Evoked Brain Potentials Research Articles

Proximal and distal esophageal sensitivity is decreased in patients with Barrett’s esophagus

To investigate sensations to multimodal pain stimulation in the metaplastic and normal parts of the esophagus in patients with Barrett's esophagus (BE). Fifteen patients with BE and 15 age-matched healthy volunteers were subjected to mechanical, thermal and electrical pain stimuli of the esophagus. Both the metaplastic part and the normal part (4 and 14 cm, respectively, above the esophago-gastric junction) were examined. At sensory thresholds the stimulation intensity, referred pain areas, and evoked brain potentials were recorded. Patients were hyposensitive to heat stimulation both in the metaplastic part [median stimulation time to reach the pain detection threshold: 15 (12-34) s vs 14 (6-23) s in controls; F = 4.5, P = 0.04] and the normal part of the esophagus [median 17 (6-32) s vs 13 (8-20) s in controls; F = 6.2, P = 0.02]. Furthermore, patients were hyposensitive in the metaplastic part of the esophagus to mechanical distension [median volume at moderate pain: 50 (20-50) mL vs 33 (13-50) mL in controls; F = 5.7, P = 0.02]. No indication of central nervous system abnormalities was present, as responses were comparable between groups to electrical pain stimuli in the metaplastic part [median current evoking moderate pain: 13 (6-26) mA vs 12 (9-24) mA in controls; F = 0.1, P = 0.7], and in the normal part of the esophagus [median current evoking moderate pain: 9 (6-16) mA, vs 11 (5-11) mA in controls; F = 3.4, P = 0.07]. Furthermore, no differences were seen for the referred pain areas (P-values all > 0.3) or latencies and amplitudes for the evoked brain potentials (P-values all > 0.1). Patients with BE are hyposensitive both in the metaplastic and normal part of esophagus likely as a result of abnormalities affecting peripheral nerve pathways.

The possibilities of the polygraph application and search for the new alternative methods of the instrumental lie detection dedicated to prevent new terrorist threats

The article treats the possibilities of creating the alternative methods to the traditional polygraph checks, new methods of the lie detection with the help of the registration and the analysis of the evoked brain potentials, their application to verify the suspected people involvement into terrorist actions. It is underlined that the new methods have high reliability and validity to discover the hidden information about the terrorist acts at the stage of their planning

Abnormal brain processing in hepatic encephalopathy

Hepatic encephalopathy (HE) is a severe and frequent complication of liver cirrhosis characterized by abnormal cerebral function. Little is known about the underlying neural mechanisms in HE and human data are sparse. Electrophysiological methods such as evoked brain potentials after somatic stimuli can be combined with inverse modeling of the underlying brain activity. Thereby, information on neuronal dynamics and brain activity can be studied in vivo. The aim of this study was to investigate the sensory brain processing in patients with HE. Twelve patients with minimal or overt HE and 26 healthy volunteers were included in the study. Cerebral sensory processing was investigated as (i) an auditory reaction time task; (ii) visual and somatosensory evoked brain potentials, and (iii) reconstruction of the underlying brain activity. Somatosensory evoked potentials were reproducible (all P>0.05), whereas flash evoked potentials were not reproducible (all P<0.05). Compared with healthy volunteers, the patient group had a prolonged reaction time index (P=0.03) along with increasing prolongation of latencies of median nerve evoked potentials (P<0.03). Reconstruction of the underlying brain sources showed a lateral shift in source localization of the P45 (P<0.001) and N60 components (P=0.02). A correlation between the psychometric hepatic encephalopathy score and the dipole shift corresponding to the N60 (P=0.003) component was seen. HE patients have evidence of prolonged intracerebral nerve conduction, along with lateralization of brain activity following median nerve stimulation. This possibly represents cortical reorganization and may be important in our understanding of this condition.

Gastrointestinal symptoms in type-1 diabetes: Is it all about brain plasticity?

