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Temporal coding of envelopes and their interaural delays in the inferior colliculus of the unanesthetized rabbit.

1. The difference in the time of arrival of a sound at the two ears can be used to locate its source along the azimuth. Traditionally, it has been thought that only the on-going interaural temporal disparities (ITDs) produced by sounds of lower frequency (approximately less than 2 kHz) could be used for this purpose. However, ongoing ITDs of low frequency are also produced by envelopes of amplitude-modulated (AM) tones. These ITDs can be detected and used to lateralize complex high-frequency sounds (1, 8, 12, 15, 22, 24, 26). Auditory neurons synchronize to the modulation envelope, but do so at progressively lower modulation frequencies at higher levels of the auditory pathway. Some neurons of the cochlear nucleus synchronize best to frequencies as high as 700 Hz, but those of the inferior colliculus (IC) exhibit their best synchrony below 200 Hz. Even though synchrony to higher modulation frequencies is reduced at higher levels of the auditory pathway, is information about ITDs retained? 2. We answered this question by extracellularly recording the responses of neurons in the IC of the unanesthetized rabbit. We used an unanesthetized preparation because anesthesia alters the responses of neurons in the IC to both monaurally presented tones and ITDs. The unanesthetized rabbit is ideal for auditory research. Recordings can be maintained for long periods, and the acoustic stimulus to each ear can be independently controlled. 3. We studied the responses of 89 units to sinusoidally AM tones presented to the contralateral ear. For each unit, we recorded the response at several modulation frequencies. The degree of phase locking to the envelope at each frequency was measured using the synchronization coefficient. Two measures were used to assess the range of modulation frequencies over which phase locking occurred. The "best AM frequency" was the frequency at which we observed the greatest phase locking. The "highest AM frequency" was the highest frequency at which significant phase locking (0.001 level) was observed. We could not assess synchrony to ipsilateral AM tones directly, because most units did not respond to ipsilateral stimulation. 4. We studied the sensitivity of 63 units to ITDs produced by the envelopes of AM tones. Sensitivity to ITDs was tested by presenting AM tones to the two ears that had the same carrier frequency, but modulation frequencies that differed by 1 Hz. Units that were sensitive to ITDs responded to this stimulus by varying their response rate cyclically at the difference frequency, i.e., 1 Hz.(ABSTRACT TRUNCATED AT 400 WORDS)

Animals↗

An integrity test battery for the Nucleus Mini 22 Cochlear Implant System.

The probability of system failures increases as the number of cochlear implants increases throughout the world. Whether a malfunction is a technical or physiological problem remains to be defined, particularly in very young children, while a psychogenic hearing disorder after implantation must not be excluded in adults. The battery of objective measurements used clinically at the Medizinische Hochschule, Hannover has provided useful diagnostic information for distinguishing possible causes of failure. In a normally functioning device, an electrical signal equivalent to the biphasic rectangular stimulation pulse can be recorded by measuring skin potentials from surface electrodes placed on the mastoid of the implant side and the forehead. The signal from the stimulated implanted electrodes is derived by applying a constant pulse rate. Signal averaging is not necessary. If no signals are observed, a non-functioning device should be suspected. If the device works normally, function of the auditory pathways can be examined by recording the electrically elicited stapedius reflex or electrically evoked brain-stem responses. In our experience with more than 450 cochlear implant patients, eight internal device failures occurred, while an additional three patients had either reduced or no hearing sensations due to a disorder of the auditory pathways.

Acoustic Stimulation↗

Hydrocephalus: increased intracranial pressure and brain stem auditory evoked responses in the hydrocephalic rabbit.

The auditory evoked response (AER) was used to study the effect of increased intracranial pressure (ICP) on the auditory pathway in normal New Zealand rabbits and in those made hydrocephalic by intracisternal injections of kaolin. AERs were studied: (a) in the normal and then in the hydrocephalic animal; and (b) in the hydrocephalic animal during further ICP elevation by cerebrospinal fluid infusion. The AER was obtained from ongoing electroencephalographic activity after rarefaction auditory clicks presented at 90 dB sound pressure equivalent. In comparing base line normal AERs to those found in hydrocephalic conditions, a statistically significant increase in latency for AER components N2, P2, and P5 was noted in hydrocephalic rabbits. Increased ICP in the hydrocephalic model showed an increase in the latencies of AER components for P0 and P1 at 250 mm H2O, and a prolongation of P3-P5 central conduction time at 700 mm H2O above base line cerebrospinal fluid pressure. In addition, a decrease in the P4/N5 amplitude and an increase in P1-P3 central conduction times at 700 mm H2O was observed. The differences between normal and hydrocephalic rabbit AER base lines may be the result of the chronically increased ICP and presumed chronic anatomical changes within the auditory pathway due to kaolin itself. The differences in the AER from base line hydrocephalus to acute increased ICP may indicate that the hydrocephalic system is more sensitive to acute neuropraxic pressure effects on the brain stem auditory structures than is the normal brain.

