I have built this essay on five interlocking themes: developing services, mapping the diagnostic landscape, scientific background, advances in treatment, and the political and social context. Inevitably my story refers mainly to the United Kingdom, often specifically to Oxford, sometimes only to personal experience. I apologize to the rest of the world, for neglecting the story of old age psychiatry there.
Textbooks are useful milestones on the journey, crystallizing the achievements and culture of their time (1, 2). I have drawn on successive editions of the textbook (1) edited by Robin Jacoby and myself to cover the period from 2008 back to 1991; and for the decade before that, Raymond Levy and Felix Post’s The Psychiatry of Late Life (3), my bible as a newly appointed consultant in 1984. My 50-year milestone is a major British textbook (4) of that time: Clinical Psychiatry by Mayer-Gross, Slater, and Roth. William Mayer-Gross and Martin Roth were pioneers in the psychiatry of old age, and the text itself is full of historical perspectives. (Doubtless, filial affection (5) also influenced my choice.)
Compassion for older people in want or distress is as old as humanity; and so are efforts to construct systems for meeting their needs. But it would be fair to give to the United Kingdom the credit for inventing psychogeriatrics as a distinct medical discipline. Its roots were in Scotland at the Crichton Royal Infirmary in Dumfries in the 1940s, and it spread from there to the Maudsley Hospital in London with Felix Post, Newcastle with Martin Roth, Klaus Bergmann and David Kay, Manchester with David Jolley, and Nottingham with Tom Arie.
Many of the pioneers had stumbled on the care of older people by accident; many had unconventional backgrounds and little formal training. Poorly resourced, accepting responsibility for uncharted numbers of community-living older people and for the hidden cases of depression or dementia among them, they used their charisma and determination to create pragmatic, humane services which could do something to relieve the distresses they uncovered. Often that ‘something’ proved sufficient to avert an admission to hospital, throw a lifeline to a family carer, or reassure a residential home that it would not be ignored when it asked for help.
The pioneers had no grandiose plan. They expected to build up services by small steps, seizing whatever chance opportunities arose. As pragmatists they absorbed every valuable idea of their time; and having only minimal premises and staff, they understood the need to collaborate with other local powers—social services, geriatricians, fellow-psychiatrists, and general practitioners. The founding principles of the specialty came from community and social psychiatry, recognizing the power of family and neighbourhood-networks, and of teamwork between colleagues with complementary skills. The typical scientific attitude was epidemiological—taking responsibility for whole populations of older people together with the ill people embedded in them, at home, in hospital, or in residential care.
In the 1970s, I came as a junior doctor into psychiatry from general medicine, where I had worked with Leo Wollner, a geriatrician who epitomized the dauntless approach to geriatric illness pioneered in the United Kingdom in the 1940s by Marjorie Warren. Psychiatry of old age to me meant only the long-stay asylum wards I had seen as a medical student: austere rows of white-painted hospital beds with raised cot sides; the pitiful sight of patients with contractures, remotely uncommunicative or endlessly calling for help, being carefully tended by nurses in white coats and plastic aprons.
A decade later, towards the end of my psychiatric training, I saw a different side of old age psychiatry. During the 1950s and 1960s the former county asylum, Littlemore Hospital, had developed an active programme of community nursing and resettlement of patients with chronic psychotic illness, and this emphasis on psychiatry in the home was maintained into the 1970s, when Oxford’s first old age psychiatrist and first community psychiatric nurse for older people were appointed. John Robinson, the psychiatrist, had come originally from a background in general practice; Steve Corea’s first profession was teaching. Together they travelled around Oxfordshire in John’s old green Morris Minor car, laying the foundations for older people of home assessment and community care. As a trainee in the specialty I was given responsibility for my own small patch of Oxfordshire, and from their expertise I started to appreciate the beauties of community psychiatry and the rewards of working with older people.
In 1969 Slater and Roth wrote (6):
The modern era in geriatric psychiatry began with the differentiation of senile dementia, arteriosclerotic dementia and the presenile psychoses from one another and from other organic psychoses, such as neurosyphilis.… Affective and paranoid disorders were regarded … as forms of senile psychosis which led eventually to deterioration of personality and intellect.… When the introduction of electroconvulsive therapy (E.C.T.) for elderly patients began to make it plain that some depressive … syndromes responded to this treatment, the practical importance of the distinction between the clinical varieties of mental illness in the aged became clear. The view that irreversible pathological changes of senile degenerative and arteriosclerotic nature provided the whole explanation for such disorders began to be called in question.
Systematic mapping began in the 1950s with Martin Roth’s careful analysis of older people admitted to mental hospitals. He classified them
‘… on the basis of psychiatric features into five groups: affective disorder, late paraphrenia, acute or subacute delirious states, senile psychosis (i.e. senile dementia) and arteriosclerotic psychosis, and these groups were found to differ sharply in pattern of outcome at six months and two years after admission.… Follow-up studies 7–8 years after admission to hospital revealed the differences between the groups still to be clearly evident although mortality due to ageing had to some extent blurred them …’
We can trace the evolution of Roth’s five diagnostic groups (in reverse order) over the following 50 years.
Slater and Roth distinguished this condition from senile dementia by ‘… the presence of cerebrovascular lesions, a markedly remitting or fluctuating course, the preservation of the personality, a large measure of insight until a relatively late stage, explosiveness or incontinence of emotional expression, and epileptiform attacks’. Onset was typically around the ages of 60 to 70, and men were more commonly affected than women. High blood pressure was a major cause: hypotensive medication was then risky and unpleasant to take, and was used only in severe cases.
In 1982 Levy and Post wrote ‘The term multi-infarct dementia has now displaced that of arteriosclerotic dementia, as increasing evidence has accumulated to demonstrate the presence of infarcts of various sizes and situations in postmortems of patients’. They noted the ‘well-known stepwise progression’ and the emotional lability seen in post-infarct patients, easily mistaken for affective disorder. Multi-infarct dementia was then estimated to account for 15–20% of cases of dementia in elderly people, and infarcts co-existing with ‘senile degenerative change’ for a further 10–15%.
In the 1990s a new term ‘vascular dementia’ became current, recognizing the role that cerebrovascular pathologies such as haemorrhage and vasculitis might also play in dementia; some types of vascular dementia did not have a history of strokes or focal neurological symptoms, but rather a gradual, progressive clinical decline. The advent of brain imaging (CT, MRI, SPECT, and PET) made it possible to establish the location of cerebrovascular lesions more precisely, and clarified the clinical pictures associated with them.
In 1993, the report ‘Vascular dementia: diagnostic criteria for research studies’ was published by an international working group (NINDS-AIREN), a sibling to the criteria agreed for Alzheimer’s disease (AD) by a similar consensus group (NINCDS-ARDRA) a decade earlier. But alongside these efforts towards diagnostic precision in research, accumulating epidemiological, clinical, and pathological evidence undermined the sharp distinction between the two types of dementia in clinical practice.
In his survey of this diagnosis in 2008 Robert Stewart (7) pointed out that secular change affects not only ideas and technology but also the populations of patients whom we study. Those described in the 1960s by Slater and Roth died younger and came to post-mortem with more severe pathology than do our patients now, who commonly die in their ninth and tenth decades, with mild levels of cerebrovascular disease which may make only a partial contribution to their dementia, or is merely coincidental.
Slater and Roth saw the relationship between senile dementia and normal ageing as simply quantitative—senile dementia becoming manifest when the degenerative changes of old age pass a critical threshold. ‘Though the possibility that senile dements are qualitatively apart in respect of some pathological change that remains to be discovered cannot be excluded’.
They considered AD separately under the heading of the presenile dementias (a category introduced in 1898 by Binswanger and applied to AD by Kraepelin in 1909), and commented that ‘the clinical features of Alzheimer’s disease are admittedly different from those of senile dementia, but pathologically no sharp distinction exists’.
