Effects of parietal lesions in humans on color and location priming.

To determine whether the parietal lobes contribute tot he selection of nonspatial features known to be processed in the ventral stream, the current study examined the effect of chronic unilateral parietal lobe lesions in humans on color and location priming. Patients and normal controls performed a go/no-go color discrimination task in which either the same color and different color pairs of stimuli (prime and probe) were projected sequentially either in the same hemifield or in opposite hemifields. Control subjects and patients both showed independent effects of color and location priming. In the patients, primes in either field produced color priming for target probes in the ipsilesional field but not for probes in the contralesional field. This observation implicates the parietal cortex in processing activated codes of stimulus attributes not only for spatial information but also for visual features processed in the ventral visual pathways.

Role of human prefrontal cortex in attention control.

Without a functioning dorsolateral prefrontal cortex, humans are stimulus bound and have little confidence in their ability to interact with the environment. Deficits in inhibitory control of external and internal processes coupled with impaired temporal coding of stimuli and detection capacity for novel events leave the patient functioning in a noisy internal environment without critical spatiotemporal cues. Some of these proposals are similar to those of Nauta (104). Based on connectivity of the prefrontal cortex, Nauta suggested that this region was ideally suited to generate and evaluate internal models of action. It is proposed that, in addition to this generation function, the prefrontal cortex is crucial for detecting changes in the external environment and for discriminating internally and externally derived models of the world. This chapter has described a cascade of deficits that result from damage to the dorsolateral prefrontal cortex. Awareness of the sensory world, and of the apparent stream of internal and external events, is impaired by deficits in novelty detection. Changes in the world, internal or external, may not be noticed in a noisy internal milieu. These deficits contribute to impaired reality monitoring and to a subsequent lack of confidence in behavior. An inability to bridge temporal gaps and temporally sequence internal events, together with deficits in inhibitory control systems, contribute to an impairment in the ability to generate coherent representations of alternate or counterfactual realities.

Anatomical substrates of auditory selective attention: behavioral and electrophysiological effects of posterior association cortex lesions.

Event-related brain potentials (ERPs) and reaction times (RTs) were recorded in an auditory selective attention task in control subjects and two groups of patients with lesions centered in (1) the temporal/parietal junction (T/P, n = 9); and (2) the inferior parietal lobe (IPL, n = 7). High pitched tones were presented to one ear and low pitched tones to the other in random sequences that included infrequent longer-duration tones and occasional novel sounds. Subjects attended to a specified ear and pressed a button to the longer-duration tones in that ear. IPL and T/P lesions slowed reaction times (RTs) and increased error rates, but improved one aspect of performance--patients showed less distraction than controls when targets followed novel sounds. T/P lesions reduced the amplitude of early sensory ERPs, initially over the damaged hemisphere (N1a, 70-110 ms) and then bilaterally (N1b, 110-130 ms, and N1c 130-160 ms). The reduction was accentuated for tones presented contralateral to the lesion, suggesting that N1 generators receive excitatory input primarily from the contralateral ear. IPL lesions reduced N1 amplitudes to both low frequency tones and novel sounds. Nd components associated with attentional selection were diminished over both hemispheres in the T/P group and over the lesioned hemisphere in the IPL group independent of ear of stimulation. Target and novel N2s tended to be diminished by IPL lesions but were unaffected by T/P lesions. The mismatch negativity was unaffected by either T/P or IPL lesions. The results support different roles of T/P and IPL cortex in auditory selective attention.

Prefrontal cortex gating of auditory transmission in humans.

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.

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.

The effects of lesions of superior temporal gyrus and inferior parietal lobe on temporal and vertex components of the human AEP.

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.

gamma-Aminobutyric acid-induced potentiation of cortical hemiplegia.

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.

Surface auditory evoked potentials in the unrestrained rat: component definition.

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.

Altered peripheral and brainstem auditory function in aged rats.

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.

Electrodermal responses in patients with unilateral brain damage.

Skin conductance responses (SCR) to emotional and to nonemotional stimuli were measured in 16 right and 16 left unilateral brain-damaged patients. Replicating findings by Morrow, Vrtunski, Kim and Boller (1981), those patients with a lesion in the left hemisphere showed higher SCR's to emotional than to nonemotional stimuli while those with a right lesion showed no difference between them. This pattern of results remained when variance in performance on a Facial Expression Recognition task was partialled out, suggesting that the absence of differentiated arousal in right-brain-damaged patients is unrelated to their impairment in perceptual analysis.