Animals↗

Auditory extinction following hemisphere damage.

Extinction to the simultaneous presentation of sounds to both ears was investigated in patients with acute cerebrovascular disease and found to be present in nearly half of the patients in the early stage of stroke. The occurrence of the symptom was not significantly different following damage to either hemisphere, but a higher percentage of right brain-damaged patients tended to show extinction for a longer time. However, this finding must be evaluated with caution since a greater number of left- than right-hemisphere patients had to be excluded from the investigation because aphasia precluded their understanding test instructions. The presence of auditory extinction was not related to that of visual extinction and there were patients with severe visual neglect who did not extinguish in the auditory modality. These findings and CT scan evidence, indicating that patients with long-lasting extinction had lesions encroaching upon the auditory pathways, suggest that in number of cases the phenomenon may have a sensory and not an attentional basis.

Attention↗

Patients with horizontal gaze palsy and progressive scoliosis due to ROBO3 E319K mutation have both uncrossed and crossed central nervous system pathways and perform normally on neuropsychological testing.

BACKGROUND: Horizontal gaze palsy and progressive scoliosis (HGPPS) is caused by mutations of the ROBO3 gene, which encodes a receptor associated with axonal guidance during development. Although there is evidence for uncrossed cuneatal and corticospinal tracts in HGPPS, it is unclear whether other central nervous system pathways are involved. OBJECTIVE: To study two patients with HGPPS homozygotic for the ROBO3 E319K mutation using a variety of neurophysiological and neuropsychological tests. METHODS: A battery of neuropsychological tests was applied to assess various cognitive and perceptual functions. The corticospinal, somatosensory and auditory pathways were evaluated using appropriate neurophysiological tests. To access motor pathways to the neck muscles, electromyographic recordings were obtained from the sternocleidomastoideus and splenius capitis muscle during active head rotation. RESULTS: Both patients performed normally on manual dexterity, complex sensory and visuospatial functions, reading and general intelligence tests. Motor evoked potentials in both patients showed uncrossed corticospinal tracts for the extremities, although in one patient, electromyography indicated pyramidal tract crossing for the neck muscles. Although somatosensory evoked potentials showed uncrossed somatosensory fibres subserving proprioception and light touch, right median nerve somatosensory evoked potential in one patient indicated a partial lemniscal crossing. Sympathetic skin response and blink reflex showed a midline crossing of the spinothalamic and quintothalamic tracts. Brain stem auditory evoked potentials indicated a lack of crossing in the level of the trapezoid body. CONCLUSIONS: Our patients with the ROBO3 E319Kappa mutation show normal perceptual and cognitive functions and have both crossed and uncrossed motor, sensory and auditory pathways.

Cognition↗

Auditory brainstem evoked potentials in leprosy.

An electrophysiological study of conduction in the auditory nerve and brainstem auditory pathways using the brainstem auditory evoked potential was undertaken in a group of 47 leprosy patients. There were no statistically significant differences between mean conduction times (interpeak latencies) in the leprosy and the control groups. Abnormal interpeak latencies were encountered in 3 leprosy patients, 1 of whom had a positive serological test for syphilis. In the remaining 2 patients, caudal pathway dysfunction (I-III interpeak latency abnormality) was indicated but specific auditory nerve involvement (an abnormally prolonged I-II interpeak latency) was not demonstrated. An explanation for these findings, other than the patients' disease, was not apparent.

Adolescent↗

Auditory tract asymmetry in brainstem electrical responses during binaural stimulation.

A recently developed technique to demonstrate binaural interaction in brainstem auditory electrical responses was systematically investigated. From analysis of the BSERs of eight normal hearing adults, it was found that variations in binaural interaction difference traces are related to an artificial relationship created by this technique between the true binaural and summed monaural waveforms. The present investigation employed a refinement of the binaural interaction technique whereby left and right monaural waveforms were subtracted individually from the binaural waveform to produce a difference trace. Analysis revealed that variations in the difference trace morphology are related to dependence of binaural latencies on left or right auditory tract preference in the brainstem auditory pathways. Within the subject population, 50% demonstrated an auditory tract preference for binaural latencies while 50% showed no preference. It was concluded that the difference trace is mathematically predictable from the morphological differences between the binaural and monaural waveforms and that a more accurate representation of binaural interaction can be obtained from a comparison of individual monaural waveforms within the binaural trace.

