DSM-6? Don't Get Your Hopes up.....

 

I just spent a while reading all the papers in the American Journal of Psychiatry about the future DSM (1-5).  As you might expect many people have many things to say and that is as true inside as outside the field.  We are on the cusp of another epoch of DSM articles in the popular press that will predictably vary from inadequate to horrific. Those articles will claim that the DSM is published as a source of revenue for the American Psychiatric Association (APA), as a way for pharmaceutical companies to make money, and as a “Bible” for psychiatrists.  There will be philosophical musings tangentially related to the field but extremely critical.  There will be the usual antipsychiatry screeds about how it is unscientific, how there are better systems out there, and how the diagnoses are mere labels that mean nothing. Most of those opinions will be written by people who have never practiced psychiatry or been treated for a mental illness.  It seems that just about anybody believes that they are an expert in psychiatry.

For those of us familiar with the field - our backgrounds are more uniform. A significant number of people are like me – undergrad science majors who are always interested in biological science and medicine. We practiced in acute care settings and saw people with significant medical comorbidity.  We made plenty of medical and neurological diagnoses that nobody else made and were a resource for that kind of referral.  We knew early on that many of the diagnoses listed in the DSM were questionable and we never used them. It turns out we are the last people the DSM is designed for and after reviewing recent opinion pieces I will tell you why and how it can be corrected.

The lead paper by Oquendo, et al (1) briefly reviews common cited problems with the DSM and possible remedies.  The first criticism is that it is atheoretical. That is less of a problem than described.  Any reader of the DSM sees immediately that despite the stated atheoretical stance there are clear stated etiologies for DSM listed diagnoses. To keep it simple, I refer any reader to the table Diagnoses associated with substance class (p. 482).  That table contains 127 diagnoses associated with specific substances.  There are similarly many diagnoses that identify a psychosocial factor as being involved in the etiology.  Categories versus spectrums are listed as problem 2, despite the fact there probably are no spectrums (from the genetic side) and all polygenic medical conditions (hypertension and diabetes mellitus for example) have the same limitations. There are 4 additional uninteresting points and proposed solutions.  One of the subcommittees is focused on the Dahlgren-Whitehead framework for social determinants of health.  At the same time another committee is looking at instruments to assure a more comprehensive sociocultural assessment.  It made me wonder whether anyone on the committee had ever read a current comprehensive psychiatric assessment.  Every psychiatrist should have concerns about more checklists.

The second paper by Cuthbert, et al (2) was about biomarkers and biological factors. The discussion was long on biomarkers and short on biology.  To neuropsychiatrists this section of the DSM has always been a disappointment. As an example, the section with the most biology – neurocognitive disorders has surprisingly little discussion of associated medical features (like a gross characterization of EEG in delirium) or a discussion of neuropathology without any additional discussion of what that looks like clinically.   The Oquendo committee (1) has proposed changing the name of the DSM to the Diagnostic and Scientific Manual because it is no longer used to collect statistics.  If that occurs, they need to put a lot more science into it, and this is the area for it. 

I have proposed a separate DSM for psychiatrists in the past but a separate volume on the current science of psychiatry would be as useful. I am talking about more than just a review of unproven research, but how the science-based psychiatrist translates what we know so far into clinical practice.  I would start with a rewrite of the section on Neurocognitive Disorders and all the important variations before worrying about plasma biomarkers and whether they are FDA approved. There are volumes written on this subject that have been lost on the DSM.  To cite a few examples – should a psychiatrist be able to recognize presentations of encephalitis, meningitis, and the various presentations of vascular dementia from their own assessment and available imaging and lab studies?  Should a psychiatrist be able to diagnose various forms of aphasia and do the indicated evaluation? Of course, they should – and it is all part of the rule out criteria for psychiatric disorders. It is not enough to leave the medicine and neurology of psychiatry to somebody else.  But very little is mentioned in the DSM except the rule out conditions: “the disturbance is (or is not) attributable to the physiological effects of a substance or another medical condition (or mental disorder).”  That is too vague for psychiatrists.  

The Structure and Dimensions Committee (3) is charged with coming up with the most clinically useful structure of the future DSM.  That involves incorporating recent research.  They have produced a lengthy table summarizing the total categories, named categories and prevailing frameworks and theories used for all the DSM starting with the first one. That number goes from 4 to 22 categories in the DSM 5-TR.  There is usually criticism about diagnostic proliferation – but not much about category proliferation.  When I encounter these numbers – I remind myself that we started with a unitary psychosis model in the 19^th century.  By 1918 (6) the situation not much better with the major diagnostic categories being psychosis or not psychosis. It could be argued that early diagnostic and classification efforts failed to recognize or include mental disorders that had been observed since ancient times rather than lower numbers being more ideal.

