Layered Psychiatry

 

I had this idea about how to present the complexity of the psychiatric diagnostic and treatment process.  After putting up a couple of diagrams for comment, I went ahead with a PowerPoint. For about 15 years I taught a course in how not to mistake a medical diagnosis for a psychiatric diagnosis.  My audience at the time was 3rd and 4th year medical students.  The lecture included a discussion of the research at the time in pattern matching and pattern completion, heuristics and common biases, Bayesian considerations, and inductive reasoning. It was generally well received but really cannot be appreciated until you are a senior clinician.  Over the time since I taught that course there also seems to be a distinct bias toward considering DSM criteria to be the basis for psychiatric diagnosis and decision making – and that is clearly a mistake.

The very first time I really became aware of the importance of pattern matching occurred when I was a fourth-year medical student.  I was on an Infectious Disease rotation and my job was to get the consults for the day, go out and see the patients we would be rounding on, do my basic compulsive medical student work up and present the findings and my ideas about the case to the attending physicians. ID docs are very bright people and like most impressive rotations I contemplated becoming an ID specialist for a while.  My patient that day had spontaneous bacterial peritonitis and the question for us was: “Do you agree with the diagnosis and current antibiotic treatment?”  I met with the patient, took a complete history, did a physical exam, reviewed the hospital course and labs, and had time for a little research. At the time I was carrying a copy of Phantom Notes for Medicine – basically an outline of the major medicine text of the day. I looked up the differential diagnosis.  I was also carrying a copy of Sanford’s guide to antibacterial therapy – the 1982 version and looked up the recommended antibiotics for peritonitis.  I was all set for rounds at that point.

Both of our ID attendings were very serious physicians. There was not a lot of banter or joking.  I anticipated presenting all of the dry facts and either getting a brief agreement, some questioning until I could no longer answer, or a long discussion of the diagnosis and treatment.  In this case the attending came into the patient’s room. He was 15 feet away from the patient and he said: “What am I seeing from right here that is a potential problem?”  Our team consisting of the ID fellow, two Internal Medicine residents, and myself – stopped in our tracks.  Nobody had an answer.  Weren’t we here for peritonitis?  How can you diagnose that from across the room?

“What is wrong with the patient’s shin?” Dr. R stated looking as serious as usual.  Sure enough there was a light pink confluent rash covering about 10 square inches of the patient’s left shin area. Dr. R happened to be an expert in streptococcal infections. He rattled off the type of strep he expected and suggested that we get a culture and send it to his lab for confirmation. I completed my presentation.  The primary diagnosis and treatment by the medicine team did not change, but now there was a new diagnosis and treatment that depended on Dr. R’s ability to recognize the pattern of this rash and make a rapid diagnosis – even though he was not expecting it.  But beyond that – we all saw the rash (although we had to be prompted to see it). Dr. R not only saw it, he processed it as a unique rash, and then a rash most likely caused by a specific kind of streptococcal bacteria. And over the next several days he was proven correct by the culture result.

Pattern matching and pattern completion are critical skills acquired by clinicians over the course of their training and careers that allows for not only more rapid diagnosis and treatment but also more accuracy in classifying ambiguous cases. Some of the examples I used in my course included ophthalmologists compared with primary care physicians diagnosing diabetic retinopathy and dermatologists compared with primary care physicians across a series of rashes.  In both cases the specialists had a higher degree of accuracy and were better at diagnosing ambiguous cases.

Cognitive neuroscience encompasses a broad range of perceptual studies starting with the early studies of visual processing by Hubel and Wiesel to more recent studies that look at the encoding that occurs in perceptual systems and what level of processing occurs at the level of primary sensory and association cortices, what the higher-level cortical structures may be, and whether or not top down processing influences perception. According to Superior Pattern Processing (SPP) theory (3), both perceived and mentally constructed patterns are processed by encoding and integration and at that point can be used for decision making or transferring approximations to other individuals.  In my example, Dr. R not only sees the pattern of the rash, but it is integrated into a feature set that has a time, visuospatial, social, and emotional context that makes it more likely that he will make a correct diagnosis. Experimental data suggests that he is not seeing the rash like any other person in the room – largely as a function of top-down control of his perceptual process.  The actual transfer of this pattern to his junior colleagues is limited because they see the rash as being a universal truth – that is they just “missed it” and therefore need to memorize what this rash looks like and not let it happen again.  They are also unaware of the processes involved in pattern matching or processing or they might have asked him about it.  For example, a logical question would have been: “What features of this rash do you notice that are suggestive of strep or a specific kind of strep?”

The question of what represents a pattern is critical to the idea of pattern recognition and processing.  There is a natural tendency to associate the term with visual or auditory stimuli, but without too much imagining patterns can clearly exist in any sensory modality and often involves the integration of multiple sensory inputs.  Cortical organization generally reflects primary sensory input to the cortex with adjacent sensory association areas and further information flow to heteromodal areas in the frontal and temporal cortex where additional integration occurs. Patterns can be sensed, encoded, recognized encoded and processed across theses systems.  The resulting integration yields a very complex array of patterns that are not intuitive.  For example, Mattson suggests that pattern processing in the human brain forms the basis of human intellect including problem solving, language and abstract thought and that it includes fabricated patterns.  Those fabricated patterns allow vicarious problems solving without having to conduct real world experiments.  The recent cognitive neuroscience of pattern processing is a significant advance compared with the old diagnostic paradigms I taught 20 years ago.  Those old experiments were basically a comparison of a non-expert to an expert diagnostician focused on a relatively basic clinical problem like a pathology slide, x-ray, ECG, or physical finding and the results were not a surprise – the experts typically prevailed in both accuracy and speed.  The sheer amount of information in a clinical encounter looks at what is essentially an infinite array of patterns, including patterns that are generally not even mentioned as being clinically relevant.

In considering what kind of patterns that need to be recognized and processed by a psychiatrist – the patterns that exist in clinical practice are a starting point.  These patterns and the associated phenomenology have been grossly oversimplified by an overemphasis on nosology. I talk with far too many people who see psychiatric diagnoses as phrases on a page in the DSM. I cringe when I hear: “The patient does or does not meet criteria for (DSM diagnosis x)”.  Kendler was correct when he referred to the DSM approach as an indexing system.  It gets people into the same ballpark, but it is not be very useful for predicting response to treatment or that specific person’s response to being ill.  It is also based on a fraction of the information collected in a psychiatric evaluation. When I consider the feature sets that psychiatrists are considering in evaluations it may look something the graphic below.  Of course, these features sets are simplified for the purpose of making a useful graphic. They will vary with the individual, their experience, social context, and culture. They will also be blended across space and have their own individual levels of integration and patterning.  Let me provide a couple of examples to illustrate these points.

