Diagnosa Dan Tatalaksana Dysthymia Anak Dan Remaja

CNS Drugs 2003; 17 (13): 927-946THERAPY IN PRACTICE 1172-7047/03/0013-0927/$30.00/0 Adis Data Information BV 2003. All rights reserved.

Diagnosis and Treatment ofDysthymia in Childrenand AdolescentsMaria Nobile, Giulia M. Cataldo, Cecilia Marino and Massimo Molteni

Child Psychiatry Unit, Scientific Institute Eugenio Medea, Bosisio Parini (LC), Italy

Contents

Abstract . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 9281. Diagnosis . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 929

1.1 Clinical Phenomenology and Classification . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 9291.2 Comorbidity . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 9291.3 Natural History and Clinical Outcome . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 929

1.3.1 Double Depression . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 9301.3.2 Suicidal Behaviour . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 9311.3.3 Functional Impairment . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 931

2. Epidemiology . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 9312.1 Prevalence. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 9312.2 Risk Factors . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 932

3. Treatment . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 9323.1 General Treatment Approach. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 9333.2 Assessment Procedures and Measures . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 933

4. Psychological Treatment . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 9334.1 Psychoeducational Interventions . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 9334.2 Supportive Treatment . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 9344.3 Cognitive Behavioural Psychotherapy . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 9344.4 Interpersonal Therapy . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 9354.5 Family Therapy . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 9354.6 Psychodynamic Psychotherapy . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 9354.7 Prevention Programmes . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 936

5. Pharmacological Treatment . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 9365.1 Indications . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 9365.2 Pharmacological Agents . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 937

5.2.1 SSRIs . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 9375.2.2 Tricyclic Antidepressants . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 9385.2.3 Other Antidepressants . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 938

5.3 Acute-Phase Medication . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 9395.4 Partial Response and Nonresponse . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 9395.5 Adverse Effects . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 9405.6 Continuation Treatment . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 941

928 Nobile et al.

5.7 Treatment of Comorbid Conditions . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 941

6. Conclusion . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 941

Dysthymic disorder is a chronic depressive condition occurring in 0.64.6% ofAbstractchildren and 1.68.0% of adolescents. Although symptoms are less severe thanthose observed in major depression, childhood-onset dysthymic disorder is cha-racterised by a persistent and long-term depressed or irritable mood (mean episodeduration 34 years), a worse outcome than major depression and, frequently,comorbid disorders (in around 50% of patients). Long-lasting depressive symp-toms seem responsible for long-term disabling consequences on social skilllearning, psychosocial functioning and consequent professional life, probablycontributing to a higher risk of relapse or development of major depression.Consistently, the first episode of major depression occurs 23 years after the onsetof dysthymic disorder, suggesting that the latter is one of the gateways to recurrentmood disorders.

The primary aims of treatment for dysthymic disorder should be to resolvedepressive symptoms, reduce the risk of developing other mood disorders overtime and strengthen psychosocial functioning, especially in children and adoles-cents, in order to prevent the potentially serious sequelae of this disorder. Aschildren with dysthymia often have multiple problems, interventions shouldinvolve multiple levels and measures: individual psychotherapy, family therapy/education and pharmacological treatment.

Psychotherapeutic techniques, such as cognitive-behaviour therapy and inter-personal therapy, have been found to be efficacious interventions in treatingchildren and adolescents with mild to moderate depression in studies includingpatients with either dysthmia or double depression.

SSRIs are the first-line drug treatment for children and adolescents because oftheir safety, adverse effect profile and ease of use (the safety of paroxetine iscurrently under investigation). Several nonblind studies have shown the efficacyand good tolerability of SSRIs in children and adolescents with dysthymicdisorder, but further research is needed to confirm their efficacy and that of newerantidepressants in the treatment of this disorder.

Regardless of whether psychotherapeutic or medical treatments are planned,according to clinical experience, psychoeducational interventions and psychoso-cial support should be provided to parents and other caregivers during the acutetreatment phase to help manage the childs irritable mood and foster a therapeuticalliance and better compliance with treatment.

Unfortunately, no studies have focused on continuation treatment of paediatricdysthymic disorder. Given the chronicity, recurrence, psychosocial consequencesand peculiar response pattern to treatment of dysthymic disorder, establishing

Adis Data Information BV 2003. All rights reserved. CNS Drugs 2003; 17 (13)

Dysthymia in Children and Adolescents 929

effective acute and continuation interventions in this group of patients shouldbe a priority in mental health management.

1. Diagnosis dysthymic disorder is significantly lower than thatof major depressive disorder, and the presence ofdysthymic disorder does not influence the age at

1.1 Clinical Phenomenology which the first episode of major depressive disorderand Classification develops.[3,4]

Dysthymic disorder in children occurs at theCurrently, according to DSM-IV,[1] children and same rate in boys and girls, whereas the female-male

adolescents can receive diagnoses of mood disor- ratio for dysthymia in adolescents is approximatelyders with few modifications compared with the adult 2 : 1, paralleling the ratio reported in adults.[5]criteria. A diagnosis of dysthymic disorder is metwhen either depressed or irritable mood is evident 1.2 Comorbidity(whereas adults must present with depressed mood)

Comorbidity is an evident clinical phenomenonfor most of the day, for more days than not and for ain child and adolescent dysthymic disorder. Esti-prolonged period (at least 1 year for children and 2mates of lifetime comorbid psychiatric disordersyears for adults) in the absence of major depressive,and pathological behaviours in children and adoles-manic or hypomanic episodes. Superimposed epi-cents indicate that dysthymic disorder is often asso-sodes of major depressive disorder may follow theciated either at onset or during the natural coursefirst year of dysthymic disorder; in such cases, aof the illness with numerous conditions, such asDSM-IV diagnosis of double depression is appropri-anxiety disorders, behavioural problems or sub-ate. The additional DSM-IV criteria for early-onsetstance abuse, which may complicate the clinicaland adult dysthymic disorder are identical and re-picture or response to treatment.[6] Estimates from aquire two of the following six symptoms: (i) poorcommunity-based sample of adolescents with dys-appetite or overeating; (ii) insomnia or hyper-thymia show that around 50% of them have othersomnia; (iii) low energy or fatigue; (iv) low self-pre-existing psychiatric disorders, including anxietyesteem; (v) poor concentration or difficulty making(40%), conduct disorders (30%), attention-deficitdecisions; and (vi) feelings of hopelessness.hyperactivity disorder (ADHD) [24%] and enuresisCompared with those with major depressive dis-or encopresis (15%), with 15% of them having two

order, children with dysthymic disorder appear toor more comorbid disorders.[2]have fewer melancholic symptoms and a signifi-

