Tag Archives: self-esteem

Comparing PTSD and Somatization Disorder

Comparing PTSD and Somatization Disorder shows that there are some similarities in the symptoms but for the most part they are different.  Somatization Disorder has a lot more physical symptoms while PTSD has more symptoms leaning toward emotional.  The symptoms the two disorders have in common are headaches and stomachaches.  In both cases symptoms can be so severe and last so long that it completely disrupts the person’s life.

Do you have medically unexplained physical, or somatic, symptoms?

Somatization disorder can cause a person towards an emotional reaction such as depression or even suicide because they feel so much pain and can never get a diagnosis for it.  The symptoms often lead to substance abuse.  Thereby leaving them to feel hopeless, as if they will never get the help they need.  Somatization disorder has a wide range of physical symptoms.  A person with this disorder will report many different symptoms over a period of time with no real medical explanation.  These symptoms are often pain throughout the body, but not usually all at the same time.  Pain in the form of headaches, stomach ache, joint or muscle pain.  It could also be internal, such as vomiting, or it could come about as a sexual or menstrual problem.  Neurological symptoms are also common, often occurring as problems with balance or vision and even paralysis.

Generally for a patient to be diagnosed they will have experienced a minimum of eight symptoms.  There will be a minimum number of symptoms from a given category.  An example of this is that a patient will experience four or more symptoms from the pain category, two or more symptoms from the gastrointestinal category, one or more symptoms from the sexual symptoms category, and one or more symptoms from the pseudoneurological symptoms.  When a person is showing signs of these symptoms they will be unexplainable and a medical diagnosis is not usually possible.  Generally the person will explain the pain they are having in a fashion that makes it seem as if they are in more pain than you think they should be in, as if they are over exaggerating the symptoms.

Somatization Disorder lasts for a very long time which is one thing this disorder has in common with PTSD.  PTSD symptoms can last anywhere from months to years.   Most PTSD symptoms are different from Somatization Disorder because they come from more of a psychological background than a physical background.  PTSD symptoms are generally geared more towards an emotional aspect, some examples are worry over dying, acting younger than the chronological age, having an impaired memory or obsessiveness.  It seems that PTSD actually transforms a person’s behavior instead of changing them physically.  This is because when traumatic experiences occur, the feelings they experience, such as shock, nervousness or fear continue on for a length of time and gradually get stronger.  The stronger they get the less of a normal life the person is able to lead.

These increased symptoms can include nightmares or night terrors, hypervigilance, panic attacks, hypersensitivity, low self-esteem and shattered self-confidence or a physical or mental paralysis.  There are three categories often used by clinicians in order to type or group people who are diagnosed with PTSD.  The categories used are re-living, avoiding, and increased arousal.  The people in the re-living group are people who suffer from living through the trauma they have been through over and over again.  This can happen through a flashback or a hallucination or just by being reminded even in small ways.  The people in the avoiding group tend to try to stay away from people, places or things that can remind them of the event.  Unfortunately the person can start to isolate themselves and eventually can turn completely inward from detachment.  The people in the increased arousal group lean towards either having difficulty showing their emotions or on the other end of the spectrum showing overly exaggerated emotions.  This group is also the group who has some physical symptoms such as higher blood pressure, muscle tension and nausea.

In conclusion, it has become very apparent to me that while there are some similarities between PTSD and Somatization Disorder, there are a lot more differences.  It has also become very apparent to me that the people who suffer from these disorders are dealing with a lot of pain, and whether it is physical or emotional, this pain can cause the person suffering from it to shut down and disable them from enjoying the life they were meant to lead.


Netherton, S.D., Holmes, D., Walker, C.E. (1999). Child and Adolescent Psychological Disorders.   New York, NY: Oxford University Press.

Blaney, P.H., Millon, T. (2009). Oxford Textbook of Psychopathology.

New York, NY: Oxford University Press.

