Treatment Of Emotional Disorders Research Articles

Modulation of monoamine oxidase (MAO) expression in neuropsychiatric disorders: genetic and environmental factors involved in type A MAO expression.

Monoamine oxidase types A and B (MAO-A, MAO-B) regulate the levels of monoamine neurotransmitters in the brain, and their dysfunction may be involved in the pathogenesis and influence the clinical phenotypes of neuropsychiatric disorders. Reversible MAO-A inhibitors, such as moclobemide and befloxatone, are currently employed in the treatment of emotional disorders by inhibiting the enzymatic degradation of dopamine, serotonin and norepinephrine in the central nervous system (CNS). It has been suggested that the irreversible MAO-B inhibitors selegiline and rasagiline exert a neuroprotective effect in Parkinson's and Alzheimer's diseases. This effect, however, is not related to their inhibition of MAO activity; in animal and cellular models, selegiline and rasagiline protect neuronal cells through their anti-apoptotic activity and induction of pro-survival genes. There is increasing evidence that MAO-A activity, but not that of MAO-B, is implicated in the pathophysiology of neurodegenerative disorders, but also in gene induction by MAO-B inhibitors; on the other hand, selegiline and rasagiline increase MAO-A mRNA, protein, and enzyme activity levels. Taken together, these results suggest that each MAO subtype exerts effects that modulate the expression and activity of the other isoenzyme. The roles of MAO-A and -B in the CNS should therefore be re-evaluated with respect to the "type-specificity" of their inhibitors, which may not be unconditional during chronic treatment. Mao-a expression, in particular, may be implicated in pathogenesis and phenotypes in neuropsychiatric disorders. MAO-A expression is modified by mao polymorphisms affecting its transcriptional efficiency, as well as by mutations and polymorphism of parkin, Sirt1, FOXO, microRNA, presenilin-1, and other regulatory proteins. In addition, childhood maltreatment has been shown to have an impact upon adolescent social behavior in children with mao-a polymorphisms of low transcriptional activity. Low MAO-A activity may increase the levels of serotonin and norepinephrine, resulting in disturbed neurotransmitter system development and behavior. This review discusses genetic and environmental factors involved in the regulation of MAO-A expression, in the contexts of neuropsychiatric function and of the regulation of neuronal survival and death.

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introduction: Numerous advances with regard to the specific treatments for emotional disorders have been achieved over the last few decades. Yet, they have many limitations. In order to overcome them, Barlow et al. have carried out a Unified Protocol for Transdiagnostic Treatment of Emotional Disorders (uP). goal: Improving the cognitive behavioral treatments for emotional disorders bearing in mind the axis of efficacy, as well as the axis of effectiveness and efficiency from the Transdiagnostic perspective used in group format. method: With a sample formed by 12 participants and after having administered the evaluation protocol (pre-test), the group therapy was carried out applying this protocol. The evaluation was done again after the intervention (post-test). results: The differences of pre-post averages have turned out statistically significant in the measures that evaluate depression as well as those that evaluate anxiety. Furthermore, 75 % of the participants stopped having the criteria for their principal diagnosis in the post-test evaluation. conclusions: The preliminary data show the efficacy of this protocol in the reduction of the diagnostic criteria and also in the clinical improvements obtained. Moreover, the UP in group format was valued by all participants as «very useful» and «satisfactory». keywords: uP, transdiagnostic, Emotional Disorders, group therapy, efficacy

