Middle- and long-latency auditory evoked responses recorded from the vertex of normal and chronically lesioned cats

A prolonged sequence of auditory evoked potentials with latencies ranging from 1 to 250 msec was recorded from the vertex of the awake restrained cat. This sequence was reproduceable within and across subjects and was not altered by complete neuromuscular paralysis. The effects of click rate, pentobarbital, and chronic lesions of a number of different brain areas were evaluated for each of the potentials. Vertex waves 1–5, previously shown to originate from generators in the primary auditory pathway of the brain stem, were followed by smaller and less well defined waves 6 and 7, with peak latencies in the 6–8 msec and 10–12 msec range respectively. These potentials were not abolished by fast click rates (i.e. up to 50/sec) nor by moderate levels of pentobarbital. Correlative extra- and intracranial studies indicated that wave 6 occurred in the same latency range as the medial geniculate body, pars principalis potential, and that wave 7 occurred in the same latency range as the primary ectosylvian cortical potential. The intracranial potentials showed click recovery functions and barbiturate resistance which were similar to those of waves 6 and 7, and wave 7 disappeared following aspiration of ectosylvian cortex. These data suggest that waves 6 and 7 reflec generators in medial geniculate body and ectosylvian gyrus.In contrast to the stability of potentials 1 through 7, the longer latency waves were relatively unstable. Wave A occurred in a latency range of 17–25 msec, wave B, 35–45 msec, wave C, 50–75 msec, and wave D, 150–200 msec. All of these waves showed marked amplitude fluctuations, disappeared as click rates increased to 10/sec, and were abolished by moderate levels of pentobarbital. After bilateral aspiration of middle suprasylvian gyrus, ectosylvian gyrus, or frontal lobes, wave A continued to appear. After hemispherectomy, which removed all cortex, basal ganglia and limbic lobes, wave A was not abolished and appeared enhanced in one animal. Thus, the generator system of wave A appears to be largely independent of auditory cortex and adjacent association cortex, but may be modulated by other forebrain systems. Wave C continued to appear after aspiration of suprasylvian and ectosylvian gyri and after frontal lobectomy, but disappeared after hemispherectomy. Thus, wave C reflects a generator system which differs from that of wave A, but which also appears to be largely independent of the primary geniculo-cortical auditory pathway.These data suggest the following conclusions: waves 1 through 7, which show high fidelity, rate-resistant, barbiturate-insensitive acoustic transmission, appear to reflect activation of the primary auditory system from acoustic nerve to auditory cortex. Subsequent, longer-latency vertex potentials seem to be generated through other forebrain systems which receive auditory information in parallel from the brain stem, rather than serially from the primary geniculo-cortical pathway and association cortex relays. The relevance of data in the cat model to the human vertex potentials is discussed.     

Frontal cortex stimulation evoked neostriatal potentials in rats: intracellular and extracellular analysis

Evoked potentials, action potentials and intracellular events were recorded in the neostriatum of urethane anesthetized rats to electrical stimulation of frontal cortex white matter, motor cortex and pre-limbic cortex. Five major waves of the evoked potential were identified. Wave N1 (3.9 msec latency) was small, preceded cellular events and probably represents activation of corticostriate terminals. Wave P1 (10.8 msec latency to peak following white matter stimulation) coincided with an EPSP and neuronal firing. Both wave N2 (38.0 msec latency to peak) and P2 (approximately 110 msec duration) overlapped the intracellularly recorded hyperpolarization and inhibition of cell firing. Based upon this correspondence and upon the behavior of waves N2 and P2 with changing current and during conditioning-test paired pulse stimulation, it was concluded that the waves represent different processes contributing to the cellular hyperpolarization. A late wave, N3 (175 msec onset latency) corresponded to a late rebound firing and cellular depolarization. This late wave was eliminated from the neostriatum, but not from the overlying sensorimotor cortex, by kainic acid lesions that destroyed medial thalamus but left thalamic lateral nuclei and reticular nucleus intact.     

Evidence for the presence of eye movement potentials during paradoxical sleep in cats.

