Friday Factoids: The Dangers of Synthetic Marijuana

 

 

While many states have decriminalized the possession, use, and cultivation of natural Cannabis for either medicinal or recreational purposes, a majority of states continue to follow Federal guidelines with their approach to natural Cannabis and the law.  This seems to be driving the popularity of synthetic marijuana in those states where natural Cannabis is still treated as a controlled substance.  Synthetic marijuana goes by many names such as Spice, K-2, “fake weed”, etc., and the biggest issue seems to be that although it binds to the same CB1 receptor in the brain, it acts as a full agonist, rather than just a partial agonist as in the case of THC. (NIDA, 2015; Walton, 2014)  Binding with a much greater efficiency seems to make it much more difficult for the body to process and metabolize the acting ingredient that gives the high the user is looking for, with the result that the effect is many times more powerful than that produced by THC.

 

While the active ingredients in synthetic marijuana are called “cannabinoids” due to their chemical resemblance to cannabinoids that are found in natural Cannabis, they are much more potent, and unpredictable, in their effects on the user.  Even though they are marketed as a safe and legal alternative, their effects can be so much more powerful that they can become life-threatening. (NIDA, 2015)  The fact that CB1 receptors are in every structure of the brain is a key part of what makes the issue so serious, as are the symptoms experienced during an overdose event.  CB1 receptors in the hippocampus (memory affect), temporal cortex (seizure initiation), prefrontal cortex (psychosis), and brain stem (cardiac, respiratory, and gastrointestinal affect) all contribute to the myriad of symptoms that occur during an overdose on synthetic marijuana having a lasting effect, while the effects of an “overdose” from THC in natural Cannabis tend to dissipate fairly quickly.   “Clinically, they just don’t look like people who smoke marijuana,” says Lewis Nelson, MD, at NYU’s Department of Emergency Medicine, Division of Medical Toxicology. “Pot users are usually interactive, mellow, funny. Everyone once in a while we see a bad trip with natural marijuana. But it goes away quickly. With people using synthetic, they look like people who are using amphetamines: they’re angry, sweaty, agitated.” (Walton, 2014)

 

Newly available and unregulated psychoactive compounds, including synthetic marijuana, belong to a drug group called “new psychoactive substances”, or NPS.  NPS are problematic in that as soon as a compound is added to the group for regulation, another is quickly made available, and the cycle continues.  Fundamental changes in drug policy, drug law, public perception/attitudes, and approaches to treatment will be necessary before the depth of the problem can be ascertained, and a suitable method for treatment and recovery developed and implemented.

 

References

NIDA (2015). Synthetic Cannabinoids. Retrieved November 24, 2016, from          https://www.drugabuse.gov/publications/drugfacts/synthetic-cannabinoids

 

Walton, A. G. (2014, August 28). Why synthetic marijuana is more toxic to the brain than pot. Forbes. Retrieved November 24, 2016, from http://www.forbes.com/sites/alicegwalton/2014/08/28/6-reasons-synthetic-marijuana-spice-k2-is-so-toxic-to-the-brain/#5e615f9249eb

 

Teresa King
Pennyroyal Doctoral Intern

 

 

 

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Article Review: Early Identification of and Treatment for Borderline Personality Disorder

 

Sharp and Fonagy (2015) offer a review of the phenomenology, prevalence, etiology, clinical problems, and interventions for adolescents with BPD. Borderline personality disorder (BPD) is said to capture the core of personality pathology (Sharp & Fonagy, 2015).  The symptoms of BPD usually manifest in adolescence (Chanen & Kaess, 2012, as cited in Sharp & Fogay, 2015); yet many clinicians are hesitant to diagnose personality pathology in children due to the presumed normal emotional liability during this developmental period.  Interesting though, this period of turmoil has received only limited support in the research (Cicchetti & Rogosch, 2002, as cited in Sharp & Fonagy, 2015).  Furthermore, a poor prognosis is often associated with individuals that have problems throughout adolescence, and as cited by Paris (2015), pathological symptoms greater than one year should not be dismissed and may likely be associated with BPD.   Regardless, the symptoms of BPD compared to typical adolescence are often more severe, pervasive, long-standing, and reflected in both internalizing and externalizing disorders.

 

Sharp and Fonagy (2015) report that studies for early detection of BPD in adolescence have shown that “chronic feelings of emptiness and inappropriate, intense anger” are considered the “most stable symptoms,” whereas identity disturbance, affective instability, and intense anger have the “greatest predictive power for development of BPD” (p. 1268). These characteristics are said to be consistent across age groups.  Additionally, for boys, paranoid ideation, and in girls, identity disturbance, have shown to be discriminating symptoms of BPD in adolescents.  Persistent self-harm behaviors are known to distinguish BPD from other disorders. Similar to adults with BPD, risk factors in adolescents with BPD are general impulsivity, risky behaviors, difficulty dealing with stress, and negative affect.  Impairment in social and academic functioning is also common.