Levy and Post, in The Psychiatry of Late Life (1982), while still using the term ‘senile dementia’, dealt crisply with these questions of definition. ‘Alzheimer himself considered his eponymous disease as a variant of senile dementia but opinions have been divided ever since.… The current [majority] view is that Alzheimer’s disease and senile dementia are one and the same and this is reflected by the increasing use of the term senile dementia of Alzheimer type (SDAT)’.
By the time of Wilcock’s and Jacoby’s account in Psychiatry in the Elderly (1991), the use of ‘Alzheimer’s disease’ to refer to the condition in older people was firmly established, though the previous term SDAT was mentioned in passing. The old question of the relationship to normal ageing was left open, but a different kind of boundary was clearly enunciated: ‘Strictly speaking, … AD is a pathological diagnosis, although a characteristic clinical syndrome corresponding to the distinct post-mortem appearances in the brain can often be distinguished. To assign a clinical diagnosis of AD, therefore, is to make an informed guess.’
This gradual change in nomenclature between the 1960s and the 1990s was far from trivial. To say that an older patient ‘is suffering from AD’ rather than ‘has senile dementia’ carries considerable symbolic weight. There is a dignity in being afflicted by a disease, rather than falling into predestined and ignominious decay. And where there is a disease, there may be a cure.
Besides these two major causes of dementia in old age, a number of specific dementia syndromes were recognized, some (e.g. Huntington’s disease) with ancient pedigrees, some described only in the 20th century (such as progressive supranuclear palsy in 1964, and idiopathic normal pressure hydrocephalus in 1965). Pick’s disease dates back to the early 20th century: the defining pathological changes (regional atrophy of the frontal and temporal lobes, and Pick bodies in neurons) were described by Alzheimer. Like AD, it was originally regarded as a presenile dementia, but it was recognized by neuropathologists (8) as also occurring in older people, though comparatively rarely. It was an important condition to recognize in life, not because there was any treatment available, but because of the relief that clarity could bring. Grave as the diagnosis was, it gave some meaning to the distressing and often infuriating changes endured by the afflicted family.
Meanwhile, the parallel category of ‘dementia of frontal lobe type’ was refined through the detailed clinico-pathological studies of the Lund group in Sweden and Neary in Manchester, leading to an international conference and the publication of consensus criteria in 1994. So ‘Pick’s disease’ (with a specific pathology) gave way to the clinical concept of frontotemporal dementia (FTD), and to recognition of variant forms: frontal (fv-FTD) and temporal (known also as semantic dementia and progressive non-fluent dysphasia). Though relatively rare, FTD is a fertile source of insights into regional cerebral function, but the neurobiology of the condition and its treatment are still barely understood (9).
In the 1980s, in the early years of our community team, we saw the occasional perplexing patient with striking visual hallucinations coupled with mild cognitive impairment, quite unlike the familiar AD. Some had delusional explanations for their experiences, but (unlike schizophrenic patients) they suffered severe adverse effects from antipsychotics even in low doses. Or we might be called urgently to visit a confused old person causing havoc in the home, only to find the situation calm once more, and a charmingly lucid patient quite unable to understand everyone’s anxieties.
Nowadays every medical student (if we have taught them properly) would suspect that these were people who had dementia with Lewy bodies (DLB). Recognition of this distinct form of dementia came gradually in the 1980s. Neuropathologists showed that abnormal intracellular inclusions, first described by Lewy in 1912 in the substantia nigra in Parkinson’s disease, were widely distributed in the brain, and especially in the neocortex. These cortical Lewy bodies were difficult to detect routinely and were much better revealed when immunostaining specific for ubiquitin was used. Gradually the features of the syndrome crystallized—fluctuating cognitive impairment resembling delirium, hallucinations, mild extrapyramidal signs, sensitivity to antipsychotic medication.
Diagnostic criteria defining the boundaries between AD, DLB, and Parkinson’s disease (PD), were published in the 1990s and refined thereafter. The 2005 criteria recognized data from imaging of the basal ganglia, and the association of REM sleep behaviour disorder with the condition. In 2008 McShane (10) described the ‘tautological’ process by which clinical diagnosis in DLB was used to validate pathological criteria, and pathology in turn to validate clinical criteria—a fair comment, in fact, on the nosological progression of all the dementias.
It was rewarding to witness the emergence of a new concept in old age psychiatry, which made sense of cases that had previously bewildered us, and which became established as part of our collective knowledge. The studies of DLB made sense too of the other end of the Parkinsonian spectrum. PD was regarded originally as purely a movement disorder, but as patients have lived longer, so the cognitive, emotional, and autonomic aspects of the disease have been recognized, and the dementia of PD is seen to run a different course from that of AD.
Other rarer syndromes included Creutzfeldt–Jakob disease and the dementias associated with physical disorders (such as B12 deficiency, thyroid disease, and HIV-AIDS). Because of these conditions, as well as the frequent coexistence of physical and mental disorders in older people, old age psychiatrists mostly understood the need to maintain their medical skills and their knowledge of geriatrics and neurology. Whether older psychiatric patients should routinely be investigated for medical disease was a live issue in the 1970s and 1980s, and resurfaced in the 2000s when memory clinics were becoming established. Evidence of important medical conditions being missed in older psychiatric patients is scanty, but every psychogeriatrician has their cautionary tale to tell, whether of the patient in prediabetic coma referred with ‘confusion’ or (as happened in our team) the patient with ‘hysteria’ who in fact had tertiary syphilis.
Often in the history of psychiatry, there is an interaction between new treatment possibilities and the delineation of disorders suitable for that treatment. In the 1980s there was no effective treatment for dementia, so efforts to distinguish in life between AD and vascular dementia seemed unnecessary. Later, the theoretical origins of cholinesterase inhibitors made them the choice for AD rather than for vascular dementia, and the distinction between the two conditions acquired practical significance. Public awareness of possible treatments for AD brought the question of early diagnosis into sharper focus, and people with mild or subjective failures in memory began to consult their GPs, worrying that they might have dementia, hoping for a treatment that might prevent it.
The study of mild memory loss in old age dates back to the late 1950s when Kral described ‘benign senescent forgetfulness’: loss of incidental details in recalling past events (details which might be remembered accurately on another occasion), without the disorientation, confabulation, or other types of cognitive difficulty which are seen in ‘malignant’ senescent forgetfulness (i.e. dementia). He showed that people with malignant memory loss had a mortality rate twice that of fellow-residents in the old people’s home, and that during the follow-up period, the malignant memory loss progressed, while the benign loss was unchanged.
In the 1970s and 1980s, opinions differed over the legitimacy of a diagnosis for people who did not meet the criteria for dementia but had concerns about their memory. Were these just symptoms of anxiety or depression? Should people with impaired practical or social functioning (but normal memory) be included? International efforts to produce agreed criteria for ‘age associated memory impairment’ (1987), or ‘ageing associated cognitive decline’ (1994) had little impact, on either clinical practice or research.
In our day-to-day work we assumed that some kind of mild memory loss existed which was neither ‘just age’ nor dementia proper, and that while a proportion of these people would progress to dementia, others would remain stable. Frankly sharing this understanding was often helpful to people worried about their memory, though the possibility of dementia in future was not denied.
In the 1990s Petersen and colleagues at the Mayo Clinic began their longitudinal studies of older people with carefully defined ‘mild cognitive impairment’ (MCI) (11), giving the concept a stability of meaning capable of underpinning repeatable research. Can any treatment of people with MCI reduce their risk of progression to dementia? So far, trials of treatment with cholinesterase inhibitors have been disappointing, but some vitamins (the B complex) look promising (12) and, intriguingly, also lithium (13).
