Disturbances in information processing can be established by means of evoked potentials (EP). Sensory information is transported over the white myelinated fibers towards the brain. Classification and storage will take place in the cortical grey. This kind of information processing can be made visible by means of EP's.

In 9 patients with dementia. Alzheimer's type and 7 patients with multi-infarct dementia a delay in information processing has been established by means of EP's. In multi-infarct dementia also a delay in short latency components was determined. The generators of various parts of the information processing in the cerebral cortex have been delayed and distorted. We speculate that, beside loss of neurons in the cerebral cortex, an alteration in cortical glial cells might be the cause of some disturbances in patients with dementia.

Background: Late life depression is often accompanied by slowed information processing during neuropsychological testing, and this has been related to underlying cerebrovascular disease. We investigated whether changes in electrophysiological markers of information processing might share the same pathological correlates.

Methods: Differences in power spectra frequency, contingent negative variation (CNV), post-imperative negative variation (PINV), and auditory P300a amplitude and latency in 19 patients with DSM-IV major depression aged ≥ 60 years were compared with 25 recordings in age-matched healthy controls. Associations with total brain volume and degree of white matter hyperintensities (WMH) were examined in those who had undergone additional magnetic resonance imaging (MRI).

Results: Compared with healthy controls, patients had more slow-wave delta (group difference: p = 0.024) and theta activity (p = 0.015) as well as alpha activity (p = 0.005) but no decrease in beta band frequency (p = 0.077). None of these changes related differently to brain volume or WMH in patients or controls. Patients further showed prolonged P300a latencies (p = 0.027), which were associated with decreased total brain volume in patients but not controls (interaction by group: p = 0.004). While there were no overall differences in PINV between both groups, patients showed a decrease in PINV magnitude with increasing WMH, a relation that was not seen in controls (interaction by group: p = 0.024).

Conclusion: Patients with late life depression show changes in several electrophysiological markers of cerebral arousal and information processing, some of which relate to brain atrophy and WMH on MRI.

A comparative method of studying the biological bases of personality compares human trait dimensions with likely animal models in terms of genetic determination and common biological correlates. The approach is applied to the trait of sensation seeking, which is defined on the human level by a questionnaire, reports of experience, and observations of behavior, and on the animal level by general activity, behavior in novel situations, and certain types of naturalistic behavior in animal colonies. Moderately high genetic determination has been found for human sensation seeking, and marked strain differences in rodents have been found in open-field behavior that may be related to basic differences in brain neurochemistry. Agonistic and sociable behaviors in both animals and humans and the trait measure of sensation seeking in humans have been related to certain common biological correlates such as gonadal hormones, monoamine oxidase (MAO), and augmenting of the cortical evoked potential.

The monoamine systems in the rodent brain are involved in general activity, exploratory behavior, emotionality, socialization, dominance, sexual and consummately behaviors, and intracranial self-stimulation. Preliminary studies have related norepinephrine and enzymes involved in its production and degradation to human sensation seeking. A model is suggested that relates mood, behavioral activity, sociability, and clinical states to activity of the central catecholamine neurotransmitters and to neuroregulators and other transmitters that act in opposite ways on behavior or stabilize activity in the arousal systems. Stimulation and behavioral activity act on the catecholamine systems in a brain–behavior feedback loop. At optimal levels of catecholamine systems activity (CSA) mood is positive and activity and sociability are adaptive. At very low or very high levels of CSA mood is dysphoric, activity is restricted or stereotyped, and the organism is unsocial or aggressively antisocial. Novelty, in the absence of threat, may be rewarding through activation of noradrenergic neurons.

The development of lateral inhibitory interactions in the infant visual system, as reflected by the visual-evoked potential (VEP), was studied using a radial, asymmetrical windmill-dartboard stimulus. This contrast-reversing stimulus generates VEP responses with a strong fundamental frequency component and an attenuated second harmonic component (relative to that obtained using a symmetrical stimulus). These two harmonic components reflect distinct phenomena, and appear to be the result of short-range (the fundamental) and long-range (attenuated second harmonic) lateral inhibitory interactions elicited by differential luminance-modulation of contiguous spatial regions. We studied the development of the short-and long-range interactions at 100% and 30% contrast in human infants using both VEP amplitude and phase measures. Attenuation of the second harmonic (long-range interactions) was adult-like by 8 weeks of age while the strength of the fundamental (short-range interactions) was adult-like by 20 weeks suggesting a differential development of long-range and short-range interactions. In contrast, corresponding phase data indicated significant immaturities at 20 weeks of age for both the short-and long-range components.

We have recorded steady-state visual evoked potentials (VEPs) from patients with vascular damage to their right brain hemispheres, some suffering from unilateral spatial neglect (n = 9), and some not (n = 7). VEPs were recorded in response to sinusoidal gratings of 0.56 cycle/deg contrast-reversed sinusoidally at temporal frequencies from 4–11 Hz. Stimuli were presented either to the left or to the right visual field, or to both. Confirming previous reports, reliable VEPs were recorded from stimuli in the left contralesional hemifield, of comparable amplitude to those of the ipsilesional hemifield and to those of both hemifields of brain damaged patients without neglect. However, analysis of apparent latency derived from phase data showed that the VEPs from the contralesional hemifield were systematically delayed by 30–40 ms compared with those of the ipsilesional hemifield, and compared with both hemifields of the nonneglect groups. This result suggests changes in neural processing in neglect patients.