 

As cited in Sharp and Fonagy (2015), Chanen & Kaess (2012) describe BPD as a developmental disorder. Research has indicated a mean age of onset at 18, with a standard deviation of 5- 6 years. Adolescence is said to be a critical period for the development of BPD due to the social demands (e.g., establishing stable friends, remaining close to family).  Furthermore, the social and emotional development in adolescence is associated with functional and structural brain changes.  While, BPD symptoms appear in adolescence, they are known to peak in early adulthood, with a decline in impulsive symptoms over time. Affective symptoms are more likely to persist.  Sharp and Fonagy (2015) have shown evidence for heterotypic developmental course, meaning that there is “coherence in the underlying organization or meaning of behaviors over time” (p. 1271).

 

Regarding comorbidity, BPD in adolescence is highly associated with internalizing and externalizing disorders. Sharp and Fonagy (2015) cite that around 70% of adolescents with BPD have comorbid mood disorders, 67% have anxiety disorders, and 60% have externalizing disorders.  Thus, the authors argue that BPD is a confluence of both externalizing and internalizing disorders, and is not a female expression of antisocial personality disorder.  Additionally, there is evidence that constitutional factors (i.e., temperament) and environmental factors have a role in BPD etiology.

 

Yet, it is also difficult to distinguish BPD from other clinical disorders. For identification of BPD, several measures have shown clinical utility (See Sharp & Fonagy, 2015, for a more comprehensive review).  Clinical assessment along with an objective measures is thought to be best clinical practice for precision in diagnosis. Regarding intervention, there is not a wealth of information available.  Programs such as Helping Young People Early (HYPE) and Dutch Emotion Regulation Training (ERT) are early intervention efforts for BPD.  They are based on cognitive analytic therapy and cognitive-behavioral elements and skills training, respectively. Cognitive-analytic therapy integrates psychoanalytic object relations theory and cognitive psychology and has demonstrated effectiveness and rapid recovery.  Mentalization-based treatment for adolescents has similar components to cognitive analytic therapy and has shown effectiveness by “improved mentalizing and reduced attachment avoidance” (p. 1281).  Dialectical behavior therapy (DBT) has also been adapted for treatment of BPD in adolescents. DBT targets emotional dysregulation, distress tolerance, and interpersonal difficulties.  Transference-focused psychotherapy is grounded in object relations theory and has been adapted for adolescents, but has not underwent RCT to assess its effectiveness.

 

Sharp and Fonagy (2015) conclude that successful interventions should contain extensive efforts to maintain engagement in treatment, have an evidence-based model of developmental pathology, and have an active therapist role, with a focus on validation and modeling of empathy, as well as the development of a strong attachment. Additionally, there should be a facilitation of trust and belief that something can be learned in therapy.  Treatment should focus on emotional processing and the connection between action and feelings, have structure to promote activity, proactivity, and self-agency, as well as be manualized, with supervision for deviations from the manual.   There should be a commitment to the approach in treatment between both the therapist and client.

 

Evidence-based treatments for BPD have common treatment characteristics (Bateman, Gunderson, & Mulder, 2015). They are structured (manual directed) and they encourage clients to control themselves (agency). Therapists help connect feelings and actions and are active, responsive, and validating. They also discuss cases with others (i.e., supervision and/or consultation).

 

Overall, there is a delicate balance in assessing BPD in adolescents compared to recognizing the potential for emotional liability during this developmental period. Yet, understanding the clinical picture, as well as the distinguishing pervasive features of BPD, will help differentiate it from either normal turmoil and/or other disorders.  Finally understanding treatment options can help clinicians gain confidence in identifying and providing subsequent treatment for adolescents with BPD.

 

 

References
Bateman, A. W., Gunderson, J., & Mulder, R. (2015). Treatment of personality disorder. The Lancet, 385, 735-743.

 

Sharp, C., & Fonagy, P. (2015). Practitioner review: Borderline personality disorder in adolescence – recent conceptualization, intervention and implications for clinical practice. The Journal of Child Psychology and Psychiatry, 56(12), 1266-1288.

 

Dannie S. Harris, MA
WKPIC Doctoral Intern

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Friday Factoids Catch-Up: Memory, the Real McCoy?

