Two excellent books about psychosomatic illnesses

  • January 9, 2022

There’s something both familiar and unfamiliar about neurologist Suzanne O’Sullivan’s book It’s All in Your Head:stories from the frontline of psychosomatic illness, which discusses her experience of psychosomatic illness while working as an NHS consultant.

The familiar first: O’Sullivan describes typical cases that come up in her clinical practice – seizures that aren’t due to epilepsy; weakness or paralysis when there is no identifiable neurological disease; persistent symptom states like chronic pain or fatigue when there is no apparent explanatory pathology. She is not talking about neurological diseases waiting to be diagnosed but about presentations in which “no disease is found because there is no disease to find. In those people the medically unexplained symptoms are present, wholly or partially, for psychological or behavioural reasons”. Refreshingly uninterested in worrying about terminology, she calls these conditions psychosomatic.

The book’s case histories contain some familiar details – responses to the diagnosis range from bemusement to downright hostility and rejection. And contact with a close family member or friend can provide revealing detail about likely causes or perpetuating influences.

And the unfamiliar? Like most doctors, O’Sullivan sees the cause of psychosomatic conditions as being primarily psychological and in her own practice she regards psychiatry as a part of the management plan. However, she is (far) more than usually willing to state this unambiguously and is interested herself in understanding what are the underlying problems. Here she encounters such a variety of stories – complicated bereavements, family and other interpersonal predicaments, gender discomfort, loneliness and more – that although she sees their relevance she cannot really discern a common theme.

O’Sullivan has clearly read more widely than many a clinician, for example in the history of psychosomatics and psychodynamic theories, and she is comfortable with the idea that the mechanisms driving psychosomatic presentations are unconscious and often involve a sort of dissociation – that is a disorganisation of usually-integrated mental processes. She sees the symptoms as having a function, perhaps defending against emotional breakdown or in some other way helping the patient adapt to the otherwise intolerable.

The book throws down a gauntlet in the form of a question: “If psychosomatic symptoms are so ubiquitous, why are we so ill-equipped to deal with them?” It is picked up in O’Sullivan’s second book on the topic The Sleeping Beauties and other stories of mystery illness, which describes her exploration of a number of “mass” episodes of psychosomatic illness. This could be a horrid parade of grotesques but it isn’t, instead providing a sensitive exploration of external social influences on illness and its course. Everywhere there are “…moral dilemmas, inconceivable choices, inequality” and the unenviable role of women in society.

The answer to the gauntlet question comes at least in part from the medical and other social and official responses, which do not come out of it well. They are often disparaging or dismissive, and mistrust of officialdom plays an important part in the difficulty of forming a shared therapeutic response.  An important observation is made about the part played by official responses that simultaneously confirm the absence of underlying disease while at the same time downplaying or ignoring the psychological and social. This loops back to the first book with a comment about the currently favoured label of Functional Neurological Disorder which is “…used to imply that the brain is not functioning – therefore (rather ham-fistedly, I would say) placing the source of psychosomatic disorders firmly in the biology of the brain” – where O’Sullivan believes it does not belong.

Again, psychosomatic illnesses are seen as serving a purpose: “…perhaps we need release valves and coping mechanisms, face-saving ways of addressing conflict and grappling with ambivalence. Sometimes, embodying and enacting conflict is either more manageable or more practical than articulating it”.

Where next? There is work left undone by these two books. One task is that more work is needed to link lessons about the causes of what we might call the epidemic cases in Sleeping Beauties to the sporadic cases in All in Your Head: in particular to ask – is there really no common theme to the apparently disparate adversities that lead to onset of psychosomatic illness? This links to the need to consider other explanations for the onset of symptoms in the face of such adversities. We accept that depression can follow loss, anxiety can follow threat and PTSD can follow trauma, and we usually see such conditions as symptomatic breakdowns rather than adaptive responses. Perhaps we could look at psychosomatic illnesses in the same light, as manifestations of how we break down when faced with adversities that represent (the common theme) persistent and seemingly unresolvable conflicts, challenges and dilemmas.  

Long Covid: the numbers don’t add up, so why do we keep collecting them?

