) were compared to those obtained following conventional time-locked averaging of the same data. During long-term continuous stimulation, the arithmetic averaged VEPs increased in amplitude to a steady state while the time-locked averages of the same sets of responses decreased in amplitude. This reduction was found to be closely related to the latency jitter. It may provide a better understanding of the phenomenon of habituation. This finding was confirmed in model single VEPs obtained by summing on-going pre-stimulus EEG activity with a time-locked average VEP stationary wave form. The variability of the true single VEPs was found to be less than the variability of the model single VEPs. The latency and amplitude parameters of the true single VEPs were strongly correlated with each other while those of the model single VEPs were not. These findings show that single VEPs have an inherent variability which may reflect brain processing.

Adult↗

PubMed1993

Thyroid hormone induces earlier onset of auditory function in neonatal rats.

The effect of thyroid hormone injection on the development of auditory function in neonatal rats was evaluated using auditory nerve-brainstem evoked responses (ABR). The hormone induced earlier onset of auditory function. In order to differentiate between conductive and sensorineural factors, both air-conducted (AC) and bone-conducted (BC) ABR responses were recorded. Neonatal rats were injected with thyroxine (T4), or with saline (control animals), from day of birth (post-natal day-PND-0), daily, until PND 9. AC- and BC-ABRs were recorded from PND 6 up to PND 20. It was found that both AC- and BC-ABR thresholds were lower in the T4-injected rats up to PND 15, after which no difference was found between the two groups. This indicated earlier maturity of both conductive (external and middle ears) and sensorineural (inner ear) factors and is probably due to the earlier appearance in the blood of higher T4 levels, following injection, than that occurring naturally during the neonatal period in these animals.

Animals↗

PubMed1993

Development of hearing in neonatal rats: air and bone conducted ABR thresholds.

While the human full-term neonate can hear at birth, in the rat the onset of auditory function as monitored by recording auditory nerve-brainstem evoked responses (ABR) has been reported to begin on post-natal day (PND) 12-14 and reaches adult thresholds at about 22 days. In order to determine the factors involved in this late onset and then rapid threshold improvement in rats, the ABR to both air conducted (AC) and bone-conducted (BC) auditory stimulation was determined in neonatal rats. ABR to maximal intensity BC stimuli (55 dB above adult rat ABR threshold--55 dB HL*) could be recorded from PND 7-8 while AC responses to 80 dB HL* stimuli, only from PND 11. The air-bone gap (a measure of conductive immaturities only) disappeared on PND 15. This shows that there are both conductive (external and middle ear--Air-bone gap) and sensori-neural (inner ear--BC threshold) immaturities in the neonatal rat; the conductive factors are resolved by PND 15 while the sensori-neural continue after that. With respect to conductive factors, it seems that the state of the ear canal is not important while the chief conductive factors involved probably include mesenchyme resorption and/or ossicular ossification. The chief sensori-neural factor may be the development of the endocochlear potential. It is likely that the human fetus in-utero undergoes similar stages of development.

Acoustic Stimulation↗

PubMed1992

Prolonged conductive hearing loss in rat pups causes shorter brainstem transmission time.

A carefully controlled study was conducted in rats to determine whether a reversible conductive hearing loss during the neonatal period could induce changes in central conduction and thereby perhaps contribute to an understanding of learning problems seen in children following conductive hearing loss in infancy. Ear plugs were inserted from post-natal day 9 in rat pups and auditory nerve brainstem evoked responses were recorded in the presence of ear plugs and following their removal on post-natal day 23. The I-IV interpeak latency (brainstem transmission time) was significantly shorter in the experimental rats several days after plug removal (day 28) compared to untreated control rats. This difference was not related to residual conductive loss, nor to different body weights and was present even in response to equal sensation level stimuli, and was not present in adult rats with similarly induced conductive hearing losses. It seems therefore that conductive hearing loss in the young animal (critical period?) can induce changes in central auditory conduction and may be related to the findings of smaller brainstem auditory neurons in sound deprived animals. These results have implications for neonatal hearing loss in humans.

Animals↗

PubMed1992

Influence of experimentally elevated blood viscosity on the auditory nerve-brainstem evoked response and threshold.

Blood viscosity, due to its effect on blood flow, is one of the determinants of oxygen delivery. Therefore the influence of elevated blood viscosity on hearing was studied in rats using the auditory brainstem response (ABR) threshold, wave 1 latency, brainstem transmission time (BTT) and wave 1/4 amplitude ratio. Whole blood viscosity (WBV) was elevated by 15-21% in two different ways: elevating the hematocrit (Polycythemia) by acclimation in a hypobaric chamber, or elevating the plasma viscosity by infusing a solution of Polyvinylpyrrolidone-360 (PVP). ABR was recorded before and 24 h after the blood viscosity was elevated, so that each rat served as its own control. Paired t-tests showed that there was no statistically significant difference in the ABR parameters in each of the groups as a consequence of blood viscosity elevation. In conclusion, the elevation of WBV to this degree for this duration, using two different techniques had no effect either on the function of the auditory nerve and the more peripheral sites, or on the central auditory pathway as studied by ABR.

Analysis of Variance↗

PubMed1991

The effect of stimulus repetition rate on the diagnostic efficacy of the auditory nerve-brain-stem evoked response.

