Showing posts with label CME. Show all posts
Showing posts with label CME. Show all posts

Monday, November 14, 2016

The Harvard Neuropsychiatry Course





I went to the Harvard Neuropsychiatry course for all of the wrong reasons.  I started going to HMS courses in Boston back in the late 1980s.  I have always seen myself as a medical psychiatrist knowledgeable in neurology, medical imaging and electroencephalography.  I have always liked seeing people with complicated problems that are associated with psychiatric diagnoses or who have psychiatric symptoms associated with their primary medical or neurological diagnoses.  That led me to the Behavioral Neurology courses through Harvard where the presentations were done by all of the experts at time including M-Marcel Mesulaum, Antonio Damasio, Hanna Damasio, Elliot Ross, and David Bear.  Their work is well represented in the text Principles of Behavioral and Cognitive Neurology.  At the time there were some older neuropsychiatry texts but learning about the field generally had to occur on a reference by reference basis.  I was working in a Memory Disorders and Geriatric Psychiatry Clinic and learning neuropsychiatry on a syndrome by syndrome basis.  I did not find out until this course that it is the largest meeting in the field and has been occurring on an annual basis for the past two years.  My motivation for coming was basically to see whether I missed anything.  I always need to answer the question: "Can a clinician working too many hours per week keep up with a technical field to an acceptable degree."  For the first time ever in my career I was spending a lot of money on a conference and travelling well outside my comfort zone to see presenters who I did not know that well.

There were about 320 people registered for the course.  The setting was a hotel built in the early 20th century but extensively remodeled to 4 star hotel status.  The conference itself took place in the main ballroom and it was densely populated with some overflow into balcony seats and a mezzanine area in the back.  The audiovisual effects worked with with a large projection screen over the speaker and large LEDs TVs lining each side of the ballroom.

The  overall format of the course was to present a lot of technical information on Day 1 and discuss more discrete diseases and syndromes on Day 2.  The detailed agenda for both days can be found at this link.  Day 1 was a focus on neuroanatomy, functional brain networks, neuroimaging,  neuropsychiatric and neuropsychological approaches to the complex patient, and a detailed approach to the complex patient.  These were not TED talks.  The first three presentations covered 81, 60, and 60 slides.  That is the way I like it.  An additional benefit is that all of the PowerPoints were available in PDF form online.  Even the most unreadable slides are easily visible in this form.  The PDF form is also allows the syllabus to be printed in black and white and used primarily for note taking.  Legibility of the slides depend on the print size and many in this syllabus were unreadable.  I think that all conferences should use this approach.  I would like it modified so that the original slides could be reused in lectures by Creative Commons licenses.

The early lecturers used a lot of subordinate clauses and very long sentences.  I could imagine that anyone unfamiliar with the jargon could get lost.  The lecturers were unapologetic and one of them suggested studying the slides and references to get up to speed.  The pace of the course was intense with brief coffee and lunch breaks in order to cover the advertised CME.  Several of the lecturers ended up accelerating their presentations as they realized that they were running out of time.  My focus in these conferences is on information transfer and not style points on the lectures.  At that level I consider it a success.  Key points were highlighted as well as references.  There were a couple of graphics that were not referenced.  The syllabus for the course is 453 pages long and could easily be worked into a text at some point.

In the past, I have reviewed all of the lectures at conferences.  For this conference I am going to mention a couple of high points.  There is some confusion about what neuropsychiatry is.  Barry Fogel, MD defined it at the end of Day 1: "Neuropsychiatry is a branch of clinical neuroscience more than a mental health discipline.  It is always in the context of the brain."  Every lecturer maintained that theme reviewing key brain circuits involved in pathological states including some that were considered to be functional as well as states associated with clear brain pathology.  In some cases those formulations were associated with a new conceptualization of the disorder.  A good example, is the case of traumatic brain injuries (TBI).  Tom McAllister, MD made the point that not too long ago, nobody would have showed up for a lecture on TBI.  Those were the days when it was common to consider TBIs, especially occurring in sports to be minor events.  That has been reconceptualized from the perspective of neuropathological changes, protein markers (Tau, APP, Aβ, and others), and possible progression to dementia.  The treatment of neuropsychiatric syndromes of TBI including depression, PTSD, and other psychiatric syndromes.  I am used to seeing a lot of people with bipolar like syndromes after TBIs but that was not mentioned.  Excellent reconstructions of the brain with a map of the results of a large number of TBIs were presented with an emphasis on the circuitry affected and how that can lead to symptoms.

