The relationship between reaction time and response variability and somatosensory No-go potentials

We investigated the relationship between reaction time (RT) and response variability and somatosensory Go/No-go potentials. Event-related potentials following electrical stimulation of the second (Go stimulus) or fifth (No-go stimulus) digit of the left hand were recorded from 16 subjects, and Go and No-go stimuli were presented at an even probability. The subjects were instructed to respond to the Go stimuli by pushing a button with their right thumb. We analyzed the correlation between RT and the N140 and P300 components, and between the standard deviation (SD) of RT and the N140 and P300. Neither the amplitude nor latency of the No-go-N140 (N140 evoked by No-go stimuli) or the Go-N140 (N140 evoked by Go stimuli) related significantly with RT and the SD of RT. There was a significant negative correlation between RT and the amplitude of the No-go-P300 (P300 evoked by No-go stimuli) at Fz and C3, indicating that subjects with a shorter RT had a No-go-P300 of larger amplitude. The latency of the Go-P300 (P300 evoked by Go stimuli) at Pz and C3 showed a significant correlation with RT. The SD of RT was significantly correlated with the amplitudes of the No-go-P300 at C3 and Go-P300 at Pz and C4, and the latency of the No-go-P300 at Cz and Go-P300 at Fz, Cz, Pz, C3, and C4. Our results suggest that response speed and variability for the Go stimulus in Go/No-go paradigms affect No-go-related neural activity for the No-go stimulus.     

Behavior related to trained increase in visual cortex excitability

Operant conditioning techniques were utilized to train cats to increase the amplitude of the short latency (5 msec) cortical response evoked by electrical stimulation of the optic radiation fibers. The cats learned to produce larger evoked potentials, and two distinctly different behaviors were associated with such increase. The first was a general relaxation of skeletal activity. The second was a brisk movement of the head, associated with a transient increase in excitability, lasting several hundred msec, with the maximum effect occurring about 250 msec after a warning stimulus.     

Gating of the Auditory Evoked Potential in Children and Adults

Auditory evoked potentials were recorded from 163 subjects, aged IS months to 55 years. A conditioning-testing paradigm was used to assess sensory gating. In this paradigm, click stimuli are presented in pairs to the subjects with a 0.5-second intrapair interval. In normal adults, the first stimulus activates or “conditions” sensory gating mechanisms. The strength of these mechanisms is “tested” by the second stimulus, which produces a response whose amplitude is significantly suppressed. This aspect of sensory gating was not reliably observed in our subjects until age 18 years. Younger subjects varied widely in their ability to demonstrate sensory gating. Mean levels of suppression increased during late childhood and adolescence, with no relationship to other changes in evoked potential amplitude and latency. Sensory gating would appear to be a late developing aspect of human sensory physiology.     

Effects of ISI and stimulus probability on event-related go/nogo potentials after somatosensory stimulation

The present study investigated the characteristics of the middle-latency negative potential of event-related potentials (ERPs) using somatosensory go/nogo tasks. We manipulated interstimulus interval (ISI) in Experiment 1 and stimulus probability in Experiment 2 and analyzed the subtracted difference waveform resulting from subtraction of the ERP evoked by the go stimulation from that evoked by the nogo stimulation. In Experiment 1, the peak latency of negativity became significantly longer as the ISI increased, but the peak amplitude was unchanged. The reaction time (RT) was longer with increasing ISI. In Experiment 2, manipulation of the stimulus probability yielded an increase in peak amplitude with decreasing probability of the nogo stimulus, but did not affect the latency. The RT increased as the probability of a nogo stimulus rose. Because manipulation of the ISI and stimulus probability elicited different brain activities, we hypothesized that manipulation of the ISI elicited a delay of the stimulus evaluation process including response inhibition, and that stimulus probability significantly affected the strength of the response inhibition process.     

