title: Frontal EEG predictors of treatment outcome in major depressive disorder Effects of Methylphenidate on performance of a practical pistol shooting task: a quantitative electroencephalography (qEEG) study Quantitative EEG effects of carbamazepine, oxcarbazepine, valproate, lamotrigine, and possible clinical relevance of the findings A pharmaco-EEG study on antipsychotic drugs in healthy volunteers Twenty Percent of a Representative Sample of Patients Taking Bupropion Have Abnormal, Asymptomatic Electroencephalographic Findings Comparison of the effects of vigabatrin, lamotrigine, and topiramate on quantitative EEGs in patients with epilepsy. Lamotrigine decreases EEG synchronization in a use-dependent manner in patients with idiopathic generalized epilepsy Changes in EEG order in neuroleptically treated normal volunteers during a voluntary movement task A pilot study to determine whether machine learning methodologies using pre-treatment electroencephalography can predict the symptomatic response to clozapine therapy The effect of methylphenidate on auditory information processing in healthy volunteers: a combined EEG/MEG study Effects of sertraline on autonomic and cognitive functions in healthy volunteers Does prior antidepressant treatment of major depression impact brain function during current treatment? Psychomotor and cognitive effects of a single oral dose of talnetant (SB223412) in healthy volunteers compared with placebo or haloperidol Alpha rhythm slowing during initiation of carbamazepine therapy: implications for future cognitive performance. Assessment of CNS effects of antiepileptic drugs by using quantitative EEG measures. A comparison of the central nervous system effects of haloperidol, chlorpromazine and sulpiride in normal volunteers. Quantitative EEG in Schizophrenic Patients before and during Pharmacotherapy Effects of gabapentin and carbamazepine on the EEG and cognition in healthy volunteers. Clinical, Cognitive, and Neurophysiologic Correlates of Short-Term Treatment with Carbamazepine, Oxcarbazepine, and Levetiracetam in Healthy Volunteers Evaluation of encephalotropic and psychotropic properties of gabapentin in man by pharmaco-EEG and psychometry. Pre-treatment EEG and it's relationship to depression severity and paroxetine treatment outcome. Imaging the cortical effect of lamotrigine in patients with idiopathic generalized epilepsy: A low-resolution electromagnetic tomography (LORETA) study
abstract: OBJECTIVE To investigate the role of frontal EEG as predictor of clinical response to SSRIs or venlafaxine in major depressive disorder ( MDD ) . METHOD 82 subjects ( age 35.9+/-13.0 ; 47.6 % female ) meeting DSM-IV criteria for MDD entered an 8-week prospect i ve treatment with SSRIs or venlafaxine . At baseline and week 1 we recorded serial , 4-channel EEGs ( F7-Fpz , F8-Fpz , A1-Fpz , A2-Fpz ) . We evaluated prospect ively the relative theta power as predictor of treatment outcome . We also developed an Antidepressant Treatment Response ( ATR ) index using EEG parameters assessed at baseline and week 1 . RESULTS 45 subjects ( 54.9 % ) responded to treatment ( HAM-D-17 reduction > or=50 % ) . At baseline , frontal relative theta power ( i.e. , 4 - 8 Hz power/2 - 20 Hz power ) was significantly ( p=0.017 ) lower ( 21 % ) in treatment responders than in non-responders ( 24 % ) . Baseline relative theta power predicted treatment response with 63 % accuracy [ 64 % sensitivity , 62 % specificity , 66 % area under the receiver operator curve ( AUROC ) ( p=0.014 ) ] . Relative theta power at week 1 predicted treatment response with 60 % accuracy [ 62 % sensitivity , 57 % specificity , 61 % AUROC ( p=0.089 ) ] . ATR predicted response with 70 % accuracy [ 82 % sensitivity , 54 % specificity , 72 % AUROC ( p=0.001 ) ] . CONCLUSION Using automated analysis of frontal EEG collected during the first week of antidepressant treatment it may be possible to facilitate prediction of SSRI or venlafaxine efficacy in MDD Background The present study examined absolute alpha power using quantitative electroencephalogram ( qEEG ) in bilateral temporal and parietal cortices in novice soldiers under the influence of methylpheni date ( MPH )  during the preparatory aim ing period in a practical pistol-shooting task . We anticipated higher bi-hemispheric cortical activation in the preparatory period relative to pre-shot baseline in the methylpheni date group when compared with the control group because methylpheni date has been shown to enhance task-related cognitive functions . Methods Twenty healthy , novice soldiers were equally distributed in control ( CG ; n = 10 ) and MPH groups 10 mg ( MG ; n = 10 ) using a r and omized , double blind design . Subjects performed a pistol-shooting task while electroencephalographic activity was acquired . Results We found main effects for group and practice blocks on behavioral measures , and interactions between group and phases on electroencephalographic measures for