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.
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.
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.