When I think about earth shaking information on a single slide (yes - it can happen) - the best example I can think of was a slide in the presentation: Neuropsychiatric Aspects of Frontotemporal Dementia by Brad Dickerson, MD.  For anyone who has followed it, the diagnostic approaches to this relatively common dementia have been confusing over the years (2).  In a slide FTLD (Frontotemporal lobar degeneration) clinicopathological spectrum parses the 6 major clinical  syndromes into subtypes based on biological markers.  Each category was also color coded to indicate the degree of tauopathy.  I found a modified version of this slide in an article by Irwin, et al in Frontiers in Aging Neuroscience (1).  These same authors have published a significant number of the papers in the field.  This review stood out to me because it is the clearest conceptualization of FTLD that I have seen.

The second high point of the conference was on Functional Neurological Symptom Disorder (FNSD).  This is actually a subheading under Conversion Disorder in the DSM-5 (p. 318) and the main diagnosis is the disorder known to most psychiatrists.  The disorder is one of pseudoneurological symptoms like weakness, paralysis, sensory symptoms, speech problems, or seizures with no known correlates of the medical diagnosis.  The presentation by Gaston Baslet, MD on the approach to these disorders was very informative.  Rather than take a strict DSM criteria approach, he presented the criteria and then illustrated levels of diagnostic certainty - the levels of diagnostic information that are ideal versus what is clinically available.  The example given was for Psychogenic Non-Epileptic Seizures (PNES).  The increased prevalence of these disorders in neurological practice as opposed to primary care was noted.  Most importantly, the approach to treating the disorder was discussed as well as what seems to work.  A model of predisposing, precipitating, and perpetuating factors was presented.  Like most disorders, cognitive behavioral therapy (CBT) is a useful treatment modality either as psychotherapy delivered in a  standard approach or using a self help manual.  Dr. Baslet also discussed a communication protocol on how to present the diagnosis and rationale for treatment to the patient.  Limiting factors include the low number of patients who complete treatment and there is a spontaneous improvement rate of about 20%.  A neurobiological model of PNES/FNSD was presented based on the work of van der Kruijs, et al (3).  This is important work for any psychiatrist who has not had the experience of treating PNES/FNSD on an ongoing basis with psychotherapy.  My experience is consistent with the presentation in that it takes good communication with the patient and an effective model for therapy to get results.

Forced normalization epilepsy was a term that I was unfamiliar with even though I have treated a significant number of people with seizure disorders.  It was discussed in Gaston Baslet's second presentation on the Neuropsychiatry of Epilepsy.  It is a description of a syndrome where psychotic states occur as the EEG abnormalities of the seizure disorder improve or disappear.  The neuropsychiatric symptoms that emergence when this occurs is also referred to as alternate psychosis.  There is a small but significant literature on this problem that also highlights some of the controversies.  His presentation also discussed the safety of antidepressants in epilepsy and the FDA warning on suicidality and antiepileptic drugs (AEDs).  Since I prescribed a lot of gabapentin in the treatment of addiction, anxiety, and chronic pain - that is a warning that I have to address a lot with patients.  He showed the Forest plot of odds ratios for specific AEDs and according to that reference (4) some drugs may be protective for suicidal ideation and behavior.  With the discussion of emerging and interictal psychotic symptoms an equivalent brief discussion of antipsychotic drugs in these states would also have been very useful.  Dr. Baslet also mentioned one of my favorite neuropsychiatric symptoms Alice In Wonderland Syndrome or metamorphopsia as it is sometimes known.  Like Alice, patient's experience body distortion (feeling too tall, floating, sinking into the ground) as a manifestation of infectious disease (originally Epstein Barr Virus), migraines, or epilepsy.