The fourth paper (4) is focused on Quality of Life (QOL) as an essential part of psychiatric diagnoses. They establish premises based on the often-quoted literature on disability associated with psychiatric diagnoses.  They describe a bidirectional relationship:  “… symptoms of a mental illness can impair the individual’s functioning in daily life, and poor functioning can in turn lead to or exacerbate the symptoms of a mental illness.”  The paper has two definitions of QOL.  The author’s definition is “a person’s subjective perception of their emotional, psychological, and social well-being.”  The paper also contains the World Health Organization (WHO) definition of QOL “incorporates how an individual feels about their emotional, social, and physical well-being, which can affect and be affected by their mental health condition(s).”  WHO further defines QOL as “one’s perceptions of their position in life, contextualized by the culture and value systems in which they live, in relation to their expectations, goals, and standards.”  There is a related discussion on the Global Assessment of Functioning (GAF) from previous DSMs.  QOL metrics were decided to be subjective rather than clinical ranking like the GAF.  The GAF was also thought to conflate symptoms of mental illness with functioning even though there is a clear relationship. 

The authors discuss the World Health Organization Disability Assessment Schedule 2.0) (WHODAS-2.0) and it’s use to rate psychiatric disability. It is a 36-item, 100-point self-administered, 6-dimension rating scale.  Administration and scoring in full clinical schedules was considered a limiting factor, but clinically the question is what happens with more identified problems?  Does the treatment plan expand proportionally?  Will psychiatrists be expected to either treat directly or develop referral sources for all the disabilities identified as communication, mobility, self-care, interpersonal, life and societal activities. Additional briefer QOL instruments are discussed as well as brief interventions.

A critical concept that was not mentioned was the patient’s baseline function. With every patient I saw, I had a subjective (and often other informant) description of their baseline level occupational, academic, and interpersonal functioning.  In some case it involved activities of daily living (ADLs) and instrumental activities of daily living (IADLS).  On inpatient units those ADLs were often documented by occupational therapists.  In my outpatient Alzheimer’s Disease and Memory Disorder clinic – every new patient had their ADLs documented by the RN staffing the clinic.  It required hours of work per day that were not reimbursed.  My clinic was eventually shut down because of that unreimbursed work and my refusal to do the work myself for free. The additional cost and time for these assessments is a reality factor in the modern rationed health care system.

The fifth paper is entitled: “The Future of DSM: A Strategic Vision for Incorporating Socioeconomic, Cultural, and Environmental Determinants and Intersectionality.”  The definition of intersectionality is “a framework for understanding how various social and political identities—such as race, gender, class, sexuality, and ability—overlap and intersect to create unique combinations of privilege and systemic discrimination.”  I have a problem with the use of a vague term that is used rhetorically being implemented in a DSM.  The DSM is a target of rhetoric and putting rhetoric in the manual is likely to amplify its role as a target.  I have also reviewed ample evidence that the major journal of the APA – was unable to separate rhetoric from reality in the case of clear historical evidence about racial discrimination.  This highlights the need for clear definitions and avoiding political rhetoric in any rethinking of this manual.  It also highlights the need for clear evidence rather than rhetoric and that commentaries – even in the flagship journal of the American Psychiatric Association cannot be depended upon for that evidence.

Intersectionality is unnecessary to get at what the authors hope to accomplish.  Cross cultural psychiatric evaluations are the case in point. They involve an assessment of cultural differences and how the culture affects disease definitions and presentations, the sick role in that culture, and how demographic factors affect how a person is advantaged or disadvantaged in their original or adopted culture. The authors suggest it is necessary to promote various public health prevention strategies and promote health care equity.  As far as I can tell, health care equity in the US is strictly in the purview of politics and in one year a massive amount has been destroyed by the Trump administration.  Political features should be avoided as much as rhetorical features in a DSM, especially given the abysmal track record of physician medical organizations in politics.

The authors define socioeconomic, cultural, and environmental determinants of health (SCE-DoH) as the key focus (along with intersectionality). These determinants are all well known to any psychiatrist who has recorded a social history for a detailed assessment and that should include all of us.  They conceptualize them as modifiable or non-modifiable risk factors and how they may be relevant for prevention strategies.  Much of the prevention is outside the scope of psychiatric practice and advocacy by professional organizations has questionable impacts.  They also use the Dahlgren-Whitehead model of main health determinants and cover suggestions of screening patient populations for these variables.  They conclude that the next DSM should include recommendations to use multiple “vetted instruments” to make these SCE-DoH assessments.  They give an example of how this assessment can be built into routine clinical care.  Interestingly, the psychiatric assessment is not included in the “routine diagnostic workflow” (see figure 2).  Looking at the strategy 2 where the SCE-DoH is used to determine “management as usual” versus “enhanced case management” – I made that determination myself for 40 years. For the last 25 years that “enhanced case management” was not available for most people needing it. That tells me that the suggested assessment is already being done by some people and the necessary resources are not there.  I found myself documenting that fact in too many cases.

