Weeks Of Fluoxetine Treatment Research Articles

Relationship of cognitive functioning with progenitor cells of the olfactory epithelium in patients with depression after eight weeks of fluoxetine treatment

Relationship of cognitive functioning with progenitor cells of the olfactory epithelium in patients with depression after eight weeks of fluoxetine treatment

MiR-124 Exacerbates depressive-like behavior by targeting Ezh2 to induce autophagy.

On the basis of our previous research, miR-124 and autophagy have been shown to be associated with depression and antidepressant treatment, respectively. However, whether miR-124 is involved in depressive-like behavior and antidepressant efficacy through regulating autophagy remains poorly understood. The chronic unpredictable mild stress (CUMS) depression model in mice was established, and then intraperitoneal fluoxetine injections (10 mg/kg) were administered for a duration of 4 weeks. The behavioral changes induced by CUMS were evaluated by the tail suspension test, open field test, sucrose preference test, and elevated plus maze test. Quantitative real-time PCR was used to detect expression levels of miR-124 and its three precursor genes in hippocampus of mice. Western blotting was used to detect the expressions of Ezh2 and autophagy proteins (P62, Atg3, Atg7, LC3-I, and LC3- II) in hippocampus of mice. Depression-like behaviors were successfully induced in CUMS models and reversed by SSRI treatments. The expression levels of miR-124 and its precursor gene ( miR-124-3 ) were significantly increased in the hippocampus of CUMS mice, while the expression levels were significantly decreased after 4 weeks of fluoxetine treatment. The mRNA and protein expressions of Ezh2, a validated target of miR-124, were decreased in the hippocampus of CUMS mice, and the fluoxetine treatment could reverse the expressions. A correlation analysis suggested that miR-124 had a significant negative correlation with Ezh2 mRNA expression. The protein levels of LC3-II/I, P62, and Atg7, which were found to be regulated by Ezh2, were increased in the hippocampus of CUMS mice and decreased after fluoxetine treatment. We speculated that autophagy was enhanced in the CUMS model of depression and might be mediated by miR-124 targeting Ezh2.

DNA Methylation of Fluoxetine Response in Child and Adolescence: Preliminary Results.

PurposeThe search for predictors of antidepressant response is gaining increasing attention, with epigenetic markers attracting a great deal of interest. We performed a genome-wide study assessing baseline differences in DNA methylation between Responders and Non-Responders.Patients and MethodsTwenty-two children and adolescents, receiving fluoxetine treatment for the first time, were classified as Responders or Non-Responders according to CGI-I score after 8 weeks of fluoxetine treatment. Genome-wide DNA methylation was profiled using the Illumina Infinium MethylationEPIC BeadChip Kit and analyzed using the Chip Analysis Methylation Pipeline (ChAMP).ResultsWe identified 21 CpG sites significantly (FDR<0.05) associated with fluoxetine response that showed meaningful differences (Δβ> ±0.2) in methylation level between Responders and Non-Responders. Two genes, RHOJ (Ras Homolog Family Member J) and OR2L13 (Olfactory Receptor family 2 subfamily L member 13), presented more than one significant CpG sites.ConclusionOur findings provide new insights into the molecular mechanisms underlying the complex phenotype of antidepressant response, indicating that methylation at specific genes could be a promising biomarker that needs further replication in large cohorts.

6.12 Perceived Criticism of Parents as a Predictor of Depression Severity Following 6 Weeks of Fluoxetine Treatment in Adolescents

6.12 Perceived Criticism of Parents as a Predictor of Depression Severity Following 6 Weeks of Fluoxetine Treatment in Adolescents

The impact of chronic fluoxetine on conditioned fear expression and hippocampal FGF2 in rats: Short- and long-term effects.