As for major depressive disorder, comorbid con-cantly lower prevalence of guilt, morbid preoccupa-ditions seem to be a predictor of additional treatmenttion and impaired concentration.[2] Reduced appetitein the acute phase and of a worse treatment outcomeis virtually absent in children with dysthymic disor-at follow-up.[7-9]der, and few experience hyposomnia and fatigue;

disobedient behaviour, probably as a feature of irri-1.3 Natural History and Clinical Outcome

table mood, is the most prevalent sign.[2]The mean age of onset of dysthymic disorder Evidence from longitudinal studies shows that

ranges between 10.1 4.9 and 13.8 3.1 years, as early-onset dysthymic disorder is better conceptual-reported in different studies.[3,4] The age of onset of ised as a long-lasting condition with a heightened


930 Nobile et al.

risk for relapse and later recurrent mood disorder and is a significant public health problem. Takenthan as a disorder with mild symptomatology and together, these data highlight how important it is togood outcome. Consistently, major depressive, ma- correctly identify dysthymic disorder among chil-nic or hypomanic episodes occur with a frequency dren and adolescents. The development of effectivesignificantly higher than chance at some point strategies for long-term treatment of dysthymic dis-during the natural course of the illness, with a med- order is crucial for shortening the symptomatician interval of 23 years between dysthymic disor- phase of the episode, reducing the risks of recurrentder onset and the first episode of major depressive affective illnesses (major depressive disorder anddisorder.[2,4,10] bipolar disorder) and relapse prevention.

In a naturalistic follow-up study of a cohort ofoutpatients with early-onset dysthymic disorder 1.3.1 Double Depression(before the age of 21 years), an estimated risk of

The superimposition of major depressive disor-76.9% and 5.8% was reported for superimposed der on the course of dysthymic disorder gives rise todepressive and manic episodes, respectively.[4] Be-the picture of double depression[11] that has now

cause 77.9% of the subjects with dysthymic disorderbeen incorporated into the DSM-IV as a commonhad already experienced a superimposed major de-basic course pattern of depressive illness. The rate ofpressive disorder by the beginning of the study,double depression varies across samples: two stud-94.2% of the subjects had at least one lifetime majories[2,12] reported a high rate (nearly 70%), whiledepressive disorder by the end of the follow-up.others reported moderate[6] (around 30%) to low[13]These data suggest that almost all individuals with (17%) rates among children.dysthymic disorder will eventually experience ma-

jor depressive disorder at some point in their lives.[4] There could be at least two explanations for theco-existence of the two disorders: (i) major depres-Patients with dysthymia experience mild symp-sion, dysthymia and their overlap might be differenttoms but long episodes, whereas major depressivemanifestations of the same disorder or differentdisorder shows exactly the opposite pattern. Esti-steps on a continuum of severity; and (ii) majormates of duration of dysthymia vary across differentdepressive disorder and dysthymic disorder are twostudies from 2.5 to 3.4 years in clinically referreddistinct disorders, and higher than chance co-occur-and community-based youths.[3,7]rence might be a result of either environmental orOnce patients recover from an episode of dys-genetic shared liability.

thymic disorder, they are at high risk of relapse forYouths with both major depressive disorder andthe same disorder, the estimated relapse rate being

dysthymic disorder have been found to have more45.2%.[4] It has been estimated that, given a 5-yearsevere and longer depressive episodes, a higher rateobservation span, children and adolescents with aof comorbid disorders, more suicidality and higherdiagnosis of dysthymic disorder show symptoms ofsocial impairment than youths with major depres-mood disorder for approximately 70% of the timesive disorder or dysthymic disorder alone.[2] What-for at least three reasons: (i) they develop recurrentever the nature of the relationship, it is clear thatmood disorder; (ii) they relapse into subsequentyouths with double depression do recover from epi-dysthymic episodes; and (iii) the duration of illnesssodes of major depressive disorder, but most of themis long. Although dysthymic disorder often presentsquickly relapse into a new episode, with an estimat-with mild symptoms, from a longitudinal perspec-ed 84.4% rate of second relapse.[4]tive it is more severe than major depressive disorder



1.3.2 Suicidal Behaviour impairments in relationships with peers,[4] which inThe clinical presentation of suicidal behaviour turn is a risk factor for lower functioning, especially

includes a wide range of psychopathological experi- during such a critical period of development. Psy-ences with increasing degrees of severity, such as chosocial functioning is negatively correlated withpersistent suicidal ideation, suicidal threats, suicidal the duration of dysthymic disorder and worsens withattempts and successfully completed suicide. Devel- increasing severity of diagnosis and presence ofopmental factors influence the clinical manifestation comorbidity.[19] Data are controversial regarding theof suicidal behaviours, most evident in the epidemi- impact of dysthymic disorder on academic perform-ology of suicidal behaviour: completed suicide is ance.[4,6]significantly rare before puberty and becomes in- Few studies have focused on the psychosocialcreasingly frequent through adolescence, reaching a consequences of adolescent dysthymic disorder;peak between the ages of 19 and 23 years. Complet- those that did found that adolescents with long-ed suicide is much more common among boys than lasting dysthymic disorder or double depressiongirls, while suicide attempts are more common with have a poorer outcome and more limited socialgirls.[14] interaction when they become adults compared with

Dysthymic disorder represents a common risk for subjects with a history of major depressive disordersuicide attempts, with rates varying between 9.5% only or nonaffective disorder in adolescence.[13,20,21]and 19% in the adolescent population.[4,6] The pres- These data suggest that adolescents with dysthymicence of comorbid conduct and/or substance use dis- disorder continue to experience significant difficul-orders further increases the risk of suicide at- ties in psychosocial functioning even after recovery,tempts,[15] while superimposed major depressive with a worse outcome than adolescents with pastdisorder does not.[4] General recognised risk factors major depressive disorder. This is probably a resultfor suicide that increase the likelihood of a suicide of the negative impact of the shorter disorder-freeattempt or a suicide in the context of a dysthymic periods with dysthymic disorder than with majordisorder, regardless of the associated psychopath- depressive disorder on the overall developmentalology, include a history of physical and sexual process.[4]abuse, positive family history for suicidal behav-