(2009, February 9). Anxiety & Panic Disorders Guide. WebMD.com. Retrieved October 5, 2009, from http://www.webmd.com/anxiety-panic/guide/post-traumatic-stress-disorder

(Retrieved 2009, October 5). Somatization Disorder. Intelihealth.com.  http://www.intelihealth.com/IH/ihtPrint/W/8271/25759/187986.html?d=dmtHealthAZ&hide=t&k=base

(Retrieved 2009, October 5). Posttraumatic Stress Disorder. American Academy of Child & Adolescent Psychiatry. AACAP.org


(Retrieved 2009, October 5). Somatization Disorder. PsychNet-UK.


Kinchin, D. (2005). Post Traumatic Stress Disorder The Invisible Injury.

Didcot, Oxfordshire OX11 9YS, UK.  Retrieved October 5, 2009, from http://www.successunlimited.co.uk/books/ptsympt.htm


The Effects of Exercise on Self-Esteem

How often do we hear, “Get a workout, it will make you feel better.”?

Exercise For Life – For Your Good Health

Exercise is a very broad spectrum of activities; it can be walking, hiking, bicycling, running or any one of a number of sports.  It can also be moving along to a video that has choreographed moves geared toward a traditional exercise routine, or dancing, or Yoga and Pilates.  It could also be going to a gym and lifting weights or using the cardio equipment.

People often say you always feel better after a workout, or, if you can get some exercise in, you would feel so much better.  Is this truly the case?  How can causing your muscles to work and be sore actually help you emotionally?  Some studies that support a connection between exercise and positive self-esteem are: Physical Fitness and Enhanced Psychological Health; Associations Between Physical Activity and Reduced Rates of Hopelessness, Depression and Suicidal Behavior Among College Students; and The Relationships Among Self-Esteem, Exercise and Self-Rated Health in Older Women.

Each study shows slightly different statistics, but come to a similar conclusion.  This would be that physical activity does help a person have an increase in self-esteem, be it through the lessening of depression symptoms, or having the ability to perceive one’s self as healthy and high functioning in older age or simply by an elevation in a person’s mood, which gives that person the chance to understand that things are better than they seemed an hour ago.  All of these things apply to a person’s self-esteem in one way or another and these studies show that exercise helps to put a positive spin on each of them.

I feel that more studies will confirm that exercise or physical activity will help increase traits in a person’s self-esteem.


Plante, T., & Rodin, J. (1990).  Physical fitness and enhanced psychological health.  Current Psychology,9(1), 3. Retrieved from Academic Search Premier database. (Document ID: 9701290177)

Misra, R., Alexy, B., & Panigrahi, B.. (1996). The relationships among self-esteem, exercise, and self-rated health in older women. Journal of Women & Aging, 8(1), 81.  Retrieved December 30, 2009, from ProQuest Psychology Journals. (Document ID: 9825352).

Taliaferro, L., Rienzo, B., Pigg, R., Miller, M., & Dodd, V.. (2009). Associations Between Physical Activity and Reduced Rates of Hopelessness, Depression, and Suicidal Behavior Among College Students. Journal of American College Health, 57(4), 427-36.  Retrieved February 7, 2010, from ProQuest Psychology Journals. (Document ID: 1623326411).


The diagnosis of Trichotillomania (TM) is synonymous with the act of recurrently pulling one’s own body hair resulting in noticeable thinning or baldness.  (American Psychiatric Association, Diagnostic and statistical manual of mental disorders, 2000, p. 674)  Sites of hair pulling can include any area of the body in which hair is found, but the most common sites are the scalp, eyelashes, eyebrows, and the pubis area.  (Kraemer, 1999, p. 298)  The disorder itself is categorized in the DSM-IV-TR as an “Impulse Control Disorder Not Elsewhere Classified” along with disorders like Pathological Gambling, Pyromania, Kleptomania, and Intermittent Explosive Disorder.  Although TM was previously considered to be a rare disorder, more recent research indicates that prevalence rates of TM may be as high as 2% of the general population.  (Kraemer, 1999, p. 298)  This prevalence rate is significantly higher than the lifetime prevalence rate of .6% that is cited as a potential baseline among college students the DSM-IV-TR.  (4th ed., text rev.; DSM-IV-TR; American Psychiatric Association, 2000, p. 676)  The condition appears to be more common among women and the period of onset is typically in childhood or adolescence. (Kraemer, 1999, p. 298)  As is customary with most DSM-IV-TR diagnoses, the act of hair pulling cannot be better accounted for by another mental disorder (like delusions, for example) or a general medical condition.  Like every disorder in the DSM-IV-TR, the disturbance must cause significant distress or impairment in functioning.  (4th ed., text rev.; DSM-IV-TR; American Psychiatric Association, 2000, p. 675)

