Tag Archives: personality disorder

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

Dysthymic Disorder


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

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

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

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

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

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

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

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

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

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

References

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

Personality Disorders


As is often the case, the primary take away from this chapter is the value of early intervention.  “The hope is that such interventions in the lives of children and adolescents can, at least to some extent, prevent the later development of the more serious personality disorders of adult life, especially the antisocial disorders.”  (Netherton, Holmes, & Walker, 1999, p. 477)  The issue at hand is that it is difficult to translate the benefits of early intervention into public policy/services for those at risk… especially in cases where there is no definitive causal relationship between the childhood manifestations of the disorder and the adult versions.

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Clinicians are currently wary of diagnosing personality disorders in children due to the assumption that they are, by definition, enduring.  This may suggest that we as clinicians are suitably unwilling to deliver the gloomy prognosis due to the fact that it may in fact become a self-fulfilling prophecy.  However, evidence us abound that suggests that “early diagnosis improves the chances of appropriate treatment and education and results in a prognosis that is less gloomy than it might appear.”  (Netherton et al., 1999, p. 478)  I don’t understand what the issue is, I would call a spade a spade do our best to rectify the situation, but that’s just me.

The text suggests that “equivalence between personality disorders of childhood and those of adult life must rely on a similarity of essential symptoms and signs,” just as they do with with other disorders.  (Netherton et al., 1999, p. 479)  I found it ironic that Zeitlin found personality disorder symptoms to have greater continuity over time than diagnoses… doesn’t it seem like we are systematically mis-diagnosing children in an effort not to label them?  I am starting to get that impression.

Temperament is generally regarded as one of the “constitutional” building blocks of personality, and therefore is also loosely associated with personality disorders in young adulthood.  I was particularly interested in the nine dimensions of temperament that were deemed by Chess & Thomas’s New York Longitudinal Study (1984).  Among those dimensions were activity level, approach/withdrawal to novelty, positive or negative mood, threshold of sensitivity to stimuli, intensity of reactions, rhythmicity of biological function (what does this mean?), adaptability to novel situations and people (why double load novelty?), distractability, and persistence (how do you measure this, exactly?).  Please refer to the in-line comments, as they really speak to my questions on the how and the why regarding this particular study.

I found the following suggestion to be of value in the future when suggesting how can successfully modify or change their parenting methods: “Children are best socialized when parents use inductive, that is, reasoning methods but do so with an emotional charge.”  (Netherton et al., 1999, p. 486)  This really reminded me of the “teach around a behavior” cognitive method that we are taught as direct support professionals whom support individuals with developmental disabilities.  Matter of fact, it mirrors the kind of guidance I provide every day.

I was surprised that we as a society are not doing more with regard to home visitation programs for vulnerable mothers.  “Numerous experimental programs have shown that specially trained and supported home visitors can help poor, unmarried, young mothers to achieve better health for their babies, better educational and work status for themselves, and more sensitive and less punitive care for their children, with the result that the children have better early language skills, make better school progress, and have fewer later behavior problems, including antisocial interaction.”  (Netherton et al., 1999, p. 488)  Is anyone aware of any comparable programs like this in the Omaha area?  I think this would be a great community resource, something we should investigate?

Although it is not entirely clear at the present time whether this is still valid (since the text was written in 1999), there is a consistent theme in the NHW book.  “This disorder has been adequately explored in the adult population but it’s application to children has not been fully explored.”  I am beside myself with the number of disorders that we could substitute in the above sentence for “this disorder.”  It’s literally all of them.  The other thing I notices, and maybe this is more of a personal observation than anything… but if there is any single population that clinicians choose NOT to work with, its kids.  Why is that?

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Reference

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

Personality and Its Disorders


The most contemporary definition of the word personality delves “beneath” surface impressions “and turns the spotlight on the inner, less revealed and hidden psychological qualities of the individual.”  (Blaney & Millon, 2009, p. 551)  It would suffice to say that our current understanding of personality has changed tremendously since its Greek inception, and will likely continue to change as the field of psychology continues to develop.

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I really liked Millon’s acknowledgement that “perspectives come and go, wax and wane, even though scholars maintain that human behavior is explained by psychological laws that are pristine and eternal.”  (Blaney & Millon, 2009, p. 552)  I think the statement underscores how little we really know about the complexity of the human mind, further exemplifying how much more there is to learn and know about the constituent parts of personality and their interrelationships with each other.

