The early non-increase of serum BDNF predicts failure of antidepressant treatment in patients with major depression: A pilot study Canadian Network for Mood and Anxiety Treatments (CANMAT) clinical guidelines for the management of major depressive disorder in adults. II. Psychotherapy alone or in combination with antidepressant medication. Short-term SSRI treatment normalises amygdala hyperactivity in depressed patients Does prior antidepressant treatment of major depression impact brain function during current treatment? Pre-treatment letter fluency performance predicts antidepressant response to transcranial direct current stimulation. Association Between Placebo-Activated Neural Systems and Antidepressant Responses: Neurochemistry of Placebo Effects in Major Depression. Concurrent Cognitive Control Training Augments the Antidepressant Efficacy of tDCS: A Pilot Study Depression and Chronic Obstructive Pulmonary Disease: Treatment Trials. Prediction of outcome and early vs. late improvement in OCD patients treated with cognitive behaviour therapy and pharmacotherapy Differential prediction of first clinical response to serotonergic and noradrenergic antidepressants using the loudness dependence of auditory evoked potentials in patients with major depressive disorder. Early improvement under mirtazapine and paroxetine predicts later stable response and remission with high sensitivity in patients with major depression. Amygdala Reactivity to Emotional Faces in the Prediction of General and Medication-Specific Responses to Antidepressant Treatment in the Randomized iSPOT-D Trial Onset and Early Behavioral Effects of Pharmacologically Different Antidepressants and Placebo in Depression
In the treatment of patients with major depressive disorder ( MDD ) , early non-improvement of symptoms after initiation of antidepressant treatment is a highly sensitive and specific marker for final treatment failure . On the other h and , meta-analyses of clinical studies investigating serum BDNF ( sBDNF ) concentration before and after antidepressant treatment showed an increase of sBDNF during treatment , which was correlated with amelioration of depressive symptoms . No study has yet investigated the predictive value of early changes of sBDNF for final treatment outcome of the individual patient . The aim of this study was to investigate in patients with MDD , whether i ) the non-increase of sBDNF in the early course of treatment is a specific and sensitive marker for final treatment failure , ii ) whether the sensitivity and specificity of early non-improvement for treatment failure can be increased by combining it with the marker " early non-increase of sBDNF " . For this purpose , we performed a pilot study with 41 in patients with MDD according to DSM-IV , who were treated in a naturalistic setting .  Depression severity and sBDNF were measured in weekly intervals from baseline to week six with the 21-item Hamilton Depression Rating Scale ( HAMD-21 ) and ELISA , respectively . The individual markers sBDNF non-increase and HAMD-21 non-improvement from baseline to day 7 or 14 predicted later non-response and non-remission with moderate to high specificity . The combined marker sBDNF non-increase plus HAMD-21 non-improvement at day 14 increased the specificity for non-response and non-remission to 100 % . Our data provide the first evidence that the absence of an early increase of sBDNF in conjunction with early non-improvement might be a highly specific peripheral marker predictive for treatment failure in patients with MDD . If replicated , this combined marker could be considered useful for prospect i ve confirmatory trials in patients with MDD BACKGROUND In 2001 , the Canadian Psychiatric Association and the Canadian Network for Mood and Anxiety Treatments ( CANMAT ) partnered to produce evidence -based clinical guidelines for the treatment of depressive disorders .  A revision of these guidelines was undertaken by CANMAT in 2008 - 2009 to reflect advances in the field . This article , one of five in the series , review s new studies of psychotherapy in the acute and maintenance phase of MDD , including computer-based and telephone-delivered psychotherapy . METHODS The CANMAT guidelines are based on a question -answer format to enhance accessibility to clinicians . Evidence -based responses are based on up date d systematic review s of the literature and recommendations are grade d according to the Level of Evidence , using pre-defined criteria . Lines of Treatment are identified based on criteria that included evidence and expert clinical support . RESULTS Cognitive-Behavioural Therapy ( CBT ) and Interpersonal Therapy ( IPT ) continue to have the most evidence for efficacy , both in acute and maintenance phases of MDD , and have been studied in combination with antidepressants . CBT is well studied in conjunction with computer-delivered methods and bibliotherapy . Behavioural Activation and Cognitive-Behavioural Analysis System of Psychotherapy have significant evidence , but need replication . Newer psychotherapies including Acceptance and Commitment Therapy , Motivational Interviewing , and Mindfulness-Based Cognitive Therapy do not yet have significant evidence as acute treatments ; nor does psychodynamic therapy . LIMITATIONS Although many forms of psychotherapy have been studied , relatively few types have been evaluated for MDD in r and omized controlled trials . Evidence about the combination of different types of psychotherapy and antidepressant medication is also limited despite widespread use of these therapies concomitantly . CONCLUSIONS CBT and IPT are the only first-line treatment recommendations for acute MDD and remain highly recommended for maintenance . Both computer-based and telephone-delivered psychotherapy -- primarily studied with CBT and IPT -- are useful second-line recommendations . Where feasible , combined antidepressant and CBT or IPT are recommended as first-line treatments for acute MDD Background Antidepressant drugs such as selective serotonin re-uptake inhibitors ( SSRIs ) remediate negative biases in emotional processing in depressed patients in both behavioural and neural outcome measures . However , it is not clear if these effects occur before , or as a consequence of , changes in clinical state . Method In the present study , we investigated the effects of short-term SSRI treatment in depressed patients on the neural response to fearful faces prior to clinical improvement in mood . Altogether , 42 unmedicated depressed patients received SSRI treatment ( 10 mg escitalopram daily ) or placebo in a r and omised , parallel-group design . The neural response to fearful and happy faces was measured on day 7 of treatment using functional magnetic resonance imaging .  A group of healthy controls was imaged in the same way . Results Amygdala responses to fearful facial expressions were significantly greater in depressed patients compared to healthy controls . However , this response was normalised in patients receiving 7 days treatment with escitalopram . There was no significant difference in clinical depression ratings at 7 days between the escitalopram and placebo-treated patients . Conclusions Our results suggest that short-term SSRI treatment in depressed patients remediates amygdala hyperactivity in response to negative emotional stimuli prior to clinical improvement in depressed mood . This supports the hypothesis that the clinical effects of antidepressant treatment may be mediated in part through early changes in emotional processing . Further studies will be needed to show if these early effects of antidepressant medication predict eventual clinical outcome 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 BACKGROUND Transcranial direct current stimulation ( tDCS ) is a promising new treatment for depression , however , clinical trials to- date indicate variable efficacy , thereby raising the need to identify inter-individual predictors of response . In the current study we aim ed to investigate pre-treatment neurocognitive performance as a predictor of antidepressant response to tDCS . METHODS Data was pooled from five clinical trials , including two r and omised controlled trials ( RCTs ) , which investigated the antidepressant effects of anodal tDCS administered to the prefrontal cortex . Data from 57 patients were included in the analysis . Mood was assessed before and after an acute course of treatment using the Montgomery-Åsberg Depression Rating Scale . The following neurocognitive tests were administered prior to treatment : Simple and choice reaction time , the Symbol Digit Modalities Test ( SDMT ) , Rey Auditory Verbal Memory Task ( RAVLT ) , Digit Span , and the Controlled Oral Word Association Test ( COWAT ) . RESULTS Better pre-treatment letter fluency performance measured using the COWAT predicted antidepressant response to tDCS after controlling for confounds . LIMITATIONS Small sample size and analysis included data from both RCTs and open label studies . CONCLUSION Pre-treatment letter fluency performance , an ability subserved by the left prefrontal cortex , the primary site of stimulation , is a predictor of response for tDCS treatment for depression . This study highlights the importance of inter-individual neurobiological differences in mediating tDCS antidepressant effects IMPORTANCE High placebo responses have been observed across a wide range of pathologies , severely impacting drug development . OBJECTIVE To examine neurochemical mechanisms underlying the formation of placebo effects in patients with major depressive disorder ( MDD ) . DESIGN , SETTING , AND PARTICIPANTS In this study involving 2 placebo lead-in phases followed by an open antidepressant administration , we performed a single-blinded 2-week crossover r and omized clinical trial of 2 identical oral placebos ( described as having either active or inactive fast-acting antidepressant-like effects ) followed by a 10-week open-label treatment with a selective serotonin reuptake inhibitor or , in some cases , another agent as clinical ly indicated . The volunteers ( 35 medication-free patients with MDD at a university health system ) were studied with positron emission tomography and the µ-opioid receptor-selective radiotracer [11C]carfentanil after each 1-week inactive and active oral placebo treatment . In addition , 1 mL of isotonic saline was administered intravenously within sight of the volunteer during positron emission tomographic scanning every 4 minutes over 20 minutes only after the 1-week active placebo treatment , with instructions that the compound may be associated with the activation of brain systems involved in mood improvement . This challenge stimulus was used to test the individual capacity to acutely activate endogenous opioid neurotransmision under expectations of antidepressant effect . MAIN OUTCOMES AND MEASURES Changes in depressive symptoms in response to active placebo  and antidepressant . Baseline and activation measures of µ-opioid receptor binding . RESULTS Higher baseline µ-opioid receptor binding in the nucleus accumbens was associated with better response to antidepressant treatment ( r = 0.48 ; P = .02 ) . Reductions in depressive symptoms after 1 week of active placebo treatment , compared with the inactive , were associated with increased placebo-induced µ-opioid neurotransmission in a network of regions implicated in emotion , stress regulation , and the pathophysiology of MDD , namely , the subgenual anterior cingulate cortex , nucleus accumbens , midline thalamus , and amygdala ( nucleus accumbens : r = 0.6 ; P < .001 ) . Placebo-induced endogenous opioid release in these regions was associated with better antidepressant treatment response , predicting 43 % of the variance in symptom improvement at the end of the antidepressant trial . CONCLUSIONS AND RELEVANCE These data demonstrate that placebo-induced activation of the µ-opioid system is implicated in the formation of placebo antidepressant effects in patients with MDD and also participate in antidepressant responses , conferring illness resiliency , during open administration . TRIAL REGISTRATION clinical trials.gov Identifier : NCT02178696 BACKGROUND Major depressive disorder ( MDD ) is frequently associated with underactivity of the dorsolateral prefrontal cortex ( DLPFC ) which has led to this brain region being identified as an important target for the development of neurobiological treatments . Transcranial direct current stimulation ( tDCS ) administered to the DLPFC has antidepressant efficacy , however the magnitude of antidepressant outcomes are limited . Concurrent cognitive activity has been shown to enhance tDCS induced stimulation effects . Cognitive control training ( CCT ) is a new cognitive therapy for MDD that aims to enhance DLPFC activity via behavioral methods . HYPOTHESIS We tested the hypothesis that co-administration of DLPFC tDCS and CCT would result in a greater reduction in depressive symptomology than administration of tDCS or CCT alone . METHODS 27 adult participants with MDD were r and omized into a three-arm sham-controlled between-groups pilot study comparing the efficacy of 2 mA tDCS + CCT , sham tDCS + CCT and sham CCT + 2 mA tDCS ( 5 sessions administered on consecutive working days ) . Blinded assessment s of depression severity and cognitive control were conducted at baseline , end of treatment and a three week follow up review . RESULTS All three treatment conditions were associated with a reduction in depression severity at the end of five treatment sessions . However , only administration of tDCS + CCT result ed in sustained antidepressant response at follow up , the magnitude of which was greater than that observed immediately following conclusion of the treatment course . CONCLUSIONS The results provide preliminary evidence that concurrent CCT enhances antidepressant outcomes from tDCS . In the current sample , participants receiving concurrent tDCS and CCT continued to improve following cessation of treatment . The clinical superiority of a combined therapeutic approach was apparent even in a small sample and following a relatively short treatment course Chronic obstructive pulmonary disease ( COPD ) affects over 16 million people in the United States and is a major cause of disability and death worldwide . Its prevalence and mortality are increasing disproportionately among the elderly , women , African-Americans , persons of lower socioeconomic status , and the population s of developing countries in which tobacco is aggressively marketed . In contrast to other major chronic diseases such as heart disease and cancer , medical treatments for COPD have not made decisive inroads into its morbidity or death rates over the last 20 years , result ing in continuing efforts to reduce disability in patients with established disease . Depression is a source of increased disability in COPD , and , as in other chronically ill patient population s , is often unrecognized and untreated in the primary and specialty care sectors . Nearly half of all patients experience some depressive symptoms and at least one-fifth have had one or more major depressive episodes , frequently of long duration . Evidence from r and omized controlled trials supports the thesis that patients with mild depression improve with multidisciplinary rehabilitation , whereas patients with major depression