Background and aims Autonomic neuropathy seems to play a central role in the development of gastrointestinal symptoms in diabetes. In order to explore the neuronal mechanisms behind the symptoms we evaluated the brain processing of painful visceral stimuli. Methods Evoked brain potentials were recorded to assess the response to painful oesophageal electrical stimuli in 15 healthy volunteers and 14 type-1 diabetes patients with autonomic neuropathy and related gastrointestinal symptoms. Source reconstruction analysis (fixed Multiple Signal Classification (MUSIC) algorithm) was applied to estimate the location of the evoked electrical activity in the brain. Results The patients had increased oesophageal sensory thresholds compared to the controls ( P = 0.004). The latencies of the evoked brain potentials at vertex (Cz) were increased ( P = 0.007) and amplitudes reduced ( P = 0.011) in diabetics. Compared with controls the patients had a posterior shift of the electrical sources in the anterior cingulate cortex at 54 ms, and additional sources close to the posterior insula at 95 ms and in medial frontal gyrus at 184 ms. Conclusions There is evidence of altered central processing to visceral stimulation, and both peripheral and central mechanisms seem involved. Central neuronal reorganisation may contribute to our understanding of the gastrointestinal symptoms in patients with diabetic autonomic neuropathy and this may guide development and evaluation of new treatment modalities.

Effect of acute hyperglycaemia on sensory processing in diabetic autonomic neuropathy

Acute hyperglycaemia is known to increase gastrointestinal (GI) sensitivity in healthy subjects and may contribute to the increased prevalence of GI symptoms in diabetes patients. The aim of this study was to evaluate the effect of acute hyperglycaemia on perception and brain responses to painful visceral and somatic stimuli in diabetic patients. The sensitivity and evoked brain potentials (EPs) to electrical oesophageal and median nerve stimulations were assessed in 14 type-1 diabetes patients with autonomic neuropathy and GI symptoms using a hyperinsulinaemic clamp at 6 and 15 mM. No differences between the normo- and hyperglycaemic conditions were found in sensitivity to both oesophageal (P=0·72) and median nerve (P=0·66) stimulations. The latencies and amplitudes of EPs did not differ between the normo- and hyperglycaemic conditions following oesophageal (P=0·53 and 0·57) and median nerve (P=0·78 and 0·52) stimulations. Acute hyperglycaemia itself does not contribute to the sensations in patients with longstanding diabetes and autonomic neuropathy. Any potential sensory effects of acute hyperglycaemia can likely be blurred by the neuropathic-like changes in the sensory nervous system.

Extraversion, evoked brain potentials and abstract thinking

Extraversion, evoked brain potentials and abstract thinking

Functional assessment of neuropathic pain

The assessment of the nervous system in patients with neuropathic pain is particularly challenging. Conventional electrophysiological testing, such as nerve conduction studies and somatosensory-evoked potentials, may prove normal as these techniques only evaluate large fibre function (A beta). In a clinical setting, two evaluation methods may prove useful to examine the nociceptive system or to explore small fibre function (A delta et C). First, quantitative sensory testing, derived from psychophysics, explores different sensory modalities (tactile, thermal and vibratory sensations) corresponding to different types of nerve fibres. Second, CO2 lasers allow for powerful and selective thermal stimuli to evoke brain potentials that are specifically related to the cutaneous activation of A delta and C nociceptors. Finally, other assessments of the nervous system, such as nociceptive reflexes and microneurography, are available for use in a more experimental setting.

Descending Inhibitory Pain Modulation Is Impaired in Patients With Chronic Pancreatitis

Pain is a prominent symptom in chronic pancreatitis (CP), but the underlying mechanisms are incompletely understood. We investigated the role of descending pain modulation from supraspinal structures as well as central nervous system sensitization in patients with pain from CP. Twenty-five patients with CP and 15 healthy volunteers were included. Descending pain modulation was investigated by diffuse noxious inhibitory control (a descending inhibitory response after conditioning stimulation). Central pain processing was investigated as the perceptual responses to multimodal (electrical, thermal, and mechanical) stimulations of the rectosigmoid and evoked brain potentials after electrical stimulation of the rectosigmoid. Compared with healthy volunteers, the efficacy of diffuse noxious inhibitory control was reduced in patients with CP (13% +/- 21% vs 39% +/- 22%, respectively; F = 3.8; P = .01); central sensitization was indicated by remote hyperalgesia in the rectosigmoid to electrical stimulation (21 +/- 15 mA vs 27 +/- 15 mA; F = 6.2; P = .02) and heat stimulation (51 degrees C +/- 5 degrees C vs 53 degrees C +/- 4 degrees C; F = 5.9; P = .02). Compared with controls, patients with CP had increased latency of the early P1 peak to rectosigmoid stimulation (85 +/- 21 ms vs 108 +/- 28 ms, respectively; P = .02), possibly reflecting reorganization of central pain pathways. Patients with CP have impairments in inhibitory pain modulation and evidence of central sensitization. Treatment of their pain therefore should focus not only on the pancreas, but also on descending pain modulation from supraspinal structures and central nervous system sensitization.

