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This study investigated the magneto- and electroencephalography (MEG and EEG, respectively) resting state to identify the deviations closely associated with the deficit syndrome (DS) in schizophrenia patients. Ten subjects in each group (control, DS, and nondeficit schizophrenia [NDS]) were included. Subjects underwent MEG-EEG recordings during a resting state condition. MEG coherence source imaging (CSI) in source space and spectral analysis in sensor space were performed. Significant differences were found between the 2 patient groups: (1) MEG and EEG spectral analysis showed significantly higher power at low frequencies (delta band) at sensor space in DS compared with NDS patients; (2) source analysis revealed larger power in the DS compared with NDS group at low frequencies in the frontal region; (3) NDS patients showed significantly higher MEG signal relative power in beta bands in sensor space compared with DS patients; (4) both DS and NDS patients showed higher EEG absolute power at higher beta band compared to controls; and (5) patients with DS were found to have a significantly higher MEG CSI than controls in the beta frequency band. These data support the observation of increased power in the low-frequency EEG/MEG rhythms associated with the DS. Increased power in the beta rhythms was more associated with the NDS.

Routine electroencephalograms (EEG) are not recommended as a screen for epileptic discharges (EDs) in current practice guidelines for children with autism spectrum disorder (ASD). However, a review of the research from the last three decades suggests that this practice should be reevaluated. The significant comorbidity between epilepsy and ASD, its shared biological pathways, risk for developmental regression, and cognitive challenges demand increased clinical investigation requiring a proactive approach. This review highlights and explains the need for screening EEGs for children with ASD. EEG would assist in differentiating EDs from core features of ASD and could be included in a comprehensive assessment. EEG also meets the demand for evidence-based precision medicine and focused care for the individual, especially when overlapping processes of development are present.

Despite decades of publications attesting to the role of the clinical EEG in diagnosing and managing psychiatric disorders, the procedure remains highly underutilized in the practice of psychiatry. The visually inspected EEG (vEEG) can detect various forms of abnormalities, each with its own clinical significance. Abnormalities can be paroxysmal (i.e., suggestive of an epileptic-like process) or stationary. The most important unanswered question remains the value of detecting epileptiform activity in a nonepileptic psychiatric patient in predicting favorable responses to anticonvulsant treatment. Despite the many shortcomings of vEEG, the available evidence suggests that in the presence of paroxysmal activity in a nonepileptic psychiatric patient a trial of a psychotropic anticonvulsant may be warranted if standard treatment has failed. More research on the contribution of paroxysmal EEG abnormalities to the problem of episodic psychiatric symptoms (e.g., panic attacks, dissociative episodes, repeated violence) is sorely needed. It is postulated that at least some of these conditions may represent an epilepsy spectrum disorder. Similarly, the significance of the presence of a slow-wave activity (whether focal or generalized) also deserves further well-designed research to ascertain the exact clinical significance. Nonetheless, the available data suggest that further medical workup is necessary to ascertain the nature and degree of the pathology when present.

Electroencephalogram (EEG) contains valuable information obtained noninvasively that can be used for assessment of brain's processing capacity of patients with psychiatric disorders. The purpose of the present work was to evaluate possible differences in EEG complexity between deficit (DS) and nondeficit (NDS) subtypes of schizophrenia as a reflection of the cognitive processing capacities in these groups. A particular nonlinear metric known as Lempel-Ziv complexity (LZC) was used as a computational tool in order to determine the randomness in EEG alpha band time series from 3 groups (deficit schizophrenia [n = 9], nondeficit schizophrenia [n = 10], and healthy controls [n = 10]) according to time series randomness. There was a significant difference in frontal EEG complexity between the DS and NDS subgroups ( p = .013), with DS group showing less complexity. A significant positive correlation was found between LZC values and Positive and Negative Syndrome Scale (PANSS) general psychopathology scores (ie, larger frontal EEG complexity correlated with more severe psychopathology), explained partially by the emotional component subscore of the PANSS. These findings suggest that cognitive processing occurring in the frontal networks in DS is less complex compared to NDS patients as reflected by EEG complexity measures. The data also suggest that there may be a relationship between the degree of emotionality and the complexity of the frontal EEG signal.