The Committee realizes that they cannot create an additional burden on clinicians who already have unrealistic demands and provide far too much work for free in rationed environments.  That translates to less time to do comprehensive assessments – not more.  

Even though these are very preliminary statements about the future DSM – I am not very hopeful at this point.  The commentaries so far seem directed at criticisms from outside of the field rather than what psychiatrists need.  Apart from the criticism I have offered so far what is noticeable:

1:  The lack of commentary on medical and neurological diagnoses – in any psychiatric classification it is either explicit (or implicit) that what are considered the current psychiatric diagnoses are not caused by a substance or another medical diagnosis.  The non-DSM diagnostic systems are generally just focused on the listed symptoms of these disorders and there is no provision for other medical conditions.  It is also not explicit enough in medical training. At some level this is explained away and needing to utilize whatever resources are available.  That is not enough.  The DSM should have a section of diseases by system that need to be diagnosed if they are present and at least a reference to how that should be done.  There is not nearly enough information on what medical diagnoses psychiatrists make.  This is also an important feature for resident education since it would suggest how much clinical medicine and neurology residents need to be exposed to and whether they are seeing relevant cases.

2:   Philosophical criticisms while minimizing biology and history –  in several of the papers the authors talk about “natural kinds” and “carving nature at the joints”.  This is philosophy speak that has been used to obfuscate the field. The first time I encountered these arguments they struck me as obvious nonsense.  That was first suggested by Thomas Sydenham when he made this statement in about 1640:

“In writing the history of a disease, every philosophical hypothesis whatsoever, that has previously occupied the mind of the author, should lie in abeyance. This being done, the clear and natural phenomena of the disease should be noted — these, and these only…” (7) 

DeGowin and DeGowin (8) summed up the process over the next three centuries:

"For several thousand years physicians have recorded observations and studies about their patients.  In the accumulating facts they have recognized patterns of disordered bodily functions and structures as well as forms of mental aberration.  When such categories were sufficiently distinctive, they were termed diseases and given specific names.”

It seems that the conceptual clarity here requires no reference to naturalism or essentialism.  It only requires empiricism and a determination of sufficiently distinctive.  In my long and intensive career – the only place I have encountered these philosophical arguments was in a literature that was generally critical of psychiatry.  In the process it also requires psychiatrists to suspend the idea that empirical adequacy is not all that is required, but also all that we were taught. 

Conceptual expansionism or semantic drift has been used to criticize the DSM and psychiatry and that needs to be called out wherever it happens.  By that I mean a concept that is developed within one academic silo that is suddenly applied without precedent or a clear basis to psychiatry.  On this blog I have criticized several of these applications including epistemic and hermeneutical injustice.  Although none of the Am J Psychiatry papers used the term, I did encounter folk psychology now being applied to criticize the DSM (9) in a mailing.  That is a concept I was familiar with from Andy Clark’s work (10).  If you are not familiar with the concept a generally accepted definition would be:  “The everyday ability to predict and explain the behavior of ourselves and others by attributing mental states—such as beliefs, desires, intentions, and fears.”  In other words – you see somebody doing something and come up with a theory of why they are doing it.  I have written about it on this blog as a reason why many people seem confident in their knowledge of psychiatry and psychology even though they have never been trained in either. There are several theories of how a folk psychology theory can apply, but the original debate centered on how the ascribed beliefs, desires, intentions, etc. had no neural equivalent and therefore that at some point these mental states would be replaced by more scientific terms. In other word suggesting that the DSM is folk psychology is basically saying the signs and symptoms used as descriptors have no brain equivalent and therefore it is an invalid classification. This argument is essentially the same argument that there is an explanatory gap between what most people consider consciousness to be and the neural substrates that causes it.  Consciousness is approximately represented in neural substrate and the same thing can be said for mental disorder symptoms.      

3:  The continued lack of focus on what might be useful to psychiatrists - 

When I think about a DSM that might be useful to psychiatrists or at least the kind of psychiatrists I am used to working with – there needs to be more than the usual slicing and dicing of diagnostic criteria.  Adding more work with more rating scales is also a disappointment.  A manual breaking down the current work with examples and a suggestion of the potential exhaustive data points might be. For example, pointing out that the typical phenomenology of a disorder should be adequately represented in the history of the present illness.  That obviously includes any precipitating factors irrespective of what they might be – biological or sociocultural. The next section should include a discussion of the past psychiatric and medical histories as well as comorbid conditions.  Psychiatrists should be expected to know relevant medical diagnoses, how medical comorbidity affects psychiatric treatment, and medical causes of psychiatric presentations.  The usual disclaimer about medical conditions is as inadequate as a disclaimer about sociocultural aspects of care.  The new DSM should not be a mere collection of psychosocial determinants completely devoid of medicine.

A more formal formulation section should be there.  In the DSM-5 for example it is referred to as a “concise summery of the social, psychological, and biological factors that may have contributed to developing a given mental disorder.”  (p. 19).  There are multiple ways to write a formulation (behavioral, psychodynamic, neuropsychiatric, and others) and they should all be discussed in the DSM.