Consider the above diagram as representing the possible features that must be recognized in order to assess a patient presenting to a psychiatrist and formulating and optimal diagnostic and treatment plan. My overriding concern in the first few minutes of the evaluation is whether this person really has a psychiatric disorder or a misdiagnosed medical problem and as a corollary - are they medically stable? That sounds like a basic consideration but prioritizing it is not listed anywhere in the DSM or any medical text that I know about. It does involve rapid recognition of patterns of acute medical illness particularly the most likely patterns to be misdiagnosed as psychiatric disorders and what I am seeing in real time.  It also involves pattern recognition of the thousands of psychiatric presentations that I have see that were really medical disorders.  Real life examples have included an almost immediate recognition that the patient had a stroke (many cases), seizures (many cases), meningitis, encephalitis, cerebral edema, serotonin syndrome, and neuroleptic malignant syndrome.  These rapid diagnoses were all predicated on experience-based pattern recognition rather than written criteria and these diagnoses had nothing to do with the DSM at the time.

A more cross-cutting feature in the diagram would be transference issues and defenses that can arise as soon as the initial evaluation or be indirectly evident by the patients historical description of their relationships with important people in their life.  These patterns will involve several layers in the above diagram and most importantly may suggest a psychotherapeutic intervention that can be implemented as early as the original assessment.  A similar process occurs if the patient is describing features of a major medication responsive illness.  In that situation, features from multiple layers result in a pattern that may be recognizable to the psychiatrist in terms of specific medical treatments or the urgency of those treatments.

And finally - what might the graphical representations of these pattern matching processes be?  Here are a few examples.  In the case of psychotherapeutic examples, it will depend on the exposure to specific therapies in training and practice. Each therapy has a specific pattern or series of patterns that the therapy depends up as well as patterns more specific to the conduct of therapy.  These graphics contain critical books from my library shelves with those elements.  In the case of the diagnostic and treatment process - the school of therapy and potential application are important patterns to recognize in the initial assessment.

All of these books contain symbolic representations of clinical patterns in the form of vignettes designed to assist the student of psychotherapy in learning techniques. They also contain information about the patterns of intervention that are relevant for a specific therapy and in some cases the common factors required in all successful therapies. I have graphically represented what happens in pattern processing once a theme is noted in the clinical assessment of the patient.  Clinical teaching of this process is often problem identification followed by an algorithm of features that might predict a successful course of therapy or limitations in therapy based on the students knowledge level at the time. As is true for most pattern matching and processing, the more extensive a physician's previous pattern exposure - the more likely they are to match the optimal intervention to the problem. 

I will resist making this first post of the New Year too long and wrap it up at this point with a diagram that I think pulls it all together (see below).  Each layer of this diagram consists of patterns and all of the associated pattern processing that leads to psychiatric diagnosis, formulation and treatment.  A few of the key features include the fact that diagnosis and treatment are interchangeable processes.  There will be times even during the initial information gathering that a verbal treatment intervention needs to occur and the entire interview occurs in the context of empathy and what Ghaemi, et al (4) have described as an existential psychotherapy based encounter – even if the administrative focus is on pharmacology. A second feature is that the information exchange is necessarily large if the psychiatrist and the patient are capable of it. There has been no research that I am aware of on the optimal amount of information that is required, but there are many limitations.  The advent of the electronic health record for example has led to the universal use of templates that are very restrictive in terms of information, typically dichotomous responses. A third implicit feature is the concept of patterns, what they imply for diagnosis and decision making and how there is almost a complete lack of discussion about this process in an era where diagnoses seem to have collapsed to a brief list of bullet points.  Cognitive neuroscience is a critical area of research focused these processes that I first became aware of when reading Kandel’s book “The Age of Insight” (5).  It is an area that does not typically get a lot of attention from psychiatrists, but it is a logical extension of the work done by behavioral neurologists from 20 years ago.  If we really want to focus on how psychiatrists think about diagnosis and treatment – we need to study this field, especially as the experiments get more complex.

I will wrap up this post at this point with the hope that 2021 is a much better year and that mankind is able to put this pandemic virus behind us by the summer and approach future pandemics with more science and wisdom.

 

Happy New Year!

George Dawson, MD, DFAPA

 

References:

1:  Constantine-Paton M. Pioneers of cortical plasticity: six classic papers by Wiesel and Hubel. J Neurophysiol. 2008 Jun;99(6):2741-4. doi: 10.1152/jn.00061.2008. Epub 2008 Jan 23. PMID: 18216235.

2: Poirier CC, De Volder AG, Tranduy D, Scheiber C. Neural changes in the ventral and dorsal visual streams during pattern recognition learning. Neurobiol Learn Mem. 2006 Jan;85(1):36-43. doi: 10.1016/j.nlm.2005.08.006. Epub 2005 Sep 22. PMID: 16183306.

3:  Mattson MP. Superior pattern processing is the essence of the evolved human brain. Front Neurosci. 2014 Aug 22;8:265. doi: 10.3389/fnins.2014.00265. PMID: 25202234; PMCID: PMC4141622.

4:  Ghaemi SN, Glick ID, Ellison JM. A Commentary on Existential Psychopharmacologic Clinical Practice: Advocating a Humanistic Approach to the "Med Check". J Clin Psychiatry. 2018 Apr 24;79(4):18ac12177. doi: 10.4088/JCP.18ac12177. PMID: 29701934.

5:  Kandel ER.  The Age of Insight. Random House, New York, 2012.

Graphics:

All generated by me for a PowerPoint presentation by the same name.  The photo at the top are two pamphlets that I carried as a med student along with a copy of Phantom Notes.  I was carrying them when I was in the room with Dr. R as he made the diagnosis described above.  I would not trade my medical school experience for anything. 

