I have accessed the full text which starts with this quote
"... two societies confronting each other with conflicting universes will both develop conceptual machinery to maintain their respective universes’.1
The 2019, SARS-CoV-2 pandemic was associated with significant mortality. Long COVID appeared as a term to describe a range of polymorphic
symptoms persisting 3 months or more following the initial infection and has been associated with significant clinical, social and economic consequences.2 Common experiences include fatigue, headache, anxiety, in- attention (‘brain fog’), myalgia, breathlessness, dizziness, postural orthostatic tachycardia syndrome (POTS) and gastrointestinal disturbance. It is more common in fe- males and is associated with significant morbidity. The exact mechanism behind this ongoing persistence re- mains unclear and no test is pathognomonic. Putative causes include chronic inflammation, an aberrant im- mune response and viral particle persistence.2 Manage- ment is supportive and includes symptom-based pharmacology, psychotherapy, physiotherapy and oc- cupational therapy. Prognosis is guarded. However, a number of unsettling observations have appeared.
In Long COVID, there is both a persistence and a vari- ability to the reported 203 possible symptoms. Symptoms may occur without a preceding positive test or in the presence of a negative test, and there is only a weak as- sociation between the severity of acute COVID-19 and the onset of Long COVID.2 Possible explanations include differing testing policies between countries, testing too early or too late in the disease course and an inconsistent or aberrant immune response.2 However, an older
narrative may exist, with Long COVID having similarities to a number of named, historical disorders.
In 1983, a seemingly new illness appeared in the small New Zealand town of Tapanui.3 Subsequently named chronic fatigue syndrome (CFS), symptoms of Tapanui Flu included fatigue, headache, anxiety, inattention, myalgia, breathlessness, dizziness and other subjective complaints that were difficult to substantiate objectively. No test was pathognomonic. The pathophysiology of CFS remained elusive despite continued inquiry including by inves- tigators whose lives had been significantly touched by the condition. CFS is more common amongst females, prognosis is guarded and treatment remains primarily supportive but now includes a more articulate inter- disciplinary support network, perhaps developed in re- sponse to a sceptical audience.
Even earlier, a similar unexplained epidemic occurred amongst the staff at London’s Royal Free Hospital.4 Symptoms included fatigue, headache, anxiety, in- attention, myalgia and breathlessness. No pathological basis was found and no test pathognomonic. There was again a female preponderance and whilst proving rela- tively benign, some patients were affected for up to a year. A Lancet article entitled ‘A New Clinical Entity’ followed and suggested ‘benign myalgic encephalomyelitis (ME)’ as the diagnosis. However, there was an unexpected
comment at the end of the article – ‘... we believe that its characteristics are now sufficiently clear to differentiate it from poliomyelitis, epidemic myalgia, glandular fever... and need it be said, hysteria’. McEvedy and Beard were perplexed, as the case for hysteria had not been examined and they had noted the overlapping symptoms between those reported and those they had encountered in a pre- vious epidemic of hyperventilation in 154 school children.5
The curious disregard for hysteria
‘At first glance it is extremely difficult for [anyone] to grasp how such physical symptoms... may in fact be an extension of ideas or fantasies. If the mysterious leap from the mind to the body is ever to be understood, then what is needed is an attentive and understanding approach to the entire patient’.6
It is a curious phenomenon that, every now and then, a clinical entity appears seemingly for the first time. It is given a new name, yet its signature remains identifiable – a triad of polymorphic symptomatology, an elusive pathophysiological explanation and often a dispropor- tionate defensiveness to suggestions that there may be psychological contributions.7,8 Hysteria has become pe- jorative, rather than an extraordinary attribute of an at- tuned human response. Acknowledging a female preponderance may be seen as sexist despite the obser- vation that unexplained illnesses may be associated with trauma and a unique set of societal pressures that women more often endure. Associated features of new un- explained entities include the presence of a triggering threat, re-naming of old symptoms and a personal in- vestment on the part of the investigators attempting to establish scientific legitimacy.
