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Neurology is psychiatry—and vice versa Adam Zeman
Correspondence to Professor Adam Zeman, Cognitive Neurology Research Group, University of Exeter Medical School, St Luke’s Campus, Magdalen Road, Exeter EX1 2LU, UK; [email protected]
ABSTRACT This paper explores the relationship between neurology and psychiatry. It marshals evidence that disorders of the brain typically have neurological and psychological—cognitive, affective, behavioural—manifestations, while disorders of the psyche are based in the brain. Given the inseparability of neurological and psychiatric disorders, their disease classifications should eventually fuse, and joint initiatives in training, service and research should be strongly encouraged.
ONCE THEY WERE UNITED… The idea that the brain is the source of our experience and behaviour is very ancient. In a famous passage, written around two-and-a-half-thousand years ago, Hippocrates (figure 1) stated his uncompromising view: Men ought to know that from the brain, and from the brain only, arise our pleasures, joys, laughters and jests, as well as our sorrows, pains, griefs and tears. Through it … we think, see, hear, and distinguish the ugly from the beautiful, the bad from the good, the pleasant from the unpleasant … sleeplessness, inopportune mistakes, aimless anxieties, absent-mindedness, and acts that are contrary to habit. These things that we suffer all come from the brain … Madness comes from its moistness.1
To cite: Zeman A. Pract Neurol Published Online First: [ please include Day Month Year] doi:10.1136/ practneurol-2013-000761
There were opposing theories, including Aristotle’s suggestion that the brain’s main function was to cool the blood, and, through the Middle Ages, aspects of our mental lives were often linked to organs other than the brain. The heart, for example, racing with joy, slowing with grief, can seem a natural home for the emotions, so that in the 16th century Shakespeare could ask: Tell me where is fancy bred, Or in the heart, or in the head?2
Zeman A. Pract Neurol 2014;0:1–9. doi:10.1136/practneurol-2013-000761
But the attention of seekers after the physical home of the mind refocused on the brain soon afterwards. Less than a hundred years later, after Harvey’s demonstration that the heart was a pump at the centre of the circulatory system, Thomas Willis (figure 2), Oxford physician and founding member of the Royal Society, author of De Cerebri Anatome, confessed that he was ‘addicted … to the opening of heads’, thereby to ‘unlock the secret places of men’s minds.’3 The exploration of those secret places was waylaid by the false promise of phrenology in the 18th century, but got underway in earnest during the 19th, when, for example, Broca and Wernicke, localised language to the left hemisphere and showed that separate areas control the programming of fluent speech and language comprehension. Broca (figure 3), echoing Hippocrates and Willis, was to write: ‘The great regions of the mind correspond to the great regions of the brain’.4 The pioneers of clinical neuroscience in the 19th century, like Broca and Wernicke, moved freely between the subject areas that are now delimited by neurology, neuropathology, psychiatry and psychology: their intimate interconnection was taken for granted. Charcot (figure 4) described ‘sclerose en plaques’ (multiple sclerosis) but was fascinated by hysteria. Alois Alzheimer (figure 5) was a psychiatrist and neuropathologist. Before describing the disease that bears his name, he wrote his dissertation on general paralysis of the insane, caused, of course, by syphilis. Constantin von Economo (figure 6), who documented the clinical and neuropathological features of encephalitis lethargica, held a chair of Psychiatry and Neurology in Vienna’s Clinic for Psychiatry and Nervous Diseases. Camillo Golgi (figure 7) was encouraged to pursue his fundamental research on the physical
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Figure 1
Hippocrates.
basis of mental disorders by a psychiatrist mentor, Cesare Lombroso: his ‘silver stain’ allowed Santiago Ramón y Cajal (figure 8) to show that the brain was, like other organs, built from individual cells, our neurones.
Figure 2 Thomas Willis (Portrait of Thomas Willis. History of Medicine Collections. Historical Images in Medicine. David M Rubenstein Rare Book & Manuscript Library, Duke University).
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Figure 3 Pierre Broca (Courtesy of US National Library of Medicine).
BUT THEN THEY CAME APART… By the middle of the last century, when the senior readers of this journal were entering neurology, matters had greatly changed. In the UK and the USA, and to some degree throughout the world, neurology and psychiatry had split apart from one another—
Figure 4 Jean-Martin Charcot.
Zeman A. Pract Neurol 2014;0:1–9. doi:10.1136/practneurol-2013-000761
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Figure 5
Alois Alzheimer.
they were practised by different doctors, differently trained, working in different buildings, usually in different parts of town. The era of ‘mindless neurology and brainless psychiatry’ was in full swing. How did this happen? Several influences conspired together, some originating within neurology, others within psychiatry. In the wake of the remarkable discoveries of Broca, Wernicke, Hughlings Jackson and others, neurologists became cerebral cartographers, keen to localise
Figure 6
Constantin von Economo.
Zeman A. Pract Neurol 2014;0:1–9. doi:10.1136/practneurol-2013-000761
Figure 7 Camillo Golgi (Wellcome Collection).
functions and lesions in the brain with maximum precision, preferably within a single Brodmann area (figure 9). This led quite naturally to a focus on ‘low hanging fruit’—elementary aspects of sensation and motor control lent themselves readily to this approach; some discrete cognitive functions, like face recognition for example, could also be neatly localised. But mood disorders, obsessive compulsive disorder, autism, schizophrenia were much less tractable
Figure 8 Santiago Ramón y Cajal (Reproduced with permission from Cajal Neuro Research Foundation).
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Figure 10 Sigmund Freud. Credit: PA.