Alopecia is a key concept that must be understood in order to complete the differential diagnosis of TM.  Alopecia is a condition of baldness in the most general sense.  (Shiel, Jr. & Stoppler, 2008, p. 14)  Other medically related causes of alopecia should be considered in the differential diagnosis of TM, especially when working with an individual who deny pulling their hair.  The common suspects include male-pattern baldness, Discoid Lupus Erythematosus (DLE), Lichen Planopilaris (also known as Acuminatus), Folliculitis Decalvans, Pseudopelade of Brocq, and Alopecia Mucinosa (Follicular Mucinosis).  (4th ed., text rev.; DSM-IV-TR; American Psychiatric Association, 2000, p. 676)  Comprehensive coverage of these medical conditions is beyond the scope of this article – all of the aforementioned confounding variables can be eliminated by a general practitioner.

There are a number of idiosyncratic features associated with TM that bear mentioning.  Although the constellation of features covered here is not sufficient to warrant a diagnosis in isolation, they can aid in the differential diagnosis process.  Alopecia, regardless of the cause, has been known to lead sufferers to tremendous feats of avoidance so that the hair loss remains undetected.  Simply avoiding social functions or other events where the individual (and their attendant hair loss) might be uncovered is a common occurrence.  In cases where individual’s focus of attention is on the head or scalp, it is not uncommon for affected individuals to attempt to hide hair loss by adopting complimentary hair styles or wearing other headwear (e.g., hats, wigs, etc).  These avoidance behaviors will be the target of exposure and response prevention later in this article.

In addition to avoidant behavior and elaborate attempts to “cover it up,” individuals with TM frequently present with clinically significant difficulty in areas such as self-esteem and mood.  Comorbidity, or the presence of one or more disorders in the addition to a primary diagnosis, is the rule not the exception in the stereotypical presentation of TM.  Mood disorders (like depression) are the most common (65%) – anxiety (57%), chemical use (22%), and eating disorders (20%) round out the top four mostly likely candidates for comorbidity.  (Kraemer, 1999, p. 298)  These comorbidity rates are not overly surprising since they parallel prevalence rates across the wider population – perhaps with the notable exception of the high rate of comorbid eating disorders.  We can speculate about the source of comorbidity – one possible hypothesis is that a few people who suffer TM also suffer from a persistent cognitive dissonance associated with having happy-go-lucky personality trait which leads them “let the chips fall where they may.”  They are individuals prone to impulsivity, but they are subdued and controlled the shame, guilt, frustration, fear, rage, and helplessness associated with the social limitations placed on them by the disorder.  (Ingram, 2012, p. 269)  On the topic of personality, surprisingly enough, research suggests that personality disorders do not share significant overlap with TM.  This includes Borderline Personality Disorder (BPD) despite the fact that BPD is often associated with self-harming behavior.  (Kraemer, 1999, p. 299)

Differentiating TM from Obsessive-Compulsive Disorder (OCD) can be challenging in some cases.  TM is similar to OCD because there is a “sense of gratification” or “relief” when pulling the hair out.  Unlike individuals with OCD, individuals with TM do not perform their compulsions in direct response to an obsession and/or according to rules that must be rigidly adhered to.  (4th ed., text rev.; DSM-IV-TR; American Psychiatric Association, 2000, p. 676)  There are, however, observed similarities between OCD and TM regarding phenomenology, neurological test performance, response to SSRI’s, and contributing elements of familial and/or genetic factors.  (Kraemer, 1999, p. 299)  Due to the large genetic component contributions of both disorders, obtaining a family history (vis-à-vis a detailed genogram) is highly recommended.  The comprehensive genogram covering all mental illness can be helpful in the discovery the comorbid conditions identified above as well.