  • October 5, 2021

How common is Long Covid?  Top of the range, with estimates of nearly 40% of people who’ve had Covid still being symptomatic 12 weeks later, come the REACT-2 study and a recently-published analysis from a US database. In the basement come estimates of 0% from a follow up study of children in Melbourne who had recovered from mild or asymptomatic infection, 2.3% at 12 weeks (the Zoe survey), 4% from a study of schoolchildren in Zurich, and 5% for symptoms at 12-16 weeks from a recent ONS survey. And other estimates in between…

Why is there so much variation? There are the usual suspects – results may be influenced by differences in the samples in terms of age, gender, BMI, vaccination status and so on. Many of the symptoms reported are non-specific (such as fatigue, aches and pains, difficulties with concentration) and endorsement is likely to depend upon exactly how they are asked about and whether an attribution to Covid infection is required. Response rates varied greatly – only 13% in a substantial UCL UCL study of young people and 20% in an ONS study of school children. Some attempt to adjust is possible but response bias and confounding can’t be entirely discounted.

Maybe there’s an issue of reporting threshold – the higher estimates coming from counting relatively minor experiences while the lower estimates count only more severe symptoms. Certainly there seems to be an inverse relationship between number of symptoms and prevalence, but severity (intensity, intrusiveness) is harder to gauge from readily available reports. An ONS survey from earlier this year suggested that only about 1 in 10 respondents was limited a lot by their experiences. An intriguing finding from a study of NHS general practice records suggests that GPs are recording very few cases by comparison with those reported from research surveys – in fact about 100th of the numbers, with a quarter of GPs using NHS codes for Long Covid to describe no cases at all in the study period. The headline of the Guardian’s report of the study this article was amended after publication. An earlier version said that GPs in England were “failing to recognise thousands of long Covid cases”. The headline was changed to indicate that the research concluded that “long Covid coding in primary care is low compared with early reports of long Covid prevalence”.” An acknowledgement that at least one possible explanation is that GPs are applying a clinical-severity filter not recognized by researchers.

Another way to ask about the significance of “Long Covid” symptoms is to consider the prevalence of the same sort of symptoms in the general population. For example persistent fatigue is reported by between 10 and 20% of the general population and something like 50% of people with an identified physical disorder. Not many Long Covid studies collect data from comparison groups, but one ONS survey suggested 3.4% of non-Covid respondents had the same symptoms as the Covid+ respondents and the UCL study found a figure of 16%. In both studies the Covid respondents had more symptoms than the non-Covid respondents, but between-study differences raise again the question of why so much variation – no doubt it’s down to sampling, how the questions were asked, and response rates.

So … what is the value, and what is the likely outcome, of collecting not-very-accurate information on underspecified populations of people who have had a Covid infection and who for the most part have non-specific symptoms that are common in the general population? It may be that the result will be a better understanding of the nature of longer-term problems attributable (or attributed) to Covid infection, but it isn’t clear that these surveys are the most efficient way of getting there. And there are potential pitfalls – Long Covid manifestly isn’t a single condition and it is difficult not to see, in the current approach to researching it, the process that Ian Hacking called Making Up People – the bringing into being of a new category of people with what may turn out to be a transient illness (transient as a medical category that is, not for the individual) – in ways that are not beneficial to anybody concerned.

A start would surely be to stop using the term Long Covid. It’s unlikely we’ll convince the media or pressure groups to drop it, but a move in the right direction would be if researchers and clinicians started using more specific terminology to describe exactly what it is they are studying and why.

NICE’s ME/CFS 2021 guideline: a much-needed pause for reflection

  • September 9, 2021

There’s more to the debate than disagreement about research findings: prejudice against psychological diagnoses and treatments is also a factor

NICE’s decision to defer publication of its guidance on ME/CFS is welcome, allowing as it does time for reflection about what is going wrong that prevents consensus on the management of this group of conditions.

Actually, just a read through the draft (consultation) guidance provides some clues. It reads less like a dispassionate review of the evidence and more like a one-sided position statement from the ME Association. There is talk about listening to and believing patients, about energy envelopes, and criticism of trials that use “subjective” outcome measures – like self-reported fatigue and quality of life. What exactly these ideas mean isn’t always made clear. Disbelief isn’t likely to be about somebody being ill (symptomatic with functional impairment) but more about that illness being caused by a yet-to-be-identified physical pathophysiology. The energy envelope is an interesting term that I have not come across in this context (as opposed to engineering or acoustics)  except when used by people who dislike the idea of activity pacing, but its physiological (“objective”) basis is as far as I know undefined. Treatments that “only” change symptoms are described as non-curative but then so are stroke rehabilitation, paracetamol and hip replacement.