1. Phasic activities related to eye movements in the dark in abducens nucleus (N.VI), lateral geniculate body (LGB), visual cortex, and lateral rectus muscle were analyzed in 18 cats with chronically implanted electrodes during waking and sleeping. 2. N.VI waves, both during waking and sleeping, were multiphasic, and two distinct wave forms were noticed on either side of the pons. The N.VI waves preceded each ocular movement by 10--20 msec. 3. Both during waking and paradoxical sleep (PS), N.VI waves always preceded those occurring in the LGB. During waking, eye movement potentials (EMPs) in LGB followed the onset of the N.VI wave with a long (greater than 60 msec) and variable latency, but followed the end of the same wave with a rather constant delay (about 20 msec). During PS, two distinct populations of latency were observed between onset of the pontine waves and that of LGB waves. The latency of one population was less than 35 msec, and of the other more than 66 msec. 4. Since the LGB waves following N.VI waves with a long latency were similar in a number of respects to EMPs during wakefulness (EMPw), they were judged to be EMPs (EMPps), and were distinguished from LGB PGO waves, which followed N.VI waves with a short latency. Cortical EMPps were observed as well, but occurred about 8--10 times less frequently than the PGO wave. 5. In the light of the present results, the mechanisms responsible for EMP and PGO wave activities are discussed.     

Evolution of visual evoked responses during various states of vigilance in Papio papio (author''s transl)]

Averaged evoked responses (AER) to light flashes were recorded in baboons (Papio papio) during wakefulness, slow-wave sleep and rapid eye movement (REM) periods, at the visual cortex, retrocalcarine sulcus, optic tract (OT), lateral geniculate (LG) and pulvinar.

Waking AERs were composed: in the OT, of a negative, low amplitude wave at 13.3 msec (I), a high amplitude wave at 34.8 msec (II), a negative wave at 72 msec (III) and a late component at 151 msec; in the LG, a small positive wave (II) with a peak latency of 40 msec, a high amplitude negative wave (III) with a latency of 70 msec and a late component; in the pulvinar of two low amplitude short latency waves (I and II), respectively negative and positive at 25 msec and 40 msec, then a high amplitude negative wave (III) at 75 msec and a late component; in the retrocalcarine sulcus 3 positive waves (I, II and III) were recorded at 25, 45 and 100 msec and a late component; in the visual cortex, 3 low amplitude negative waves (II, III and IV) at 40, 50 and 54 msec, then a positive wave at 80 msec and some late components.

In slow-wave sleep, AERs did not change in the OT, but in the LG and pulvinar, they showed an increase in the amplitude of wave II from stage 1 to stage 3. At the cortical level, early waves (II for the retrocalcarine sulcus, II and IV for the visual cortex) presented a marked increase in amplitude during stages 2 and 3, but only a slight increase for stage 1. Peak latency increase of each wave in cortical and subcortical AERs was seen during slow-wave sleep.

REM AERs resembled, in amplitude and peak latency, those recorded in the LG and pulvinar during wakefulness; in the visual cortex and retrocalcarine sulcus, they were similar to those obtained during wakefulness and stage 1.

In conclusion, a different evoked response was found between visual cortex and deep structures (except for the OT): firstly, during slow-wave sleep (the AERs showed a difference for stage 1 between the visual cortex or the retrocalcarine sulcus and the LG or the pulvinar), secondly, in REM (on the cortex, REM AERs looked like wakefulness and stage 1 responses); on the contrary, in the LG and pulvinar, REM AERs were similar only to those recorded during waking. Finally, it can be said that for Papio papio the differentiation and structural responses between the various stages of sleep (particularly light sleep and REM) were greater in the cortex than in the thalamic structures.     

Évolution des réponses évoquées le long de la voie visuelle au cours du sommeil nocturne chez Papio papio