2. Epidemiologyiours and a previous suicide attempt.[16-18]

1.3.3 Functional Impairment2.1 Prevalence

Psychosocial disturbances are common in dys-thymic disorder, but it is unclear whether they re- Epidemiological studies have reported pointpresent a precursor, a state condition or a long-term prevalence rates for dysthymic disorder ranging be-consequence of the disorder. In a community-based tween 1.6% and 8.0% in adolescents and 0.6% andsample of adolescents, lifetime dysthymic disorder 4.6% in children, and the 6-month prevalence ratewas more frequently associated with psychosocial for double depression is 9.9%.[22-26] In a sample ofdifficulties at onset (i.e. no sports activities, poor high-school students aged 1418 years, Lewinsohnrelationships with siblings, mother and father, and et al.[22] reported a 1-year first incidence of dys-problems with relatives).[6] In the few studies that thymia of 0.13% and 0.0% for girls and boys, re-have investigated psychosocial functioning during spectively. An epidemiological study of adolescentsthe symptomatic period, children and adolescents aged 1116 years showed a 3.4% weighted 1-yearwith dysthymia were found to frequently experience incidence of dysthymic disorder, which was found


932 Nobile et al.

by examining those individuals with no disorder at disorders over time[2,4,10] and reduce the long-termbaseline.[4] disabling consequences on their social skills learn-

ing and consequent professional lives. Intervening2.2 Risk Factors in the disorder shortly after its onset may offer a

window of opportunity to prevent its potentiallyNumerous factors are potential candidates to dif-serious sequelae (academic failure, substance abuse,ferentially influence the onset and natural course ofsuicide attempts and suicide).[31]dysthymia: demographic factors (age, sex, socioeco-

Despite the great number of children and adoles-nomic status), concurrent psychopathology (pre-ex-cents with dysthymic disorder, very few controlledisting diagnosis), familial factors (parental psycho-studies have been carried out on the psychologicalpathology, high genetic loading for mood disorders)and medical treatment of youth with dysthymic dis-and psychosocial factors (poor support, stressful lifeorder or comorbid dysthymic disorder and majorevents, poor maternal functioning). Dysthymic dis-depressive disorder. In clinical practice, the sameorder aggregates specifically in families of patientsinterventions for children and adolescents with ma-with the same disorder, and relatives of patients withjor depressive disorder are usually recommended fordysthymic disorder and those with major depressivethe treatment of paediatric dysthymia.[32] Neverthe-disorder show higher rates of major depressive dis-less the peculiar aspects of this disorder should beorder compared with the relatives of healthy controltaken into account when developing a specific treat-individuals, thus suggesting that dysthymic disorder

and major depressive disorder show strong familial ment plan. Improvement of depressive symptomsrelationships, although they may have distinct pat- may not necessarily parallel functional improve-terns of familial transmission.[27] ment (which is particularly impaired).[4] On the oth-

er hand, as a result of its chronicity, dysthymicAbnormal family interactions might intuitivelydisorder may require longer treatment and moreincrease the risk of developing dysthymic disorder,

even though the exact mechanism underlying this frequent sessions than other depressive disorders,[33]relationship is not known and could be a nonspecific which imply greater economic impact on either therisk factor for child psychopathology. However, families of patients or healthcare systems. So far, nodysthymic disorder was associated with high levels study has been able to define the optimal duration ofof adverse early home environments in childhood an effective treatment for children and adolescentsand parental psychopathology, even though no dis- with dysthymic disorder.tinction could be made clearly between genetic and Furthermore, few studies have focused on theenvironmental effects.[28,29] Among life events, treatment outcome of patients with dysthymic disor-physical abuse and illness or death of a close relative der and comorbid conditions. As for major depres-seem to be specifically related to the onset of dys- sive disorder, comorbid conditions are likely tothymic disorder during adolescence.[6,30] worsen the treatment outcome. For instance, Kovacs

et al.[7] found that externalising disorders affect the3. Treatmentduration of dysthymia and suggested implementinginterventions for behaviour problems to shorten thisThe primary aim of treatment of dysthymic disor-type of depression. Brent et al.[8] found that subsyn-der is to resolve depressive symptoms (i.e. remis-dromal depressive symptoms, behavioural problemssion). This would be especially desirable in individ-and family conflicts at the end of acute treatmentuals at an early developmental age, because it could

prevent the high risk of their developing other mood predicts the need for further treatment at follow-up.



Finally, Brent et al.[34] found that comorbid anxiety Nation Outcome Scale for Children and Adolescentsamong depressed children (major depressive disor- (HoNOSCA).[40]der and dysthymic disorder) was associated with

4. Psychological Treatmentpoorer treatment response.

The general aims of psychological treatments in3.1 General Treatment Approach

childhood and adolescence are to modify maladap-A comprehensive diagnostic evaluation of chil- tive personality organisation that may determine

dren and adolescents with dysthymia requires sepa- long-term change in mood,[41] to enhance behav-rate interviews with the patient and the parents, ioural, cognitive and emotional management skillssince children are often more aware of internalising to cope with present and future stressful life events,symptoms, whereas their parents are more aware of and to obtain full remission of symptoms as well asbehavioural problems.[35] Assessment should in- prevent recurrence.clude a careful evaluation of psychosocial stressors, Psychological treatment is the only interventionfamily functioning, school environment and the in- possible when a family refuses pharmacologicaldividuals coping ability.[36] medication or when the patient is not responsive to

The frequently comorbid diagnoses[4] (about 50% antidepressants.[42]of patients have comorbid diagnoses) should be Response to psychotherapy is related to severaladdressed concurrently in the treatment of a child factors, including age at onset, severity of depres-with dysthymia. sion, presence of comorbid psychiatric disorder, de-

