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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.

References

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

What Kind of Therapy is Out There?


In reviewing treatments for depression, it seems the three most common, two of which are very broad, treatments are anti depressant medications, electro-convulsive therapy or ECT, and psychotherapy. Each of these treatments has their own purpose and regimen and can be combined in various ways even though they are different. In fact it is most likely because they are so different that they work well together.

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Antidepressant medication gives a therapist and a patient many options. These options have both positive and negative effects. There are different side effects with each type of medication, some tolerable, some need to be managed with other medications. It is different for everyone; this is why it is important to continue trying different combinations until an agreeable treatment plan is found. One example of medication is SSRIS, which are Selective Serotonin Reuptake Inhibitors. This medication is usually the first choice for treatment. The reasoning behind this is that SSRI’s are the most tolerated with very little side effects and most people find they work very well for them. Some side effects are headache or insomnia, but often any side effects subside in the first month. This medication allows a high amount of serotonin to be blocked in the synapse. By doing this, the cells that are neglected are resaturated allowing relief from depression symptoms.

Tricyclic anti-depressants or TCAs are a second choice in medications, if for some reason the SSRI is unable to help the patient. This medication was developed sometime during the 1950’s and 60’s. TCAs seem to be used for more moderate or severe depression because the side effects are more likely to be serious. TCAs work in the brain synapses and increase norepinephrine. Some of the side effects include dry mouth or visual focus, but the more serious side effects include things such as urinary obstruction or delirium. People who have had a lot of strokes or have been diagnosed as having seizure disorders should not be given any TCAs as medication.

MAOIs or monoamine oxidase inhibitors are another common medication prescribed to depression patients. These are generally a last choice because the side effects are often serious. MAOIs are usually effective in treating depression and were actually the first anti-depressant. It works by blocking monoamine oxidase in the brain synapses and increasing norepinephrine. MAOIs inhibit the body’s ability to break down tyramine which is found in very common foods such as wine, nuts, and chocolate. When this food is consumed while the person is taking an MAOI, it is possible for the tyramine to cause blood pressure to rise to dangerous levels.

While anti-depressants can be mixed or left as a single treatment, they do provide a lot of options to help deal with side effects or other issues that may come up.  They are always the best option; another treatment option for depression is electroconvulsive therapy or ECT.

When electroconvulsive therapy is chosen as treatment the patient receives an electrical current which is passed through the brain causing a seizure. The seizure usually continues for twenty to ninety seconds. This treatment is said to offer a patient a quick relief of their depression symptoms. A common side effect of this treatment is confusion that can last up to several hours and short term memory loss, both of which are short term.

Psychotherapy is the last type of treatment discussed and is often referred to as talk therapy. There are various types of psychotherapy such as cognitive behavioral therapy, interpersonal therapy, and psychodynamic therapy. The most common type of talk therapy is the cognitive behavioral therapy. During sessions a patient not only talks about their depression, they have the opportunity to learn more about it. The patient is then able to focus on knowing what their negative patterns are and changing those into positive behaviors. Interpersonal therapists’ help their patients look at the destructive relationships a person is in that may be helping to grow the depression instead of helping to keep it at bay. Psychodynamic therapy helps a patient work through and resolves whatever internal conflicts the patient may be living with.

All of these types of psychotherapy focus on one thing, helping the patient talk through and learn how to deal with events in their lives so they don’t feel like they are drowning in depression.

Out of all of these treatments I would actually think electroconvulsive therapy to be the quickest and most effective. I can’t imagine going under sedation in order to endure treatment and then waking up not only with memory loss but also being confused about your whereabouts, among other things, even if only temporarily.

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References:

Child and Adolescent Psychological Disorders.

Oxford Textbook of Psychopathology.

Depression. medicinenet.com. http://www.medicinenet.com/script/main/art.asp?articlekey=342&pf=3&page=6

Depression (Major Depression).  Mayoclinic.com. http://www.mayoclinic.com/health/depression/DS00175/METHOD=print&DSECTION=all

Eating Disorders = BIG BUSINESS


“Weight discrimination and the resulting obsession with thinness are rampant and recalcitrant.  I believe that, in order to make any kind of a dent in this field, we all need to combat these pernicious influences.”  (Netherton, Holmes, & Walker, 1999, p. 412)  Amen.  The weight of the media, the “diet food industry,” and the purveyors of a “healthy lifestyle” propagate this issue… without a doubt.  Losing weight is BIG BUISINESS, and there are huge profits to be made for those that offer obese people the glimmer of a stereotypically thin body.