the electrodes T3 , T4 , P3 and P4 . Regarding the behavioral measures , the MPH group demonstrated significantly poorer in shooting performance when compared with the control and , in addition , significant increases in the scores over practice blocks were found on both groups . In addition , regarding the electroencephalographic data , we observed a significant increase in alpha power over practice blocks , but alpha power was significantly lower for the MPH group when compared with the placebo group . Moreover , we observed a significant decrease in alpha power in electrodes T4 and P4 during PTM . Conclusion Although we found no correlation between behavioral and EEG data , our findings show that MPH did not prevent the learning of the task in healthy subjects . However , during the practice blocks ( PBs ) it also did not favor the performance when compared with control group performance . It seems that the CNS effects of MPH dem and ed an initial readjustment period of integrated operations relative to the sensorimotor system . In other words , MPH seems to provoke a period of initial instability due to a possible modulation in neural activity , which can be explained by lower levels of alpha power ( i.e. , higher cortical activity ) . However , after the end of the PB1 a new stabilization was established in neural circuits , due to repetition of the task , result ing higher cortical activity during the task . In conclusion , MPH group performance was not initially superior to that of the control group , but eventually exceeded it , albeit without achieving statistical significance UNLABELLED Quantitative EEG ( QEEG ) effects of therapeutic doses of carbamazepine ( CBZ ) , oxcarbazepine ( OXC ) , valproate ( VA ) and lamotrigine ( LA ) monotherapy were investigated in patients with beginning epilepsy . Baseline waking EEG ( EEG1 ) was recorded in the untreated state , the second EEG ( EEG2 ) was done after 8 weeks of reaching the therapeutic dose . Left occipital data were used for analysis . QEEG target parameters were absolute b and -power ( delta : AD , theta : AT , alpha : AA , beta : AB ) , and alpha mean frequency ( AMF ) . Group effects ( untreated versus treated condition in the CBZ , VA , OXC , LA groups ) were computed for each target parameter . One group with benign rol and ic epilepsy remained untreated for clinical reasons and served to estimate the QEEG test-retest differences . In addition , the individual QEEG response to each drug was calculated as ( EEG2-EEG1 ) . RESULTS statistically significant ( p<0.05 ) group differences indicated the QEEG domain systematic ally affected by the drugs . CBZ caused AT increase and AMF decrease . OXC caused AMF decrease . VA and LA did not decrease AMF ( LA even increased it ) , but reduced broad-b and power . Individual power and AMF changes showed considerable variability in each group . > 0.5 Hz AMF decrease ( that was reported to predict cognitive impairment in prior studies ) occurred in 10/41 patients in the CBZ group but never in the OXC , VA , LA groups . The results may be utilized in planning further studies addressing the relationship between antiepileptic drugs and their CNS effects . In addition , the relationship of AED-related cognitive impairment and AMF changes was discussed Rationale Both psychotropic drugs and mental disorders have typical signatures in quantitative electroencephalography ( EEG ) . Previous studies found that some psychotropic drugs had EEG effects opposite to the EEG effects of the mental disorders treated with these drugs ( key – lock principle ) . Objectives We performed a placebo-controlled pharmaco-EEG study on two conventional antipsychotics ( chlorpromazine and haloperidol ) and four atypical antipsychotics ( olanzapine , perospirone , quetiapine , and risperidone ) in healthy volunteers . We investigated differences between conventional and atypical drug effects and whether the drug effects were compatible with the key – lock principle . Methods Fourteen subjects underwent seven EEG recording sessions , one for each drug ( dosage equivalent of 1 mg haloperidol )  . In a time-domain analysis , we quantified the EEG by identifying clusters of transiently stable EEG topographies ( microstates ) . Frequency-domain analysis used absolute power across electrodes and the location of the center of gravity ( centroid ) of the spatial distribution of power in different frequency b and s. Results Perospirone increased duration of a microstate class typically shortened in schizophrenics . Haloperidol  increased mean microstate duration of all classes , increased alpha 1 and beta 1 power , and tended to shift the beta 1 centroid posterior . Quetiapine decreased alpha 1 power and shifted the centroid anterior in both alpha b and s. Olanzapine shifted the centroid anterior in alpha 2 and beta 1 . Conclusions The increased microstate duration under perospirone and haloperidol was opposite to effects previously reported in