Memories develop starting at birth and continue to develop throughout the life cycle as we age. The brain remembers by association, strengthening neural connections through repetition (“use it or lose it principle”) (Willingham, 2007).  Research has shown that, although memory is often considered to be a singular ability in and of its self, it is actually a process of at least three inter-related functions: encoding, storage, and retrieval.  The first step to creating a memory is encoding, a crucial step involving the conversion of the perceived item of interest into a construct that can be stored, and then later recalled through retrieval processes, from either short- or long-term memory at some point in the future.  The process of storage occurs between encoding and retrieval, when the memory exists only as a possibility for remembrance. (Arbuthnott, et al., 2001)  Memories are, in a sense, us; they chart our life details.  There are several types of memory processes that deal with differing aspects of how memories are formed.  Short- and long-term memory are the two most common forms people tend to recognize, but there are others, such as associative, elaborative, and autobiographical, that come into play.

 

The study of memory in early childhood is centered around development as it relates to the cognitive self, and a particularly important aspect of early memory centers on childhood amnesia, specifically the fading ability to recall events that occur during early childhood.  Although children may remember events prior to ages 3-4, those memories also tend to fade with time as we age. (Goleman, 1993; Willingham, 2007)  Most adults remember very little prior to age 3 or 4, since this is the age at which our cognitive memory first begins to truly function.  Prior to that age, the cognitive and language skills that are necessary for the processing of external events are not yet developed fully enough to allow this processing to occur, which is essential to the storing of events as memories. (Kihlstrom, 1994)   As aging occurs and cognitive and language skills improve, new knowledge is also being acquired, as well as the establishment of a sense of self.  During the aging process in children, major developments occur in the expansion of memory, perhaps with less processing being required to enable long-term storage.  According to a study published by the New York Times, memories that are autobiographical in nature begin when children learn about themselves and their early years through their parents. (Goleman, 1993)  Over time, as we navigate through the aging process, some memories fade, some are lost, and others are distorted as a natural result of the progression of time and aging.

 

Traditionally, faulty memory has often been associated with either the elderly or those who have suffered a traumatic brain injury, but the ongoing research that has occurred over the last couple of decades tells a different story.  There are certainly instances where people’s memories are obviously faulty, and often this is due to such factors as dementia, Alzheimer’s, concussion, or some other such factor exerting an influence on the brain’s ability to manifest an effective and accurate recall of prior events.  However, the distortion of memories, from the changing of details to the outright planting of false memories, has become an area of real interest and research due to the fact that the accuracy of memories can have much greater implications than just those that directly affect the individual in their quest for resolution of a particular psychological issue.  The likelihood of false memories, in conjunction with the fact that there is still much about the mind that we do not yet understand, make it a dangerous prospect for the therapist to suggest too much.  The evidence exists that people can be led to believe that they have experienced events in their lives that are patently untrue, or at the least, highly unlikely to ever have occurred. (Loftus, 2004)  One particular study showed that even a brief exposure to a false memory of a childhood event serves to boost their confidence that the event actually occurred. (Sharman, Powell, 2012; Garry, et al., 1996; Sharman, et al., 2005)  This was attributed to a phenomenon called imagination inflation.  The study participants were asked to rate their confidence levels on a range of childhood events that occurred prior to 10 years of age.  They were then asked two weeks later to imagine events that they indicated did not occur, and rate their confidence of the event occurrences a second time.  The confidence ratings of the events that did not happen were rated higher in confidence of their occurrence the second time around than the events that actually occurred, which were used as control events.

 

There are several techniques that have been used to attempt to determine the validity of false memories through “planting” of events that were false and never actually occurred, including hypnosis, guided imagery/imagination, dream interpretation, and picture cuing, and all proved successful at inducing false memories in research study participants in statistically significant numbers.  One of the earliest studies that specifically attempted to plant false memories for an entire event used a technique that came to be called the “lost in the mall” technique, which utilized stories about events that happened to participants as related by their parents, and included one wholly false story that was verified as having never occurred, usually lost in a mall, or, alternatively, spilling punch on a bride’s parents at a wedding or having a serious accident.  Based on the results of a series of interviews that utilized memory recovery techniques, 20%-25% of the study participants confirmed a memory of these false events even though they never actually occurred. It was also determined that these false memories exhibited high levels of detail and emotional responses in those that developed them. (Laney, Loftus, 2013)

 

Scoboria et al. (2004) posited a model for autobiographical beliefs and memories that, based on their research, indicated the memories, thoughts, and beliefs concerning plausibility of an event are of a “nested” format.  For a person to remember an event, they necessarily have to believe that it occurred, meaning that the memory itself is nested within confidence.  It also needs to be personally plausible, so confidence is nested within personal plausibility.  The event has to be plausible generally, so personal plausibility is nested within general plausibility. While the research shows that false beliefs and memories will increase due to repeated exposures, brief exposure to false events does not increase confidence or implant false memories. (Sharman, Powell, 2012)

 