The Bureaucratic Takeover of American Psychiatry

 

This interview was posted on the Psychiatric Times web site today.  It contains bit and pieces from blog posts here over the past 8 years. It is a rare opportunity for people to see what is wrong with American psychiatry and that is - it is not run by American psychiatrists. It is run by managed care companies, pharmaceutical benefit managers, and government bureaucrats who all have the common goals of restricting access to psychiatric services.  And by psychiatric services, I am including substance use disorders and their treatment as well as the considerable amount of treatment of organic brain disorders that is provided by psychiatrists. 

I expect that some people will say: "What is special about psychiatry? Aren't these same rationing techniques applied to all of medicine?"  To a certain extent that is true.  Primary care physicians, medical specialists, and surgical specialists have to contend with similar rationing techniques.  It is however a question of scale.  I have talked with physicians who were around when the psychiatric rationing started and psychiatric services were chosen as the target of the express purpose of elevating the stock price of a company.  I was there when the Hay Report was released in the 1990s showing disproportionate rationing of psychiatric services relative to any other specialty.  I saw the original figures released in 2002 showing that Cardiology services were reimbursed at a 20% premium, while psychiatric inpatient services were discounted by 60%.  That led to some immediate closures of psychiatric hospitals and a continued trend of lower and lower bed availability.   There are endless examples of this disproportionate rationing on this blog and as I point out in the interview it is one of many reasons I write this blog.

One of the key questions that any observer of psychiatry should ask themselves is: "Why is George Dawson the only guy writing about this issue?"  Apart from the fact that this rationing has impacted my care of patients nearly every day of my professional life there are some obvious considerations.

1.  The people who self identify as the critics of psychiatry - clearly know very little about the practice environment or its constraints. I have seen two articles now that use the same example that psychiatrists believe that every mental disorder should be treated with a medication and that this is biological psychiatry.  The model of care they are referring to is not how psychiatrists are trained (see the above figure).  It represents a blended government and managed care model of how patients are scheduled, seen, and billed.  That bureaucratic model at one point employed an M code meaning a 5-10 minute visit with a psychiatrist.

2.  The critics similarly ignore highly innovative and individualized therapies that were invented by psychiatrists such as the Assertive Community Treatment  model that I mentioned in this interview as well as the myriad ways that psychiatrists have figured out how to talk in therapeutic ways with patients in rationed time slots and how those relationships result in recovery.

3.  The critics systematically ignore the lack of infrastructure to support psychiatric treatment.  There are very few inpatient units in each state that allow for the treatment of people with severe mental illnesses. By contrast, there appears to be no shortage of state-of-the-art facilities to treat heart disease, cancer, and gastrointestinal problems.  There is no shortage of state-of-the-art surgical facilities to treat any condition where surgery may be indicated.  In the mean time, mental illness and substance use disorders are the number 1 debilitating disease condition in the United States.  Rather than invest in the necessary infrastructure to provide an equivalent level of care, people with severe mental illnesses are incarcerated instead.  Rather than reversing that trend, several Sheriffs in the country propose designated parts of county jails as psychiatric hospitals and treating people in jail who should not have been incarcerated in the first place. 

I could keep going with additional points like I have in the past, but at this point would encourage any interested reader to take a look at the interview at this link.  Then take a look at the summary at the top of this post and consider my point. Psychiatrists are well trained to do a lot for people with mental illnesses and substance use disorders. We want our patients and their families to have access to the same amount of resources that other medical or surgical specialists have. Don't accept any criticism of psychiatry that does not address these basic points.  

George Dawson, MD, DFAPA 

Reference:

Awais Aftab, MD.  The Bureaucratic Takeover of American Psychiatry: George Dawson, MD, DFAPA
Psychiatric Times.  November 13, 2020    Link

Supplementary 1:

Dr. Allen's comment made me realize a critical deficiency in my graphic and also the interview and that is impact on the academic environment. One of the most exciting aspects of medical school and residency was learning to understand the medical literature and apply it to patient care. I met hundreds of physicians and colleagues with their own unique approaches. In training environments in the 1980s and early 1990s the expectation was that you were researching and reading about your patient's problems and diagnoses and were prepared to intelligently discuss it.  As an attending you had to keep on top of the literature to be a competent teacher and also as a marker of professional competence. Teaching rounds, grand rounds and other teaching based meetings were the most exciting aspects of going to work each day.  I modified my managed care timeline to illustrate the impact on the academic side of the work environment.  

Book Review of The Great Pretender by Susannah Cahalan

 

 This is the second book review of this book on my blog.  I was asked by the editor of The Philosophy Special Interest Group of the Royal College of Psychiatrists - Dr. Abdi Sanati to write another review for this newsletter.  I looked at it as an opportunity to cover some things I may have missed in the first review.  I agreed to not put it on my blog until the newsletter came out.  The latest review follows:

The Great Pretender (1) is written as an exposé of a famous experiment conducted by Rosenhan (2) that purported to discredit psychiatric diagnoses.  The original article was published in in the journal Science in 1973.  Whether you we aware of the original article or not depended on when you were trained and the extent to which you followed that literature. I was just finishing my undergraduate degree at that point and did not complete psychiatric training until 1986.  We had a community psychiatry seminar for 6 months during my last year that was taught by some of the innovators in the field.  It was common to analyze and discuss controversial papers of the day.  A good example would have been the paper that suggested that people with schizophrenia had a much better outcome in the developing countries (3).  At no point did we hear about or discuss the Rosenhan paper.  In fact, for the next 24 years the paper never came across my desk. It was only when I started writing a psychiatry blog that I realized it played a major role in psychiatric criticism and antipsychiatry rhetoric.  At that point, I read the paper and the associated criticism and concluded independently that the methodology was extremely weak and that pseudopatients were not really a good test of medical or psychiatric diagnoses.  I thought it would just fade away on that basis.

I was as surprised as anyone when I heard that investigative reporter Susannah Cahalan had written a book about this experiment, the author, and the methods used.  The investigation begins with a visit to one of Rosenhan’s former colleagues. This colleague shows her a stack of anti-psychiatry books that he thinks “were the key to his thinking”. There is also a file labeled “pseudopatients” that contain the names of all eight pseudopatients and details surrounding their hospitalizations. All the names or aliases and the hospital names had also been changed.