There is some suggestion that knowledge of events associated with onset is “intriguing, but unnecessary for successful treatment.”  (Kraemer, 1999, p. 299)  I call shenanigans.  There is a significant connection between the onset of TM and the patient enduring loss, perceived loss, and/or trauma.  Time is well spent exploring the specific environmental stressors that precipitated the disorder.  Although ignoring circumstances surrounding onset might be prudent when employing strict behavioral treatment paradigms, it seems like a terrible waste of time to endure suffering without identifying some underlying meaning or purpose that would otherwise be missed if we overlook onset specifics.  “Everything can be taken from a man but one thing: the last of human freedoms – to choose one’s attitude in any given set of circumstances, to choose one’s own way.”  (Frankl, 1997, p. 86)  If we acknowledge that all behavior is purposeful, then we must know and understand the circumstances around onset if we will ever understand the purpose of said behavior.  I liken this to a difference in professional opinion and personal preference because either position can be reasonably justified, but in the end the patient should make the ultimate decision about whether or not to explore onset contributions vis-à-vis “imagery dialogue” or a similar technique.  (Young, Klosko, & Weishaar, 2003, p. 123)  If such imagery techniques are unsuccessful or undesired by the client, a psychodynamic conversation between “internal parts of oneself” can add clarity to the persistent inability of the client to delay gratification.  (Ingram, 2012, p. 292)  Such explorations are likely to be time consuming, comparatively speaking, and should not be explored with patients who are bound by strict EAP requirements or managed care restrictions on the type and length of treatment.  Comorbid developmental disabilities and cognitive deficits may preclude this existential exploration.  I employ the exploration of existential issues of origin in the interest of increasing treatment motivation, promoting adherence, enhancing the therapeutic milieu, and thwarting subsequent lapses by anchoring cognitive dissonance to a concrete event.

TM represents a behavioral manifestation of a fixed action patterns (FAPs) that is rigid, consistent, and predicable.  FAPs are generally thought to have evolved from our most primal instincts as animals – they are believed to contain fundamental behavioral ‘switches’ that enhance the survivability of the human species.    (Lambert & Kinsley, 2011, p. 232)  The nature of FAPs that leads some researchers to draw parallels to TM is that FAPs appear to be qualitatively “ballistic.”  It’s an “all or nothing” reaction that is comparable to an action potential traveling down the axon of a neuron.  Once they are triggered they are very difficult to suppress and may have a tendency to “kindle” other effects.  (Lambert & Kinsley, 2011, p. 233)

There are some unique considerations when it comes to assessing a new patient with TM.  Because chewing on or ingesting the hair is reported in nearly half of TM cases, the attending clinician should always inquire about oral manipulation and associated gastrointestinal pain associated with a connected hair mass in the stomach or bowel (trichobezoar).  Motivation for change should be assessed and measured because behavioral interventions inherently require a great deal of effort.  Family and social systems should not be ignored since family dynamics can exacerbate symptomatlogy vis-à-vis pressure to change (negative reinforcement), excessive attention (positive reinforcement), or both.  (Kraemer, 1999, p. 299)

What remains to be seen is the role of stress in the process of “triggering” a TM episode.  Some individuals experience an “itch like” sensation as a physical antecedent that remits once the hair is pulled.  This “itch like” sensation is far from universal.  Some clinicians and researchers believe that the abnormal grooming behavior found in TM is “elicited in response to stress” with the necessary but not sufficient condition of “limited options for motoric behavior and tension release.”  (Kraemer, 1999, p. 299)  Although this stress hypothesis may materialize as a tenable hypothesis in some cases, it’s by no means typical.  Most people diagnosed with TM report that the act of pulling typically occurs during affective states of relaxation and distraction.  Most individuals whom suffer from TM do not report clinically significant levels of anxiety as the “trigger” of bouts of hair pulling.  We could attribute this to an absence of insight regarding anxiety related triggers or, perhaps anxiety simply does not play a significant role in the onset and maintenance of hair pulling episodes.  Regardless of the factors that trigger episodes, a comprehensive biopsychosocial assessment that includes environmental stressors (past, present and anticipated) should be explored.