Figure 9 A colourised version of Brodmann’s cytoarchitectonic map (with acknowledgment to Professor Emeritus Mark Dubin, University of Colorado-Boulder).
to localisationalists, and were exiled from neurology partly for this reason. Powerful forces within psychiatry had also been pulling neurology and psychiatry apart. One of these forces owed much to a man whose initial training, interests and ambitions were neurological—Sigmund Freud (figure 10). Educated in Vienna toward the close of the 19th century, the young Freud was fascinated by the relationship between mind and brain. He investigated the local and systemic properties of cocaine, dissected the nervous system of lamprey and crayfish, studied aphasia and wrote an early manuscript on the neurological basis of mind, his ‘Project for a Scientific Psychology’. But after studying with Charcot in Paris, and encountering the puzzling phenomena of hysteria and hypnosis, his intellectual direction changed. While he never lost his interest in neurology, he developed the hugely influential theory of psychoanalysis which interpreted mental disorder in primarily psychological terms, and sent 20th century psychiatry on its own unique trajectory. A third influence was fed by a recurring line of thought about psychiatry, which crystallised in the 20th century in the ‘antipsychiatry movement’ associated with Laing5 (figure 11) and Szasz.6 This 4
movement rejected the ‘medical model’ of mental disorders, downplaying the role of the brain and the body. Instead, antipsychiatry underlines the importance of the social and economic environment in engendering mental illness, and recognises the (real) risk that psychiatry may be abused by oppressive regimes, as it was in the last century in Russia, China and elsewhere. The moving 1960s film ‘One Flew over the Cuckoo’s Nest’, which depicts psychiatry as a tool of control and oppression in the USA, captured the spirit of antipsychiatry (figure 12). Whatever view one takes of mental illness, antipsychiatry provides a salutary reminder that conceptions of mental illness cross the uncertain boundary between science and society. One other influence may have played a part. Though attitudes to the relationship between mind and body have varied from culture to culture and time to time, the broad distinction may be a ‘human universal’. Surveys, including one conducted among Edinburgh undergraduates 10 years ago7 (figure 13), reveal notably ‘dualistic’ view of mind and brain among scientists and laymen. If we are indeed all ‘Descartes’ babies’8 at the start of our lives, we have a predisposition to oppose mind and body, or mind and brain, despite their intimate inter-relationships. This can lead to an unreasonably sharp distinction between the specialists who care for their disorders. NEUROLOGY IS PSYCHIATRY There is a sense in which all illness is ‘psychosomatic’—the processes by which we detect, ponder
Zeman A. Pract Neurol 2014;0:1–9. doi:10.1136/practneurol-2013-000761
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Figure 13 Attitudes to mind and brain, from Demertzi et al 7.
Figure 11 R D Laing.
and report the symptoms of illness are all thoroughly ‘psychological’, and these have a major effect on the experience and the outcome of disease. Neurology has an especially close relationship with the psyche because the brain is the central organ of neurological and psychological processes. Indeed, whereas we tend to be educated in medicine in the belief that neurology and psychiatry are correctly allocated separate chapters in our student textbooks, disorders of the central nervous system typically have neurological and psychological—cognitive, affective, behavioural— manifestations.9 Even brain regions that were once regarded as safely ‘neurological’, like the basal ganglia and cerebellum, are proving to be deeply involved in psychological processes and psychiatric disorder.10 11 Here are four types of relationship between neurology and psychiatry/psychology—I will give some examples of each: ▸ Neurological disorder can present with psychological symptoms.
Figure 12 Screen shot of Jack Nicholson in ‘One Flew Over the Cuckoo’s Nest’.
Zeman A. Pract Neurol 2014;0:1–9. doi:10.1136/practneurol-2013-000761
▸ Psychological disorder can present with neurological symptoms. ▸ Neurological disorder can cause a psychological reaction. ▸ Psychological disorder can cause a neurological reaction. Neurological disease can present with psychological symptoms
In cognitive neurology, neurological disease presenting with psychological symptoms, mostly cognitive and behavioural ones, is the rule, not the exception, but such symptoms crop up in every neurology clinic. Cases I have encountered personally as a general neurologist over the years have included a patient sectioned because of his chaotically dangerous behaviour caused, we later discovered, by his neuroacanthocytosis12; a man delivered to hospital by the police with intermittent fluent dysphasia and a background thought disorder, whose left temporal arteriovenous malformation was probably responsible for both13; a woman unable to recognise close members of her family by sight, whose prosopagnosia had been caused by epilepsy arising from a venous angioma in the left fusiform gyrus.14 Examples of neurological conditions presenting with psychological symptoms abound in every category of disorder9 15: cerebrovascular disease can cause cognitive decline, acute mood disorder, sudden behavioural change; multiple sclerosis can present with depression, mania or subcortical dementia; epilepsy can give rise to transient and persistent memory impairment, abrupt changes of mood, ictal, postictal and interictal psychosis; the early symptoms of variant Creutzfeldt-Jakob disease takes sufferers to the psychiatrist’s office16; the recently described encephalitis associated with antibodies to NMDA receptors typically causes psychotic symptoms at the outset17; many neurodegenerative disorders are primarily conditions of the psyche—Alzheimer’s disease, dementia with Lewy bodies, frontotemporal dementia. A recent monograph on the differential diagnosis of psychosis devotes 141 pages to its general medical and 5
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Psychological disorder can present with neurological symptoms
