Tag Archives: anhedonia

Dysthymic Disorder

My choice of Dysthymic Disorder for purposes of this essay was both personal and professional.  First and foremost, I was attracted to this disorder because it resides in the gray area somewhere between an Axis I disorder and a personality disorder.  Because of this unique diagnostic positioning I feel as though I could reasonably justify techniques that are traditionally associated with all of the major schools of psychotherapy I have studied to date: Behavior Therapy, Cognitive Behavior Therapy, Schema Therapy, Existential Psychotherapy, and/or (perhaps most importantly) my own personal brand of psychotherapy that shall remain unnamed.  With some amalgamation of techniques derived from the above, as dictated by individual client needs, I have confidence I would have a reasonable chance of having “success” (however we mutually choose to define that) with the majority of clients that present with Dysthymic Disorder.  Secondly, it seems to me a young clinician’s time is best spent on the disorders he is mostly likely to encounter.  Prevalence rates of Dysthymic Disorder could be as high as 6% in a nationally representative sample, and as high as 22% in outpatient mental health settings.  (Dougherty, Klein, & Davila, 2004)  It’s extremely unlikely that I will not encounter Dysthymic Disorder during the course of my professional life.  Third and finally, this disorder is close to me because someone I love endured it for the better part of 10 years.  Thankfully – I can report at this time that it is in full remission.  The journey to full remission was one that tested all of our capacities for change and growth.  This essay represents a personal and professional journey that is has led to significant gains in my own understanding of mood disorders.  Successfully navigating through the dark forest that is Dysthymic Disorder is no easy task.  It is my hope that my clients don’t have to endure the dark thoughts any longer than is absolutely necessary.

The essential feature of Dysthymic Disorder is a chronically depressed mood that occurs for most of the day, more days than not, for at least two years.  (American Psychiatric Association, Diagnostic and statistical manual of mental disorders, 2000, p. 376)  During periods of depressed mood, at least two of the following additional symptoms are present: poor appetite or overeating, insomnia (sleep too little?) or hypersomnia (sleep too much?), low energy or fatigue, low self-esteem, poor concentration or difficulty making decisions, and feelings of hopelessness.  (4th ed., text rev.; DSM-IV-TR; American Psychiatric Association, 2000, p. 377)  In my example case the individual was laden with hypersomnia, fatigue, and poor concentration.  It is noteworthy that are over 700 different combinations of symptoms that any single individual could potentially present with and still have the same diagnosis of Dysthymic Disorder.  As a result, it bears mentioning that the following analysis is in no way suggesting that this is the only right way to treat the disturbance.  Manualized treatment is probably doomed to failure when it comes to treating Dysthymic Disorder.  Any reasonable attempt to work toward complete remission of Dysthymic Disorder should be guided by a professional.

Differential diagnosis can be a challenge with Dysthymic Disorder.  “This is the way it’s always been” is not an unexpected response from patients whom suffer from Dysthymic Disorder.  There is no rest for the wicked: During the two year period of the disturbance, the individual may not have been without the qualifying symptoms in for more than 2 consecutive months.  Furthermore, no major depressive episode should be present during the first two years of the disturbance and the disturbance cannot be better accounted for by the diagnoses of chronic Major Depressive Disorder, or Major Depressive Disorder, In Partial Remission.  (4th ed., text rev.; DSM-IV-TR; American Psychiatric Association, 2000, p. 380)  Double depression, or the comorbid combination of Major Depressive Disorder and Dysthymia, is also a very real consideration since major depressive episodes are often superimposed on mild chronic depression.  (Dougherty et al., 2004, p. 1012; Morrison, 2007, p. 139)  There should never have been a manic, hypomanic, or mixed episode that would be contraindicative of Dysthymic Disorder and indicative of either Cyclothymic Disorder or Bipolar Disorder (I or II).  The disturbance should not occur exclusively during the course of a chronic psychotic disorder (like schizophrenia, for example) or be the direct physiological effects of a substance (like methamphetamine, for example) and/or general medical condition (like a traumatic brain injury, for example).  As is the case with most DSM diagnoses, the disturbance should cause clinically significant distress or impairment in social, occupational, or other important areas of functioning.  (4th ed., text rev.; DSM-IV-TR; American Psychiatric Association, 2000, p. 381)  This differential diagnosis quandary is further exacerbated by the fact that depression “shares borderlands with bereavement and other losses, problems of living, and adjustment disorders.”  (Morrison, 2007, p. 127)  A thorough investigation of antecedents and mitigating factors is absolutely critical to accurately “anchor your boat” so you can “wade into the river” with a correct diagnosis.