Acid hypersensitivity in patients with eosinophilic oesophagitis

Objective. Painful symptoms are prevalent in patients with eosinophilic oesophagitis but experimental data are sparse. The aim of this study was to compare the pain response to experimental oesophageal stimulation in 14 patients with eosinophilic oesophagitis and 15 healthy volunteers. Material and methods. A multimodal probe was placed in the oesophagus. The participants were subjected to mechanical, thermal and electrical pain stimuli followed by perfusion with 0.1 M HCl. Pain scores, referred pain areas and evoked brain potentials to electrical stimulation of the oesophagus were recorded. Results. Patients tolerated significantly less acid perfused in the oesophagus (median 123 versus 200 ml; P = 0.02) and felt the burning sensation evoked by the acid earlier (median 2.0 versus 5.0 min; P = 0.01). Eight patients had coexisting gastro-oesophageal reflux disease. Six patients had pure eosinophilic oesophagitis, and this group felt the acid earlier than those with concomitant reflux or the healthy volunteers (median 0.8 versus 2.0 and 5.0 min; P = 0.03). There were no differences between patients and controls in the responses to mechanical or thermal stimulation (P > 0.4). Furthermore, no differences were found for the proxies of central nervous system sensitization (response to electrical stimulations, referred pain areas or evoked brain potentials; P > 0.1). Conclusions. Patients with eosinophilic oesophagitis are hypersensitive to acid perfused in the oesophagus, and pathophysiologic findings are likely confined to the peripheral tissue. Reflux from physiological acid may play a role in the symptoms of eosinophilic oesophagitis.

Sleep loss does not aggravate the deteriorating effect of hypoglycemia on neurocognitive function in healthy men

Sleep deprivation (SD) impairs neurocognitive functions. Assuming that this effect is mediated by reduced cerebral glucose supply due to prolonged wakefulness inducing a progressive depletion of cerebral glycogen stores, we hypothesized that short-term sleep loss amplifies the deteriorating effects of acute hypoglycemia on neurocognitive functions. Seven healthy men were tested in a randomized and balanced order on 3 different conditions spaced 2 weeks apart. After a night of total SD (total SD), 4.5h of sleep (partial SD) and a night with 7h of regular sleep (regular sleep), subjects were exposed to a stepwise hypoglycemic clamp experiment. Reaction time (RT) and auditory evoked brain potentials (AEP) were assessed during a euglycemic baseline period and at the end of the clamp (blood glucose at 2.5mmol/l). During the euglycemic baseline, amplitude of the P3 component of the AEP was lower after total SD than after partial SD (9.2+/-3.2microV vs. 16.6+/-2.9microV; t(6)=3.2, P=0.02) and regular sleep (20.2+/-2.1microV; t(6)=18.8, P<0.01). Reaction time was longer after total SD in comparison to partial SD (367+/-45ms vs. 304+/-36ms; t(6)=2.7, P=0.04) and to regular sleep (322+/-36ms; t(6)=2.41, P=0.06) while there was no difference between partial SD and regular sleep condition (t(6)=0.60, P=0.57). Hypoglycemia decreased P3 amplitude by 11.2+/-4.1microV in the partial SD condition (t(6)=2.72, P=0.04) and by 9.3+/-0.7microV in the regular sleep condition (t(6)=12.51, P<0.01), but did not further reduce P3 amplitude after total SD (1.8+/-3.9microV; t(6)=0.46, P=0.66). Thus, at the end of hypoglycemia P3 amplitudes were similar across the 3 conditions (F(2,10)=0.89, P=0.42). RT generally showed a similar pattern with a significant prolongation due to hypoglycemia after partial SD (+42+/-12ms; t(6)=3.39, P=0.02) and regular sleep (+37+/-10ms; t(6)=3.53, P=0.01), but not after total SD (+15+/-16; t(6)=0.97, P=0.37), resulting in similar values at the end of hypoglycemia (F(1,6)=1.01, P=0.36). One night of total SD deteriorates neurocognitive function as reflected by indicators of attentive stimulus processing, but does not synergistically aggravate the impairing influence of acute hypoglycemia. The findings are not consistent with the view that neurocognitive deteriorations after SD result from challenged cerebral glucose metabolism.