Acoustic Stimulation↗

Progressive deterioration of central components of auditory brainstem responses during postnatal development of the myelin mutant taiep rat.

Auditory brainstem responses (ABRs) were evaluated during the postnatal development (P10-P180) of taiep rats, neurological mutants characterized by early abnormal myelin development and subsequent demyelination of the CNS. The disorder is produced by an autosomal recessive mutation trait that affects the oligodendrocytes but not the Schwann cells. After onset of ABRs (P12-P14), taiep rats and their nonaffected heterozygous littermates that served as controls showed a similar pattern of maturation for wave I. The central waves (In-IV) showed significantly longer latencies in the mutants. By P60-P180, the later waves (III and IV) were frequently difficult to discern. From the onset of ABRs, the interpeak latency I-IV, corresponding to the central conduction time (CCT) of the auditory pathway, showed in taiep rats significantly longer values than controls. After an initial reduction, proportional to that of control rats, the CCT value increased progressively during the second month of the mutants' lives. The electrophysiological results of the present study strongly support the hypothesis that mutation in the taiep rat impairs neuromaturation of the central auditory pathway in the brainstem by affecting the myelination process in the CNS.

Animals↗

Brain stem auditory-evoked responses in suspected central pontine myelinolysis.

Central pontine myelinolysis was suspected in two chronic alcoholics who developed and recovered from a progressive spastic paresis of all muscles, that derived innervation at and below the level of the pons. In both cases, short-latency auditory-evoked responses aided in the diagnosis by indicating a slowing of conduction in the pontine auditory pathway, which varied in degree with the severity of the clinical manifestations of pontine demyelination.

Alcoholism↗

Brain stem auditory evoked response development in the kitten.

The development of brain stem auditory evoked responses (BAERs), recorded from a surface electrode as short-latency, volume-conducted potentials, was studied in a series of kittens over a postnatal period ranging from birth to 60 days. Repeated, longitudinal observations on particular kittens were supplemented with observations on additional kittens during the first and second postnatal week to determine age of onset of the BAERs. The position of the animal and sound source within the recording chamber were held constant across recording sessions, as was click intensity except during recordings in which intensity effects were specifically studied. Click rates of 1, 10, 50 and 100/sec were routinely presented. Reference electrodes at the tongue, pinna and neck showed volume-conducted responses to the click stimuli and resulted in considerable distortion of the activity recorded by the vertex electrode; the forepaw, in contrast, showed no activity and a vertex-forepaw electrode configuration provided good resolution of the BAERs across development. A number of new observations were made. BAERs were first observed at 4 days of age, approximately the same age at which depth evoked potentials are first recorded in brain stem auditory nuclei. Initially the BAERs were diffuse, high threshold and fatigued rapidly, characteristics shared with depth evoked potentials in the early postnatal period. Over the first two weeks, the potentials showed marked decrease in threshold, increased resistance to fast click rates, and better definition of wave forms. All BAER components showed exponential decreases in latency. Because all of the brain stem evoked potentials could be recorded concurrently and longitudinally in the same subject a number of developmental comparisons were possible among the BAER components. Wave 1, related to the acoustic nerve in the adult cat, showed a developmental time course and adult latency similar to that reported for N1. Wave 2, related to the cochlear nucleus in the adult, showed a marked bimodality over the first month; wave 2a was a large amplitude clearly separated wave which gradually fused as an inconspicuous leading shoulder on wave 2b. Wave 2b developed with a time course and adult latency similar to that reported for the ventral cochlear nucleus. Wave 3, related to the region of the superior olivary complex in the adult, showed a clear but transient bimodality during the third week of development. Wave 5, related to the inferior colliculus in the adult, appeared later than waves 1-4 and showed a significantly slower rate of development than waves 1-4. These data indicate that differential developmental changes occur within the brain stem auditory pathway and that the BAERs provide a dynamic probe of concurrent maturational interactions.

Acoustic Stimulation↗

Inner hair cell loss leads to enhanced response amplitudes in auditory cortex of unanesthetized chinchillas: evidence for increased system gain.