The options for treatment of TM are limited at best.  SSRIs have demonstrated some potential in the treatment of TM, but more research is needed before we can consider SSRIs as a legitimate first-line treatment.  SSRIs are worth a shot as an adjunct treatment in cases of chronic, refractory, or treatment resistant TM.  I would consider recommending a referral to a psychiatrist (not a general practitioner) for a medication review due in part to the favorable risk profile of the most recent round of SSRIs.  Given the high rate of comorbidity with mood and anxiety disorders – if either is anxiety or depression are comorbid, SSRIs will likely be recommended regardless.  Killing two birds with one stone is the order of the day, but be mindful that some medication can interfere with certain treatment techniques like imaginal or in vivo exposure.  (Ledley, Marx, & Heimberg, 2010, p. 141)  Additional research is needed before anxiolytic medications can be recommended in the absence of comorbid anxiety disorders (especially with children).  Hypnosis and hypnotic suggestion in combination with other behavioral interventions may be helpful for some individuals, but I don’t know enough about it at this time to recommend it.  Call me skeptical, or ignorant, but I prefer to save the parlor tricks for the circus…

Habit reversal is no parlor trick.  My goal isn’t to heal the patient; that would create a level of dependence I am not comfortable with… my goal is to teach clients how to heal themselves.  Okay, but how?  The combination of Competing Response Training, Awareness/Mindfulness Training, Relaxation Training, Contingency Management, Cognitive Restructuring, and Generalization Training is the best hope for someone who seeks some relief from TM.  Collectively I will refer to this collection of techniques as Habit Reversal.

Competing Response Training is employed in direct response to hair pulling or in situations where hair pulling might be likely.  In the absence of “internal restraints to impulsive behavior,” artificial circumstances are created by identifying substitute behaviors that are totally incompatible with pulling hair.  (Ingram, 2012, p. 292)  Just like a compulsive gambling addict isn’t in any danger if spends all his money on rent, someone with TM is much less likely to pull hair if they are doing something else with their hands.

Antecedents, or triggers, are sometimes referred to as discriminative stimuli.  (Ingram, 2012, p. 230)  “We sense objects in a certain way because of our application of priori intuitions…”  (Pirsig, 1999, p. 133)  Altering the underlying assumptions entrenched in maladaptive priori intuitions is the core purpose of Awareness and Mindfulness Training.  “There is a lack of constructive self-talk mediating between the trigger event and the behavior. The therapist helps the client build intervening self-messages: Slow down and think it over; think about the consequences.”  (Ingram, 2012, p. 221)  The connection to contingency management should be self evident.  Utilizing a customized self-monitoring record, the patient begins to acquire the necessary insight to “spot” maladaptive self talk.  “Spotting” is not a new or novel concept – it is central component of Abraham Low’s revolutionary self help system Recovery International.  (Abraham Low Self-Help Systems, n.d.)  The customized self-monitoring record should invariably include various data elements such as precursors, length of episode, number of hairs pulled, and a subjective unit of distress representing the level of “urge” or desire to pull hair.  (Kraemer, 1999)  The act of recording behavior (even in the absence of other techniques) is likely to produce significant reductions in TM symptomatlogy.  (Persons, 2008, p. 182-201)  Perhaps more importantly, associated activities, thoughts, and emotions that may be contributing to the urge to pull should be codified.  (Kraemer, 1999, p. 300)  In session, this record can be reviewed and subsequently tied to “high risk circumstances” and “priori intuitions” involving constructs such as anger, frustration, depression, and boredom.

Relaxation training is a critical component if we subscribe to the “kindling” hypothesis explained previously.  Relaxation is intended to reduce the urges that inevitably trigger the habit.  Examples abound, but diaphragmatic breathing, progressive relaxation, and visualization are all techniques that can be employed in isolation or in conjunction with each other.