may require specific pharmacotherapy to achieve significant improvement in mood disorder and day-to-day function . In addition to its impact on disability , depression may contribute indirectly to the etiology and progression of COPD through its relationship to addictive smoking . Mood disorder in adolescence and early adulthood contributes to early smoking and failure to quit , even after the onset of respiratory disease in later life . Patients with a history of major depression are more likely to fail in smoking cessation programs and to develop a major depressive episode when they do stop . This relationship calls for psychiatrically informed intervention models to improve long-term abstinence rates . The functional impairments associated with COPD are themselves potential promoters of depressive morbidity and chronicity , acting through complex causal pathways . Progressive hypoxia due to respiratory insufficiency leads to structural brain changes and neurocognitive deficits that impair day-to-day function and reduce adaptive potential ;  and oxygen therapy , as now practice d , offers minimal neurocognitive and mood benefits to most patients . Limited data from studies of experimental hypoxia in animals suggest that relatively mild lack of oxygen impairs the function and plasticity of critical neurotransmitter systems implicated in both cognition and mood , although current practice st and ards withhold oxygen therapy until late in the course of disease when the damaging effects of hypoxia on the brain have become well established . Neuropsychiatric approaches to the prevention , delay , and treatment of brain dysfunction should be a primary objective of research to improve patient outcomes . A comprehensive relational model that links pulmonary disease , hypoxia , neurocognitive impairment , and structural brain disease with depression provides a useful framework for the design of such studies . The near-term research agenda should include three components : ( 1 ) practical methods for improving physician and patient recognition of depression and neurocognitive impairment as targets for intervention ; ( 2 ) additional trials of st and ard antidepressant treatment approaches for both major and minor depression ; and ( 3 ) tests of the hypothesis that late-onset depression in patients with COPD is a marker for the presence of neurocognitive deficits and structural brain changes . The long-range research agenda must aim at preventive interventions design ed to forestall brain deterioration . Controlled clinical trials of supplemental oxygen in patients with mild hypoxia and minimal cognitive deficits are needed to determine whether early treatment can reverse or moderate decline , reduce the incidence and chronicity of depression , and improve response to antidepressant treatment . Novel neuroprotective therapies such as antioxidant supplementation and modulation of monoaminergic neurotransmission , coupled with overall improvements in long-term respiratory disease management that minimize episodes of increased systemic oxidative stress , should be considered for multisite trials design ed to define optimal treatment and prevention In this study , follow‐up results of cognitive‐behaviour therapy and of a combination of cognitive‐behaviour therapy with a serotonergic antidepressant were determined . The study also examined factors that can predict this treatment effect , both in the long term and in the short term . In addition , it investigated whether differential prediction is possible for cognitive‐behaviour therapy vs. a combination of cognitive‐behaviour therapy with a serotenergic antidepressant .  A total of 99 patients were included in the study . Treatment lasted 16 weeks , and a naturalistic follow‐up measurement was made 6 months later . Of the 70 patients who completed the treatment , follow‐up information was available for 61 subjects . Significant time effects were found on all outcome measures at both post‐treatment measurement and follow‐up . No differences in efficacy were found between the treatment conditions . Effectiveness at post‐treatment measurement appears to predict success at follow‐up . However , 17 of the 45 non‐responders at the post‐treatment measurement had become responders by the follow‐up . The severity of symptoms , motivation for treatment and the dimensional score on the PDQ‐R for cluster A personality disorder appear to predict treatment outcome . No predictors were found that related specifically to cognitive‐behaviour therapy or combined treatment . These results indicate that the effectiveness  of cognitive‐behaviour therapy or a combination of cognitive‐behaviour therapy and fluvoxamine at the post‐treatment measurement is maintained at follow‐up . However , non‐response at post‐treatment does not always imply non‐response at follow‐up . Patients with more severe symptoms need a longer period of therapy to become responders . Although predictors for treatment success were found , no evidence was found to determine the choice of one of the treatment modalities OBJECTIVE Predictors of treatment response to serotonergic versus