A  final brief point was noted in the presentation on neuropsychology by Aaron Nelson, PhD.  It is useful at a time when I think there is a lot of controversy about these assessments and what they show.  The commonest reason I see patients getting a neuropsychological assessment these days is Attention Deficit-Hyperactivity Disorder.  It is generally presented to me as proof of the disorder and proof that a person needs stimulant medications.  The patient generally reports that they were "tested" for ADHD and found to have it despite a normal development history, normal and typically good academic performance, and good vocational achievement.  I have previously posted that Russell Barkley, PhD one of the leading authorities on ADHD has stated that neuropsychological testing is neither necessary or sufficient to make a diagnosis of ADHD and as it is based on clinical criteria.  Of course the main reason for neuropsychological testing of individuals suspected of having ADHD is to test for any associated learning disorders and in the adult patients I see - very few people recall any information of that sort.  Dr. Nelson points out that intraindividual variation in neuropsychological test performance is common with 66% or participants in his study (6) producing maximal discrepancies that exceeded 3 standard deviations on test performance.  His conclusion is that score variability alone is not enough to base diagnostic inferences on.  Dr. Nelson also called for a show of hands to see if any clinicians had access to neuropsychological testing in a time frame of less than 3 months.  There were few if any hands raised.            

Those were a few of my favorite highlights from this conference.  There are many more, but I am trying to keep this post contained to the highlights and overall focus.  This is an intense conference but a good one.  In the follow up assessment, they asked if the course should be three days rather than two and I endorsed that approach.  I think that the inflammatory section of neuropsychiatric disorders could be reinforced by having any of the psychiatrists who write the sections in Lahita's text on Systemic Lupus Erythematosus present on that topic. If your priorities in conferences are similar to mine (information transfer, non-experiential, and a direct comparison of your skills to the experts are a priority) - you might want to attend this conference next year.  The course organizers did have question and answer sessions regularly throughout the program and questions were actively solicited by course staff and read and answered by the lecturers.

And it turns out my approach to self-study has paid off.  There were several points where I could have stood up and given the lecture.  That may seem immodest if you believe that practicing psychiatrists need to be constantly tested and reassessed by some higher authority to prove that they are competent.   I don't and never have.  It turns out all you have to do is practice medicine, think a lot about what you are doing and try to keep up on the literature.  At one point the lecturers asked about how many people in the audience were psychiatrists and then how many have treated people with frontotemporal dementia.  Most of the people were psychiatrists and most of them have assessed and treated frontotemporal dementia, despite the fact that the diagnostic classification has been in a state of flux for the past 20 years.  Thinking about that, there was a tremendous amount of knowledge about neuropsychiatric disorders in that room.  I can't imagine that this disorder or the general importance cerebral atrophy on imaging  is well recognized in primary care settings.  That is just one of the reasons why neuropsychiatrists are needed out there and why these concepts need to be taught and understood in residency training.



George Dawson, MD, DFAPA
 
 

References:

1:  Irwin DJ, Trojanowski JQ, Grossman M. Cerebrospinal fluid biomarkers for differentiation of frontotemporal lobar degeneration from Alzheimer's disease. Front Aging Neurosci. 2013 Feb 21;5:6. doi: 10.3389/fnagi.2013.00006. PubMed PMID: 23440936; PubMed Central PMCID: PMC3578350.

2:  Kertesz A, Munoz DG.  Frontotemporal Dementia; in:  Alzheimer Disease. RD Torrey, R Katzman, KL Bick, SS Sisodia (eds); Lippincott Williams and Wilkins; New York; 1999; pp 133-145.