Family history is an important consideration when determining the hypothetical etiology of a disturbance, especially in the case of mood disorders.  “Family history is more useful in starting the train of diagnostic thought than in determining its final destination.”  (Morrison, 2007, p. 133)  Research suggests that the strongest predictors for Dysthymic Disorder include a history of sexual abuse, quality of the patient’s relationship with both parents, and higher familial loadings for drug abuse and ‘Cluster A’ personality disorders.  Unfortunately, we could use that same laundry list of antecedent events for just about every personality disorder in the DSM-IV-TR… so that doesn’t tell us much.  Childhood adversity and familial psychopathology and have greater predictive utility for Dysthymic Disorder when compared with demographic and clinical variables.  (Durbin, Klein, & Schwartz, 2000)  Translation: nurture appears to trump nature.  Nature continues to play a significant role in the development and maintenance of the disturbance, however.  A patient with a parent (or parents) with unipolar depression exhibited significantly higher rates of Affective/Mood Disorders including Major Depressive Disorder and Dysthymic Disorder – yet another marker that can guide the patient-clinician dyad in the right direction.  (Klein, Clark, Dansky, & Margolis, 1988)

A full exploration of the potential therapeutic interventions is beyond the scope of this paper, but there are a few empirically supported treatments that are noteworthy.  Supportive therapies, coupled with cognitive behavioral interventions, have been effective in extinguishing negative verbalizations and normalizing daily functioning.  (Elligan, 1997)  This is consistent with my “necessary but not sufficient” position when it comes to person centered therapies practiced by the late great Carl Rogers (1902-1987).  Although I concede that the research I found doesn’t specifically point to Schema Therapy as a potential treatment modality for Dysthymic Disorder, I would consider it based in part on event-related brain potential research.  (Yee, Deldin, & Miller, 1992)  Processing deficits including selective attention may be modified and corrected vis-à-vis Schema therapy.  Since research suggests that resource allocation is the issue, not resource capacity, the goal of Schema Therapy would be to allow for attention resources to be more effectively and efficiently focused on task performance.  (Yee & Miller, 1994)  Pharmacological interventions have been less effective on Dysthymic Disorder when compared with other mood disorders, so I would not consider this to be a first line of defense except in cases of Double Depression or in cases where talk therapy would be otherwise unproductive without the value added by antidepressant medications.  Other noteworthy psychological treatments that have garnered empirical support for the treatment of clinical depression include Behavior Therapy (Behavioral Activation), Cognitive Therapy, Cognitive Behavioral Analysis System of Psychotherapy, Interpersonal Therapy, Problem-Solving Therapy, Self-Management/Self-Control Therapy, Acceptance and Commitment Therapy, Behavioral Couples Therapy, Emotion-Focused Therapy (Process-Experiential), Reminiscence/Life Review Therapy, Self-System Therapy, and Short-Term Psychodynamic Therapy.  (Hayes & Strunk, n.d.)  In the end, the choice is one that will be made based on the training and expertise of the respective therapist and the needs of the individual patient.  Not all therapists are created equal.  In the end, every clinician should know a little about most of the treatment options above so they can make a referral if your particular variant of Dysthymia will not be well served by the treatment modalities that your clinician is versed in.