Phenotypic differences in conditioned fear expression may be a marker of vulnerability to the development of anxiety disorders. Hippocampal FGF2 correlates negatively with conditioned fear expression, and antidepressants, the first-line pharmacological treatment for anxiety, increase hippocampal FGF2. In the present study, we assessed whether treatment with the selective serotonin reuptake inhibitor fluoxetine reduces conditioned fear expression in rats that naturally express lower (Low fear) or higher (High fear) levels of fear following a single-trial conditioning session. Experiment 1 demonstrated that phenotypic differences in fear expression were highly stable over a two-week interval. Experiment 2 demonstrated that two weeks of fluoxetine treatment (administered via drinking water) reduced conditioned fear expression in both Low and High fear rats. Experiment 3 demonstrated that two weeks of fluoxetine reduced conditioned fear expression even when treatment commenced two weeks after fear conditioning, but not when conditioned fear was assessed following a two-week drug-free washout period. Additionally, fluoxetine increased hippocampal FGF2 levels relative to vehicle-treated rats, but only when measured immediately after fluoxetine treatment, and not two weeks after treatment termination. Together, these results provide further indirect evidence that endogenous hippocampal FGF2 may mediate individual differences in conditioned fear expression. They also suggest that fluoxetine may be effective in reducing conditioned fear expression in both vulnerable and resilient populations when administered immediately, or sometime after, aversive experiences, but these effects do not persist once treatment is terminated.

The Effects of Short-Term Stress and Long-Term Fluoxetine Treatment on the Expression of Apoptotic Proteins in the Brain

The effects of 2- or 8-week-long daily treatment with fluoxetine at a dose of 7.26–7.70 mg/kg given with drinking water and short-term forced-swim stress on the levels of mRNAs of anti- and pro-apoptotic proteins, that is, Bcl-xL and Bax, respectively, were studied in the brains of adult male rats using the RT-PCR method. Antiapoptotic effects of stress on the expression of these proteins were observed in the hippocampus of rats that were not treated with fluoxetine and in the midbrain after 2 weeks of the antidepressant treatment. Pro-apoptotic effects of stress were revealed in the frontal cortex of animals that were not treated with fluoxetine and after 2 weeks of fluoxetine treatment. An 8-week-long fluoxetine treatment resulted in an increase in the basal Bax expression in the hippocampus and in anti-apoptotic effects in the neocortex, which were more clearly seen after stress. The observed interaction of the effects of stress and fluoxetine on the expression of proteins of neuronal survival and plasticity may provide anti- or proapoptotic action of the antidepressant on the cells of the emotiogenic structures of the brain.

Predictors and Moderators of Relapse in Children and Adolescents With Major Depressive Disorder.

To identify predictors and moderators of relapse during continuation treatment among depressed youth randomly assigned to fluoxetine or placebo. Potential predictors and moderators of relapse that were identified by a literature review were examined in 102 youth (aged 7-18 years), diagnosed with major depressive disorder as defined by DSM-IV criteria, who were considered responders after 12 weeks of fluoxetine treatment (acute phase). This randomized controlled trial was conducted from June 2000 through October 2005. Each candidate predictor and moderator was evaluated with a multiple logistic regression model to examine the main and interaction effects of 12 weeks of continuation treatment on relapse status (at week 24) while controlling for age, sex, and depression severity. Relapse was defined as a Children's Depression Rating Scale-Revised total score ≥ 40 with worsening of depressive symptoms for at least 2 weeks. Youth with comorbid dysthymia (adjusted odds ratio [OR] = 2.88, P = .03) and low levels of family leadership (adjusted OR = 1.39, P = .006) at baseline are more likely to relapse than their counterparts. Higher levels of depression (OR = 1.21, P = .003) and higher levels of residual sleep disturbance (insomnia) (OR = 6.74, P = .006) and irritability (OR = 7.40, P = .01) at the end of acute treatment (12 weeks) increased the odds of relapse. Higher levels of depressive symptoms at baseline in youth who remained on fluoxetine for continuation treatment were associated with increased odds of relapse (adjusted OR = 1.14, P = .03). Females who remained on fluoxetine for the duration of continuation treatment were almost 9 times more likely to relapse than males (adjusted OR = 8.86, P = .007). This is the first large continuation study for treatment of depression in youth to examine predictors and moderators of relapse. Youth with greater improvement by the end of 3 months of treatment were less likely to relapse than those with continued depressive symptoms. In addition, youth with comorbid dysthymia had 3 times greater risk of relapse that those without. Targeting residual symptoms, particularly sleep disturbance and irritability, earlier in treatment may reduce relapse rates. ClinicalTrials.gov identifier: NCT00332787.

Glucocorticoid Receptor Genetic Variants and Response to Fluoxetine in Major Depressive Disorder.