Around one-third of the patients who come to our neurology clinics have symptoms that are either ‘not at all’ or only ‘somewhat’ explained by neurological disease.19 Such symptoms are not, therefore, a side issue for neurologists but among the common problems we encounter. These symptoms are perfectly real to those who experience them, and it can be difficult, especially in the course of a relatively brief neurological consultation, to distinguish symptoms due to neurological disease from those due to psychological disorder. There is a temptation which many of us will recognise from hard experience, to label symptoms that we find mysterious as ‘functional’, when this reflects the limitations of our knowledge of neurology rather than the nature of the problem—as Thomas Willis wrote in the 17th century, ‘hysteria’ can be ‘the subterfuge of ignorance’.20 However, we should not shy away from making the diagnosis of ‘symptoms without disease’ in the large group of patients in whom it is accurate: there is reassuring evidence that misdiagnosis is rare.21 Patients with ‘functional disorder’ are, as a group, just as disabled as patients with neurological disease, but more likely to have given up work.22 They are distinguished by their relatively high symptom count, often including pain. They are more likely to be suffering from depression, anxiety or panic than matched controls with neurological disorder. They are, interestingly, less willing to entertain the possibility that stress might be relevant to their symptoms, and less eager that their doctor should enquire about their emotional state. Neurologists, not surprisingly, differ in their enthusiasm for managing patients with such problems. Some find the phenomenon of disabling symptoms in the absence of disease—often linked to an individual’s life story, personality and mood—intriguing and challenging; others prefer to focus on treating the neurological diseases in which they have particular expertise. But any neurologist with a ‘general neurology’ clinic must be able to recognise, explain and make a plan for patients presenting in this way. In my experience, the chances of achieving this are raised by making it clear from the start, for example, by asking appropriate questions in the functional enquiry, that every patient’s psychological state is of interest and might be relevant to diagnosis. This facilitates later discussion of ‘functional disorder’, if it proves necessary, and opens the door to psychological or psychiatric approaches to treatment if these are required. But as we are about to see, these approaches are often needed, also, in patients with neurological disease. 6
Neurological disease can cause a psychological reaction
Disorders of the brain often disturb the processes which govern mood and behaviour and thereby give rise directly to psychological symptoms. But the diagnosis of a neurological disorder and its consequences for the sufferer’s life—the resulting impairment, disabilities and handicaps—are also potentially major life events. These can cause reactive anxiety, panic, depression and sometimes psychosis, which will warrant attention in their own right. Rates of psychiatric diagnosis among patients seeing neurologists are correspondingly high. The risk of depression in, for example, epilepsy, multiple sclerosis and Parkinson’s disease is markedly higher than in the background population.15 These sequelae are sometimes more readily treated than the underlying neurological problem, and doing so can greatly improve a patient’s quality of life. Psychological disorder can cause a neurological reaction
The opposite relationship—the effect of psychological state on neurological processes and symptoms—may be less obvious but is increasingly well documented. For example, depression proves to be a risk factor for new onset epilepsy, and is linked, possibly by way of elevated levels of circulating corticosteroids, to hippocampal atrophy and memory impairment.23 Indeed, the study of neurological and psychiatric comorbidities has become a focus of cutting edge research. But this relationship, between symptoms we regard as ‘psychological’ and disorders we regard as ‘neurological’, seriously understates the importance of the relationship between our psychological lives and neural processes: for if one can reasonably argue that neurology is psychiatry, just as strong a case can be made for the opposite assertion. PSYCHIATRY IS NEUROLOGY Psychiatry has been described as ‘neurology without signs’, but the link between the two disciplines is not always obvious. The common psychiatric disorders are not caused by straightforwardly identifiable lesions in the brain—a normal MRI scan of the brain in a patient with devastating psychiatric disorder is a familiar and sobering sight; psychiatric illnesses are often highly sensitive to social factors, as the antipsychiatrists insisted; they are usually suspected and almost always confirmed on the basis of ‘subjective’ symptoms—patients’ reports of their altered experience. But, on reflection, none of these features sharply distinguishes psychiatric from neurological disorders, and contemporary neuroscience has begun to furnish the techniques required to illuminate the neurological dimensions of psychiatric illness. I will briefly mention some examples of findings from structural and functional imaging, neurogenetics and neuropharmacology.
Zeman A. Pract Neurol 2014;0:1–9. doi:10.1136/practneurol-2013-000761
REVIEW The profound effects of schizophrenia on perception, thought, intellectual capacity, emotion and behaviour strongly suggest that there must be a pervasive, underlying, neurological disorder—but this has been very hard to identify. Early reports of ventricular enlargement in sufferers led to much controversy. A meta-analysis of structural imaging studies of 1424 patients with a first-episode psychosis indicated that at this early stage of the disorder, there was ventricular enlargement and corresponding whole brain and hippocampal atrophy, though close to the limits of detecAutism, like tion by existing methods.24 schizophrenia, is a pervasive disorder which often lacks obvious neural correlates. A recent study measuring five morphological variables in the brains of people with autism and then applying a sophisticated statistical approach (support vector machine analysis) distinguished ‘autistic’ from control brains with a sensitivity of 90% and specificity of 80%.25 Meta-analyses suggest that there are reductions of hippocampal volume in depression,26 and changes in hippocampal, amygdalar and cingulate volumes in post-traumatic stress disorder.27 Functional imaging, more than any other approach to understanding the brain, has revolutionised thinking about mind and brain over the past 30 years by rendering vividly visible the neural basis of previously invisible mental processes. The techniques are in some respects crude, and the apparent localisation of cognitive activity by functional MRI (fMRI) in the brain of a dead salmon urges caution in the interpretation of its results.28 Yet, functional imaging approaches hold out great promise in understanding the elusive neural basis of psychiatric disorder, with notable results, for example, in the study of Charles Bonnet syndrome, where the content of hallucinations associated with visual loss correlates with regional activations29; depression, in which there is evidence for network dysfunction with areas of hyperactivation and hypoactivation30; and even in the study of hysteria where there are reversible changes in thalamus, caudate and putamen contralateral to regional sensory symptoms.31 The developing study of the human ‘connectome’,32 the architecture of connections that creates the functional networks of the brain, and the novel techniques that facilitate this, such as resting-state fMRI33 and analysis using ‘graph theoretical analysis’,34 are likely to be especially valuable in psychiatry, for which the previous approach to neurological analysis—mapping the brain small area by area—was probably inappropriate. The genetic study of psychiatric disorder is in the midst of a growth spurt, but there are already suggestive findings and a likelihood that these will lead to a restructuring of psychiatric diagnoses over time.35 Risk factors for psychosis have been identified at the level of single genes, and in relation to disorders caused by these. For example, the lifetime risk of