4:  A theory section on the biology of psychiatric diagnoses – why they are complex and how that complexity should be approached.  There are experts in the field who can comment on how polygenes produce quantitative diagnoses that can blend imperceptibility into the normative states.  Some of those same experts can discuss the statistical methods used to try to improve classifications and how that works clinically.  There should be a comparison with other commonly described quantitative disorders like hypertension and diabetes mellitus Type 2.  The classification system of rheumatology could be discussed as a direct comparison to the DSM.

I have written about the problem with the term transdiagnostic. I do not think it adds any specificity to interventions.  In psychiatry what is considered a transdiagnostic symptom can also conceal a potential primary problem. One of the most common scenarios I encountered in practice was longstanding insomnia prior to the onset of depression. In the transdiagnostic scenario, insomnia could be considered just that or a symptom of another disorder rather than a primary sleep disorder. All these issues including categorical versus dimensional diagnoses should be covered in this theory section written by our experts.  There are plenty of reasons not to blindly accept the transdiagnostic jargon as being that relevant.    

Psychometrics can be discussed in the theory section.  We have all heard and read about reliability of diagnoses for decades and a lack of validity. Reliability statistics are available for a range of DSM categories and that could be included as a single graphic with a brief discussion.  The discussion of validity needs to be more extensive and nuanced rather than just dismissed.  Study groups from DSM-5 were working on 11 validity indicators.  It is time to see them on graphics like what can be constructed for reliability. The data should be included where it exists.

5:  A genetics section:  Genetics and the associated molecular biology is the future of medicine and psychiatry. A summary of that data should be available in the DSM as well as the clear importance of this information.  At the biological level, the discussion should be clearly focused on changes in brain systems associated with disorders and the problem of many genes affecting these systems.   

6:  Definition/Threshold of a disorder:

There is always criticism about the dysfunction threshold for making a diagnostic assessment.  There is never much discussion about why it is necessary or why there are consensus diagnoses.  Even a superficial look at other specialties that treat polygenic heterogeneous entities invites comparison.  Rheumatology is a case in point:   

“Rheumatologists face unique challenges in discriminating between rheumatologic and non-rheumatologic disorders with similar manifestations, and in discriminating among rheumatologic disorders with shared features.  The majority of rheumatic diseases are multisystem disorders with poorly understood etiology; they tend to be heterogeneous in their presentation, course, and outcome, and do not have a single clinical, laboratory, pathological, or radiological feature that could serve as a “gold standard” in support of diagnosis and/or classification.”

A recent review of polymyalgia rheumatica (PMR) in the NEJM (11) looked at diagnostic algorithms for both acute PMR and treatment.  The introduction involved the statement:  “The diagnosis of polymyalgia rheumatica is made on the basis of clinical grounds by combining characteristic signs and symptoms with laboratory findings and ruling out common mimickers such as late-onset gout and pseudogout and others.”  (p. 1099).  I counted 23 conditions in the differential diagnosis.  One of the criteria for the diagnosis is “functional impairment”.  The implication is that it is due to morning stiffness or possible pain but that is not specific.  There are limited reviews of how to establish diagnostic criteria for diseases and disorders that lack objective tests (12).  I think the degree of dysfunction is obviously relevant when assessing disorders that are based on purely subjective signs and symptoms.  It factors into routine clinical care of both known and unknown diagnoses. On this blog I have documented examples from numerous medical and surgical specialties.

That is my criticism after reading 5 current papers on the direction of the DSM.  I really do not want the next volume to look like what has been described so far. When I think about my final 1500-2500 word assessments that contain just about everything the authors of these papers discuss and much more – I do not want to see all that good work sacrificed because somebody wants to include more checklists or dimensions of questionable value. I have had people tell me years and in some cases decades later, that they found those assessments to be valuable and useful for future evaluation and treatment of that same person.  

If I had to capture three elements that the future DSM planning seems to miss it is that phenomenological assessments can easily contain as much or more data than checklists, that psychiatry is a medical specialty, and that like all medical specialties the field has boundaries. The current suggestions from these papers stretch those boundaries into activism, politics, and importing criticism from other academic silos rather than a restatement of what is relevant for psychiatric assessment and classification. 

That should be the priority…    

 

George Dawson, MD, DFAPA

 

 

 

References:

1:  Oquendo MA, Abi-Dargham A, Alpert JE, Benton TD, Clarke DE, Compton WM, Drexler K, Fung KP, Kas MJH, Malaspina D, O'Keefe VM, Öngür D, Wainberg ML, Yonkers KA, Yousif L, Gogtay N. Initial Strategy for the Future of DSM. Am J Psychiatry. 2026 Jan 28:appiajp20250878. doi: 10.1176/appi.ajp.20250878. Epub ahead of print. PMID: 41593833

2:   Cuthbert B, Ajilore O, Alpert JE, Clarke DE, Compton WM, Drexler K, Fung KP, Gogtay N, Kas MJH, Kumar A, Malaspina D, O'Keefe VM, Öngür D, Tamminga C, Wainberg ML, Yonkers KA, Yousif L, Abi-Dargham A, Oquendo MA. The Future of DSM: Role of Candidate Biomarkers and Biological Factors. Am J Psychiatry. 2026 Jan 28:appiajp20250877. doi: 10.1176/appi.ajp.20250877. Epub ahead of print. PMID: 41593830.