Knowing nothing about my potential client, I would begin the treatment from a cognitive behavioral perspective because I believe that it is the “best bang for the buck” in a brief therapy environment.  The most likely scenario for a first session could be summed up in the word “triage.”  Something brought the client into therapy and we need to “stop the bleeding.”  Behavioral activation in the form of cognitive behavioral homework is absolutely critical to get the ball rolling.  Although we can only speculate without a specific case study to reference, we would likely begin with some simple behavioral activation like “going on a walk with a friend for one hour, once a week.”  Ideally the target behavior would be specific, measurable, and relatively easy to complete (at least at the beginning).  Reversing that “downward spiral” as soon as is possible is an important first step in the treatment of Dysthymic Disorder.  (Beck, 2011, p. 80)  After identifying avoidance behaviors and potential reinforcing activities, I would endeavor to implement some form of self-reinforcement whereby transfer, generalization, and long-term maintenance of the desired behavior can be established and maintained.  (Spiegler & Guevremont, 2010, p. 135)  It should be a foregone conclusion but it bears mentioning that the homework should be customized for the specific patient and, if deemed necessary, “contracted” to increase the likelihood of compliance.

Furthermore, I would work to identify chronic stressors that appear to be contributing to the maintenance and onset-recurrence of the disturbance.  (Dougherty et al., 2004, p. 1012)  I typically engage in a series of assessments including interviews, behavioral checklists, assessments (ex: Beck Depression Inventory), and direct ecological observation to obtain both direct and indirect data regarding the antecedent variables and functional relations that serve to perpetuate the disturbance.  (Cooper, Heron, & Heward, 2007, p. 50)  I would pay particular attention to social, medical, family circumstances in the past, present, and anticipated future.  I would also make certain to note any vested friends and family without whom behavior change cannot be successful.  (Cooper et al., 2007, p. 51)  Parallel to that search for natural supports, I would engage in a systematic search for pool of appropriate people whom the individual could potentially model.  (Cooper et al., 2007, p. 413)  Finally, it bears mentioning that the continued inclusion of data from multiple sources (people) and situations (cultural contexts and mediating factors) makes the process of culturally competent cognitive behavioral therapy a possible since “identification of important, controllable, causal functional relationships” is an intimately subjective process laden with unique cultural issues and challenges.  (Hays & Iwamasa, 2006, p. 255-256)

The next logical step after the aforementioned behavioral interventions is a series of cognitive interventions that help the patient establish a bridge between automatic thoughts and behavior.  The cognitive elements of belief modification may need to be undertaken in parallel with behavioral interventions if the patient isn’t “buying the rationale” or is repeatedly unable to traverse unforeseen cognitive obstacles.  (Beck, 2011, p. 295)  The process of teaching a patient to identify and monitor automatic thoughts is of paramount importance for long term success and maintenance.  If the patient-clinician dyad comes to consensus about a longer treatment course, Schema Therapy would be my personal tool of choice since we can reasonably anticipate it will take at least 12-24 months to modify an individual’s core belief system.

There are a number of anticipated complications that we can reliably predict before treatment commences.  The first and most obvious complication is that negative self talk and poor self image are so much a part of the typical patient with Dysthymic Disorder that compliance is likely to be a huge issue.  Resistance is likely to be moderate to high, especially once core issues are identified.  Metaphorically, we are talking about convincing someone that gravity doesn’t exist… it’s sure to be an uphill battle.  By virtue of the fact that I have endured the disorder myself, countertransference is a real and pertinent issue.  I would personally address this by attending my own individual sessions to ensure that I don’t get in the way of the best interest of my patient.  Finally, it must be noted that an individual with Dysthymic Disorder should be considered extremely vulnerable and handled with the utmost care.  For example, individuals with Dysthymic Disorder often exhibit symptoms such as fatigue and low self-esteem.  These symptoms may lead to tension in interpersonal relationships, thereby increasing the probability of terminating therapy.  Although these life events may appear to be the “cause” a major depressive episode, the episode is often predated by deficits in informational processing that lead to pre-morbid deterioration of the relationship.  (Harkness & Luther, 2001)