What is being played out in these guidelines is a long-standing opposition to (sometimes expressed as hostility, anger or aggression) treatments such as CBT and GET. What is that opposition about? The debate is sometimes framed as being about the status of trials’ evidence but I don’t think that explains the emotional tone. I detect in the background a drive to reject these therapies because they suggest there is a large psychological or motivational element to the illness.

We live in a society in which the idea is not widely accepted that physical illness can have predominantly psychological causes or treatments, and of course the personal experience of physical symptoms is so pressing that psychological ideas can just not seem to work as explanations. Beyond that starting point there is something more going on and I think it is an active prejudice against the idea of psychological (and specifically psychosomatic) diagnosis. There are several reasons for such an aversion. The diagnosis may be misunderstood as meaning that an illness is imagined or even deliberately feigned. No doubt this is also part of the “not believed” complaint. On the other hand it is assumed that if the diagnosis is accurate, the person so diagnosed must be really odd. This idea has its roots, I think, in the history of hysteria and its conflation of the hysterical illness with the hysterical personality. And of course there is a threat inherent in the idea that somebody can be so lacking self-awareness that their body generates an illness in a mysterious way that is outside their control.

Is prejudice too strong a word? I don’t think so: it explains the animus in the reaction to psychological research and practice in the field, which clearly reflects more than disagreement about the interpretation of trial results. And it surfaces even in some of the milder critical responses to NICE’s decision, such as use of the word “relegated” to describe people offered psychological diagnosis or input, with its implications of inferiority and failure.

How can professionals with an interest respond? Of course there is a continuing need to engage with constructive critical appraisal of the research literature, including discussion of the use of so-called PROMs (patient-reported outcome measures) in applied health research. In addition there is a need to explore new ways to discuss attitudes to psychological causes and treatment for functional or psychosomatic illnesses, tackling the idea that these are somehow disreputable or demeaning approaches.

This last question is sensitive because of the anger and resistance it can provoke in some quarters. My own sense is that the result of this sensitivity is some professional foot-shuffling. Too much is made of findings that many functional states are not preceded by severely threatening or traumatic life experiences; psychotherapy is discussed at times as if it is synonymous with CBT which in this context functions largely as an adjunct to rehabilitation rather than as a way of exploring more widely into the psychosocial context of illness development and maintenance; a welcome interest in the physiological mediators of symptom production is unnecessarily and incorrectly accompanied by claims that such research heralds the end of dualism (implication, using a psychological vocabulary is so passé…).

Time will tell, but my own prediction is that for these reasons the impasse will not be resolved merely by a renewed critical appraisal of the literature. Maybe a “form of words” will be found, but a more useful conclusion would be an acceptance that psychological treatments are important because psychological disorders are important – real, potentially serious, treatable and not inferior to physical diseases.

Dualism is dead! Well, maybe…

  • December 22, 2020

I have been struck by how often academics and clinicians writing about functional disorders feel the need to announce the death of dualism – aka mind-body dualism or even Cartesian dualism, depending on the author. It isn’t easy to understand what is meant exactly by this claim and I have been doing a bit of reading between the lines to clarify, at least for myself.

Dualism in philosophy

First, it is worth saying that Descartes understood the mind and body not as radically separate but as in some way highly integrated.  Here he is in the VI Meditation on First Philosophy:

‘Nature also teaches me, by these sensations of pain, hunger, and thirst, that I am not merely present in my body as a sailor is present in a ship, but that I am very closely joined and intermingled with it, so that I and the body form a unit. If this were not so, I, who am nothing other than a thinking thing, would not feel pain when the body was hurt, but would perceive the damage only by intellect, just as a sailor perceives by sight if anything in his ship is broken.’

Or again:

I now understand the mind to be coextensive with the body – the whole mind in the whole body and the whole mind in any of its parts.

