Archive for the 'psychiaty' Category

Proposed DSM-5 Cultural Formulation guidelines: A report from the SSPC

Last week saw the annual meeting of the Society for the Study of Psychiatry and Culture (SSPC) in New York City. SSPC’s mission includes “furthering research, clinical care and education in cultural aspects of mental health and illness,” and although somewhat small includes some of the most prominent thinkers in the world of psychiatry and culture. These are the people who go beyond simplistic cultural diatheses (e.g., individualism versus collectivism), incorporating multidimensional frameworks that include political factors as well as ethnicity and race.

Among the livelier presentations was a report by Roberto Lewis-Fernandez, Neil Aggarwal (both at Columbia), Laurence Kirmayer (McGill), and Renato Alarcón (Mayo Clinic and Universidad Peruana Cayetano Heredia) on much needed updates to the Cultural Formulation guidelines in the upcoming DSM-5. The DSM — Diagnostic and Statistical Manual — is the American Psychiatric Association’s official guidebook to human psychopathology, and the current version, DSM-IV-TR, is largely accepted as the last word on mental health problems in psychiatry, psychology, social work, and related disciplines. Cultural Formulation guidelines are suggestions for how clinicians should conceptualize the role of culture in patients’ mental health problems. The guidelines appeared first in the pages of the DSM-IV (1994), but, along with a short and messy list of “Culture-Bound Syndromes,” were placed in the back of the book where few practitioners would ever find them.

This time around there is a widespread effort to place the Cultural Formulation front and center in the DSM-5. Drs. Lewis-Fernandez and Aggarwal reported on a tool designed to make cultural formulation quicker and easier, the Cultural Formulation Interview, or CFI. The CFI is meant to be administered during patients’ initial assessment, and consists of 14 questions. Many of these questions are just good clinical practice. For instance, the first question is, “What problems or concerns bring you to the clinic?” Although there are hints at what might be considered culture by question three (“People often understand their problems in their own way, which may be similar or different from how doctors explain the problem. How would you describe your problem to someone else?”), it’s not until the seventh question that culture is explicitly mentioned: “Is there anything about your background, for example your culture, race, ethnicity, religion or geographical origin that is causing problems for you in your current life situation?”

The point of framing the questions this way  is to not make a big deal of culture while at the same time getting a good person-centered assessment that considers culture as important to how patients view their problems. This is meant to avoid the stereotyping that considering culture often leads to in situations in which clinician and patient differ on some cultural dimension. The CFI seems to provide space for individuals to define their problems as they see fit — i.e., to make explicit their own explanatory models — and then relate this to how others within their social networks (including family members and those that don’t share their culture) may see their problems.

My favorite exchange came after one audience member looked over the CFI and asked, “For whom would these questions not be relevant?”

Dr. Lewis-Fernandez replied: “Yes, exactly.”

The CFI is currently undergoing field trials. Read more about the proposed DSM-5 Cultural Formulation and the CFI, and express your opinion as to whether it should be emphasized (or not, I suppose), by following this link to the DSM-5 commentary website. Common sense needs advocates.

On a related note: If you haven’t read it yet, Allen Frances’ Op-Ed in Saturday’s New York Times, provocatively titled Diagnosing the DSM, is worth it. In it Dr. Frances, one of the architects of the DSM-IV, argues strongly that the DSM-5 development process should be untethered from professional psychiatry in order to build a better product. A teaser:

Until now, the American Psychiatric Association seemed the entity best equipped to monitor the diagnostic system. Unfortunately, this is no longer true. D.S.M.-5 promises to be a disaster — even after the changes approved this week, it will introduce many new and unproven diagnoses that will medicalize normality and result in a glut of unnecessary and harmful drug prescription. The association has been largely deaf to the widespread criticism of D.S.M.-5, stubbornly refusing to subject the proposals to independent scientific review.

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Two press pieces on the science (and anti-science) of PTSD in the military

The past weekend saw two articles in the popular press concerning PTSD among U.S. soldiers that are worth a read. First, the Seattle Times reported that the Army’s new PTSD screening guidelines fault the established screening tests designed to root out PTSD fakers. Why would anyone fake PTSD? The Army pays an average of $1.5 million in disability benefits per soldier (over his/her lifetime) with PTSD. It is estimated that 22 percent of returning soldiers have PTSD. The difference between those who have it and those who may be faking is no small chunk of change.

In part because of pressure by Senator Patty Murray (D-Washington) to investigate screening at the Madigan Army Medical Center (in Tacoma, Washington), the Army Surgeon General has issued new guidelines that criticize the use of the Minnesota Multiphasic Personality Inventory — or, MMPI, as most psychologists know it. The MMPI is one of the most venerated of psychological screening questionnaires, holding up pretty well in over 60+ years of research (it has been revised several times, most recently in 2008). At issue in this case is the MMPI’s “lie scale,” which has been shown to detect malingerers of various stripes in multiple studies.