Treatment should be individualised and based on gree of support, parental psychopathology, familyneeds as well as resources and assessment of stres- conflict, exposure to stressful life events, socioeco-sors. As children with dysthymia often have multi- nomic status, quality of treatment, the therapistsple problems, interventions should occur at multiple expertise and motivation of both patient and thera-levels, including individual psychotherapy, family pist,[32] as well as the familys understanding oftherapy/education and pharmacological treatment. depressed mood and their ways of managing it. AllPsychoeducational interventions and psychosocial these aspects should be taken into account whensupport are an essential component of an individual- devising treatment plans, since they can influenceised treatment plan, regardless of whether specific the initiation, maintenance and recurrence of depres-psychotherapy or medication is used.[36] sion. For instance, Kovacs et al.[7] found that the

duration of dysthymic disorder in children and ado-3.2 Assessment Procedures and Measures lescents was predicted by comorbid externalising

disorders (conduct, oppositional, attention-deficit)Severity of symptoms and global functioningand suggested addressing behavioural problems to

should be evaluated before treatment, at clinical re-shorten depression, since depressive symptoms may

evaluation and at follow-up. Severity of depressivebe a way of coping with the negative social reactions

symptoms can be assessed by one of the availablethat conduct disturbances elicit.depression scales, such as the self-administered

Childrens Depression Inventory (CDI)[37] or the4.1 Psychoeducational Interventions

observer rated Hamilton Depression Rating Scale(HAM-D).[38] Impairment in global functioning can On the basis of clinical experience and in linebe evaluated using scales such as the Children Glob- with the Practice Parameters for Assessment andal Assessment Scale (CGAS)[39] or Health of the Treatment of Children and Adolescents with De-


934 Nobile et al.

pressive Disorders,[32,43,44] psychoeducational inter- the number of school demands and focusing less onventions should always be provided to the child, his/ deficits when the dysthymic disorder is diagnosedher parents and other caregivers during the acute with a comorbid learning disability.treatment phase regardless of whether psychologicaltreatments or medication are used. The aims of 4.2 Supportive Treatmentpsychoeducational interventions are to inform the

The goals of supportive interventions are to es-child, the family and the school about symptoms,tablish, maintain and build rapport and provide sup-their consequences, prognosis, treatment durationport, as well as improve self-concept by aiding theand adverse effects of medication as well as topatients in the identification and expression of feel-provide educational guidelines in order to help theings through reflective listening and empathy. Inchild cope with depressed mood and foster a betterthis type of treatment, the therapists refrain fromcompliance with treatment.giving advice, setting limits and teaching skills.The child is encouraged to divert from the ten-

Although individual supportive treatment wasdency to ruminate on bad feelings and to spend asnot found to be as effective as other more structuredmuch of the day as possible functioning normally,therapies such as cognitive behavioural therapyregardless of how he/she may feel inside by reduc-(CBT),[43] supportive group treatment was found toing his/her time alone, and by attending school andbe more helpful than a problem-solving group in thecontinuing weekly activities.[36]reduction of depressive symptoms in adolescents

Parents and family members need to be informedwith either dysthymia or major depressive disor-

about clinical aspects and biological/psychological der.[46]determinants of depression and instructed about thechilds need for reassurance and support, rather than

4.3 Cognitive Behavioural Psychotherapypunishment for unacceptable behaviour. Educationof all family members is essential because the symp- Controlled studies on the psychotherapy of de-toms of depression (lack of interest, fatigue, isola- pression are mostly within the cognitive-behaviour-tion and irritability) may affect the response of each al framework.[47] CBT is generally a time-limitedmember of the family to the patient and increase intervention, primarily targeting cognitive, behav-their emotional involvement, causing more stress, ioural patterns and affecting management skills;[48]guilty or angry feelings for the patients to cope it is delivered in either individual or group formats.with.[32] Furthermore, these instructions decrease The duration of CBT in studies on child and adoles-self-blaming (Im a bad parent) and the tendency cent depression ranges from 5 to 16 weeks.[48] Theto blame the youth (He is just lazy). Finally, the theoretical assumption of this approach is that auto-family should be involved in the development of matic, irrational thoughts and maladaptive copingtreatment plans and the identification of areas for behaviours are responsible for depressive symptomschange.[36] and mood[49] and that their replacement with more

There is evidence that depressed youth often do adaptive self-statements and coping skills will re-not seek treatment,[45] and clinical experience has duce depressive symptoms. The interventions areshown that withdrawal from treatment greatly di- based on various techniques to help patients self-minishes with the addition of an educational compo- monitor, set goals, identify and change distortednent. The school setting should be adapted as much cognitions, increase their social problem-solvingas possible to reduce stress, for instance by limiting skills and engage in more pleasant activities as well



as manage affects through relaxation and impulse 4.5 Family Therapycontrol techniques.

Family therapy is recommended for youth be-No studies of psychological treatments in youthcause of the frequent association between depres-have focused on dysthymic disorder only. Mostsive symptoms and family dysfunction,[62] which

studies include subjects with a diagnosis of majorcan reflect both environmental mechanisms and ge-

depressive disorder or dysthymic disorder or both,netic factors. High parental criticism,[63] family dis-

without differentiating the effects[50-53] and thuscord[64] and poor parent-child communication[65] are

making it difficult to identify differential responseoften observed in families of depressed children and

rates according to clinical conditions.[47] However,adolescents. Durbin et al.[66] found that familial

several studies have tested CBT on adults with dys- psychopathology, including the patients poor rela-thymic disorder only,[54] showing response rates at tionship with their own parents and high familialthe end of treatment ranging from 20% to 67% after loading for drug abuse and personality disorders, is4 months of CBT.[55,56] The rates of recurrence or the most effective predictive variable of outcome inrelapse at follow-up after treatment are not clear for dysthymic disorder, thus stressing the need for fami-children and adolescents with dysthymic disorder ly involvement in treatment plans.since no distinction is made from patients with ma- Most therapists working with children and ado-jor depressive disorder. However, all clinical stud- lescents involve parents in the treatment at someies of CBT on depressed children and adolescents point, but systematic clinical guidelines on how tohave found a high rate of relapse on follow-up, involve them are needed. Only a few controlledsuggesting the need for continuation treatment.[32] studies have been carried out on the effect of family