Multiple sclerosis, emotions and social cognition

A. Tourbah*, N. Ehrle, N. Henry, S. Bakchine, M.P. Chaunu,M. MontreuilCHRU de Reims, service de neurologie, hopital Maison-Blanche, 45, rueCognacq Jay, URCA LPN UE 2027, Paris VIII, 51092 Reims, France*Corresponding author.E-mail address: atourbah@chu-reims.frKeywords: Multiple sclerosis; Alexithymia; Theory of mind; Emotion;CognitionEmotional processes are governed by the areas and neural systems that can beexplored MRI (amygdala, orbitofrontal cortex, cingulate cortex, insula). It isnowpossibletoexplorebyMRI,usingtechniquesbasedonfunctionalMRIanddiffusion tensor including (anatomical and functional connectivity).These processes seem disturbed in MS. Indeed, the motor and neurosensorydisabilityisassociatedwithcognitivedisorders,mooddisorders,andemotionaland socio-cognitive deficit.Emotions play a critical role in the organization of social processes in differentareas of cognition (memory, attention decision). Besides alexithymia (difficultyverbalizing emotional experiences, fantasy poverty), social cognition is the skillsetthatallows ustointerpret and predictthebehaviorofothers.Their disruptioninvolvedinthesepatientswithbehavioralproblemsandsocialadjustment.Toolstoexplorethesedisturbances,includingthestudyoffacialexpressions(perceptionof primary emotions), and theory of mind (attribution of thoughts to others).Their management is insufficient. The detection and treatment of emotionaldisorders (in addition to cognitive impairment, fatigue and mood disorders) isdesirable for these patients to maintain social and family life, and improvequality of life. It has not been shown that treatments, currently used in MS, areeffective in this area. The establishment of workshops rehabilitation would beuseful.Further readingBanati M, Sandor, J., Mike, A., Illes, E., Bors, L., Feldmann, A., Herold, R. &Illes Z. (2009). Social cognition and Theory of Mind in patients withrelapsing-remitting multiple sclerosis. European Journal of Neurology, 17(3),426-433.Henry A, Tourbah A, Chaunu MP, Rumbach L,Montreuil M, Bakchine S.Social Cognition Impairments in Relapsing-Remitting Multiple Sclerosis. J IntNeuropsychol Soc (2011), 17, 1122-1131.http://dx.doi.org/10.1016/j.rehab.2013.07.906CO04-002-e

An Evaluation of the Effects of Diagnostic Composition on Individual Treatment Outcome Within Transdiagnostic Cognitive–Behavioral Group Therapy for Anxiety

Recently, studies have supported the efficacy of treating anxiety disorders utilizing a transdiagnostic, or non-diagnosis-specific, framework (Erickson, D. H. (2003). Group cognitive behavioural therapy for heterogeneous anxiety disorders. Cognitive Behaviour Therapy, 32, 179–186; Garcia, M. S. (2004). Effectiveness of cognitive-behavioural group therapy in patients with anxiety disorders. Psychology in Spain, 8, 89–97; Norton, P. J., & Hope, D. A. (2005). Preliminary evaluation of a broad-spectrum cognitive-behavioral group therapy for anxiety. Journal of Behavior Therapy and Experimental Psychiatry, 36, 79–97). Transdiagnostic group treatment packages focus on the common aspects inherent across the anxiety disorders such as behavioral and cognitive avoidance, and faulty cognitive appraisals of threat potential or meaning (Barlow, D. H., Allen, L. B., & Choate, M. L. (2004). Toward a unified treatment for emotional disorders. Behavior Therapy, 35, 205–230). Although research supports the overall efficacy of transdiagnostic cognitive behavior therapy (CBT) for anxiety disorders (Norton, P. J., & Philipp, L. M. (2008). Transdiagnostic approaches to the treatment of anxiety disorders: A quantitative review. Psychotherapy: Theory, Research, Practice and Training, 45, 214–226), the effect of diagnostically mixed group composition on individual outcomes is less clear. This study investigated the relationship between group composition and treatment outcome within diagnostically heterogeneous groups with the purpose of determining if diagnostic heterogeneity differentially impacted treatment outcome for 84 individuals during a 12-week transdiagnostic cognitive–behavioral group anxiety treatment program (Norton, P. J. (2012a). Group cognitive-behavioral therapy of anxiety: A transdiagnostic treatment manual. New York: Guilford). The diagnostic makeup of the treatment group was examined at the beginning of treatment and at the end of treatment, and the results indicated that the diagnostic makeup of the treatment group had no significant impact on individual treatment outcome. These findings have direct implications for the delivery of transdiagnostic treatments, and are discussed in terms of their global implications for the transdiagnostic approach to the treatment of anxiety disorders.