Averaged evoked responses (AER) to light flashes were recorded in baboons (Papio papio) during wakefulness, slow-wave sleep and rapid eye movement (REM) periods, at the visual cortex, retrocalcarine sulcus, optic tract (OT), lateral geniculate (LG) and pulvinar.Waking AERs were composed: in the OT, of a negative, low amplitude wave at 13.3 msec (I), a high amplitude wave at 34.8 msec (II), a negative wave at 72 msec (III) and a late component at 151 msec; in the LG, a small positive wave (II) with a peak latency of 40 msec, a high amplitude negative wave (III) with a latency of 70 msec and a late component; in the pulvinar of two low amplitude short latency waves (I and II), respectively negative and positive at 25 msec and 40 msec, then a high amplitude negative wave (III) at 75 msec and a late component; in the retrocalcarine sulcus 3 positive waves (I, II and III) were recorded at 25, 45 and 100 msec and a late component; in the visual cortex, 3 low amplitude negative waves (II, III and IV) at 40, 50 and 54 msec, then a positive wave at 80 msec and some late components.In slow-wave sleep, AERs did not change in the OT, but in the LG and pulvinar, they showed an increase in the amplitude of wave II from stage 1 to stage 3. At the cortical level, early waves (II for the retrocalcarine sulcus, II and IV for the visual cortex) presented a marked increase in amplitude during stages 2 and 3, but only a slight increase for stage 1. Peak latency increase of each wave in cortical and subcortical AERs was seen during slow-wave sleep.REM AERs resembled, in amplitude and peak latency, those recorded in the LG and pulvinar during wakefulness; in the visual cortex and retrocalcarine sulcus, they were similar to those obtained during wakefulness and stage 1.In conclusion, a different evoked response was found between visual cortex and deep structures (except for the OT): firstly, during slow-wave sleep (the AERs showed a difference for stage 1 between the visual cortex or the retrocalcarine sulcus and the LG or the pulvinar), secondly, in REM (on the cortex, REM AERs looked like wakefulness and stage 1 responses); on the contrary, in the LG and pulvinar, REM AERs were similar only to those recorded during waking. Finally, it can be said that for Papio papio the differentiation and structural responses between the various stages of sleep (particularly light sleep and REM) were greater in the cortex than in the thalamic structures.     

Electrophysiology of the frontal granular cortex. I. Patterns of focal field potentials evoked by stimulations of dorsomedial thalamus in conscious monkey

Focal field potentials and unit discharges of impulses evoked by low frequency (2–10/sec) stimulations of dorsomedial thalamus (DM) were simultaneously recorded with microelectrodes in the middle and inferior frontal gyri of the dorsal frontal granular cortex (FC) in the normal unanesthetized monkey.The depth profiles and sequences of responses of the FC evoked by the stimulations of DM were observed to be generally similar to the augmenting type of responses reported previously by others in the sensorimotor cortex of encéphale isoléor paralyzed cat.Stimulations of DM evoked short latency (3.2–4.0 msec) negative waves at a depth of 0.6–1.7 mm and correlated positive waves on the surface of the FC. Additional waves of alternating polarity succeeded the primary waves during augmenting sequences according to variations of stimulus strength and frequency. Unit discharges recorded with the same electrode simultaneously with field potentials revealed that a brief burst of 2–4 impulses occurred in association with each of the short latency deep negative waves evoked by repetitive stimuli. The latency of the earliest of the spikes of a burst was in the range of 6.5–9 msec. Following the burst of spikes, there was a long period of absence of spikes in each response.Surface corticograms of FC and nearby precentral cortex revealed that the evoked responses were highly pronounced and restricted to the frontal granular cortex and did not spread diffusely to the agranular cortex. Only a prolonged (40–60 sec) stimulation caused a synchronizing tendency in the corticogram of the agranular area. Furthermore, the evoked potentials in the corticogram of FC were presently only during quiet wakeful states, and became highly disorganized and almost indecipherable during states of synchronizing EEG and decreased consciousness as in natural slow-wave sleep or under Nembutal anesthesia.From these results, it is concluded that the dorsomedial thalamus is organized more like a specific thalamic nucleus to the frontal association cortex, and less like an integral part of the diffuse projection system.     

Postsynaptic reactions of neurons of the sensomotor cortex of the cat during evoked and self-sustained rhythmic activity of the "peak-wave" type

Intracellular correlates of evoked rhythmic cortical "spike-and-wave" potentials produced in sensorimotor cortex during 3/s stimulation of the thalamic relay nucleus (VPL) and of self-sustained "spike-and-wave" afterdischarges following 8-14/s stimulation of the same nucleus were studied in acute experiments on cats immobilized by myorelaxants. Intracellular recordings of pyramidal tract neurons revealed that different components of evoked "spike-and-wave" potentials, i. e. the spike-like negative wave and the long lasting negative wave, are postsynaptic in origin: the first is due to EPSPs with spike discharges, and the latter--to IPSPs of cortical neurons. Components of "spike-and-wave" afterdischarge mostly reflect the paroxysmal depolarizing shifts of the membrane potential of cortical neurons. After cessation of sustained "spike-and-wave" activity the long-lasting hyperpolarization accompanied by inhibition of spike discharges and subsequent recovery was observed in cortical neurons. It is presumed that the negative wave of the evoked "spike-and-wave" potential as well as slow negative potentials of direct cortical and primary responses reflect IPSPs of deeper parts of pyramidal tract neurons, while the waves of the sustained "spike-and-wave" afterdischarges are due to paroxysmal depolarizing shifts in cortical neurons.     