Rationale Limited research is available on electrophysiological abnormalities such as epileptiform EEG or EEG slowing in depression and its association with antidepressant treatment response. Objectives We investigated the association between EEG abnormalities and antidepressant treatment response in the international Study to Predict Optimized Treatment in Depression (iSPOT-D). Methods Of 1008 participants with major depressive disorder randomized to escitalopram, sertraline, or venlafaxine-XR, 622 completed 8 weeks of treatment per protocol. The study also recruited 336 healthy controls. Treatment response was established after 8 weeks using the 17-item Hamilton Rating Scale for Depression (HRSD 17 ). The resting-state EEG was assessed at baseline with eyes closed. EEG abnormalities including epileptiform activity, EEG slowing, and alpha peak frequency (APF) were scored for all subjects, blind to treatment outcome. Results Patients and controls did not differ in the occurrence of EEG abnormalities. Furthermore, in the per protocol sample the occurrence of epileptiform EEG and EEG slowing (as a combined marker) were associated with a reduced likelihood of responding to escitalopram (P = .019; odds ratio [OR] = 3.56) and venlafaxine-XR (P = .043; OR = 2.76), but not sertraline (OR = 0.73). The response rates for this "any EEG abnormality" groups versus the "no-abnormality" group were 33% and 64% for escitalopram and 41% and 66% for venlafaxine-XR, respectively. A slow APF was associated with treatment response only in the sertraline group (P = .21; d = .027). Conclusions EEG abnormalities are associated with nonresponse to escitalopram and venlafaxine-XR, but not sertraline, whereas a slow APF is associated to response for sertraline only., (© EEG and Clinical Neuroscience Society (ECNS) 2015.)

Electroconvulsive therapy (ECT) remains to be one of the most effective treatment options in treatment-resistant major depressive disorder (MDD). From the early days, researchers have embarked on extracting information from electroencephalography (EEG) recordings before, during, and after ECT to identify neurophysiological targets of ECT and discover EEG predictors of response to ECT in patients with MDD. In this article, we provide an overview of visually detected and quantitative EEG features that could help in furthering our understanding of the mechanisms of action of ECT in MDD. We further discuss the EEG findings in the context of postulated hypotheses of ECT therapeutic pathways. We introduce an alternative and unifying hypothesis suggesting that ECT may exert its therapeutic efficacy through resetting the aberrant functional connectivity and promoting the generation of new and healthy connections in brain regions implicated in MDD pathophysiology, a mechanism that may be in part mediated by the ECT-induced activation of inhibitory and neuroplasticity mechanisms. We further discuss the added value of EEG markers in the larger context of ECT research and as complementary to neuroimaging and genetic markers. We conclude by drawing attention to the need for longitudinal studies in large cohort of patients and the need for standardization and validation of EEG algorithms of functional connectivity across studies to facilitate the translation of EEG correlates of ECT response in routine clinical practice.

The efficacy of antiepileptic drugs (AEDs) in treating behavioral symptoms in nonepileptic psychiatric patients with abnormal EEGs is currently unknown. Although isolated epileptiform discharges have been reported in many psychiatric conditions, they are most commonly observed in patients with aggression, panic, or autistic spectrum disorders. The literature search was guided by 3 criteria: (1) studies had patients who did not experience seizures, (2) patients had EEGs, and (3) an AED was administered. Most important finding is that the number of "controlled" studies was extremely small. Overall, most reports suggest that the use of an AED can be associated with clinical and, at times, improved EEG abnormalities. Additionally, six controlled studies were found for other psychiatric disorders, such as learning disabilities with similar results. Overall, the use of anticonvulsants to treat nonepileptic psychiatric patients needs further controlled studies to better define indications, adequate EEG work-up, best AED to be used, and optimal durations of treatment attempts.