Intolerance of Uncertainty: A Common Factor in the Treatment of Emotional Disorders

Intolerance of uncertainty (IU) is a characteristic predominantly associated with generalized anxiety disorder (GAD); however, emerging evidence indicates that IU may be a shared element of emotional disorders. This study aimed to examine IU across diagnostic categories, change in IU during transdiagnostic treatment, and the relationship between change in IU and treatment outcome. Patients diagnosed with heterogeneous anxiety and depressive disorders received up to 18 weeks of a transdiagnostic cognitive-behavioral therapy intervention. Patient self-reported IU and self-report and clinician-rated symptom/functioning measures were administered at pretreatment and posttreatment. When controlling for negative affectivity, IU correlated with measures of depressive symptoms and worry severity at pretreatment. Patients with GAD and panic disorder exhibited the highest pretreatment IU scores, yet IU scores did not differ significantly based on the presence or absence of a specific diagnosis. A significant decrease in IU was observed, and change in IU was related to reduced anxiety and depressive symptom levels at posttreatment across diagnostic categories. Change in IU can be observed across problem areas in transdiagnostic treatment and such change is correlated with treatment outcome.

Neural Correlates of Three Neurocognitive Intervention Strategies: A Preliminary Step Towards Personalized Treatment for Psychological Disorders

Brain-based behavioral interventions targeting specific neurocognitive mechanisms show initial promise in the treatment of emotional disorders, but personalization of such approaches will be facilitated if brain targets are empirically established. As a preliminary step, we conducted a proof-of-concept study to test whether particular emotion regulatory neural circuitry can be differentially targeted by specific neurocognitive tasks, and whether these tasks effectively inhibit amygdala activity. Eleven healthy individuals underwent an idiographic sadness and guilt induction. Brain response was measured via fMRI during 4 subsequent emotion regulation conditions: fixation, cognitive reappraisal (selected to target the ventrolateral prefrontal cortex), working memory practice (selected to target the dorsolateral prefrontal cortex), and visual distraction (Tetris; selected to target occipital cortex). In whole-brain comparisons to fixation, hypotheses were upheld. Reappraisal uniquely activated left ventrolateral prefrontal cortex, working memory practice uniquely activated left dorsolateral prefrontal cortex, and Tetris uniquely activated bilateral occipitoparietal cortex, activations that were largely robust at the single-subject level. All tasks inhibited amygdala activity relative to fixation. Data support examining whether repeated exposure to these tasks in psychiatric patients affects neural abnormalities implicated in emotional disorders. Ideally, psychiatric treatment will be accelerated by matching specific treatments to patients with specific neural profiles.

Transdiagnostic CBT for anxiety disorder: Efficacy, acceptability, and beyond = TCC transdiagnóstica para los trastornos de ansiedad: Eficacia, aceptabilidad, y otros aspectos

Interest in transdiagnostic approaches to the cognitive-behavioral treatment (CBT) ofemotional disorders has been increasing over the past decade. The purpose of this paper was toreview the rationale behind transdiagnostic treatment models, describe one such group-based treatmentprotocol in detail, and report on the building evidence base to date. The evidence suggests thattransdiagnostic CBT for anxiety is associated with symptom improvement, performs better thanwaitlist controls, is associated with improvements in comorbid disorders, and performs equivalentlyto established diagnosis-specific treatments. Transdiagnostic protocols are also associatedwith good client satisfaction, high levels of therapeutic alliance and group cohesion, and positivetreatment perceptions during and following treatment. Limitations and directions for future researchare discussed.

A unified protocol for the group treatment of chilhood anxiety and depression = Protocolo unificado de grupo para el tratamiento de la ansiedad y la depresión en la infancia

Childhood anxiety and mood disorders are common and are associated with high levels ofimpairment. These disorders share a common etiology and risk factors, and are often experiencedconcurrently. While evidence-based interventions for youth anxiety and depressive disorders do exist,children experiencing this common comorbidity tend to experience weaker treatment outcomes inanxiety or depression focused treatments as compared to youth suffering from either disorder alone.Researchers are now investigating transdiagnostic interventions, which have potential to target commonvulnerability factors and address a wider range of concerns. The Unified Protocol for the Treatmentof Emotional Disorders in Children: Emotion Detectives (UP-C: ED) is a transdiagnostictreatment that implements a set of core principles to address common factors underlying youth anxietyand depressive disorders in a group setting. Theoretical underpinnings of the UP-C: ED are discussedalong with an in-depth presentation of treatment content. A case study is also presented detailinginitial intake, treatment conceptualization, treatment, and treatment outcomes using this modality.