Double stimulation modulates afterhyperpolarization phase following action potentials evoked in rat motoneurones

The influence of a pair of stimuli running in time sequence between 5-10 ms (a doublet) on the basic parameters of antidromic action potentials was studied in rat motoneurones. Electrophysiological experiments were based on stimulation of axons in the sciatic nerve and intracellular recording of antidromic action potentials from individual motoneurones located in L4-L5 segments of the spinal cord. The following parameters were analyzed after application of a single stimulus and a doublet: amplitude and duration of the antidromic spike, amplitude, total duration, time to minimum, half-decay time of the afterhyperpolarization (AHP). It was demonstrated that application of a pair of stimuli resulted in: (1) a prolongation of action potentials, (2) a prolongation of the total duration and half-decay time of the AHP, (3) a decline of the time to minimum of the AHP, (4) an increase of the AHP amplitude of the spike evoked by the second stimulus. Significant differences in AHP parameters were found either in fast or slow motoneurones. We suppose that doublet-evoked changes in the AHP amplitude and duration are linked to intrinsic properties of individual motoneurones and may lead to the prolongation of the time interval to subsequent motoneuronal discharges during voluntary activity.     

Projection from the thalamic intralaminar nuclei on the isocortex of the rat: a surface potential study

Summary Cortical surface potentials evoked from thalamic intralaminar nuclei have been studied in rats anaesthetized with chloralose. Stimulation with low current intensity in central lateral nucleus (CL), evoked potentials in large areas of the rat isocortex. In the posterior parietal cortex responses with a short latency negativity were evoked which followed high frequency repetitive stimulation. Its latency and ability to follow high frequency stimulation indicated a monosynaptic connection from CL to this part of the cortex. The short latency potential was followed by a second negativity with longer latency and varying amplitude. This second negativity did not follow repetitive stimulation exceeding 10 Hz, and was also reduced by supplementary doses of anaesthetics, indicating a polysynaptic origin. Stimulation at different CL sites elicited cortical potentials with short latency in a topographical pattern. Laminar analysis in the parietal and motor cortex suggested both a superficial and a deep layer termination of afferents from CL. Similar topografical relations and afferent layer distributions have previously been found in cats. The role of the thalamocortical projection from CL to parietal cortex in arousal, attention and pain mechanisms is discussed.     

Scalp topography and analysis of intracranial sources of face-evoked potentials

Several reports have described that a positive vertex peak of an evoked potential varied in amplitude and latency specifically when images of faces were the eliciting stimulus. The scalp topography and the possible underlying dipole sources of this peak are the subject of this report. We presented black-and-white photographs of human faces, flowers and leaves to 16 healthy subjects and recorded the evoked brain potentials from 31 scalp electrodes. We found the previously described higher amplitude of the positive vertex peak when faces were the crucial stimulus, but the latency of this peak was the same (180 ms) for all three categories of stimulus. At the posterior temporal electrodes, the face waveforms showed a negative peak at 175 ms, which was only rudimentary in the waveforms elicited by the other stimuli. Since in most previous reports a mastoid reference was used, it is most likely that the previously described latency shift of the positive vertex peak associated with face stimuli was due to the interaction with this posterior temporal peak. The dipole analysis of the possible generators of the recorded potentials suggested the sequential activation of occipital, lateral temporal and mesio-temporal brain structures during the perception of a human face.     

The three-neuron corneal reflex circuit and modulation of second-order corneal responsive neurons

Neurons located in the border region between the interpolaris and caudalis subdivisions of the spinal trigeminal nucleus (Vi/Vc) are second order neurons of the corneal reflex, receiving corneal afferents and projecting to the lid closing, orbicularis oculi (OO) motoneurons. Recordings of Vi/Vc neurons identified by antidromic activation from stimulation of the facial nucleus and non-identified Vi/Vc neurons reveal two neuron types, phasic and tonic. Corneal stimulation elicits Aδ latency action potentials that occur early enough to initiate OO contraction and C-fiber latency action potentials that can modulate the end of the blink in phasic Vi/Vc neurons. Tonic Vi/Vc neurons exhibit a constant irregular, low frequency discharge as well as the cornea-evoked activity exhibited by phasic neurons. For both phasic and tonic neurons, blink amplitude increases with the total number of spikes evoked by the corneal stimulus. Peak firing frequency predicts peak orbicularis oculi EMG activity. Paradigms that suppress cornea-evoked blinks differentially affect Vi/Vc neurons. Microstimulation of the border region between the spinal trigeminal caudalis subdivision and the C1 spinal cord (Vc/C1) significantly reduces the number of spikes evoked by corneal stimulation and suppresses blink amplitude. In the paired stimulus paradigm, a blink evoked by a corneal stimulus 150 ms after an identical corneal stimulus is significantly smaller than the blink elicited by the first stimulus. Vi/Vc neuron discharge, however, is slightly larger for the second blink. Our data indicate that second-order Vi/Vc neurons do not determine the specific pattern of OO muscle activity; rather Vi/Vc neurons initiate OO motoneuron discharge and program the activity of another circuit that generates the late phase of the blink. The Vc/C1 suppression of Vi/Vc neurons suggests that the Vc/C1 region provides an “internal model” of the intended blink.     