I had not considered the limitations of the categorical model of personality.  It would appear that Millon is correct, “there are potentially as many types as there are individuals to be typed.”  (Blaney & Millon, 2009, p. 554)  This statement seems to lend credibility to the dimensional model where personality characteristics are expressed on a continuous gradient.  The dimensional model differs from the categorical in the respect that there are no residual cases, meaning everyone regardless of situation can be accounted for.  However, even the dimensional model cannot escape the weight of the categorical model, primarily because the dimensions themselves need to be anchored to a theory… a theory the will invariably choose dimensions to cover relevant categories or personality traits.

Prototypal models seem to be the latest trend because they acknowledge the synthesis between the categorical and the dimensional models.  “To be used successfully, however, the prototype requires (1) a willingness on the part of the professional to move flexibly between categorical and dimensional paradigms as utility requires, regarding each as what it essentially is- a clinical point of departure and nothing more and (2) valid criteria sets.”  (Blaney & Millon, 2009, p. 557)

On the whole, I was most impressed with the mathematical methods of data analysis.  I am suitably impressed with the factor models and their lack of a sharp division between normality and pathology.  Gray areas in which it is clearly a matter of opinion whether someone is “normal” or not seems to be the rule, not the exception.  This is especially true when we take multiculturalism into consideration.  I am particularly impressed with the fact that “factor models are explicitly mathematical and provide some assurance that they fuzzy domain of the social sciences can be quantified like the harder sciences of chemistry and physics.”  (Blaney & Millon, 2009, p. 558)  The limitation of the factor models is that the data chosen for inclusion must be supplied by the scientist… and the inclusion (or exclusion) of specific types of data introduces bias into an otherwise unbiased mathematical process.  I, too, am tempted by the feeling that something “real” is being uncovered by this factor model process… although I question the long term utility if there is no way to prove or disprove them as Millon suggests on page 561.

No conversation or essay on personality would be complete without discussing cognitive theories of personality and Aaron Beck.  I have to admit, the suggestion that cognitive schemas shape experience, and experience shapes behavior… is attractive.  The idea that schemas “introduce a persistent and systematic bias into the individual’s processing machinery” gives those of us that intend to practice psychoanalysis hope that maladaptive behaviors can be changed or modified… and it’s that hope that I am most attracted to.  (Blaney & Millon, 2009, p. 572)

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Reference

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

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.

Comorbidity: Substance Abuse Disorders (SUDs)


Comorbid, or comorbidity, is literally defined as “recurring together.”  (Shiel, Jr. & Stoppler, 2008, p. 94)  For our purposes, comorbidity will refer to cases where two or more psychiatric conditions coexist, and where one of the conditions is a substance abuse disorder (SUD).  “There are 11 groups of substances specifically discussed in the DSM-IV: alcohol; amphetamines and related sympathomimetics; caffeine; cannabis; cocaine; hallucinogens; inhalants; nicotine; opiates; phencyclidine and related drugs (PCP); and sedatives, hypnotics, and anxiolytics.”  (Colman, 2009, p. 741)  Any one of the above substances, or combination of the above substances, can contribute to and be related this discussion of comorbidity with SUDs.

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Although this list is by no means exhaustive, “long-term substance use is related to psychiatric conditions such as suicide and depression, affective disorders, eating disorders (ED), and personality disorders (PD).”  (Netherton, Holmes, & Walker, 1999, p. 248)  Increased risk of mood disorders has been documented across all substance categories and across all mood related diagnoses.  (Blaney & Millon, 2009, p. 287)  Substance-Related Disorders are commonly comorbid with many mental disorders, including Conduct Disorder in adolescents; Antisocial and Borderline Personality Disorders, Schizophrenia, Bipolar Disorder.  (American Psychiatric Association, Diagnostic and statistical manual of mental disorders, 2000, p. 204)   Schneier et al. (2010) also concluded that alcohol use disorders and social anxiety disorder (SAD) is a prevalent dual diagnosis, associated with substantial rates of additional co-morbidity.

ADHD represents a risk factor for substance abuse.  ADHD patients with a high degree of nicotine consumption may be consuming large quantities as a form of self-medication.  Nicotine and alcohol, when combined, pose a markedly greater risk for the development of other addictions.  (Ohlmeier et al., 2007, p. 542)  There is “high comorbidity between heavy drinking and heavy smoking.”  (Blaney & Millon, 2009, p. 266)  These admissions seem to support the premise that alcohol and nicotine continue to serve as “gateway drugs” for people whom suffer from ADHD.