Current generators and properties of late components evoked in rat olfactory cortex

Following main olfactory bulb (MOB) stimulation at frequencies of 0.1-0.3 Hz, in addition to early field potentials, a frequency-sensitive, surface negative late N2 wave (latency range: 63-96 msec) followed occasionally by a late N3 transient, was evoked in the piriform cortex and endopiriform nucleus of the rat. The N2 wave inverted polarity at the Ib-II cortical layer interface (P2 wave) and was associated with late unit discharges 200 to 1200 microns deep to the turnover point. Response probability, peak latency, recovery curve and frequency-sensitivity of the P2 wave were not significantly different in animals under urethane or pentobarbital. Current-source-density (CSD) analysis revealed that the N2 wave generators were localized to the Ib-II layer interface. Since inhibitory activity does not contribute substantially to the second derivative curve, CSD analysis strengthens the assumption that late components (LCs) are excitatory events (compound EPSPs) presumably generated on the proximal apical dendritic segments of pyramidal cells by association axons. The early "b" wave in a test response was facilitated, rather than occluded, when a LC was present in the conditioning response, or when the priming volley was delivered to the mediodorsal thalamic nucleus. Clustering of unit and field activity in two distinct periods of the evoked response separated by a prolonged interval of cell silence suggests that cortical coding of olfactory cues might be more efficiently achieved by temporal modulation of the neuronal response rather than by spatial distribution of firing patterns.     

Electrophysiology of the frontal granular cortex. III. The cingulate-prefrontal relation in primate

An investigation of the nature of laminar potentials and impulse discharges of units of dorsolateral prefrontal cortex (FC) evoked by stimulations of cingulate gyrus was made in rhesus monkey.Anterior cingulate stimulations evoked 1.0–1.5 msec latency waves, positive on pial surface and negative at FC depths of about 500–2000 μm with about the same time scale. Following the positive wave there was also a negative wave response.The amplitude and duration of the surface positive wave and negative wave of response varied according to the state of background EEG of the area. During steady EEG the positive wave was well developed and the negative wave was incipient but during EEG oscillations, the positive wave was markedly diminished and the negative wave enlarged. The alteration of responsiveness was also confirmed in depths by changes of reversed polarity potentials corresponding temporally to surface potentials.Discrete responses of FC were evoked at stimulus frequencies of up to 20 Hz. Higher frequencies resulted in depression of responsiveness. Alternate responses were depressed between 20 and 40 Hz and all responses were progressively depressed with still higher frequencies.Impulse discharges of FC units were evoked either singly or in bursts by the cingulate stimulations. Single impulse responses were commonly found. Presumably monosynaptic responses were in the latency range of 1.2–3.0 msec. They were found at depths of about 500 μm and 1000 μm. Long latency (7 msec) responses were also observed in the upper levels of cortex. The latency of the unitary response of a multi-impulse burst was in the range of 6.5–16 msec and the frequency of impulses in burst was in the order of 500–750 Hz. Such burst responses occurred on the declining phase of the depth negative wave evoked by the cingulate stimulation.The anterior cingulate effects were found to be distributed on the prefrontal cortex from arcuate sulcus to two-thirds distance rostrally. The unit responses were more commonly found in laminae between 0.4 and 1.0 mm depth than at other depths. The cingulate effects on FC were not affected by lesion of nucleus medialis dorsalis thalami or by ablation of the pre-motor cortex.The study discloses a basis by which functional states of limbic cortex can powerfully modulate the functioning of prefrontal neocortex of primate.     

Cat-P300 present after association cortex ablation

The cat-P300 is a positive endogenous potential, larger to a stimulus when rare than when frequent, with a latency of 200-500 msec. The role of polysensory association cortex, postulated to be important in human P300 generation, was assessed in the cat. EEG was recorded in 13 awake cats from a skull screw at the vertex. Stimuli included frequent (P = 0.80) 1 kHz and rare (P = 0.10) 2 kHz tone pulses with probabilities counterbalanced across 260-trial blocks. After 12 preoperative sessions, bilateral ablations were made of pericruciate cortex (4 cats), anterior lateral and medial suprasylvian gyri (4 cats) and all 3 areas (5 cats). Postoperatively, all 13 cats showed a P300 across 12 recording sessions. Thus polysensory association cortex is not essential for generation of the cat-P300.     