In contrast to sensory gating, the brain's ability to re-respond to relevant stimuli and the potential differences between healthy and schizophrenic participants have not been studied in great detail. Here, we explore what auditory paradigms are useful to measure this re-responding ability. Evoked potentials (EPs) were obtained from the Cz channel using 3 paired stimulus paradigms (pairs with equal stimuli {PE}, the second stimulus being lower {PL} or higher {PH} in frequency) and 2 short-train paradigms in which 5 identical stimuli were followed by a lower frequency stimulus (train lower {TL}) or higher frequency stimulus (train higher {TH}). Data were collected from 17 healthy control participants (NC) and 17 age and gender-matched patients with schizophrenia (SZ). Up to 4 data sets obtained on 4 different days were available for each participant. Ensemble averages were computed for each session, from which the P50, N100, and P200 latencies and amplitudes were obtained. No significant differences in amplitude or latency of the various EP components were found between the responses to the second stimulus obtained with the 5 paradigms. Neither did the responses to the fifth and sixth stimuli differ for the TL and TH paradigm, with the exception of the N100 latency of the fifth stimulus, which was longer for TH than TL for NC. Healthy participants had larger amplitudes and shorter latencies than the patients with schizophrenia for the responses to the first stimuli, with the latency differences continuing for the fifth and sixth response. Also, the amplitude and latency of the first response was larger than for the second response in both populations. In conclusion, none of the paradigms studied here, with the employed parameters, are useful to measure the re-responding ability of the brain. Also, the shorter latencies for the repeated stimulus suggest that the neural mechanism underlying attenuation of repeated stimuli is of a facilitating nature.

Recent findings indicate that binding and synchronization of distributed activities are crucial for the mechanism of consciousness, and there is increased evidence that disruptions in feature binding produce disintegration of consciousness in schizophrenia. These data suggest that the disrupted binding and disintegration of consciousness could be related to dissociation, which is historically linked to Bleuler's concept of splitting in schizophrenia. In the present study we aimed to investigate relations among electroencephalogram (EEG) activities of cortical sites and used psychometric measures of positive and negative schizophrenia symptoms (Positive and Negative Syndrome Scale) and the Dissociative Experiences Scale (DES) in 58 patients with paranoid schizophrenia. The results show statistically significant Spearman correlations of the DES with cross-correlation function in nine (of 16) EEG pairs. Positive symptoms display significant Spearman correlation with mean of cross-correlation function in only one EEG pair (F4-C4). Results of the Mann-Whitney test between patients with higher (DES > or = 30) and lower dissociation show statistically significant differences between the groups for cross-correlations in nine EEG pairs. The results of this study provide the first supportive evidence for a negative relationship between cross-correlation indices and symptoms of dissociation in schizophrenia., (Copyright 2009 Elsevier Ltd. All rights reserved.)