Cahalan’s approach is to write about three parallel subjects.  The most thorough and objective analysis is about the pseudopatient experiment. She covers everything from the available remaining data and the problems with it to the likelihood that the experiment actually occurred the way it was described in the Science paper.  The second broad subject was a character study of Rosenhan.  How did people describe him?  What was he like? Did people especially his colleagues believe that he conducted the experiment.  And finally, the book is a vehicle for Cahalan to comment on psychiatry.  She comes to this work with the direct experience of having experienced autoimmune encephalitis and writing about that experience in the book Brain on Fire.

Reading the original paper is a good starting point for understanding the book.  If you do pull up that article, a few details are immediately evident. The author begins the introduction using the terms “sane” and “insane” as though this is technical language used by psychiatrists. That use of language is interesting because he is listed as a professor of both psychology and law at Stanford.  Since the days of my training, insanity is a strictly legal term and it is without meaning in psychiatry.  The use of these legal terms allows him to point out the unreliability of the “sane”-“insane” dichotomy based on expert witnesses disagreeing in adversarial court hearings.  That has nothing to do with the clinical diagnoses in psychiatry. To what extent were formal diagnoses used in 1973? Rosenhan refers to the Diagnostic and Statistical Manual in the body of his paper.  Interestingly, the authors of my community psychiatry paper (3) reported on the 2-year follow-up of patients from the International Pilot Study of Schizophrenia (1973) and concluded that schizophrenia could be reliably diagnosed so that international comparisons and follow up were possible.  A sanity metric during the same time frame is crude by comparison. There are many additional examples of a lack of objectivity toward the issue of psychiatric diagnosis in the introductory section of the paper (paragraphs 4-7) and the discussion. Excellent critiques of the scientific merit of the paper were available at the time most notably by Robert Spitzer. 

The author describes his pseudopatient experiment as consisting of 8 people – three women and four men of various occupations. Cahalan identifies Rosenhan as pseudopatient number 1.  Twelve hospitals in various locations were chosen.  One was a private hospital.  Pseudopatients were supposed to call the hospital, present for an intake appointment, and then complain that they were hearing voices. When asked to elaborate they were supposed to say the voices were unclear except for the words “empty”, “hollow”, and “thud”.  Rosenhan provides a rationalization for this symptom choice about how on the one hand these symptoms were supposed to have existential meaning and yet there was not a single report of existential psychosis in the literature. Once admitted, the patient was supposed to cease simulating any symptoms and give their actual social history and behave “normally”. They were to take notes and be as cooperative as possible to get discharged. The length of stay was 7-52 days with an average of 19 days. 

Rosenhan also claims in the body of this paper that a second experiment occurred at a “research and teaching hospital” where the staff were informed ahead of time that pseudopatients were going to seek admission during a 3-month period.  Staff were asked to rate whether a patient was a pseudopatient or not.  Of 193 admissions during that time 41 were ranked as likely being a pseudopatient. In this case, Rosenhan did not send any pseudopatients to the facility and claims this false experiment represents “massive errors”.  

One of the elements of the paper that is really never discussed is it structure. The primary data points were eight pseudopatients were admitted and discharged from psychiatric hospitals without being discovered. The secondary data points were a series of observations of the staff that is largely unstructured, highly anecdotal, and contrasted with other situations that seem to lack relevance. The bulk of Rosenhan’s discussion is judgmental and there is no discussion of the limitations of the experimental design or data. Instead the author leaps to clear-cut conclusions that are in some cases only peripherally connected to the data.

Cahalan expends a lot of effort to try to identify and find the pseudopatients and ask them what their experience was like. She locates the records of Rosenhan’s own admission as a pseudopatient. The first real sign of a departure from the research protocol described in Science, occurs in Rosenhan’s recorded admission interview. He recited the voices script and said the symptoms had been going on for four months. He was admitted on an involuntary commitment and discharged nine days later. The hospitalization ended in 1969 - four years before the article came out. The first major sign that the experiment described in Science was not quite the way it was described in the paper occurs when Cahalan looks at the record of the admission interview. In addition to the vague description of hallucinations, Rosenhan states that he believes he can “hear what people are thinking”, that he has tried to “insulate out the noises by putting copper over my ears”, and that he has “suicidal thoughts”. These are all more serious psychiatric symptoms than factitious “existential hallucinations”. Rosenhan also altered his occupational history during one assessment to say that his psychiatric illness led him to give up a job in economics 10 years earlier. At one point he stated that his wife is probably unaware of how useless he felt and that “everyone would be better off if he was not around”.  Considering the seriousness of his fake history, I was surprised that he was discharged in 9 days.

What about the other 8 pseudopatients?  Cahalan was able to locate two – only one of whom was part of the research protocol and shared Rosenhan’s experience. The second patient started out as a psychologist and co-authored a couple of papers with Rosenhan. The author was surprised at how little preparation went into the pseudopatient role. Patient 2 was taught to cheek medications and spit them out. He was reassured by Rosenhan that he had filed a writ of habeus corpus to get him out of the hospital at any time.  When Cahalan tracked down that attorney who said the writs had been discussed but never prepared and that he did not consider himself to be “on call” to get pseudopatients immediately released. Patient 2 was also in the hospital for 9 days and basically released upon his request.  There was no reason for discharge given on the official form but he recalled a psychiatrist approaching him prior to discharge and making remarks to suggest that there was still some concern that he may still be suicidal. Despite that concern there was apparently no discharge plan.

The third pseudopatient discovered by Cahalan was interesting in that he was eliminated from the original protocol and not counted by Rosenhan.  Cahalan discovered that the ninth uncounted pseudopatient was a research psychologist named Harry Lando.  Dr. Lando is well represented in the smoking cessation literature and had published an article in the Professional Psychologist (4) stressing the positive aspects of his pseudopatient experience.  His observations were in direct contrast to Rosenhan and he states as much in the observation: “My overall impressions of the hospital are overwhelmingly positive. The powerlessness and depersonalization of patients so strongly emphasized by Rosenhan simply did not exist in this setting.” He goes on to suggest that using better hospitals as models may be a way to improve the quality of care.  He also questions the ethics of placing pseudopatients in “already overcrowded and understaffed institutions”.  Lando does express a concern about the diagnostic process since all three pseudopatients received diagnoses of schizophrenia.

The key question about why the data of the ninth pseudopatient was omitted from the original paper is answered as a footnote number 6 on page 258 of the original paper:

“Data from a ninth pseudopatient are not included in this study because although his sanity went undetected, he falsified aspects of his personal history. Including marital status and parental relationships. His experimental behaviors therefore were not identical to the other pseudopatients.” 