Because Dysthymic Disorder is largely defined and distinguished by its protracted course, longitudinal studies are uniquely positioned to investigate the prognosis of the disorder.  Due to the staggering costs associated with longitudinal studies, few have been conducted on the naturalistic course of Dysthymic Disorder.  (Klein, Norden, Ferro, Leader, & Kasch, 1998)  The overall consensus is that success treating Dysthymic Disorder is better addressed on a case by case basis – making a generalization about expected treatment outcomes and prognosis is probably ill advised.  However, we can reasonably expect that there will be some measure of improvement in cognitive functioning, motivation, mood, and affect.  I would be cautious about setting expectations for full recovery or total remission until the underlying core beliefs are identified.  Assuming I could obtain permission from the patient, I would endeavor to track relevant data over the course of treatment as we consider the transition to schema therapy together, if applicable.  Individuals whom suffer from Dysthymic Disorder often find that the minor daily hassles that happen to everyone may spiral into more serious life events that trigger depression.  (Harkness & Luther, 2001, p. 570)  Tracking those hassles seems to a reasonably simple way to measure the effectiveness of the therapy being provided and adjusting it if necessary.


American Psychiatric Association. (2000). Diagnostic and statistical manual of mental disorders (4th ed., text rev.). Washington, DC: Author.

Beck, J. S. (2011). Cognitive behavior therapy: Basic and beyond (2nd ed.). New York, NY: Guilford Press.

Cooper, J. O., Heron, T. E., & Heward, W. L. (2007). Applied Behavior Analysis (2nd ed.). Upper Saddle River, NJ: Pearson Education.

Dougherty, L. R., Klein, D. N., & Davila, J. (2004, Dec). A growth curve analysis of the course of dysthymic disorder: The effects of chronic stress and moderation by adverse parent-child relationships and family history. Journal of Consulting and Clinical Psychology, 72(6), 1012-1021. doi: 10.1037/0022-006X.72.6.1012

Durbin, E. C., Klein, D. N., & Schwartz, J. E. (2000, Feb). Predicting the 21/2-year outcome of dysthymic disorder: The roles of childhood adversity and family history of psychopathology. Journal of Consulting and Clinical Psychology, 68(1), 57-63. doi: 10.1037/0022-006X.68.1.57

Elligan, D. (1997). Culturally sensitive integration of supportive and cognitive behavioral therapy in the treatment of a bicultural dysthymic patient. Cultural Diversity and Mental Health, 3(3), 207-213. doi: 10.1037/1099-9809.3.3.207

Harkness, K. L., & Luther, J. (2001, Nov). Clinical risk factors for the generation of life events in major depression. The Journal of Abnormal Psychology, 110(4), 564-572. doi: 10.1037/0021-843X.110.4.564

Hayes, A., & Strunk, D. (n.d.). Depression. Retrieved May 28, 2012, from http://www.div12.org/PsychologicalTreatments/disorders/depression_main.php

Hays, P. A., & Iwamasa, G. Y. (Eds.). (2006). Culturally responsive cognitive-behavioral therapy. Washington DC: American Psychological Association.

Klein, D. N., Clark, D. C., Dansky, L., & Margolis, E. T. (1988, Aug). Dysthymia in the offspring of parents with primary unipolar affective disorder. The Journal of Abnormal Psychology, 97(3), 265-274. doi: 10.1037/0021-843X.97.3.265

Klein, D. N., Norden, K. A., Ferro, T., Leader, J. B., & Kasch, K. L. (1998). Thirty-month naturalistic follow-up study of early-onset dysthymic disorder: Course, diagnostic stability, and prediction of outcome.. The Journal of Abnormal Psychology, 107(2), 338-348. doi: 10.1037/0021-843X.107.2.338

Morrison, J. (2007). Diagnosis made easier: Principles and techniques for mental health clinicians. New York: Guilford Press.

Spiegler, M. D., & Guevremont, D. C. (2010). Contemporary Behavior Therapy (5th ed.). Belmont, CA: Wadsworth: Cengage Learning.