The research on false memory has firmly established that people can be led to believe that they have experienced events that have never actually occurred.  Not only can these false memories be wrapped in exquisite detail and sensory associations of recollection, conveying all the characteristics of being the genuine article, but they can be extremely far-fetched in their subject matter such that they are extremely unlikely to be true, yet people will still insist on having experienced them.  The consequences of false memories can have far-reaching, and often unintended, consequences.  There are documented cases of people having spent decades of their lives in prison based on testimony that relied on what turned out to be an instance of false memory, and were only exonerated because of DNA evidence.  While this is an extreme example of the consequences of reliance on memory to be infallible, it clearly illustrates that memory is fluid, malleable, and completely vulnerable to improper influence and subsequent dubious recall.  As a Clinical Psychology student, I previously held to the belief that a memory which is uncovered during therapy is more than likely to be true.  After all, why would a profession devoted to helping people end up doing harm by implanting false memories?  In my opinion, it is not intentional harm on the part of the therapist but, rather, a misuse of techniques which can, and sometimes does, lead to disastrous consequences.  Knowing that memories can become twisted and confused should be reason enough to become skeptical of any method of regression treatment or therapy.

 

References
Arbuthnott, K. D., Arbuthnott, D. W., Rossiter, L. (2001). “Guided imagery and memory: implications for Psychotherapists”. Journal of Counseling Psychology Vol. 48, No. 2, 123-132. Retrieved from Ebscohost, November 17, 2016.

 

Durbin, P. G., Ph.D. Beware false memories in regression hypnotherapy. Retrieved November 16, 2016, from http://alchemyinstitute.com/false-memory.html

 

Goleman, D. (1993, April 6). Studying the secrets of childhood memory. The New York Times. Retrieved from http://www.nytimes.com

 

Kihlstrom, J. E. (1994). “Hypnosis, delayed recall and the principles of memory”. The International Journal of Clinical & Experimental Hypnosis. 1994, Vol. XLII, No. 4, 337-344. Retrieved from Ebscohost, November 15, 2016.

 

Laney, C., Loftus, E. F. (2013). “Recent advances in false memory research”. South African Journal of Psychology 43(2) 137-146. Retrieved from Ebscohost, November 17, 2016.

 

Loftus, Elizabeth F. (2004). ”Memories of things unseen”. Current Directions in Psychological Science. 2004. Vol. 13, No. 4, 145-147. Retrieved from Ebscohost, November 15, 2016.

 

Sharman, S. J., Powell, M. B. (2012). “Do cognitive interview instructions contribute to false beliefs and       memories?”. Journal of Investigative Psychology and Offender Profiling. 10: 114-124 (2013).

 

Willingham, D. T. (2007). Cognition: The thinking animal (3rd ed.). Upper Saddle River, New Jersey: Pearson.

 

Teresa King
Pennyroyal Doctoral Intern

 

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Friday Factoids Catch-Up: Heroin and Fentanyl–A Match Made in Hell

 

Heroin use has always been a serious issue where drug abuse is concerned, but in the last few years it has become even more deadly due to fentanyl being added to give it more “kick”.  Dealers have begun including fentanyl to improve the potency of their product; however, the equipment they use to measure out amounts for trafficking don’t usually measure at levels fine enough to ensure that the amount of fentanyl that has been added stays below overdose levels.  To add to the danger, fentanyl sold at the street level is usually manufactured in “underground” labs which produce a far less pure product than pharmaceutical-grade labs, which can cause unpredictable effects on the body (Bond, 2016).

 

Heroin is classified by the DEA (Drug Enforcement Agency) as a Schedule I drug, while fentanyl is classified as a Schedule II drug.  Both are opioid derivatives; however, while heroin is synthesized directly from morphine, fentanyl is a synthetic opioid analgesic, with a potency of 50x to 100x that of morphine (NIDA, 1969, 2011, 2014).  While both have a high potential for abuse, there is a wide gulf between the two drugs with regard to the amount required to induce an overdose.  An average sized adult male would take around 30g of heroin to produce an overdose situation, roughly an amount similar to 7 packets of sugar.  By contrast, it would only take around 3g of fentanyl (little more than a ½ packet) to produce an overdose (Bond, 2016).

 

Fentanyl-laced heroin quickly reached crisis levels as it began to gain popularity among users.  In March of 2015, the (DEA) issued a nationwide alert in response to a surge in overdose deaths from heroin laced with fentanyl (19 March 2015).  While heroin has been recognized as having a high potential for abuse since the mid-1900s, fentanyl wasn’t added as a Schedule II substance until 2015, after recognizing that a variant, acetyl fentanyl, was being manufactured by Mexican cartels and smuggled stateside for distribution (10 September 2015).  The problem has surged so much that “the National Forensic Laboratory Information System, which collects data from state and local police labs, reported 3,344 fentanyl submissions in 2014, up from 942 in 2013” (Leger, 2015).