“In terms of clinical presentation, a concurrent Personality Disorder (PD) diagnosis is associated with an earlier age of onset of alcohol-related problems, increased addiction severity, more secondary drug use, more psychological distress, and greater impairment in social functioning.  As for course in addiction treatment, a concurrent PD diagnosis has been associated with premature discontinuation of treatment, earlier relapse, poorer treatment response, and worse long-term outcome.”  (Zikos, Gill, & Charney, 2010, p. 66)  Cluster B (Antisocial, Borderline, Histrionic, and Narcissistic) Personality Disorders (PDs) appear to be particularly prevalent, perhaps because the link between substance dependency and antisocial behavior can be found genetically.  (Blaney & Millon, 2009, p. 263)

“Among individuals with schizophrenia, between 40% and 50% also meet criteria for one or more substance use disorders.”  (Blaney & Millon, 2009, p. 288)  Comorbid substance use complicates adherence to sometimes complex schizophrenia treatment regimens.  Poor adherence to treatment results in worsening of schizophrenia symptoms, relapse, worsening of overall condition, increased utilization of health care facilities, re-hospitalization, reduced quality of life, social alienation, increased substance abuse, unemployment, violence, high rates of victimization, incarceration, and death.  (Hardeman, Harding, & Narasimhan, 2010, p. 405-406)  The compounding effect of substance abuse on the quality of life for individuals with schizophrenia can’t be understated.  Substance abuse is particularly common and also worsens the course of schizophrenia.  (Buckley, Miller, Lehrer, & Castle, 2009, p. 396)

Differential diagnosis and treatment can sometimes be a troublesome proposition.  Comorbidity complicates the diagnosis, treatment, and clinical course of Substance Abuse Disorders (SUDs).  (Blaney & Millon, 2009, p. 287)  “If symptoms precede the onset of substance use or persist during extended periods of abstinence from the substance, it is likely that the symptoms are not substance induced.”  (4th ed., text rev.; DSM-IV-TR; American Psychiatric Association, 2000, p. 210)  Carbaugh and Sias (2010) concluded that successful outcomes can be increased through proper diagnosis and early intervention, at least in the case of comorbid Bulimia Nervosa and substance abuse.  Prevention of substance use disorders can help alleviate or decrease much impairment in psychiatric patients in particular.  (Powers, 2007, p. 357)  Furthermore, a review of treatments for patients with severe mental illness and comorbid substance use disorders concluded that mental health treatment combined with substance abuse treatment is more effective than treatment occurring alone for either disorder or occurring concurrently without articulation between treatments.  (Hoblyn, Balt, Woodard, & Brooks, 2009, p. 54)

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References

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

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

Buckley, P. F., Miller, B. J., Lehrer, D. S., & Castle, D. J. (2009, Mar). Psychiatric comorbidities and schizophrenia. Schizophrenia Bulletin, 35(2), 383-402. doi: 10.1093/schbul/sbn135

Carbaugh, R. J., & Sias, S. M. (2010, Apr). Comorbidity of bulimia nervosa and substance abuse: Etiologies, treatment issues, and treatment approaches. Journal of Mental Health Counseling, 32(2), 125-138. Retrieved from http://ezproxy.bellevue.edu:80/login?url=http://proquest.umi.com.ezproxy.bellevue.edu/pqdweb?did=2026599321&sid=2&Fmt=3&clientId=4683&RQT=309&VName=PQD

Colman, A. M. (2009). Oxford dictionary of psychology (3rd ed.). Oxford, NY: Oxford University Press.

Hardeman, S. M., Harding, R. K., & Narasimhan, M. (2010, Apr). Simplifying adherence in schizophrenia. Psychiatric Services, 61(4), 405-408. Retrieved from http://ezproxy.bellevue.edu:80/login?url=http://proquest.umi.com.ezproxy.bellevue.edu/pqdweb?did=2006767471&sid=3&Fmt=3&clientId=4683&RQT=309&VName=PQD

Hoblyn, J. C., Balt, S. L., Woodard, S. A., & Brooks, J. O. (2009, Jan). Substance use disorders as risk factors for psychiatric hospitalization in bipolar disorder. Psychiatric Services, 60(1), 50-55. Retrieved from http://ezproxy.bellevue.edu:80/login?url=http://proquest.umi.com.ezproxy.bellevue.edu/pqdweb?did=1654365811&sid=6&Fmt=3&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.