Age Dynamics of Evoked Brain Potentials in Involuntary and Voluntary Attention to a Deviant Stimulus in Schoolchildren from the Northern Region

The central mechanisms of involuntary and voluntary regulation of attention in schoolchildren from the northern region were studied using a method based on the P300 wave of evoked brain potentials (the oddball paradigm). Data were compared with results obtained from psychological tests. Differences in the organization of EP were seen in the "passive" and active (counting) perception of deviant stimuli. Three components were identified within the time envelop of the P300 wave, two of which dominated in the frontal and one in the parietal area of the cerebral cortex. The latency of the P300 wave decreased with age in the children, reflecting increased rates of information processing and increases in the volume of operative memory. In passive perception, the statistical relationship characterized by a reduction in P300 latency with age was significant for leads in the central, temporal, parietal, and occipital areas; in active perception, this applied to all areas including the frontal. The most significant changes in P300 parameters were seen in children aged from seven to 12 years, indicating that this period can be regarded as "critical" in the development of learning skills. The roles of the parietal and frontal areas of the cortex in the mechanisms of involuntary and voluntary regulation of attention are discussed, along with the possibility of using the P300 method to identify children with delayed rates of development of voluntary attention in population studies.

At which processing level does extrinsic speaker information influence vowel perception?

The interpretation of vowel sounds depends on perceived characteristics of the speaker [e.g., average first formant (F1) frequency]. A vowel between /ɪ/ and /ε/ is more likely to be perceived as /ɪ/ if a precursor sentence indicates that the speaker has a relatively high average F1. Behavioral and electrophysiological experiments investigating the locus of this extrinsic vowel normalization are reported. The normalization effect with a categorization task was first replicated. More vowels on an /ɪ/-/ε/ continuum followed by a /papu/ context were categorized as /ɪ/ with a high-F1 context than with a low-F1 context. Two experiments then examined this context effect in a 4I-oddity discrimination task. Ambiguous vowels were more difficult to distinguish from the /ɪ/-endpoint if the context /papu/ had a high F1 than if it had a low F1 (and vice versa for discrimination of ambiguous vowels from the /ε/-endpoint). Furthermore, between-category discriminations were no easier than within-category discriminations. Together, these results suggest that the normalization mechanism operates largely at an auditory processing level. The mismatch negativity (an automatically evoked brain potential) arising from the same stimuli is being measured, to investigate whether extrinsic normalization takes place in the absence of an explicit decision task.

Assessing efficacy of non‐opioid analgesics in experimental pain models in healthy volunteers: an updated review

Experimental pain models may help to evaluate the mechanisms of analgesics and target the clinical indications for their use. This review, the second in a series of two, addresses how the efficacy of non-opioid analgesics have been assessed in human volunteers using experimental pain models. A literature search was completed for randomized controlled studies that included human experimental pain models, healthy volunteers and non-opioid analgesics. Nonsteroidal anti-inflammatory drugs worked against various types of acute pain as well as in hyperalgesia. Analgesia from paracetamol was difficult to detect in experimental pain and the pain needed to be assessed with very sensitive methods like evoked brain potentials. The N-methyl-D-aspartate antagonists exemplified by ketamine generally needed strong, long-lasting or repeated pain in the skin for detectable analgesia, whereas pain in muscle and viscera generally was more easily attenuated. Gabapentin worked well in several models, particularly those inducing hyperalgesia, whereas lamotrigine was weak in modulation of experimental pain. Imipramine attenuated pain in most experimental models, whereas amitriptyline had weaker effects. Delta-9-tetrahydrocannabinol attenuated pain in only a few models. Pain induction and assessment are very important for the sensitivity of the pain models. Generally, experimental pain models need to be designed with careful consideration of the pharmacological mechanisms and pharmacokinetics of analgesics. The drawback with the different study designs is also discussed. This knowledge can aid the decisions that need to be taken when designing experimental pain studies for compounds entering Phase I and II trials.