3:  van der Kruijs SJ, Bodde NM, Vaessen MJ, Lazeron RH, Vonck K, Boon P, HofmanPA, Backes WH, Aldenkamp AP, Jansen JF. Functional connectivity of dissociation in patients with psychogenic non-epileptic seizures. J Neurol Neurosurg Psychiatry. 2012 Mar;83(3):239-47. doi: 10.1136/jnnp-2011-300776. PubMed PMID: 22056967.   JNNP has a collection of Neuropsychiatry articles up until 2015.

4:  Hesdorffer DC, Kanner AM. The FDA alert on suicidality and antiepilepticdrugs: Fire or false alarm? Epilepsia. 2009 May;50(5):978-86. doi: 10.1111/j.1528-1167.2009.02012.x. Review. PubMed PMID: 19496806.

5: Hesdorffer DC, Berg AT, Kanner AM. An update on antiepileptic drugs andsuicide: are there definitive answers yet? Epilepsy Curr. 2010 Nov;10(6):137-45. doi: 10.1111/j.1535-7511.2010.01382.x. PubMed PMID: 21157540.   

6: Schretlen DJ, Munro CA, Anthony JC, Pearlson GD. Examining the range of normal intraindividual variability in neuropsychological test performance. J Int Neuropsychol Soc. 2003 Sep;9(6):864-70. PubMed PMID: 14632245.



Attribution:

The graphic at the top of this post is the cover of my syllabus for this course.  I have no affiliation with the course or Harvard Medical School, I just paid the fee to take the course like everybody else.  The graphic is included here is to provide information about the course that I reviewed in this post.




Tuesday, June 3, 2014

The Issue With Patient Management Problems

So-called patient management problems have been building up on us over the past 30 years.  I first encountered them in the old Scientific American Medicine Text.  They are currently used for CME and more importantly, Maintenance of Certification.  To nonphysicans reading this they are basically hypothetical patient encounters that claim to be able to rate your responses to fragments of the entire patient story in such a way that it is a legitimate measure of your clinical acumen.  I am skeptical of that claim at best and hope to illustrate why.

Consider a recent patient management problem for psychiatrists in the most recent issue of Focus, the continuing education journal of the American Psychiatric Association (APA).  I like Focus and consider it to be a first rate source of the usual didactic continuing medical education (CME) materials.  Read the article, recognize the concepts and take the CME test.  This edition emphasized the recognition and appropriate treatment of Bipolar II Disorder and it provided an excellent summary of recent clinical trials and treatment recommendations. The patient management problem was similarly focused.  It began with a brief descriptions of a young women with depression, low energy, and hypersomnia.  It listed some of her past treatment experience and then listed for the consideration of the reader, several possible points in the differential diagnosis including depression and bipolar disorder, but also hypersomnia-NOS, obstructive sleep apnea, disorder and a substance abuse problem.  I may not be the typical psychiatrist but after a few bits of information, I would not be speculating on a substance abuse problem and would not know what to make of a hypersomnia-NOS differential diagnosis.  I would also  not be building a tree structure of parallel differential diagnoses in my mind.  Like most experts, I have found that the best way to proceed is to move form one clump of data to the next and not go through and exhaustive checklist or series of parallel considerations.  The other property of expert diagnosticians is their pattern matching ability.  Pattern matching consists of rapid recognition of diagnostic features based on past experience and matching them to those cases, treatments and outcomes.  Pattern matching also leads to rapid rule outs based on incongruous features, like an allegedly manic patient with aphasia rather than a formal thought disorder.