Contingency Management is inexorably tied to the existential anchor of cognitive dissonance described above.  My emphasis on this element is where my approach might differ from some other clinicians.  “You are free to do whatever you want, but you are responsible for the consequences of everything that you do.”  (Ingram, 2012, p. 270)  This might include the client writing down sources of embarrassment, advantages of controlling the symptomatlogy of TM, etc.  (Kraemer, 1999)  The moment someone with pyromania decides that no fire worth being imprisoned, they will stop starting fires.  The same holds true with someone who acknowledges the consequences of pulling their hair.

How do we define success?  Once habit reversal is successfully accomplished in one setting or situation, the client needs to be taught how to generalize that skill to other contexts.  A hierarchical ranking of anxiety provoking situations can be helpful in this process since self-paced graduated exposure is likely to increase tolerability for the anxious client.  (Ingram, 2012, p. 240)  If skills are acquired, and generalization occurs, we can reasonably expect a significant reduction in TM symptomatlogy.  The challenges are significant, cognitive behavioral therapy is much easier said than done.  High levels of treatment motivation are required for the behavioral elements, and moderate to high levels of insight are exceptionally helpful for the cognitive elements.  In addition, this is an impulse control disorder… impulsivity leads to treatment noncompliance and termination.  The combination of all the above, in addition to the fact that TM is generally acknowledged as one of the more persistent and difficult to treat disorders, prevents me from providing any prognosis other than “this treatment will work as well as the client allows it to work.”


Abraham Low Self-Help Systems. (n.d.). Recovery international terms and definitions. Retrieved August 2, 2012, from http://www.lowselfhelpsystems.org/system/recovery-international-language.asp

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

Frankl, V. E. (1997). Man’s search for meaning (rev. ed.). New York, NY: Pocket Books.

Ingram, B. L. (2012). Clinical case formulations: Matching the integrative treatment plan to the client (2nd ed.). Hoboken, NJ: John Wiley & Sons.

Kraemer, P. A. (1999). The application of habit reversal in treating trichotillomania. Psychotherapy: Theory, Research, Practice, Training, 36(3), 298-304. doi: 10.1037/h0092314

Lambert, K. G., & Kinsley, C. H. (2011). Clinical neuroscience: Psychopathology and the brain (2nd ed.). New York: Oxford University Press.

Ledley, D. R., Marx, B. P., & Heimberg, R. G. (2010). Making cognitive-behavioral therapy work: Clinical process for new practitioners (2nd ed.). New York, NY: Guilford Press.

Persons, J. B. (2008). The case formulation approach to cognitive-behavior therapy. New York, NY: Guilford Press.

Pirsig, R. M. (1999). Zen and the art of motorcycle maintenance: An inquiry into values (25th Anniversary ed.). New York: Quill.

Shiel, W. C., Jr., & Stoppler, M. C. (Eds.). (2008). Webster’s new world medical dictionary (3rd ed.). Hoboken, NJ: Wiley Publishing.

Young, J. E., Klosko, J. S., & Weishaar, M. E. (2003). Schema therapy: A practitioner’s guide. New York: Guilford Press.

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

Substance Abuse: Etiological Considerations

Over the course of the last few decades prevalence of substance abuse has increased on a global scale.  The lifetime prevalence of a substance use disorder in the general population is approximately 24%.  The lifetime prevalence of any mental disorder (excluding substance abuse/dependence) is approximately 22.5%.  (McDowell & Clodfelter Jr., 2001)  Despite the increase, no single etiological path has been identified as a precipitating cause.  “Many interrelated factors influence a person’s decision to use substances.  These include psychological (intrapersonal and interpersonal), biological, environmental, and cultural factors.”  (Netherton, Holmes, & Walker, 1999, p. 245)  This essay will attempt to address some of the more predominant etiologies as related to substance abuse, with the express understanding that no single explanation is solely plausible due to the interactional and interdependent natures of the etiologies themselves.