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psychosis in velo-cardio-facial syndrome is around 30%.18 In general, psychiatric risk is likely to be determined by contributions from many genes which are individually of small effect: genome-wide association studies are locating such genes including ZN804A which influences the risk of schizophrenia and CACNA1C which modulates the risk of bipolar disease.35 Variations in ‘copy numbers’ are proving to be common risk factors for disorders previously regarded as distinct, for example, autism, schizophrenia and learning disability.35 The path leading from genotype to psychiatric phenotype will undoubtedly be a complex one in which gene–gene and gene–environment interactions will play a key role. ‘Imaging genetics’ is identifying the effects of genetic variation on patterns of brain activity.36 Neuropharmacology provides a final example of the seamless boundary between neurology and psychiatry. However difficult it is to define their relationship in theory, the indispensable British National Formulary quietly but logically includes drugs working on the central nervous system in a single chapter, regardless of which specialism predominantly uses them—and, of course, many drugs cross the divide: neurologists prescribe ‘antidepressants’ to reduce migraine and cataplexy; psychiatrists prescribe ‘antiepileptics’ to stabilise mood. This is not surprising as the systems based in the brain stem that neurologists-in-training come to know as the ‘ascending activating system’, regulating conscious state, overlap massively with the systems psychiatrists-in-training encounter as key regulators of motivation and mood (figure 14). SOME RELEVANT SIDE ISSUES: ORGANISM AND FUNCTION; MIND AND MATTER; BIOPSYCHOSOCIAL MEDICINE Medicine and medics tend to be suspicious of philosophy, but just a few abstract points require a mention here. First, we should be cautious, at least, in our use of the terms ‘functional’ and ‘organic’. We continue to deploy these, despite Kinnier Wilson’s comment in his 1940 textbook that the ‘antithesis between “organic” and “functional” disease states … lingers at the bedside and in medical literature, though it is transparently false and has been abandoned long since by all contemplative minds.37’ It is ‘transparently false’ because all our patients are organisms, and all their disorders involve upsets of functioning: this distinction presumes and perpetuates the misleading, dualistic distinction between mindless matter and matterless mind. It is surely revealing that we find it so difficult to do without a distinction that makes so little sense. The rather different distinction between ‘functional’ and ‘structural’ disorder is more coherent.38 The second general point is that in the background of the debate over the relationship between neurology and psychiatry lies the philosophical debate over the
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Figure 14 The pharmacology of the brainstem activating systems: A shows the origin and distribution of the central noradrenergic pathways in the rat brain; B the dopaminergic pathways; C the cholinergic pathways; D the serotonergic pathways. CTT, central tegmental tract; dltn, dorsolateral tegmental nucleus; DNAB, dorsal noradrenergic ascending bundle; DR, dorsal raphe; DS, dorsal striatum; HDBB, horizontal limb nucleus of the diagonal band of Broca; Icj, islands of Calleja; IP, interpeduncular nucleus; LC, locus ceruleus; MFB, medial forebrain bundle; MS, medial septum; NBM, nucleus basalis magnocellularis (Meynert in primates); OT, olfactory tubercle; PFC, prefrontal cortex; SN, substantia nigra; tpp, tegmental pedunculopontine nucleus; VDBB, vertical limb nucleus of the diagonal band of Broca; VNAB, ventral noradrenergic ascending bundle; VS, ventral striatum (from Robbins & Everitt 1995).
relationship between mind and matter.39 This is a fascinating and possibly insoluble philosophical conundrum, but the main argument of this article does not depend at all on reaching a solution to this ancient philosophical question. The argument that ‘neurology is psychiatry and vice versa’ doesn’t make any assumptions about the nature of matter or mind, and, in particular, is not ‘mind-denying’. Rather, it insists that to understand and manage disorders of the brain, we need to take into account experience, behaviour and physiology at all times. This is a practical message, usefully encapsulated in the concept of biopsychosocial medicine40: every disorder—indeed every moment of healthy functioning—has biological, psychological and social dimensions. Doctors ignore any one of these at their peril. SO WHAT? The first practical upshot of the argument made here is that neurological and psychiatric disease classifications should be fused.41 This would draw the two professions together and encourage them to collaborate more intensively, with benefits for service and research. But however good an idea this may be, the massive institutional barriers mean that it will not happen anytime soon. There are more realistic short-term and middle-term goals. Neurologists-in-training should spend some time, at least 6 months, working in an appropriate psychiatric training post, probably in a department of
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‘psychological medicine’ rather than on a psychiatry ward, from which the lessons learned would be less easily transferred to the neurology clinic. Psychiatrists-in-training, likewise, should, where possible, spend a similar period working in a neurology service. This innovation would meet a felt need among trainees, enhance collaboration between the specialties and ensure that neurologists develop some psychiatric skills, and psychiatrists gain confidence in neurology. More or less everyone agrees that this is a good idea but few training programmes have achieved it. Excuses involving the differing lengths of junior attachments in the two specialties are feeble. Let’s do it! Among patients with disorders that plainly cross the traditional divide—for example, in the dementias or in the case of patients with ‘symptoms without disease’—joint consultations, though expensive, can be highly effective and should be arranged more often. In general, liaison between neurologists and psychiatrists should increase, and psychological services, which are often needed but in short supply, should be made more available and be more fully integrated into neurology departments. Finally, the intimate relationship between these specialisms implies that joint research should be encouraged by research leaders and funding bodies. Neurology and psychiatry have much to learn from one another. This message is old news in neuroscience: basic research tends to move freely between
Zeman A. Pract Neurol 2014;0:1–9. doi:10.1136/practneurol-2013-000761
REVIEW neurological and psychiatric contexts, and many neuroscientists would regard the kernel of this paper as plumb obvious. Things are very different in the clinic. Medicine should not be left behind. Acknowledgements I am very grateful to Nick Craddock, Jon Stone, Michael Trimble and Peter White for their penetrating comments on this paper, and to Joanne Veale for her help with permissions. Competing interests None.
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Provenance and peer review Commissioned; externally peer reviewed. This paper was reviewed by Jon Stone, Edinburgh, UK.