 

Due to the resurgence in popularity of heroin among IV drug users in recent years, it would seem that fentanyl-laced heroin and the associated use risks and health issues with regard to overdosing are going to be an issue for some time to come.

 

References
Bond, A. (2016, September 29). Why fentanyl is deadlier than heroin, in a single photo. Retrieved November 10, 2016, from https://www.statnews.com/2016/09/29/fentanyl-heroin-photo-fatal-doses/

 

DEA Issues Alert on Fentanyl-Laced Heroin as Overdose Deaths Surge Nationwide – Partnership for Drug-Free Kids. (2015, March 19). Retrieved November 10, 2016, from http://www.drugfree.org/news-service/dea-issues-alert-fentanyl-laced-heroin-overdose-deaths-surge-nationwide/

 

Fentanyl-Laced Heroin Worsening Overdose Crisis, Officials Say – Partnership for Drug-Free Kids. (2015, September 10). Retrieved November 10, 2016, from http://www.drugfree.org/news-service/fentanyl-laced-heroin-worsening-overdose-crisis-officials-say/

 

Leger, D. L. (2015, March 18). DEA: Deaths from fentanyl-laced heroin surging. Retrieved November 10, 2016, from http://www.usatoday.com/story/news/2015/03/18/surge-in-overdose-deaths-from-fentanyl/24957967/

 

NIDA (2011). Fentanyl. Retrieved November 10, 2016, from https://www.drugabuse.gov/drugs-abuse/fentanyl

 

NIDA (1969, rev. October 2014). Heroin. Retrieved November 10, 2016, from https://www.drugabuse.gov/publications/drugfacts/heroin

 

Teresa King
Pennyroyal Doctoral Intern

 

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Friday Factoids Catch-Up: New Treatments For Tic Disorders Associated With Tourette’s

 

Tics, which are characterized by sudden, repetitive, non-rhythmic body movements and/or vocalizations associated with tic disorders and Tourette’s syndrome, are involuntary movements that may involve the hands, shoulder shrugging, eye blinking, etc.  In many cases, these tics do not get in the way of living a relatively normal life and consequently little if any treatment is required.  At the other end of the spectrum, the tics may be so severe that they require treatment with medication and behavioral therapy, especially if they are causing pain/injury, are interfering with a normal daily routine in one’s education, job performance, or social life, or are responsible for inducing excessive stress. Prior to the treatment of the presenting tics, the presence of other movement-related disorders like chorea, dystonia, as well as the movements displayed by those with autism (stereotypic movement disorder), or those movements manifested as compulsions of OCD or seizure-related activity, must be ruled out to ensure the patient receives the proper care and treatment that is best suited to address his or her needs.

 

There are various methods for treating the tics that are so often associated with Tourette’s syndrome, including medication, behavioral therapies, and habit reversal.  While medication is most often the go-to panacea for controlling tics, the medications themselves may carry side effects that are as bad, or even worse, than the condition that they may be used to treat.  Behavioral therapies can also be effective as well by teaching those with Tourette’s to manage their tics.  While these can be effective in reducing the number, severity, and impact of the tic behaviors, it is important to realize that behavioral therapy is not a cure, and that although effective it does not mean that tics are merely psychological in their nature.  While these treatment methods are effective in aiding the treatment of, and helping to manage, the tic symptoms of Tourette’s syndrome, it is important to note that they are varied in their efficacy, are not one-size-fits-all in their nature, and in the case of medication, may produce unwanted side effects ranging from mild to debilitating in and of themselves.

 

One of the most promising methods recently developed for the treatment of tics associated with Tourette’s is the Comprehensive Behavioral Intervention for Tics, or CBIT.  This new, evidence-based therapy includes the use of education, teaching relaxation techniques, and habit reversal in a combination that is shown to be effective in reducing symptoms of tics and their related impairments, and seems to work equally well for both children and adults. CBIT involves those with Tourette’s working with a therapist to gain a greater understanding of their particular type of tic and learning to recognize situations that worsen tic symptoms.  When possible, a change in environment may be initiated, and using habit reversal, a new behavior is modeled so that when the urge to tic occurs, the new behavior is substituted.  This method helps to lessen tic occurrences through substituting the new behavior for the tic through repetition, under the guidance of an experienced therapist.

 

Over the last few years, the number of health professionals that have come to know and appreciate the benefits and effectiveness of CBIT has increased; however, there are still relatively few therapists that have the specific training in these methods of treatment targeted specifically at tic disorders and Tourette’s, and work is currently being done by The Tourette Association of America and the Centers for Disease Control and Prevention to provide education for more health professionals with the training necessary to incorporate and apply this method in their treatment approach to managing the symptoms of Tourette’s and other tic disorders.