Hyperactivity of the hypothalamic pituitary adrenocortical (HPA) axis is one of the main clinical findings in depression. The HPA axis is interrelated with glucocorticoid signaling via glucocorticoid receptors (GCRs). Thus, functional genetic variants on GCRs might influence therapeutic outcomes in depression. The aim of the present study was to investigate the association between three functional polymorphisms (rs41423247, rs6195, and rs6189/rs6190) on GCR and response to fluoxetine in a group of depressed patients. One hundred newly diagnosed patients completed 6 weeks of fluoxetine treatment. Response to treatment was defined as a 50% decrease in the Hamilton Depression Rating Scale score. Variants of rs41423247, rs6195, and rs6189/rs6190 polymorphisms were determined in extracted DNAs using PCR-RFLP method. Regarding rs41423247 polymorphism, carriers of the CG and GG genotype responded significantly better to fluoxetine compared with CC carriers (p=0.008, OR=3.3, 95% CI=1.35-8.07). Moreover, the G allele of rs41423247 polymorphism was strongly associated with response to fluoxetine (p=0.032, OR=2.2, 95% CI=1.09-4.44). There was no significant association between different genotypes and alleles of rs6195, rs6189/rs6190 variants, and response to fluoxetine (p=0.213 and 0.99, respectively). In conclusion, rs41423247 polymorphism might be a predictor for better response to fluoxetine. These findings support the idea that some variants of the GCR might contribute to interindividual variability of response to antidepressants.

Pharmacogenetic study focused on fluoxetine pharmacodynamics in children and adolescent patients: impact of the serotonin pathway.

Pharmacogenetic studies of fluoxetine in children and adolescents are scarce. After reporting the effect of genetic variants in genes related to the fluoxetine pharmacokinetics on clinical response in a pediatric population, we now evaluate the impact of genetic markers involved in its pharmacodynamics. The assessment was performed in 83 patients after 12 weeks of fluoxetine treatment. The genetic association analysis included a total of 316 validated single nucleotide polymorphisms in 45 candidate genes involved in six different pathways. Clinical improvement after treatment with fluoxetine in our pediatric population was associated significantly with two polymorphisms located in genes related to the serotonergic system: the 5-hydroxytryptamine receptor 1B (HTR1B) and the tryptophan 5-hydroxylase 2 (TPH2). Although a wide range of candidate genes related to different pathways were assessed, the results show that genetic markers directly related to serotonin have an important effect on fluoxetine response.

Evidence for Pretreatment LICI Deficits Among Depressed Children and Adolescents With Nonresponse to Fluoxetine

BackgroundResearch suggests that alterations in gamma-aminobutyric acid receptor functioning have a role in depression. Paired-pulse transcranial magnetic stimulation (TMS) paradigms are noninvasive measures of cortical inhibitory and excitatory circuits. Objective/hypothesisThe present study examined pretreatment short-interval intracortical inhibition (SICI), long-interval cortical inhibition (LICI), and intracortical facilitation (ICF) in children and adolescents with major depressive disorder who were initiating fluoxetine treatment. The primary objective was to examine the relationship of these measures with subsequent treatment response. It was hypothesized that alterations in pretreatment GABA and glutamate mediated neurotransmission, would be associated with fluoxetine nonresponse. MethodsSixteen children and adolescents with major depressive disorder underwent paired-pulse TMS testing before beginning fluoxetine treatment. Response was prospectively characterized by scores of 1 or 2 on the Clinical Global Impression Scale and less than 40 on the Children's Depression Rating Scale-Revised after 6 weeks of fluoxetine treatment (20–40 mg/day). ResultsEight patients responded to treatment. Least-squares mean LICI values were consistently higher bilaterally for treatment nonresponders. Higher LICI values indicate less inhibition and impaired GABAB functioning. There was no significant effect of treatment response on the measures of SICI and ICF. ConclusionsOur findings suggest that deficits in pretreatment GABAB may be related to fluoxetine nonresponse in depressed youth. This is congruent with prior work demonstrating that GABAB interneurons have serotonergic input and antidepressants modulate GABAB receptors. These findings also show that TMS paradigms have utility in studying the neurophysiology and treatment of childhood mood disorders. RegistrationsCortical Excitability and Inhibition in Children and Adolescents With Major Depressive Disorder, http://www.clinicaltrials.gov/ct2/show/NCT00896090?term=cortical+excitability+and+inhibition&rank=2, NCT00896090; Sequential Treatment of Pediatric MDD to Increase Remission and Prevent Relapse, http://www.clinicaltrials.gov/ct2/show/NCT00612313?term=Sequential+Treatment+and+MDD&rank=1, NCT00612313.

