Biomedical subjects
Publications and source records attributed to D Scabini.
Middle-latency auditory evoked potentials (MAEPs) were recorded in controls and patients with focal lesions in dorsolateral prefrontal cortex. Unilateral prefrontal lesions increased the amplitude of the Pa component of the MAEP beginning at 25-35 ms poststimulus. The data suggest that prefrontal cortex exerts early inhibitory modulation of input to primary auditory cortex in humans.
The P3 component of the event-related potential (ERP) is generated in humans and other mammalian species when attention is drawn to infrequent stimuli. We assessed the role of subregions of human posterior association cortex in auditory P3 generation in groups of patients with focal cortical lesions. Auditory P3s were recorded to target (P3b) and unexpected novel stimuli (P3a) in monaural and dichotic signal detection experiments. Two groups of patients were studied with lesions of: (1) temporal-parietal junction including posterior superior temporal plane and adjacent caudal inferior parietal cortex; and (2) the lateral parietal lobe including the rostral inferior parietal lobe and portions of superior parietal lobe. Extensive lateral parietal cortex lesions had no effect on the P3. In contrast, discrete unilateral lesions centered in the posterior superior temporal plane eliminated both the auditory P3b and P3a at electrodes over the posterior scalp. The results indicate that auditory association cortex in the human temporal-parietal junction is critical for auditory P3 generation.
We recorded auditory evoked potentials (AEPs) to 1 kHz tone bursts in controls and patients with unilateral lesions centered in posterior superior temporal gyrus and adjacent caudal inferior parietal lobule (STG) or in rostral inferior parietal lobule (IPL). Controls generated a vertex maximal N94 (N1b) and P200 (P2) and additional P45, N78 and N127 temporal AEP components (P45, N1a, N1c). Similar to prior reports, in controls the N1a was most prominent over the left temporal lobe and the P45 was largest over the right temporal lobe consistent with behavioral and anatomical data indicating differential organization of left and right human temporal lobe. The N1c was recorded equally from both T3 and T4 electrodes and was enhanced in the temporal site contralateral to the ear of stimulation. The patient groups had differential effects on AEPs. Unilateral STG lesions resulted in bilateral reductions of the N1b and P45 and marked unilateral reductions of the N1a and N1c over lesioned hemisphere. IPL lesions resulted in bilateral but non-significant reductions of the N1b and N1c. The scalp topography results in normal subjects combined with the effects of unilateral STG lesions provide supportive evidence that the temporal maximal components of the human AEP (P45, N1a, N1c) are generated by radially oriented neuronal dipole sources located in STG. The bilateral reduction of the N1b vertex response by unilateral STG lesions is compatible with a unilateral disruption of a vertically oriented dipole situated in the posterior superior temporal plane. The results emphasize the critical role of the superior temporal plane and lateral superior temporal gyrus in generation of human long latency AEPs.
A novel model of hemiplegia in young and aged rats is described. Osmotic minipumps were used to deliver a chronic (7 days), localized application of gamma-aminobutyric acid (GABA) (100 micrograms/microliter/h), to the somatomotor cortex of unrestrained rats. This resulted in an easily quantifiable, contralateral and reversible motor syndrome in both young and aged animals. In the young group, the motor deficit cleared over 5-day period, while in the aged animals it persisted for at least a 2-week period. Control animals treated with saline-filled minipumps did not develop a long-lasting motor deficit. The GABA-induced facilitation of hemiplegia due to small motor cortex lesions and the age effects on behavioral recovery of function are discussed. Cortical inhibitory mechanisms may play a role in debilitating syndromes such as stroke or post-epileptic paralysis.
A technique for conducting free-field brainstem auditory evoked potential (BAEP) audiometry in unanesthetized, unrestrained rats revealed a non-recruiting 18 dB elevation of click threshold in aged rats. BAEPs were first recorded in young and aged rats to clicks of equal intensity (80 dB SPL). Compared to the young group, aged animals exhibited longer wave I and wave IV latencies with no difference seen in the I-IV central conduction time. The prominent negative wave (No) following wave IV was also delayed and the I-No and IV-No conduction times increased in the aged group. When BAEPs were recorded to clicks with intensities adjusted to 35 dB above individual threshold, no differences in wave I or wave IV latencies or in the I-IV central conduction time were found between groups. However, the No component was delayed and the I-No and IV-No conduction times remained prolonged in the aged group. The results suggest that in addition to changes in peripheral auditory structures, changes in the rostral auditory brainstem accompany age-related hearing loss in rats.
Auditory evoked potentials (AEPs) to click and pure tone stimuli were recorded in unrestrained, unanesthetized rats. The middle latency rat AEPs (N17, P23, N38) had midline scalp distributions similar to human MAEPs and were recorded to within 15 dB above BAEP threshold. In contrast to human MAEPs, rat MAEPs were decreased in amplitude at high stimulation rates and only the N17 component was unaltered by slow wave sleep. The longer latency N50, N80 and P130 components had several response properties comparable to human N100-P200 vertex potentials. These included restricted midline fronto-central scalp distributions, progressive increases in amplitude at ISIs up to 4-8 sec and marked attenuation during slow wave sleep. The frequency sensitivity of the rat AEP revealed a decreased response to pure tones below 4 kHz but robust responses for stimuli up to at least 45 kHz. There was a notch in the rat audiogram with decremented component amplitudes to pure tone stimuli centered at 35 kHz. When equated for intensity, click and pure tone stimuli in the range of the rats maximal audiometric sensitivity (8-20 kHz) generated comparable AEP components. These results provide normative data on rat surface recorded AEPs. It is suggested that these surface recorded rat AEPs are generated by subcortical neural systems involved in the detection of auditory transients.