Yee, C. M., & Miller, G. A. (1994, Nov). A dual-task analysis of resource allocation in dysthymia and anhedonia. The Journal of Abnormal Psychology, 103(4), 625-636. doi: 10.1037/0021-843X.103.4.625

Yee, C. M., Deldin, P. J., & Miller, G. A. (1992, May). Early stimulus processing in dysthymia and anhedonia. The Journal of Abnormal Psychology, 101(2), 230-233. doi: 10.1037/0021-843X.101.2.230

Paranoid & Delusional Disorders

The boundary between normal and abnormal appears to be largely subjective.  “One person’s excessive suspiciousness is another’s due caution, and one person’s trust is another’s gullibility.”  (Blaney & Millon, 2009, p. 362)  The “trade-off between vigilance and vulnerability” is something I had not considered… that balance is perceived to be the issue when it comes to paranoid personality disorder (PDD), paranoid schizophrenia (PS), and or delusional disorder (DD).  “Any stubborn genius will have ideas that happen to be wrong as well as those that happen to be right.”  This observation seems to suggest that the people who often suffer from these disorders are extremely intelligent, and thus, may have some beliefs that are in fact sane, relevant, and true.  It would suffice to say that I am going to use caution when pursuing this diagnosis… Einstein was considered to be delusional!

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Most studies that have been done to date have focused on persecutory delusions… either by design or because they are more common and subsequently easier to find suitable samples.  Persecutory delusions involve a degree of suspiciousness, or are generally mistrustful and/or wary.  It is suitably difficult to measure the tangible levels of suspiciousness via self report, however, since some sufferers may be too guarded to admit that they are suspicious.  The very process of self report is likely to “trip the defenses of” and subsequently increase guardedness.  Further compounding the efficacy of self-report inventories is the issue that sufferers may be reporting reality, betraying hypersensitivity, or some combination of both.  This highlights the necessity of multiple-peer reports that can confirm the interpersonal difficulties of the sufferer.  We, as clinicians, will have to be diligent about securing 3rd party sources (schools, work environment, relatives, other individuals whom are close to the client) in order to get as many perspectives on the conditions as possible.

There are several dimensions of delusions… most notably belief certainty (emotional commitment, conviction), self-monitoring (insight), distress, and frequency.  I was particularly interested in the “double awareness phase” in which a patient wavers between embracing a delusion and recognizing that its delusionality.  Of note, is the observation that psychotropic medications reduce engagement in delusions, thereby improving overall functionality, but ultimately leave actual beliefs untouched?  This seems to parallel the overall trend of medications “treating the symptoms and not the cause.”

Some patients may possess some distinctly protective attributes that account for the fact that they do not become delusional.  As a result, quasi-delusional or aberrant beliefs may not always be associated with clinical conditions indicative of a general mental disturbance or distress.  For example, low levels of anhedonia and high levels of openness are commonly thought to be a psychological asset… despite the fact that they may be quasi-delusional.  Such individuals may demonstrate greater levels of control over their unusual perceptions.  (Blaney & Millon, 2009, p. 366)  Perhaps this natural protection can be leveraged to direct treatment of people whom do not have that natural protection.  It seems to me that if we know what can prevent delusions, we should make every attempt to instill those protections in our clients whom suffer without them?

Paranoia and delusions are thought to arise from several different situations or events.  One possible event is migration, in which an individual finds themselves in a new environment that does not provide a sense of security.  Growing frustration with the new locale may leave migrants vulnerable to paranoid disorders.  As is the case with many other disorders, abuse and trauma during childhood often precede delusional experiences in adulthood.  In some cases the delusions are related to that specific event, like trauma flashbacks, or they may be more generalized due to negative schematic models of the self and the world.  This manifests in high levels of self-reported suspiciousness and/or resentment.  Paranoid individuals tend to be characterized by experiences involving victimization or stigmatization by others, whereas depressed individuals were characterized by interpersonal losses.  (Blaney & Millon, 2009, p. 369)  Personally, I am not at all surprised by the childhood abuse antecedent.  The toll of child abuse rises again this week… I am hard pressed to find a disorder that can NOT be predicated by child abuse.

