Tag Archives: mood disorders

Comorbidity of Personality Disorders and Substance Abuse Disorders


There are an estimated 44%-60% of people who have been diagnosed with substance use disorder who also qualify with symptoms pertaining to a minimum of one personality disorder.  Personality disorders include antisocial personality disorder, avoidant personality disorder, borderline personality disorder, obsessive-compulsive personality disorder and schizoid personality disorder.  Each of these personality disorders have their own symptoms and characteristics, but generally speaking any personality disorder affects people cognitively, which is the way people look at themselves and the world in general, affectation, which is the level of reaction to any one thing, as well as interpersonal functioning and the level of impulse control a person has.  A person can suffer from mood swings, anger outbursts or alcohol or substance abuse.

A person who is diagnosed with a personality can also have a second diagnosis of substance abuse disorder.  This is defined as:

 

 

 

 

 

 

“A complex behavioral disorder characterized by preoccupation with obtaining                     alcohol or other drugs (AOD) and a narrowing of the behavioral repertoire towards          excessive consumption and loss of control over consumption.  It is usually also           accompanied by the development of tolerance and withdrawal and impairment in social and occupational functioning.” (www.cdad.com)

A patient must present with certain symptoms in order to be diagnosed with substance abuse disorder, the symptoms are the behaviors someone would expect from anyone with a substance abuse disorder, but they are not usually so obvious to the patient.  The symptoms include a tolerance of the substance or a need for more and more of the substance because it is harder and harder to feel the effects of the substance, withdrawal when the substance is not used on a regular basis, the substance being used for longer than the patient thought they would be using it for, the patient having a continuous desire to control the habit of using the substance but is unsuccessful at doing so, the patient spending a lot of time trying to find or use the substance or coming off of the substance, the patient giving up activities in multiple areas of their life in order to have the opportunity to use the substance, and continuing use even though it is causing health problems to the patient.

The diagnosis of substance abuse disorder comes about when the patient has become increasingly more tolerant and dependent on their chosen substance.  After the body becomes accustomed to having that substance available on a regular basis, the body will react with withdrawal symptoms which can include headaches, insomnia, and hallucinations and could include aggression, paranoia or promiscuous behavior.  Most patients live in denial when it comes to admitting they have a problem and have to get past that denial in order for any type of treatment to help them.

When a patient is diagnosed with both of these disorders at the same time it is considered co-morbidity of substance abuse disorder and personality disorder.  A little over half of patients who have been seen for substance use disorder have also been diagnosed with a minimum of one personality disorder.

There are two treatments that have been established for this type of co-morbidity.  One is called dual focus schema therapy and it combines different life skills such as functional analysis and coping skills training.  This treatment involves 24 sessions and plans for two stages.  The first of these stages is called early relapse prevention and helps the patient develop life skills that will aid the patient in dealing with temptation or actual relapses.  The second stage is called schema change therapy and coping skills work, this stage helps the patient make the changes more concrete and helps the patient develop methods for coping once abstinence is achieved.

Looking at co-morbidity of substance abuse and personality disorders has shown how difficult it can be to diagnose a patient with multiple disorders, especially when it involves substance abuse because substance use is so common and it seems there really is a fine line between the two.

References

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

(Retrieved 2009, October 28). Co-occurring Mental Health and Substance Abuse Disorders. www.dshs.wa.gov.com.   http://www.dshs.wa.gov/pdf/hrsa/mh/cobestpract.pdf

(Retrieved 2009, October 28). Axis II Personality Disorders and Mental Retardation.  Psyweb.com.   http://psyweb.com/Mdisord/DSM_IV/jsp/Axis_II.jsp

(Retrieved 2009, October 28). Frequently Asked Questions (FAQ’s) About Substance Abuse Disorders.  www.cdad.org  http://www.cdad.org/FAQSubstanceUseDisorders.htm

Trichotillomania


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.”

References

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.

Sleep/Wake Disorders


Historically, sleep disorders have long been commonly recognized within the context of other psychopathological conditions, but they have been frequently minimized or otherwise ignored as distinct entities or stand-alone psychopathological situations.  Research supporting the current DSM-IV-TR classification system is extremely limited, despite the common sense approach (in my opinion) of grouping sleep disorders primarily on the basis of underlying constellation of symptoms.

