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

 

 

 

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

 

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

 

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

 

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