Eeg Coherence between Prefrontal and Posterior Cortical Regions is Related to Negative Personality Traits

Eeg Coherence between Prefrontal and Posterior Cortical Regions is Related to Negative Personality Traits

Calidad de vida en niños y adolescentes sobrevivientes de leucemia linfoblástica aguda

Quality of life in children and adolescents surviving acute lymphoblastic leukemia Objective: Describe the quality of life of patients cured of acute lymphoblastic leukemia (ALL) treated at the Oncology Unit at Roberto del Rio Children’s Hospital. Method: With a transversal design, the Kidscreen-27 questionnaire was applied to a selected sample of 41 patients. Results were compared with a random sample of school children paired for age and sex. Results: Children cured from ALL had lower scores than the control group, although ANOVA showed differences were not signifi cant. ALL children tended to self report as ill, signifi cantly lower in physical well-being. Average followup time was 8 years. Conclusions: Quality of life of chilean children cured from ALL is similar to school children of similar age and gender. To preserve the quality of life, it is suggested that the following measures be taken: prevention of sequelae, detection and treatment of emotional disorders, and discharge at a reasonable time. (Key words: Lymphoblastic leukemia, quality of life, cancer survivalr, Kidscreen-27). Rev Chil Pediatr 2011; 82 (2): 113-121

Cognitive–behavioral therapy: what benefits can it offer people with multiple sclerosis?

Cognitive–behavioral therapy (CBT) originated as a treatment for emotional disorders. However, it is increasingly used to help people with chronic illnesses manage symptoms and improve psychosocial outcomes, such as depression and quality of life. In this article, we focus on uses of CBT in patients with multiple sclerosis, an incurable neurological disease that causes potentially debilitating symptoms and poses numerous challenges to psychological well-being. We examine the rationale for using CBT to deal with distress, symptoms, impairment and disease exacerbation and progression, and discuss examples of existing research on the efficacy and acceptability of these interventions. Finally, we consider areas where CBT could potentially benefit people with multiple sclerosis in the future. Ongoing challenges in this field are discussed.

Real-time support vector classification and feedback of multiple emotional brain states

An important question that confronts current research in affective neuroscience as well as in the treatment of emotional disorders is whether it is possible to determine the emotional state of a person based on the measurement of brain activity alone. Here, we first show that an online support vector machine (SVM) can be built to recognize two discrete emotional states, such as happiness and disgust from fMRI signals, in healthy individuals instructed to recall emotionally salient episodes from their lives. We report the first application of real-time head motion correction, spatial smoothing and feature selection based on a new method called Effect mapping. The classifier also showed robust prediction rates in decoding three discrete emotional states (happiness, disgust and sadness) in an extended group of participants. Subjective reports ascertained that participants performed emotion imagery and that the online classifier decoded emotions and not arbitrary states of the brain. Offline whole brain classification as well as region-of-interest classification in 24 brain areas previously implicated in emotion processing revealed that the frontal cortex was critically involved in emotion induction by imagery. We also demonstrate an fMRI-BCI based on real-time classification of BOLD signals from multiple brain regions, for each repetition time (TR) of scanning, providing visual feedback of emotional states to the participant for potential applications in the clinical treatment of dysfunctional affect.

Differential regulation of CaMKII inhibitor β protein expression after exposure to a novel context and during contextual fear memory formation

Understanding of the molecular basis of long-term fear memory (fear LTM) formation provides targets in the treatment of emotional disorders. Ca(2+)/calmodulin-dependent protein kinase II (CaMKII) is one of the key synaptic molecules involved in fear LTM formation. There are two endogenous inhibitor proteins of CaMKII, CaMKII N alpha and N beta, which can regulate CaMKII activity in vitro. However, the physiological role of these endogenous inhibitors is not known. Here, we have investigated whether CaMKII N beta protein expression is regulated after contextual fear conditioning or exposure to a novel context. Using a novel CaMKII N beta-specific antibody, CaMKII N beta expression was analysed in the naïve mouse brain as well as in the amygdala and hippocampus after conditioning and context exposure. We show that in naïve mouse forebrain CaMKII N beta protein is expressed at its highest levels in olfactory bulb, prefrontal and piriform cortices, amygdala and thalamus. The protein is expressed both in dendrites and cell bodies. CaMKII N beta expression is rapidly and transiently up-regulated in the hippocampus after context exposure. In the amygdala, its expression is regulated only by contextual fear conditioning and not by exposure to a novel context. In conclusion, we show that CaMKII N beta expression is differentially regulated by novelty and contextual fear conditioning, providing further insight into molecular basis of fear LTM.