schizophrenic patients , suggesting a key – lock mechanism . The opposite centroid changes induced by olanzapine and quetiapine compared to haloperidol might characterize the difference between conventional and atypical antipsychotics The risk of dose-dependent seizures is a safety issue with bupropion hydrochloride . To evaluate the presence of specific electroencephalographic ( EEG ) waveforms , 210 adult subjects taking stable doses of bupropion hydrochloride  were recruited to undergo 2 EEGs in a prospect i ve , single-center cohort study . The occurrence of spike waves , sharp waves , and focal slowing was recorded and assessed with a continuation ratio logit model for polytomous responses . This model showed that there was a relationship between sex and the incidence of these waveforms , such that the odds of female subjects having sharp waves was increased by a factor of 2.53 ( P = 0.05 ) when compared with male subjects and controlled for both age and dose . Similarly , female subjects were 2.45 ( P = 0.09 ) times more likely than males to have focal slowing on EEG . Overall , 19.8 % ( 39/197 ) of this representative population was found to have abnormal , asymptomatic EEG findings . The presence of these waveforms in individuals taking a medication known to lower the seizure threshold may be a risk factor for developing seizures Information on the effects of newer antiepileptic drug ( AEDs ) on the electroencephalogram ( EEG ) is sparse and contradictory . Quantitative EEG ( qEEG ) provides a method of estimating the effects of drugs on the central nervous system . Twenty-three adult patients with difficult-to-control complex partial seizures , with or without secondary generalization , participated in an add-on study with one of three newer AEDs : vigabatrin ( n = 10 ) , lamotrigine ( n = 6 ) , and topiramate ( n = 7 ) . Frequency analysis and topographic mapping of awake EEGs before and during treatment with the drug were compared . Statistical analysis was performed using 2-way analysis of variance ( ANOVA ) with repeated measures . Vigabatrin administration was followed by a diffuse decrease in the absolute alpha ( p < 0.05 ) and beta ( p < 0.02 ) activities and a decrease in the absolute theta in the frontal and parieto-occipital regions ( p < 0.03 ) . Lamotrigine caused a significant diffuse increase in the faster frequencies ( relative alpha p < 0.04 and relative beta p < 0.02 ) , and decrease in the slower activities ( relative theta in the posterior head regions p < 0.03 and relative delta diffusely p < 0.05 ) . Topiramate increased the absolute beta ( p < 0.05 ) and theta ( p < 0.02 ) activities diffusely and decreased the relative alpha activity over the left hemisphere ( p < 0.03 ) . The different effect profiles of the newer AEDs on the electrical brain activity may reflect their different mechanisms of action OBJECTIVE To investigate the quantitative EEG effects of lamotrigine ( LTG ) monotherapy . HYPOTHESIS LTG was predicted to decrease thalamo-cortical neuronal synchronization in idiopathic generalized epilepsy ( IGE ) . METHODS Waking EEG background activity of 19 IGE patients was investigated before treatment and in the course of LTG monotherapy .  Raw absolute power ( RAP ) , raw percent power ( RRP ) , and raw mean frequency ( RMF ) were computed for 19 electrodes and four frequency b and s ( delta=1.5 - 3.5Hz , theta=3.5 - 7.5Hz , alpha=7.5 - 12.5Hz , and beta=12.5 - 25.0Hz ) . Inter- and intrahemispheric coherence was computed for eight electrode pairs and the four frequency b and s. In addition , scalp-averages were calculated for each variable . Group differences were computed by means of nonparametric statistics including correction for multiple comparisons . RESULTS Main results were decreased delta and theta RAP ( p<0.05 for scalp-averages ) . LTG compressed the delta , theta , and alpha RAP data sets , reducing the upper limit of the scatter in particular . Spearman r-values indicated marked correlation between the starting values ( RAPuntreated ) and the LTG-related decrease ( RAPtreated-RAPuntreated ) in three b and s : delta ( r=-0.72 ; p=0.0005 ) , theta ( r=-0.59 ; p=0.007 ) , and alpha ( r=-0.61 ; p=0.006 ) . Thus , the greater the baseline neuronal synchronization , the marked the dampening effect of LTG on it . The remaining findings were decreased theta RRP , theta RMF , and increased alpha RMF ( p<0.05 for scalp-averages ) . The electrode-related changes were small but topographically consistent across the 19 electrode sites . LTG did not affect coherence . CONCLUSIONS 1 . LTG partially normalized the spectral composition of EEG background activity . LTG decreased pathological thalamo-cortical synchronization in use-dependent manner . 