I cannot do justice here to this category of illness. Of course the phenomenon of altered consciousness should be profoundly interesting to psychiatrists, and it is essential for every practising doctor to have the skills to recognize it. But most of the causes of delirium, both acute and subacute, and the means for investigating and treating the patients, are the province of general physicians and geriatricians in particular. Practice has rightly changed since the time of Slater and Roth, and patients with delirium no longer form a major category in the work of psychiatric hospitals. Instead, old age psychiatry has tried to develop ways of meeting the psychiatric needs of patients in general hospitals, whether through joint units (as pioneered in Nottingham by Tom Arie), liaison teams, or individual consultation. Although these practical arrangements have been difficult to achieve and to sustain, nevertheless the understanding of delirium, its prevention and its management, has made significant progress (14).
Paranoid illnesses arising in old age were included indiscriminately with ‘non-organic psychoses of the senium’, until Roth in the 1950s classified them in a separate category—‘late paraphrenia’. He showed that these patients had a lower mortality than their coevals with dementia, but higher rates of institutionalization than those with affective disorders. Understanding of these patients was subsequently enriched by Post’s detailed long-term study in the 1960s of ‘Persistent persecutory states of the elderly’.
This work raised several new questions. First, was paranoid illness with onset in old age a condition distinct from schizophrenia, or the same condition but with delayed onset? Post classified his patients into groups defined by their phenomenology and their similarity to schizophrenia; but in fact these groups were not stable over time, and in a given patient the index illness and later relapses might fall under different descriptive headings. Second, was delusional disorder in old age always a consequence of degenerative brain disease, or were pathological findings at post-mortem (such as vascular damage) merely incidental? Naming was also a problem: critics argued that ‘late paraphrenia’ was a misleading reminder of Kraepelin’s ‘paraphrenia’, which described a very different condition.
Arguments rumbled on through the 1980s and 1990s, not helped by international systems of classification: the third edition of the Diagnostic and Statistical Manual (DSM-III), for instance, restricted the diagnosis of ‘schizophrenia’ to cases with onset below the age of 45. The dilemmas were summarized by Naguib and Levy (15): ‘For day-to-day clinical purposes, it does not matter what we call these states, provided that we make it clear what we mean. For research and statistical purposes, it is essential that we adopt a … classification which allows for the retrieval of cases with late-onset delusional states, whatever these are called.’
Eventually in 1998 an international consensus group considered all the available evidence and agreed that cases of schizophrenia with age of onset from 40 to 59 should be called ‘late onset schizophrenia’, while illnesses with onset after 60 were different in significant ways and should have their own name—‘very late onset schizophrenia-like psychosis’ (VLOSLP). As Robert Howard wrote (16), ‘The latter term is long-winded and unmemorable but is at least unambiguous, and it received the unprecedented support of both European and North American old age psychiatrists.’ And for us watching on the sidelines of this long academic wrangle, it seemed a significant moment for the international and scientific standing of our specialty.
Conceptual progress has here come not through the invention of diagnostic entities but through clarification. In old age we see the affective disorders familiar to us from younger patients, but it has taken time to understand the effects of ageing on their expression.
‘Involutional depression’ as a diagnostic category has disappeared. ‘Depressive pseudo-dementia’ is no longer a live concept, and the differential diagnosis between severe forms of dementia and depression, much discussed in the literature of the 1970s and 1980s, has become less problematic—perhaps because we more often see patients close to the onset of their illness, and (as Felix Post taught) it is the early histories of the two conditions that help us to distinguish them.
A different perspective on mixed affective and cognitive symptoms is captured in the concept of ‘vascular depression’, proposed on clinical grounds in 1997 by Alexopoulos and colleagues, and later amplified by the demonstration on MRI scans in these patients of ischaemic lesions in subcortical areas of the brain, in both white matter and grey. Typically in vascular depression the symptoms are more apathetic than melancholic, cognitive impairment lies mainly in executive function, and the response to treatment is disappointing. The more severe the radiological findings, the worse the outcome appears to be. However, not all authorities accept the idea of a specifically vascular depressive syndrome, seeing the brain instead as subject to a variety of damaging pathological processes, interacting together to precipitate the illness.
‘Manic-depressive psychosis in the senium’ was well-recognized by the pioneers of old age psychiatry, although manic episodes were then thought to be rare. In The Psychiatry of Late Life Post, referring to the study he carried out with Shulman at the Maudsley, described ‘the preponderance of surly, hostile affects in elderly manics’ by contrast with the euphoria often seen in younger patients; and he called attention to the phenomenon of ‘slow flight of ideas’ in which the characteristic thought disorder of mania is coupled with depressive retardation. Later studies found no consistent difference in the symptoms of mania between young and old, but they confirmed Post’s observations on mixed affective states, and showed that in old-age bipolar affective disorder these are at least as common as are pure manic or depressive presentations.
Patients who bear the lifelong burden of bipolar affective disorder are both a reward and a challenge for an old age psychiatrist. Those in whom the illness was recognized in youth reflect in their case-histories the whole story of 20th-century psychiatry. One of my 80-year-old patients had her first episode of manic illness in 1916, which was recorded as ‘nymphomania’ and treated with belladonna and tincture of opium. And those in whom bipolar disorder is finally recognized can be given some explanation for the chaotic unpredictability of their lives, and can benefit from the stability offered by treatments developed over recent decades for young and old alike.
During the 1960s and 1970s in Britain there was a steady growth of ideas, creative practice, concrete evidence, and national policy on the theme of community care for older people. Typically it was individual practitioners who saw the possibilities for new services, striking examples being Joshua Carse and his day hospital in Worthing, and Duncan Macmillan and his integrated assessment unit at Mapperley Hospital in Nottingham. But the support of local powers (both in the NHS and in social care) was also crucial. The final necessary ingredient was evidence. It tells us something important about the climate of those years that these innovations were properly studied and the findings fed directly into policy: a process well illustrated by a government-sponsored seminar on community old age psychiatry in 1982 (17).
At this time of optimistic growth in services at a national level, Oxfordshire also saw developments in its psychogeriatric service, precipitated by changes in the county boundary. The new segment of the county, till then minimally provided for, acquired half a consultant, a dedicated community psychiatric nurse, six beds on an old long-stay ward, and an enlightened charge nurse (with experience as a district nurse) to lead the hospital team. Full of enthusiasm for the model of early ascertainment and community provision, fortified by The Psychiatry of Late Life, we went out to meet the general practitioners in our new sector. They were welcoming and courteous; some were already convinced of the value of supporting older people at home instead of in hospital, others were deeply sceptical, predicting that within months our beds would be immovably filled, the waiting lists as long as before, and the new model of care an empty promise.
Our best allies at this time were the staff of the local social services department, already blazing the trail for home support for older people; and a voluntary day centre in a church hall, nurtured from birth by Steve Corea, by then a senior nurse in the Oxfordshire service.
In the 1980s, collaboration between the NHS and social care was encouraged by new legislation. ‘Joint funding’ grants became available for projects created in partnership by local medical and social services. Our joint invention was ‘patch teams’—local outposts of the parent services—the key professionals in a patch team being a community psychiatric nurse and a social worker for older people. Each received training from the ‘opposite’ parent, so that, as far as possible, nurse and social worker could each offer the same range of skills, information, and networks. They sat together in an office located in the community they served, helped and taught each other, and managed a joint case-load. They shared in the time of the sector consultant, occupational therapist, and (when possible) psychologist, and everyone met weekly in their premises. The model worked well. The patients, their families, and general practitioners approved.
These patch teams, granted creative freedom, invented the ‘flexible carer’: carers employed simply to give time, doing whatever tasks the person concerned identified as their priority. (The idea was sparked when a grieving client asked for someone to help dig a grave for her beloved cat.) At first employed opportunistically, flexible carers were later adopted and managed as a service by Oxfordshire Age Concern.