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Primary insomnia is the hallmark diagnosis in this category.  It is “characterized by chronic difficulty initiating and/or maintaining sleep or persistent poor-quality sleep.”  (Blaney & Millon, 2009, p. 508)  Individually commonly suffer from mild anxiety, mood disturbances, concentration/memory dysfunction, somatic concerns, and general malaise… but these conditions are generally viewed as symptoms rather than causes.  Insomnia prevalence increases with age, in contrast with sleep onset difficulties are more common in young adults.  It has also been suggested that, generally speak, women are more susceptible than men.  Societal prevalence is between 1% and 2%.  (Blaney & Millon, 2009, p. 508)

I was intrigued by the statement that “the majority of insomnia sufferers tend to overestimate the time it takes them to fall asleep and to underestimate the time they actually sleep to some degree.”  (Blaney & Millon, 2009, p. 510)  This might give some basis to a cognitive-behavioral approach if we can reset those expectations.  A stated by the text, the main problem is that most clinicians don’t have access to the raw data to confirm or refute this subjective complaint.  My question… is it out of the realm of possibility for us to send a client home with a measurement device so we can accumulate that data?

Narcolepsy is characterized by recurrent, irresistible day time sleep episodes.  The “classic tetrad” indicative of narcolepsy includes excessive daytime sleepiness and unintended sleep episodes during situations where most persons could stay awake, abrupt and reversible decrease or loss of muscle tome (without loss of consciousness, also known as cataplexy), and/or awakening from nocturnal or diurnal sleep with an inability to move (sleep paralysis), and finally vivid images and dreams that are evoked just as sleep develops (hypnagogic hallucinations).  (Blaney & Millon, 2009, p. 510)  Narcolepsy generally first appears during adolescence or young adulthood, and is believed to be genetically predisposed.   Life events may precipitate the onsite of this disorder… although it is not clear to me whether they are causes or effects?

Breathing related sleep disorders encompass what is widely known as sleep apnea.  This condition manifests as loud snorting, pauses in breathing, gasping for breath during sleep, headaches on wake, and automatic behaviors during wakefulness or excessive daytime sleepiness.  The headaches on waking part turned my head because I get that all the time… although I haven’t really noticed any other signs or symptoms.  Odd…

Circadian Rhythm Sleep Disorders (CRSDs) represent a mismatch between natural sleep/wake rhythms and the schedule imposed by occupational or social demands.  (Blaney & Millon, 2009, p. 512)  Individuals typically report insomnia at certain times of the day (generally when they want to be sleeping) and excessive sleepiness at other times (generally when they should be awake).

Parasomnias encompass nightmares, night terrors, and sleepwalking.  Nightmare disorder is characterized by repeated awakenings by disturbing dreams.  Sleepwalking and Night Terrors both occur early in the sleep period and appear to represent incomplete arousals from the deepest states of sleep (states 3-4), known as slow wave sleep (SWS).  All of the above are more prevalent in children when compared with adults, and more common in males than in females. (I honestly would have expected it to be more common in females?)

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Reference

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

Is There More Than One Kind Of Depression?


Dysthymic Disorder and Major Depressive Disorder are actually two different versions of depression.  Dysthymic Disorder is noted for chronic depression.

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The definition for Dysthymic Disorder is that it is a “mood disorder with chronic depressive symptoms that are present most of the day, more days than not, for a period of at least two years.”  (Minddisorders.com).  The symptoms are usually present for years and can include low self esteem, decreased motivation, change in sleeping patterns and change in appetite patterns.  Causes of this type of depression are things like a person’s upbringing.  If a person is brought up in a home where abuse is prevalent an adult can suffer from depression for their entire life.  Treatment for this type of depression is generally psychotherapy but sometimes is combined with antidepressants.

Similarly Major Depressive Disorder is the next level of depression and is defined as, “a condition characterized by a long lasting depressed mood or marked loss of interest or pleasure in all or nearly all activities” (Minddisorder.com).   This form of depression has an intense impact on a person’s life.  It usually comes about when a person suffers a traumatic event, but this does not always happen.  Symptoms can include a disturbed mood throughout most of the day, a change in the sleep pattern, a change in the appetite pattern, a loss of interest in things that are considered pleasurable, but then go further to include problems when trying to concentrate or think in depth, psychomotor retardation or agitation and thoughts of suicide.  If this form of depression is left untreated it can last longer than four months and recurrence is eminent.  Treatments for Major Depressive Disorder include psychotherapy or talk therapy, electroconvulsive therapy or ECT and antidepressant medications or a combination of these treatments.