3:  Öngür D, Abi-Dargham A, Clarke DE, Compton WM, Cuthbert B, Fung KP, Gogtay N, Kas MJH, Kumar A, Malaspina D, O'Keefe VM, Oquendo MA, Wainberg ML, Yonkers KA, Yousif L, Alpert JE. The Future of DSM: A Report From the Structure and Dimensions Subcommittee. Am J Psychiatry. 2026 Jan 28:appiajp20250876. doi: 10.1176/appi.ajp.20250876. Epub ahead of print. PMID: 41593835.

4:  Drexler K, Alpert JE, Benton TD, Fung KP, Gogtay N, Malaspina D, O'Keefe VM, Oquendo MA, Wainberg ML, Yonkers KA, Yousif L, Clarke DE. The Future of DSM: Are Functioning and Quality of Life Essential Elements of a Complete Psychiatric Diagnosis? Am J Psychiatry. 2026 Jan 28:appiajp20250874. doi: 10.1176/appi.ajp.20250874. Epub ahead of print. PMID: 41593851.

5:  Wainberg ML, Alpert JE, Benton TD, Clarke DE, Drexler K, Fung KP, Gogtay N, Malaspina D, O'Keefe VM, Oquendo MA, Yonkers KA, Yousif L. The Future of DSM: A Strategic Vision for Incorporating Socioeconomic, Cultural, and Environmental Determinants and Intersectionality. Am J Psychiatry. 2026 Jan 28:appiajp20250875. doi: 10.1176/appi.ajp.20250875. Epub ahead of print. PMID: 41593836.

6: American Medico-Psychological Association. Statistical Manual for the Use of Institutions for the Insane.  1918:  https://dn790008.ca.archive.org/0/items/statisticalmanu00assogoog/statisticalmanu00assogoog.pdf

7:  Sydenham, Thomas, 1624-1689; Greenhill, William Alexander, 1814-1894; Latham, R. G. (Robert Gordon), 1812-1888.  The works of Thomas Sydenham, M.D.  Volume 1, London. Sydenham Society.  1848-1850. P. 14  https://archive.org/details/worksofthomassyd01sydeiala/page/lv/mode/1up?q=abeyance

Translation of Medical Observations by Thomas Sydenham, London, 1669. The Preface.  Original was in Latin.

8:  DeGowin EL, DeGowin RL.  Bedside Diagnostic Examination, 3^rd ed.  New York.  Macmillan Publishing Company, Inc.  1976. P. 1.

9:  Aftab A. The Future DSM: Bold redesign, lingering blind spots.  Psychiatric Times. March 2026: 12-16.

10:  Clark A.  Microcognition: Philosophy, cognitive science, and parallel distributed processing.  Cambridge, MA.  The MIT press. 1989.   

11:  Dejaco C, Matteson EL. Polymyalgia Rheumatica. N Engl J Med. 2026 Mar 12;394(11):1097-1109. doi: 10.1056/NEJMcp2506817. PMID: 41812194.

12:  White SJ, Barker TH, Merlin T, Holland G, Sanders S, O'Mahony A, Pathirana T, Theiss R, Pollock D, Reid N, Munn Z. Methods for developing diagnostic criteria for conditions without objective tests, biomarkers, or reference standards: a scoping review. J Clin Epidemiol. 2026 Feb;190:112052. doi: 10.1016/j.jclinepi.2025.112052. Epub 2025 Nov 18. PMID: 41265667.

New Onset Headaches In An Old Man - What Should Be Done?

 

 

In November of 2022, I started to experience headaches that were new and unusual. They would start out as a dull ache behind the left eye to varying degrees and generally persist until I took 1,000 mg of acetaminophen. Acetaminophen (APAP) works like a miracle for me for most kinds of pain and it would reliably knock the headache out in 1-2 hours. Back in my early 20s I experienced more severe headaches that were quite debilitating and most likely cluster headaches. For a couple of years, I would get them every spring and would have to take aspirin (ASA) or APAP and take a nap until they went away.  I make that diagnosis in retrospect after learning quite a bit about headaches and learning how to treat them. The new headache was nothing like those cluster headaches.  I could still read, exercise and function well. I also noticed that sleep alone had no effect on the new headache. I would still wake up with it if I did not take APAP.  Only recently I had an episode where the new retroorbital headache worsened with coughing and that seemed to be an isolated event. The headache could occur at any time of the day, was not related to stress, or any activity.