Long-term fluoxetine treatment induces input-specific LTP and LTD impairment and structural plasticity in the CA1 hippocampal subfield

Antidepressant drugs are usually administered for several weeks for the treatment of major depressive disorder. However, they are also prescribed in several additional psychiatric conditions as well as during long-term maintenance treatments. Antidepressants induce adaptive changes in several forebrain structures which include modifications at glutamatergic synapses. We recently found that repetitive administration of the selective serotonin reuptake inhibitor (SSRI) fluoxetine to naïve adult male rats induced an increase of mature, mushroom-type dendritic spines in several forebrain regions. This was associated with an increase of GluA2-containing α-amino-3-hydroxy-5-methylisoxazole-4-propionate receptors (AMPA-Rs) in telencephalic postsynaptic densities. To unravel the functional significance of such a synaptic re-arrangement, we focused on glutamate neurotransmission in the hippocampus. We evaluated the effect of four weeks of 0.7 mg/kg fluoxetine on long-term potentiation (LTP) and long-term depression (LTD) in the CA1 hippocampal subfield. Recordings in hippocampal slices revealed profound deficits in LTP and LTD at Schaffer collateral-CA1 synapses associated to increased spine density and enhanced presence of mushroom-type spines, as revealed by Golgi staining. However, the same treatment had neither an effect on spine morphology, nor on LTP and LTD at perforant path-CA1 synapses. Cobalt staining and immunohistochemical experiments revealed decreased AMPA-R Ca2+ permeability in the stratum radiatum (s.r.) together with increased GluA2-containing Ca2+ impermeable AMPA-Rs. Therefore, 4 weeks of fluoxetine treatment promoted structural and functional adaptations in CA1 neurons in a pathway-specific manner that were selectively associated with impairment of activity-dependent plasticity at Schaffer collateral-CA1 synapses.

Effects of an antidepressant on neural correlates of emotional processing in patients with major depression

We measured brain activation in patients with major depressive disorder when exposed to emotional pictures before and after antidepressant treatment. The participants included 18 first-episode unmedicated patients with current major depressive disorder and 18 age- and gender-matched control subjects. All subjects performed an emotional task during functional magnetic resonance imaging scanning at baseline and after 8 weeks of fluoxetine treatment. Unmedicated depressed patients showed lower accuracy rates (0.53±0.26) than did subjects in the control group (0.71±0.18) while viewing positive pictures. During exposure to positive stimuli, decreased activations were seen in the right insula (BA13) and left anterior cingulate cortex (BA32) in patients after antidepressant treatment. After antidepressant treatment, patients exhibited greater activation in the right middle frontal gyrus (BA8,9) in response to negative stimuli. Our results suggest that the prefrontal cortex, anterior cingulate cortex and insula may play key roles as biological markers for treatment response and as predictors of therapeutic success.

Neurogenomic Evidence for a Shared Mechanism of the Antidepressant Effects of Exercise and Chronic Fluoxetine in Mice

Several different interventions improve depressed mood, including medication and environmental factors such as regular physical exercise. The molecular pathways underlying these effects are still not fully understood. In this study, we sought to identify shared mechanisms underlying antidepressant interventions. We studied three groups of mice: mice treated with a widely used antidepressant drug – fluoxetine, mice engaged in voluntary exercise, and mice living in an enriched environment. The hippocampi of treated mice were investigated at the molecular and cellular levels. Mice treated with fluoxetine and mice who exercised daily showed, not only similar antidepressant behavior, but also similar changes in gene expression and hippocampal neurons. These changes were not observed in mice with environmental enrichment. An increase in neurogenesis and dendritic spine density was observed following four weeks of fluoxetine treatment and voluntary exercise. A weighted gene co-expression network analysis revealed four different modules of co-expressed genes that were correlated with the antidepressant effect. This network analysis enabled us to identify genes involved in the molecular pathways underlying the effects of fluoxetine and exercise. The existence of both neuronal and gene expression changes common to antidepressant drug and exercise suggests a shared mechanism underlying their effect. Further studies of these findings may be used to uncover the molecular mechanisms of depression, and to identify new avenues of therapy.