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I also appreciated the acknowledgement on the pressure exerted by managed care.  Eating disorders appear to be particularly “deep seated” and ill suited for half a dozen one hour sessions.  Correcting inaccurate perceptions, relabeling cognitions of visceral and affective states, and redrawing boundaries… this kind of work takes time… more time than managed care often provides.  This is yet another example of the effect managed care will continue to have for as long as it is the primary method of seeking out psychological assistance.

I was suitably surprised at the long-term mortality rate… suggested to be over 10%.  (Netherton et al., 1999, p. 399)  With a roughly 1 in 10 shot of succumbing to starvation, suicide, or electrolyte imbalance; you would think this particular set of disorders would get more research attention.  The fact that there is still limited epidemiological data is frustrating… perhaps the difficulty obtaining the data is related to the relative secrecy and shame associated with the disorders themselves?

Like the BM text, NHW jumps on the multi-determined etiology bandwagon.  It’s hard to disagree with since biological, familial, sociocultural, and personality factors all seem to be plausible.  The differences in family characteristics were particularly interesting.  “Bulimic families tend to be characterized as disengaged, chaotic, and highly conflictual and as having a high degree of life stress.”  Conversely, “anorexic families tend to be characterized as enmeshed, overprotective, and conflict avoidant.”  (Netherton et al., 1999, p. 400)  That’s a strange clinical picture that seems to suggest that there might be a single underlying biological cause for EDs in general, but that familial and personality factors may play a role in its manifestation.

The list of comorbid disorders we need to consider during the assessment process is long and fairly inclusive.  “Depression, anxiety disorders, dissociative disorders, substance abuse, and personality disorders” are on the forefront of the disorders we should be checking for.  (Netherton et al., 1999, p. 401)  Furthermore, NHW suggest we assess treatment history, as well as suicide attempts and self mutilative behaviors (cutters).

Pharmacological interventions employing antidepressants have been particularly successful.  This text only cites 3 studies that have employed SSRI class antidepressants, but they report “significant improvement with 60-80 mg dosages (of Prozac) compared to placebo.”  (Netherton et al., 1999, p. 407)  I think I am going to dig deep into some more recent research to see of this trend holds up, there has to be more than three studies on it by now.

I like the idea of a behavioral contract… not just for eating disorders, but for any disorders which involve “behavior.”  I am inclined to agree with the statement “the contract provides structure and predictability.  Expectations, rewards, and consequences are delineated so that all people involved (patient, treaters, families) know what is expected at all stages of treatment.”  (Netherton et al., 1999, p. 407)  My question is this… realistically, what “consequences” are there if we are dealing with outpatient treatment?

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Reference

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

Sexual Dysfunctions


Sexual dysfunctions are conditions that impair sexual satisfaction.  This can manifest as reduced desire to initiate or sustain sexual activity, or lack of ability to achieve sexual satisfaction.  Epidemiological data suggests that the prevalence rate for all sexual disorders is approximately 31% for men and 43% for women.  (Blaney & Millon, 2009, p. 399)  That rate is given to fluctuate, however, depending on the definition of what a “dysfunction” actually entails.  The reality, for Blaney & Millon, is that any particular label or operational definition is imperfect and subject to alterative interpretations.  The key consideration for the therapist is that we must been seen as nonjudgmental.

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I am not overly surprised by the suggestion that Americans have never learned to be comfortable talking about things sexual.  “Even couples who have been together for many years, and experienced physical intimacy hundreds of times, are still often most reluctant to reveal their sexual desires, fears, and concerns to each other.”  (Blaney & Millon, 2009, p. 400)  This is the 21st Century; it’s perfectly acceptable (even desirable)… this is foreign to me.

