human
***TASK*** the task is to summarize an input biomedical literature in six sentences 
    ***INPUT*** the input is a biomedical literature 
    ***OUTPUT*** the output is the summary of an input biomedical literature in six sentences 
    ***DOCUMENTATION*** 
    ***EXAMPLES*** 
    Input: 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 
    Output:
    
agent
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 .
***TASK*** the task is to summarize an input biomedical literature in six sentences 
    ***INPUT*** the input is a biomedical literature 
    ***OUTPUT*** the output is the summary of an input biomedical literature in six sentences 
    ***DOCUMENTATION*** 
    ***EXAMPLES*** 
    Input: 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 
    Output:
    