I was seeing optometrists at the time – initially for an annual eye exam and then for severe dry eyes. I asked both optometrists if any of the eye diagnoses (Meibomian gland dysfunction, ocular rosacea, blepharitis, punctate keratitis, dry eyes, and astigmatism of the left eye) could be causing the headaches and was told it was a possibility but that I should follow up with primary care and neurology. By January of 2023, I tried to get an appointment to see a neurologist – but could not get in until September 2023.  I saw my primary care MD twice during this period and his diagnosis was tension type headaches because I had no other neurological symptoms. The plan was to keep taking APAP.

Digressing a moment to diagnosing and treating headaches as a psychiatrist. As an acute care psychiatrist, I was in the position of diagnosing and treating many people with severe chronic headaches. They were typically admitted because of associated severe depression, suicidal thoughts or behavior, or a complete inability to function at home. Many of those patients started out with migraine headaches that were eventually complicated by medication overuse headaches. Frequent use of medications like APAP, triptans, and non-steroidal anti-inflammatory medications (NSAIDs) resulted in a headache that would not longer resolve. That diagnosis led to a different treatment plan that was moderately successful until a better plan for headache prophylaxis could be established. I had excellent back up by neurology and often consulted with a friend of mine who is a local neurologist and pain specialist.

Diagnosing headaches is not too far removed from making a psychiatric diagnosis in that the phenomenology of the headache it critically important.  What is the pain like, how is it described, does it radiate, are there any associated events or sensory phenomenon?  History is a critical part of the headache evaluation. The physical exam can contribute in the case of autonomic findings, making an underlying diagnosis that is a cause of the headache, or in some cases  a finding that suggests an underlying pathophysiological mechanism.  An example would be tenderness in the facet joints of the cervical spine (C-spine) for cervicogenic headaches.  Associated testing can be diagnostic but in most cases it is supportive.  That is degenerative disk disease and arthropathy of the facet joints of the C-spine supports the diagnosis but other elements need to be there like the characteristic pain distributions associated with this headache. A complete list of the common forms of headaches can be found at the National Headache Foundation and much more detailed discussion in headache specialty texts. The list is not exhaustive since headaches can occur across many settings and can be the general result of chemical alterations (alcohol, alcohol withdrawal, medication side effects, etc) and inflammation (influenza, coronavirus, etc).  As far as I know neurologists have not embraced the transdiagnostic term that we see cropping up in the psychiatric literature, but headaches are both a disease and a transdiagnostic symptom.

An illustration of the complexity of these headaches uses my specific example.  The table below illustrates the onset and frequency of these headaches from October 2022 to June 17, 2023).  Headaches are recorded only if they were treated with APAP.

 

	Generalized Bilateral	Left Retroorbital
OCT	7	1
NOV	8	4
DEC	1	6
JAN	2	4
FEB	5	5
MAR	4	3
APR	3	14
MAY	3	10
JUN (to June 17)	0	5

 

I will attempt to correlate various comorbidities to see if there are any possible explanations:

C-spine disease – I was diagnosed with C-spine disease by clinical exam and MRI about 20 years ago. The MRI showed stenosis but EMG studies were normal and physical therapy resolved the neurological symptoms I had at the time – primarily numbness in the C7-C8 distribution of both arms.  I have been doing the PT exercises for the past 20 years.  From the chart I do get episodic bilateral occipital headaches that radiate up from the neck and I attribute these to C-spine disease.  I typically treat them with physical therapy maneuvers and occasionally APAP.  Cervicogenic headaches have three reported pain distributions - occipital, occipital temporal maxillary, and supraorbital (most common).  Other sources say that the pain can be experienced anywhere on the face (1).  Retroorbital headaches from this cause seem unlikely.

BPPV- my only other MRI of the brain was done when I developed benign paroxysmal positional vertigo about 25 years ago.  Although that brain scan was normal, a polyp was noted in the frontal sinus but no further evaluation or treatment was recommended. I typically have episodes that seem to be improving over time.  Not debilitating.  

Astigmatism- severe in the left eye – causes visual distortion and seems to contribute to vertigo.

Dry eyes – multiple diagnoses as noted

Paroxysmal atrial fibrillation – have had about 20 episodes lifetime.  Much better control recently with a brief episode every 1-2 years. On an antiarrhythmic for 16 years. The main non-cardiac risk is embolic stroke.  I have had highly variable experiences with the physicians I have consulted about this disorder over the years.  There appears to be no consensus on the time frame necessary for cardioversion to prevent strokes.  I have been cardioverted initially in time frames of up to 15 hours both with medications and electrical cardioversion. In one case, I was anticoagulated and in other cases not. I have had patients who were in permanent atrial fibrillation and were not anticoagulated. Primary care seems to have a fairly casual approach to atrial fibrillation possibly because early studies showed there was no difference in outcomes based on rate control or rhythm control (normal sinus rhythm). Since then, studies have shown that people with rhythm control may have a higher quality of life. I decided to start anticoagulation 18 months ago because the pandemic had seriously compromised physician access and I did not want to end up in atrial fibrillation with no access to cardioversion. For the purpose of this post the question is: “Is it possible that a silent stroke occurred and caused this headache?”  At least one reference suggests that silent strokes are common in the elderly but not a cause of headaches, but deep white matter lesions on MRI may be. (2)

ATM and other risk genotypes- In a previous post I explained the ATM genotype and how it significantly increases the risk for pancreatic cancer.  I also have genotypes associated with increased risk for epithelial cells cancers.