“Rewarding sexual activity requires the adequate functioning of at least three organ systems: cardiovascular, hormonal, and neurological.”  (Blaney & Millon, 2009, p. 401)  These systems can be adversely affected by medications, particularly SSRI Antidepressants.  Virtually any medical condition that affects those systems; including illnesses, treatments, procedures, and changes- could also serve as precipitating factors.  Finally, culture and psychosocial variables weigh in as contributing factors, although “many people with sexual dysfunctions report none of these factors and many with one or more of these risk factors report satisfying and functional sexual lives.”  (Blaney & Millon, 2009, p. 402)

If a regular partner is a variable, it is preferable to have them present and willing to participate in the process.  “The involvement of the partner of the symptomatic client in treatment is widely believed to play an important (even critical) facilitative role in sex therapy.”  (Blaney & Millon, 2009, p. 404)  Even if the partner is unwilling or unable to be present for the office visits, partner cooperation and participation (along with sensitivity to partner issues on the part of the therapist) are “good enough” to make reasonable progress.

Knowing what is at stake is a key consideration for therapists to measure or ascertain.  What if they therapy fails?  Will the relationship end or will it continue?  “Having more at stake in treatment (i.e., the continuation of the relationship) can sometimes serve as an important motivator for one or both partners.”  (Blaney & Millon, 2009, p. 404)  However, this presents negative aspects as well… primarily because it is an outward indication that there is serious dissatisfaction with the relationship.

Sexual pain disorders are another dimension of sexual dysfunctions that are often neglected.  Recurrent or persistent genital pain in a female, typed dyspareunia, often causes marked distress.  Vulvodynia, characterized by chronic vulvar discomfort or pain, is also not uncommon.  The third common complaint is involuntary contractions or spasms of the outer third of the vaginal barrel, called vaginismus.  This condition makes intercourse painful or impossible.

Treatment of sexual pain disorders always begins with a careful and comprehensive gynecological exam.  “Among the many medical treatments that have been used, with at least some success, are the following:  topical creams, oral medications, biofeedback, physical therapy, cognitive behavioral sex therapy, pain management, local anesthetic agents, topical estrogen, electrical stimulation of the vestibular area, and surgery.”  (Blaney & Millon, 2009, p. 422)

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Reference

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

Major Depressive Disorder (MDD) treatment options – Examining the STAR*D Trial


When weighing the effectiveness of Major Depressive Disorder (MDD) treatment options, the most logical place to start is the largest open-label pragmatic trial ever rendered; The Sequenced Treatment Alternatives to Relieve Depression (STAR*D) trial.  The STAR*D trial concluded that there were no statistically significant differences in short term remission or response rates between tested treatment options, including both CBT and pharmacological remedies, but that some treatment options had advantages over others in terms of side effects and/or mean time to remission.  (Sinyor, Schaffer, & Levitt, 2010)

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There are many different flavors of CBTs intended to treat mood disorders.  Those flavors include those predominantly focused on learning theory or behavioral activation (BA), predominantly cognitive models such as Cognitive Therapy (CT/CBT), and models incorporating additional elements such as Cognitive Behavioral Analysis System Psychotherapy (CBASP) and Mindfulness-Based Cognitive Behavioral Therapy (MCBT).  (Meyer & Scott, 2008, p. 685)  CBT, when practiced by inexperienced STAR*D clinicians, was at least equally effective in short term follow-ups when compared with pharmacological remedies.  CBT was also associated with significantly fewer side effects.  Those facts alone should serve as reasonable justification in recommending CBT over all other treatment methods.

CBT was associated with longer times to remission when compared with pharmacological remedies, when they were effective, so if speed of improvement is of critical importance the client could potentially benefit the pharmacological treatment option.  Despite the apparent speed with which the pharmacological agents worked, choosing which drug is no easy task.  STAR*D found no clear medication “winner” for patients whose depression does not remit after one or more aggressive medication trials.  (Gaynes, Warden, Trivedi, & Wisniewski, 2009, p. 1443)  Matter of fact, every drug and combination of drugs showed the same effect as every other drug and drug combination.  (Leventhal & Antonuccio, 2009)  Some studies suggest that use of multiple antidepressant medications may double the likelihood of remission compared with use of a single medication.  (Blier, Ward, Tremblay, & Laberge, 2010)  Guess who funded that study?