 If I see a pattern that looks like it may be bipolar disorder, the feature that I immediately hone in on is whether or not the patient has ever had a manic episode.  That is true whether they tell me that they have a diagnosis of bipolar disorder or not.  I am looking for a plausible description of a manic episode and the less cued that description the better.  I have seen evaluations that in some cases say: "The patient does not meet criteria for bipolar disorder."  I don't really care whether the specific DSM-5 criteria are asked or not or whether the patient has read them.  I need to hear a pretty good description of a manic episode, before I start asking them about specific details.  I should have enough interview skills to get at that description.  The description of that manic episode should also meet actual time criteria for mania.  Not one hour or four hours but at least 4 days of a clear disturbance in mood.  I recall reading a paper by Angst, one of Europe's foremost authorities on bipolar disorder when he proposed that time criteria based on close follow up of his research patients and I have been using it ever since.  In my experience practically all substance induced episodes of hypomania never meet the time criteria for a hypomanic episode.  There is also the research observation that many depressed patient have brief episodes of hypomania, but do not meet criteria for bipolar disorder.  I am really focused on this cluster of data.

On the patient management problem, I would not get full credit for my thinking because I am only concerned about hypersomnia when I proceed to that clump of sleep related data and I am only concerned about substance use problems when I proceed to that clump of data.  The patient management problem seems more like a standardized reading comprehension test with the added element that you have to guess what the author is thinking.

The differential diagnosis points are carried forward until additional history rules them out and only bipolar II depression remains.  At that point the treatment options are considered, three for major depression (an antidepressant that had been previously tried, an antidepressant combination, electroconvulsive therapy, and quetiapine) and one for bipolar II depression.  The whole point of the previous review is that existing evidence points to the need to avoid antidepressants in acute treatment and that the existing relatively weak data favors quetiapine.  The patient in this case is described as a slender stylishly dressed young woman.  What is the likelihood that she is going to want to take a medication that increases her appetite and weight?  What happens when that point comes up in the informed consent discussion?

The real issue is that you don't really need a physician who can pass a reading comprehension test.  By the time a person gets to medical school they have passed many reading comprehension tests.  You want a physician who has been trained to see thousands of patients in their particular specialty so they have a honed pattern matching and pattern completion capability.  You also want a physician who is an expert diagnostician and who thinks like an expert.  Experts do not read paragraphs of data and develop parallel tree structures in their mind for further analysis.  Experts do not approach vague descriptions in a diagnostic manual and act like they are anchor points for differential diagnoses.  Most of all experts do not engage in "guess what I am thinking" scenarios when they are trying to come up with diagnoses.  Their thinking is their own and they know whether it is adequately elaborated or not.

This patient management program also introduced "measurement based care".  Ratings from the Inventory of Depressive Symptomatology (IDS) were 31 or moderately depressed at baseline with improvements to a score of 6 and 4 at follow up.  Having done clinical trials in depression myself,  and having the Hamilton Depression Rating Scores correlated with my global rating score of improvement, I have my doubts about the utility of rating scale scores.  I really doubt their utility when I hear proclamations about how this is some significant advance or more incredibly how it is "malpractice" or not the "standard of care" if you don't give somebody a rating scale and record their number.  In some monitored systems it is even more of a catastrophic if the numbers are not headed in the right direction.  Rating scales of subjective symptoms remain a poor substitute for a detailed examination by an expert and I will continue to hold up the 10 point pain scale as the case in point.  The analysis of the Joint Commission 14 years ago was that this was a "quantitative" approach to pain.  We now know that is not accurate and there is no reason to expect that rating scales are any more of a quantitative approach to depression.

Those are a couple of issues with patient management problems.  The articles also highlight the need for much better pharmacological solutions to bipolar II depression and more research in that area.

George Dawson, MD, DFAPA


Cook IA.  Patient Management Exercise - Psychopharmacology.  Focus Spring 2014, Vol. XII, No. 2: 165-168.

Hsin H, Suppes T.  Psychopharmacology of Bipolar II Depression and Bipolar Depression with Mixed Features.  Focus Spring 2014, Vol. XII, No. 2:  136-145.  