Comorbidity and the Treatment of Principal Anxiety Disorders in a Naturalistic Sample

This study examined the impact of comorbidity on treatment outcome and the effects of cognitive behavioral therapy (CBT) for anxiety and depressive disorders on comorbid disorders in a naturalistic sample of 150 patients presenting to an anxiety disorders clinic. The following results were observed across principal (i.e., most severe) diagnoses. Patients with comorbid anxiety and depressive disorders presented for treatment with higher severity of their principal disorder than patients without comorbidity. However, the presence of comorbidity did not predict dropout or poor treatment response, and patients demonstrated significant improvement in their principal disorders regardless of comorbidity. The frequency of clinically severe and subclinical (i.e., not severe enough to meet diagnostic criteria) comorbid conditions decreased significantly over the course of treatment. The implication of these findings for the classification and treatment of emotional disorders is discussed.

A test of shame in outpatients with emotional disorder

Background: Shame is an acknowledged part of several psychopathological conditions, but is underrepresented in clinical research. Cook's Internalized Shame Scale (ISS) is the most promising measure, but has mostly been used for testing small clinical samples biased toward depressive pathology and female participants. Aims: To contribute to establishing indicators of pathological shame in outpatients with depression and anxiety disorder, and to contribute to establishing norms for the ISS in Scandinavia. Method: The ISS was administered to n = 200 gender balanced non-patient and outpatient samples. A total of 100 patients each were diagnosed as suffering from a depression or anxiety disorder. The diagnoses were supported by Beck's Depression (BDI) and Anxiety Inventory (BAI). The analyses used were the principal component analysis (PCA) and confirmatory factor analysis (CFA) for item structure and sample equivalence, ANOVAs, t-tests and Mann–Whitney non-parametric statistics for index scores, and the receiver operating curve (ROC) for break-off. Results: Patients' ISS score were similar to the results from previous research, the effect size of patient–non-patient difference was 0.68, correlations indicated a higher level of shame in depression than in anxiety, and the BDI–BAI correlation was 0.56 for both clinical samples. The PCA showed three factors that were identified as: “Inadequacy”, “Emptiness”, and “Vulnerability”. Conclusions: The ISS is a viable instrument, which indicates a widespread shame pathology in both depressive and anxious out-patients. The instrument may not be uni-dimensional, but exploration of factor variation may be a promising goal for further research. Clinical implications: Assessment of shame should be included in diagnosis and treatment of emotional disorder.

Relationship of Exposure to Clinically Irrelevant Emotion Cues and Obsessive-Compulsive Symptoms

Research has highlighted the role of emotion regulation as a common factor underlying emotional disorders. The current study examined the relationship of emotion regulation skills to obsessive-compulsive disorder (OCD) symptoms. Seven participants with a principal diagnosis of OCD in a multiple-baseline across subjects design were taught the skill of prevention of emotional avoidance in the context of emotion provocation procedures to clinically irrelevant (nonspecific) cues prior to practicing this skill with clinically relevant (OCD-specific) cues. Results suggested successful acquisition of emotion regulation skills (as evidenced by decreased thought suppression and increased acceptance of thoughts and feelings) in clinically irrelevant contexts. Acquisition of this skill was associated with decreases in obsessive-compulsive symptoms, even though clinically relevant cues were not introduced during this phase. Implementation of skills in clinically relevant contexts was associated with greater reductions in OCD symptoms. Discussion focuses on implications for emotion regulatory processes in the maintenance and treatment of emotional disorders.

Location of the Antidepressant Binding Site in the Serotonin Transporter

The serotonin transporter (SERT) regulates extracellular levels of serotonin (5-hydroxytryptamine, 5HT) in the brain by transporting 5HT into neurons and glial cells. The human SERT (hSERT) is the primary target for drugs used in the treatment of emotional disorders, including depression. hSERT belongs to the solute carrier 6 family that includes a bacterial leucine transporter (LeuT), for which a high resolution crystal structure has become available. LeuT has proved to be an excellent model for human transporters and has advanced the understanding of solute carrier 6 transporter structure-function relationships. However, the precise structural mechanism by which antidepressants inhibit hSERT and the location of their binding pockets are still elusive. We have identified a residue (Ser-438) located within the 5HT-binding pocket in hSERT to be a critical determinant for the potency of several antidepressants, including the selective serotonin reuptake inhibitor citalopram and the tricyclic antidepressants imipramine, clomipramine, and amitriptyline. A conservative mutation of Ser-438 to threonine (S438T) selectively increased the K(i) values for these antidepressants up to 175-fold. The effects of introducing a protein methyl group into the 5HT-binding pocket by S438T were absent or reduced for analogs of these antidepressants lacking a single methyl group. This suggests that these antidepressants interact directly with Ser-438 during binding to hSERT, implying an overlapping localization of substrate- and inhibitor-binding sites in hSERT suggesting that antidepressants function by a mechanism that involves direct occlusion of the 5HT-binding site.

