Contributions of temporal-parietal junction to the human auditory P3.

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.

Sensory and cognitive evoked potentials in a case of congenital hydrocephalus.

We studied auditory and visual evoked potentials in D.W., a patient with congenital stenosis of the cerebral aqueduct. Head CT scans revealed marked hydrocephalus with expanded ventricles filling more than 80% of the cranium and compressing brain tissue to less than 1 cm in thickness. Despite the striking neuroanatomical abnormalities, however, the patient functioned well in daily life and was attending a local community college at the time of testing. Evoked potentials provided evidence of preserved sensory processing at cortical levels. Pattern reversal visual evoked potentials had normal latencies and amplitudes. Brain-stem auditory evoked potentials (BAEPs) showed normal wave V latencies. Na and Pa components of middle-latency AEP had normal amplitudes and latencies at the vertex, although amplitudes at lateral electrodes were larger than at the midline. In contrast to the normal sensory responses, long-latency auditory evoked potentials to standard and target tones showed abnormal P3 components. Standard tones (probability 85%), evoked N1 components with normal amplitudes (-3.7 microV) and latencies (103 msec), but also elicited large P3 components (17 microV, latency 305 msec) that were never observed following frequent stimuli in control subjects. Target stimuli (probability 15%) elicited P3s in D.W. and controls, but P3 amplitudes were enhanced in D.W. (to more than 40 microV) and the P3 showed an unusual, frontal distribution. The results are consistent with a subcortical source of the P300. Moreover, they suggest that the substitution of controlled for automatic processes may help high-functioning hydrocephalics compensate for abnormalities in cerebral structure.

Generators of middle- and long-latency auditory evoked potentials: implications from studies of patients with bitemporal lesions.

We recorded middle- and long-latency auditory evoked potentials (AEPs) in 5 patients (ages 39-72 years) with bilateral lesions of the superior temporal plane. Reconstructions of CT sections revealed that primary auditory cortex had been damaged bilaterally in four of the patients, while in the fifth an extensive left hemisphere lesion included primary auditory cortex while a right hemisphere lesion had damaged anterior auditory association areas but spared primary auditory cortex. Normal middle-latency AEPs (MAEPs) were recorded at the vertex electrode in all of the patients. In 3 of the 5 patients, MAEPs also showed normal coronal scalp distributions and were comparable in amplitude following stimulation of either ear. Two patients showed abnormalities. In one case, Na (latency 17 msec)-Pa (latency 30 msec) amplitudes were reduced over both hemispheres following stimulation of the ear contralateral to the more extensive lesion. In another, with both subcortical and cortical involvement, the Pa was abolished over the hemisphere with the more extensive lesion. Long-latency AEPs were normal in 2 patients whose lesions were largely confined to the superior temporal plane. In 2 patients with lesions extending into the inferior parietal lobe, N1s were abolished bilaterally. In the fifth patient, the N1 showed a slight reduction over the hemisphere with the more extensive lesion. Middle- and long-latency AEPs were differentially affected by some lesions. For example, patients with absent N1s could produce normal Pas. A review of these results and those of previous studies of bitemporal patients suggests that abnormalities in middle- and long-latency AEPs do not necessarily reflect damage to primary auditory cortex per se, but rather the degree of damage to adjacent areas. Abnormalities in MAEPs are associated with subcortical lesions, or cortical lesions extensive enough to denervate thalamic projection nuclei. Abnormalities in the long-latency N1 reflect lesion extension into the multi-modal areas of the inferior parietal lobule. This area appears to exert a critical modulatory influence over N1 generators outside of the superior temporal plane.

Age-related changes in human middle latency auditory evoked potentials.

We recorded middle latency auditory evoked potentials (MAEPs) in young (20-40 years) and elderly (60-80 years) subjects with normal hearing. The Pa component was prolonged in latency and markedly enhanced in amplitude in the elderly subjects. No changes were found in Na, or in the binaural interaction of the MAEP. Differences in Pa amplitude and latency were not due exclusively to changes in auditory thresholds, since they were not duplicated by changes in stimulus intensity, and persisted when MAEPs from selected young and old subjects were compared at similar SPL levels. The enhancement of Pa amplitude appears to reflect age-related central modifications in auditory processing.

Click spatial position influences middle latency auditory evoked potentials (MAEPs) in humans.

Middle latency auditory evoked potentials (MAEPs) were elicited by monaural and binaural clicks. The Na component (latency 15.8 msec) was larger in amplitude and shorter in latency at electrodes contralateral to the stimulated ear in monaural conditions, but showed no evidence of binaural occlusion. The Pa (28.4 msec) and Nb (42.0 msec) components did not change in amplitude or distribution as a function of the ear of stimulus delivery, but were smaller following binaural stimulation than would have been predicted from separately recorded monaural responses. These results indicate that functionally distinct generator systems are responsible for different components of the MAEP. The generators of the Na are more effectively activated by contralateral inputs. In contrast, the generators of the Pa and Nb receive equally effective and convergent inputs from the two ears.