Saturday, September 15, 2012

Borderline Personality Disorder - DBT versus GPM

I just got back from a Mayo Clinic CME course "Clinical Management of Borderline Personality Disorder". I went to see John G. Gunderson, MD.  He and I go way back in a peripheral sort of way to the days before the Internet.  About 20 years ago I sent him a letter and he mailed me a copy of his "Diagnostic Interview for Borderlines." That was about three years after Marsha Linehan mailed me a rough copy of her research protocol for Dialectical Behavior Therapy. I like to see and hear from the experts.

The course was excellent and the logical summation of work done in this field for the past two decades. It was accessible and the faculty that included Dr. Gunderson and Brian Palmer, MD were enthusiastic and optimistic about treatment outcomes. Dr. Gunderson pointed out that sampling bias has led to therapeutic nihilism and stigmatization in the past and that more recent outcome studies show very positive results. The basic tenets of therapy that you learn in psychiatry school can go a long way. Therapeutic neutrality, and active interest in with the patient has to say, the therapeutic alliance, and technical skill with specific interventions are common elements in working with patients across all diagnostic categories.  If the diagnosis is accurate psychopharmacology is a secondary intervention.  The primary focus is psychotherapy and case management.

One of the significant points in the presentation was the concept of General Psychiatric Management (GPM) in the treatment of borderline personality disorder. In the years since I received the DBT manual, in many areas that therapy has become the de facto standard of care for borderline personality disorder. There is research evidence that it is effective.  DBT treatment programs seem to have popped up everywhere in the past decade. My experience in inpatient units led me to observe that many of these patients seem to have been misdiagnosed or DBT was being applied to the wrong diagnosis. There are fairly specific selection criteria for DBT, but it seems that anyone with a difficult problem was being put in a DBT program.

Dr. Gundersen referenced an article in the American Journal of Psychiatry comparing GPM versus DBT.  General Psychiatric Management is a variation of what we used to call supportive psychotherapy and it was defined by the researchers as:

"General psychiatric management was implemented as a comprehensive approach to borderline personality disorder, developed and manualized for this trial, consisting of psychodynamic psychotherapy, case management, and pharmacotherapy (P.S. Links, Y. Bergmans, J. Novick, J. LeGris, unpublished 2009 manuscript). The psychotherapeutic model in this approach emphasized the relational aspects of the disorder and focused on disturbed attachment patterns and the enhancement of emotion regulation in relationships. Case management strategies were integrated into weekly individual sessions. No restrictions were placed on ancillary pharmacotherapy in either condition; in general, pharmacotherapy was based on a symptom-targeted approach but prioritized mood lability, impulsivity, and aggressiveness as presented in APA guidelines (16)." (see link below to McMain 2012)"

The study showed that the outcomes of both treatment modalities across several outcome measures (suicidal and non-suicidal self injurious behavior, depression, anger, interpersonal functioning) were comparable.  GPM was delivered as once a week hourly psychotherapy with additional case management and coordination of care.  This is important research because the logical extension of this research is to look at ways to improve functional capacity as well as symptomatology.

Take a look at the references and attend the seminar in the future if you have the chance.

George Dawson, MD, DFAPA

John G. Gunderson and Brian A. Palmer.  Clinical Management of Borderline Personality Disorder.  Mayo Clinic CME, September 14, 2012.

McMain SF, Links PS, Gnam WH, Guimond T, Cardish RJ, Korman L, Streiner DL. A randomized trial of dialectical behavior therapy versus general psychiatric management for borderline personality disorder. Am J Psychiatry. 2009 Dec;166(12):1365-74. Epub 2009 Sep 15.

McMain SF, Guimond T, Streiner DL, Cardish RJ, Links PS. Dialectical behavior therapy compared with general psychiatric management for borderline personality disorder: clinical outcomes and functioning over a 2-year follow-up. Am J Psychiatry. 2012 Jun;169(6):650-61