According the the Seattle Times, the Army’s new policy “specifically discounts tests used to determine whether soldiers are faking symptoms of post-traumatic stress disorder. It says that poor test results do not constitute malingering.” Technically this is true; malingering scale scores on any normed test like the MMPI are associated with higher or lower probabilities of malingering, and not absolute certainty. Still, by throwing out the best tool they have to detect whether soldiers are malingering or not, what the Army really seems to be doing is trying to avoid appearing callous by relying on scientific methods.

Ironically, the same guidelines include empirically-based treatment improvements regarding medication:

The document found “no benefit” from the use of Xanax, Librium, Valium and other drugs known as benzodiazepines in the treatment of PTSD among combat veterans. Moreover, use of those drugs can cause harm, the Surgeon General’s Office said. The drugs may increase fear and anxiety responses in these patients. And, once prescribed, they “can be very difficult, if not impossible, to discontinue,” due to significant withdrawal symptoms compounded by PTSD, the document states.

Score one for research on meds, zero for research on screening questionnaires (or maybe: psychiatrists one, psychologists zero).

The second article of note wasn’t a report, but an editorial. Writing in the New York Times’ Sunday Review, Weill Cornell Psychiatrist Richard Friedman builds the case that one possible reason for the increase in cases of PTSD among returning soldiers from Afghanistan and Iraq is an increase in stimulants prescribed to them on the battlefield. With the help of the Freedom of Information Act, Dr. Friedman found that military spending on stimulants increased 1,000 percent over five years.

Stimulants do much more than keep troops awake. They can also strengthen learning. By causing the direct release of norepinephrine — a close chemical relative of adrenaline — in the brain, stimulants facilitate memory formation. Not surprisingly, emotionally arousing experiences — both positive and negative — also cause a surge of norepinephrine, which helps to create vivid, long-lasting memories. That’s why we tend to remember events that stir our feelings and learn best when we are a little anxious.

Since PTSD is basically a pathological form of learning known as fear conditioning, stimulants could plausibly increase the risk of getting the disorder.

Dr. Friedman goes on to explain the neurochemistry behind the proposed interaction of stimulants and trauma, review new research showing ameliorative effects of beta-blockers, and (appropriately) call for more transparency and more research on the topic.

More from McGill’s Summer Program: The Affliction Film Series

McGill University’s Summer Program in Social and Cultural Psychiatry is not just about the differences between Swedes and Irish. As part of the summer program’s keynote course, Cultural Psychiatry, McGill luminary Laurence Kirmayer includes a number of film clips in the syllabus to give students a chance to observe some of the phenomena that gets diagnosed by psychiatrists using Western psychiatric categories, but may perhaps make more sense by examining the patient’s cultural and historical context.

One of the most striking films shown (so far) comes from Robert Lemelson’s psychiatric anthropology series, Afflictions: Culture and Mental Illness in Indonesia. In “Shadows and Illuminations,” a man presents with visual and auditory hallucinations of Balinese spirits, disorganized behavior and inappropriate dress. His family and neighbors regard him as odd, so it’s not the case that he is just odd to our foreign eyes. Our psychiatric practice tells us to look for schizophrenia. He reports the symptoms began with the death of his daughter, and we think perhaps it is a posttraumatic stress reaction of some sort. He is examined by two traditional healers and a psychiatrist, all of which have their own treatments, but none of which seem to help. Accommodations are made for the man’s behavior in his own home, and he seems to get a little better. Improvement had nothing to do with our diagnosis, or lack thereof.

Each story in the series situates behavior and concepts of illness within the families and societies in which they occur. Not satisfied with biological explanations of these patients’ problems, Lemelson’s films remind us that psychiatric practices have non-psychiatric implications, specifically around family relations, historical meaning-making, and even implications related to the freedom of the individuals with mental health problems.

Stressed mice moms, less licking & grooming, DNA methylation, & sad mouse dads: An epigenetic model of intergenerational transmission of psychopathology

The recent special issue of Biological Psychiatry on Stress, Neuroplasticity and Posttraumatic Stress Disorder (September 1, 2010) includes an intriguing piece on the transmission of the impact of stressed child-rearing among mice across generations: “Epigenetic transmission of the impact of early stress across generations.” This article was announced by the publisher’s regular newsletter as having implications for intergenerational trauma, and so I figured I better take a look.