Brain Activity in Adolescent Major Depressive Disorder Before and After Fluoxetine Treatment

Major depression in adolescents is a significant public health concern because of its frequency and severity. To examine the neurobiological basis of depression in this population, the authors studied functional activation characteristics of the brain before and after antidepressant treatment in antidepressant-naive depressed adolescents and healthy comparison subjects. Depressed (N=19) and healthy (N=21) adolescents, ages 11 to 18 years, underwent functional MRI assessment while viewing fearful and neutral facial expressions at baseline and again 8 weeks later. The depressed adolescents received 8 weeks of open-label fluoxetine treatment after their baseline scan. Voxel-wise whole brain analyses showed that depressed youths have exaggerated brain activation compared with healthy comparison subjects in multiple regions, including the frontal, temporal, and limbic cortices. The 8 weeks of fluoxetine treatment normalized most of these regions of hyperactivity in the depressed group. Region-of-interest analyses of the areas involved in emotion processing indicated that before treatment, depressed youths had significantly greater activations to fearful relative to neutral facial expressions than did healthy comparison subjects in the amygdala, orbitofrontal cortex, and subgenual anterior cingulate cortex bilaterally. Fluoxetine treatment decreased activations in all three regions, as compared with the repeat scans of healthy comparison subjects. While effective treatments are available, the impact of depression and its treatment on the brain in adolescents is understudied. This study confirms increases in brain activation in untreated depressed adolescents and demonstrates reductions in these aberrant activations with treatment.

Fluoxetine for the Treatment of Childhood and Adolescence Social Phobia: Factors playing a role in Efficacy

Objective: The aim of this study was to investigate the stepwise efficacy, after 8 and 12 weeks of fluoxetine treatment, on social anxiety disorder (SAD) in 7 to 17 year-old children and adolescent...

The involvement of distinct neural systems in patients with obsessive–compulsive disorder with autogenous and reactive obsessions

To investigate the regional metabolite abnormalities and changes after treatment in patients with OCD with autogenous and reactive obsessions. We assessed right anterior cingulate cortex (ACC) and amygdala-hippocampal region (Am + Hpp) N-acetyl-aspartate (NAA), choline (Cho) and creatine (Cr) concentrations and NAA/Cr and Cho/Cr ratios using single-voxel proton magnetic resonance spectroscopy in 15 patients with autogenous obsessions (OCD-A), 15 patients with reactive obsessions (OCD-R) and 15 healthy controls (HC). Measurements were repeated after 16 weeks of fluoxetine treatment. Baseline ACC NAA/Cr ratios of both OCD groups were significantly lower than HC. OCD-A group had significantly lower baseline NAA/Cr ratios in the Am + Hpp than other groups. These differences were more likely to be explained by higher Cr levels in ACC. We found no significant differences and changes for Cho levels and Cho/Cr ratios between groups and within groups. Significant increase in NAA/Cr ratios of OCD-A group found in the Am + Hpp was more likely to be explained by increased NAA levels. No significant changes were found in ACC NAA/Cr ratios. While disturbed energy metabolism in ACC might reflect a common pathology in patients with OCD regardless of symptom dimension, alterations in mesiotemporal lobe are more likely for autogenous obsessions.

Psychometric Properties of the Children's Depression Rating Scale–Revised in Adolescents

The aim of this study was to present the reliability and validity of the Children's Depression Rating Scale-Revised (CDRS-R) in the adolescent age group. Adolescents with symptoms of depression were assessed using the CDRS-R and global severity and functioning scales at screening, baseline, and after 12 weeks of fluoxetine treatment. Global improvement was also assessed at week 12 (or exit). Reliability and validity were analyzed using Classical Test Theory (item-total correlations and internal consistency) and correlations between the CDRS-R and other outcomes. Adolescents (n = 145) were evaluated at screening; 113 (77.9%) met criteria for major depressive disorder, 8 (5.5%) had subthreshold depressive symptoms, and 24 (16.6%) had minimal depressive symptoms. Ninety-four adolescents had a baseline visit after 1 week, and 88 were treated with fluoxetine. Internal consistency for the CDRS-R was good at all three visits (screening: 0.79; baseline: 0.74; exit: 0.92), and total score was highly correlated with global severity (r = 0.87, 0.80, and 0.93; p < 0.01). Only exit CDRS-R score was significantly correlated with global functioning (Children's Global Assessment Scale; r = -0.77; p < 0.01). Reductions on the CDRS-R total score were highly correlated with improvement scores at exit (Clinical Global Impressions-Improvement; r = -0.83; p < 0.01). The results demonstrate good reliability and validity in adolescents with depression.