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Individualized personality traits have been inexorably linked to problem drug behavior.  The “addictive personality” has come to represent individuals whom demonstrate significant levels of neuroticism; disinhibitory tendencies; anti-sociality; novelty seeking; negative affect; low self-esteem; anxiety sensitivity; hopelessness; sensation seeking; and impulsivity.  All of these individualized variables and personality traits can be employed to predict both nature and course of substance use.  (Blaney & Millon, 2009, p. 271, p. 260)  “Drug abusers show deficits in impulsive choice and inhibition, although it is impossible to know whether difference in impulsivity caused or were caused by drug abuse.”  (Perry & Carroll, 2008, p. 19)  Reyno and associates (2006) found that anxiety sensitivity was strongly related to alcohol consumption in certain high risk situations.

Genetically speaking, “having a biological parent who was or is alcoholic increases one’s risk for alcoholism about 2.5 times, regardless of whether one was raised by that parent.”  (Blaney & Millon, 2009, p. 261)  Drug availability, when coupled with permission parental attitudes (up to and including parental drug use), has been shown to facilitate adolescent initiation and use of substances.  (Blaney & Millon, 2009, p. 258)  Parental smoking has been shown to increase risk for substance use in adolescent offspring.  (Keyes, Legrand, Iacono, & McGue, 2008)  As severity of substance abuse in the family increases, the negative consequences on adolescent development increase and are manifested in physical symptoms and negative mood.  (Gance-Cleveland, Mays, & Steffen, 2008)  It has been suggested that removal of the child from the substance abusing household can result in significant gains in child cognitive functioning.  McNichol & Tash (2001) found that children placed in forster care presented with low to average cognitive skills, but that they made disproportionate and significant improvement during placement.  Furthermore, they found that children with prenatal exposure to drugs scored significantly lower at the beginning of the placement, but made significantly more progress than the other children during placement.  This research seems to suggest that prenatal exposure to drugs, while regrettable, is not a “life sentence” for children.

Since adolescents place great value on peer opinions and struggle to fit in, peers contribute to the onset of drug use first by providing access to the substance by contributing to developing attitudes regarding expectancy.  (Blaney & Millon, 2009, p. 258; Netherton et al., 1999, p. 247)  Early expectancies of personal response to drug use have been shown to predict later use.  (Blaney & Millon, 2009, p. 268)  Research suggests that doing things in order to be popular with others is strongly related to feeling pressured by others, and that peer pressure is a far stronger predictor of risk behaviors and potential psychosocial difficulties than popularity.  (Santor, Messervey, & Kusumakar, 2000)

There is considerable evidence that severe trauma (e.g., disaster, assault, combat) greatly increase the risk for drug use and abuse.  (Blaney & Millon, 2009, p. 260)  In an exemplary study, Brave Heart (2003) leveraged the Lacota population to demonstrate that historical trauma (HT) has substance abuse ramifications, deemed to be a historical trauma response (HTR).  HT represents the cumulative emotional and psychological wounding over the lifespan and across generations.  HTR manifests in traumatized populations as depression, self-destructive behavior, suicidal thoughts and gestures, anxiety, low self-esteem, anger, difficulty recognizing and expressing emotions, and substance abuse.  (Brave Heart, 2003)  There is also evidence to the contrary, with research that suggests that among homeless men, trauma experiences are strong indicators of mental health problems, but are not indicators of either physical health or substance abuse problems.  (Kim, Ford, Howard, & Bradford, 2010)

The weight of cultural influences is colossal, as demonstrated by relative conformity of subcultures within a specific society, and by the wide comparative variability between and among cultures and subcultures.  (Blaney & Millon, 2009, p. 255)  For example, “the holocaust experienced by American Indian and Alaska Native (AI/AN) peoples during the past five centuries includes ravaged communities, destroyed families, the brutal murder of hundreds of thousands of AI/AN people, organized attempts to erase rich cultures and beautiful languages, and trans-generational scars that affect AI/ANs to this day.”  The subsequent introduction of alcohol and other substances have resulted in high rates of sexual and physical trauma, high death rates from physical complications of substance abuse, suicide, homicide, depression, grief, poor school performance, and low employment rates.  (Gray & Nye, 2001)