Effects of intensity of repetitive acoustic stimuli on neural adaptation in the ventral cochlear nucleus of the rat

To study neural adaptation as a function of stimulus intensity, auditory near-field evoked potentials were recorded from the ventral cochlear nucleus in awake Long Evans rats. Responses to 250-ms trains of repetitive clicks (pulse rates ranging from 100 to 1000 pulses per second) were collected at stimulus intensities of 5, 10, 30, 50 and 70 dB SPL. The amplitude of the first negative (N₁) component of the average evoked potentials to individual pulses in the train was measured by using a subtraction method. The N₁ responses were normalized with respect to the highest cochlear nucleus potential observed in the train, and then plotted as a function of click position in the train. As expected, the general trend of the curves was an exponential decay reaching a plateau more or less rapidly as a function of both intensity and rate of stimulation. Fitting these curves with exponential decay equations revealed that the rapid time constant decreased for increasing stimulus intensities whereas the short-term time constant is relatively independent of intensity. The amount of adaptation (expressed as the ratio of the plateau to the first peak amplitude) was substantially less prominent at low intensities (5–10 dB SPL) and low rates (100–200 pulses per second) than at higher intensities and high rates. These results indicate that adaptation patterns obtained in the ventral cochlear nucleus by using near-field evoked potentials exhibit properties comparable to those already present at the level of the auditory nerve.     

Auditory N1 as a change-related automatic response

To test the hypothesis that the N1 component of auditory evoked potentials (AEPs) is one form of the change-related response elicited by an abrupt change in sound pressure from a silent background, two AEP experiments were conducted. Change-N1 was evoked by a test stimulus at 70 dB following a 3-s conditioning stimulus of 0-69 dB. On-N1 was evoked by the test sound alone at various sound pressures. As the physical difference between stimuli increased, the amplitude of Change-N1 increased, and the latency shortened. The amplitude and latency of On-N1 showed a similar pattern to the Change-N1 response. These results support the idea that On-N1 is a change-related component elicited by a sound pressure change.     

CORTICAL RESPONSE TO A TACTILE STIMULUS DURING ATTENTION, MENTAL ARITHMETIC AND FREE ASSOCIATIONS

Attention to a stimulus appears to be associated with amplitude fluctuations in 100-msec or later components of the cortical compound evoked potential (CEP). In this study, changes in amplitude and latency of the CEP to the same tactile stimulus were investigated under three conditions: attention, free associations, and mental arithmetic. In the attention condition Ss were asked to estimate varying time intervals between stimuli on a 2- to 6-sec scale. Ss were 12 pairs of twins. It was found that the amplitudes of two negative electrocortical potentials were greater when Ss were estimating lengths of time intervals between stimuli than during free association or mental arithmetic. Peak latency of the second negative potential was greater in attention than in the other two conditions. Free association CEPs were distinguished by the incidence of a bursts. The results support the hypothesis that attention is associated with certain parameters of the electrocortical response and suggest which aspects of the electrocortical response are most likely to be related to attention.     