Mapping the effects of motor cortex stimulation on somatosensory relay neurons in the rat thalamus: Direct responses and afferent modulation

Single unit recordings were used to map the spatial distribution of motor (MI) cortical influences on thalamic somatosensory relay nuclei in the rat. A total of 215 microelectrode penetrations were made to record single neurons in tracks through the medial and lateral ventroposterior (VPM and VPL), ventrolateral (VL), reticular (nRt), and posterior (Po) thalamic nuclei. Single units were classified according to their: 1) location within the nuclei, 2) receptive fields, and 3) response to standardized microstimulation in deep layers of the forepaw-forelimb areas of MI cortex. For mapping purposes, only short latency (1-7 msec) excitatory neuronal responses to the MI cortex stimulation were considered. Percentages of recorded thalamic neurons responsive to the MI stimulation varied considerably across nuclei: VL: 42.6%, nRt: 23.0%, VPL: 15.7%, VPM: 9.3%, and Po: 3.9%. Within the VPL, most responsive neurons were found in "border" regions, i.e., areas adjacent to the VL, and (to a lesser extent) the nRt and Po thalamic nuclei. The same parameters of MI cortical stimulation were used in studies of corticofugal modulation of afferent transmission through the VPL thalamus. A condition-test (C-T) paradigm was implemented in which the cortical stimulation (C) was delivered at a range of time intervals before test (T) mechanical vibratory stimulation was applied to digit No. 4 of the contralateral forepaw. The time course of MI cortical effects was analyzed by measuring the averaged evoked unit responses of the thalamic neurons to the T stimuli, and plotting them as a function of C-T intervals from 5-50 msec. Of the 30 VPL neurons tested during MI stimulation, the average response to T stimulation was decreased a mean 43%, with the suppression peaking at about 30 msec after the C stimulus. This suppression was more pronounced in the VPL border areas (-52% in areas adjacent to VL and nRt) than in the VPL center (-25%).     

Place of the thalamus in the network of interconnections between the association and limbic cortices in the monkey

Anatomophysiological criteria underlying the definition of associative cortex as well as limbic cortex include some imprecise data. The original notion of "cortical association spheres" (Flechsig) with no connections with the thalamus has rightly been abandoned, and that of the macroscopic "large limbic lobe" (Broca) fails to stand up to histologic or hodologic findings. However, the concept of cortical areas implicated specifically in multiple sensorial integration, sensory-motor coupling and control of behavior lasts due to necessity. In the monkey, the posterior parietal cortex of area 7 (PG area), the cortex of the upper slope of the superior temporal sulcus (STS) and the prefrontal cortex anterior to the sulcus arcuatus exchange direct corticocortical connections, receive afferents from sensory cortex and are not connected to specific thalamic relays. The term "associative" in its widest sense applies more particularly therefore to these cortical areas organized in networks. On the internal surface of the hemisphere, the cingular gyrus, retrosplenial cortex and parahippocampic gyrus (TF and TH areas) which occupy the major part of the limbic lobe, participate in the formation of this network and exchange direct cortico-cortical connections with the associative cortex defined above. The use of anterograde (labelled aminoacids) and retrograde (peroxidases) markers and of fluorescent dyes, allowing double retrograde labelling, demonstrates that the median pulvinar nucleus is connected with the knots of the associative cortical network. This thalamic nucleus, of a relatively increased size from phylogenetic evolution, is therefore excluded from the classification opposing specific and diffuse projection nuclei. In contrast to the thalamic reticular nucleus, which lacks cortical projections, and to the nuclei of the internal medullary band, which have the striatum as main target, the median pulvinar is a thalamic structure connected directly and specifically with each of the cortical areas, lesions of which result in negligence behavior.     