Descartes was writing nearly 400 years ago, so it’s not surprising that the terms used in the debate have changed somewhat. Modern philosophy of mind concerns itself, in this context, with the nature of consciousness or intentionality and how subjective experiences are to be explained, and (typically) with the question of how such experiences are related to something physical in the structures and functions of the brain. I think it’s fair to say that philosophers (well, the ones I’ve read) regard the idea that studying the brain can sort this out as bordering on the absurd. Tim Crane for example suggests that in exploring the mind-body relationship we should stop “considering those options which frustrate our understanding of our minds – for example…that we should look for consciousness by inspecting the sticky fatty matter of the brain”. Putting it slightly differently, Galen Strawson comments that even accepting that “…the known phenomena of experience are wholly a matter of the physical nature of ordinary matter under mild conditions (the mild of special conditions that obtain in the brain), … the physics and neurophysiology of the brain don’t enable us to understand how this is so”.

Dualism in clinical thinking

Actually, I don’t think that “dualism” is being used, in the context of clinical writings about functional disorders, in the philosophical sense at all. Rather it refers to the idea that a comprehensive account should include both mind and body mechanisms as expressed here: “A dualistic mind-body understanding of functional neurological disorders (FNDs), also known as conversion disorders, has led to the view that the cause of the symptom should be either psychological (psychogenic) or physical (neurogenic-“organic”).” … “The authors argue that the conversion concept is consistent with recent neuroscientific research findings, and the model allows psychological and neurobiological concepts to be reconciled within a single account of FND that begins to resolve the dualistic mind-body dichotomy.”

In one sense this is not at all a new idea – we have known for a long time that brain states accompany mental states and no doubt this is what Tony David meant when he said that dualism between mind and body “went in the nineteenth century”.

Looking further at this idea…here is an anecdote from the memoir of Geoffrey Keynes, a surgeon who served in the Great War:-

“On one occasion, when I happened to be in my dressing station …. a message came that a gunner had been wounded and was lying beside his gun at the edge of the lake.  Would I, please, come at once?  I then experienced a feeling which it is hard to describe. It was my duty to walk immediately with stretcher-bearers from a position of comparative safety to a gun pit, which was being accurately shelled every few minutes.  I ordered my legs to take me there, but at first they refused to move.  My mind was equal to the ordeal, but another part of my brain declined to pass on the necessary instructions….”

Geoffrey Keynes  The Gates of Memory  1983

Can we describe a mechanism whereby the brain declines to pass on the mind’s instructions? The dualism abolitionists would say – perhaps not perfectly but we’re getting there. I think that’s wrong, and here’s a different vignette to explain why.  Suppose I am crying at a funeral and three friends are discussing my plight. A psychiatric friend says – he has been bereaved (a social state), and he is crying because he is grieving (a mental state).  The neurologist standing next to her says – ah, but he is crying because of activation of a multi-component pathway in the brain that includes the anterior cingulate gyrus.  Wretched dualists! says the third, can you not see that the mental state of grief causes activation of the neural pathway and you need both elements to answer your question? Apart from noting what odd friends I have, you might wonder if my anti-dualism friend is really contributing anything apart from putting the two accounts (psychological and neurological) into the same sentence.

Dualism in clinical discussions

This points to what I take it the end-to-dualism claim actually means in practice: not that we have resolved the mind-body problem nor that we can produce a genuinely unitary account of functional disorders – how could we without solving the mind-body problem?  Instead it means that when we speak about functional disorders we know longer use highly-articulated psychological explanations for what is going on.  We pull this off in one of two ways.

One approach is to drop the psychological altogether or to trivialise or marginalise it. We should understand instead that for functional neurological disorders the problem “lies within the brain and its complex networks” and we should communicate this to patients in ways that enable them to say to themselves “I have a real dysfunction of networks in my brain”. If we use analogies they should be mechanical ones like the computer hardware-software distinction, or other neurological problems like phantom limb.

The other approach is to use a sort of language mash-up, as in a recent review  that summarised studies from neuroimaging, cognitive psychology, biological markers, and epigenetic studies to generate a model that “…allows psychological and neurobiological concepts to be reconciled within a single account of FND that begins to resolve the dualistic mind-body dichotomy”.  This is a (well-meaning) fudge: What happens is that a faux-integrated accounts allows for a misleading impression that the psychological side has been properly worked out because the neural mechanisms associated with it are now better understood.  It would better to say that there are likely psychological mechanisms at play and likely neurological mechanisms, and we don’t understand how the one acts on the other.

Dualism lives – in philosophy, in clinical practice and (hidden in plain sight) in the accounts we offer of functional disorders. Nothing to be embarrassed about, even if some people are made uncomfortable by thinking about psychological causes for illnesses.

