Tag Archives: anxiolytics

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.

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