That a psychological process may have a somatic effect has been long documented in both the clinical and non- clinical fields. In a review of epidemic hysteria that dated back to 1374, threats have included environmental fac- tors (contaminated water, chemical exposure and gas leaks) as well as conflict that was both high and in- escapable.8 In 1859, Briquet speculated on untoward development and life experiences including parental mistreatment and spousal abuse and described his first series in men.9 In the workplace, stress related to bore- dom, production pressures, labour-management rela- tions, job dissatisfaction or conflict between one’s job and other obligations, particularly those at home, were noted.8 When there was a fear of toxic gas being released in Tokyo’s subway, more than 85% of the 5500 people seeking hospital treatment were found to have a psy- chogenic aetiology.10 Fear was heightened by the unique challenges associated with COVID-19, including com- municated global mortality, protracted lockdowns, vac- cine hesitancy and misinformation. In the non-clinical realm, similar symptoms were reported following the extraordinarily realistic, 1938 War of the Worlds radio
broadcast where listeners panicked, believing they were being invaded from Mars.11 In 1954, fear of a local ra- diation leak causing car windscreen pitting took hold.11 In 2016, fear of a Russian-initiated, invisible ray attack on United States12 personnel in Cuba, known as the Havana Syndrome, appeared.13 Spreading easily, contagion ap- pears enhanced by the general excitement of emergency personnel and equipment, the media, rumours and in- terestingly, labelling the illness with a specific diagnostic term.8
In order to evaluate epidemiological observations, Brad- ford Hill suggested that for A to cause B, specific criteria might be met.14 These include a strong association that intuitively is plausible, coherent, specific and consistent in other populations. Further, the stimulus must precede the outcome and that the relevant outcome could be reproduced experimentally. With respect to Long COVID, a follow-up study of 54,960 patients showed that pre- infection psychological distress predicted an increased risk of Long COVID.15 The mortality of acute COVID-19 and persistence of Long COVID stand in contrast to the Havana Syndrome where no deaths occurred.13 The ex- perimental induction of a similar psychogenic illness has recently been reported and, interestingly, demonstrated no gender differences.16 Despite these observations, psychogenic factors often polarise rather than contribute to the understanding and management of these disabling conditions.
Getting the name right by understanding the problem
‘Refusing to acknowledge its existence or changing its name will not make it go away. The way we formulate the diagnosis and the way society responds to patients with the disorder do have consequences for course and outcome’.17
Described as the social construction of reality, knowledge is not just made up of objective inquiry but also of the result of communicable social perceptions, values and beliefs. In an attempt to comprehend complexity and uncertainty, differing narratives may reflect the prevailing discourse in the only available currency at the time. For example, given the predominance of gynaecological- and obstetric-related symptoms, Hippocrates suggested the uterus (‘hyster’) was a central factor in ‘female com- plaints’. When spirit possession was at the fore, exorcism dominated. Influenced by the notion of planetary and magnetic forces on the human body, Mesmer suggested magnetism as a treatment. In 1697, Sydenham conceived hysteria as an emotional condition, moving the source of the disorder from the uterus to the brain with Freud emphasising unbearable conflicts presenting as physical manifestations.18 Comparing the similar symptoms of neurasthenia in the East and CFS in the West, social in- fluences were described, including the respect accorded to neurasthenia which confirmed those affected were often hard working and high achieving.19"
then comes the table pasted in an above comment. more copy and paste...