That footnote is exactly what Rosenhan did when he was admitted as pseudopatient 1 as documented in the existing medical record.  Rosenhan’s lapses were discovered and discussed by Cahalan and are included in the following table.

 

Rosenhan’s Lapses

1.  Data was improperly recorded. The two pseudo-patients interviewed by Cahalan pointed out that their durations of stay in the hospital were not correctly recorded.

2.  His private notes indicated strong influence by Szasz and Laing. Prior to the pseudopatient experiment he assigned work to his students describing psychiatric hospitals as “authoritarian”, “degrading”, and “illness-maintaining”.

3.  He told a pseudopatient that a writ of habeas corpus was prepared and an attorney was on call to get them out of the hospital if necessary. That was not true.

4.  Professional and possibly “unethical” mistakes (p. 173) about length of stay in pseudopatient number two (7 days versus 8) and pseudopatient number 9 (26 days versus 9 days), patient population in the hospital 8,000 vs 1,510), the specific discharge diagnoses of pseudopatients 2 and 9, and details of staff behavior on the ward.

5.  Sending a pseudo-patient into a hospital that was in disarray because it was closing.

6.  Rosenhan at one point lied in correspondence to Spitzer about his stay in the hospital and said it was part of a “teaching exercise” that had nothing to do with research(p. 180). Cahalan describes this as “an outright lie”.

7.  During his admission Rosenhan “goes off script” and gives far more fabricated symptoms and history than the “empty, hollow, thud” existential hallucinations he described in the protocol. Additional symptoms suggest a significant psychiatric disorder. He describes suicidal ideation and significant conflict with his employer – the same falsification of personal history that led him to eliminate the data of the ninth pseudopatient.

8.  Rosenhan fabricated an excerpted portion of the medical record and both the original record and the excerpt are published for A - B comparison on page 190. Cahalan concludes that the facts “were distorted intentionally by Rosenhan himself.”

9.  Inadequate preparation of the research subjects. Patient 2 ended up taking a dose of chlorpromazine and patient 9 was given liquid chlorpromazine so it could not be cheeked as instructed.  Pseudopatient 9 estimated the preparation time for hospital admission by Rosenhan was about 15 minutes.

10.  When patient 9 was eliminated from the study none of the data about pills dispensed or staff contact time in the paper was changed.

11.  In an National Public Radio program that aired before the publication of his paper (December 14, 1972) he misstated his time in the hospital as a pseudopatient (several weeks versus 9 days) and the amount of medications dispensed to pseudopatients (5,000 pills versus 2,000 pills) while building to the conclusion that psychiatric hospitals are non-therapeutic and should be closed (p.234)

12.  Pseudopatient 9 commented that what Rosenhan had written about him in the experiment was “total fiction” (p.269)

13.  Rosenhan did not complete a book about the pseudopatient experience, despite an advance from the publisher, a subsequent lawsuit from the publisher and what is described as plenty of publicity around the time the paper came out in Science. He also never published on the topic again (p. 295).

 

Rosenhan did continue to publish a description and discussion of his study in the text Abnormal Psychology (5). The discussion emphasized that the simple hallucinations described with nothing else being unusual would have been detected outside of a hospital. In the context dependent setting it was not.  In other words – he maintained one of the same themes as in the original paper.

One of the areas that really piqued my interest was why Science published this paper in the first place.  Cahalan got the opinion from an academic psychologist that the peer review in a non-psychology journal would be less rigorous.  When she approached the journal she was told that records were confidential and that they were not kept back that far.  Accessing Retraction Watch (6) demonstrated that there has been a total of 120 papers retracted from Science since 1963. The reasons for the retractions are given as data errors, errors in methods, result errors, errors in conclusions, errors due to contaminated experiments, falsification/fabrication of data, irreproducible results, misconduct by the author, ethical violations by the author, investigation by a company, institution, or third-party.  Only three of these papers had anything to do with psychiatry and those papers were primarily about the neurobiology of the brain. Cahalan’s investigation suggests that several of the reasons for retraction have been met.

Apart from the details of the Science paper, Cahalan also does a character study of Rosenhan. We learned that his brother had bipolar disorder and did well on lithium. It was suggested that was why he became interested in psychology. He was described as bright and charismatic. He was clearly influenced by the work of anti-psychiatrists and assigned work to his students that “describe psychiatric hospitals as authoritarian, degrading, and illness maintaining among other terms”. (p 73).  The title of the book highlights Rosenhan’s characteristics as a raconteur who would occasionally pretend to be someone who he was not. His son described an incident in New York City where he introduced himself as a professor of engineering at Stanford in order to get a tour of an interesting construction site with his son. In another scene he is joking about the wig he wore to get into the psychiatric hospital.  Cahalan finds the admission photo showing that he is bald without a wig. The people who knew him the best – acknowledge the he was difficult to know and just like Rosenhan’s arguments about psychiatric diagnoses being context dependent – his personality was as well.   

Apart from academic books about the history of psychiatry – most books review sensational history and arguments that by their very nature diminish the field.  This book is intermediate in that tone with those arguments interspersed through the investigative journalism about Rosenhan. They touch on the familiar themes of biological reductionism as opposed to a clinical psychiatry where patients are actually listened to with no reference to how clinical psychiatrists really practice every day. Some psychiatrists end up being caricatured and some are acknowledged as being highly motivated and humanistic. I am probably far too invested in clinical psychiatry and the good I have seen done to tolerate a journalist’s approach to the field.  I give Cahalan credit for touching on the current situation that has resulted in severely rationed care and the transinstitutionalization of patients in jails.  The overall concept that psychiatrists have little to do with the systems of care that are controlled by businesses and governments is not emphasized even though it was recognized as a problem by two of the pseudopatients.  She also points out that the pseudopatient experiment is irrelevant to psychiatric practice today but her resounding theme throughout the book was that it was extremely relevant irrespective of what actually happened.  The book also gives Rosenhan too much credit for psychiatric criticism. Like many books of this nature – there is little to no evidence that psychiatrists might be their own best critics or that outrage might be a legitimate reaction to outrageous criticism rather than defensiveness.