Carboplatin preferentially destroys inner hair cells (IHCs) in the chinchilla inner ear, while retaining a near-normal outer hair cell (OHC) population. The present study investigated the functional consequences of IHC loss on the compound action potential (CAP), inferior colliculus potential (ICP) and auditory cortex potential (ACP) recorded from chronically implanted electrodes. IHC loss led to a reduction in CAP amplitude that was roughly proportional to IHC loss. The ICP amplitude was typically reduced by IHC loss, but the magnitude of this reduction was generally less than that observed for the CAP. In contrast to the CAP and ICP, ACP amplitudes were generally not reduced following IHC loss. In some animals, the ACP amplitude remained at pre-carboplatin values despite substantial IHC loss. However, in other animals, IHC loss led to an increase ('enhancement') of ACP amplitude. ACP enhancement was greatest at 1-2 weeks post-carboplatin, returning towards baseline amplitudes at 5 weeks post-carboplatin. In other animals, the ACP remained enhanced up to 5 weeks post-carboplatin. We interpret the transient and sustained enhancement of ACP amplitude following partial IHC loss as evidence of functional reorganization occurring at or below the level of the auditory cortex. These results suggest that the gain of the central auditory pathway increases following IHC loss to compensate for the reduced input from the cochlea.

Action Potentials↗

[Coding of the acoustic information in the superior auditory centers].

The internal ear may be considered analysing acoustical signals in the frequency domain. This spectral analysis appears in the auditory pathways as a place code, each neuron being activated for a narrow and well defined frequency band. But in addition to this place code, temporal information on the phase and the period of low frequency signals is preserved in the low auditory centers. In the medial geniculate body, the last relay before the cerebral cortex, the place code shows the same properties as in lower centers but with a greater diversity in the response patterns and tuning properties. The tonotopic organization is less precise and, for the pars lateralis, follows the histological lamellar organization of this region. The most lateral laminae are composed of cells responding to low frequencies, the most medial ones of high frequency cells. In the auditory cortex intracellular recordings confirm the importance of an active inhibition underlying the diverse response patterns observed. Persistance of a time code is shown by certain cells presenting responses precisely time-locked to individual clicks in a train for rates ranging from 50 to 1000 Hz. Other cells respond selectively for certain click train frequencies without marking the temporal structure of the stimuli. Thus a temporal and a place code are still both present at the cortical level for this particular kind of signals.

Acoustic Stimulation↗

Generation of auditory brain stem responses (ABRs). III. Effects of lesions of the superior olive, lateral lemniscus and inferior colliculus on the ABR in guinea pig.

Auditory brain stem potentials were recorded between the skull (vertex) and a non-cephalic reference in guinea pig before and after making discrete lesions of the auditory pathway in the pons and midbrain. Lesions of the superior olivary complex were accompanied by attenuation of P3 and N3 to contralateral input. Lesions of the lateral lemniscus were accompanied by attenuation of N3 to contralateral input. Lesions of the lateral portion of the pons adjacent to the lateral superior olivary nucleus were accompanied by attenuation of P4 to ipsilateral input. Lesions of the inferior colliculus were without effect on the ABR. These data are interpreted as supporting the hypothesis that each component of the ABR arises from a focal region of the brain stem auditory pathway.

Animals↗

Auditory neuropathy/dys-synchrony and its perceptual consequences.

Auditory neuropathy/dys-synchrony is a form of hearing impairment in which cochlear outer hair cell function is spared but neural transmission in the auditory pathway is disordered. This condition, or group of conditions with a common physiologic profile, accounts for approximately 7% of permanent childhood hearing loss and a significant (but as yet undetermined) proportion of adult impairment. This paper presents an overview of the mechanisms underlying auditory neuropathy/dys-synchrony-type hearing loss and the clinical profile for affected patients. In particular it examines the perceptual consequences of auditory neuropathy/dys-synchrony, which are quite different from those associated with sensorineural hearing loss, and considers currently available, and future management options.

Adult↗

Auditory cortical onset responses revisited. II. Response strength.