Tectal evoked potentials (TEPs) in response to sinusoidal gratings of different contrast, spatial and temporal frequency have been recorded from the tectal surface of the pigeon. Responses have been digitally filtered in order to isolate transient oscillatory (fast) potentials (50–150 Hz), transient slow potentials (1–50 Hz), and the steady-state second-harmonic component (16.6 Hz). Transient slow potentials, as well as the steady-state second-harmonic component, are band-pass spatially tuned with a maximum at 0.5 cycles/deg and attenuation at higher and lower spatial frequencies. The high spatial frequency cutoff is 4–5 cycles/deg. Both transient slow potentials and the steady-state second-harmonic component increase in amplitude as a function of log contrast and saturate at about 20% contrast. The contrast sensitivity, as determined by extrapolating TEP amplitude to 0 V is 0.1–0.2%. These characteristics of spatial-frequency selectivity and contrast sensitivity are similar to those reported for single tectal cells. Unlike slow potentials, oscillatory potentials are not band-pass spatially tuned. In addition, their contrast response function does not saturate at moderate contrast. These differences suggest that tectal evoked slow and fast potentials reflect the activity of different neuronal mechanisms.

We recorded visual evoked potentials in response to square-wave contrast-reversal checkerboards undergoing a transition in the mean contrast level. Checkerboards were modulated at 4.22 Hz (8.45-Hz reversal rate). After each set of 16 cycles of reversals, stimulus contrast abruptly switched between a “high” contrast level (0.06 to 1.0) to a “low” contrast level (0.03 to 0.5). Higher contrasts attenuated responses to lower contrasts by up to a factor of 2 during the period immediately following the contrast change. Contrast-response functions derived from the initial second following a conditioning contrast shifted by a factor of 2–4 along the contrast axis. For low-contrast stimuli, response phase was an advancing function of the contrast level in the immediately preceding second. For high-contrast stimuli, response phase was independent of the prior contrast history. Steady stimulation for periods as long as 1 min produced only minor effects on response amplitude, and no detectable effects on response phase. These observations delineate the dynamics of a contrast gain control in human vision.

Visual tasks that are perceptually diverse might be expected to elicit unique evoked-potential waveforms that exhibit differing topographic maps. To investigate this possibility, multichannel visual-evoked potentials (VEPs) were recorded in response to several dot spatial localization stimuli that are physically similar yet produce different percepts (vernier offsets, stereoscopic disparity, bisection, orientation, and relative displacement) to determine if the unique percepts arising from these stimuli reflect the activation of different cortical neural populations. The resulting evoked potentials were all similar in waveform, although the stereoscopic VEPs were relatively delayed. Topographic maps of the evoked-potential activity to each stimulus revealed a late major component with two independent foci: one 7 or more centimeters above the inion lateral to the midline, and the other at least 6 cm lateral to Oz. The scalp localization of both peaks was independent of both the position of the stimulus in the visual field and the particular stimulus cue presented. An asymmetric response to pattern appearance vs. disappearance indicated strong pattern specificity for each stimulus type except unreferenced motion. The timing of the VEP responses and relative insensitivity to retinal locus of stimulation suggest the involvement of higher cortical areas. The two map foci might be interpreted as activation of inferotemporal and parietal cortices whose roles are thought to be visual object interpretation and spatial attention and localization, respectively.

We investigated the intracortical organization of neuronal mass activity that is related to texture segregation on the basis of orientation contrast. Evoked potentials were recorded to a stimulus, signalling a contribution from texture segregation-sensitive mechanisms by means of specific response components. The specific components could only be recorded when textons had a spatial organization that leads to the percept of image segmentation. Equivalent dipole estimations of the specific response components suggested the presence of texture segregation-related activity in the primary visual cortex. These results were corroborated by current-source-density analysis of intracortical recordings in the awake monkey. A specific involvement of layers 2/3 and 5 of area 17 in the global process of image segmentation could be demonstrated.

The most informative neurophysiological techniques available in the neurosurgical intensive care unit are electroencephalograph and somatosensory evoked potentials. Such tools, which give an evaluation of cerebral function in comatose patients, support clinical evaluation and are complementary to neuroimaging. They serve both diagnostic/prognostic and monitoring purposes. While for the former, discontinuous monitoring is sufficient, for the latter, to obtain increased clinical impact, continuous monitoring is necessary. To perform and interpret these examinations in the neurosurgical intensive care unit, both the technician and the neurophysiologist need specific training in the intensive care field. There is sufficient evidence to show that somatosensory evoked potentials are the best single indicator of early prognosis in traumatic and hypoxic-ischaemic coma compared to the Glasgow Coma Score, computed tomography scan and electroencephalograph. Indeed, somatosensory evoked potentials should always be combined with clinical examination to determine the prognosis of coma. Despite widespread use of somatosensory evoked potentials and their prognostic utility in acute brain injury, few studies exist on continuous somatosensory evoked potential monitoring in the intensive care unit. We carried out a pilot study of continuous electroencephalograph-somatosensory evoked potential monitoring in the neurosurgical intensive care unit (traumatic brain injury and intracranial haemorrhage, Glasgow Coma Score <9, intracranial pressure monitoring). All patients stable from a clinical and computed tomography scan point of view showed no significant somatosensory evoked potential modifications, while in the case of clinical deterioration (23%), somatosensory evoked potentials always showed significant modifications. While somatosensory evoked potentials correlated with short-term outcome, intracranial pressure showed a poor correlation. We believe neurophysiological monitoring is an ideal complement to the other parameters monitored in the neurosurgical intensive care unit. Whereas intracranial pressure is simply a pressure index, electroencephalograph-somatosensory evoked potential monitoring reflects to what extent cerebral parenchyma still remains metabolically active during acute brain injury.