2 . LTG did not cause quantitative EEG alterations suggesting worsening of the physiological brain functions . Instead , its profile suggested a mild psychostimulant effect . SIGNIFICANCE The results contribute to the underst and ing of the effect of LTG at the network level Summary 15 normal volunteers were treated over three weeks with haloperidol ( HAL ) and in the third week additionally with biperidene ( BIP ) . The order of the EEG spectra at different topographical locations and in different frequency b and s during a movement task was analyzed using uncertainty analysis ( UA ) , a multivariate analysis technique based on informationtheoretical methods . Different patterns of drug-induced changes were found . HAL decreases the theta and alpha b and order at the fronto- central lateral areas but increases it at the fronto- central midline in the theta b and and at the parietal areas in the alpha b and . With the exception of the fronto- central midline locations , BIP more or less counterbalances the effect of HAL . Volunteers felt unwell and had motor disturbances during HAL and felt well again during HAL + BIP .  Reaction time values were increased during HAL and normalized during HAL + BIP OBJECTIVE To investigate whether applying advanced machine learning ( ML ) method ologies to pre-treatment electroencephalography ( EEG ) data can predict the response to clozapine  therapy in adult subjects suffering from chronic schizophrenia . METHODS  Pre-treatment EEG data are collected in 23 + 14 schizophrenic adults . Treatment outcome , after at least one year follow-up , is determined using clinical ratings by a trained clinician blind to EEG results . First , a feature selection scheme is employed to select a reduced subset of features extracted from the subjects ' EEG that is most statistically relevant to our treatment-response prediction . These features are then entered into a classifier , which is realized in the form of a kernel partial least squares regression method that performs response prediction . Various scales , including the positive and negative syndrome scale ( PANSS ) are used as treatment-response indicators . RESULTS We determined that a set of discriminating EEG features do exist . A low-dimensional representation of the feature space showed significant clustering into clozapine responder and non-responder groups . The minimum level of performance of the proposed prediction methodology , tested over a range of conditions using the leave-one-out cross-validation method using the original 23 subjects , with further testing in an independent sample of 14 subjects , was 85 % . CONCLUSIONS These findings indicate that analysis of pre-treatment EEG data can predict the clinical response to clozapine in treatment resistant schizophrenia . SIGNIFICANCE If replicated in a larger population , this novel approach to EEG analysis may assist the clinician in determining treatment-efficacy Introduction The psychomotor stimulant methylpheni date ( MPH ) has been shown to improve attentional processes , reflected in behavioural measures such as vigilance , reaction time and visual attention tasks . The neural mechanisms of MPH action on sensory information processing , however , remain poorly understood . To the authors ’ knowledge , this present study is the first to investigate whether a single dose of MPH affects neural substrates of passive attention in healthy adults studied with simultaneous whole-head magnetoencephalography ( MEG ) and electroencephalography ( EEG ) . Methods Monaural left-ear auditory stimuli were presented in an oddball paradigm with infrequent deviant tones differing in frequency and duration . Neuronal activity was recorded with simultaneous whole-head MEG and EEG in 13 healthy subjects ( five females ; aged 27 ± 5 years ) after oral administration of 40 mg MPH or placebo in a r and omised , double-blind , cross-over design . We analysed both electric and magnetic N100 , P200 and mismatch negativity ( MMN ) components . Results MPH  increased arousal levels in visual analogue scales  . MPH had no effect on the dipole strength of MMN or MMNm in either frequency or duration deviations . MPH did , however , reduce P200 amplitudes in EEG . Conclusions The lack of effect of MPH on either MMN or MMNm suggests no association between catecholaminergic activities and MMN generation . However , our findings imply that MPH may change the neural bases of auditory information processing such as the early stimulus evaluation reflected in the P200 component . Dopamine and noradrenaline neurotransmitter systems could be responsible for the modulation of these processes . The exclusive effect of MPH on the P200 component could have a clinical application Rationale Though sertraline , a selective serotonin reuptake inhibitor ( SSRI ) , causes autonomic and cognitive adverse events such as dry mouth and somnolence , there is a paucity of appropriately design ed studies on the cognitive and autonomic effects of the drug in the literature . Objective To compare the effects of sertraline on cognitive and autonomic functions with those of placebo in healthy humans . Method A r and omized , double blind , cross over study of 12 healthy