This study investigates the hypothesis that an increase in the click presentation rate during diagnostic testing with the auditory nerve-brain-stem response (ABR) will increase the efficiency with which lesions may be detected in the nervous system. Cats were exposed to conditions of hypoxia, hypercapnia and acidemia, and hypoglycemia was induced in rats. ABR was recorded using the standard 10/sec click rate and also a higher (55/sec) rate during both the control state and experimental state. Various parameters of the ABR were compared at the two click rates in the control and experimental states to see if the higher click rate was more effective in detecting pathology in the nervous system. It was found that in only a very few cases was the higher stimulus presentation rate more effective, and that in general ABR recordings at one stimulus rate only is quite sufficient for work in a clinical setting.

Acidosis↗

PubMed1991

Hypoxia induced hearing loss in animal models of the fetus in-utero.

The human fetus in-utero has low arterial oxygen tension. It has, therefore, been suggested that at greater than 28 weeks gestational age, the fetus may have a sensori-neural hearing loss comparable to that seen in adult cats exposed to similar degrees of hypoxia. This is due to hypoxia induced depression of the endocochlear potential. However, fetal blood is provided with compensatory mechanisms (elevated hematocrit and hemoglobin and special fetal hemoglobin) which enable pick up and transport of more oxygen from the placenta than adult blood under the same physiological conditions. Therefore, the hypothesis of a fetal sensori-neural hearing loss due to oxygen lack was tested in the following animal models: a) Adult cats to which feline red blood cells were infused thus causing a polycythemia similar to fetal conditions; b) Adult rats acclimated to altitude in a hypobaric chamber, inducing erythropoiesis with elevated hematocrit and hemoglobin; c) Neonatal guinea pigs and goats studied when they were less than 12 hours old so that the fetal compensatory mechanisms were still present. In each model, hypoxia (PaO2 20-30 mmHg) induced an ABR threshold elevation resembling that obtained in the uncompensated adult animal. Thus these experiments seem to have confirmed the hypothesis of a fetal, hypoxic induced sensori-neural hearing loss even though such experiments have not been conducted directly on fetal animals.

Animals↗

PubMed1991

Short latency vestibular evoked response to angular acceleration impulse in human beings.

Vestibular evoked response (VsEP) to acceleration stimuli were recorded in experimental animals and in human beings by scalp electrodes. The stimuli are angular acceleration impulses (up to 30,000 deg/sec2) transmitted to the skull by special devices. The short latency vestibular evoked response consisted of several waves during the first 10 msec. The first two waves (P1 and P2), which are the most consistent, have been shown in cats to originate from the vestibular nerve and nucleus, respectively. The middle latency response is believed to be of myogenic origin. It is hoped that the recording of VsEP in human beings will enable the localization of the site of lesion in vertiginous patients.

Adolescent↗

PubMed1991

Postnatal development of flash visual evoked potentials in the jaundiced Gunn rat.

In this study, the postnatal development of flash visual evoked potential (VEP) has been monitored in the jaundiced (jj) Gunn rat model of neonatal hyperbilirubinemia to determine whether this evoked response is affected by bilirubin-induced neurotoxicity. VEP could first be recorded at 16 d of age. The jj rats exhibited prolonged wave latencies and lower wave amplitudes during the 3rd wk of postnatal life, when compared with their nonjaundiced littermates. There was no correlation at 21 d of age between VEP parameters and either bilirubin levels or body weight. About one third of the jj animals died between 21 and 28 d of age. The average VEP wave latencies at 21 d of age of the rats who were to die was prolonged compared with those of rats who survived till at least 28 d of age. Thus, the latency of VEP waves at the age of 21 d appears to be related to the further outcome of jj Gunn rats. Although wave amplitudes were lower in jj as compared with nonjaundiced 21-d-old animals, there were no amplitude differences between the jj rats who would die and those who would survive during the 4th wk of life. These findings may contribute to the understanding of the pathogenesis of bilirubin encephalopathy in the neonatal period.

Age Factors↗

PubMed1991

Auditory brainstem response (ABR) latency shifts in animal models of various types of conductive and sensori-neural hearing losses.

Clinical ABR studies in patients with peripheral hearing loss have led to conflicting results, some reporting increases in brainstem transmission time (BTT), some decreases, and others no change. In order to study this in a carefully controlled fashion, various types of peripheral hearing losses were induced in experimental animals: conductive hearing loss by occluding auditory meatus (rats) (CHL), noise induced temporary sensori-neural hearing loss (rats) (NI-SNHL), stimulus intensity attenuation (rats), (Atten.), and controlled hypoxemia induced temporary sensori-neural hearing loss (cats) (HI-SNHL). ABR latencies and thresholds were determined in each animal before (control) and during the induced hearing loss (experimental) states. The data in each group in each state were analyzed by calculating group average values for latency of waves 1 and 4, their interpeak latency (BTT), paired t-tests for changes between the control and experimental states and linear regression analysis of latency changes on threshold shift. In each group, there were small decreases in BTT in the experimental state (not significant in the CHL group only). This was caused by the prolongation of latency of wave 1 to a greater extent than that of wave 4. These changes were smaller than the standard deviation of the BTT in the control state. Therefore, in attempting to apply these results to the human clinical situation, these small decreases in BTT would not be considered abnormal. Possible mechanisms of these BTT changes are considered.

Animals↗

PubMed1990

The influence of sound stimulus parameters on the acoustic reflex waveform.

The transient increase in admittance seen at the beginning of the acoustic reflex response in man was investigated with a view to reaching a better understanding of its possible mechanisms. The sound stimulus intensity, its duration and its off-time were varied to investigate their effects on the morphology of the admittance waveform. The results found suggest that the transient increase may not be due to a temporary partial decoupling of the ossicular chain during the initial stages of stapedial contraction, but rather that it may be caused by a slight improvement in the coupling between the middle ear components.

Acoustic Stimulation↗