In the 1990s and the new millennium, upheavals in culture and politics occurred at levels of power beyond our ability to influence. Funding was constrained in both health and social services, and their partnership was undermined. New managers dictated nationwide changes in policy and in the shape of services. A small local invention could not survive, and the patch teams were closed down. Though we still visited patients at home, and tried to work collaboratively with social service colleagues (for whom we had much respect and affection), we could no longer give our patients a service as ‘close to home’ as we had always intended.
National leaders at this time were celebrating ‘reform’ in the NHS. At the coal face we did not feel we had anything to celebrate. Rather, these centralized reforms signalled for us a doctrinaire eradication of local partnership, and the erosion of responsiveness to actual needs.
Just as technical advances (especially the use of silver stains for microscopy of brain tissue) allowed Alois Alzheimer in 1906 to describe the ‘peculiar appearances’ in the brain of his patient Auguste D., so further technical developments have illuminated the histopathology, chemistry, and genetics of the pathological features that he described.
The 1960s began a new era in the study of the brain. Electron microscopy helped to visualize the fine structure of neurons and the neurofibrillary tangles (NFTs) and inclusion bodies within them. Examining neural tissue stained with Congo red under polarized light identified amyloid as a component of AD pathology, especially in plaques and in the walls of blood vessels. Counting cells under the microscope by hand, and later by automated methods, brought a quantitative approach to the differentiation of dementia from normal ageing.
Corsellis (18), reviewing the pathology of dementia in 1969, predicted that ‘an amyloid substance in the aged brain … could well repay further study, particularly by biochemists and immunologists’. Concerning the relation between cerebral degeneration and dementia, he wrote: ‘it has often been contended … that the structural state of the brain is of relatively minor importance when compared with the influence of environmental and psychological factors’; but himself argued for the opposite view, quoting the work of Blessed and Tomlinson who had shown in 1965 that intensity of degeneration, measured by counting the plaques in brain tissue, correlated with the clinical severity of dementia.
The quantitative approach was developed further during the 1970s. Initially, laboratories each devised their own criteria for diagnosis in ‘senile dementia’, based on the distribution and density of plaques and tangles; in later decades shared criteria, such as the CERAD protocol (1991), were gradually accepted.
Meanwhile, neurochemical studies were establishing new ground. I remember as a medical student in the 1960s being told that the chemical study of neurotransmission in the brain (by contrast with peripheral organs) might never be possible, because of the speed with which self-digestion of brain tissue takes place after death. It was wonderful later to find that this pessimism had not prevailed—it acted only as a provocation to scientists to find ways round the problem. By studying the relevant enzymes rather than the transmitters directly, by carefully matching post-mortem tissue samples according to the physiological conditions at the time of death, and by exploiting rare opportunities to study brain biopsies taken for diagnostic purposes, abnormalities in noradrenergic and cholinergic neurotransmitter systems were identified. Through the 1970s, scientists in different centres—Bowen, Davies, the Perrys, and others—made crucial observations linking the clinical and pathological signs of dementia to the laboratory finding of impaired cholinergic neurotransmission. Thus in 1983 the ‘cholinergic hypothesis’ (that AD is ‘a disorder of cortical cholinergic innervation’) was formulated. But in time it became clear that this could not be the whole story.
Meanwhile, animal studies revealed the anatomy of the cells implicated in these chemical changes. As the Perrys explained in The Psychiatry of Late Life, in 1982, ‘the majority of cholinergic nerve processes [in the cortex] are terminal axonal processes thought to be derived … from cell bodies situated in the nucleus of Meynert … in the substantia innominata region’, and by 1997 (19) textbooks were depicting four distinct groups of neurons, each arising from its own subcortical nucleus, each releasing its particular neurotransmitter from axons projecting diffusely into the cortex.
A significant form of connectivity between different brain regions was studied by Pearson and Powell, Braak and Braak, and others in the 1980s. They found a gradient in the severity of lesions of AD, in a logical sequence along known anatomical pathways from one region to the next, suggesting a spread of the disease process from origins in the entorhinal cortex to hippocampus, to the temporal cortex, and thence to other cortical association areas. The olfactory cortex and olfactory mucosa also show pathological changes very early in AD. Clues, perhaps, to the unknown aetiology of the disease?
Also through the 1980s, the structure, chemistry, and origins of NFTs and of the amyloid in senile plaques were being clarified. Electron microscopy in the 1960s had shown NFTs to be helically paired filaments formed from abnormal protein. Now they were found to be derived from microtubules (part of the internal transport structure of neurons). In the early 1990s the microtubule-associated protein tau was extracted from NFTs, and was found to be highly phosphorylated in that situation, possibly making it functionally different from normal tau.
The amyloid protein identified as beta-A4 (or beta-amyloid) was isolated from senile plaques in 1985, and in 1987 was shown to be derived from a much larger molecule, amyloid precursor protein (APP). During the normal metabolism of APP it is divided enzymatically at specific points along its length; if cleavage occurs at a different point, an abnormal fragment of APP is produced which is then deposited as amyloid. Hardy and Higgins in 1992 proposed the ‘amyloid cascade hypothesis’, suggesting that ‘the mis-metabolism of APP and deposition of beta-A4 is the seminal pathogenic event in AD’.
In the 1990s, studies of intracortical signalling showed that glutamate, a metabolically important molecule, acts also as a cortico-cortical and hippocampal neurotransmitter. The pathways concerned degenerate quite early in AD. Glutamate can be toxic to neurons, and such excitotoxicity, probably important in cerebrovascular disease, may be relevant to AD as well.
Finally the genetic discoveries of the 1990s must be mentioned. The genetic coding for APP is found on chromosome 21 (recalling the raised incidence of AD in trisomy 21); and mutations affecting the structure of tau are associated with chromosome 17. In 1995, studies of families with early-onset AD yielded the genes presenilin-1 and presenilin-2, on chromosomes 14 and 1 respectively. The gene for a protein (Apolipoprotein E) which is secreted by astrocytes and binds to beta-amyloid was shown to influence the prevalence of late-onset AD—possibly by accelerating its onset. This gene was found on chromosome 19.
These are the bare bones of the discoveries in the last 50 years. Four areas of current ignorance call for future exploration. First, the relationship between plaques and NFTs is still obscure. Diffuse plaques precede NFTs in the course of AD, but plaques alone, unlike NFTs alone, are not always associated with dementia. Secondly, the study of glial cells (oligodendrocytes, astrocytes, microglia) has barely begun. Equally difficult is the exploration at subcellular level of whole neurons, from cell body to furthest dendrites, which means that the connection between pathological events in different parts of a cell that spans different regions of the nervous system can only be inferred. Lastly, the distinction between phenomena (chemical or histological) which signal the direct effect of disease and those which reflect adaptive responses is only gradually being unravelled.
David Smith (professor of pharmacology), Margaret Esiri (neuropathologist), Kim Jobst (clinical director of the project), and Elizabeth King (senior research nurse) were the initiators in 1988 of this meticulously planned and executed study, in volunteer patients and healthy controls, of the natural history of cognitive and non-cognitive decline in dementia. A founding principle of the study was that, since no treatment was on offer, participants must be given instead the best care then available—warm and expert support, regular contact, truthful information, and the knowledge that they and their families were contributing to research at the forefront of scientific knowledge. Participants received a complete medical and radiological examination initially and annually till death, and were visited regularly by their own Optima research nurse. At entry to the study they were invited to consider donating their brain for autopsy after their death. The success of this approach was shown by the very high rate (97%) of participants who agreed to brain donation and in whom (with their relatives’ permission) autopsy was eventually carried out (20).
The studies generated by the Optima project (in neuropathology, in imaging, in clinical syndromes such as depression and DLB, in therapeutics and prevention) are too many to list here. What I most affectionately remember is the strong collaborative ethos of the research group—both internally and in its relationships with local colleagues. For the old age clinicians in the region, Optima’s monthly clinico-pathological meetings were a source of knowledge and inspiration, giving a level of importance to our daily work that only participation in active research can provide.