In research on schizophrenia electrophysiological measures have been investigated to identify biomarkers of the disorder, indices enabling differential diagnosis among psychotic disorders, prognostic indicators or endophenotypes. The present systematic review will focus on the most largely studied electrophysiological indices, i.e., qualitative or quantitative (limited to spectral analysis) EEG and the P300 event-related potential. The PubMed clinical query was used with research methodology filters for each of the following categories: diagnosis/prognosis/ aetiology and a broad sensitive search strategy. The key-words: SCHIZOPHRENIA AND EEG/P3/P300 were used. The search results were then narrowed by including the terms "human" and "English language", and cross-referenced. Systematic reviews and meta-analyses, when available, were also used for cross-referencing. Case reports and studies irrelevant to the topics and methodologies under examination were excluded. The remaining papers were screened to verify the eligibility for this systematic review. Inclusion criteria were: a) a diagnosis of schizophrenia confirmed by DSM-III/ICD-9 criteria (or later editions of the same classification systems); b) the inclusion of both a schizophrenia study group and an healthy control group (when appropriate, i.e., for P300 and quantitative EEG); c) qualitative or spectral EEG findings and amplitude measures for P300. The included studies were then reviewed to verify homogeneity of the results, as well as the presence of the information needed for the present systematic review and meta-analysis. Previous reviews and studies meeting the above requirements (n = 22 for qualitative EEG; n = 45 for spectral EEG and n = 132 for P300) were classified according to the Oxford Centre for Evidence-based Medicine (EBM) levels of evidence criteria. For qualitative EEG as a diagnostic test, the majority of studies predated the introduction of DSM-III and were excluded from the review. Few post DSM-III studies investigated the usefulness of qualitative EEG in the differential diagnosis between schizophrenia and psychosis due to general medical condition. None of them was Oxford CEBM level 3b (non-consecutive-study or cohort-study without consistently-applied reference standard) or better (exploratory or validating cohort-study). No meta-analysis could be conducted due to the lack of reliable quantification methods in the reviewed studies. For spectral EEG as a diagnostic test, most studies qualified as level 4 (case-control study with poor reference standard), and only 24% as level 3b or better. An increase of slow activity in patients is reported by most of these studies. As to meta-analyses examining 29 studies, with 32 independent samples for the delta band and 35 for the theta band, a moderate effect size was found and only 1 study yielded findings in the opposite direction for both measures. There was no identified source for the discrepancy. The analysis of moderator factors included medication, band frequency limits, spectral parameters and disease stage. The medication status was significant for the theta band but the effect was unclear as findings for drug-naïve and drug-free patients were in a different direction. Chronicity had a significant effect on both delta and theta bands, with slow activity increase larger in chronic than in first episode patients. For P3 amplitude reduction as a diagnostic index, 63% of the studies qualified as level 3b or better. Meta-analysis (52 studies, 60 independent samples) results demonstrated a large effect size. None of the studies reported opposite findings. The analysis of moderator factors, including medication status and disease stage, revealed no significant effect on data heterogeneity. In conclusion, the examined indices are good candidates but are not ready yet for clinical applications aimed to improve present diagnostic standards for schizophrenia. Further research carried out according to adequate methodological standards and based on large scale multi-center studies is mandatory.

For patients with schizophrenia, a deficient gating (or filtering) of sensory input has been described. One major approach to study this sensory gating is to measure event-related potentials (ERPs) in response to paired clicks. In these experiments, sensory gating is quantified as amplitude reduction of the ERP components P50 and N100 from the 1st to the 2nd stimulus. In ERP studies brain electrical signals are averaged over single trials. Alterations in phase locking might be one factor contributing to the observed deficits in sensory gating, but findings have been inconclusive as yet. In particular, the contribution of different frequency bands to the deficit required further investigation. We studied N100 gating by intracranial recordings in a sample of epilepsy patients and subdivided the group into good and poor gators of the intracranial ERP component N100. Data were evaluated by frequency specific wavelet-based phase and power analyses. Poor N100 gators had an increased phase locking in the frequency range from 6.0-15.1 Hz after the 2nd stimulus, as compared to good gators. Other group differences were apparent already before the 2nd stimulus. Poor gators had less phase locked beta band activity (20.2-30.0 Hz) than good gators 200-315 ms after the onset of the 1st stimulus. Within the group of poor gators, lower values of phase locking in this frequency range were also associated with lower gating ratios. The reduced beta band response in response to the 1st stimulus may reflect poorer memory encoding of the 1st stimulus in poor gators. This in turn might lead to increased demands to process the 2nd stimulus.

Subclinical electroencephalographic epileptiform discharges in neurobehavioral disorders are not uncommon. The clinical significance and behavioral, diagnostic, and therapeutic implications of this EEG cerebral dysrhythmia have not been fully examined. Currently the only connotation for distinctive epileptiform electroencephalographic patterns is epileptic seizures. Given the prevailing dogma of not treating EEGs, these potential aberrations are either disregarded as irrelevant or are misattributed to indicate epilepsy. This article reappraises the literature on paroxysmal EEG dysrhythmia in normative studies of the "healthy" nonepileptic general populations, neuropsychiatry, and in neurobehavioral disorders. These EEG aberrations may be reflective of underlying morpho-functional brain abnormalities that underpin various neurobehavioral disturbances.