 

References

  1. Cook CR, Blacher J. Evidence-based psychosocial treatments for tic disorders. Clin Psychol: Science and Practice. 2007;14(3):252–67.
  2. Piacentini J, Woods DW, Scahill L, Wilhelm S, Peterson AL, Chang S. Behavior therapy for children with Tourette disorder: a randomized controlled trial. JAMA. 2010;303(19):1929–37.
  3. Harris, Elana, MD, PhD. Children with tic disorders: How to match treatment with symptoms. Current Psychiatry. 2010 March; 9(3):29-36
  4. Qasaymeh MM, Mink JW. New treatments for tic disorders. Current Treat Options Neurol. 2006 Nov;8(6):465-473

 

Teresa King
Pennyroyal Intern

 

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Interviewing at WKPIC

 

WKPIC’s staff has begun the process of reviewing applications for the 2017-2018 intern year. We’re excited!

 

Soon, letters will go out, and we hope that we will meet many of you who applied to our program. If you accept, you’re probably wondering what our interview will be like.

 

For basic info, check out our Interview Information section. Note the “wear comfortable shoes” bit, if you plan to participate in the tour of the 165+ year-old Western State Hospital.

 

No, you really don’t have to study or prepare. We trust you have done that in graduate school. Ours is not a cut-throat or competitive process. We want you to see if you could be happy here and learn from us, and we want to see if we can teach you, and if you would enjoy being in our area and having the experiences we can offer. Seriously, you can wear comfortable shoes. If you Match with us, you’ll definitely want to wear them to work, too!

 

Just brings yourselves, and what you’ve learned. That’s enough. We look forward to meeting you!

 

 

Susan R. Redmond-Vaught, Ph.D.
Director of Psychology, Western State Hospital
Director, WKPIC

 

 

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Friday Factoids: Disruptive Mood Dysregulation Disorder

Disruptive mood dysregulation disorder (DMDD) is a newer diagnosis in childhood that is depicted by extreme irritability, anger, and frequent outbursts (National Institute of Mental Health [NIMH], 2016).  Irritability is a clinical symptom of both bipolar disorder and DMDD (Wiggins et al., 2016).  Comparatively, irritability in DMDD is “severe and relatively invariant over time,” yet irritability experienced with bipolar disorder may occur while a child is euthymic and may increase during manic or depressive episodes (Wiggins et al., 2016, p. 722). Thus the inclusion of DMDD in part allows for appropriate diagnosis for children with “severe, nonepisodic irritability” that is distinct from bipolar disorder (Wiggins et al., 2016, p. 722).

 

With DMDD being a new diagnosis, treatment is often based on other disorders with shared symptomatology (e.g., attention-deficit/hyperactivity disorder, anxiety disorders, oppositional defiant disorder, and major depression; NIMH, 2016). Cognitive-behavior therapy (CBT), parent training, and computer-based training are recommended psychological interventions (NIMH, 2016) for DMDD, where as medications may also be considered.  For instance, stimulants may help address irritability, antidepressants may mitigate irritability and mood problems, and atypical antipsychotics could be used to alleviate severe outbursts with physical aggression (NIMH, 2016).

 

The potential for adverse effects with some treatments limit their use in children, resulting in the necessity to explore noninvasive means for treatment (Wiggins et al., 2016).  For instance, the use of a video game to reduce the misinterpretation of ambiguous faces in children with irritability has shown to help reduce anger-based reactions found in DMDD.  The literature has shown that children with DMDD and bipolar disorder tend to rate neutral faces as angry (Wiggins et al., 2016). Research conducted by Wiggins et al. (2016) has demonstrated that a computer game helped to change the tendency to misinterpret ambiguous faces as angry in irritable children.  After training, children were more likely to rate ambiguous faces as happy (Wiggins et al., 2016).  Such an intervention may appear superficial, however this research has demonstrated that brain activation patterns when labeling emotional faces differs between DMDD and bipolar disorder (Wiggins et al., 2016).  Specifically, amygdala activation related to irritability differed between children with DMDD and bipolar disorder; and temporo-occipital regions of the brain had “associations between irritability and activation in response to ambiguous angry faces” (Wiggins et al., 2016, p. 728).

 

Thus, differing brain activation patterns helped distinguish the clinical presentation of DMDD versus bipolar disorder (Wiggins et al., 2016).  As a result, the authors conclude that though irritability is a common symptom of both DMDD and bipolar disorder, they are in fact distinct disorders and given the different neural correlates, treatments may also be different (Wiggins et al., 2016).