In the early years of geriatric psychiatry, options for imaging the brain were extremely limited. Plain radiographs of the skull could show only its bones and its cavities. Occasionally a tumour might be detected, but living brain was virtually terra incognita for radiology. Electroencephalography (EEG) seemed to promise better, and was used by some researchers and enthusiasts, but in the United Kingdom at least (except when epilepsy was suspected) it never entered routine psychogeriatric practice.
It was different when CT emerged in the 1970s, first as a research tool, and much later for clinical use. In 1980 Jacoby and Levy employed this new technology in a study of patients with dementia and patients with affective disorder, compared to age-matched cognitively normal people. They confirmed that the cerebral atrophy of dementia would show up on CT scans; and devised a reliable method for quantifying brain volume which allowed patients and controls to be validly compared.
In routine practice the diagnosis of dementia was based on patients’ histories and their clinical features. CT (then an expensive investigation) gave little additional information in straightforward cases, so its use was limited to excluding other intracranial disease. But participants in Optima did get scanned as part of the protocol, and the research staff found that showing the images to patients and their families and explaining their interpretation was therapeutic in itself. Opinions at that time were strongly divided as to whether patients with dementia should be told their diagnosis, but in this population of research volunteers, freely sharing the clinical information was undoubtedly beneficial.
Optima developed a technique for imaging the medial temporal lobe by angling the CT scan along its length, and with this method hippocampal atrophy (now an accepted diagnostic feature in AD), could be quantified. In some of the cases, serial scans showed an accelerated rate of atrophy accompanying a sharp deterioration in the patient’s cognitive state.
The next advance in imaging concerned the physiology of the living brain, using radioemitting chemicals in PET and (more practically) SPECT, to provide information about metabolic function in different brain regions. The characteristic picture on SPECT scans of parietal hypometabolism, combined with atrophic changes demonstrated by CT, made the diagnosis of AD more accurately than either technique on its own.
In the 1990s as brain MRI came into use it tended to supplant the older methods (except that confused patients find CT less frightening). We take for granted the precision and beauty of its images, which would have astounded researchers just a few decades ago. They could not have conceived it possible to read the neurochemical activity of a brain while it engages in active thought—as is nowadays made possible by functional MRI.
This most stigmatizing of Roth’s five diagnostic categories has become the domain of high-prestige research. Few conditions offer the same transparency of connection between disordered brain and afflicted mind. The exploration of that connection becomes ever more arcane, the world of the super-scientist not the everyday clinician, but the discoveries of impaired neurotransmission in dementia also led directly to the development of practical drug regimes, promising alleviation, if not cure, for a disease formerly thought beyond therapeutic reach (21).
Tacrine was the first compound targeted on defective cholinergic neurotransmission (22) that could be used in dementia, and clinical trials in the 1980s and 1990s showed clear, though limited, benefit to patients. The drug could cause serious side effects (especially hepatotoxicity) and never entered routine psychogeriatric practice, but it led the way for the ‘second-generation’ cholinesterase inhibitors, donepezil, rivastigmine, and galantamine.
Donepezil was licensed in the United Kingdom in 1997, but it was clearly not curative. The evidence that it could at least help to delay the progression of AD accumulated only gradually, and the cholinesterase inhibitors were not accepted for prescription by the NHS until 2001. The body responsible for this decision, the National Institute for Health and Care Excellence (NICE), bases its reasoning less on the efficacy of a drug under research conditions than on its cost-effectiveness in practice—i.e. the health benefit attributable to the drug as opposed to an implicit alternative use of the same money. This is often a controversial position to adopt, and NICE’s successive recommendations on the treatments for dementia provoked fierce scientific, economic, and political argument. Public opinion (led by the patients’ advocacy organizations) was roused; a campaign of legal challenge funded by the drug companies began; and in 2011 NICE removed its restrictions on the prescribing of cholinesterase inhibitors in the NHS.
Other experimental approaches to treatment are being investigated. The demonstration of a link between cognition and alterations in glutamate and aspartate neurotransmission in the cortex (the ‘glutamatergic hypothesis’) underpin the development of memantine, used in moderate and severe AD. Experimental attempts to reduce the deposition of amyloid beta-peptide in the brain by immunotherapy looked promising until a trial in 2001 was aborted when some subjects developed severe side effects. Gordon Wilcock, reviewing these developments (23), concluded: ‘Not only is symptomatic treatment a reality, albeit at a modest level …, but disease-modifying, i.e. neuroprotective, treatments may be on the horizon. There is considerable hope for the future.’
By contrast, the search for drugs to modify behaviour in dementia has been less rational. From the 1960s onwards, doctors have turned mainly to the antidepressants and antipsychotics to treat the agitation, aggression, confusion, paranoia, sleeplessness, and wandering of their older patients. There was little reason for preferring one drug over another, but the pressure on the doctor from struggling families or exasperated nursing staff to do something to help could be very intense. Occasionally the effects of medication were almost miraculous—for example, when a depressive illness had been unrecognized in the context of the patient’s dementia. The counter-argument to using medication was concern over side effects, given added force when the exceptional vulnerability to antipsychotics in Lewy body dementia was discovered. For patients with depressive symptoms the newer antidepressants (SSRIs and others) had been a decided improvement over the tricyclics, and for a time the atypical antipsychotics were similarly welcomed, until it was found, first, that they accelerate the dementing process (24) and second, that they carry an increased risk of serious cardiovascular events in people with dementia (25).
In the last few decades, there has been a second counter-force to the use of medication in dementia—recognition of the power of a psychological approach. In severe dementia the necessary shift in perspective was to consider the patient’s behaviour as a meaningful response to their situation (which includes the specific cognitive limitations imposed by their illness), rather than simply as a symptom determined by neurobiological factors. Interpretation of troublesome behaviour requires a detailed contextual analysis by the psychologist, while the help must come from people surrounding the patient (family or care staff) with their responses shaped by the understanding derived from the analysis (26).
General opinion, especially that of family carers, is usually sympathetic to psychological approaches and wary of medication—rightly so where antipsychotics are concerned. Expert advice and guidelines now set strict limits to the use of antipsychotics in dementia, but practice is slow to change, and vigilance by carers and specialists remains essential.
Older people have shared in the advances over the last half-century in the pharmacological treatment of depression, particularly from the emergence of safer drugs with fewer side effects. In the 1990s, ahead of practice at younger ages, many old age psychiatrists kept their patients on antidepressant medication for at least 2 years after a severe depressive illness, and often for life, to prevent relapse or recurrence. A multicentre trial (in which many of us participated) of such a continuation regime (27) showed that older patients on placebo were more than twice as likely as treated patients to suffer relapse or recurrence over the 2 years of the trial.
Mayer-Gross’s introduction of electroconvulsive treatment (ECT) was an important advance at the dawn of old age psychiatry, and it has continued as a safe and effective treatment for older patients, especially in severe depression and when pharmacological treatment has failed. Post in 1982 recommended unilateral (non-dominant) application to minimize post-treatment confusion and to prevent memory impairment afterwards. But in 1991 Baldwin (in Psychiatry in the Elderly) noted ‘the negative public image suffered by ECT’, the reluctance of clinicians and the practical obstacles to its use, and he feared that patients were sometimes left ineffectively treated.
In the 1970s and 1980s public suspicion and opposition to ECT were strong enough to influence policy. Fortunately these pressures during the preparation of the 1983 Mental Health Act did not succeed in outlawing ECT altogether, and the legal mechanisms enacted to constrain its use proved workable. In those years it was often hard to convince staff who had no experience of ECT and who were appalled at the thought of such ‘barbaric’ treatment of a gravely ill old patient, that the cruelty lay rather in withholding effective relief for their suffering. With families, likewise upset at the idea of ECT for their relative, each discussion had to begin at the beginning, and indeed one could sympathize with their disbelief that electricity would be safer than medication for a frail and unreachable 90-year old. One form of treatment which we practised without the benefit of hard evidence was maintenance ECT in patients with recurrent episodes of medication-resistant depression. (Maintenance ECT involved treatment of the patient, with perhaps one application per month, on a regular basis without waiting for any sign of relapse of the depression, in order to prevent relapse.) Such patients and their families often became the strongest supporters of the treatment plan.