 In conclusion The Great Pretender identifies very specific problems with the original Rosenhan paper that have been listed in the narrative and table in this report. He gained initial celebrity status from the study and signed a book contract. Even though he was given an advance on the book and wrote a manuscript he never produced a book.  The author suggests that may have been due to the fact that Robert Spitzer was aware of Rosenhan’s nonadherence to the research protocol during his admission. As Rosenhan withdrew from the pseudopatient limelight he also stated that none of his research should lead to the conclusion that psychiatric hospitals were unnecessary and that represented a complete turnaround form earlier statements.

The controversy, the original paper and the book could be the subject of seminars in the history or philosophical aspects of psychiatry. It touches on a number of themes primarily the ethics of research and how it should be conducted. It also touches on psychiatric criticism and may be useful in discussing how future generations of psychiatrists can prepare to deal with it. 

 

George Dawson, MD, DFAPA

 

References:

 

1: Susannah Cahalan.  The Great Pretender. Grand Central Publishing. New York, 2019. 382 p.

2: Rosenhan DL. On being sane in insane places. Science 1973 Jan 19;179(4070):250-258.

3: Sartorius N, Jablensky A, Shapiro R. Cross-cultural differences in the short-term prognosis of schizophrenic psychoses. Schizophr Bull. 1978;4(1):102‐113. doi:10.1093/schbul/4.1.102

4: Lando, H. A. (1976). On being sane in insane places: A supplemental report. Professional Psychology, 7(1), 47–52. https://doi.org/10.1037/0735-7028.7.1.47

5: David E. Rosenhan, Martin E.P. Seligman. Abnormal Psychology- 2^nd Ed. WW Norton and Company, New York City, 1984, 1989; p 181-183.

6: Retraction Watch: Retractions from Science.  Accessed on May 22, 2020: http://retractiondatabase.org/RetractionSearch.aspx#?jou%3dScience

7:  Gaudino M, Robinson NB, Audisio K, et al. Trends and Characteristics of Retracted Articles in the Biomedical Literature, 1971 to 2020. JAMA Intern Med. Published online May 10, 2021. doi:10.1001/jamainternmed.2021.1807

The authors cite retracted literature (5209 papers) back to the year 1923. Scientific misconduct like fabrication of data was cited as the most common reason.  

Supplementary:

The review was written for Philosophy Special Interest Group of the Royal College of Psychiatrists September 2020 newsletter and it can be found starting on page 8.

Additional Reference posted on July 17, 2021:

Justman, Stewart, "Below the Line: Misrepresented Sources in the Rosenhan Hoax" (2021). Global Humanities and Religions Faculty Publications. 13. https://scholarworks.umt.edu/libstudies_pubs/13

This author fact checks Rosenhan's references and footnotes and finds they do not support his points.

 

 

 

 

Covid-19 Up Close and Personal

 On September 4, I started to feel typical symptoms of a flu-like illness. I have been a student of flu-like illnesses for at least the past 15 years. Some may say that I am obsessed with flu-like illnesses. By definition these illnesses start out as acute upper respiratory infections but also lead to systemic symptoms like malaise, weakness, and muscle pains or myalgias. In some cases, the symptoms can build to a disabling intensity. About five years ago I developed a flu-like illness after returning from Alaska that led to an exacerbation of asthma. I had not taken any asthma medications for 20 years but have been on those medications ever since. Researching that area suggested that flu-like illness was probably a rhinovirus. Some researchers think that rhinovirus is one of the main precipitants of asthma. Rhinovirus also happens to be a common circulating respiratory virus along with about 20 others that cause respiratory infections every year.  There are several non-COVID-19 coronaviruses in this group.

There were definite early signs even before the first respiratory symptoms. I have a fairly set exercise routine that I do every week and I noticed that my baseline heart rate (54 bpm) and blood pressure (105-110 mm Hg systolic) were increased and my exercise capacity was decreased by about 40%. That occurred about 48 hours before the onset of symptoms. As the symptoms increased my first thought was that I needed to get tested for coronavirus. That took an additional four days. It wasn’t from a lack of trying, but more a lack of resources going into the weekend. That delay highlights a significant weakness in the American healthcare system. I self-quarantined during that time but there are a lot of people who would need to see the test result before they could.  I did get positive test on day seven, I canceled the rest of the day at work and have been home recovering ever since.

The overall course of the illness has been very similar to a moderate case of influenza with the exception that I did not get a fever. It measured every day in the normal range. I also did not get shortness of breath.  Having the risk factors of asthma and old age, I was fairly anxious about any shortness of breath as a symptom. My symptoms are basically as graphed with a few exceptions of what I would refer to as atypical symptoms. The first one would be feeling flushed or like the skin temperature is elevated. That has been a fairly consistent feature that I have not seen mentioned anywhere. My skin was always cool to the touch and not moist. Another atypical symptom is laryngitis.  I have observed that in several COVID-19 patients in the media.  It can be fairly limiting if you have to talk all day at work like I do. The third atypical symptom was viscous mucus in the nose and throat. It was not abundant but difficult to clear and never reached the volumes typically seen in bronchitis.

One of the questions that I have been asked is: “How does a guy as careful as you end up catching COVID-19?”  It turns out that is an excellent question. As noted elsewhere on this blog I have essentially self-quarantined at home since the end of March or the start of the pandemic. I have had limited contact with people. I do not go into stores, supermarkets, coffee shops, or any public space. I pick up groceries ordered online and then collect them from a site where a masked attendant loads them into the back of my SUV.  All of my clinical work, continuing education, and professional meetings are done online.  I prepared a timeline of all contacts in or around my home for the previous 19 days (click to enlarge).  

From the summary, of the 18 total contacts I had direct contact with 6, only 4 of them about 6 days prior to the onset of symptoms.  All 4 of those contacts were wearing masks and none have tested positive for COVID-19.  My wife had contact with the other 12 and 9 of them were socially distanced or masked.  Only the electrician and three of the appliance repair/installers were not but they were socially distanced.  In addition, we made an effort to air out the house when they were there and after the left.  There was a total of 5 tradesmen in the house. They were all there for an average of about 1 hour.  I greeted one of them at a distance of about 12 feet and he was not wearing a mask. According to a recent hierarchy of transmission risk, I had no high-risk contacts for transmission (3).