involvement on treatment of depressed children andadolescents, none of them showing significant ef-4.4 Interpersonal Therapyfects compared with the control conditions repre-sented by CBT and supportive therapy only.[43,50]Like CBT, interpersonal therapy (IPT) is time

limited and manual based; the therapist helps the4.6 Psychodynamic Psychotherapypatients recognise links between mood and current

interpersonal experiences, focusing on different Psychodynamic therapy of depression has beenproblem areas[54] such as grief, interpersonal roles, reported as being effective by some but not alldisputes, role transitions and interpersonal difficul- clinicians. Some positive case reports are avail-ties. Its efficacy is proven for the acute treatment of able,[67] but it has been argued that gathering strongadolescents with major depressive disorder[57-59] and evidence in favour of or against the efficacy of thisfor adult patients with dysthymic disorder.[60] In a approach through controlled clinical studies wouldstudy by Rossello` and Bernal,[61] adolescents with be time consuming and expensive. Additional re-major depressive disorder or major depressive disor- search with standardised measures and controlder with dysthymia were randomly assigned to groups is surely needed. Psychodynamic psycho-CBT, IPT or a wait-list condition. IPT and CBT therapy may help youth understand themselves,reduced overall depressive symptoms when com- identify feelings, improve self-esteem, change mal-pared with the wait-list condition. Youth treated adaptive patterns of behaviour, interact more posi-with IPT improved more in self-esteem and social tively with others and cope with ongoing and pastadaptation compared with the wait-list condition. conflicts.[67]


936 Nobile et al.

4.7 Prevention Programmes studies for a specific disorder in a specific agegroup. There are no data from controlled trials in

Prevention programmes are implemented to pre- paediatric dysthymia. Only a few open studies havevent dysthymia (primary prevention) and recurrence evaluated the therapeutic effect of SSRIs (fluoxe-after remission of symptoms. tine, paroxetine, fluvoxamine, citalopram and sertra-

Programmes on primary prevention are of two line) in children and adolescents with dysthymia.types: universal and targeted. Universal program- Nevertheless, the use of antidepressants in the treat-mes involve all individuals in a population regard- ment of child and adolescent dysthymia appearsless of their level of risk; they consist of education- reasonable in light of the significant impairmental group sessions aiming to develop social skills associated with this disorder, the multiple lines ofwith a view to develop strengths against depres- evidence suggesting continuity from child and ado-sion.[68] This type of intervention did not show sig- lescent dysthymia to adult mood disorders and thenificant benefits compared with a no-intervention well established efficacy of antidepressants (tricy-condition.[68] Targeted prevention programmes tar- clic antidepressants [TCAs], monoamine oxidaseget a population of children and adolescents with inhibitors [MAOIs], SSRIs and serotonin/nora-high levels of risk for depressive disorders. These at- drenaline (norepinephrine) reuptake inhibitorsrisk individuals are selected on the basis of high [SNRIs])[71-73] in the treatment of adult chronic de-scores on self- or parent-reports and/or have a fami- pression.ly history of depression or report parental conflict. Considering that the majority of the studies inAgain, programmes focus on social skills training childhood depression have focused on major depres-and sometimes education of parents and teachers sive disorder and only a few on dysthymia or bothabout depressive symptoms. Encouraging results major depressive disorder and dysthymic disorder,were achieved in some studies with these high-risk general principles for the pharmacological treatmentpopulations, leading to a significant reduction in of paediatric major depressive disorder may also bedepressive symptoms at follow-up.[69,70] applied to the treatment of dysthymia with some

A further case for the implementation of preven- specific caveats as discussed in the next sections.tion programmes may be seen in the findings ofrelatively poor treatment response and relapse rate at 5.1 Indicationsfollow-up in childhood and adolescence dys-

The initial decision is whether or not to start athymia.[46,52] There is no strong evidence yet for thetrial of antidepressants. Unlike major depression,preventive effects of psychological treatmentwhere the severity of depressive symptomatologyagainst recurrence, but available results suggest thatand recurrence[36,74] are the main criteria for med-booster sessions should be included in treatmentication, in dysthymic disorder, criteria could be theprogrammes to limit the risk of relapse and acceler-severity of psychosocial impairment in family andate recovery among patients who were still de-peer functioning or school performance and the co-pressed at the end of the treatment.[53]occurrence of a major depressive episode (doubledepression) [table I]. Functional impairment appears5. Pharmacological Treatmentto be greater for double depression than for pureepisodic major depression.[75]The decision on whether or not to treat a child

with pharmacotherapy should ideally be based on Prior to the initiation of medication, the impair-data about the efficacy of a given drug in controlled ment in global functioning and the severity of symp-



SSRIs in children and adolescents with dysthymicdisorder.

Fluoxetine

Waslick et al.[80] used fluoxetine (20mg daily) totreat 19 paediatric patients with dysthymic disorder(n = 7) or double depression (n = 12) whose symp-toms had not responded to brief (4 weeks) psychoso-

Table I. Indications for initiating medication in childhood dysthymia(reproduced from Emslie and Mayes,[36] with permission)Severity of psychosocial impairment in family and peerfunctioning or school performanceOther family members responseDouble depressionComorbidityNo response to psychotherapyConvenience for familyPsychosocial stressors

cial treatment alone. After 8 weeks of treatment withfluoxetine, 73% of patients no longer met the criteria

toms should be measured using one of the available for dysthymic disorder or major depressive disorderscales, as discussed in section 3.2. There is no need (67% and 78%, respectively). It was noted thatfor baseline laboratory testing prior to initiating treatment was associated with significant improve-treatment with SSRIs or SNRIs except for a review

ment in depressive symptoms, but the overall im-of the last menstrual period and a pregnancy test in provement in terms of functioning was rather mod-adolescent girls if indicated;[76] before starting one

est. This could certainly be explained in terms ofof the TCAs, a baseline ECG, resting blood pressure

residual impairment in school, interpersonal or fam-and heart rate (supine, sitting and standing) as well ily functioning that could be expected after the pa-as bodyweight should be recorded. No other tests are tients had been depressed for a significant part ofusually indicated in a healthy child before starting their early developmental years.antidepressant therapy.[77]