nonserotonergic , e.g. , noradrenergic , antidepressants are of considerable clinical relevance as they could help to reduce the occurrence of patients ' receiving weeks or even months of unsuccessful treatment . Several studies show that the response to selective serotonin reuptake inhibitors can be successfully predicted by using the loudness dependence of auditory evoked potentials ( LDAEP ) , which denotes change in the amplitudes in response to different stimulus intensities and is to date one of the best vali date d indicators of the central serotonergic system . The aim of the current r and omized prospect i ve study was to investigate whether or not LDAEP also allows the differential prediction of treatment response to serotonergic versus noradrenergic antidepressants . METHOD Electrophysiologic recordings were performed on 48 subjects between 1999 and 2001 . After exclusions due to artifacts , the study sample consisted of 35 unmedicated in patients with a DSM-IV or ICD-10 diagnosis of major depressive disorder ( mean + /- SD age = 42.5 + /- 10.8 years ; 13 male , 22 female ; mean + /- SD score of 28.9 + /- 5.7 on the Hamilton Rating Scale for Depression [ HAM-D ] , the primary measure for psychopathology ) . The patients were then treated for 4 weeks with either the selective serotonin reuptake inhibitor citalopram or the noradrenaline reuptake inhibitor reboxetine . RESULTS Analysis of variance ( F = 5.05 , df = 1,31 ; p = .03 ) revealed that responders ( 50 % improvement in HAM-D score ) to the citalopram treatment were characterized by a strong LDAEP at baseline , and responders to reboxetine were characterized by a weak LDAEP at baseline . Non-responders to citalopram or reboxetine showed the inverse LDAEP characteristics , respectively . CONCLUSION This study is one of the first to demonstrate differential prediction of response to different classes of antidepressants . Patients at the beginning of an antidepressant treatment who show an initially strong LDAEP have a greater probability of responding to a serotonin-agonist antidepressant , whereas patients with a weak LDAEP will probably benefit more from a nonserotonergic , e.g. , noradrenergic , antidepressant . If these results were replicated in a larger sample , this simple electroencephalographic method could be more broadly used in clinical practice to support clinicians in replacing the trial and error method with a more targeted and individualized approach to antidepressant treatment OBJECTIVE Current clinical knowledge holds that antidepressants have a delayed onset of efficacy . However , the delayed onset hypothesis has been question ed recently by survival analytical approaches . We aim ed to test whether early improvement under antidepressant treatment is a clinical ly useful predictor of later stable response and remission . METHOD We analyzed data from a r and omized double-blind controlled trial with  mirtazapine and paroxetine  in patients with major depression ( DSM-IV ) .  Improvement was defined as a 17-item Hamilton Rating Scale for Depression ( HAM-D-17 ) score reduction of > or = 20 % . Stable response was defined as > or = 50 % HAM-D-17 score reduction at week 4 and week 6 , and stable remission as a HAM-D-17 score of < or = 7 at week 4 and week 6 . Sensitivity , specificity , positive predictive value ( PPV ) , and negative predictive value ( NPV ) were calculated . RESULTS Improvement occurred in a majority of the analyzed patients within 2 weeks ( mirtazapine : 72.7 % of 109 patients ; paroxetine : 64.9 % of 103 patients ) . Early improvement was a highly sensitive predictor of later stable response or stable remission for both drugs . NPV approached maximum values as early as week 2 for mirtazapine and week 3 for paroxetine . After 2 weeks of treatment with mirtazapine and 3 weeks with paroxetine , almost none of the patients who had not yet improved became a stable responder or stable remitter in the later course . CONCLUSION Our results strongly suggest that early improvement predicts later stable response with high sensitivity . These empirically derived data question the delayed onset hypothesis for both antidepressants tested and provide important clinical clues for an individually tailored antidepressant treatment Although the cost of poor treatment outcomes of depression is staggering , we do not yet have clinical ly useful methods for selecting the most effective antidepressant for each depressed person . Emotional brain activation is altered in major depressive disorder ( MDD ) and implicated in treatment response . Identifying which aspects of emotional brain activation are predictive of general and specific responses to antidepressants may help clinicians and patients when making treatment decisions . We examined whether amygdala activation probed by emotion stimuli is a general or differential predictor of response to three commonly prescribed antidepressants , using functional magnetic resonance imaging ( fMRI ) . A test – retest design was used to assess patients with MDD in an academic setting as part of the International Study to Predict Optimized Treatment in