Before going into the article itself, a couple of terms. First, epigenetics. Genetics is the study of how traits are passed on from one generation to the next via genes (in DNA) and epi is a prefix indicating essentially “related to but not of” (from the Greek preposition meaning on, around, above, nearby, outer, etc.), so epigenetics concerns those phenomena that result in traits being passed from one generation to the next that are not directly due to genetic material alone. In other words, those things that affect the phenotype without affecting the genotype (for those of you in High School biology). Epigenetics has been a hot field in mental health research for a few years now, particularly among those who want to explain how childhood adversity might influence the ability to tolerate stress later in life.

Second term, DNA methylation (I’ll admit I had to look this one up). Methylation is the addition of a methyl group — a group of chemical characterized by CH3 (for those of you in High School Chemistry) — to DNA. The addition of a methyl group to DNA is critical to development, and the amount and location influences how a gene will be expressed. Importantly, (1) methylation happens because of phenomena external to the gene — i.e., it is epigenetic — and (2) it can be passed on to later generations.

Okay, the article. A group of researchers in Switzerland set up an animal model of transgenerational transmission of the impact of early life stress using mice. (Animal models are useful to mental health research because they allow researchers to manipulate aspects of research design.) How did the Swiss operationalize early life stress in this model?

Dams and litters were subjected to unpredictable maternal separation combined with unpredictable maternal stress (MSUS). (p. 408)

Essentially, they stressed out the new mice mothers (“dams”) and took them away from their mice children (“litters”) at irregular intervals (“MSUS”) throughout the first two weeks following birth. They also left a separate group of dams and litters alone. They observed these two groups of mice, and found what others have found, that among the “treated group” (i.e., the ones with unpredictably separated and stressed mothers) there were fewer of the behaviors associated with healthy mouse development — arched-back nursing, regular licking and grooming, and time hanging out on the nest — when the moms were in contact with their litters. In addition, when the little mice grew up, males in the treated group spent more time floating passively in a “forced swim” test (dropping mice in water and seeing how fast they swim, essentially), spent more time immobile in a “tail suspension” test (holding mice by their tails), and ate less sugar (a “sucrose consumption test”) than mice in the nontreated group. These traits were seen as “depressive-like” behavior. Notably, females were not different from all the mice who were raised without the unpredictable and stressed mothering.

Once the two groups of litters were old enough to breed, the researchers bred the males of the stressed group with a new set of female mice (who grew up normally) quickly separated them from their litters and female partners so as not to influence the behavior of their children once born, did not stress the mothers, and then observed the behaviors of their offspring — i.e., the second generation. Then they did the same thing with the next — the third — generation as well. With some slight variability, results from the first generation were replicated in both second and third generations, suggesting that not only is there an effect of early life maternal child-rearing practices that persists across (mice) generations, but also that this effect is independent of how subsequent mothers rear their litters, and thus it must be carried by the father.

So how is this done? What is the mechanism of transmission? Combining their findings and the knowledge about epigenetics, our Swiss friends thought that maternal separation combined with unpredictable maternal stress might be altering gene expression through DNA methylation in sperm cells. So:

To determine whether DNA methylation was altered by early stress in the male germline, we examined its level in the promoter of the several candidate genes in sperm from F1 MSUS males. (p. 412)

The “several candidate genes” here were genes that are associated with the regulation of depressive-like behavior. What did they find?

Methylation of the CpG island surrounding the transcription initiation site of MeCP2 and CB1 genes was increased in F1 MSUS sperm. In contrast, for the CRFR2 gene, methylation in a stretch of the CpG island located 5′ of the transcription initiation site was decreased. Methylation was not changed in target regions of the 5-HT1A or MAOA gene. (p. 413)

What did they find? Essentially, DNA methylation was different for some of the genes in the group that had been subjected to maternal separation combined with unpredictable maternal stress than in the group that had been allowed to lead a normal mouse childhood.

So early maternal separation and distress can have effects at the epigenetic level that are carried through paternal lines to subsequent offspring. This is important news for developmental psychologists studying depression and other disorders, and should not be underestimated. That someone has figured out how care-taking behavior affects gene expression and can be carried across generations to me is simply phenomenal. But what does it all mean for trauma studies? I mentioned above this article was advertised as important for trauma studies, but the term trauma never comes up once in the manuscript — rather, the authors focus on “depression-like” behavior. This may be relevant to trauma studies — most people who develop PTSD also develop depressive disorders as well — but the research doesn’t show that somehow PTSD is passed along intergenerationally.