male volunteers aged 24 ( 21– 32 ; median ; range ) years . Subjects orally received 50 mg sertraline and placebo once daily for periods of 14 days each with at least 14 days in between . Heart rate variability ( HRV ) , skin conductance level ( SCL ) and skin conductance response ( SCR ) following sudden deep respiration were employed as parameters for autonomic function . Quantitative EEG ( qEEG ) and psychometric tests served as parameters for cognitive function . Measurements were performed repeatedly before the start of drug administration and on the last treatment day . Results Sertraline caused a significant reduction of heart rate and SCL ( P<0.05 ) , whereas HRV and SCR were not changed . Cognitive functions such as flicker fusion frequency , memory , choice reaction time and psychomotor performance were not influenced by sertraline but slow and fast beta power density in the qEEG was increased . Conclusion Cognitive and psychomotor performance are not altered in healthy humans receiving multiple dosing with sertraline . The observed decreases in heart rate and SCL may be due to a sympatho-inhibitory effect of sertraline The relationship between prior antidepressant treatment and prefrontal brain functional response to subsequent treatment with antidepressant medication or placebo is unknown . Eighty-nine adults with Major Depressive Disorder ( MDD ) , characterized as antidepressant-experienced or antidepressant-naive , received one week of single-blind placebo treatment prior to eight weeks of r and omized treatment with medication ( fluoxetine or venlafaxine ; n = 47 ) or placebo ( n = 42 ) in one of three similar placebo-controlled trials . Brain function was assessed at baseline , end of placebo lead-in , and during r and omized treatment using quantitative electroencephalography ( qEEG ) . The authors assessed change in prefrontal theta-b and cordance ( PFC ) in antidepressant-experienced vs. antidepressant-naive subjects . Treatment history groups differed significantly on PFC change during the placebo lead-in even when controlling for clinical and demographic variables ( F(1,62 ) = 4.27 , p = .04 ) . As assessed in linear mixed models that examined treatment history ( antidepressant-experienced or antidepressant-naive ) , treatment assignment ( medication or placebo ) , and their interaction as predictors , treatment history also predicted PFC change during the r and omized phase of treatment even when controlling for pretreatment clinical and demographic and symptom improvement during treatment ( F(1,5o ) = 5.20 , p = .03 ) . The interaction was not significant . Post hoc analyses showed that antidepressant-experienced subjects treated with placebo showed PFC changes that did not differ from PFC changes seen in the medication group . Results suggest that prefrontal brain functional changes during treatment for MDD may differ depending upon prior treatment with antidepressant medication Central Nervous System ( CNS ) effects of talnetant , an NK-3 antagonist in development for schizophrenia , were compared to those of haloperidol and placebo . The study was r and omised , double-blind , three-way crossover of talnetant 200 mg , haloperidol 3 mg or placebo .  Twelve healthy males participated  and EEG , saccadic and smooth pursuit eye movements , adaptive tracking , body sway , finger tapping , hormones , visual analogue scales ( VAS ) for alertness , mood and calmness and psychedelic effects , left/right distraction task , Tower of London and Visual and Verbal Learning Task were assessed . Haloperidol showed ( difference to placebo ; 95 % CI ; p-value ) decreases in EEG α power ( −0.87μV ; −1.51/−0.22 ; p = 0.0110 ) , saccadic inaccuracy ( 2.0 % ; 0.5/3.6 ; p = 0.0133 ) , smooth pursuit eye movements ( −7.5 % ; −12.0/−3.0 ; p = 0.0026 ) , adaptive tracking ( −3.5 % ; −5.4/−1.7 ; p = 0.0009 ) , alertness ( −6.8 mm ; −11.1/−2.4 ; p = 0.0039 ) , negative mood ( −4.6 mm ; −8.6/−0.6 ; p = 0.0266 ) , the ability to control thoughts ( 1.2 mm ; 0.2/2.3 ; p = 0.0214 ) , and an increase of serum prolactin ( ratio 4.1 ; 3.0/5.6 ; p < 0.0001 ) . Talnetant  showed decreased alpha power ( −0.69 μV ; −1.34/−0.04 ; p = 0.0390 ) , improved adaptive tracking ( 1.9 % ; 0.1/3.7 ; p = 0.0370 ) and reduced calmness on VAS Bond and Lader ( −4.5 mm ; −8.0/−1.0 ; p = 0.0151 ) . Haloperidol effects were predominantly CNS-depressant , while those of talnetant were slightly stimulatory . The results suggest that talnetant penetrates the brain , but it remains to be established whether this dose is sufficient and whether the observed effect profile is class-specific for NK3-antagonists A prospect i ve study comparing the immediate changes in occipital electroencephalographic ( EEG ) frequency following institution of carbamazepine therapy to long-term alterations of neuropsychological performance is reported . The patient group consisted of 16 previously untreated children in the 5 - 14-year age range who had recent onset partial seizures and were managed for at least 1 year with carbamazepine monotherapy .  