In the 2000s, the Royal College of Psychiatrists, aware of failings in the quality of ECT practice across the United Kingdom, took action to improve it by creating a system of regular and rigorous audit to which hospitals could subscribe. In the Oxford ECT service this brought about striking improvements, thanks to the leadership of a committed psychiatrist invested by management with the authority to carry the audit and its recommendations through in every detail.
The College also sought out the views of patients who had undergone ECT, and their own accounts of memory loss. It is now clear that loss of autobiographical memories, invisible to routine memory tests, is a genuine effect of ECT and the one that most distresses patients. The risk of this memory loss is not increased by age; ECT can safely be given for depression in patients with dementia; and it still holds an important place in the practice of old age psychiatry (28).
Psychological and psychotherapeutic treatments were not considered in the first textbooks of old age psychiatry. It was assumed that clinicians would apply the same generic skill to older people that they had learned in the setting of general psychiatry. But from the late 1990s and early 2000s, psychological techniques devised for younger age-groups were increasingly adopted into work with older people. Most systematic studies of psychological interventions in old age date from those years, and by 2008 the subject occupied 55 pages (29) of the Oxford Textbook of Old Age Psychiatry. Older people are now most often offered cognitive-behaviour therapy, interpersonal psychotherapy, or problem-solving therapies. Family and systemic therapies and psychodynamic psychotherapy are less widely available. Psychological and pharmacological treatments are often used together, and it is also common to offer psychological help to a patient and to their caring relative in parallel. The greatest obstacle to the use of psychological treatments in old age is the shortage of staff with appropriate skills—not only psychologists but also members of other disciplines who elect to train in these methods.
Should services for older people be subsumed under (or integrated into) the ‘mainstream’ psychiatric service in each area? Or is there still a case for old age psychiatry as a specialism in its own right? An integrated service might ensure better access to psychological treatments, since a special interest in old age is relatively new among psychologists. The United Kingdom Department of Health in 2005 strongly advocated integration on this principle, declaring that separate specialist services perpetuate ageism. Against this view, clinicians in the specialty argued that psychiatric illness in old age frequently coexists with physical illness or disability, often together with cognitive impairment, so that clinical practice is genuinely different from that in ‘adults of working age’, and its practitioners need a different range of attitudes and skills. These clinicians also suspected that pursuit of an age-blind principle would instead separate dementia services from mainstream psychiatry, disadvantaging the many older patients who need help from both disciplines. Where psychological therapies are concerned, these arguments are fairly evenly balanced, and different providers will resolve the question in different ways.
The creation of the NHS in 1948 united three different categories of health provision: general practitioners and primary care; secondary care in hospitals, including the mental hospitals; and services provided by the local authorities (which included hospitals for the chronic sick, the seed-bed for the future development of geriatric medicine). In a history of the NHS written for its 50th anniversary, Geoffrey Rivett wrote (30):
At the outset the NHS had accepted responsibility for the long-term care of the chronic sick, although the standard of care was often unacceptably low. Over the years the NHS service improved, with an accent on rehabilitation. Categorization of people into those needing health provision (that was free) and those requiring social support (that was chargeable) was difficult. Although frail elderly people often required both social support and health care, such responsibilities increasingly passed to the social services and the private sector.
This uneasy boundary between health and social provision runs through the story of older people’s care in the United Kingdom, along with the constant battle to ensure that psychiatric illness is not forgotten when strategies for older peoples’ health are written.
The national strategy for psychiatry in the 1960s was to move provision out of the large old mental hospitals and into small assessment units situated in district general hospitals, backed by care ‘in the community’ supported by local authority services. Statistical predictions from the Department of Health of a continuing steep decrease in the number of beds required for psychiatric admissions underpinned this strategy. Clinicians doubted whether the kind of community support needed by relocated patients would materialize, and whether anyone had thought about elderly or chronically ill patients left behind in long-stay wards while resources went to the young and newly ill in the general hospital units.
Politicians did recognize that not everything ideal could be afforded. In 1976 the Department of Health and Social Security published Priorities for Health and Personal Social Services, in an attempt to ‘move resources to the care of elderly people and those who were mentally ill’. At ground level, psychogeriatric teams struggled especially with inadequate provision for long-term care, at that time confined mainly to the back wards of hospitals under pressure to close, and to residential homes run by the local authorities.
In the late 1970s, funding of long-term care underwent a major political change. Previously, local authorities had funded places in residential homes which they provided and controlled. Now the funding was to come from the national social security budget, by means-tested allocation to individuals, regardless of the ownership of the home in which they sought a place. This move uncovered a relentlessly growing demand (partly reflecting demographic forces) for long-term care. The independent sector duly responded, so that from the 1970s to the end of the 1990s there was a fivefold increase in the number of places in independent sector homes, and correspondingly enormous pressure on the social security budget.
So in 1990 the politics changed again. Responsibility for funding people in residential and nursing homes was taken away from the Department of Social Security and given back to the local authorities. ‘An open-ended and rapidly expanding budget was replaced by a limited one based on individual assessment of need … Local authorities became the principal budget-holders for state-financed long-term-care’ (31).
No country has yet found an ideal and affordable arrangement for funding the care of its elderly. In the United Kingdom a Royal Commission proposed a solution in 1999 which was quietly shelved, and new recommendations made by the Dilnot Commission in 2011 still await a political response.
Since the reforms to the NHS in 1989–90, repeated reorganizations have largely been premised on the model of acute services and have done little to help older people with mental illness, though exceptions exist. The 1990 contract with general practitioners required annual health checks for all patients over 75, and though many GPs thought this a fruitless exercise, on balance its effects have been positive. 1999 saw a National Service Framework for Mental Health, backed by funds to ensure the implementation of its directives. Older people with mental illness were supposedly included, but the prescribed models of care were not designed for their needs. The National Service Framework for Older People in 2001 was less prescriptive, but it had no money behind it.
Only in 2009 did the psychiatric needs of (some) older people take centre stage, with the publication of the National Dementia Strategy. (Functional psychiatric illness in old age was not included.) From this strategy emerged the National Dementia Declaration, and the launch of the Dementia Action Alliance, which ‘seeks radical change in the way that our society responds to dementia.’
The declaration listed the shortcomings of current social arrangements, and outlined in detail the seven desired outcomes of the strategy, couched in the imagined voice of a person with dementia. Whether these outcomes can be achieved is questionable, but the language alone is interesting for the light it throws on historical change in culture and perspective. It is hard to imagine the words ‘I live in an enabling and supportive environment where I feel valued and understood’ (outcome 5) being formulated in 1969.
‘Elder abuse’, the maltreatment of older people, became a serious topic of research only in the 1980s, yet neglect and cruelty have surely as long a history as do care and benevolence. In 1967 Barbara Robb wrote Sans Everything, documenting much neglect and mindless cruelty towards elderly people in long-stay institutions. The next year, a government enquiry into standards of care at Ely Hospital in Cardiff revealed similar abuses, and in response to its recommendations the Hospital Advisory Service was created, with responsibility for investigating hospitals for mentally ill, elderly and learning disabled patients. Revelations of the abuse of vulnerable patients in hospital continued through the 1970s, and in a book published in 1984 (32) the part repeatedly played in these scandals by incompetent management, inadequate staffing, professional isolation, and internal corruption was convincingly depicted. For a few decades there were no further horror stories on this scale, and many hoped that the closure of the old inward-looking institutions would likewise eliminate the conditions that led to abuse.