Sensory gating refers to the preattentional filtering of irrelevant sensory stimuli. This process may be impaired in schizotypy, which is a trait also associated with cigarette smoking. This association may in part stem from the positive effects of smoking on sensory gating and attention. The relationship among sensory gating, smoking, schizotypy and attention was examined in 39 undergraduates. Sensory gating was indexed by the P50 suppression paradigm, and attention was measured by the Attention Network Test (ANT) and a Stroop task. Results showed sensory gating to be positively correlated with performances on ANT and Stroop reflected in better alerting, less conflict between stimuli, faster reaction time, and greater accuracy. Smokers showed a pattern of a greater number of significant correlations between sensory gating and attention in comparison to non-smokers, although the relationship between sensory gating and attention was not affected by schizotypy. The majority of significant correlations were found in the region surrounding Cz. These findings are discussed relative to the potential modifying influence of smoking and schizotypy on sensory gating and attention.

Objective: A literature review was conducted to ascertain whether or not EEG spectral abnormalities are consistent enough to warrant additional effort towards developing them into a clinical diagnostic test for schizophrenia., Methods: Fifty three papers met criteria for inclusion into the review and 15 were included in a meta-analysis of the degree of significance of EEG deviations as compared to healthy controls. Studies were classified based on a 4-step approach based on guidelines for evaluating the clinical usefulness of a diagnostic test., Results: Our review and meta-analysis revealed that most of the abnormalities are replicated in the expected directions with the most consistent results related to the increased preponderance of slow rhythms in schizophrenia patients. This effect remained consistent in un-medicated patients. Only a small number of studies provided data on the sensitivity and specificity of the findings in differentiating among the psychiatric disorders that frequently appear on the same differential diagnostic list as schizophrenia (Step 3 studies). No multicenter studies using standardized assessment criteria were found (Step 4 studies)., Conclusions: Additional Step 3 and Step 4 studies are needed to draw conclusions on the usefulness of EEG spectral abnormalities as a diagnostic test for schizophrenia.

Rationale: Suppression of middle latency auditory evoked responses is considered an index for the multistage sensory gating process. This has been observed in sequentially occurring P50, N100 and P200 components in a dual-click procedure. Since P50 sensory gating deficits have been observed in schizophrenic patients and first degree relatives, this parameter was suggested as an intermediate phenotype of the disease. However, most studies only show a low reliability for P50 sensory gating and neither N100 nor P200 sensory gating have been sufficiently tested., Methods: Reliability of P50, N100 and P200 sensory gating was measured in 41 healthy subjects in two sessions, four weeks apart, using intra-class correlation. Sensory gating was calculated as ratio-gating (second response magnitude/first response magnitude x100) as well as difference-gating (first response magnitude minus second response magnitude)., Results: The difference-gating showed good to excellent reliabilities independently of the amplitude-measurement method applied (P50 peak-to-peak 0.75 and baseline-to-peak 0.74, N100 peak-to-peak 0.63 and baseline-to-peak 0.70, P200 peak-to-peak 0.82 and baseline-to-peak 0.79). Regarding ratio-gating, best temporal stability was observed for the P200 (peak-to-peak 0.58 and baseline-to-peak 0.62). Reliability of P50 ratio-gating strongly depends on the amplitude-measurement method (peak-to-peak 0.0 and baseline-to-peak 0.46)., Conclusion: Regarding long-term reliability in healthy subjects the difference-gating of all three evoked responses and the ratio-gating of the P200 component may be useful tools for clinical or intermediate phenotype studies measuring different stages of the auditory sensory gating process. In contrast, the reliability of the P50 and N100 ratio-gating component seems to be insufficient for this purpose. However, long-term reliability remains to be confirmed in clinical samples.