Currently, inquiry is typically molecular with virological, immunological and intracellular mechanisms attracting most attention.2 Described as the seductive allure of neu- roscience, even explanations based upon fallacious science are preferred over those without a scientific component.20 Thus, despite an inability to explain or to replicate features outlined in the historical clinical and non-clinical examples above, microscopic mechanisms are preferentially endorsed. Psychiatry itself seems to have retreated and created a series of euphemisms including ‘medically unexplained symp- toms’ and ‘functional neurological disorder’ (Table 1). Thisflight may be a genuine response to not knowing but also to the fear of repeating historical errors. Of the 85 patients in Slater’s series who had an illness labelled as hysteria, 12 died, 4 of whom by suicide.21 Bradford Hill makes an important observation: ‘All scientific work is incomplete. All scientific work is liable to be upset or modified by advancing knowledge. That does not confer upon us a freedom to ignore the knowledge we already have, or to postpone the action that it appears to demand at a given time’.14
Conclusion
There has been an uneasiness in writing this article. An un- easiness for fear of its misinterpretation and in so doing of being distracted from its overall aim, namely, to contextualise social and psychological factors in unexplained illnesses, both current and historical. The narrative offered here necessarily reflects the values and beliefs of the authors, all of whom are psychiatrists. Long COVID has similarities to other historical, clinical and non-clinical events that have appeared across time and cultures. The clinician can be alerted to this pos- sibility by recognising familiar polymorphic presentations that remain pathologically elusive but are associated with a disproportionate defensiveness. Reacquaintance with his- torical lessons may offer an appreciation of the agility of the mind and body and an opportunity to intervene early with a focus less on the molecular and more on the context from which the person presents.
Disclosure
The author(s) declared no potential conflicts of interest with respect to the research, au- thorship, and/or publication of this article.
Funding
The author(s) received no financial support for the research, authorship, and/or publication of this article.
References
1. Berger PL and Luckman T. The social construction of reality. NY: Anchor Books, 1966. 2. Davis HE, McCorkell L, Vogel JM, et al. Long Covid: major findings, mechanisms and
recommendations. Nat Rev Microbiol 2023; 21: 133–146.
3. PooreM,SnowPandPaulC.AnunexplainedillnessinWestOtago.NZMedJ1984;97:
351–354.
4. The Medical Staff of the Royal Free Hospital. An outbreak of encephalomyelitis in the
royal free hospital group, London in 1955. Br Med J 1957; 2: 895–904.
5. McEvedyCPandBeardAW.Royalfreeepidemicof1955:areconsideration.BrMedJ1970;1:7–11.
6. Weintraub MI. Hysteria – a clinical guide to diagnosis. Clin Symp 1977; 29: 1–31.
7. Newman M. Chronic fatigue syndrome and long Covid. Br Med J 2021; 373: n1559.
8. BossLP.Epidemichysteria:areviewofthepublishedliterature.EpidemiologicalReviews 1997; 19: 233–243.
9. Millon T. Masters of the mind. New Jersey: John Wiley & Sons, 2004.
10. OkumuraT,SuzukiK,FukuyamaA,etal.TheTokyosubwaysarinattack.AcadEmergMed
1998; 5: 613–628.
11. Heyer P. America under attack. Can J Commun 2003; 28: 149–165.
12. Medalia NZ and Larsen ON. Diffusion and belief in a collective delusion: the Seattle windshield pitting epidemic. Am Socio Rev 1958; 23: 180–186.
13. Bartholemew RE and Baloh RW. Challenging the diagnosis of ‘Havana Syndrome’ as a novel clinical entity. J R Soc Med 2020; 113: 7–11.
14. Bradford AB. The environment and disease: association or causation. Proc Roy Soc Med 1965; 58: 295–300.
15. Wang S, Quan BA, ScD C, et al. Associations of depression, anxiety, worry, perceived stress and loneliness prior to infection with risk of post COVID-19 conditions. The Journal of the American Medical Association Psychiatry 2022; 79: 1081–1091.
16. Broderick JE, Kaplin-Liss E and Bass E. Experimental induction of psychogenic illness in the context of a medical event and media exposure. American Journal of Disaster Medicine 2011; 6: 163–172.
17. Eisenberg L. The social construction of mental illness. Psychol Med 1988; 18: 1–9.
18. Trimble M and Reynolds EH. A brief history of hysteria. Handb Clin Neurol 2016; 139: 3–10.
19. AbbeySEandGarfunkelPE.Neurasthenicandchronicfatiguesyndrome.AmJPsychiatr 1991; 148: 1638–1646.
20. Hopkins EJ, Weisberg DS and Taylor JCV. The seductive allure is a reductive allure. Cognition 2016; 155: 67–76.
21. Slater E. Diagnosis of “hysteria”. Br Med J 1965; 1: 1395–1399.