Most neurons of the auditory pathway discharge spikes locked to the onset of an acoustic stimulus, but it is largely unknown in which way the acoustic parameters of sound onsets shape the neuronal responses. In this paper is analyzed the number of spikes discharged by single neurons in primary auditory cortex of barbiturate-anesthetized cats to the onsets of tones of characteristic frequency. The time course of the peak pressure (i.e., the envelope) was altered by parametrically varying sound pressure level (SPL), rise time, and rise function (linear or cosine-squared). For both rise functions, rise time had manifold, and in some cases dramatic, effects on conventional spike count-level functions. In general, threshold SPL, dynamic range, and the lowest SPL at which monotonic spike count functions saturated increased with prolongation of the rise time. In neurons with mostly nonmonotonic spike count-level functions, "best SPL" increased and the descending high-SPL arms flattened, so that functions obtained with long rise times were often monotonic whereas those obtained with shorter rise times were highly nonmonotonic. Consequently, the "tuning" to SPL was less sharp for longer rise time tones, and spike count versus rise time functions changed from "short-pass" to "long-pass" with an increase in SPL. Systematic effects of rise time persisted when spike counts were plotted against the rate of change of peak pressure or against the maximum acceleration of peak pressure. However, when spike counts were plotted as a function of the instantaneous peak pressure at the time of response initiation, the functions obtained with different rise times, and even with different rise functions, were in close register. This suggests that the stimulus-dependent component of first-spike latency can be viewed as an integration window, during which rate of change of peak pressure is integrated. The window commences with tone onset and its duration is inversely related to the maximum acceleration (or, for linear rise functions, the rate of change) of peak pressure and the neuron's transient sensitivity. The present findings seriously question, for onset responses, the usefulness of the spike count-level function and measures derived from it, such as threshold SPL, dynamic range, best SPL, or degree of nonmonotonicity. They further cast doubt onto the validity of current concepts of intensity coding at cortical levels, because most neurons' onset responses are not indicative of a signal's steady-state SPL. However, they suggest a mechanism by which a neuronal population will sample a given transient in an orderly, sensitivity-dependent, temporal sequence. The sampling rate is automatically adjusted to, and adjusted by, the rapidity of the signal's change. And the instantaneous properties of the transient could be represented by the ratios and spatial distribution of responses across the simultaneously active subpopulation. Such a mechanism could provide the basis for the demonstrated capability of discrimination of rapid transients.

Animals↗

Postnatal expression of the serotonin transporter in auditory brainstem neurons.

To investigate the putative role of serotonin (5-HT) in auditory brainstem development, the expression of the 5-HT transporter (5-HTT) was evaluated in the normal mouse brainstem at 6 different postnatal ages. The brains of C3H/HeJ mice at birth (P0) and P1, P8-P9, P13, P21-P22, P35-P36 and P48-P50 were collected and processed immunohistochemically with an antibody raised against the 5-HTT. 5-HTT immunoreactivity (5-HTT-IR) was first observed in P8 mice and was localized to cell bodies in the ventral cochlear nucleus (VCN) and principal nuclei of the superior olivary complex, including the medial nucleus of the trapezoid body. Labeled neurons were found in similar regions in older mice except at P48-50, where labeled neurons were observed in the VCN only. 5-HTT-IR was especially prominent in VCN neurons at P21 and was observed in all of the brains examined at this age. These results indicate that auditory brainstem neurons of the normal inbred mouse express the 5-HTT postnatally. The presence of 5-HTT-IR in neurons located in the VCN indicates a regional expression of the 5-HTT that is related to the ascending auditory pathway. The timing of 5-HTT expression indicates that 5-HT may modulate developmental processes that rely on cochlear input.

Aging↗

[Evoked response audiometry in circulatory disorders in the brainstem (author's transl)].

In the case of retrocochlear lesions evoked potentials from different stages of the auditory pathway were recorded. Four Patients with nearly normal hearing threshold and normal cortical potentials show reduced medium latency potentials show reduced medium latency potentials due to circulatory dysfunction in the brainstem. Desynchronisation effects on the brainstem level are completely compensated in the cortex. The damage of the auditory pathway could not be found by X-ray or other usual clinical methods. In the two cases described improvement under medical treatment can be demonstrated.

Audiometry↗

[Effect of body temperature changes on evoked potentials].

Short-latency somatosensory (SSEPs) and brainstem auditory evoked potentials (BAEPs) were recorded in 12 patients with fever due to respiratory infection (age, 44.3 +/- 20.9 years, mean +/- SD) to clarify the effect of body temperature change on conduction in the central somatosensory and brainstem auditory pathways. Subjects were studied during episodes of fever (37.9 +/- 0.8 degrees C) and after their body temperature had decreased (36.6 +/- 0.3 degrees C). The central conduction time (CCT), which is the peak latency between N 13 and N 20, was significantly longer after body temperature had decreased than during fever. Likewise the interpeak latency between waves I and V (I-V IPL) was significantly prolonged following decrease in body temperature. These results suggest that increases in body temperature have an effect upon conduction in the central somatosensory and brainstem auditory pathways.

Body Temperature↗