The filtering of sensory information, also referred to as "sensory gating", is impaired in various neuropsychiatric diseases. In the auditory domain, sensory gating is investigated mainly as a response decrease of the auditory evoked potential component P50 from one click to the second in a double-click paradigm. In order to relate deficient sensory gating to anatomy, it is essential to identify the cortical structures involved in the generation of P50. However, the exact cerebral topography of P50 gating remains largely unknown. In a group of 17 patients with drug-resistant focal epilepsy, P50 was recorded invasively via subdural electrodes, and the topography of functionally indispensable ("eloquent") cortices was obtained by electrical stimulation mapping. These eloquent areas were involved in language, motor, and sensory functions. P50 could be identified in 13 patients in either temporal (n=8) or midfrontal sites (n=5). There were six occurrences (in five patients) of overlap of sites with maximal P50 responses and eloquent areas. Those were auditory (n=1), supplementary sensorimotor (n=3), primary motor (n=1), and supplementary negative motor (n=1). Results suggest that the early stage of sensory gating already involves a top-down modulation of sensory input by frontal areas.

Early (P50) and late (P200) auditory sensory gating were assessed in low and high schizotypal personality groups using Raine's Schizotypal Personality Questionnaire. We also assessed the impact of smoking as it relates to low and high schizotypal personalities. Low and high schizoptypal personality groups were divided into subgroups of participants who either smoked or did not smoke tobacco cigarettes. Participants were 39 (18 men) right-handed undergraduates. Using a paired-tone paradigm (40 pairs, 70 dB, 1000 Hz), smokers were tested while abstaining from smoking, and 5 min after smoking. Non-smokers were tested similarly without smoking. Midline and hemispheric sites were evaluated at frontal (F3/Fz/F4), fronto-central (FC3/FCz/FC4), central (C3/Cz/C4), centro-parietal (CP3/CPz/CP4), and parietal (P3/Pz/P4) regions. P50 sensory gating was better at midline sites than left/right hemispheric sites, whereas there was no difference in activation with respect to location for P200 sensory gating. Cz had better P50 sensory gating than other midline regions, whereas Fz, FCz and Cz had better P200 sensory gating than CPz and Pz. Hemispheric comparisons were made. At the central region for non-smokers, high schizotypys showed poorer P50 sensory gating than low schizotypys. Among low schizotypys, smokers showed poorer P50 sensory gating than non-smokers at the fronto-central and central regions smokers showed better P200 sensory gating than non-smokers at the central region. Smoking had no acute impact on either early (P50) or late (P200) sensory gating. Our data support the notion that early sensory gating and late sensory gating represent different sensory gating mechanisms with respect to low and high schizotypy personalities. Individual differences in early and late sensory gating need further investigation.

The authors evaluate quantitative electroencephalography (qEEG) as a laboratory test in clinical psychiatry and describe specific techniques, including visual analysis, spectral analysis, univariate comparisons to normative healthy databases, multivariate comparisons to normative healthy and clinical databases, and advanced techniques that hold clinical promise. Controversial aspects of each technique are discussed, as are broader areas of criticism, such as commercial interests and standards of evidence. The published literature is selectively reviewed, and qEEG's applicability is assessed for disorders of childhood (learning and attentional disorders), dementia, mood disorders, anxiety, panic, obsessive-compulsive disorder, and schizophrenia. Emphasis is placed primarily on studies that use qEEG to aid in clinical diagnosis, and secondarily on studies that use qEEG to predict medication response or clinical course. Methodological problems are highlighted, the availability of large databases is discussed, and specific recommendations are made for further research and development. As a clinical laboratory test, qEEG's cautious use is recommended in attentional and learning disabilities of childhood, and in mood and dementing disorders of adulthood.