EEG changes following initiation of carbamazepine therapy , as compared to baseline , were determined by a computer-based quantitative method . Neuropsychological factors were assessed at baseline and after 1 year of therapy . While the alpha frequency decreased following institution of carbamazepine in most subjects , a greater decline ( typically > 0.5 Hz ) was observed in the subset who subsequently demonstrated decreased neuropsychological performance at 1 year . The major effects could be attributed to the Arithmetic and Picture Completion subtests of the Wechsler Intelligence Scale for Children-Revised ( WISC-R ) . The findings suggest that quantitative EEG analysis may be useful for identifying individuals at increased risk for developing anticonvulsant-related long-term cognitive changes PURPOSE Antiepileptic drugs ( AEDs ) can be associated with adverse neurologic effects including cognitive dysfunction . Objective methods for recognizing AED effects on the brain could be valuable for long-term management . We compared quantitative EEG measures and cognitive tests in a group of patients beginning or ending AED therapy .  METHODS Subjects included 20 patients beginning AED therapy ( AEDon ) , 12 patients stopping AED therapy ( AEDoff ) , 33 patient controls receiving stable AED therapy ( AEDco ) , and 73 healthy controls ( Nco ) . All subjects underwent structured EEG recording and a cognitive test battery before change in AED dose and again 12 - 16 weeks later , > or=4 weeks after the last dose change . Four occipital EEG measures ( peak frequency , median frequency , relative theta and delta power ) were analyzed . Cognitive test changes were scored by using test-retest regression equations based on the Nco subjects . Wilcoxon tests were used for two-group comparisons . RESULTS AEDons had a significant decrease , and AEDoffs , a significant increase in the peak frequency of the EEG rhythm , as compared with controls . Results for median frequency and theta power were similar . Change in the EEG peak frequency correlated with an aggregate cognitive change measure ( r2= 0.71 ; p < 0.001 ) , individual cognitive measures , and subjective complaints . Of the combined AEDon/AEDoff patients , 58 % exceeded the 95 % confidence interval for test-retest change in EEG peak frequency . CONCLUSIONS Quantitative measures derived from the occipital EEG are sensitive to AEDs and correlate with AED-related cognitive effects and subjective complaints . Although this correlation does not indicate a direct relation , quantified EEG may be a practical measure of AED impact on the brain 1 . Twelve healthy male volunteers participated in four experimental occasions during each of which they were dosed with one of the following anti-psychotic drugs : chlorpromazine ( 50 mg ) , haloperidol ( 3 mg ) , sulpiride ( 400 mg ) and placebo . Drugs were allocated to subjects in a double-blind , crossover fashion . 2 . The subject 's mood state , psychometric performance and electroencephalogram ( EEG ) were assessed pre-dose , and at 2 , 4 , 6 , 8 , 24 and 48 h post-dose . Mood states were assessed using 16 visual analogue scales and psychomotor performance was measured using the following tests : elapsed time estimation , tapping rate , choice reaction times , a rapid information processing task , flash fusion threshold , a manipulative motor task , digit span , body sway and tremor . 3 . Chlorpromazine and haloperidol significantly reduced subjective ratings of ' alertness ' and ' contentedness ' , and haloperidol significantly reduced feelings of ' calmness ' .  Sulpiride did not significantly affect any of the visual analogue scales . 4 . All three anti-psychotic drugs had similar EEG effects with peak effect 2 to 4 h postdose . The profile was characterised by an increase in the proportion of slow wave activity ( delta and theta ) as well as decreased alpha ( 8 - 14 Hz ) and faster ( beta ) wave activity . 5 . Chlorpromazine reduced tapping rate and increased choice reaction movement times . Haloperidol reduced the flash fusion threshold frequency at 6 h post-dose . Sulpiride prolonged the duration of the manipulative motor task , particularly at 48 h post-dose . 6 . All three anti-psychotic drugs impaired performance on the rapid information processing task . Chlorpromazine significantly reduced the number of correct letter pair identification s at 2 , 4 and 6 h post-dose , haloperidol at 4 , 6 , 8 , 24 and 48 h post-dose , and sulpiride at 24 h post-dose . ( ABSTRACT TRUNCATED AT 250 WORDS The aim of the study was to determine the possible differences in quantitative EEG parameters of schizophrenic patients before and during therapy with neuroleptics .  