Nearly everything about these two disorders are similar, the main difference is that major depressive disorder is an extension of Dysthymic Disorder in that symptoms and moods are more severe therefore treatments need to be more involved and more inclusive.

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References:

Netherton, S.D., Holmes, D., Walker, C.E., Child and Adolescent Psychological Disorders

Blaney, P.H., Millon, T., Oxford Textbook of Psychopathology.

Depression (Major Depressive Disorder) http://psychcentral.com/disorders/sx22.htm

Dysthymic Disorder. minddisorder.com.  http://www.minddisorders.com/Del-Fi/Dysthymic-disorder.html

Dissociative Identity Disorder. Psychnet-uk.com. http://www.psychnet-uk.com/dsm_iv/dissociative_identity_disorder.htm

Major Depressive Disorder. minddisorder.com. http://www.minddisorders.com/Kau-Nu/Major-depressive-disorder.html

Eating Disorders


“Eating disorders (EDs) are polysymptomatic syndromes, defined by maladaptive attitudes and behaviors around eating, weight, and body image.”  (Blaney & Millon, 2009, p. 431)  The primary disorders in this category are anorexia nervosa (AN), bulimia nervosa (BN), and eating disorders no otherwise specified (EDNOS).  Examples of EDNOS might include “AN-like” with preoccupations with thinness, normal-weight people purging food without binging or simply binging without purging (Binge Eating Disorder, or BED).  (Blaney & Millon, 2009, p. 432)

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Epidemiological data suggests that EDs occur more often in women than in men (by a factor of roughly 10); although there is some evidence indicating that the gender gap is closing.  Although AN/BN tend to be most prevalent in late adolescence and early adulthood, BED defies the stereotype by manifesting in an older age group (typically around 40 years of age).  There is also little linkage to socioeconomic status, despite the common belief that Eds are disorders of the affluent.  (Blaney & Millon, 2009, p. 433)  This totally astounds me… how can people who are already undernourished give up what sustenance they are offered?

EDs frequently co-occur with mood, anxiety, substance-abuse, personality, and other psychiatric disorders.  There are so many comorbid mood disorders noted in individuals with EDs that it is easier to exclude mood disorder (singular) that is unrelated… bi-polar disorders.  Personally, I believe the single mood disorder that is currently excluded should be considered.  “The disorders are believe to depend on similar family/developmental determinants (e.g., attachment problems or trauma), and both have been thought to have similar neurobiological substrates.”  (Blaney & Millon, 2009, p. 434)  Social phobias and OCD were among the most prevalent anxiety related comorbid disorders.  Since anxiety disorders often precede ED onset, it has been suggested that an anxious or obsessive-compulsive attitude predisposes an individual to ED development.  (Blaney & Millon, 2009, p. 435)

Not only are PTSD and substance abuse disorders often comorbid with EDs, but they are often comorbid with each other.  “Substance abusers in an eating-disordered population show significantly more Social Phobia, Panic Disorder, and Personality Disorders.  In addition, comorbid substance abuse was found to predict elevations in Major Depression, Anxiety Disorders, Cluster B personality disorders, as well as greater impulsivity and perfectionism.”  (Blaney & Millon, 2009, p. 435)

Finally, personality disorders are frequently present in individuals whom suffer from EDs.  Restrictive type EDs seem to be associated with Anxious-Fearful PD diagnosis (anxiousness, orderliness, introversion, preference for sameness and control).  Binge-purge types have a pronounced affinity for the dramatic-erratic PDs including attention/sensation seeking, extroversion, mood lability, and proneness to excitability or impulsivity.  (Blaney & Millon, 2009, p. 435)

EDs are assumed to be multiply determined by complex interactions including constitutional factors, psychological/developmental processes, social factors, and secondary effects in the biological, psychological and social spheres of maladaptive eating practices themselves.  (Blaney & Millon, 2009, p. 443)  All of the above features generally manfest in eating-specific cognitions related to bodily appearance and appetite regulation, body image or weight considerations, and social values that heighten concerns with all of the above.  As a result, it is currently conceived that EDs represent a “tightly woven” expression of causes and symptoms that have an interrelationship between and among each other.

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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