Depression . A total of 80 MDD out patients were scanned prior to treatment and 8 weeks after r and omization to the selective serotonin reuptake inhibitors escitalopram and sertraline and the serotonin – norepinephrine reuptake inhibitor , venlafaxine-extended release ( XR ) . A total of 34 matched controls were scanned at the same timepoints . We quantified the blood oxygen level-dependent signal of the amygdala during subliminal and supraliminal viewing of facial expressions of emotion . Response to treatment was defined by ⩾50 % symptom improvement on the 17-item Hamilton Depression Rating Scale . Pre-treatment amygdala hypo-reactivity to subliminal happy and threat was a general predictor of treatment response , regardless of medication type ( Cohen ’s d effect size 0.63 to 0.77 ; classification accuracy , 75 % ) . Responders showed hypo-reactivity compared to controls at baseline , and an increase toward ‘ normalization ’ post-treatment . Pre-treatment amygdala reactivity to subliminal sadness was a differential moderator of non-response to venlafaxine-XR ( Cohen ’s d effect size 1.5 ; classification accuracy , 81 % ) . Non-responders to venlafaxine-XR  showed pre-treatment hyper-reactivity , which progressed to hypo-reactivity rather than normalization post-treatment , and hypo-reactivity post-treatment was abnormal compared to controls . Impaired amygdala activation has not previously been highlighted in the general vs differential prediction of antidepressant outcomes . Amygdala hypo-reactivity to emotions signaling reward and threat predicts the general capacity to respond to antidepressants . Amygdala hyper-reactivity to sad emotion is involved in a specific non-response to a serotonin – norepinephrine reuptake inhibitor . The findings suggest amygdala probes may help inform the personal selection of antidepressant treatments This study was aim ed at resolving the time course of clinical action of antidepressants ( ADs ) and the type of early behavioral changes that precede recovery in treatment-responsive depressed patients . The first goal was to identify , during the first 2 weeks of treatment , the onset of clinical actions of the selective serotonin reuptake inhibitor ( SSRI ) , paroxetine , and the selective noradrenergic reuptake inhibitor , desipramine ( DMI ) . The second aim was to test the hypothesis that the two pharmacologic subtypes would induce different early behavioral changes in treatment-responsive patients . The design was a r and omized , parallel group , placebo-controlled , double-blind study for 6 weeks of treatment following a 1-week washout period . The study utilized measures of the major behavioral components of the depressive disorder as well as overall severity . The results indicated that the onset of clinical actions of DMI ranged from 3 to 13 days , averaged 13 days for paroxetine , and was 16–42 days for placebo . Furthermore , as hypothesized , the different types of ADs initially impacted different behavioral aspects of the disorder . After 1 week of treatment , DMI produced greater reductions in motor retardation and depressed mood than did paroxetine and placebo , and this difference persisted at the second week of treatment . Early improvement in depressed mood – motor retardation differentiated patients who responded to DMI after 6 weeks of treatment from those that did not . Paroxetine initially reduced anxiety more in responders than in nonresponders , and by the second week , significantly improved depressed mood and distressed expression in responders to a greater extent . Depressed patients who responded to placebo showed no consistent early pattern of behavior improvement . Early drug-specific behavioral changes were highly predictive of ultimate clinical response to the different ADs , results that could eventually be applied directly to clinical practice
The available evidence suggests the early changes in cognition may predict treatment response in individuals with MDD .
The results depict an emerging trend towards early changes in facial emotion recognition ( i.e. , a hot cognitive process ) as a predictor of treatment outcome .
Conclusion : The identification of reliable early treatment predictors of antidepressant response would be clinical ly significant , enabling clinicians to more accurately evaluate the efficacy of selected treatment avenues .
HIGHLIGHTSCognitive dysfunction is a principal feature and determinant of health outcome in MDD.Cognitive changes have shown to occur prior to improvements in mood symptoms .
Early changes in emotional processing may predict treatment response in MDD
Background : Despite the widespread use of antidepressants in clinical practice , the current trial‐ and ‐error approach to medication selection contributes to treatment failure and underscores the need to identify reliable predictors of antidepressant response .
Since changes in measures of cognition have been reported to occur early in treatment and prior to improvements in overall mood symptoms , the present review aims to determine whether early changes in measures of cognition can predict response in individuals with MDD .