PubMed HealthSearch

Biomedical subjects

H Sohmer

Publications and source records attributed to H Sohmer.

At least 19 recordsLinked to original sources

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

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

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

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

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

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

A functional measure of brain activity: brain stem transmission time.

Surface-recorded auditory nerve and brain stem responses are being used routinely for diagnostic purposes in man. When interest is in auditory diagnosis, the electric response threshold is of primary importance. However, when used in neurological diagnosis, the wave form of the response is important. As a measure of one aspect of response wave form, this paper suggests the use of brain stem transmission time (BTT), defined as the time interval between the first earlobe-negative wave (response of the auditory nerve--the 'input' to the brain stem) and the earlobe-positive wave from the region of the inferior colliculus (the 'output' of the brain stem). The paper shows that BTT is longest in neonates, approaches adult values at the age of about 3 years, is relatively independent of click intensity, conductive hearing loss (middle ear lesion), click rate (except for high rates) and click frequency (filtered clicks). The finding that in a given age group, BTT is generally independent of most stimulus conditions, makes it a useful functional test of brain stem activity.

Adolescent

Auditory nerve and brain stem responses. Comparison in awake and unconscious subjects.

The recording of auditory nerve and brain stem responses to click stimuli is being used for the diagnosis of several conditions such as suspected hearing loss and suspected neurological disorders. The responses obtained in the patient group (often infants and children) are compared with those obtained in normal subjects of similar age who, for ethical reasons, are not sedated. In this study, recordings were made in normal subjects while they were awake and when they were unconscious in drug-induced sleep (being prepared for dental surgery). No significant difference could be observed between the recordings obtained in the awake state and when unconscious in the same subjects. Therefore, one is justified in using recordings made in awake subjects as controls for recordings made in other unconscious patients.

Brain Stem

Evidence from auditory nerve and brainstem evoked responses for an organic brain lesion in children with autistic traits.

In an attempt to resolve the question as to whether children with autistic traits have an organic nervous system lesion, auditory nerve and brainstem evoked responses were recorded in a group of 15 children with autistic traits. The most obvious results included a longer response latency of the auditory nerve and a longer brainstem transmission time, compared to normal children. Five of the autistic children were found to be profoundly deaf. These results strengthen the theory that an organic lesion of the nervous system can give rise to autistic traits.

Autistic Disorder

Brain lesion diagnosis by recording cochlear and brainstem responses to sound stimuli.

A technique has been developed for the recording of the cochlear action potential (electrocochleography) and the brainstem evoked responses to click stimuli by means of earlobe and scalp electrodes with an average response computer. This technique has already proved its usefulness in diagnosis of hearing loss. Since the brainstem responses are generated in the successive brainstem auditory nuclei and since the auditory nuclei and pathways constitute a relatively large volume of brainstem tissue, there is reason to believe that this same technique can also contribute to the diagnosis of brain stem lesions and their localization. When these recordings were made in patients with clinical signs of brain stem involvement, one (or more) of the usual response waves was smaller in amplitude, prolonged in latency, or completely absent. Recording of the cochlear and brainstem evoked potentials thus seems to be a new, simple and rapid tool for the diagnosis of brainstem lesions.

Acoustic Stimulation

Usher's syndrome: electrophysiological tests of the visual and auditory systems.

The symptoms of Usher's syndrome - congenital hearing impairment and tapetoretinal dystrophy - are difficult to detect in young children. The electroretinogram (ERG), visual evoked potential (VEP), auditory nerve and brain-stem responses as well as the cochlear microphonic potentials were used to evaluate the defects of the visual and auditory systems in 20 patients, 3-45 years of age. This study demonstrates the usefulness, reliability and convenience of the electrophysiological tests for early diagnosis and functional evaluation of Usher's syndrome.

Adolescent

Correlations between psychophysical magnitude estimates and simultaneously obtained auditory nerve, brain stem and cortical responses to click stimuli in man.

Responses from the auditory nerve, brain stem auditory nuclei and cortex, as well as subjective responses to click stimuli at 10 intensities, were recorded simultaneously in the same human subjects. For various measures of the responses, the power-law exponents of their intensity functions were calculated, along with their statistical significances. The electrophysiological and psycho-physical functions were compared for similarity. On average, the exponents of the intensity functions of amplitudes of the auditory nerve and earlier brain stem responses were highly significant, showing similarity across subjects and similarity with the exponents of the subjective estimates. However, a closer examination proved this similarity to be superficial, since magnitude estimates showed an appreciable intersubject and intersession variability while the auditory nerve and brain stem responses were approximately constant. All other electric response measures either had exponents which were not significant or showed even poorer correlation with the subjective response. It is proposed that the type of electrical activity recorded in this study may not be the proper set of neural parameters which give rise to the loudness estimate.