FluvoxamineThe decision to initiate drug treatment must ac-Rabe-Jablonska[81] studied the therapeutic effecttively involve adequately informed parents with the

of fluvoxamine (150200mg daily) in 21 adoles-childs assent. It is vital to educate parents andcents with dysthymia in a 26-week open-label study.patients about adverse effects and toxicity.[77]Good clinical response as determined by a 50%decrease in HAM-D baseline scores was noted in5.2 Pharmacological Agents56% of patients at 8 weeks. Relapse of dysthymicsymptoms occurred in 34% of patients after 26

5.2.1 SSRIsweeks of receiving medication. Fluvoxamine was

SSRIs are the first-line treatment for child andwell tolerated in 76.2% of adolescents; poor tolera-

adolescent depression because of their safety, ad- bility resulted in a discontinuation rate of 14.2%.verse effect profile, ease of use and efficacy.[42,77,78] (The reported response rate of 34% at 26 weeks isSSRIs have been shown to selectively block the difficult to interpret, as the author reported that 3 ofpresynaptic neuronal reuptake of serotonin with lit- the 18 patients had discontinued fluvoxamine some-tle or no affinity for adrenergic, cholinergic or hista- time after week 8).minic receptors.[79] Currently available SSRIs are

Paroxetinefluoxetine, paroxetine, sertraline, citalopram andfluvoxamine. At present, fluoxetine is the only drug Nobile et al.[82] examined the efficacy of paroxe-officially approved by the US FDA to treat major tine in the treatment of seven children and adoles-depressive disorder in children and adolescents cents with dysthymic disorder over a period of 3717 years of age. Several nonblinded studies have months. Seventy-one percent of patients had a satis-shown the efficacy and good tolerability profile of factory response, defined as both a 50% improve-


938 Nobile et al.

ment from baseline HAM-D score and a Clinical depressive disorder group. The mean average dailyGlobal Impression Improvement (CGI-I) score of dose was only slightly higher in the dysthymic dis-much or very much improved. Clinical evaluation of order group (140 vs 125mg).responders at 6 months after the beginning of ther-

Citalopramapy suggested stability of improvement over time.

Bostic et al.[85] assessed the effectiveness of cita-The mean dosage of 20.12 mg/day was similar to thelopram in 21 adolescents with depressive disorderdosage of paroxetine prescribed for children with (major depressive disorder, n = 14; bipolar disorder,

major depression,[83] and the pattern and incidencen = 4; dysthymic disorder, n = 3) treated naturalisti-

of adverse effects were similar to those of othercally in a community mental health centre over aSSRIs[79] in depressed children and adolescents.1-year interval. Seventy-six percent of the wholeThe efficacy of 8 weeks treatment with paroxe-group were much to very much improved on the

tine was also assessed in a retrospective study of CGI-I scale, while all patients with dysthymia wereseven adolescents with dysthymia (from a total sam-

very much improved. The median dosage of citalo-ple of 25 depressed adolescents).[73] Seventy-onepram was 25 mg/day; mild adverse effects, includ-percent of patients treated with paroxetineing headaches, dizziness, nausea, sedation, agitation(2040mg daily), administered either as monother-and sweating, were reported by 33% of patients.

apy or with benzodiazepines, showed a satisfactoryresponse (three total remissions and two improve- 5.2.2 Tricyclic Antidepressantsments with residual symptoms). Adverse effects in Several well designed trials of treatment withthe whole group did not differ from those expected TCAs in depressed children and adolescents havefor SSRIs in adults and adolescents. failed to demonstrate the effectiveness of the drugs

The safety of paroxetine is currently under inves- compared with placebo.[77,86] No data are availabletigation (see section 5.5) and, as a result, use of the regarding the use of TCAs for the treatment ofdrug in patients


venlafaxine and placebo.[87] Venlafaxine has been and adolescents; see section 5.5). Starting dosagesfound to be more efficacious than paroxetine in should be lower than those used in adults and slowlytreating adult dysthymic disorder,[73] but so far this increased to target dosages[42,76,77,79,93] as specifiedhas not been shown in children and adolescents. in table II. In our clinical experience, this reduces

the incidence of adverse effects, particularly sleepIn two open naturalistic trials,[88,89] nefazodoneand gastrointestinal disturbances, thus enhancingwas well tolerated and associated with a significantthe collaboration of patients and their families withreduction in depressive symptoms in children andtreatment.adolescents with major depressive disorder.

Patients should be treated with adequate and tol-Bupropion is a novel antidepressant with agonis-erable doses for at least 8 weeks to assess treatmenttic effects on the noradrenergic system and, to aresponse. A regular review of symptoms, globallesser extent, the dopaminergic system,[90] each be-functioning and adverse effects using one of theing potentially relevant for the treatment of depres-available scales with the child and the parents ission and ADHD. Arredondo[91] evaluated its effi-recommended; it is believed that close monitoringcacy in adolescent major depressive disorder andresults in more favourable outcome (as a result offound a significant improvement in eight of tenincreased patient adherence). In addition, more fre-adolescent inpatients.quent contact enhances the engagement of the childDaviss et al.[92] evaluated a sustained release (SR)and family in treatment and provides additional op-formulation of bupropion in 24 adolescents withportunities for education.[74,94]ADHD and major depressive disorder (n = 2) or

If at 4 weeks there is minimal improvement,dysthymic disorder (n = 7) or both (n = 15). Theincreasing the dose could be an option. On the otherstudy was open-label in design and used doses flexi-hand, if an aggravation of symptoms or severe ad-bly titrated up to 3 mg/kg twice daily, after a single-verse effects are observed, it is advisable to considerblind placebo lead-in. The authors noted final globalchanging medication (see section 5.4). For patientsresponse rates of 88% for depressive disorders andshowing minimal or no response, the total trial63% for ADHD, with 58% of patients appraised asshould not exceed 48 weeks. For patients with asimultaneous responders for both disorder groups.partial response, the trial may last up to 12Bupropion SR was generally well tolerated, al-weeks.[42,74]though various adverse effects were reported more

frequently during active medication than during the5.4 Partial Response and Nonresponsepatients placebo lead-in phase, including rashes,

irritability, tremors and tics; no patients discontin- Patients with symptoms not responding to ade-ued the medication because of adverse effects. quate treatment should be assessed for the quality of

the therapeutic relationship, adverse effects, dose,5.3 Acute-Phase Medication

Although further controlled studies are needed onlarger samples, the results reported in section 5.2.1suggest that SSRIs should be considered first-lineagents in the acute-phase treatment (i.e. the first812 weeks of treatment) of dysthymic disorder inchildren (the UK MHRA and US FDA have advisedthat paroxetine should not be prescribed for children