Phasic pupil dilation response to noxious stimulation in normal volunteers: relationship to brain evoked potentials and pain report

Pupillary response to noxious stimulation was investigated in men (n = 11) and women (n = 9). Subjects experienced repeated trials of noxious electrical fingertip stimulation at four intensities, ranging from faint to barely tolerable pain. Measures included pupil dilation response (PDR), pain report (PR), and brain evoked potentials (EPs). The PDR began at 0.33 s and peaked at 1.25 s after the stimulus. Multivariate mixed-effects analyses revealed that (a) the PDR increased significantly in peak amplitude as stimulus intensity increased, (b) EP peaks at 150 and 250 ms differed significantly in both amplitude and latency across stimulus intensity, and (c) PR increased significantly with increasing stimulus intensity. Men demonstrated a significantly greater EP peak amplitude and peak latency at 150 ms than did women. With sex and stimulus intensity effects partialled out, the EP peak latency at 150 ms significantly predicted PR, and EP peak amplitude at 150 ms significantly predicted the PDR peak amplitude.     

The evoked K-complex: all-or-none phenomenon?

The functional significance and topographical variation of the different components of the evoked K-complex were examined. In the first experiment, the intensity of the stimulus (80 and 60 dB SPL) and its rise-and-fall time (2 and 20 milliseconds) were manipulated during nonrapid eye movement sleep. In the second experiment the tonal frequency (500, 1,000 and 2,000 Hz) of the stimulus was manipulated. In the first experiment, nine stimuli were presented every 10 seconds, whereas in the second, 20 consecutive stimuli were presented. The evoked K-complex consisted of two different negative components peaking at approximately 350 and 550 milliseconds, respectively, and followed by a positive component peaking at approximately 900 milliseconds. K-complexes were easier to elicit for high-intensity fast rise-and-fall time stimuli than for low-intensity slow rise-and-fall time stimuli. The probability of occurrence was not affected by the tonal frequency of the stimulus. When a K-complex was evoked, the amplitude and latency of N350, N550 and P900 remained invariant regardless of its intensity, rise-and-fall or its tonal frequency. The N550-P900 portion of the K-complex therefore appears to be an all-or-none phenomenon. On trials in which a K-complex could not be elicited, N350 was still visible although much attenuated. In these trials, its amplitude was further reduced when stimulus intensity was lowered. N350 might need to reach a certain critical threshold before the much larger N550-P900 complex is elicited.     

Transducer action of isolated frog muscle spindle evoked by pseudorandom noise stimuli

The dynamic response properties of the isolated frog muscle spindle receptor were investigated by recording the receptor potential evoked by pseudorandom noise (PRN) stimuli. The entire dynamic range of the receptor was determined by measuring the sensory response either at different intensities of the PRN stimulus (sigma = 8-30 microns) around a constant mean length or at the same intensity while varying the mean length from resting length L0 up to L0 + 150 microns. The 3-dB bandwidth of the test signal was 130 Hz. Random stimuli often evoked brief receptor potentials with variable size but characteristic shape. This shape contained a fast depolarization transient of the receptor potential during the stretching phase of the stimulus and a slowly decaying repolarization transient during release of stretch. The depolarization transient rose faster in proportion to the increasing amplitude of the receptor potential, so that larger receptor potentials were more phasic in character than smaller ones. The repolarization transient exhibited two segments of different exponential decay: The first brief repolarization phase lasted for 5 ms; its decline (tau = 2-5 ms) was faster for larger receptor potentials. The second slowly decaying repolarization transient was the same for different receptor potential amplitudes (tau = 47 ms). Consequently, the slow repolarization transients of succeeding receptor potentials displayed temporal summation. Since the amplitude and shape of the receptor potential remained constant during repeated sequences of PRN stimuli, this test stimulus was the most appropriate for the investigation of dynamic response properties under stationary conditions. Long-term stimulation caused a small shift of the mean membrane voltage towards hyperpolarizing values. This finding together with the marked "off effect" after termination of the stimulus indicate the action of an electrogenic pumping mechanism. The dynamic range of the muscle spindle receptor extended from resting length L0 up to L0 + 100 microns. Within this range static prestretches placed a bias upon the transducing site and effectively enhanced the amplitude of the receptor potential. Further prestretch beyond the dynamic region kept the receptor potential constant at its maximum amplitude. The receptor potential amplitude distribution was not symmetrical about the mean but was skewed in favor of depolarization values responding to the stretch trajectories of the PRN stimulus. Variation of the operating point by increasing the static prestretch also shifted the mode of the response distribution towards depolarization.(ABSTRACT TRUNCATED AT 400 WORDS)     