Biologically speaking, some researchers have attempted to attribute these behaviors to processing defects or bias.  Theory of Mind (ToM), for example, suggests that the human mind is characterized by a system that facilitates inferences about the mental processes of other persons.  (Blaney & Millon, 2009, p. 377)  In essence, patients have difficulty discerning others’ intentions correctly.  Some have suggested that delusion-prone individuals are overconfident and quick to reach certainty in the face of incomplete information.  Other research suggests that delusional individuals may have a proposed tendency to attribute specific persons as a source of danger (personalization), thereby revealing an inability to distinguish between external negative events that are situational as opposed to interpersonal.  It has been posited that they may have an exaggerated version of self-consciousness in which they continually preoccupy themselves with how they are seen by others… and subsequently generalize that everyone feels like that.  (Blaney & Millon, 2009, p. 379)  On the whole, there are several theories… all of which seem “plausible.”  I can’t wait to get into the field to test the theory.

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Blaney, P. H., & Millon, T. (2009). Oxford textbook of psychopathology (2nd ed.). New York, New York: Oxford University Press.

Schizophrenia, Downward Social Drift, and Interpersonal Adjustment

Everyday social encounters present people with schizophrenia a considerable amount of difficulty.  They show significant impairment in both “instrumental relationships” and social-emotional relationships.  This impairment is demonstrated by “downward social drift” and, perhaps more importantly, the fact that the majority of people with schizophrenia never marry.  Of note is that interpersonal adjustment issues are much more prevalent in the male portion of the schizophrenia population that in the female portion.

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Social competence is a global or “macro” measurement of social role performance.  Global social competence issues continue to be a marker not only for people who have schizophrenia, but for people who are considered “high risk.”  I still don’t quite understand the etiology of these social deficits however… which came first, the social deficits or the disorder?

Social skills are less global and more molecular, thereby representing skills that enable a person to competently perform a social task.  They include “specific verbal, non-verbal and paralinguistic (e.g., voice tone) behavioral components that together form the basis for effective communication.”  (Blaney & Millon, 2009, p. 335)  To my own personal delight, I really enjoy any opportunity to utilize role-play… and this is one of them.  Typically, people with schizophrenia will show weaker verbal and nonverbal skill development, they tend to be less assertive, and they tend to deny making errors or lie as opposed to apologize or explain.  I am really looking forward to utilizing role-play with this population, I believe it to be one of my strong suits (and one of the pieces I really enjoy).

People with schizophrenia can have remarkably impaired ability to solve social problems.  This might manifest in difficulty recognizing interpersonal problems, formulating solutions to that problem, or perhaps most importantly implementing a solution that has a probably degree of success.  They are generally less able to recognize poor problem solutions (e.g., solutions that are unlikely to work).

Gender is an often neglected variable when studying schizophrenia.  Female patients typically have later onset, shorter and less frequent psychotic episodes, and show better response to treatment when compared to make counterparts.  They are more likely to be marked, to live independently, and to be employed (despite having similar symptoms to men).  Women often require less antipsychotic medication to stabilize them.  This leads some authors to speculate about the neuroprotective properties of estrogen… interesting concept to say the least.  This might be off-base, but could this possibly explain the late life crisis that women often experience around menopause?

Positive and negative symptoms should not be viewed in the context of “good and bad.”  Positive symptoms are “added,” like delusions or hallucinations for example.  Negative symptoms are typically features that are removed, reduced, or blunted.  This typically manifests as emotional withdrawal or anhedonia.  Negative effects have been shown to predict both unemployment and reduced social network size.  In total, positive symptoms, negative symptoms, and “disorders of relating” represent three distinct dimensions of schizophrenia.  (Blaney & Millon, 2009, p. 340)

Of particular interest to me is the discussion on interpersonal stress, relapse, and the apparent foundation of the above in family systems theory.  Specifically, “the social environment into which schizophrenia patients were discharged after they left the hospital was significantly associated with how well patients fared psychiatrically over the next several months.”  (Blaney & Millon, 2009, p. 349)  Expressed emotion (EE) reflects the extent to which the relatives of a psychiatric patient talk about that patient in a critical, hostile, or emotionally over-involved way.  EE has been found to be a reliable predictor of relapse, and as a result, family therapy focused on dealing with living with a schizophrenic patient is definitely in order.  This can assist family members in overcoming their apparent difficulty in accepting, and understanding, the disorder.

