Tag Archives: impulsivity

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.

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.

Substance Abuse: Etiological Considerations


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

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

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

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

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

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

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References

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

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

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

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

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

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

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

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

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

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

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

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

ADHD


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With the increased prevalence of ADHD in the Western world, there is an immediate and pressing need to justify and explain the underlying cause of explosive growth in the ADHD population.  This justification comes with high stakes, since critics of the pharmaceutical industry and psychiatry in general have implicated greed on the part of North American mental health providers.

At stake is ADHD’s identity as a bona fide mental disorder (as opposed to a social construction).  When initial reports of ADHD prevalence emerged, higher prevalence in North American than European samples was remarked upon. This observation spawned a 10-year debate, exemplified by articles with titles such as “Is Childhood Hyperactivity the Product of Western Culture?” and, more recently, “ADHD Is Best Understood as a Cultural Construct?”  Having an explanation for inconsistencies in the cross-national prevalence of ADHD is important because such inconsistencies fuel assertions that ADHD is a fraud propagated by the “profit-dependent pharmaceutical industry and a high-status profession [psychiatry] looking for new roles.”  (Moffitt & Melchior, 2007)

Later, in the same article, it is suggested that prevalence in North America is elevated primarily because of differences in the definition of ADHD.  Specifically, the DSM-IV-TR is more lenient in its definition of ADHD when compared to the ICD-10.

The ICD-10 strictly requires that a child must show symptoms in all three dimensions (inattention, hyperactivity, and impulsivity) and must meet all criteria at home and at school. The ICD-10 also excludes children with co-occurring disorders. DSM-IV is more lenient. It is possible to diagnose a child who shows symptoms in only one dimension (inattention). Some impairing symptoms – but not all- must be shown at home and at school. DSM-IV allows diagnosing ADHD alongside co-occurring disorders.  (Moffitt & Melchior, 2007)

Although differences in clinical definition can have an impact over space (geography), can they also have an impact over time?  Leon Eisenberg, M.D. would assert that the continued refinement of the definition has contributed to a broader interpretation of what constitutes ADHD.  Hyperkinetic reaction of childhood appeared as a category in DSM II in 1968.  It was not, however, until DSM III (1980) that attention-deficit/hyperactivity disorder (ADHD) entered the official lexicon.  (Eisenberg, 2007)  The end result is a shift from diagnosing the presenting features of ADHD as symptoms of other classified disorders, to a new and entirely separate diagnosis.  And so, ADHD was “staking a claim” to the prominent clinical features it encompassed, thus differentiating itself as a clinically valid diagnosis and not a sub-type of an underlying behavior disorder.  ADHD has morphed from a relatively un-common condition 40 years ago to one whose current prevalence is estimated to be just under 8% of U.S. children 4–17 years of age.  (Eisenberg, 2007, p. 283)

Societal expectations and parental influences continue to play a significant role in the search for the etiological roots of all pathologies, including ADHD.  We as a culture have a long history of implicating parental inadequacies in child psychopathology.  The continued search for biological causes serves to reinforce our convictions that we are indeed good parents.

In many public school jurisdictions, the diagnosis led to additional services for such children because of the implication that their problems were organic or endogenous, as opposed to psychological or psychogenic. For this very reason, parents welcomed it. Furthermore, the term proved they were not responsible for their child’s problems (no small victory at a time when parent blaming was widespread in child psychiatry and education).   (Eisenberg, 2007)

Parental pressures, when taken in conjunction with recent advances in brain imaging and the relative effectiveness of pharmacological interventions, have contributed to a “consensus that neurochemical imbalances play a central role in the etiology of ADHD.”    (Netherton, Holmes, & Walker, 1999, p. 103)  This biological model is further supported by evidence that, in a limited number of cases, “it can be acquired after birth, via head injury, neurological illness, elevated lead levels, and other biological complications.”  (Netherton et al., 1999, p. 103)

Recent technological advances in brain imaging have served as catalysts to futher underscore attempts to localize the etiology of ADHD in the brain.  In a recent morphological study of ADHD, researchers incorporated the novel measures of local shape, complexity, volume, and thickness and align structural MRI with other imaging modalities, such as the delineation of white matter tracts by diffusion tensor imaging and maps of brain activation generated by functional MRI.  The study’s most striking finding was marked volume loss in the region of the pulvinar nuclei bilaterally in the ADHD group.  (Shaw, 2010, p. 363)

Despite mounting evidence that ADHD can be attributed to biological factors, there remains a contingent of dedicated psychological practitioners who would assert that familial deficiencies do serve to exacerbate the biological predispositions of ADHD.  (Netherton et al., 1999, p. 104)  If we aim to address the etiological causes of ADHD, we have to do so with a conscious widening of our world view.  We need to take the entirety of geographic, historical, societal, technological, and pharmacological information into consideration before passing judgment on the etiology of Attention-Deficit/Hyperactivity Disorder (ADHD).  Although it is not within the scope of this article to drill down on any one specific aspect, it should serve as a baseline by which we can all being to explore the complexities of the etiology of ADHD.

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References

Eisenberg, L. (2007, Jun). Commentary with a historical perspective by a child psychiatrist: When “ADHD” was the “brain-damaged dhild”. Journal of Child and Adolescent Psychopharmacology, 17(3), 279–283. doi: 10.1089/cap.2006.0139

Moffitt, T. E., & Melchior, M. (2007, Jun). Why does the worldwide prevalence of childhood attention deficit hyperactivity disorder matter?. The American Journal of Psychiatry, 164(6), 856-859. Retrieved from http://ezproxy.bellevue.edu:80/login?url=http://proquest.umi.com.ezproxy.bellevue.edu/pqdweb?did=1288245351&sid=3&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.

Shaw, P. (2010, April). The shape of things to come in attention deficit hyperactivity disorder. The American Journal of Psychiatry, 167(4), 363-366. Retrieved from http://ezproxy.bellevue.edu:80/login?url=http://proquest.umi.com.ezproxy.bellevue.edu/pqdweb?did=1996846691&sid=2&Fmt=3&clientId=4683&RQT=309&VName=PQD