Acoustic Stimulation

Identification and separation of acoustic frequency following responses (FFRS) in man.

Frequency following responses (FFRs) to monaural tone bursts were recorded in normal and hearing impaired subjects as the potential difference between an ipsilateral earlobe electrode and a scalp vertex electrode. Whenn the rubber tube coupler between the earphone and the subject's ear was clamped, a stimulus artefact FFR was occasionally recorded. The "biological" FFR had a latency of about 1 msec and an irregular wave form which was made more sinusoidal by the addition of white noise. When the responses to tone bursts of opposite onset phases were added together, a "double frequency" FFR was obtained which had a latency of about 6 msec and whose amplitude was appreciably reduced by white noise. In some hearing impaired subjects (with no neural responses to clicks), this longer latency double frequency component could not be recorded, while in those cases in which the cochlear microphonic potential could be recorded, the shorter latency FFR was also present. It is concluded that the FFR in normally hearing subjects is made up of a short latency cochlear microphonic component and a longer latency neural component.

Adolescent

Sources of frequency following responses (FFR) in man.

In order to study the sources and pathways which are responsible for the frequency following response (FFR), records were made in control subjects and in patients with special types of lesion and response. It has already been shown that the FFR in normal subjects to tone bursts with single onset phases is made up of a short latency cochlear microphonic potential (CM) and a longer latency neural component (neural FFR). No neural FFR could be recorded in patients with upper brain-stem lesions (absence of click-evoked responses from the inferior colliculus along with clinical signs of such a lesion). Their FFR was exclusively a cochlear microphonic potential, thus demonstrating that the neural FFR with a latency of 6 msec is generated in the region of the inferior colliculus. Also in subjects with large post-auricular muscle (PAM) responses, the PAM can contribute to the FFR, with a latency of 10 msec. In patients with high-tone hearing loss due to acoustic trauma, no CM could be recorded while a neural FFR with a latency of 6 msec was present. This indicates that the CM recorded by this technique may be generated in the basal turn. It also demonstrates that the pathway of the neural FFR begins in the apical turn of the cochlea.

Adult

Intensity and rate functions of cochlear and brainstem evoked responses to click stimuli in man.

The complex of five waves, which are the responses to click stimuli of the auditory nerve and the brainstem auditory nuclei, were recorded in ten human subjects by means of earlobe and scalp electrodes. The rate of the stimuli was varied from 5/s to 80/s and their intensity was varied over a 70 dB intensity range in order to study the rate and intensity functions of each of the response components. With increasing click intensity, the amplitude of the first wave (generated by the auditory nerve) increased proportionally while the amplitudes of the later waves (generated by the brainstem auditory nuclei) reached their maximum amplitudes at intermediate click levels (saturation), and at high intensities occasionally even decreased in amplitude. The latency of each of the waves decreased by similar amounts as the intensity was increased. With increasing click rates, the amplitude of the first wave decreased the most, while there were smaller effects on the amplitude of the later waves. There was no effect of click rate on the latency of the first wave, but the latency of the later waves increased with click rate, the effect being greater on the later waves. In the rate functions, the latency change of a wave was greater than that of the waves preceding it (accumulative effect). These results are explained by overlapping convergence and divergence in the ascending auditory pathway. These results support the notion that the principal component of each wave is activated by the principal component of the previous wave. These results may explain the relative ease with which several workers record the fourth wave of the complex, and their preference for this response.

Auditory Pathways

Recording of the cochlear microphonic potential with surface electrodes.

The cochlear microphonic potential was recorded in human subjects with surface electrodes (earlobe clip and scalp vertex disc) and an averaging procedure. Special precautions were taken to identify and separate artefactual, neural and microphonic components. These included shielding of the earphone, a rubber tube to introduce a time delay between artefact and biological response and white noise to mask the neural component. The cochlear microphonic potential was larger in amplitude in response to low frequency sounds and had a high threshold. Two clinical cases of cochlear hearing loss are presented, both lacking neural responses. The cochlear microphonic potential was present in one of them (i.e., neural hearing loss) and absent in the other (i.e., sensory hearing loss).

Adult

Neonatal auditory brain-stem response threshold and latency: 1 hour to 5 months.

Auditory brain-stem evoked responses were recorded in normal neonates and infants ranging in age from less than 1 h to 5.5 months. The average threshold in neonates 0-5 h old was 29 dB greater than that in adults, reaching the adult threshold range within 2 weeks. The latency of wave I in 0-5 h neonates was 1.81 msec and reached the adult range within 2 weeks. The V-I interpeak latency in 0-5 h neonates was 5.3 msec and did not reach adult values within the period of this study.

Brain Stem