Phases in the development of a penicillin epileptiform focus in rat neocortex

Somatosensory evoked potentials and potentials evoked by direct cortical stimulation were recorded from layer IV of the somatosensory area of the cerebral cortex in urethane anaesthetised rats. Penicillin was expelled electrophoretically from the tip of a drug-filled micropipette at constant rates into layer IV. Small fluxes of penicillin (with electrophoretic currents of -50 to -90 nA) resulted in the appearance, after a delay of 1–2 min, of an enhancement of amplitude in the voltage of both types of evoked potential, unaccompanied by any prolongation of the waveform or spontaneous focal epileptiform discharges. The amplitude of the enhanced evoked potential exhibited a strength-response curve which was a scaled-up version of the curve before penicillin, the scaling factor reflecting the enhancement of amplitude. As the interval between a pair of stimuli was increased, the magnitude of the response to the second stimulus recovered, following a time course similar to that before penicillin. With larger fluxes of penicillin (with electrophoretic currents of -250 to -1000 nA) the amplitude of evoked potentials rose more rapidly and to a higher level; as the concentration of penicillin rose, this enhancement of amplitude led into a second phase, in which there was additionally an increase in the duration of the evoked potentials and the appearance of spontaneous epileptiform discharges. The evoked potentials in this situation showed physiological properties different from those before penicillin application. The strength-response curve exhibited a discontinuity, indicating the evoked potential to be the sum of a physiological response and an epileptiform discharge, the former being graded with stimulus strength and the latter being all or none. With paired stimuli, the response to the test stimulus was profoundly depressed for long conditioning-test intervals by comparison with the relatively rapid recovery exhibited by normal brain. When a cuboid of cortex measuring 0.6 mm² or less was partially isolated subpially by incisions extending through the upper half of the cortical mantle, all the features of hyperexcitability produced by penicillin in intact cortex were blocked. This shows that even the simple enhancement of evoked potentials, which is the earliest indicator of hypersynchronous activity, differs from an exaggeration of normal evoked activity in requiring a larger community of neurones with their horizontal intracortical connections intact.     

Afferent control of human stance and gait: evidence for blocking of group I afferents during gait

Summary The cerebral potentials (c.p.) evoked by electrical stimulation of the tibial nerve during stance and in the various phases of gait of normal subjects were compared with the c.p. and leg muscle e.m.g. responses evoked by perturbations of stance and gait. Over the whole step cycle of gait the c.p. evoked by an electrical stimulus were of smaller amplitude (3 V and 9 V, respectively) than that seen in the stance condition, and appeared with a longer latency (mean times to first positive peak: 63 and 43 ms, respectively). When the electrical stimulus was applied during stance after ischaemic blockade of group I afferents, the c.p. were similar to those evoked during gait. The c.p. evoked by perturbations were larger in amplitude than those produced by the electrical stimulus, but similar in latencies in both gait and stance (mean 26 V and 40 V; 65 ms and 42 ms, respectively) and configurations. The large gastrocnemius e.m.g. responses evoked by the stance and gait perturbations arose with a latency of 65 to 70 ms. Only in the stance condition was a smaller, shorter latency (40 ms) response seen. It is concluded that during gait the signals of group I afferents are blocked at both segmental and supraspinal levels which was tested by tibial nerve stimulation. It is suggested that the e.m.g. responses induced in the leg by gait perturbations are evoked by group II afferents and mediated via a spinal pathway. The c.p. evoked during gait most probably reflect the processing of this group II input by supraspinal motor centres for the coordination of widespread arm and trunk muscle activation, necessary to restablish body equilibrium.     