Epileptogenesis alters gene expression pattern in rats subjected to amygdala-dependent emotional learning

Here we tested a hypothesis that epileptogenesis influences expression pattern of genes in the basolateral amygdala that are critical for fear conditioning. Whole genome molecular profiling of basolateral rat amygdala was performed to compare the transcriptome changes underlying fear learning in epileptogenic and control animals. Our analysis revealed that after fear conditioning procedure 26 genes were regulated differently in the basolateral amygdala of both groups. Thus, our study provides the first evidence that not only the damage to the neuronal pathways but also altered composition or activity level of molecular machinery responsible for formation of emotional memories within surviving pathways can contribute to impairment in emotional learning in epileptogenic animals. Understanding the function of those genes in emotional learning provides an attractive avenue for identification of novel drug targets for treatment of emotional disorders after epileptogenesis-inducing insult.

Behavior analysts and counseling: Why are we not there and how can we get there?

Behavioral psychology is a broad field that encompasses a range of topics from working with individuals with severe self-injurious behaviors through professional management in the workplace. While the range of topics is broad, the interventions or programs that are put into place have common elements: behaviorists work to modify by using the principles of behavior. The degree that I (the first author) hold is in developmental and child psychology, with my doctorate-level education focusing on analysis. Thus, I hold two credentials: I am a board certified analyst (BCBA) as well as a licensed psychologist (LP). The BCBA signifies that I understand (or it should) while the LP indicates that I hold the credential necessary to bill insurance companies for my work with clients. I work with families and children that have behavioral challenges and continually come in contact with views of the diagnosis, development, and treatment of emotional and behavioral challenges in children. Because of this, I attended a workshop on the treatment of emotional disorders in children at the most recent Association for Behavior Analysis International conference in order to further develop my understanding of the treatment of these disorders from a analytic perspective. I came away with the sense that, with a few exceptions, analysis continues to avoid addressing some of the issues that traditional psychology and address. This is apparent even in the way behaviorists talk about between the two divisions of the field: one goes to a psychologist or counselor for or counseling; one receives from a behavioral psychologist or analyst (Baker, Blumberg, Freeman, & Wieseler, 2002; Dougher & Hackbert, 2000). Even for a single individual working as a BCBA and an LP, the two are separate. When working with insurance companies, the language that is used determines if the service receives reimbursement: if interactive therapy with a descriptive narrative of what transpired during the psychologist/client interaction is provided the service receives compensation; if services are provided with data sheets and a graph the are not compensated: insurance companies do not pay for behavior modification or intervention--they pay for and therapy. Thus, I feel that an understanding of the dichotomy between behavioral intervention and is critical to increasing the availability of quality analytic and is worthy of discussion. In my experience, while our unwillingness to foray into counseling areas is multivariate, there are a few basic areas that are fundamental to this unwillingness. First, because our education does not include psychological training, analysts do not learn how to present intervention in such a way as to receive third party reimbursement. Consequently, the contingencies that operate on our as we provide treatment for challenging in an applied setting tend to be aversive--we either need to learn how to use non-behavioral terms to describe behavior/environment interaction (requiring an increased response effort) or we do not receive payment. A case in point is my recent experience with Medicaid. I had been supplying for four families over a three-year period. When Medicaid conducted their audit of my files I was denied payment for these services, based in part on the type of notes I had (e.g. change schedule of SR+ to a VR3). Consequently, a recoupment process was started, and I was required to reimburse Medicaid the roughly $16,000 I had been paid over the three year period. This event was (and continues to be) quite punishing! Secondly, as analysts, we receive our professional recognition (social reinforcement) from the community within which we operate. …

P.7.030 Efficacy of valproic acid in the treatment of emotional disorders in children with abnormalities in EEG

P.7.030 Efficacy of valproic acid in the treatment of emotional disorders in children with abnormalities in EEG