There is increasing evidence that the biological explanation and pharmacological treatment of depressions is a failure.  STAR*D provides compelling evidence to that the placebo effect is the prime explanation for favorable outcomes that occur with antidepressants.  Of the patients that were found to respond positively to pharmacotherapy on the short term, the STAR*D study found that at the end of a year’s time almost all of the patients (97%) had either relapsed or dropped out.  (Leventhal & Antonuccio, 2009)  Even if we continue to leverage the pharmacological remedies, the long-range outcomes of clients with MDD are better when CBT is included, regardless of whether CBT is concurrent with or follows pharmacotherapy.  (Friedman, Wright, Jarrett, & Thase, 2006, p. 327)  The beneficial effects of CBT persist several years into post treatment and are strongly associated with preventing relapse (Kuyken, Dalgleish, & Holden, 2007), especially among individuals discontinuing medication use.  (Friedman, 2004)

As controversial as they are, “brain stimulation therapies” like electroconvulsive treatment (ECT) are effective in days, not weeks, and most have a higher response rate than any treatment tested in the STAR*D trial.  (Insel & Wang, 2009)  While ECT is still the gold standard in brain stimulation therapies, clinicians now have a growing list of FDA approved brain stimulation interventions. “These interventions include new modifications of ECT, vagus nerve stimulation, transcranial magnetic stimulation (TMS), magnetic seizure therapy, deep brain stimulation, transcranial direct current stimulation, implanted cortical stimulation, and others on the horizon.”  (Lisanby & Novakovic, 2009, p. 734)  Studies that utilized brain stimulation therapies to treat depression revealed significant increases in the release of norepinephrine as well as increased serotonergic activity, both of which are purported to have antidepressant effects.  (Weaver, 2009)  However, ECT is use is “limited by its invasive nature, which includes the requirement of general anesthesia and the risk of retrograde amnesia, which may be irreversible in some patients.”  (Rot, Mathew, & Charney, 2009, p. 311)  As a result, brain stimulation therapies are usually reserved for cases where depression is resistant to conventional treatments.  In addition, use of brain stimulation therapy is entirely dependent on the prescribing clinician believing in a tenuous underlying premise that norepinephrine plays a key role in depression onset and recurrence.

It would suffice to say that I favor the CBT methodology of treatment for unipolar depression, in most, if not all cases.  Personally, I would endeavor to enhance the CBT experience by utilizing cutting edge technological alternatives to traditional CBT… like virtual reality, or VR, simulations.  VR simulations are computer generated environments constructed to elicit an appropriate emotional response from clients… responses we as therapists can use in therapy.  (David, 2010)  Coupling responses that rival in vivo responses with well trained and knowledgeable CBT methods, we could usher in a new alternative to the placebo effect that passes for pharmacological intervention today.  The failure of antidepressants to provide lasting benefit, and the underlying truth that 100 years of research has failed to identify an underlying physical cause for mental disorders (including depression) leads me to believe that a “biopsychosocial model may be more useful than a disease model for conceptualizing and treating depression.”  (Leventhal & Antonuccio, 2009, p. 199)

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References

Blier, P., Ward, H. E., Tremblay, P., & Laberge, L. (2010, Mar). Combination of antidepressant medications from treatment initiation for major depressive disorder: A double-blind randomized study. The American Journal of Psychiatry, 167(3), 281-288. Retrieved from http://ezproxy.bellevue.edu:80/login?url=http://proquest.umi.com.ezproxy.bellevue.edu/pqdweb?did=1976013231&sid=18&Fmt=4&clientId=4683&RQT=309&VName=PQD

David, D. (2010, Mar). Cutting edge deveopments in psychology: Virtual reality applications. Interview with two leading experts. Journal of Cognitive and Behavioral Psychotherapies, 10(1), 115-126. Retrieved from http://ezproxy.bellevue.edu:80/login?url=http://proquest.umi.com.ezproxy.bellevue.edu/pqdweb?did=2010171911&sid=2&Fmt=3&clientId=4683&RQT=309&VName=PQD

Friedman, E. S., Wright, J. H., Jarrett, R. B., & Thase, M. E. (2006, May). Combining cognitive therapy and medication for mood disorders. Psychiatric Annals, 36(5), 320-329. Retrieved from http://ezproxy.bellevue.edu:80/login?url=http://proquest.umi.com.ezproxy.bellevue.edu/pqdweb?did=1069483751&sid=4&Fmt=3&clientId=4683&RQT=309&VName=PQD