An initial report of a new biological marker for bipolar disorder: P85 evoked brain potential

Progress toward understanding the neurobiological and genetic underpinnings of bipolar disorder has been limited by the scarcity of potential biological markers that predict its occurrence. A measure of the integrity of brain inhibitory function, sensory gating, measured using the amplitude of the evoked potential at 50 ms to the first of two paired clicks divided by the response to the second, has been characterized as a biological marker for schizophrenia. Currently, no such biological marker exists for bipolar disorder. The goal of this research was to determine how gating of an auditory brain potential at 85 ms (P85), not previously examined in sensory gating studies, differentiated control and patient groups. P50 and P85 auditory evoked potentials were collected from individuals diagnosed with schizoaffective disorder (n = 45), paranoid schizophrenia (n = 66), and bipolar I disorder (n = 42) using DSM-IV criteria and the Structured Clinical Interview for DSM-IV; and from 56 healthy controls. The P85 gating ratio was significantly larger in the bipolar disorder group compared to each of the other groups (F(3,204) = 5.47, p = 0.001, and post-hoc tests). The P50 gating ratio was significantly larger for the schizoaffective group than for the control group (F(3,204) = 2.81, p = 0.040), but did not differ from the ratio for the schizophrenia, paranoid type (p = 0.08) and bipolar groups. The previously unstudied P85 gating ratio may provide a new marker specific to bipolar disorder. The findings will promote further studies to investigate the unique contribution of this measure as an endophenotype.

Early Static Pressure-Related Evoked Brain Potentials Indications of Central Middle Ear Pressure Control in Humans

The aim of this study was to investigate the possibility of afferent subcortical components related to static pressure changes of the human middle ear. The normal middle ear function depends on a proper regulation of middle ear pressure, whereas an inadequate regulation with negative pressures is considered a major pathogenetic factor responsible for a variety of middle ear disorders. However, although studies on middle ear pressure and related clinical problems are common, studies on the role of its central control have been remarkably few. Hence, we attempted recording evoked brain potentials in response to static pressure stimulation of the middle ear in normal adult humans. The experiments were conducted by stimulating the middle ear in 6 subjects with a novel computer-controlled static pressure triggering system for rapid synchronized pressure loads of +3 kPa. The resulting brain evoked responses were recorded from 64 surface electrodes using a standard electroencephalogram cap. A wide-band electroencephalogram acquisition method was adopted, signals were sampled at 20,000 Hz, and band-pass filtered between 150 and 3,000 Hz. Repeatable pressure evoked brain potentials and topographies were described for the first time. Hence, source localization could be adopted on a realistic head model, which showed the location of these early neural generators in the brainstem, followed by activity generated by the cerebellum. The findings are in agreement with previous animal experiments and provide basic information for further investigations on central components related to static pressure changes of the human middle ear.

Central pain mechanisms following combined acid and capsaicin perfusion of the human oesophagus

Visceral afferents originating from different gut-segments converge at the spinal level. We hypothesized that chemically-induced hyperalgesia in the oesophagus could provoke widespread visceral hypersensitivity and also influence descending modulatory pain pathways. Fifteen healthy volunteers were studied at baseline, 30, 60 and 90 min after randomized perfusion of the distal oesophagus with either saline or 180 ml 0.1 M HCl + 2 mg capsaicin. Electro-stimulation of the oesophagus, 8 cm proximal to the perfusion site, rectosigmoid electrical stimulation and rectal mechanical and heat stimulations were used. Evoked brain potentials were recorded after electrical stimulations before and after oesophageal perfusion. After the perfusion, rectal hyperalgesia to heat ( P < 0.01, 37%) and mechanical ( P = 0.01, 11%) stimulations were demonstrated. In contrast, hypoalgesia to electro-stimulation was observed in both the oesophagus ( P < 0.03, 23%) and the sigmoid colon ( P < 0.001, 18%). Referred pain areas to electro-stimulation in oesophagus were reduced by 13% after perfusion ( P = 0.01). Evoked brain potentials to rectosigmoid stimulations showed decreased latencies and amplitudes of P1, N1 and P2 ( P < 0.05), whereas oesophagus-evoked brain potentials were unaffected after perfusion. In conclusion, modality-specific hyperalgesia was demonstrated in the lower gut following chemical sensitization of the oesophagus, reflecting widespread central hyperexcitability. Conversely, hypoalgesia to electrical stimulation, decreases in referred pain and latencies of evoked brain potentials was seen. This outcome may reflect a counterbalancing activation of descending inhibitory pathways. As these findings are also seen in the clinical setting, the model may be usable for future basic and pharmacological studies.