There is another, more subtle critique to be made here as well. The title of the article mentions “early stress” and the authors consistently refer to “chronic and unpredictable stress in early postnatal life” (p. 413) and the like. But I think it’s a mistake to apply these findings to childhood adversity in general, or even neonatal adversity in general. Their model of early stress was particular to one key developmentally crucial relationship: that of an offspring to it’s mother. Although there is good reason to believe that several types of early life adversity can affect one’s proclivity towards depression and other disorders, it does not follow that among these several types that there is one pathway for all, and certainly not that all are best seen as versions of being unpredictably separated from a stressed mother.

Brain-mind or heart-mind; TMS or MST; DSM-5 or DSM-V? The American Psychiatric Association in New Orleans

This weekend and the first part of this week the American Psychiatric Association held its annual meeting in New Orleans, LA. In addition to staying out of the way of drifting gulf oil and seeing a lot of great music, I sat in on a few sessions in the monstrous Morial Convention Center to hear the latest from my psychiatric cousins. Psychiatrists in general fascinate me. On the one hand they rely heavily on the biomedical model to explain psychological phenomena (they are, after all, doctors), on the other they talk even more impressionistically than my psychologist compatriots (one of the presentations this year is on Chopin). As doctors, they know so much stuff (doctors have to memorize an amazing number of facts about the body), yet as researchers they can hardly handle more than two-by-two tables in their analyses (to be honest, most psychologists don’t do a whole lot better — they just don’t get published). I get asked all the time whether I’m a psychologist or a psychiatrist, and then, regardless of the answer, if I can prescribe; for those of you wondering: psychologist, and no.

On Saturday, I attended a session run by Devon Hinton (of Mass General) on cultural assessment of non-Western patients. In addition to Devon, his brother Ladson, Roberto Lewis-Fernandez, and myself, Brandon Kohrt of Emory University presented a paper on culture and symptoms. Brandon’s done a lot of work with child soldiers in Nepal, and presented on “child-led indicators” of distress among this population. Lots of good things in there, but my favorite was a distinction made among Nepalis between problems of the “brain-mind” and problems of the “heart-mind.” Your heart-mind is where your emotions are, your brain-mind where your thinking and cognition happen. Heart-mind problems are normal, brain-mind problems stigmatized. Although heart-mind problems can lead to brain-mind problems, they usually can be addressed successfully with appropriate social support. Critically, Brandon reported that Western psychosocial NGOs working with Nepalis affected by the civil war (which ended in 2006) had translated posttraumatic stress disorder into a term associated with brain-mind problems, and thus found it very hard to get people to participate in their interventions. It was only when they started using a heart-mind term that they got more people to participate.

TMS stands for transcranial magnetic stimulation. MST stands for magnetic seizure therapy. I’ll admit here that I am way out of my league here, but I’ll give you the synopsis. Both are new treatments for depression, and both involve magnets applied to your skull (falling under the somewhat euphemistic category of “brain stimulation”). In TMS you are awake, in MST you are under anesthesia. Okay, why do you want to do either of these things? Well, the treatment with the strongest therapeutic effects on people who have suffered multiple bouts of severe depression is well known to be electroconvulsive therapy, ECT. Yes, that means administering electric shocks to people’s brains. The problem with ECT is that associated with shocking people’s brains is some retrograde amnesia. So, electrotherapists have searched for more focal treatments at lower doses, and have found some success by putting strong magnets on the surface of people’s heads. I’m being a bit glib here, but really, this is pretty exciting stuff — particularly for those suffering from depression that is resistant to medication. For more on TMS, see the work of William McDonald; for MST, see Sarah Lisanby (she’s also done TMS work as well).

The development of DSM-5 was a big topic at APA 2010. The publication of the DSM-5 in May of 2013 (at APA San Francisco) is already a much-heralded event, and those on the various subcommittees have been doing due diligence throughout the various mental health conference circuits. I heard a lot about DSM-5 at APA 2010, but perhaps the most interesting proposed conceptual change I heard was the decoupling of disability from the notion of mental disorder. Since DSM-III (1980), criteria for diagnosing most disorders has included a functional criterion; i.e., you can’t just have some symptoms, the symptoms have to keep you from doing the things you want or need to do. So, someone with depression who is really sad but gets everything done cannot really have clinical depression. Decoupling symptom criteria from functional disability would put DSM-5 in line with the World Health Organization’s ICD-10/ICF system (ICD-10 is the WHO’s classification disorders manual; ICF is their functional disability manual). It would also clearly expand the number of people with disorders, as the functional criterion limits the application of a given disorder. Over-diagnosis will likely result. However, leaving things as they are means that the functional criteria limits prevention efforts: if you have to wait to diagnose a disorder before it becomes disabling, how can you administer (or more to the point, how can you pay for the administration of) prevention efforts? Stay tuned… or just check out the DSM-5 website. (By the way, it’s settled: DSM-5, not DSM-V.)


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