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1 Jones WHS. Hippocrates. Cambridge, MA: Harvard University Press, 1923:175. 2 Shakespeare W. The alexander text of the complete works of Shakespeare, the merchant of venice (Act 3 Scene 2). London: Collins, 1623:238. 3 Willis T. Cerebri anatome: Cui accessit nervorum descriptio et usus. 1666. https://archive.org/details/cerebrianatomecu1666will (accessed 20 Nov 2013). 4 Broca P. Remarks on the seat of the faculty of articulate language, following an observation of Aphemia (loss of speech). Bulletin de la Société Anatomique 1861;6:330–57. 5 Laing RD. The divided self: an existential study in sanity and madness. London: Penguin, 1960. 6 Szasz T. The myth of mental illness: foundations of a theory of personal conduct. New York, NY: Harper and Row, 1961. 7 Demertzi A, Liew C, Ledoux D, et al. Dualism persists in the science of mind. Ann N Y Acad Sci 2009;1157:1–9. 8 Bloom P. Descartes’ baby. London: Arrow Books, 2004. 9 Butler C, Zeman AZ. Neurological syndromes which can be mistaken for psychiatric conditions. J Neurol Neurosurg Psychiatry 2005;76(Suppl 1):i31–8. 10 Schmahmann JD, Caplan D. Cognition, emotion and the cerebellum. Brain 2006;129(Pt 2):290–2. 11 Bejjani BP, Damier P, Arnulf I, et al. Transient acute depression induced by high-frequency deep-brain stimulation. N Engl J Med 1999;340:1476–80. 12 Zeman A, Daniels G, Tilley L, et al. McLeod syndrome: life-long neuropsychiatric disorder due to a novel mutation of the XK gene. Psychiatr Genet 2005;15:291–3. 13 Zeman A, Carson A, Rivers C, et al. A case of evolving post-ictal language disturbance secondary to a left temporal arteriovenous malformation: jargon aphasia or formal thought disorder? Cogn Neuropsychiatry 2006;11:465–79. 14 Wright H, Wardlaw J, Young AW, et al. Prosopagnosia following nonconvulsive status epilepticus associated with a left fusiform gyrus malformation. Epilepsy Behav 2006;9:197–203. 15 David A, Fleminger S, Kopelman M, et al. Lishman’s organic psychiatry. Oxford: Wiley-Blackwell, 2009. 16 Spencer MD, Knight RS, Will RG. First hundred cases of variant Creutzfeldt-Jakob disease: retrospective case note review of early psychiatric and neurological features. BMJ 2002;324:1479–82. 17 Dalmau J, Gleichman AJ, Hughes EG, et al. Anti-NMDA-receptor encephalitis: case series and analysis of the effects of antibodies. Lancet Neurol 2008;7:1091–8. 18 Cardinal R, Bullmore ET. The diagnosis of psychosis. Cambridge University Press, 2011. 19 Carson A, Stone J, Hibberd C, et al. Disability, distress and unemployment in neurology outpatients with symptoms
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Neurology is psychiatry—and vice versa Adam Zeman
Correspondence to Professor Adam Zeman, Cognitive Neurology Research Group, University of Exeter Medical School, St Luke’s Campus, Magdalen Road, Exeter EX1 2LU, UK; [email protected]
ABSTRACT This paper explores the relationship between neurology and psychiatry. It marshals evidence that disorders of the brain typically have neurological and psychological—cognitive, affective, behavioural—manifestations, while disorders of the psyche are based in the brain. Given the inseparability of neurological and psychiatric disorders, their disease classifications should eventually fuse, and joint initiatives in training, service and research should be strongly encouraged.
ONCE THEY WERE UNITED… The idea that the brain is the source of our experience and behaviour is very ancient. In a famous passage, written around two-and-a-half-thousand years ago, Hippocrates (figure 1) stated his uncompromising view: Men ought to know that from the brain, and from the brain only, arise our pleasures, joys, laughters and jests, as well as our sorrows, pains, griefs and tears. Through it … we think, see, hear, and distinguish the ugly from the beautiful, the bad from the good, the pleasant from the unpleasant … sleeplessness, inopportune mistakes, aimless anxieties, absent-mindedness, and acts that are contrary to habit. These things that we suffer all come from the brain … Madness comes from its moistness.1
To cite: Zeman A. Pract Neurol Published Online First: [ please include Day Month Year] doi:10.1136/ practneurol-2013-000761
There were opposing theories, including Aristotle’s suggestion that the brain’s main function was to cool the blood, and, through the Middle Ages, aspects of our mental lives were often linked to organs other than the brain. The heart, for example, racing with joy, slowing with grief, can seem a natural home for the emotions, so that in the 16th century Shakespeare could ask: Tell me where is fancy bred, Or in the heart, or in the head?2
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But the attention of seekers after the physical home of the mind refocused on the brain soon afterwards. Less than a hundred years later, after Harvey’s demonstration that the heart was a pump at the centre of the circulatory system, Thomas Willis (figure 2), Oxford physician and founding member of the Royal Society, author of De Cerebri Anatome, confessed that he was ‘addicted … to the opening of heads’, thereby to ‘unlock the secret places of men’s minds.’3 The exploration of those secret places was waylaid by the false promise of phrenology in the 18th century, but got underway in earnest during the 19th, when, for example, Broca and Wernicke, localised language to the left hemisphere and showed that separate areas control the programming of fluent speech and language comprehension. Broca (figure 3), echoing Hippocrates and Willis, was to write: ‘The great regions of the mind correspond to the great regions of the brain’.4 The pioneers of clinical neuroscience in the 19th century, like Broca and Wernicke, moved freely between the subject areas that are now delimited by neurology, neuropathology, psychiatry and psychology: their intimate interconnection was taken for granted. Charcot (figure 4) described ‘sclerose en plaques’ (multiple sclerosis) but was fascinated by hysteria. Alois Alzheimer (figure 5) was a psychiatrist and neuropathologist. Before describing the disease that bears his name, he wrote his dissertation on general paralysis of the insane, caused, of course, by syphilis. Constantin von Economo (figure 6), who documented the clinical and neuropathological features of encephalitis lethargica, held a chair of Psychiatry and Neurology in Vienna’s Clinic for Psychiatry and Nervous Diseases. Camillo Golgi (figure 7) was encouraged to pursue his fundamental research on the physical
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Figure 1
Hippocrates.
basis of mental disorders by a psychiatrist mentor, Cesare Lombroso: his ‘silver stain’ allowed Santiago Ramón y Cajal (figure 8) to show that the brain was, like other organs, built from individual cells, our neurones.
Figure 2 Thomas Willis (Portrait of Thomas Willis. History of Medicine Collections. Historical Images in Medicine. David M Rubenstein Rare Book & Manuscript Library, Duke University).
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Figure 3 Pierre Broca (Courtesy of US National Library of Medicine).
BUT THEN THEY CAME APART… By the middle of the last century, when the senior readers of this journal were entering neurology, matters had greatly changed. In the UK and the USA, and to some degree throughout the world, neurology and psychiatry had split apart from one another—
Figure 4 Jean-Martin Charcot.
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Figure 5
Alois Alzheimer.
they were practised by different doctors, differently trained, working in different buildings, usually in different parts of town. The era of ‘mindless neurology and brainless psychiatry’ was in full swing. How did this happen? Several influences conspired together, some originating within neurology, others within psychiatry. In the wake of the remarkable discoveries of Broca, Wernicke, Hughlings Jackson and others, neurologists became cerebral cartographers, keen to localise
Figure 6
Constantin von Economo.