Table II. Approximate suggested dosages for antidepressants inchildren and adolescents with dysthymia[42,76,77,79,93]

Medication Initial dosage Paediatric dosage(mg/day) range (mg/day)

Fluoxetine 5 1030Sertraline 25 50200Fluvoxamine 2550 50200Citalopram 10 1030Venlafaxine 12.525 37.575


940 Nobile et al.

duration and, particularly, adherence.[32] In addition, higher rates of suicidal thoughts and behaviour inthe recommendations of the Texas Consensus Con- the patients who took paroxetine (25 of 738; 3.4%)ference Panel on Medication Treatment of Child- compared with those who took placebo (8 of 647;hood Major Depressive Disorder[74] should also be 1.2%). There was no case of an actual suicide in theconsidered for patients with dysthymic disorder: (i) patients in these studies. Nine studies into the drugreassess the diagnosis for previously unrecognised had been conducted, but the result of only one wascomorbid conditions; (ii) consider the possibility of in the public domain, and researchers andan unrecognised general medical condition; (iii) re- clinicians cannot access the data on which theevaluate the patients exposure to negative psycho- MHRA recommendations are based. GlaxoSmith-social stressors; (iv) assess the quality of treatment; Kline, the manufacturer of paroxetine, noted thatand (v) re-evaluate family functioning or look for conclusions drawn from their data differ to thosepsychopathology in other family members. drawn by the MHRA.

For patients with symptoms not responding to The US FDA is currently reviewing these data.their initial medication, three strategies can be pur- Although the US FDA has not completed its evalua-sued: optimisation, substituting with another drug, tion, it is recommending that paroxetine not be usedand augmentation or combining antidepres- in children and adolescents for the treatment ofsants.[42,74] Optimisation involves increasing the major depressive disorder until further evidencedosage gradually, adverse effects permitting, and from the scientific community is available and in themaintaining the increased dosage for 68 weeks. meantime suggests the use of other approved treat-The second strategy (substitution) is based on the ment options available for depression in children.fact that a lack of response to one SSRI does not

The most common adverse effects seen with SS-necessarily predict a lack of response to another

RIs are gastrointestinal disturbances, headache, diz-agent of the same class. In the third, lithium aug-

ziness and initial insomnia.[77,79] Some of these dis-mentation has been described in adolescent depres-

turbances (in particular, gastrointestinal disorders)sion.[95,96] Only a few noncontrolled data are avail- have been reported to be more frequent in patientsable on augmentation treatment in adult dys-

with dysthymia.[84] On the other hand, somatic com-thymia,[97,98] and no data are available for children plaints are common symptoms of paediatric dys-and adolescents with dysthymia.

thymia. Gastrointestinal adverse effects may beeased by a low starting dose or by taking medication

5.5 Adverse Effectswith food.[76,79]

Available data indicate that SSRIs are well toler- Another important adverse effect of all antide-ated in the short term, but further research is needed pressants is induction of mania or hypomania. Thisto provide the necessary information on long-term is not to be confused with akathisia and restlessness,effects in children and adolescents. which can be adverse effects of the rapid induction

In June 2003, the UK Medicines and Healthcare of SSRI treatment. In about 13%[2] of patients, dys-Products Regulatory Agency (MHRA) advised that thymia will evolve into a bipolar disorder (and theparoxetine should not be prescribed for children and patients will probably develop manic symptomsadolescents.[99] It did so on the recommendation of when treated with SSRIs or other antidepressants).an independent expert working group commissioned For the majority of patients, manic symptoms sub-by the Committee on Safety of Medicines (CSM). side quickly after discontinuation of antidepres-The advice is based on studies showing that there are sants.



5.6 Continuation Treatment more major depressive episodes in comorbidity withdysthymia or persistent functional impairment.

All recommendations for continuation-phase Antidepressants should be discontinued gradu-treatment for children and adolescents with dys- ally over 6 weeks under close supervision andthymia are based on adult data[100-103] and studies of planned with patients and parents to avoid discontin-child and adolescent major depressive disor- uation syndromes and relapse.[105] As a relapse ofder.[36,42,74,77] However, evidence suggests that the dysthymic symptoms or a new major depressivemean duration of dysthymia is up to 3 years and that episode[4] is likely to occur, the patient should bethere is an estimated 76.9% risk[4] of developing a seen every 24 months; patients and their parentssuperimposed major depressive episode. Therefore, should be taught to monitor for recurrence of de-continuation of medication for 69 months is recom- pressive symptoms.mended after symptom remission at the full thera-peutic dose used in the acute phase. 5.7 Treatment of Comorbid Conditions

Pharmacological data from the only two 6-monthIn addition to the treatment of depressive symp-studies[81,84] reported in the literature suggest that

toms, it is crucial to treat the comorbid conditionschildren and adolescents with dysthymia have athat frequently accompany dysthymic disorder. Asdifferent response pattern from those with majormentioned in section 1.2, comorbid conditions maydepressive disorder: patients with dysthymic disor-influence the initiation, maintenance and recurrenceder did not maintain acute-phase treatment responseof dysthymic disorder, with externalising, disruptiverates like those with major depressive disorder, withdisorders predicting a worse outcome. Specifica 34% relapse rate. Another study on paediatrictreatment guidelines for each of the comorbid disor-dysthymia[80] suggests that during the acute phaseders should be considered. If possible, a clinicianonly, depressive symptoms improved, while theshould choose the medication that optimises res-overall improvement in terms of functioning is rath-ponse for dysthymia and the comorbid disorder. Forer modest. As mentioned in section 5.2.1, this couldexample, SSRIs may help relieve both anxiety andbe explained by residual functional impairment,dysthymia in children and adolescents.[106] Bupro-which could determine relapse or recurrence of thepion SR appears to be useful for treating ADHD thatillness.[72,103,104]is comorbid with dysthymia and major depression inThe authors believe that, during the continuationchildren and adolescents.[92] Nevertheless, at times itphase, the introduction of CBT or booster sessionsmay be necessary to use two medications to treatto consolidate the skills learned in the acute phasetwo concomitant conditions (i.e. SSRIs and stimu-