Migraine Aura without Headache- I have experienced this in the past but not recently as a single episode of visual phenomenon.  The ophthalmologist I consulted with knew what had happened immediately and no specific treatment was recommended.

 Obstructive sleep apnea (OSA) – Diagnosed 18 years ago and I have been 100% compliant with CPAP/APAP ever since. I get a daily report on hypopneic episodes/hours and they are always well withing the target range.  OSA can be a cause of headaches, typically in the morning (3) but improve with treatment and are unlikely in this case.

Not all these factors were considered by the physicians I consulted about these headaches. The protocol was basically a cursory (or detailed) neurological review of systems and neurological exam.  In all cases I was told that it was a “non-focal” neurological exam.  My primary care physician saw that as a reason for no imaging and continuing the current treatment with APAP for a diagnosis of “tension headaches”.  The neurologist initially said he thought I had a migraine but on further consultation the diagnosis was “inflammatory headache” and I was given a standard tapering dose of methylprednisolone.  I filled the prescription but decided not to take it until after the imaging study.  None of the physicians suggested that it could be pain due to C-spine disease and I have found that unless you are talking with a rheumatologist, a lot of physicians do not spend a lot of time discussing or treating arthritis. The neurologist also ordered an MRI scan of the brain and two of the images are at the top of this post.  It was read as a normal MRI scan of the brain. The headaches persist.

This exercise in the differential diagnosis and treatment of headaches is instructive for several reasons:

1:  It highlights the complexity of medical conditions and everything that needs to be considered.  I could argue that 20 or even 30-minute visits with a generalist or even a neurologist might not result in an adequate assessment just based on the information that needs to be considered.  I described 50 years of medical history as succinctly as possible but it also requires somebody to put that together as rapidly as possible and look for the relevant patterns of disease. There are headache specialists out there who do this – but they are rarer than child psychiatrists and that is rare.

2:  The complexity is compounded by the fact that there can be more than one type of headache present and that each requires a separate diagnosis and treatment. In my case I came in with my own ideas that I had one type of cervicogenic headache and a new headache of undetermined etiology.  There are studies available that attempt to differentiate migraine headaches from cervicogenic headaches by selective injections of various cervical vertebrae.  In some cases that clarifies the source of the headache and in others the patient has both types. Similarities to the psychiatric diagnostic process are noted.  There are some who suggest that there should only be one treatable diagnosis.  If you can have more than one headache I don’t see why you could not have more than one psychiatric diagnosis.  

3:  Testing is a wild card – but should it be?  In this case my primary care physician opted to not order brain imaging but the neurologist did.  The kind of testing done in psychiatry and in much of neurology is non-diagnostic.  In other words, if a lesion is detected there is still a question of whether it is causative. The best example is degenerative disk disease and arthritis of the spine. It is easy to detect degenerative changes but the question is how they relate to the clinical problem. At the same time, the prevalence of serious secondary causes of headaches in the elderly such as tumors, vascular, inflammatory and other space occupying lesions like hematomas is significantly higher than in younger population – making any primary headache diagnosis in an older person - a diagnosis of exclusion.  I have certainly imaged patients in my practice based on various combinations of neuropsychiatric, cognitive, and neurological symptoms for this reason. It is no different in neurology.  In addition to the central nervous system secondary causes of headaches, orbital lesions need to be considered and that list is also extensive.

4:  Are headaches a disease?  With all of the repetitive rhetoric from the anti-science and anti-psychiatry crowd – my mind wandered to this question.  I had also recently encountered the term “Szaszian binaries” in a philosophical paper that was mildly critical of the disease arguments from antipsychiatrists that to this day are based on Szasz’s 60-year-old definition – that diseases must be based on morphology or a known pathophysiological mechanism – like infection from an organism.  It turns out that headaches are indisputably called diseases even though the mechanisms are as speculative and no morphological lesions are seen on brain imaging.  Like psychiatrists – the only positive findings will be the identification of secondary causes and that is no small accomplishment.  As I searched this topic, I found an article written by Ron Pies, MD on this very topic (5).  Szasz never wrote a Myth of Migraine Headache or commented on why headaches were not diseases.  