Functional neurological disorders

  • November 11, 2020

Research and treatment should involve understanding why and not just how they develop

The group of clinical conditions that are now described as Functional Neurological Disorder (FND) used to be known by more uncomfortable names – hysteria, conversion disorder, or the hybrid hysterical-conversion. The change of terminology is welcome, although perhaps not its usage in the singular; after all the category brings together some quite disparate conditions.

With this change in terminology comes a change in the academic and clinical discourse. For the last century or so, the majority view has been that these functional disorders have psychological causes:  how they develop comes about through a process of loosening and disconnection between usually connected functions that need to be co-ordinated for effective motor or sensory function – dissociation; why they develop is explained as a response to some sort of psychological conflict that cannot be satisfactorily resolved – the emergence of disorder representing either symptomatic breakdown or a defensive manoeuvre to contain the conflict.

A shift in emphasis

The current FND discourse is relatively uninvolved with ideas about why FND occurs. Its focus is on antecedents that seem relatively trivial psychologically and upon mechanisms of symptom production – the how. Modern approaches in neuroscience allow studies of the physiology of symptom production that give new meaning to older ideas like dissociation and somatosensory amplification and more recent ideas about interoception, helping to explain some of the specifics of presentation – how some symptom states are generated – or to suggest why some individuals are especially susceptible.  Such research may yield interesting insights into the nature of these conditions and perhaps offers the future possibility of new therapeutic approaches.

A corollary has been a tendency to downplay the role of interpersonal factors in aetiology or maintenance: early or later life experience is hardly discussed as having a potentially meaningful relationship to onset or persistence of FND. Enthusiasts for a quasi-neurological cause for FND are keen to quote a systematic literature review1 which found that many people do not report severe life events as antecedents to onset. Three of the most widely used patient-facing resources2 lead on “problems with functioning of the nervous system” in their definitions of FND, while not offering the possibility that an important cause might be psychological. Psychological intervention, if any is offered, is focussed on overcoming barriers to social and physical rehabilitation and formal psychological therapy may not even mentioned as an option3-4.

There are apparent clinical benefits to this approach, which no doubt account for its current popularity. Most significantly it can facilitate engagement during consultations and thereby rehabilitation efforts, especially in those cases where a less medical-sounding diagnosis is “not well accepted by patients who feel that (it) implies that their symptoms are inauthentic…”5

Where does psychotherapy fit in now?

Against this background a recent systematic literature review6 has summarised evidence for the effectiveness of psychological therapies in FND – 12 studies of CBT and seven of psychodynamic therapy. Therapy trials ought to be a test of some of the ideas about causes of FND and its associated disability, because CBT sits mainly as an adjunct to rehabilitation whereas psychodynamic therapy is aimed at the interpersonal distress that, putatively, has a causal as well as maintaining role.

The results are, frustratingly but not surprisingly, inconclusive. Most of the studies are small and had methodological weaknesses that prevent us getting a definitive answer. The lumping together of participants with quite different clinical presentations makes it impossible to answer the question “what might work for whom?”. We don’t know what proportion of eligible patients will accept either therapy when it is offered in an encouraging and supportive way.

Even so, two results stand out from this useful and well-conducted review. The first is that psychotherapy, including psychodynamically-informed therapy, can be acceptable to people with a range of functional disorders. The second is that the CODES trial7 – by far the largest and best conducted in the field – produced a number of non-specific benefits in mood, wellbeing, quality of life and so on, but had no effect on the frequency or severity of the primary presenting problem which was non-epileptic (functional) seizures.

Where next?

The discourse on FND needs to be rebalanced. A full formulation should include an understanding of psychological and social factors in the generation and maintenance of functional states – not just as coincidental co-morbidities or as natural consequences of disability but as meaningfully related to the disorder. Current evidence on life adversity is not robust enough to dismiss this possibility:  severe threatening events are not what one would typically expect to find as the explanatory exposure in this context8, and life events interviewing is a blunt tool for exploring more nuanced interpersonal conflicts.

The framing of FND as primarily a problem of nervous system function may get in the way of this broader formulation, making it harder for people to discuss and understand the psychosocial aspects of their illness.