Changes in cortical sensory responses with a cryogenic blockade of nucleus ventralis posterolateralis

The contribution of nucleus ventralis posterolateralis (VPL) to sensory responses in the cortex of the cat was investigated. Averaged evoked potentials (AEP) were collected in response to paw, click, and light stimuli from primary sensory area S1 and the precruciate (PCA), anterior lateral (ALA), and posterior middle suprasylvian (PMSA) cortical association areas. Activity in VPL was reversibly blocked using a cryoprobe system to produce localized cooling. Reduction in amplitude of the short latency component of the AEP in S1 in response to the paw stimulus indicated that VPL was blocked. The short latency component of responses in the three association cortices was also blocked by cooling VPL, but the latency of this component was 20 msec longer than that of S1. Cross-correlation analyses of AEPs were performed to evaluate waveform similarity. Responses in a single cortical area to two different stimulus modalities or responses in two different cortical areas to one stimulus modality had about the same degree of waveform similarity. The effect of cooling VPL on waveform similarity was minimal and was not consistent for either stimulus pairs or cortical pairs. We concluded that VPL contributes to short latency responses in association cortices, but by a projection system differing from that to S1 since the latency to the changed response component was 20 msec longer than that observed for S1 cortex. Some similarity of sensory response waveform was found, but VPL makes little or no contribution to this similarity. No evidence was found for covariation of response excitability in cortical areas.     

Somatosensory evoked potentials (SEPs) and cortical single unit responses elicited by mechanical tactile stimuli in awake monkeys

The origins of surface recorded evoked potentials have been investigated by combining recordings of single unit responses and somatosensory evoked potentials (SEPs) from the postcentral gyrus of 4 alert macaque monkeys. Responses were elicited by mechanical tactile stimuli (airpuffs) which selectively activate rapidly adapting cutaneous mechanoreceptors, and permit patterned stimulation of a restricted area of skin. Epidurally recorded SEPs consisted of an early positive complex, beginning 8-10 msec after airpuff onset, with two prominent positive peaks (P15 and P25), succeeded by a large negative potential (N43) lasting 30 msec, and a late slow positivity (P70). SEPs, while consistent in wave form, varied slightly between monkeys. The amplitude of the early positive complex was enhanced by increasing the number of stimulated points, or by placing the airpuffs in the receptive fields of cortical neurons located beneath the SEP recording electrode. SEP amplitude was depressed when preceded 20-40 msec earlier by a conditioning stimulus to the same skin area. Single unit responses in areas 3b and 1 of primary somatosensory (SI) cortex consisted of a burst of impulses, beginning 11-12 msec after the airpuff onset, and lasting another 15-20 msec. Peak unitary activity occurred at 12-15 msec, corresponding to the P15 wave in the SEP. No peak in SI unit responses occurred in conjunction with the P25 wave. Although SI neurons fired at lower rates during P25, the lack of any peak in SI unit responses suggests that activity in other cortical areas, such as SII cortex, contributes to this wave. Most unit activity in SI cortex ceased by the onset of N43, and was replaced by a period of profound response depression, in which unit responses to additional tactile stimuli were reduced. We propose that the N43 wave reflects IPSPs in cortical neurons previously depolarized and excited by the airpuff stimulus. Late positive potentials (P70) in the SEP had no apparent counterpart in SI unit activity, suggesting generation at other cortical loci.     

Visual evoked potentials in monkeys.

Visual evoked potentials (VEPs) were recorded from 2 cortical sites in stump-tailed macaques. VEPs recorded from striate cortex were basically consistent between animals (especially at low light intensity), remained remarkably stable over time, and compared favorably to VEPs reported by other investigators. We concluded that the VEP recorded from the striate cortex of day-active monkeys consists of 5 major peaks within the first 250 msec. The potentials recorded from post-central gyrus were simpler and more individualized and did not show intensity-related latency changes or increases in inter-subject variability. However, amplitudes of potentials recorded from both electrode placements increased with light intensity apparently reflecting the amplitude of individual potentials rather than the variability of these potentials from which the average VEPs were derived.     

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.     