First EEG recordings were obtained from schizophrenic patients ( n = 50 ) who had not been taking any medicaments during the preceding 2 months . Second EEG recordings were obtained during the administration of neuroleptic therapy . Amplitude values of particular spectral segment , i.e. delta , theta , alpha 1 , alpha 2 , beta 1 and beta 2 ( after fast Fourier transformation ) were analyzed . The F3 , F4 , C3 , C4 , T3 , T4 , P3 , P4 , O1 and O2 regions were observed . The effect of pharmacotherapy manifested as a decrease in delta and beta 2 activities . The alterations of the delta spectrum were recorded in each patient subgroup ( regardless of the neuroleptic used ) . The changes in beta 2 activity were registered in patients on haloperidol and fluphenazine PURPOSE Antiepileptic drug ( AED ) therapy can be associated with neurotoxic side effects including cognitive dysfunction . Objective methods for detection of neurotoxicity in individual patients would be useful . We studied the effects of gabapentin ( GBP ) and carbamazepine ( CBZ ) on neurophysiologic and cognitive/behavioral measures in healthy volunteers . METHODS In a 12-week , r and omized , double-blind , parallel-group study of CBZ and GBP in healthy volunteers , 23 subjects completed the protocol . All achieved the target dose of 1,200 mg CBZ or 3,600 mg GBP . A structured EEG for quantitative analysis and a cognitive test battery were administered before AED therapy and again after 12 weeks of therapy . Test-retest differences were compared with those of 72 untreated control subjects . RESULTS Both CBZ and GBP significantly decreased the peak frequency of the posterior ( alpha ) rhythm , with CBZ exerting a greater effect . Ten CBZ and six GBP subjects exceeded the 95 % confidence interval ( CI ) for an individual . Cognitive tests revealed AED vs. control group effects for two of seven measures ( Digit Symbol , Stroop ) and all subjective measures . However , few subjects exceeded the 95 % CI for any objective test . Differences between CBZ and GBP were not significant . Greater EEG slowing was associated with greater subjective neurotoxicity and poorer test-retest performance on a cognitive test summary measure . CONCLUSIONS Prolonged CBZ and GBP therapy induced EEG slowing that correlated with cognitive complaints and often exceeded the confidence interval for individual subjects . Quantitative EEG measures may be useful in the objective determination of AED-related neurotoxicity BACKGROUND The adverse effects of the antiepileptic drugs ( AEDs ) originally developed are well known , while those of the newer AEDs remain unclear . OBJECTIVE To investigate clinical , cognitive , and neurophysiologic effects of carbamazepine , oxcarbazepine , and levetiracetam in healthy volunteers . METHODS A double-blind crossover study was conducted in 10 volunteers . Eight-day treatment with carbamazepine , oxcarbazepine , levetiracetam , or placebo was administered in r and om order . Drug doses were titrated gradually to the daily target doses on day 7 : carbamazepine 800 mg , oxcarbazepine 1200 mg , and levetiracetam 1500 mg . At baseline and at the end of each treatment period , participants underwent cognitive and neurophysiologic assessment . A washout period of 14 days between treatment periods was conducted . RESULTS More adverse events were self-reported with carbamazepine ( 63 % ) than the other treatments ( oxcarbazepine 12 % , levetiracetam 20 % , placebo 5 % ; p < 0.001 between the 4 groups ) . Carbamazepine induced the greatest motor slowing ( p = 0.002 ) , followed by oxcarbazepine ( p = 0.01 ) . Levetiracetam left baseline motor speed unchanged . All AEDs increased attention span from baseline values as shown on the Stroop test . Quantitative electroencephalogram ( EEG ) analysis showed that carbamazepine significantly increased the delta – theta power and reduced the frequency of alpha rhythm ; oxcarbazepine induced smaller changes than carbamazepine . Levetiracetam did not change any EEG measurements . On color visually evoked potential ( VEP ) tests , carbamazepine induced a constant slowing of P1 latency , while oxcarbazepine induced changes only after the blue – black pattern . All color VEP measures for volunteers receiving levetiracetam were almost unchanged . CONCLUSIONS After short-term treatment in healthy volunteers , carbamazepine induced major clinical and neurophysiologic changes . Oxcarbazepine was better tolerated than carbamazepine . Levetiracetam interfered least with clinical and neurophysiologic test results In a double-blind , placebo-controlled study the encephalotropic and psychotropic properties of gabapentin - a new gaba-analogue with anticonvulsant and antispastic properties penetrating the blood brain barrier easily - were studied in 10 normal subjects by means of quantitative pharmaco-EEG and psychometric analyses . They received r and omized and in weekly intervals single oral doses of 50 mg , 100 mg , 200 mg and 400 mg gabapentin as well as placebo .  