It was too much to hope. As the patients needing long-term care moved from hospitals into residential and nursing homes, or returned to their own homes to be looked after there, the potential for abuse moved with them. Once again, as risk was recognized, systems for inspection and regulation were created, initially in local social service departments and later through national regulatory bodies. Once again there were media reports of cruel or incompetent treatment of vulnerable people, where regulators had failed to intervene. In 2011 the Equality and Human Rights Commission found ‘that the care of elderly people in their own homes is so poor that it breaches basic human rights’; while in the same year the Health Service Ombudsman (33) found poor communication, a dismissive response to suffering, and ‘an apparent indifference … to deplorable standards of care’ among staff caring for older people. Governments would sooner respond by redesigning the systems for inspection, than by probing the factors identified in Martin’s 1984 analysis. The effectiveness of this approach cannot be assumed, and the voices of relatives, of staff prepared to be whistleblowers, and of the media are still indispensable.
In the 1990s a different approach to raising standards was tried. Clinical audit was incorporated into ‘clinical governance’, a mechanism established (by analogy with corporate governance in business) in the NHS for safeguarding the quality of its services. Good audit depends crucially on choosing the right measure of the qualities that need improvement. When badly chosen, measuring instruments become parasitic and divert resources from the service into their own growth and renown. In our field the national audit of ECT overcame this danger, but many aspects of psychiatric care in old age are less clear-cut, and suitable measures are harder to find. The quality of the care given to people with dementia comes down to the details of practice, to sound training, to the moral attributes of care staff, and the nurturance and respect that the staff receive. Measurement of these intangibles, without letting measurement itself distort the care, is difficult. The best and most influential instrument so far devised is Dementia Care Mapping, the work of Tom Kitwood and the Bradford Dementia Group (34).
Older psychiatric patients were beneficiaries (equally with younger patients) in the replacement of the 1959 Mental Health Act by the 1983 Mental Health Act in England and Wales. It is beyond the scope of this essay to discuss those legal arrangements, though they were important in securing better treatment for older people under detention, and in protecting their rights under the law.
An important area not covered adequately by the 1983 Act was the status of people who lacked capacity to consent, whether to hospital admission or to treatment. The two most important groups of patients affected by this lack of legal provision were those with learning disability and people with dementia. The 1959 Act had marked a decided move away from involuntary committal, and enlarged the scope for voluntary psychiatric treatment. The 1983 Act, libertarian rather than paternalist in its philosophy, sought to constrain infringements of rights within legal boundaries. People who did not object to admission or treatment simply because they could not understand enough either to give or to withhold their consent were poorly served by that framework.
In 1989 the Law Society published a discussion document on Decision-Making and Mental Incapacity, calling for new legislation. After 18 years of repeated consultations, delays and redraftings—a salutary example of the obstacles which confront even widely welcomed reforms—the Mental Capacity Act 2005 was brought into force in 2007.
During this long gestation, ‘non-competent non-objecting’ patients were still treated as if they were voluntarily consenting. Few advocates for such patients were happy with this. When the United Kingdom’s Human Rights Act 1998 was enacted, it became obvious that these rights applied fully to psychiatric patients, and a route was opened up for legal challenge by the advocates of patients who had not been formally detained when perhaps they should have been. The Mental Capacity Act 2005 and its 2008 Code of Practice were therefore written to ensure that proper process is followed, when patients who lack capacity are necessarily deprived of their liberty.
Though critics of the Mental Capacity Act view its procedures as legalistic and cumbersome, its system of prescribed visits may supplement with its own searchlight the roles of national inspectorates. And the status of intellectually impaired people—whether impaired from birth or in old age—has been enhanced, I believe, by the prolonged and respectful attention that was given to their rights by parliament, the relevant professions, and the public at large.
The word ‘carer’ does not appear in the index of Clinical Psychiatry in 1969, nor in The Psychiatry of Late Life in 1982. Of course this does not mean that the role of families and friends was then ignored—quite the opposite. From its beginning, geriatric psychiatry understood its dependence on collaboration with the social networks which sustained the patient at home.
Systematic epidemiological and social surveys of older people living in the community were published in the 1960s and 1970s, and the enormous role played by family members (and others) in sustaining older people in their homes began to be measured. These people were unpaid, usually unsupported, subject to desperate pressures, their work unrecognized. An influential report on carers commissioned by the National Institute for Social Work was published in 1989 (35), initiating a large and growing field of research. The term ‘carer’ (with its ambivalent connotations of both love and toil) was not ideal, but no better alternative was found. For the resident daughter of a parent with late dementia to be called an ‘informal carer’ seemed only to trivialize the weight of her emotional and practical burden; while others were offended by the implication that anyone not giving physical help to a relative did not ‘care’ for them, however loving their relationship.
A phenomenon of increasing importance has been the emergence of national charities to represent the interests of carers and their dependants. Carers UK was founded in 1965, and Age Concern in 1971, merging with Help the Aged in 2009 to become Age UK. The first branch of the UK Alzheimer’s Disease Society (following the example of the United States) was initiated in Oxford in 1979. Originally the influence of such charities was through their local branches, bringing together groups of carers for mutual support and education. These soon engaged with the health and social providers in their area, and advocated (or themselves established) new facilities such as daycare centres. The national organizations gradually raised their public profile, providing a point of reference, a newsletter, education and advice for their members; political lobbying and media contacts; publicity for the cause and an accessible website; and fundraising for research.
Medicine has long taught us to learn from our patients, and personal accounts of illness have been a precious source of insight down the ages. In old age psychiatry we have the accounts of carers as well; they do not substitute for the voice of the person with dementia, but they are invaluable in themselves. In hearing these stories, new carers see the reflection of their own struggles and know that they are recognized. An early excellent source in 1985 was Mace and Rabins’ The 36-hour day: caring at home for confused elderly people (36). Although compiled by professionals, it is in essence a direct and honest expression by carers of all the problems and rewards of caring. I cannot count how often I have lent my copy to families I was seeing at home, or taught my students from it.
It is rare to find personal accounts of dementia written while the disease takes hold of the writer. My journey into Alzheimer’s disease by Robert Davis, an American pastor, was published in 1989 by his wife (37). It is a revelation to read his ‘view from inside’ of the signs of dementia coolly described by clinicians 50 or 100 years earlier, and since enshrined in textbooks. Especially memorable are his descriptions of the panic-stricken exhaustion that comes simply from sensory or cognitive overload, and the security that a stable routine provides.
When John Bayley, Professor of English at Oxford, wrote the memoir of his wife Iris Murdoch, the novelist (38), the depiction of dementia moved into mainstream literature (and subsequently into film). Other well-known figures such as Ronald Reagan had AD or, like the author Terry Pratchett, have been willing to say openly that they have it and to help in the fight against misunderstanding and stigma. In general, public sympathy for older people with mental illness is growing, for a combination of reasons: with greater numbers surviving into advanced old age, younger people are more likely to be acquainted with (or caring for) an old person with some form of psychological need; advances in neuroscience make good-news stories and are widely reported; and discrimination against any disadvantaged group has steadily become socially unacceptable.
I have tried to depict the evolution of old age psychiatry as both a scientific discipline and a social entity enmeshed in its specific place and time. Sustained by commitment to the welfare of mentally ill older people, it has tried to reach out further—to the earliest stages of illness or to the end of life, to independent people or to those in institutional care—and to a society which recognizes their needs, even while trying sometimes to deny them.
1 Jacoby, R. and Oppenheimer, C. (1991). Psychiatry in the elderly. Oxford: Oxford University Press. Also (1997) second edition; and (2002) third edition.
2 Jacoby, R., Oppenheimer, C., Dening, T., and Thomas. A. (2008). Oxford textbook of old age psychiatry. Oxford: Oxford University Press.