Where does all of this leave me today?  First relieved that there is no life threatening or debilitating brain pathology and that my brain looks pretty good for an old man.  I previously documented a serious traumatic brain injury in my 20s and my C-spine problems are likely the result of playing high school football and compression injuries transmitted through my helmet and head and into my neck. I was also involved in a collision playing third base that resulted in my neck being locked up for several hours that did not help. Second, it adds to my long-term health plan.  Despite that list of health problems, I have exercise and physical therapy plans to deal with most of it. Maintenance measures will take care of the rest.  I have a follow-up with neurology in October and if the retroorbital headaches start to increase in frequency I might try the methylprednisolone, but I don’t have high expectations. I had an asthma flare after a trip to Alaska about 8 years ago and had to take prednisone at a substantial dose and that did not seem to do much for the cervicogenic headaches.  My primary treatment modalities will remain exercise, physical therapy, and APAP.

It may seem like that is a significant list of problems, but after working in the field for 40 years they seem expected to me.  As long as they are manageable and I am tracking them and making necessary adjustments life is good. I also have a high index of suspicion for future problems and hope to identify any that come up, but I am also not fooling myself that I can control everything or that new problems will always be manageable. 

 

George Dawson, MD, DFAPA

Supplementary on Neck Pain:

I did a previous post of the importance of the spine in psychiatric practice largely because of bidirectional considerations.  I was seeing a large number of people who had sleep problems that were either caused by neck pain or had insomnia that seemed to cause neck pain. My interest in the mechanical and neurological spine dates back to excellent neurosurgical rotations in medical school and the associated radiology rounds with the late Sanford J. Larson, MD, PhD.  Even though neurosurgery was a tough rotation for students, residents, and attendings - every Saturday morning Dr. Larson would meet all of us in the Radiology reading room at Froedtert Hospital and would spend the morning reviewing all of the films from the last week.  I say films because all of the images were on large films placed on a device that could rotate them all in order.  The standard film in those days was 35 x 43 cm (14“ x 17“) so each row on that machine held about 8 films.  I was able to continue that practice when I worked at an acute care hospital but outside of that setting - it was always difficult to access films and later digital images. 

Another outcome of that early experience was continuing to read papers on common spinal problems and way to address them.  The epidemiology of neck pain has progressed significantly over time (6.7). In 2015 it was noted to be the 4th leading cause of disability.  Most acute neck pain resolves in a couple of weeks but in 50% of those cases it recurs over the next year. Annual prevalence is estimated to be 15-50% with an average of about 37.2%.  There have also been some studies of the impact of structured exercises on neck pain that typically show improvement.  I have not seen any estimate on the percentage of people with neck pain who have associated headaches but expect that would depend on risk factors and degree of mechanical and neurological impairment. This also seems to be a medical education issue. In my experience very few physicians know how to do a back and neck examination and interpret the findings. 

 

References:

1:  Al Khalili Y, Ly N, Murphy PB. Cervicogenic Headache. 2022 Oct 3. In: StatPearls [Internet]. Treasure Island (FL): StatPearls Publishing; 2023 Jan–. PMID: 29939639.

2:  Fujishima M, Yao H, Terashi A, Tagawa K, Matsumoto M, Hara H, Akiguchi I, Suzuki K, Nishimaru K, Udaka F, Gyoten T, Takeuchi J, Hamada R, Yoshida Y, Ibayashi S. Deep white matter lesions on MRI, and not silent brain infarcts are related to headache and dizziness of non-specific cause in non-stroke Japanese subjects. Intern Med. 2000 Sep;39(9):727-31. doi: 10.2169/internalmedicine.39.727. PMID: 10969904.

3: Verbraecken J. More than sleepiness: prevalence and relevance of nonclassical symptoms of obstructive sleep apnea. Curr Opin Pulm Med. 2022 Nov 1;28(6):552-558. doi: 10.1097/MCP.0000000000000915. Epub 2022 Sep 14. PMID: 36101923; PMCID: PMC9553267.

4:  Vongvaivanich K, Lertakyamanee P, Silberstein SD, Dodick DW. Late-life migraine accompaniments: A narrative review. Cephalalgia. 2015 Sep;35(10):894-911.

5:  Pies RW.  Why Thomas Szasz did not write about the myth of migraine. Psychiatric Times.  July 29, 2021.  https://www.psychiatrictimes.com/view/thomas-szasz-myth-migraine

6:  Cohen SP. Epidemiology, diagnosis, and treatment of neck pain. Mayo Clin Proc. 2015 Feb;90(2):284-99. doi: 10.1016/j.mayocp.2014.09.008. PMID: 25659245.

7:  Kazeminasab S, Nejadghaderi SA, Amiri P, Pourfathi H, Araj-Khodaei M, Sullman MJM, Kolahi AA, Safiri S. Neck pain: global epidemiology, trends and risk factors. BMC Musculoskelet Disord. 2022 Jan 3;23(1):26. doi: 10.1186/s12891-021-04957-4. PMID: 34980079; PMCID: PMC8725362.