Friedman, M. A. (2004, Spring). Combined psychotherapy and pharmacotherapy for the treatment of major depressive disorder. Clinical Psychology: Science and Practice, 11(1), 47-68. Retrieved from http://proquest.umi.com.ezproxy.bellevue.edu/pqdweb?index=40&did=526558591&SrchMode=1&sid=5&Fmt=10&VInst=PROD&VType=PQD&RQT=309&VName=PQD&TS=1272666830&clientId=4683

Gaynes, B. N., Warden, D., Trivedi, M. H., & Wisniewski, S. R. (2009, Nov). What did STAR*D teach us? Results from a large-scale, practical, clinical trial for patients with depression. Psychiatric Services, 60(11), 1439-1445. Retrieved from http://ezproxy.bellevue.edu:80/login?url=http://proquest.umi.com.ezproxy.bellevue.edu/pqdweb?did=1921563151&sid=2&Fmt=3&clientId=4683&RQT=309&VName=PQD

Insel, T. R., & Wang, P. S. (2009, Nov). The STAR*D trial: Revealing the need for better treatments. Psychiatric Services, 60(11), 1466-1467. Retrieved from http://proquest.umi.com.ezproxy.bellevue.edu/pqdweb?index=28&did=1921563061&SrchMode=1&sid=6&Fmt=6&VInst=PROD&VType=PQD&RQT=309&VName=PQD&TS=1272667182&clientId=4683

Kuyken, W., Dalgleish, T., & Holden, E. R. (2007, Jan). Advances in cognitive-behavioural therapy for unipolar depression. Canadian Journal of Psychiatry, 52(1), 5-14. Retrieved from http://ezproxy.bellevue.edu:80/login?url=http://proquest.umi.com.ezproxy.bellevue.edu/pqdweb?did=1203220561&sid=5&Fmt=3&clientId=4683&RQT=309&VName=PQD

Leventhal, A. M., & Antonuccio, D. O. (2009). On chemical imbalances, antidepressants, and the diagnosis of depression. Ethical Human Psychology and Psychiatry, 11(3), 199-214. Retrieved from http://ezproxy.bellevue.edu:80/login?url=http://proquest.umi.com.ezproxy.bellevue.edu/pqdweb?did=1923231211&sid=19&Fmt=3&clientId=4683&RQT=309&VName=PQD

Lisanby, S. H., & Novakovic, V. (2009, Jun). Brain stimulation therapies for clinicians. The American Journal of Psychiatry, 166(6), 734-736. Retrieved from http://ezproxy.bellevue.edu:80/login?url=http://proquest.umi.com.ezproxy.bellevue.edu/pqdweb?did=1738370431&sid=14&Fmt=3&clientId=4683&RQT=309&VName=PQD

Meyer, T. D., & Scott, J. (2008, Nov). Cognitive behavioural therapy for mood disorders. Behavioural and Cognitive Psychotherapy, 36(6), 685-693. doi: 10.1017/S1352465808004761

Rot, M. A., Mathew, S. J., & Charney, D. S. (2009, Feb 3). Neurobiological mechanisms in major depressive disorder. Canadian Medical Association. Journal, 180(3), 305-313. Retrieved from http://ezproxy.bellevue.edu:80/login?url=http://proquest.umi.com.ezproxy.bellevue.edu/pqdweb?did=1634710771&sid=14&Fmt=3&clientId=4683&RQT=309&VName=PQD

Sinyor, M., Schaffer, A., & Levitt, A. (2010, Mar). The sequenced treatment alternatives to relieve depression (STAR*D) trial: A review. Canadian Journal of Psychiatry, 55(3), 126-136. Retrieved from http://ezproxy.bellevue.edu:80/login?url=http://proquest.umi.com.ezproxy.bellevue.edu/pqdweb?did=2016794701&sid=2&Fmt=3&clientId=4683&RQT=309&VName=PQD

Weaver, D. F. (2009, Summer). Self-induced “therapeutic seizures” for the treatment of depression. The Journal of Neuropsychiatry and Clinical Neurosciences, 21(3), 355-357. Retrieved from http://proquest.umi.com.ezproxy.bellevue.edu/pqdweb?index=71&did=1868802651&SrchMode=1&sid=14&Fmt=3&VInst=PROD&VType=PQD&RQT=309&VName=PQD&TS=1272668233&clientId=4683