 

References
National Institute on Drug Abuse (NIDA). (2016). Disruptive Mood Dysregulation Disorder. Retrieved from http://www.nimh.nih.gov/health/topics/disruptive-mood-dysregulation-disorder-dmdd/disruptive-mood-dysregulation-disorder.shtml

 

Wiggins, J. L., Brotman, M. A., Adleman, N. E., Kin, K., Oakes, A. H. Reynolds, R. C.,…Leibenluft, E. (2016).  Neural correlates of irritability in disruptive mood dysregulation and bipolar disorders.  American Journal of Psychiatry, 173, 722-730.

 

 

Dannie S. Harris, MA
WKPIC Doctoral Intern

 

 

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Massive WOOHOOs and CONGRATULATIONS!

WKPIC would like to extend giant happy dances to the following brilliant folks:

 

First, former intern and current post-doc Crystal Bray successfully defended her dissertation!

 

20160825-DSC_2098

 

 

 

 

 

 

20160901-DSC_2315Seconnd, current intern Dannie Harris passed the EPPP–at the doctoral level!

 

 

 

 

 

 

 

 

 

 

 

 

YOU LADIES ROCK!!!

 

Susan Redmond-Vaught, Ph.D.
Director, WKPIC

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Friday Factoids: Methamphetamine Psychosis

 

As reported by the National Institute on Drug Abuse (NIDA; 2013) methamphetamine use continues to be a significant problem, with over 12 million people or 4.7 percent of the population having tried methamphetamine at least one time.  According to NIDA (2013), methamphetamine use can cause memory loss, aggression, psychotic behavior, damage to one’s cardiovascular system, malnutrition, and dental problems.

 

Chronic use may cause an individual to have difficulty feeling pleasure outside of use, as well as anxiety, confusion, insomnia, mood disturbance, and violent behavior. Psychotic features experienced include paranoia, delusions, and visual, auditory, and tactile hallucinations.  Stress has also been related to spontaneous methamphetamine psychosis in individuals who have abused methamphetamine in the past (NIDA, 2013).  With acute methamphetamine intoxication individuals may experience hallucinations (auditory, visual, tactile), persecutory, influence, and control delusions, as well as are prone to violence (Zarrabi, Khalkhali, Hamidi, Ahmadi, & Zavarmousavi, 2016).

 

Even after intoxication passes, psychosis may occur over a prolonged period of time (Zarrabi et al., 2016).  Acute psychosis usually has a maximum period of four to five days (Zarrabi et al., 2016); yet, a differing course of psychosis has been documented in the literature. For instance, three clinical groups for stimulant-induced psychosis have been identified:  the first group is characterized by transient psychosis, where the duration of symptoms is limited to four or five days and may be associated with withdrawal; with the second group, psychosis is typically resolved in less than one month; and in the third group, psychosis may last several months or years (Zarrabi et al., 2016).  It has been estimated that between 5-10% of individuals with methamphetamine-induce psychosis may not fully recover (as cited in Zarrabi et al., 2016).

 

Risk factors for methamphetamine-induced psychosis are duration, frequency, and amount of use, history of sexual abuse, family history, other substance use, and co-occurring personality and mood disorders (Grant et al., 2012). Of note, substance intoxication is differentiated from a substance/medication-induced psychotic disorder if reality testing for altered perceptions remains intact (American Psychiatric Association, 2013).

 

Zarrabi, Khalkhali, Hamidi, Ahmadi, and Zavarmousavi (2016) indicate there are no structured treatment guidelines for methamphetamine-induced psychosis.  In their study, risperidone and olazapine were most frequently used, as well as benzodiazepines to reduce restlessness. Antipsychotics were reportedly preferred due to better control of violent behaviors.  Another study indicated that quetiapine could also be used as an antipsychotic treatment with comparable effects to haloperidol (Verachai et al., 2014). Electroconvulsive therapy (ECT) has been used to control severe aggression and violent behaviors, as well as thoughts of suicide and homicide in methamphetamine-induced psychosis (Zarrabi et al., 2016).  Results indicated that after six to nine sessions of ECT, symptoms began to disappear.  Though limited by constraints of a case study, Grelotti, Kanayama, and Harrison (2010) again demonstrated the positive effects of ECT on methamphetamine-induced psychosis.

 

Overall, the most common symptoms with methamphetamine-induced psychosis are paranoid delusions and auditory hallucinations, and such symptoms may prove resistant or refractory to antipsychotic medications (Grelotti, Kanayama, & Pope, 2010).  As indicated in the literature, clinicians faced with refractory cases of methamphetamine-induced psychosis may consider ECT as a treatment option.

 

 

References
American Psychiatric Association. (2013). Diagnostic and statistical manual of mental disorders (5th ed.). Washington, DC: Author.