Previous studies have shown alterations of eyeblink reflex in patients with various psychiatric disorders. It has previously been demonstrated by our group that EEG measures of the reactivity to eye opening could effectively predict patient-reported startle response in patients with acute stress reaction. In our present study, EEG spectral power analysis and eyeblink electrical startle responses were acquired from a total of 39 patients diagnosed with various psychiatric disorders: 7 patients with schizophrenia, 10 patients with major depressive disorder (MDD), 10 patients with panic disorder, 5 patients with posttraumatic stress disorder (PTSD) and 7 patients with generalized anxiety disorder (GAD). EEG percent power data of each frequency band (delta, theta, alpha, beta) obtained from the 19 leads under open or closed eyelid conditions were used to calculate the arithmetical difference between eyes-open and eyes-closed states as representative of "EEG reactivity to eye opening". Data was analyzed separately for each diagnostic group. For all of the disorders, right-sided R2c (contralateral secondary component) latency was the single eyeblink startle measure that was found to be significantly correlated with EEG reactivity to eye opening. The correlation was most significant for right temporal theta frequency in schizophrenia, right temporal theta frequency in MDD, left central beta frequency in panic disorder, left parietotemporal delta frequency in PTSD and right occipital alpha frequency in GAD. Findings showed a newly identified pattern that has potential scientific and clinical value with respect to psychiatric medicine.

The extent of medical follow-up of abnormal screening EEGs secured from psychiatric patients, particularly those reporting slow wave dysrhythmias as the single finding, still varies widely. From an earlier routine EEG screening program for psychiatric inpatients, 103 consecutive cases of abnormal EEGs with generalized, focal, or paroxysmal slowing as the only EEG finding were identified. Despite suggestions for medical follow-up, less than half (44.6%) of the patients received subsequent study. However, 74.2% of patients considered to be without organic pathophysiology at the time of the EEG had positive organic findings on medical follow-up.

Evidence for a role for drugs of abuse in the development of chronic psychotic syndromes is scattered throughout 40 years of literature. Electrophysiological studies examining groups believed to have chronic drug-induced psychotic symptoms yielded interesting findings. To our knowledge, no studies directly compared schizophrenia patients whose drug use preceded and those whose drug use followed the onset of psychotic symptoms. Twenty-six schizophrenia patients and 10 healthy control subjects were recruited for the study. Based on the SCID interview, schizophrenia subjects were classified into a Psychosis First (Psy 1st) group (N=11), Drugs First (Drugs 1st; N=8), and No Drug Use (No Drugs; N=7). Schizophrenia subjects were administered the Positive and Negative Symptoms Scale (PANSS). The P300 evoked response and sensory gating were measured for all subjects. Despite the small sample sizes significant differences were found between the groups. Most significantly, the P300 amplitude was smallest in the Drugs 1st as compared to the No Drugs groups, while sensory gating deficit was worst in the Psy 1st group. The data suggest that significant clinical and electrophysiological differences between these groups can be identified. Further research to better define these differences seems warranted.

In the field of psychiatry diagnoses are primarily based on the report of symptoms from either the patient, parents, or both, and a psychiatrist's observations. A psychiatric diagnosis is currently the most widely used basis for medication selection and the brain is seldom investigated directly as a source of those symptoms. This study addresses the request from the National Institute of Mental Health (NIMH) Research Domain Criteria Project (RDoC) for scientific research into neurological abnormalities that can be linked to psychiatric symptoms for the purpose of predicting medication response. One such neurological abnormality that has been the focus of many studies over the last three decades is isolated epileptiform discharges (IEDs) in children and adolescents without seizures. We conducted a systematic review of the literature to determine prevalence rates of IEDs within diagnostic categories. We then compared the prevalence of IEDs in the selected literature to our IRB-approved data archive. Our study found a consistent high prevalence of IEDs specifically for ADHD (majority > 25%) and ASD (majority > 59%), and consistent low prevalence rates were found for Depression (3%). If children and adolescents have failed multiple medication attempts, and more than one-third of them have IEDs, then an EEG would be justified within the RDoC paradigm. [ABSTRACT FROM AUTHOR]