Symptom Improvement and Residual Symptoms during Acute Antidepressant Treatment in Pediatric Major Depressive Disorder

Knowing the timing of specific depressive symptom improvement will enable clinicians to prepare their patients well and improve treatment outcome, whereas recognizing which depressive symptoms may show delayed improvement will help clinicians to provide additional interventions early in treatment. In a prospective open-label fluoxetine study, we investigated the timing of depressive symptom improvement during acute treatment, and identified common remaining symptoms following 4, 8, and 12 weeks of acute treatment in depressed youths. A total of 168 children and adolescents, aged 7-18 years, with primary diagnoses of major depressive disorder (MDD) received 12 weeks of fluoxetine treatment. Youths were evaluated using the Kiddie Schedule for Affective Disorders and Schizophrenia. The outcome measure included the Children's Depression Rating Scale-Revised. All depressive symptoms improved, particularly during the first 4 weeks of acute treatment. Forty-seven percent of remitters reported at least one residual symptom following 12 weeks, with most common residual symptoms being impaired school performance, insomnia, and irritability. Residual symptoms are common, even among remitters, at the end of 12 weeks of acute treatment. There is a need for clinicians to monitor symptom improvement and potentially provide additional interventions for the more resistant symptoms, such as insomnia and school performance.

Early Prediction of Acute Antidepressant Treatment Response and Remission in Pediatric Major Depressive Disorder

Objective Less than half of youths achieve remission (minimal to no symptoms) after acute antidepressant treatment. Early identification of who will or will not respond to treatment and achieve remission may help clinicians formulate treatment decisions and shorten the time spent on ineffective treatments. In a prospective open-label fluoxetine study, we investigate indicators of acute treatment response and remission. Method One hundred sixty-eight children and adolescents, ages 7 to 18 years, with primary diagnoses of major depressive disorder received 12 weeks of fluoxetine treatment. The youths were evaluated using the Kiddie Schedule for Affective Disorders and Schizophrenia. The outcome measure included the Children's Depression Rating Scale-Revised. Results Positive first-degree family history of depression was the only baseline demographic and clinical characteristic that predicted a favorable treatment response ( p = .01). The rate of symptom improvement, however, is a good indicator of acute treatment response. A significant symptom reduction (approximately 50%) by week 4 is needed to achieve remission at the end of acute treatment. Conclusions This study demonstrated that the rate of symptom improvement during early weeks of acute fluoxetine treatment is a good indicator of remission. Treatment approach may be reevaluated and modified as early as week 4 during acute treatment.

Electroencephalographic Alpha Measures Predict Therapeutic Response to a Selective Serotonin Reuptake Inhibitor Antidepressant: Pre- and Post-Treatment Findings

There is growing evidence that individual differences among depressed patients on electrophysiologic (EEG), neuroimaging, and neurocognitive measures are predictive of therapeutic response to antidepressant drugs. This study replicates prior findings of pretreatment differences between selective serotonin reuptake inhibitor (SSRI) responders and nonresponders in EEG alpha power or asymmetry and examines whether these differences normalize or are stable after treatment. Resting EEG (eyes open and closed) was recorded from 28 electrodes (nose reference) in 18 depressed patients when off medication and at the end of 12 weeks of fluoxetine treatment. Clinical response was assessed by an independent rater with the Clinical Global Impression Improvement scale. The EEG data were also obtained for 18 healthy adults matched to patients in gender and age. Treatment responders had greater alpha power compared with nonresponders and healthy control subjects, with largest differences at occipital sites where alpha was largest. There were also differences in alpha asymmetry between responders and nonresponders at occipital sites. Responders showed greater alpha (less activity) over right than left hemisphere, whereas nonresponders tended to show the opposite asymmetry. Neither alpha power nor asymmetry changed after treatment, and test-retest correlations were high, particularly for alpha power. Alpha power and asymmetry showed reasonable positive predictive value but less negative predictive value. The findings confirm reports of alpha differences between antidepressant responders and nonresponders and raise hopes for developing EEG tests for selecting effective treatments for patients. The stability of alpha power and asymmetry differences between SSRI responders and nonresponders after treatment suggests that they represent state-independent characteristics.