Evidence for multiple generators in evoked responses using finite difference field mapping: Auditory evoked fields

Summary Electric potential maps and magnetic field maps have been used to study brain electrical activity. During the temporal course of an evoked cortical response, the electrical activity of specific neuronal subpopulations change in a sequential manner giving rise to measurable electrical potentials and magnetic fields. For these potentials and fields, both the amplitude and rate of amplitude change have characteristic, time-dependent waveforms. Presently, amplitude waveforms from multiple locations are used to generate magnetic field and electric potential maps which have been found to be useful in understanding the activity of the neurons which give rise to these maps (Romani 1990). This paper introduces a data transformation technique which results in a derived map that we have termed a "finite difference field map" (FDFM). This mapping technique provides information associated with the rate at which the amplitude of the neuronal electric activity changes. In this paper, some advantages of FDFM analysis are illustrated by application of this technique to the study of the auditory evoked cortical field (AECF) N1m waveform. Using data obtained from normal subjects it will be demonstrated that application of the FDFM technique allows the localization of the primary N1m source at an earlier latency than is possible using the conventional waveform data. The source location determined at an early latency by FDFM analysis was identical to that obtained at later latency from the conventional field data. These data suggest that the primary N1m source is stationary. In addition, analysis of the time sequence of FDFM field maps contains evidence of a second spatially separate source which is co-active with primary N1m source.     

Changes of motor cortical excitability in human subjects from wakefulness to early stages of sleep: a combined transcranial magnetic stimulation and electroencephalographic study

The effect of sleep on human motor cortical excitability was investigated by evaluating the latency and amplitude of motor evoked potentials in ten subjects using transcranial magnetic stimulation. Motor evoked potentials and electroencephalographic data were recorded simultaneously and analyzed. Recordings were performed before, during and after a sleep period. A significant decrease in motor evoked potentials amplitude and a slight change in motor evoked potentials latency were noted in the recordings during the different sleep stages with a return to baseline values on awakening. A decrease in motor cortical excitability is suggested as explaining the effect of sleep.     

Cerebral Dynamics of SEPs to Non-Painful and Painful Cutaneous Electrical Stimulation of the Thenar and Hypothenar

Early, middle and late latency somatosensory evoked potentials (SEPs) elicited by cutaneous electrical stimulation (painful vs. non-painful) of right and left hands were recorded. The aims were to study (1) if lifelong use of dominant right hand would result in different SEP topographies compared to non-dominant left hand stimulation, (2) if painful and non-painful stimuli resulted in different SEP activation patterns for the different latency components and (3) if these results were consistent between two areas of the hand. Electrical stimuli were applied cutaneously above the thenar and hypothenar muscles of the left and right hand. A two-way repeated measures ANOVA was used to test the effects of laterality and intensity for a given peak amplitude and latency. Statistical results yielded no significant difference in peak amplitude for either thenar and hypothenar between the two hands. In contrast, a significant difference in amplitude was observed for 6 components for each stimulus location when the two intensities were compared. These components were found at early, middle and late latencies. No significant latency shift was observed between the two hands. Only the P30 component showed a significant latency shift for both locations with the painful condition having the shorter latency. Thus, life-long use of the dominant hand does not generate detectable changes in cortical evoked activity to sensory input from the skin above thenar and hypothenar muscles. Several SEP components across the time course (0-400 ms) showed increased amplitude when the stimulus was increased from non-painful to painful intensity.     

Emitted and Evoked P300 Potentials and Variation in Stimulus Probability

There have been a number of reports of a cerebral potential occurring at about the time of an expected but absent stimulus when absence provided significant information for the subject. This potential consists primarily of a positive peak occurring with a latency of about 300 msec with respect to the time of stimulus absence and is referred to as an emitted P300 potential. It has been conjectured that the emitted P300 is a manifestation of the same process that underlies the evoked P300 . Evidence supporting this hypothesis is provided by demonstrating that both the evoked and emitted P300 potentials are similarly affected by variation in event probability. A paradigm was used in which click presence and absence provided information. The relative probability of click presence and absence was experimentally manipulated. Both evoked and emitted p300 amplitude responded in the same way to event probability, larger for the less frequent event and smaller for the more frequent event.