 

Gerlotti, D., Kanayama, G., & Pope, H. G. (2010). Remission of persistent methamphetamine-induced psyhcosis after electroconvulsive therapy: Presentation of a case and review of literature. The American Journal of Psychiatry, 167(1), 17-23.

 

Grant, K. M., LeVan, T. D., Wells, S. M., Li, M., Stoltenberg, S. F., Gendelman, H. E.,…BEvins, R. A. (2012). Methamphetamine-associated psychosis. Journal of Neuroimmune Pharmacology, 7(1), 113-139.

 

National Institute on Drug Abuse (NIDA). (2013).  Methamphetamine. Retrieved from https://www.drugabuse.gov/publications/research-reports/methamphetamine

 

Verachai, V., Rukngan, W., Chaswanakrasaesin, K., Nilaban, S., Suwanmajo, S., Thanateerabunjong, R.,…Kalayasiri, R. (2014). Treatment of methamphetamine-induced psychosis: a double-blind randomized controlled trial comparing haloperidol and quetiapine. Psychopharmacology, 231(16), 3099-3108.

 

Zarrabi, H., Khalkhali, M., Hamidi, A., Ahmadi, R., & Zavarmousavi, M. (2016). Clinical features, course and treatment of methpahetamine-induce psychosis in psychiatric inpatients. BMC Psychiatry, 16, 1-8.

 

Dannie S. Harris, MA
WKPIC Doctoral Intern

 

 

 

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Friday Factoids: Motivational Interviewing as a Clinical Option for Generalized Anxiety Disorder

Cognitive-behavior therapy (CBT) has shown to be efficacious for treating anxiety, yet some clients “either fail to respond, respond only partially, or relapse at follow-up” (Westra, Constantino, & Antony, 2016, p. 768).  As reported by Hunot, Churchhill, Teixeria, and Silva de Lima (2007; as cited in Westra et al., 2016), only 46% of clients with Generalized Anxiety Disorder (GAD) demonstrated significant improvement after therapy.  One factor that may contribute to poorer outcomes is ambivalence.  Ambivalence in anxiety is holding positive beliefs about worry and being reluctant to change or let go of the worry (Westra & Arkowitz, 2010; as cited in Westra et al., 2016).  Additionally, therapeutic directness or demands related to change might be met with resistance (Westra et al., 2016).  Thus, additional components that work with ambivalence may boost treatment outcomes by working through resistance, all while remaining anchored in CBT.

 

Motivational Interviewing (MI) is a treatment with a focus on ambivalence (Miller & Rollnick, 2002).  Here the therapist is not the advocate for change, rather therapists assist clients to be their own advocate for change (Westra et al., 2016).   With specific strategies, MI helps reduce resistance and “increases intrinsic motivation” for change (Westra et al., 2016, p. 769).  In their study, Westra, Constantino, and Antony  (2016) investigated the effects of integrating MI and CBT for severe GAD.  In the study, one group received 15 weekly session of CBT alone (CBT-alone) and another group had 4 sessions of MI followed by 11 sessions of CBT integrated with MI (MI-CBT).  Initially, there were no posttreatment differences between groups; yet, at the 6- and 12-month follow-up, several group differences emerged. The MI-CBT group reported a continued improvement on self-reported worry and general distress after treatment ended.  MI-CBT clients also had significantly higher rates of recovery and clinically significant change (five times as likely to not meet diagnostic criteria for GAD).   Westra et al. (2016) indicated that similar sleeper-type effects are often reported with MI use in treating other disorders.

 

So, why did clients continue to improve after treatment?  Westra et al. (2016) indicated that the opportunity to explore ambivalence and becoming more committed to change might help clients not respond to worry, thus reducing relapse rates.  Additionally, the authors suggested that MI techniques fostered the development of personal agency, which may have led to the client’s belief that they are capable of change, resulting in internalization of this belief.  By “rolling with resistance” and viewing the “client-as-expert” helped to “promote internal attributions for progress” (Westra et al., 2016, p. 777).  With this model, the efficacy of CBT treatment for GAD is maintained, yet by integrating MI where clients can openly explore resistance may help clients become more receptive to traditional CBT techniques.

 

 

References
Miller, W. R., & Rollnick, S. (2002). Motivational interviewing: Preparing people for change (2nd ed.). New York, NY: Guilford Press.

 

Westra, H. A., Constantino, M. J., & Antony, M. M. (2016). Integrating motivational interviewing with cognitive-behavioral therapy for severe generalized anxiety disorder: An allegiance-controlled randomized clinical trial. Journal of Consulting and Clinical Psychology, 84(9), 768-782.

 

Dannie S. Harris, MA
WKPIC Doctoral Intern

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