Caricaturing of psychological perspectives doesn’t help.  If clinicians really say to their patients  “It’s all in your head”9  or describe them (presumably to colleagues) as work-shy hysterics10 then what’s needed is some re-education of those clinicians rather than reformulating functional disorders so that patients learn to say “I have a real dysfunction of networks in my brain”9.  We must be careful not to collude with the stigmatising of mental health problems by a reluctance to acknowledge that they too are respectable states with which to be diagnosed.  When I first started in medicine, patients were frequently not told they had cancer – as a way of avoiding distressing and uncomfortable consultations. Nobody accepts that now, but it feels as if that’s where we are with FND.

It is a mistake to believe that everybody wants a disease-like diagnostic label and not everybody is offended by sensitively handled discussion of psychological causes of physical illness. For example Markus Reuber and colleagues in Sheffield have shown, as does the latest literature review, that if care is taken with early introduction of the ideas then psychological therapy, even when informed by psychodynamic principles, can be delivered in brief and acceptable formats to people with functional symptoms. Of course not everybody will accept a psychological approach, but an early over-emphasis on mechanistic explanations and short-term goals in therapy just makes it more difficult to address important psychological and social issues at a later stage, if all is not going well.

Writing a little while ago, Anthony David11 talked about a happy “we’re-all-friends-together-let’s get-rid of Cartesian-dualism” camaraderie that pervades this field. He was talking about something a bit different, but it’s still true that “an end to dualism” won’t do to explain where we are now. Apart from the misunderstanding of dualism that the slogan implies, it’s wrong because what we need is more openness about discussing with patients the possible primarily psychological causes and treatments that are relevant in FND even if that may bring uncomfortable consultations – a part of the continuing confrontation of stigmatisation in psychological illness. These ideas need to be tested in careful clinical trials that allow for testing of the value of psychological formulation and intervention as a substantial rather than adjunctive part of treatment, and involve evaluation of mediators and moderators of outcomes that can help unpack the complex nature of this group of disorders. We should do no less – we are still a long way from understanding functional disorders and treating them effectively, and the prognosis for FND is certainly not good as things stand12.

  1. Ludwig L, Pasman JA, Nicholson T, Aybek S, David AS, Tuck S, Kanaan RA, Roelofs K, Carson A, Stone J. Stressful life events and maltreatment in conversion (functional neurological) disorder: systematic review and meta-analysis of case-control studies. The Lancet Psychiatry. 2018 Apr 1;5(4):307-20.
  2. FND Action; FND Hope;   Neurosymptoms
  3. Johns R. I feel I am missing a piece of the puzzle. BMJ. 2020 Apr 8;369.
  4. Wong M. Telling me you don’t know is ok. BMJ. 2020 Jan 8;368.
  5. Dimsdale J, Creed F, Escobar J, Sharpe M, Wulsin L, Barsky A, Lees S, Irwin M, Levensen J (2013). Somatic symptom disorder: an important change in DSM. Journal of Psychosomatic Research, 75, 223-228.
  6. Gutkin M, McLean L, Brown R, Kanaan RA. Systematic review of psychotherapy for adults with functional neurological disorder. Journal of Neurology, Neurosurgery & Psychiatry. 2020 Nov 5.
  7. Goldstein LH, Robinson EJ, Mellers JD, Stone J, Carson A, Reuber M, Medford N, McCrone P, Murray J, Richardson MP, Pilecka I. Cognitive behavioural therapy for adults with dissociative seizures (CODES): a pragmatic, multicentre, randomised controlled trial. The Lancet Psychiatry. 2020 Jun 1;7(6):491-505.
  8. Kanaan RA, Craig TK. Conversion disorder and the trouble with trauma. Psychological Medicine. 2019 Jul;49(10):1585-8.
  9. Burke MJ. “It’s All in Your Head”—Medicine’s Silent Epidemic. JAMA Neurology. 2019 Sep 16.
  10. Popkirov S, Baguley DM, Carson AJ, Brown RJ, Stone J. The neurology of the Cuban” sonic attacks”. The Lancet Neurology. 2019 Sep;18(9):817.
  11. David AS. Functional disorders, Cartesian dualism and stigma: where does the dualism really lie? Journal of Neurology, Neurosurgery & Psychiatry 2012;83:869.
  12. Edwards MJ. Functional neurological disorder: an ethical turning point for neuroscience. Brain 2019 Jun 26;142(7):1855-7.

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