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

Brave Heart, M. Y. (2003, Jan-Mar). The historical trauma response among natives and its relationship with substance abuse: A Lakota illustration. Journal of Psychoactive Drugs, 35(1), 7-13. Retrieved from http://ezproxy.bellevue.edu:80/login?url=http://proquest.umi.com.ezproxy.bellevue.edu/pqdweb?did=338232111&sid=18&Fmt=3&clientId=4683&RQT=309&VName=PQD

Gance-Cleveland, B., Mays, M. Z., & Steffen, A. (2008, Jan). Association of adolescent physical and emotional health with perceived severity of parental substance abuse. Journal for Specialists in Pediatric Nursing, 13(1), 15-25. Retrieved from http://ezproxy.bellevue.edu:80/login?url=http://proquest.umi.com.ezproxy.bellevue.edu/pqdweb?did=1418986821&sid=20&Fmt=3&clientId=4683&RQT=309&VName=PQD

Gray, N., & Nye, P. S. (2001). American indian and alaska native substance abuse: Co-morbidity and cultural issues. American Indian and Alaska Native Mental Health Research (Online), 10(2), 67-84. Retrieved from http://ezproxy.bellevue.edu:80/login?url=http://proquest.umi.com.ezproxy.bellevue.edu/pqdweb?did=1077011111&sid=19&Fmt=3&clientId=4683&RQT=309&VName=PQD

Keyes, M., Legrand, L. N., Iacono, W. G., & McGue, M. (2008, Oct). Parental smoking and adolescent problem behavior: An adoption study of general and specific effects. The American Journal of Psychiatry, 165(10), 1338-1344. Retrieved from http://ezproxy.bellevue.edu:80/login?url=http://proquest.umi.com.ezproxy.bellevue.edu/pqdweb?did=1567487491&sid=7&Fmt=4&clientId=4683&RQT=309&VName=PQD

Kim, M. M., Ford, J. D., Howard, D. L., & Bradford, D. W. (2010, Feb). Assessing trauma, substance abuse, and mental health in a sample of homeless men. Health & Social Work, 35(1), 39-48. Retrieved from http://ezproxy.bellevue.edu:80/login?url=http://proquest.umi.com.ezproxy.bellevue.edu/pqdweb?did=1969768361&sid=18&Fmt=3&clientId=4683&RQT=309&VName=PQD

McDowell, D. M., & Clodfelter Jr., R. C. (2001, Apr). Depression and substance abuse: Considerations of etiology, comorbidity, evaluation, and treatment. Psychiatric Annals, 31(4), 244-251. Retrieved from http://ezproxy.bellevue.edu:80/login?url=http://proquest.umi.com.ezproxy.bellevue.edu/pqdweb?did=71687723&sid=22&Fmt=4&clientId=4683&RQT=309&VName=PQD

McNichol, T., & Tash, C. (2001, Mar/Apr). Parental substance abuse and the development of children in family foster care. Child Welfare, 80(2), 239-256. Retrieved from http://ezproxy.bellevue.edu:80/login?url=http://proquest.umi.com.ezproxy.bellevue.edu/pqdweb?did=70552258&sid=20&Fmt=4&clientId=4683&RQT=309&VName=PQD

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

Perry, J. L., & Carroll, M. E. (2008, Sep). The role of impulsive behavior in drug abuse. Psychopharmacology, 200(1), 1-26. doi: 10.1007/s00213-008-1173-0

Reyno, S. M., Stewart, S. H., Brown, C. G., Horvath, P., & Wiens, J. (2006, Aug). Anxiety sensitivity and situation-specific drinking in women with alcohol problems. Brief Treatment and Crisis Intervention, 6(3), 268-282. doi: 10.1093/brief-treatment/mhl007

Santor, D. A., Messervey, D., & Kusumakar, V. (2000, Apr). Measuring peer pressure, popularity, and conformity in adolescent boys and girls: Predicting school performance, sexual attitudes, and substance abuse. Journal of Youth and Adolescence, 29(2), 163-182. Retrieved from http://ezproxy.bellevue.edu:80/login?url=http://proquest.umi.com.ezproxy.bellevue.edu/pqdweb?did=53959633&sid=17&Fmt=4&clientId=4683&RQT=309&VName=PQD