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Figure 7 Camillo Golgi (Wellcome Collection).
functions and lesions in the brain with maximum precision, preferably within a single Brodmann area (figure 9). This led quite naturally to a focus on ‘low hanging fruit’—elementary aspects of sensation and motor control lent themselves readily to this approach; some discrete cognitive functions, like face recognition for example, could also be neatly localised. But mood disorders, obsessive compulsive disorder, autism, schizophrenia were much less tractable
Figure 8 Santiago Ramón y Cajal (Reproduced with permission from Cajal Neuro Research Foundation).
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Figure 10 Sigmund Freud. Credit: PA.
Figure 9 A colourised version of Brodmann’s cytoarchitectonic map (with acknowledgment to Professor Emeritus Mark Dubin, University of Colorado-Boulder).
to localisationalists, and were exiled from neurology partly for this reason. Powerful forces within psychiatry had also been pulling neurology and psychiatry apart. One of these forces owed much to a man whose initial training, interests and ambitions were neurological—Sigmund Freud (figure 10). Educated in Vienna toward the close of the 19th century, the young Freud was fascinated by the relationship between mind and brain. He investigated the local and systemic properties of cocaine, dissected the nervous system of lamprey and crayfish, studied aphasia and wrote an early manuscript on the neurological basis of mind, his ‘Project for a Scientific Psychology’. But after studying with Charcot in Paris, and encountering the puzzling phenomena of hysteria and hypnosis, his intellectual direction changed. While he never lost his interest in neurology, he developed the hugely influential theory of psychoanalysis which interpreted mental disorder in primarily psychological terms, and sent 20th century psychiatry on its own unique trajectory. A third influence was fed by a recurring line of thought about psychiatry, which crystallised in the 20th century in the ‘antipsychiatry movement’ associated with Laing5 (figure 11) and Szasz.6 This 4
movement rejected the ‘medical model’ of mental disorders, downplaying the role of the brain and the body. Instead, antipsychiatry underlines the importance of the social and economic environment in engendering mental illness, and recognises the (real) risk that psychiatry may be abused by oppressive regimes, as it was in the last century in Russia, China and elsewhere. The moving 1960s film ‘One Flew over the Cuckoo’s Nest’, which depicts psychiatry as a tool of control and oppression in the USA, captured the spirit of antipsychiatry (figure 12). Whatever view one takes of mental illness, antipsychiatry provides a salutary reminder that conceptions of mental illness cross the uncertain boundary between science and society. One other influence may have played a part. Though attitudes to the relationship between mind and body have varied from culture to culture and time to time, the broad distinction may be a ‘human universal’. Surveys, including one conducted among Edinburgh undergraduates 10 years ago7 (figure 13), reveal notably ‘dualistic’ view of mind and brain among scientists and laymen. If we are indeed all ‘Descartes’ babies’8 at the start of our lives, we have a predisposition to oppose mind and body, or mind and brain, despite their intimate inter-relationships. This can lead to an unreasonably sharp distinction between the specialists who care for their disorders. NEUROLOGY IS PSYCHIATRY There is a sense in which all illness is ‘psychosomatic’—the processes by which we detect, ponder
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Figure 13 Attitudes to mind and brain, from Demertzi et al 7.
Figure 11 R D Laing.
and report the symptoms of illness are all thoroughly ‘psychological’, and these have a major effect on the experience and the outcome of disease. Neurology has an especially close relationship with the psyche because the brain is the central organ of neurological and psychological processes. Indeed, whereas we tend to be educated in medicine in the belief that neurology and psychiatry are correctly allocated separate chapters in our student textbooks, disorders of the central nervous system typically have neurological and psychological—cognitive, affective, behavioural— manifestations.9 Even brain regions that were once regarded as safely ‘neurological’, like the basal ganglia and cerebellum, are proving to be deeply involved in psychological processes and psychiatric disorder.10 11 Here are four types of relationship between neurology and psychiatry/psychology—I will give some examples of each: ▸ Neurological disorder can present with psychological symptoms.
Figure 12 Screen shot of Jack Nicholson in ‘One Flew Over the Cuckoo’s Nest’.
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▸ Psychological disorder can present with neurological symptoms. ▸ Neurological disorder can cause a psychological reaction. ▸ Psychological disorder can cause a neurological reaction. Neurological disease can present with psychological symptoms
In cognitive neurology, neurological disease presenting with psychological symptoms, mostly cognitive and behavioural ones, is the rule, not the exception, but such symptoms crop up in every neurology clinic. Cases I have encountered personally as a general neurologist over the years have included a patient sectioned because of his chaotically dangerous behaviour caused, we later discovered, by his neuroacanthocytosis12; a man delivered to hospital by the police with intermittent fluent dysphasia and a background thought disorder, whose left temporal arteriovenous malformation was probably responsible for both13; a woman unable to recognise close members of her family by sight, whose prosopagnosia had been caused by epilepsy arising from a venous angioma in the left fusiform gyrus.14 Examples of neurological conditions presenting with psychological symptoms abound in every category of disorder9 15: cerebrovascular disease can cause cognitive decline, acute mood disorder, sudden behavioural change; multiple sclerosis can present with depression, mania or subcortical dementia; epilepsy can give rise to transient and persistent memory impairment, abrupt changes of mood, ictal, postictal and interictal psychosis; the early symptoms of variant Creutzfeldt-Jakob disease takes sufferers to the psychiatrist’s office16; the recently described encephalitis associated with antibodies to NMDA receptors typically causes psychotic symptoms at the outset17; many neurodegenerative disorders are primarily conditions of the psyche—Alzheimer’s disease, dementia with Lewy bodies, frontotemporal dementia. A recent monograph on the differential diagnosis of psychosis devotes 141 pages to its general medical and 5
REVIEW neurological causes, but only 17 pages to primary psychiatric disease.18
Psychological disorder can present with neurological symptoms