Brain responses evoked by high-frequency repetitive transcranial magnetic stimulation: An event-related potential study

Many recent studies have used repetitive transcranial magnetic stimulation (rTMS) to study brain-behavior relationships. However, the pulse-to-pulse neural effects of rapid delivery of multiple TMS pulses are unknown largely because of TMS-evoked electrical artifacts limiting recording of brain activity.ObjectiveIn this study, TMS-related artifacts were removed with independent component analysis (ICA), which allowed for the investigation of the neurophysiologic effects of rTMS with simultaneous electroencephalographic (EEG) recordings. Repetitive TMS trains of 10 Hz, 3 seconds (110% of motor threshold) were delivered to the postcentral gyrus and superior parietal lobule in 16 young adults. Simultaneous EEG recordings were made with a TMS-compatible system. The stereotypical pattern of TMS-related electrical artifacts was identified by ICA. Removal of artifacts allowed for identification of a series of five evoked brain potentials occurring within 100 milliseconds of each TMS pulse. With the exception of the first potential, for both areas targeted, there was a quadratic relationship between potential peak amplitude and pulse number within the TMS train. This was characterized by a decrease, followed by a rise in amplitude. ICA is an effective method for removal of TMS-evoked electrical artifacts in EEG data. With the use of this procedure we found that the physiologic responses to TMS pulses delivered in a high-frequency train of pulses are not independent. The sensitivity of the magnitude of these responses to recent stimulation history suggests a complex recruitment of multiple neuronal events with different temporal dynamics.

Brain-evoked potentials as a tool for diagnosing neuropathic pain

Neuropathic pain is a complex subject, not completely understood yet, and it is quite common in clinical practice, even outside of a neurological context. Neuropathic pain, often being a chronic process, alters and profoundly affects the quality of life. Therefore, the management of neuropathic pain involves a multidimensional approach, as physicians have to take care not only of the objective aspects of the problem, but also of the subjective experiences of pain. This explains why the attainment of a diagnosis becomes so important, as it allows clinicians to treat the patients with the best therapeutic approach. Several studies report the use of brain-evoked potentials for studying patients suffering from neuropathic pain. In particular, laser- and contact heat-evoked potentials have proved useful for the diagnosis of clinical conditions characterized by neuropathic pain. However, although these tools are reliable and safe instruments to assess function of the nociceptive system, their use is still largely confined to research purposes.

Central Processing of Gut Pain in Diabetic Patients With Gastrointestinal Symptoms

OBJECTIVETo evaluate the brain's responses to painful visceral and somatic stimuli in diabetic patients with gastrointestinal symptoms.RESEARCH DESIGN AND METHODSThe sensitivity to electrical esophageal and median nerve stimulations was assessed in 15 healthy volunteers and 14 type 1 diabetic patients with autonomic neuropathy and gastrointestinal symptoms using a euglycemic-hyperinsulinemic clamp. Evoked brain potentials were recorded.RESULTSPatients had reduced sensitivity to esophageal (48%; P < 0.001) and median nerve (80%; P < 0.001) stimulations. They also had increased (8.8%; P = 0.007) and nonreproducible (P = 0.006) latencies of evoked potentials in response to esophageal stimulations, with 26% reduction in amplitude (P = 0.011). No potential differences were seen to median nerve stimulations. In diabetic patients, the topographic location of the first peak in potentials was more central (P < 0.001) and gastrointestinal symptoms correlated with characteristics of brain potentials (P = 0.049).CONCLUSIONSThis study supports that diabetes induces changes in peripheral visceral nerves as well as in the central nervous system.

Two semantic systems in the brain for rapid and slow differentiation of abstract and concrete words

Most studies of semantic processing address changes in the late (300-800 msec) components of evoked potentials. However, recent years have seen the appearance of data showing that humans can perceive the sense of stimuli presented to them in significantly shorter periods of time. We report here studies of the mechanism of semantic analysis of written abstract and concrete words in four series of experiments: 1) reading of words on a monitor screen; 2) simple classification of all presented words into the categories "abstract" and "concrete;" 3) complex, i.e., selective classification of words written only in a specified color with a prompt as to which color would be used for the word; 4) complex classification of words of only a specified color without a prior prompt. Early (40-100 msec) differences in evoked brain potentials were seen on comparison of responses to abstract and concrete words, predominantly in the frontal areas in the case of simple reading of words and in the more dorsal areas in the case of tasks with simple classification. All cases of explicit classification of words were characterized by differences in late (450-700 msec) components in the left frontal zone. The results indicate the existence of two semantic systems: a rapid, implicit system associated with activation of the right frontal area, and a slow, explicit system of word classification which is predominantly associated with activity in the left frontal area. The relationship between the two systems is to a certain extent reciprocal: the rapid system can by inhibited by introduction of a word classification task.