Ohlmeier, M. D., Peters, K., Kordon, A., Seifert, J., Wildt, B. T., Weise, B., … Schneider, U. (2007, Aug). Nicotine and alcohol dependence in patients with comorbid attention-deficit/hyperactivity disorder (ADHD). Alcohol and Alcoholism : International Journal of the Medical Council on Alcoholism, 42(6), 539-543. doi: 10.1093/alcalc/agm069

Powers, R. A. (2007, May). Alcohol and drug abuse prevention. Psychiatric Annals, 37(5), 349-358. Retrieved from http://ezproxy.bellevue.edu:80/login?url=http://proquest.umi.com.ezproxy.bellevue.edu/pqdweb?did=1275282831&sid=5&Fmt=3&clientId=4683&RQT=309&VName=PQD

Schneier, F. R., Foose, T. E., Hasin, D. S., & Heimberg, R. G. (2010, Jun). Social anxiety disorder and alcohol use disorder co-morbidity in the National Epidemiologic Survey on Alcohol and Related Conditions. Psychological Medicine, 40(6), 977-988. doi: 10.1017/S0033291709991231

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

Zikos, E., Gill, K. J., & Charney, D. A. (2010, Feb). Personality disorders among alcoholic outpatients: Prevalence and course in treatment. Canadian Journal of Psychiatry, 55(2), 65-73. Retrieved from http://ezproxy.bellevue.edu:80/login?url=http://proquest.umi.com.ezproxy.bellevue.edu/pqdweb?did=1986429431&sid=1&Fmt=3&clientId=4683&RQT=309&VName=PQD

Substance Abuse Grab-bag


On the subject of terminology, I thought it was rather odd that NHW made the statement that “the phrases ‘chemical dependency, addiction, and habit’ are still in use but less so than ‘substance abuse, use, or misuse;’” and then later citing “changes in the thinking in the field of chemical dependency.”  (Netherton, Holmes, & Walker, 1999, p. 241)  Perhaps that’s an indication that old habits are not easily broken.

The text again acknowledges that “the use of substances to cope, alter moods, or reach another level of consciousness has been an acceptable form of communication and expression for most of humankind.”  (Netherton et al., 1999, p. 242)  This statement alone suffices to encapsulate the difficulty of the task at hand.  Quite simply, there is a significant portion of the population that doesn’t recognize there is a problem.  “Substance use has become less stigmatizing among adolescents and is fiend less as a problem among their peers.”  (Netherton et al., 1999, p. 242)  Check and checkmate.

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I have trouble “getting behind” the disease model for substance use and abuse.  To my eyes, substance use appears more like a behavior than a disease.  In my experience, alcoholism is typically a secondary symptom stemming from another underlying physical cause or emotional disorder.  The degree and the prevalence of comorbidity would appear to support this position.  While I don’t disagree that the behavior needs to be recognized and addressed, I believe that addressing the underlying emotional disorder is critical to the long term success of these individuals.

Other substance-related models include the developmental model, the gateway model, problem behavior theory, cognitive models, the social learning model, and finally… the addictive behavior model.  I believe that social learning weighs heavily on the adolescent mind, and I wholly support the statement that “adolescents place great value on peer opinions and struggle to fit in.”  (Netherton et al., 1999, p. 247)  This serves as an entry point for the behavior, which then sets the tone for the addictive behavior model, which subsequently suggests that behaviors are a series of bad habits that have been over-conditioned to the extent that they become detrimental.

“Long-term substance use is related to psychiatric conditions such as suicide and depression, affective disorders, eating disorders, and personality disorders.”  (Netherton et al., 1999, p. 248)  This is only the second time in this class where we have listed entire categories as being comorbid with a specific disorder.  Is this the first mention of dual diagnosis in this class, or have we previously addressed that?

Addressing treatment, the treatment options range from pretreatment services, through outpatient treatment, to intensive inpatient treatment and/or residential care.  “Some of the fundamental treatment services include structure, dual diagnosis capabilities, pharmacological interventions, arrangements with medical care, role modeling, client participation in the therapeutic milieu, family groups, individual and group therapy, school/vocational training, recreational programs, relapse prevention, and 12-step support.”  (Netherton et al., 1999, p. 255)

Of the specific treatment approaches and interventions, I most identified with the harm reduction approach.  “Harm reduction, harm minimization, and risk reduction are terms that describe methods based on the assumption that habits can be placed along a continuum ranging from lowest risk to highest amount of risk.”  (Netherton et al., 1999, p. 258)  The object, or the goal, is the transition the individual along the continuum to a behavior that is less harmful.  It seems to be more progressive in its approach, with its intent to “normalize rather than marginalize substance abusers.”  I don’t think this is necessarily the ideal treatment for all people who suffer from alcohol-related problems, but I think it would be a less invasive and potentially better received option than some of the more stringent measures.

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Reference

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