Around one-third of the patients who come to our neurology clinics have symptoms that are either ‘not at all’ or only ‘somewhat’ explained by neurological disease.19 Such symptoms are not, therefore, a side issue for neurologists but among the common problems we encounter. These symptoms are perfectly real to those who experience them, and it can be difficult, especially in the course of a relatively brief neurological consultation, to distinguish symptoms due to neurological disease from those due to psychological disorder. There is a temptation which many of us will recognise from hard experience, to label symptoms that we find mysterious as ‘functional’, when this reflects the limitations of our knowledge of neurology rather than the nature of the problem—as Thomas Willis wrote in the 17th century, ‘hysteria’ can be ‘the subterfuge of ignorance’.20 However, we should not shy away from making the diagnosis of ‘symptoms without disease’ in the large group of patients in whom it is accurate: there is reassuring evidence that misdiagnosis is rare.21 Patients with ‘functional disorder’ are, as a group, just as disabled as patients with neurological disease, but more likely to have given up work.22 They are distinguished by their relatively high symptom count, often including pain. They are more likely to be suffering from depression, anxiety or panic than matched controls with neurological disorder. They are, interestingly, less willing to entertain the possibility that stress might be relevant to their symptoms, and less eager that their doctor should enquire about their emotional state. Neurologists, not surprisingly, differ in their enthusiasm for managing patients with such problems. Some find the phenomenon of disabling symptoms in the absence of disease—often linked to an individual’s life story, personality and mood—intriguing and challenging; others prefer to focus on treating the neurological diseases in which they have particular expertise. But any neurologist with a ‘general neurology’ clinic must be able to recognise, explain and make a plan for patients presenting in this way. In my experience, the chances of achieving this are raised by making it clear from the start, for example, by asking appropriate questions in the functional enquiry, that every patient’s psychological state is of interest and might be relevant to diagnosis. This facilitates later discussion of ‘functional disorder’, if it proves necessary, and opens the door to psychological or psychiatric approaches to treatment if these are required. But as we are about to see, these approaches are often needed, also, in patients with neurological disease. 6
Neurological disease can cause a psychological reaction
Disorders of the brain often disturb the processes which govern mood and behaviour and thereby give rise directly to psychological symptoms. But the diagnosis of a neurological disorder and its consequences for the sufferer’s life—the resulting impairment, disabilities and handicaps—are also potentially major life events. These can cause reactive anxiety, panic, depression and sometimes psychosis, which will warrant attention in their own right. Rates of psychiatric diagnosis among patients seeing neurologists are correspondingly high. The risk of depression in, for example, epilepsy, multiple sclerosis and Parkinson’s disease is markedly higher than in the background population.15 These sequelae are sometimes more readily treated than the underlying neurological problem, and doing so can greatly improve a patient’s quality of life. Psychological disorder can cause a neurological reaction
The opposite relationship—the effect of psychological state on neurological processes and symptoms—may be less obvious but is increasingly well documented. For example, depression proves to be a risk factor for new onset epilepsy, and is linked, possibly by way of elevated levels of circulating corticosteroids, to hippocampal atrophy and memory impairment.23 Indeed, the study of neurological and psychiatric comorbidities has become a focus of cutting edge research. But this relationship, between symptoms we regard as ‘psychological’ and disorders we regard as ‘neurological’, seriously understates the importance of the relationship between our psychological lives and neural processes: for if one can reasonably argue that neurology is psychiatry, just as strong a case can be made for the opposite assertion. PSYCHIATRY IS NEUROLOGY Psychiatry has been described as ‘neurology without signs’, but the link between the two disciplines is not always obvious. The common psychiatric disorders are not caused by straightforwardly identifiable lesions in the brain—a normal MRI scan of the brain in a patient with devastating psychiatric disorder is a familiar and sobering sight; psychiatric illnesses are often highly sensitive to social factors, as the antipsychiatrists insisted; they are usually suspected and almost always confirmed on the basis of ‘subjective’ symptoms—patients’ reports of their altered experience. But, on reflection, none of these features sharply distinguishes psychiatric from neurological disorders, and contemporary neuroscience has begun to furnish the techniques required to illuminate the neurological dimensions of psychiatric illness. I will briefly mention some examples of findings from structural and functional imaging, neurogenetics and neuropharmacology.
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REVIEW The profound effects of schizophrenia on perception, thought, intellectual capacity, emotion and behaviour strongly suggest that there must be a pervasive, underlying, neurological disorder—but this has been very hard to identify. Early reports of ventricular enlargement in sufferers led to much controversy. A meta-analysis of structural imaging studies of 1424 patients with a first-episode psychosis indicated that at this early stage of the disorder, there was ventricular enlargement and corresponding whole brain and hippocampal atrophy, though close to the limits of detecAutism, like tion by existing methods.24 schizophrenia, is a pervasive disorder which often lacks obvious neural correlates. A recent study measuring five morphological variables in the brains of people with autism and then applying a sophisticated statistical approach (support vector machine analysis) distinguished ‘autistic’ from control brains with a sensitivity of 90% and specificity of 80%.25 Meta-analyses suggest that there are reductions of hippocampal volume in depression,26 and changes in hippocampal, amygdalar and cingulate volumes in post-traumatic stress disorder.27 Functional imaging, more than any other approach to understanding the brain, has revolutionised thinking about mind and brain over the past 30 years by rendering vividly visible the neural basis of previously invisible mental processes. The techniques are in some respects crude, and the apparent localisation of cognitive activity by functional MRI (fMRI) in the brain of a dead salmon urges caution in the interpretation of its results.28 Yet, functional imaging approaches hold out great promise in understanding the elusive neural basis of psychiatric disorder, with notable results, for example, in the study of Charles Bonnet syndrome, where the content of hallucinations associated with visual loss correlates with regional activations29; depression, in which there is evidence for network dysfunction with areas of hyperactivation and hypoactivation30; and even in the study of hysteria where there are reversible changes in thalamus, caudate and putamen contralateral to regional sensory symptoms.31 The developing study of the human ‘connectome’,32 the architecture of connections that creates the functional networks of the brain, and the novel techniques that facilitate this, such as resting-state fMRI33 and analysis using ‘graph theoretical analysis’,34 are likely to be especially valuable in psychiatry, for which the previous approach to neurological analysis—mapping the brain small area by area—was probably inappropriate. The genetic study of psychiatric disorder is in the midst of a growth spurt, but there are already suggestive findings and a likelihood that these will lead to a restructuring of psychiatric diagnoses over time.35 Risk factors for psychosis have been identified at the level of single genes, and in relation to disorders caused by these. For example, the lifetime risk of