3 Levy, R. and Post, F. (1982). The psychiatry of late life. Oxford: Blackwell Scientific Publications.
4 Slater, E. and Roth, M. (1969). Mayer-Gross, Slater and Roth, Clinical psychiatry (3rd edn). London: Bailliere, Tindall and Cassell.
5 Eliot Slater had four children, of whom I am the third.
6 Slater, E. and Roth, M. (1969). Clinical psychiatry (3rd edn), London: Bailliere, Tindall and Cassell, pp. 548–9.
7 Stewart, R. (2008). Clinical aspects of dementia: vascular and mixed dementia. In: Jacoby, R., Oppenheimer, C., Dening, T., and Thomas, A. (eds.) Oxford textbook of old age psychiatry, Oxford: Oxford University Press, pp. 443–52.
8 Perry, R. and Perry, E. (1982). The ageing brain and its pathology. In: Levy, R. and Post, F. (eds.) The psychiatry of late life, Oxford: Blackwell Scientific Publications, pp. 9–67.
9 Pasquier, F., Deramecourt, V., and Lebert, F. (2008). Frontotemporal dementia. In: Jacoby, R., Oppenheimer, C., Dening, T., and Thomas, A. (eds.) Oxford textbook of old age psychiatry, Oxford: Oxford University Press, pp. 461–72.
10 McShane, R. (2008). Dementia in Parkinson’s disease and dementia with Lewy bodies. In: Jacoby, R., Oppenheimer, C., Dening, T., and Thomas, A. (eds.) Oxford textbook of old age psychiatry, Oxford: Oxford University Press, pp. 453–9.
11 Petersen, R. C., Smith, G. E., Waring, S. C. et al. (1999). Mild cognitive impairment: clinical characterization and outcome. Archives of Neurology 56, 303–8.
12 De Jager, C., Oulhaj, A., Jacoby, R., Refsum, H., and Smith, A. D. (2012). Cognitive and clinical outcomes of homocysteine-lowering B vitamin treatment in mild cognitive impairment: a randomized controlled trial. International Journal of Geriatric Psychiatry 27, 592–600.
13 Forlenza, O. F., Diniz, B. S., Radanovic, M. et al. (2011). Disease-modifying properties of long-term lithium treatment for amnestic mild cognitive impairment: randomised controlled trial. British Journal of Psychiatry 198, 351–6.
14 Hogg, J. (2008). Delirium. In: Jacoby, R., Oppenheimer, C., Dening, T., and Thomas, A. (eds.) Oxford textbook of old age psychiatry, Oxford: Oxford University Press, pp. 506–17.
15 Naguib, M. and Levy, R. (1991). Paranoid states in the elderly and late paraphrenia. In: R. Jacoby and C. Oppenheimer (eds.) (1991). Psychiatry in the elderly. Oxford: Oxford University Press, pp. 758–778.
16 Howard, R. (2008). Late onset schizophrenia and very late onset schizophrenia like psychosis. In: Jacoby, R., Oppenheimer, C., Dening, T., and Thomas, A. (eds.) Oxford textbook of old age psychiatry, Oxford: Oxford University Press, pp. 617–26.
17 Bergmann, K. and Jacoby, R. (1983). The limitation and possibilities of community care for the elderly demented. In: Research contributions to the development of policy and practice. Essays based on the seminar ‘Support for elderly people living in the community’ sponsored by DHSS and held at the University of East Anglia, September 1982. London: Her Majesty’s Stationery Office, pp. 141–67.
18 Corsellis, J. A. N. (1969). The pathology of dementia. Reprinted in Silverstone, T. and Barraclough, B. (eds.) (1975). Contemporary psychiatry: selected reviews from the British Journal of Hospital Medicine. British Journal of Psychiatry Special Publication No. 9. Ashford, Kent: Headley Brothers, pp. 110–18.
19 Procter, A. W. (1997). Neurochemical pathology of neurodegenerative disorders in old age. In: Jacoby, R. and Oppenheimer, C. (eds.) Psychiatry in the elderly (2nd edn), Oxford: Oxford University Press, pp. 104–22.
20 King, E. M.-F., Smith, A. and Jobst, K. (1993). Autopsy: consent, completion and communication in Alzheimer’s disease research. Age and Ageing 22, 209–14.
21 Francis, P. T., Palmer, A. M., Snape, M., and Wilcock, G. K. (1999). The cholinergic hypothesis of Alzheimer’s disease: a review of progress. Journal of Neurology, Neurosurgery and Psychiatry 66, 137–47.
22 The ‘cholinergic hypothesis’ proposes that the activity of the neurotransmitter acetylcholine in the brain is reduced in AD. If the enzyme acetyl cholinesterase, which catalyses the destruction of acetylcholine, can be prevented from acting, then the level of acetylcholine at the synapse can be maintained for longer, and so achieve more effective transmission of the nervous impulse. Hence the use of inhibitors of acetyl cholinesterase in Alzheimer’s disease.
23 Wilcock, G. K. (2008). Clinical aspects of dementia: specific pharmacological treatments for Alzheimer’s disease. In: Jacoby, R., Oppenheimer, C., Dening, T., and Thomas, A. (eds.) Oxford textbook of old age psychiatry, Oxford: Oxford University Press, pp. 483–91.
24 McShane, R., Keene, J., Gedling, K. et al. (1997). Do neuroleptic drugs hasten cognitive decline in dementia? Prospective study with necropsy follow-up. BMJ 314, 266–70.
25 Schneider, L. S., Dagerman, K. S., and Insel, P. (2005). Risk of death with atypical antipsychotic drug treatment for dementia: meta-analysis of randomised placebo-controlled trials. JAMA 294, 1934–43.
26 James, I. A. and Fossey, J. (2008). Psychological treatments: non-pharmacological interventions in care homes. In: Jacoby, R., Oppenheimer, C., Dening, T., and Thomas, A. (eds.) Oxford textbook of old age psychiatry, Oxford: Oxford University Press, pp 285–96.
27 OADIG (Old Age Depression Interest Group) (1993). How long should the elderly take antidepressants? a double-blind placebo-controlled study of continuation/prophylaxis therapy with dothiepin. British Journal of Psychiatry 162, 157–82.
28 O’Connor, D. W. (2008). Electroconvulsive therapy. In: Jacoby, R., Oppenheimer, C., Dening, T., and Thomas, A. (eds.) Oxford textbook of old age psychiatry, Oxford: Oxford University Press, pp. 201–14.
29 Wilkinson, P. (2008). Psychological treatments. In: Jacoby, R., Oppenheimer, C., Dening, T., and Thomas, A. (eds.) Oxford textbook of old age psychiatry, Oxford: Oxford University Press, pp 241–96.
30 Rivett, G. (1998). From cradle to grave, fifty years of the NHS, London: King’s Fund, p. 406.
31 Rivett, G. (1998). From cradle to grave, fifty years of the NHS, London: King’s Fund, p. 407.
32 Martin, J. P. (1984). Hospitals in trouble. Oxford: Basil Blackwell.
33 The Parliamentary and Health Service Ombudsman (2011). Care and compassion. Report of the Health Service Ombudsman on ten investigations into NHS care of older people. London: The Stationery Office.
34 Brooker, D. (2008). Person centred care. In: Jacoby, R., Oppenheimer, C., Dening, T., and Thomas, A. (eds.) Oxford textbook of old age psychiatry, Oxford: Oxford University Press, 229–40.
35 Levin, E., Sinclair, J., and Gorbach, P. (1989). Families, services and confusion in old age. Aldershot: Avebury.
36 Mace, N. L. and Rabins, P. V. (1985). The 36-hour day: caring at home for confused elderly people. London: Hodder & Stoughton.
37 Davis, R. (1989). My journey into Alzheimer’s disease. Helpful insights for family and friends. Wheaton, IL: Tyndale House.
38 Bayley, J. (1998), Iris. A memoir of Iris Murdoch. London: Gerald Duckworth.