EEG recordings and evaluation of pulse , blood pressure and side effects were carried out after 0 , 1 , 2 , 4 , 6 and 8 hours ; psychometric tests were done at the same times except for the first hour . Computer-assisted spectral analysis of the EEG showed moderate though significant central effects of gabapentine in doses of 200 - 400 mg as compared with placebo , which were maximally pronounced in the 2nd hour post drug . These alterations were generally characterized by an attenuation of total power , augmentation of delta and theta activity and a decrease of alpha activity indicating CNS-inhibitory properties . Only at the late hours did the type of changes shift towards a vigilance-promoting one . Beta activity showed alternating changes . Psychometric and psychophysiological evaluations demonstrated subtle psychotropic effects as compared with placebo characterized mostly by an improvement in concentration , numerical memory , complex reaction and performance in the alphabetical reaction test while performance variability increased as well . Subjectively experienced well-being changed dose-dependently . CFF decreased after 100 mg as did pupil size after 50 - 200 mg . Evaluation of pulse , blood pressure and side effects demonstrated good tolerability of the drug An array of variables have been assessed as potential early predictors of antidepressant response in depressed patients . This exploratory study examined the relationship of clinical outcome , following pharmacotherapeutic treatment , with quantitative  electroencephalographic ( EEG ) features assessed prior to treatment onset . In 70 major affective disorder patients , pre-treatment spectrum-analysed topographic EEG indices ( absolute power , relative power , mean frequency , inter-hemispheric power asymmetry and coherence for 4 frequency b and s ) were assessed in relation to baseline HAM-D ratings and HAM-D rating changes following 6 weeks of open-label paroxetine treatment .  EEG slow wave ( theta ) activities were positively correlated with depression ratings prior to treatment . Of the patients ( n = 51 ) completing treatment , 80 % evidence d a > 50 % reduction in HAM-D ratings . Improved rating changes in general were found to be negatively related to slow ( delta and theta ) wave activity and positively related to fast ( beta ) activity at frontal recording sites . Findings are discussed in relation to the neurochemistry and neurobiology of depressive disorders PURPOSE Anatomical localization of the cortical effect of lamotrigine ( LTG ) in patients with idiopathic generalized epilepsy ( IGE ) . METHODS 19 patients with untreated IGE were investigated .  EEG was recorded in the untreated condition and 3 months later when LTG treatment abolished the seizures . 19-channel EEG was recorded , and a total of 2min artifact-free , waking EEG was processed to low-resolution electromagnetic tomography ( LORETA ) analysis . Activity ( that is , current source density , A/m(2 ) ) was computed in four frequency b and s ( delta , theta , alpha , and beta ) , for 2394 voxels that represented the cortical gray matter and the hippocampi . Group differences between the untreated and treated conditions were computed for the four b and s and all voxels by multiple t-tests for interdependent data sets . The results were presented in terms of anatomical distribution and statistical significance . RESULTS p<0.01 ( uncorrected ) changes ( decrease of activity ) emerged in the theta and the alpha b and s. Theta activity decreased in a large cluster of voxels including parts of the temporal , parietal , occipital cortex bilaterally , and in the transverse temporal gyri , insula , hippocampus , and uncus on the right side . Alpha activity decreased in a relatively smaller cortical area involving the right temporo-parietal junction and surrounding parts of the cortex , and part of the insula on the right side . CONCLUSIONS LTG  decreased theta activity in several cortical areas where abnormally increased theta activity had been found in a prior study in another cohort of untreated IGE patients [ Clemens , B. , Bessenyei , M. , Piros , P. , Tóth , M. , Seress , L. , Kondákor , I. , 2007b . Characteristic distribution of interictal brain electrical activity in idiopathic generalized epilepsy . Epilepsia 48 , 941 - 949 ] . These LTG-related changes might be related to the decrease of seizure propensity in IGE
target: RESULTS Following an extensive review of selected studies from the 201 articles , the studies indicate that each of the psychotropic medications review ed impact alpha , beta , delta and theta waves independently and differently from each other .
  Additionally , certain medications , particularly haloperidol and valproic acid , have dissimilar results exemplified in all waveforms .
background: OBJECTIVES It is known that psychotropic medications have an impact on the readings found in Electroencephalogram ( EEG ) .
  In the field of psychiatry , there are several psychotropics utilized by clinicians .
  This review seeks to investigate all the available data for psychotropic drugs and their impact on EEG changes .