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psychosis in velo-cardio-facial syndrome is around 30%.18 In general, psychiatric risk is likely to be determined by contributions from many genes which are individually of small effect: genome-wide association studies are locating such genes including ZN804A which influences the risk of schizophrenia and CACNA1C which modulates the risk of bipolar disease.35 Variations in ‘copy numbers’ are proving to be common risk factors for disorders previously regarded as distinct, for example, autism, schizophrenia and learning disability.35 The path leading from genotype to psychiatric phenotype will undoubtedly be a complex one in which gene–gene and gene–environment interactions will play a key role. ‘Imaging genetics’ is identifying the effects of genetic variation on patterns of brain activity.36 Neuropharmacology provides a final example of the seamless boundary between neurology and psychiatry. However difficult it is to define their relationship in theory, the indispensable British National Formulary quietly but logically includes drugs working on the central nervous system in a single chapter, regardless of which specialism predominantly uses them—and, of course, many drugs cross the divide: neurologists prescribe ‘antidepressants’ to reduce migraine and cataplexy; psychiatrists prescribe ‘antiepileptics’ to stabilise mood. This is not surprising as the systems based in the brain stem that neurologists-in-training come to know as the ‘ascending activating system’, regulating conscious state, overlap massively with the systems psychiatrists-in-training encounter as key regulators of motivation and mood (figure 14). SOME RELEVANT SIDE ISSUES: ORGANISM AND FUNCTION; MIND AND MATTER; BIOPSYCHOSOCIAL MEDICINE Medicine and medics tend to be suspicious of philosophy, but just a few abstract points require a mention here. First, we should be cautious, at least, in our use of the terms ‘functional’ and ‘organic’. We continue to deploy these, despite Kinnier Wilson’s comment in his 1940 textbook that the ‘antithesis between “organic” and “functional” disease states … lingers at the bedside and in medical literature, though it is transparently false and has been abandoned long since by all contemplative minds.37’ It is ‘transparently false’ because all our patients are organisms, and all their disorders involve upsets of functioning: this distinction presumes and perpetuates the misleading, dualistic distinction between mindless matter and matterless mind. It is surely revealing that we find it so difficult to do without a distinction that makes so little sense. The rather different distinction between ‘functional’ and ‘structural’ disorder is more coherent.38 The second general point is that in the background of the debate over the relationship between neurology and psychiatry lies the philosophical debate over the
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Figure 14 The pharmacology of the brainstem activating systems: A shows the origin and distribution of the central noradrenergic pathways in the rat brain; B the dopaminergic pathways; C the cholinergic pathways; D the serotonergic pathways. CTT, central tegmental tract; dltn, dorsolateral tegmental nucleus; DNAB, dorsal noradrenergic ascending bundle; DR, dorsal raphe; DS, dorsal striatum; HDBB, horizontal limb nucleus of the diagonal band of Broca; Icj, islands of Calleja; IP, interpeduncular nucleus; LC, locus ceruleus; MFB, medial forebrain bundle; MS, medial septum; NBM, nucleus basalis magnocellularis (Meynert in primates); OT, olfactory tubercle; PFC, prefrontal cortex; SN, substantia nigra; tpp, tegmental pedunculopontine nucleus; VDBB, vertical limb nucleus of the diagonal band of Broca; VNAB, ventral noradrenergic ascending bundle; VS, ventral striatum (from Robbins & Everitt 1995).
relationship between mind and matter.39 This is a fascinating and possibly insoluble philosophical conundrum, but the main argument of this article does not depend at all on reaching a solution to this ancient philosophical question. The argument that ‘neurology is psychiatry and vice versa’ doesn’t make any assumptions about the nature of matter or mind, and, in particular, is not ‘mind-denying’. Rather, it insists that to understand and manage disorders of the brain, we need to take into account experience, behaviour and physiology at all times. This is a practical message, usefully encapsulated in the concept of biopsychosocial medicine40: every disorder—indeed every moment of healthy functioning—has biological, psychological and social dimensions. Doctors ignore any one of these at their peril. SO WHAT? The first practical upshot of the argument made here is that neurological and psychiatric disease classifications should be fused.41 This would draw the two professions together and encourage them to collaborate more intensively, with benefits for service and research. But however good an idea this may be, the massive institutional barriers mean that it will not happen anytime soon. There are more realistic short-term and middle-term goals. Neurologists-in-training should spend some time, at least 6 months, working in an appropriate psychiatric training post, probably in a department of
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‘psychological medicine’ rather than on a psychiatry ward, from which the lessons learned would be less easily transferred to the neurology clinic. Psychiatrists-in-training, likewise, should, where possible, spend a similar period working in a neurology service. This innovation would meet a felt need among trainees, enhance collaboration between the specialties and ensure that neurologists develop some psychiatric skills, and psychiatrists gain confidence in neurology. More or less everyone agrees that this is a good idea but few training programmes have achieved it. Excuses involving the differing lengths of junior attachments in the two specialties are feeble. Let’s do it! Among patients with disorders that plainly cross the traditional divide—for example, in the dementias or in the case of patients with ‘symptoms without disease’—joint consultations, though expensive, can be highly effective and should be arranged more often. In general, liaison between neurologists and psychiatrists should increase, and psychological services, which are often needed but in short supply, should be made more available and be more fully integrated into neurology departments. Finally, the intimate relationship between these specialisms implies that joint research should be encouraged by research leaders and funding bodies. Neurology and psychiatry have much to learn from one another. This message is old news in neuroscience: basic research tends to move freely between
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REVIEW neurological and psychiatric contexts, and many neuroscientists would regard the kernel of this paper as plumb obvious. Things are very different in the clinic. Medicine should not be left behind. Acknowledgements I am very grateful to Nick Craddock, Jon Stone, Michael Trimble and Peter White for their penetrating comments on this paper, and to Joanne Veale for her help with permissions. Competing interests None.
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Provenance and peer review Commissioned; externally peer reviewed. This paper was reviewed by Jon Stone, Edinburgh, UK.
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