Surface negative waves in penicillin-induced epileptogenesis in cats

The "surface negative (SN) wave" produced by pyramidal tract stimulation and recorded at the cortical surface has been identified as a reflection of postsynaptic potentials generated through recurrent inhibitory pathways (Humphrey, et al.). We studied changes in SN wave in an attempt to examine inhibitory mechanisms underlying epileptogenesis in immobilized cats. 1) A single shock applied to the cerebral peduncle evoked alpha and beta wave at the surface of ipsilateral anterior sigmoid gyrus (Fig.1 A). A train of 4 shocks with 4 msec shock-interval elicited SN wave which had a peak latency of 20 msec and decayed in 60-80 msec (Fig. 1 B,C,D). 2) The spindle-like after-discharges elicited by direct cortical shock were markedly suppressed with conditioning stimulation of the ipsilateral pyramidal tract (Fig. 2). Spike-and-wave complexes and other ECoG paroxysms produced by intramuscular administration of penicillin (Pc) were also depressed by repeated stimulation of the cerebral peduncle (Fig. 3). These facts revealed that the inhibitory effects of pyramidal tract stimulation caused to suppress the occurrence of epileptic discharges. 3) SN wave gradually diminished in amplitude after topical application of Pc at the anterior sigmoid gyrus (Fig. 4 A-D). It disappeared completely when tonic-clonic sustained paroxysms occurred at the focus (Fig. 4 E). These effects are due presumably to depression of recurrent postsynaptic inhibition caused by topical penicillin. 4) SN wave observed at the contralateral secondary focus was almost unchanged during interictal and ictal stage (Fig. 5).(ABSTRACT TRUNCATED AT 250 WORDS)     

A non-thalamic olfactory pathway to the orbital gyrus in the cat

Extracellular unit responses were recorded from the cortical layer of the orbital gyrus following stimulation of the piriform cortex fronting on that gyrus. The responses were obtained only from the dorsal bank of the rhinal sulcus. The responses were presynaptic axon and postsynaptic soma spikes with latencies of about 4 and 4.8 msec, respectively. When the dorsal bank of the rhinal sulcus was stimulated, antidromic responses with a latency of about 4.4 msec were recorded from the superficial and deep soma layers of the piriform cortex. Following injections of horseradish peroxidase into the dorsal bank of the rhinal sulcus, labeled cells were found in the piriform cortex, the lateral, basolateral and central amygdaloid nuclei, and the prelimbic area. These results indicate that the piriform cortex projects directly to part of the orbital gyrus by way of association fiber pathways.     

Cortical sources of the early components of the visual evoked potential

This study aimed to characterize the neural generators of the early components of the visual evoked potential (VEP) to isoluminant checkerboard stimuli. Multichannel scalp recordings, retinotopic mapping and dipole modeling techniques were used to estimate the locations of the cortical sources giving rise to the early C1, P1, and N1 components. Dipole locations were matched to anatomical brain regions visualized in structural magnetic resonance imaging (MRI) and to functional MRI (fMRI) activations elicited by the same stimuli. These converging methods confirmed previous reports that the C1 component (onset latency 55 msec; peak latency 90-92 msec) was generated in the primary visual area (striate cortex; area 17). The early phase of the P1 component (onset latency 72-80 msec; peak latency 98-110 msec) was localized to sources in dorsal extrastriate cortex of the middle occipital gyrus, while the late phase of the P1 component (onset latency 110-120 msec; peak latency 136-146 msec) was localized to ventral extrastriate cortex of the fusiform gyrus. Among the N1 subcomponents, the posterior N150 could be accounted for by the same dipolar source as the early P1, while the anterior N155 was localized to a deep source in the parietal lobe. These findings clarify the anatomical origin of these VEP components, which have been studied extensively in relation to visual-perceptual processes.     

Somatosensory evoked potentials in the term newborn.

Median nerve somatosensory evoked potentials (SEPs) were recorded from surface electrodes in 40 healthy term infants (range 36.5-43 weeks postmenstrual age). Electrical stimulation at 5 Hz was used, averaging the response to several runs of 1024 stimuli to each median nerve, bandpass 10-3000 Hz, sweeptime 100 msec. Identifiable potentials were collected over the cervical cord on all runs in all 40 infants and from the cortex in at least some runs in 39 out of 40 infants. The cervical response showed little variation and consisted of a clear negative wave with up to 3 peaks, mean latency of the largest 10.2 +/- 0.7 msec, followed by a positive deflection. The cortical response was very variable in form and latency between infants and to a lesser degree within infants. Four types of cortical wave form were found, symmetrical, asymmetrical, plateau and M shaped, of increasing complexity. In 11% of trials the response was absent or indistinct but could usually be uncovered by alteration in stimulus frequency or intensity. In the whole group, the mean latency for N1 was 30.0 +/- 6.8 msec and for the central conduction time 19.8 +/- 6.5 msec. Significant differences were found between the 4 cortical wave forms in the main variables measured, which gave support for form S being the most primitive and form M the most mature response.