could be the best way to prevent relapse and long-lants for comorbid dysthymic disorder and ADHD).term sequelae.[42,53,103] It could be hypothesised that

remission of depressive symptoms may enable the 6. Conclusionchild to gradually return to higher levels of function-ing and a normal developmental trajectory. The All cases of dysthymic disorder require carefulpeculiar response pattern of dysthymic disorder in evaluation of depressive symptoms, comorbidity,acute- and continuation-phase treatment highlights chronicity, functional impairment, psychosocialthe importance of investigating both acute and con- stressors, family functioning, school environmenttinuation phases in treatment outcome studies of this and the individuals coping ability. The treatmentdisorder. Long-term maintenance pharmacotherapy plan should be individualised and, possibly, shouldmay be considered for patients who have had two or involve multiple levels and measures: individual


942 Nobile et al.

Continuation treatment(69 months):

booster sessions

Continuation treatment (69 months):full therapeutic dose + psychotherapy

booster sessions

Optimisation Substitution Augmentation

Diagnostic evaluation

Psychoeducational support

Remission Partial or no response RemissionPartial or no response

Psychotherapy(812 weeks): CBT IPT family therapy

Pharmacologicaltreatment (812 weeks): SSRIs TCAs other antidepressants

Fig. 1. Hypothetical integrated approach to the management of dysthymic disorder in children and adolescents. CBT = cognitive behaviour-al therapy; IPT = interpersonal therapy; TCAs = tricyclic antidepressants.

psychotherapy, family therapy/education and, even- be considered in case of nonresponse or comor-bidity.tually, pharmacological treatment (figure 1).

According to clinical experience and clinicalPsychotherapies have been shown to be effica-guidelines for depressive disorders in children andcious for the treatment of children and adolescentsadolescents,[32,42] psychoeducational interventionswith mild to moderate depression (including dys-and psychosocial support should be provided tothymic disorder and double depression). Thus, weparents and other caregivers during the acute-treat-would recommend initially an 8- to 12-week trial ofment phase to help them manage the childs irritablepsychotherapy. For patients with symptoms that domood and foster a therapeutic alliance and better

not respond to psychotherapy, who are not suitablecompliance with treatment during both pharmaco-

for psychotherapy or who still have severe function-therapy and psychotherapy.

al impairment after an adequate trial of psychothera-When evaluating the response to the acute-phasepy, pharmacological treatment should be planned. In

intervention and planning the continuation phase, acase of partial response to psychotherapy, the clini-

careful evaluation of functional improvement (notcian should consider combining psychotherapy with

only the improvement of depressive symptoms) isdrug treatment.

needed. The authors believe that during the continu-Given their efficacy, adverse effect profile and ation phase, the introduction of CBT or booster

ease of use, SSRIs are the first-line pharmacological sessions to consolidate the skills learned in the acutetreatment for children and adolescents with dys- phase could be the best way to prevent relapse and

long-term sequelae.[38,90,107]thymia, even though further studies are needed toconfirm their acute and long-term efficacy (the safe- So far, most acute studies have focused on thety of paroxetine is currently under investigation). symptom profile; more information should be gath-Other medications (i.e. TCAs or bupropion) should ered on the profile and changes concerning the de-



12. Ferro T, Carlson GA, Grayson P, et al. Depressive disorders:gree of psychosocial impairment of children withdistinctions in children. J Am Acad Child Adolesc Psychiatry

dysthymic disorder. Given the lack of data about the 1994; 33: 664-7013. Goodman SH, Schwab-Stone M, Lahey BB, et al. Majorresponse pattern after the acute phase of treatment,

depression and dysthymia in children and adolescents; dis-prospective evaluation of response in children andcriminant validity and differential consequences in a com-

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14. American Academy of Child and Adolescent Psychiatry. Prac-tice parameter for the assessment and treatment of children andadolescents with suicidal behavior. J Am Acad Child AdolescAcknowledgementsPsychiatry 2001; 40 Suppl. 7: 24S-51S

15. Kovacs M, Goldston D, Gatsonis C. Suicidal behaviors andThis study was supported by the Italian National Institutechildhood-onset depressive disorders: a longitudinal investiga-of Health Current Research Grant R.C.02. The authors havetion. J Am Acad Child Adolesc Psychiatry 1993 Jan; 32 (1):

no conflicts of interest that are directly relevant to the content 8-20of this manuscript. 16. Brent DA, Oquendo M, Birmaher B, et al. Familial pathways to

early-onset suicide attempt. Arch Gen Psychiatry 2002; 59:The authors wish to thank Professor M. Battaglia for his 801-7

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Contents 927Abstract 9281. Diagnosis 9291.1 Clinical Phenomenology and Classification 9291.2 Comorbidity 9291.3 Natural History and Clinical Outcome 9291.3.1 Double Depression 9301.3.2 Suicidal Behaviour 9311.3.3 Functional Impairment 931

2. Epidemiology 9312.1 Prevalence 9312.2 Risk Factors 932

3. Treatment 9323.1 General Treatment Approach 9333.2 Assessment Procedures and Measures 933

4. Psychological Treatment 9334.1 Psychoeducational Interventions 9334.2 Supportive Treatment 9344.3 Cognitive Behavioural Psychotherapy 9344.4 Interpersonal Therapy 9354.5 Family Therapy 9354.6 Psychodynamic Psychotherapy 9354.7 Prevention Programmes 936

5. Pharmacological Treatment 9365.1 Indications 9365.2 Pharmacological Agents 9375.2.1 SSRIs 9375.2.2 Tricyclic Antidepressants 9385.2.3 Other Antidepressants 938

5.3 Acute-Phase Medication 9395.4 Partial Response and Nonresponse 9395.5 Adverse Effects 9405.6 Continuation Treatment 9415.7 Treatment of Comorbid Conditions 941

6. Conclusion 941Acknowledgements 943References 943Correspondence 946Email 946

Diagnosa Dan Tatalaksana Dysthymia Anak Dan Remaja

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