My wife on the other hand was in a couple of higher risk scenarios (but not much higher).  As an extrovert, she was also out talking with people every day and exercising with several of her health club friends at their homes. She did however test negative for COVID-19 on the exact same test that I took. There are various estimates that 20-40% of COVID-19 infections result in asymptomatic carriers. It may be possible that she was a carrier and subsequently cleared the virus so that no viral RNA was detected on the nasal swab.  We are both currently trying to get antibody testing to COVID-19. It will confirm that I have short term immunity and possibly that my wife was an asymptomatic carrier.

When I did find out that I tested positive, I self-quarantined in the house pending my wife’s test and have been quarantined ever since.  The health plan recommendation is to wait for day 14 and if asymptomatic at that point, the self-quarantine can end. My wife is using the same date to end her quarantine and remained asymptomatic.  We have the luxury of having a large enough house where we can occupy separate areas and have separate bathrooms that are exhausted to the outside of the house.  I also kept an electronic air filter with a UVC germicidal light at the entrance to my office and between us in any public areas.  Several questions arise from this experience including:

1.  Why were my symptoms so mild (relatively speaking)?

Considering the actual statistics of the pandemic in the United States – my outcome is not that surprising.  About 1 in 34 cases have died and that number increases to 1 in 13 in my age range and 1 in 5 in the next highest age decile.  At the time of this posting there have been 197,000 deaths and 6.7 million cases.  There is a lot of comparison with influenza, but at this time there should be no mistake that while influenza typically generates more cases and more hospitalizations – there has only been one year where influenza mortality exceeded current SARS-CoV-2 mortality and that was the pandemic of 1918. 

The second consideration are the physical parameters of the environment. Assuming that my wife is not an asymptomatic carrier, the only time I was at a distance of less than 4 meters I was wearing a mask and so were the people I was in proximity to.  The contact lasted less than 10 minutes. And not a lot was said. We know that masks, distancing, and dilution in outdoor air probably works be reducing the concentration of airborne viral particles.  With that reduced concentration, any inhaled inoculum will be less resulting in a less severe infection. The estimated number of viral particles necessary to precipitate a case of COVID-19 is about 280 particles. That is 2-3 orders of magnitude higher than more virulent and lethal viruses like smallpox.

A few other lifestyle considerations. I eat a high-protein, high fiber, high whole grain, and low fat/low sugar diet.  I try to maintain a healthy weight.  I drink a lot of fluids every day.  I have been doing that for at least 30 years on the advice of a rheumatologist in order to maximize uric acid secretion and decrease the risk of gout attacks (I am an undersecretor of uric acid and had my first gout attack in medical school). Anyone reading this should drink a lot of fluid only based on their physician’s advice.  The only relevant factor in this paragraph in surviving the virus is probably maintaining a healthy weight and a good diet.  I was able to maintain my usual fluid intake during the course of this illness.

I take Vitamin D every day because my levels are typically marginal.  I take famotidine daily to prevent anaphylactic reactions. I only take it because the original H-2 antagonist recommended by my allergist (ranitidine) was taken off the market because of contamination in the manufacturing process. There has been some suggestion that famotidine is useful in the prevention or treatment of COVID-19 and for a while it nearly disappeared off the generic market.  I am not aware of any randomized clinical trial (RCT) results of famotidine and it has been demonstrated to not have any direct antiviral effect in vitro.  There is current speculation that in combination with H-1 antagonists that it may reduce histamine associated cytokine effects (13). At this point I would not consider it to be too relevant.

Exercise is a big part of my life and has been for the past 30 years. I typically exercise vigorously for 90 to 120 minutes per day.  Recent research (11,12) suggests that people who exercise vigorously into old age have better acute adaptive immunity (T-cell response) due to a better thymic environment.  One of the purported mechanisms is IL-7 production by skeletal muscle.  IL-15 is also an exercise responsive interleukin that enhances T-cell survival.  The net effect of these changes in the older person who exercises vigorously has a greater input of thymocyte progenitor cells and an enhanced output of CD4 and CD8 cells that are recent thymic emigrants (RTE). Both of these cells populations are critical for the acute adaptive response to novel viruses.  If I had to speculate about the lifestyle factors that are important it would probably be the effects of exercise, diet, not smoking and no alcohol intake on immunity and pulmonary function.

 2.  Why is there such heterogeneity in responses?

The host determinants of response are not well characterized at this point- other than the suggestion that previous exposure to common circulating coronaviruses could possibly lead to an enhanced antibody effect and either apparent asymptomatic carrier status or a less severe case as an adult.  Is it possible that the severe respiratory infection that I got in January was a coronavirus that was not SARS-CoV-2 and that it conferred some immunity?  This is one of the theories about why children are less affected by COVID-19 than adults – they tend to get more respiratory virus infections per year. Human coronaviruses and rhinoviruses are generally considered to cause up to 50% of common cold infections per year (10).  The Minnesota Influenza Incidence Surveillance Project, (MIISP) 3 of the 4 normally circulating human Coronaviruses – NL63, HKU1, and 229E (not OC43) since last September. Although these coronaviruses are now considered all part of the collection of common cold viruses they have been fairly recent discoveries with NL63 discovered in 2004 (7) and HKU1 discovered in 2005 (8).  The common coronaviruses have considerable RNA sequence homology with SARS-CoV-2 suggesting cross immunity can exist (9).  For example, pre-existing T-cell immunity in blood donors to SARS-CoV-2 is documented and is thought to be due to exposure to beta-coronaviruses that are in circulation (4).  But there is also evidence suggesting that pre-existing coronavirus immunity is not effective with SARS-CoV-2 (15).

One the genetic side, there are essentially no data at this point about genetic factors that favor successful recovery from the pandemic virus (click to enlarge).

 

3.  Given the exposures – is it possible that some other exposure (packaging, mail, aerosols from washing packing or mail) is more important than suggested by conventional wisdom?

Even though handwashing and washing of frequently touched surfaces is a top recommendation the current opinion is that transmission is unlikely from either groceries or mail based on studies that look at virus survival on different materials over time.  To me that is somewhat inconsistent with the hand washing advice.  The original theory was that a person could touch a contaminated surface, touch their face, and then end up with the infection through mucus membranes.  Groceries and the mail seem to be designated as infrequently touched surfaces relatively free from contamination.  An additional question for consideration is whether aerosols generated in washing the surfaces of groceries can transmit. SARS-CoV-2.  I use a UV sanitizer for mail and any objects the size of a large book or smaller. That method has limitations in terms of how accessible the surfaces of any contaminated object are.