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Blaney, P. H., & Millon, T. (2009). Oxford textbook of psychopathology (2nd ed.). New York, New York: Oxford University Press.

Major Depression Disorder (MDD)

There are some significant differences between diagnosing a child with MDD and diagnosing an adult.  First and foremost, symptom duration must be at least 1 year (as opposed to 2 for adults).  Secondly, the presentation is likely to be different… with children exhibiting somatic complaints, irritability, and social withdrawal much more often their adult counterparts.  In both cases, one symptom must be depressed or irritable mood and/or inability to experience pleasurable emotions from normally pleasurable life events such as eating or social interaction (anhedonia).

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The likelihood that comorbid conditions will appear increases with the severity of the depression.  (Netherton, Holmes, & Walker, 1999, p. 266)  Often MDD is comorbid with anxiety disorders, ADHD, behavior disorders, eating disorders, and/or substance abuse.  There does appear to be a distinct lack of a “developmental perspective” in the DSM-IV-TR, but that is not exclusive to this particular category or disorder…  I suspect that’s just an effort to remain “atheoretical.”

I am not at all surprised that rates of depressive disorders increase with age, since frequency, duration, and severity of previous episodes seem to be an indicator of risk.  Also, for lack of a better explanation, the longer you live, the more likely you are to have to endure a negative life event.  I was surprised to see that by age 15, females are twice as likely as males to receive a depressive disorder diagnosis.

Theoretically speaking, I came to favor the interpersonal/cognitive/behavioral models of development for depression.  There was a continued lack of a developmental model, however, for all the theories.  On the whole, I got the impression that we were really selling the childhood cohort short due to lack of research (or, perhaps that’s just the Netherton text working, not sure which… will definitely check this out when I get knee deep into the journal reading).

Attachment theory rears its ugly head again, condemning insecure parental attachment as being significant in the etiology of depression related cognitive processes.  (Netherton et al., 1999, p. 269)  The text suggests that this leads to a more depressive perspective on self, world, and future… culminating in a sense of helplessness and hopelessness.  It would appear that depression is a possible marker for RAD?  I would like to see some comorbity rates.

I understand that self assessment has to be a key component for assessment, but I wouldn’t bet the house on those results alone.  I really like the idea of a multi-trait, multi-method, multi-informant approach to increase diagnostic reliability and validity.  I really believe that you need to take a big picture approach to the complete child, accessing cognitive, affective, interpersonal, adaptive, genetic, and environmental effects to be able to diagnose this disorder effectively.  In addition to a full batter of testing and semi-structured interviews, if able we should dig into a medical history and eliminate underlying organic causes… paying special attention to drug history since many anticonvulsants and some antibiotics are associated with depressive symptoms.

Although I will give treatment only cursory coverage, at this early stage I am very much in favor of cognitive restructuring and development of more adaptive cognitions.  Although the text didn’t really address it, I would also take a “top down” approach and see if I couldn’t convert this to a family intervention.  I am increasingly aware that families are systems and that children tend to play a specific role in that system.

Depression is one area where I am a proponent of pharmacological intervention, despite the fact that I have come out against the pharmacological means to the end on some other diagnosis.  It would appear to me that SSRI’s were made specifically for depression, success rates are relatively high, and side effects are minimal.  I’m not sure I could consider TCAs and MAOIs unless SSRI+CBT failed.  ECT is our last resort… but the degree of impairment would have to be pretty serious for me to suggest it.

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Netherton, S. D., Holmes, D., & Walker, C. E. (1999). Child and adolescent psychological disorders: A comprehensive textbook. Oxford, NY: Oxford University Press.