Patients with GET have plastic changes in multiple neural systems that allow neural activity associated with eye movement, including those associated with the neural integrator, to stimulate the auditory system. Anomalous auditory activation is enhanced by the failure of cross-modal inhibition to suppress auditory cortical activity. The time course for the development of GET suggests that it may be due to multiple mechanisms.
Most functional imaging studies of the auditory system have employed complex stimuli. We used positron emission tomography to map neural responses to 0.5 and 4.0 kHz sine-wave tones presented to the right ear at 30, 50, 70 and 90 dB HL and found activation in a complex neural network of elements traditionally associated with the auditory system as well as non-traditional sites such as the posterior cingulate cortex. Cingulate activity was maximal at low stimulus intensities, suggesting that it may function as a gain control center. In the right temporal lobe, the location of the maximal response varied with the intensity, but not with the frequency of the stimuli. In the left temporal lobe, there was evidence for tonotopic organization: a site lateral to the left primary auditory cortex was activated equally by both tones while a second site in primary auditory cortex was more responsive to the higher frequency. Infratentorial activations were contralateral to the stimulated ear and included the lateral cerebellum, the lateral pontine tegmentum, the midbrain and the medial geniculate. Contrary to predictions based on cochlear membrane mechanics, at each intensity, 4.0 kHz stimuli were more potent activators of the brain than the 0.5 kHz stimuli.
Steady-state evoked potentials were measured from unanesthetized chinchillas both before and after carboplatin-induced selective inner hair cell loss. Recordings were made from both the inferior colliculus (IC) and the auditory cortex (AC). The steady-state potential was measured in the form of the envelope following response (EFR), obtained by presenting a two-tone stimulus (f1 = 2000 Hz; f2 = 2020, 2040, 2080, 2160, or 2320 Hz), and measuring the magnitude of the Fourier coefficient at the f2-f1 difference frequency. From the IC, precarboplatin, EFR amplitude vs difference tone frequency showed a bandpass pattern, with maximum amplitude at either 160 or 80 Hz, depending upon stimulus level. Postcarboplatin, the preferred difference frequency was 80 Hz for all stimulus levels. From the AC, EFR amplitude versus difference tone frequency also showed a bandpass pattern, with the maximum amplitude at 80 Hz both pre- and postcarboplatin. EFR amplitude from the IC was decreased for some conditions postcarboplatin, while the amplitude from the AC showed no significant change.
The auditory evoked potential f2-f1 difference tone (DT) and the 2 f1-f2 cubic difference tone (CDT) were recorded from electrodes implanted in the inferior colliculus in a group of chinchillas. The purpose of this study was to measure normative aspects of AEP distortion products in awake chinchillas, by comparing the DT and CDT under a variety of stimulus conditions. For experiment 1, f1 was held constant at 1998 Hz, while the f2/f1 ratio was varied from 1.05 to 1.50. Input-output functions were measured over a range of primary tone levels up to 80 dB SPL. The amplitude of the DT was greatest for the smallest f2/f1 ratio, and decreased systematically as f2/f1 ratio increased. DT amplitude was greater than CDT amplitude for all primary tone pairs. Experiment 2 was conducted to determine the effect of f1 frequency upon the DT and CDT for a constant f1-f2 difference frequency of 102 Hz (f1-999, 1998, 4999, and 9998 Hz). The DT input-output functions were overlapping for all f1 frequencies. For the CDT, amplitude decreased with increasing f1 frequency, which corresponded to an increase in CDT frequency. In experiment 3, the relationship between ear of stimulation and inferior colliculus recorded from was investigated. DT input-output functions (f1 = 1998 Hz, DT = 102 Hz) were measured for monaural contralateral, monaural ipsilateral, and dichotic stimulus conditions. DT amplitude was largest for the contralateral condition, followed by the ipsilateral condition. A smaller, dichotic component to the DT was observed as well.
In a previous paper (Arnold and Burkard, 1998) a dichotic f2-f1 difference tone (DT) auditory evoked potential from the chinchilla inferior colliculus (IC) was measured while presenting f1 (2000 Hz) to one ear and f2 (2100 Hz) to the other ear. This measurement paradigm could be used as a means to study binaural processing in an unanesthetized animal model. However, it is possible that this response is actually generated peripherally, as a result of acoustic crossover. The purpose of the present set of experiments was to investigate whether the dichotic DT is a true binaural phenomenon. Recordings were made from chronically implanted IC electrodes in unanesthetized, monaural chinchillas (left cochlea destroyed). In experiment 1, interaural attenuation (IA) was measured in two ways. First, IA was measured by comparing IC evoked potential thresholds obtained when stimulating the normal right ear and the dead left ear, using tone bursts (0.5-8 kHz). Mean values of interaural attenuation ranged from 50-65 dB across frequency (55 dB at 2000 Hz). Next, the DT was measured monaurally using f1 = 2000 and f2 = 2100 (L1 = L2). By comparing the mean DT input/output functions for monaural stimulation of the right and left ears, a mean value of IA for the tonal pair was estimated (approximately 69 dB). In experiment 2, the DT was measured with right monaural stimulation, while varying the relative levels of the primaries. A small DT could be seen with primary levels up to 30 dB apart, but not for greater level differences. Differences substantially greater than 30 dB would be expected in the crossover situation based upon IA. In experiment 3, the stimuli were presented dichotically (f1 to right ear, f2 to left ear and vice versa, L1 = L2) to determine whether acoustic crosstalk to the normal right ear would generate a DT. No DT was reliably observed in this condition. Taken together, these results suggest that the dichotic DT is a true binaural phenomenon, and not simply attributable to acoustic crossover.
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