One final critical consideration is the person you are in quarantine with. Do they share your goals and risk tolerance or not?  In my particular case, I am not risk tolerant at all if the risk is contracting a virus that has a 1 in 13 chance of killing me.  The prior probability of an adverse outcome is higher due to me having asthma, but the exact numbers are probably not known at this time. I would happily remain at home, not get a haircut (I have not), and just go out for groceries and necessary medical care.  My wife on the other hand is very social, and has maintained an active schedule with her friends and associates over the entire pandemic.  She spends her days exercising, socializing, and attending limited activities with friends.  She is distanced and wears a mask when necessary. Despite our ability to pick up groceries without having to enter a store she will spontaneously stop at these stores, put a mask on, and pick up a few items. This difference in approaches to the pandemic does create some tension.

Whether our different approaches produced predictable outcomes or not is up in the air at this point.  She was just approved for antibody testing and I still have to get approval at an appointment next week. All we know is that I was positive for SARS-CoV-2 on a PCR test and she was not. That leaves either airborne transmission, contaminated surfaces, or aerosols from washing contaminated services.

Getting through this does provide a sense of relief.  Even though immunity to this virus does not seem to be permanent at this point I am very grateful to have made it through these two weeks.  My boss sent me an email and asked what that sense of relief was like and I told him:

“It feels like I dodged a bullet.”

And it does…..

 

George Dawson, MD, DFAPA

 

References:

1:  Stephens DS, McElrath MJ. COVID-19 and the Path to Immunity. JAMA. Published online September 11, 2020. doi:10.1001/jama.2020.16656

2:  Gandhi M, Beyrer C, Goosby E. Masks Do More Than Protect Others During COVID-19: Reducing the Inoculum of SARS-CoV-2 to Protect the Wearer [published online ahead of print, 2020 Jul 31]. J Gen Intern Med. 2020;1-4. doi:10.1007/s11606-020-06067-8

3:  Jones Nicholas R, Qureshi Zeshan U, Temple Robert J, Larwood Jessica P J, Greenhalgh Trisha, Bourouiba Lydia et al. Two metres or one: what is the evidence for physical distancing in COVID-19? BMJ 2020; 370 :m3223 Link

4:  Stephens DS, McElrath MJ. COVID-19 and the Path to Immunity. JAMA. Published online September 11, 2020. doi:10.1001/jama.2020.16656 Link

5:  Fischer EP, Fischer MC, Grass D, Henrion I, Warren WS, Westman E. Low-cost measurement of face mask efficacy for filtering expelled droplets during speech. Sci Adv. 2020;6(36):eabd3083. Published 2020 Sep 2. doi:10.1126/sciadv.abd3083 Link

6:  Bar-On YM, Flamholz A, Phillips R, Milo R. SARS-CoV-2 (COVID-19) by the numbers. Elife. 2020 Apr 2;9:e57309. doi: 10.7554/eLife.57309. PMID: 32228860.

7:  Fouchier RA, Hartwig NG, Bestebroer TM, Niemeyer B, de Jong JC, Simon JH, Osterhaus AD. A previously undescribed coronavirus associated with respiratory disease in humans. Proc Natl Acad Sci U S A. 2004 Apr 20;101(16):6212-6. doi: 10.1073/pnas.0400762101. Epub 2004 Apr 8. PMID: 15073334; PMCID: PMC395948.

8:  Woo PC, Lau SK, Chu CM, Chan KH, Tsoi HW, Huang Y, Wong BH, Poon RW, Cai JJ, Luk WK, Poon LL, Wong SS, Guan Y, Peiris JS, Yuen KY. Characterization and complete genome sequence of a novel coronavirus, coronavirus HKU1, from patients with pneumonia. J Virol. 2005 Jan;79(2):884-95. doi: 10.1128/JVI.79.2.884-895.2005. PMID: 15613317; PMCID: PMC538593.

9:  Yaqinuddin A. Cross-immunity between respiratory coronaviruses may limit COVID-19 fatalities. Med Hypotheses. 2020 Jun 30;144:110049. doi: 10.1016/j.mehy.2020.110049. Epub ahead of print. PMID: 32758887; PMCID: PMC7326438.

10:  Greenberg SB. Update on Human Rhinovirus and Coronavirus Infections. Semin Respir Crit Care Med. 2016 Aug;37(4):555-71. doi: 10.1055/s-0036-1584797. Epub 2016 Aug 3. PMID: 27486736; PMCID: PMC7171723.

11:  Duggal NA, Pollock RD, Lazarus NR, Harridge S, Lord JM. Major features of immunesenescence, including reduced thymic output, are ameliorated by high levels of physical activity in adulthood. Aging Cell. 2018;17(2):e12750. doi:10.1111/acel.12750

12:  Lazarus NR, Lord JM, Harridge SDR. The relationships and interactions between age, exercise and physiological function. J Physiol. 2019;597(5):1299-1309. doi:10.1113/JP277071

13:  Hogan Ii RB, Hogan Iii RB, Cannon T, et al. Dual-histamine receptor blockade with cetirizine - famotidine reduces pulmonary symptoms in COVID-19 patients [published online ahead of print, 2020 Aug 29]. Pulm Pharmacol Ther. 2020;63:101942. doi:10.1016/j.pupt.2020.101942.

14:  Minnesota Influenza Incidence Surveillance Project,  (MIISP). Minnesota Department of Health.  Correspondence on circulating common coronaviruses in Minnesota.  Received on 9/19/2020. 

15:  Loos C, Atyeo C, Fischinger S, Burke J, Slein MD, Streeck H, Lauffenburger D, Ryan ET, Charles RC, Alter G. Evolution of Early SARS-CoV-2 and Cross-Coronavirus Immunity. mSphere. 2020 Sep 2;5(5):e00622-20. doi: 10.1128/mSphere.00622-20. PMID: 32878931; PMCID: PMC7471005. 

Supplementary 1:

My wife tested negative for SARS-CoV-2 IgG antibodies today (9/22/2020) in addition to the negative nasal swab PCR tests - making her an unlikely source of infection.

Supplementary 2:

COVID-19 follow-up: 

Saw my internist yesterday (9/25/2020). 

My course of the illness was "average" for all of the patients he has seen. He agreed that PCR false positives are not likely but false neg are. He declined Ab testing. I applied to the Red Cross convalescent plasma program.