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001 WHERE IS DEMENTIA IN ENGLISH HEALTH POLICY?
A. Barker.Department of Health, London, UK
The title is intentionally ambiguous, to allow discussion of several themes:
Where can dementia policy be found? How far has policy on dementia developed, and where is it going? Why hasn’t it achieved a higher priority?
Such is the scope of dementia’s mental, physical, and social impact, that policy addressing its management necessarily includes diverse streams of work from various governmental departments. While spanning many priority areas therefore, it may also be said to suffer from lack of focus. Equally, policy cuts across organisational and professional boundaries, lending itself to huge opportunities for integrated working but providing equally large challenges to those responsible for implementation.
This presentation will place dementia policy in the context of national health and social care policy, explore some strengths and weaknesses of its current position, and give a personal view from a Department of Health (England) advisor of progress over the last few years and its likely future direction.
002 EPIDEMIOLOGY OF DEMENTIA
A. Hofman.Erasmus Medical Centre, Dept of Epidemiology & Biostatistics, 3000 DR Rotterdam, The Netherlands
This presentation will address the frequency and risk of dementia and Alzheimer’s disease. The prevalence of dementia increases strongly with age, from about 1% at age 65 years to at least 30% at the age of ⩾85 years. Alzheimer’s disease accounts for about two-thirds of all dementia cases. The prevalence of Alzheimer’s disease is higher in women than in men. Our findings suggest that currently about 2 500 000 men and 3 000 000 women living in the European Union suffer from dementia. The incidence of dementia also increases markedly with age, from about 1 per 1000 person years at the age of 65 years to about 10 per 1000 person years at the age of ⩾85 years. There is evidence that northwest Europe has a slightly higher incidence of dementia than southern Europe. Our findings indicate that over half a million new dementia patients will be diagnosed each year in the European Union.
003 IMPACT OF CHARITIES ON RESEARCH AND POLICY
S. Sorensen, C. Ballard.Quality Research in Dementia, Alzheimer’s Society, London, UK
A disease specific charity allows the voices of people affected by the disease to be heard by policy makers and researchers.
The Alzheimer’s Society has been a major force in shifting the public perception of dementia being a social care issue associated with ageing to being a health issue – a condition caused by disease. Dementia is now a political hot topic and the Alzheimer’s Society has helped generate a serious debate about free care for people with dementia. Free care is an example of an issue where the charity got a problem to the top of the agenda but where we have not shifted the political power despite putting the case consistently over a long period.
The Alzheimer’s Society put patient defined outcomes in focus with its first submission to NICE in 2000 and was very influential in the resulting recommendation of prescribing drugs for people with early to mid stage Alzheimer’s disease. We are still re-enforcing the view that what people think about a drug matters as much in the overall evaluation as health economics. This approach has had some influence on clinical trial designs where the patients’ and carers’ views are now more often included in the outcome measures.
Medical research charities including the Alzheimer’s Society have had major influence on the legal framework for research in UK. Most disease charities acknowledge the need for animal models in research and provide consistent support for basic research in this debate. It is likely that the UK’s regulations for stem cell research would have been more like that of the USA if a number of medical charities had not got involved in the debate. The association of medical research charities were heavily involved in securing extra funding for basic science research from the government in 2003.
Dementia research is at an exciting point with key advances in our understanding of molecular biology, important advances in techniques for early diagnosis, and a number of novel therapies either in development or being evaluated in clinical trials. However, there is still so much to do. The lack of research capacity and the limitation of funding is putting major constraints upon what can be achieved within the UK. The Alzheimer’s Society share with other disease charities the concern that the absence of a comprehensive structure enabling the development of promising new scientists is leading to many of the best young researchers moving abroad or leaving academia. If the opportunities for major developments are to be capitalised upon there is a need for a major injection of new funding, better strategic planning to coordinate the efforts of the major funders and the key research groups, and a cohesive system to nurture promising young scientists.
A new initiative, the Clinical Research Network (CRN) for dementia, will provide a substantial new research infrastructure for clinical trials. However, without additional investment to directly fund clinical trials and without similar initiatives to prioritise research developing the underpinning science, it is a worry that the CRN will enable little other than more efficient patient recruitment for commercially sponsored clinical trials.
The Alzheimer’s Society funds an active, consumer led research programme (Quality Research in Dementia). Recent initiatives include a plan to develop a UK dementia Brain Bank jointly with the Alzheimer Research Trust to support an infrastructure for clinico-pathological research. Government funding channels might be worried about taking on a brain banking project in the present climate but this project received the highest level of priority given to any project by the QRD consumers.
Response funding for the best science, competing for ever diminishing resources is not sufficient to optimise progress in dementia research. It is essential that the charities with an interest in dementia, the research councils, people with dementia and their carers, and scientists cooperate to determine the key objectives and formulate a strategic plan with ring fenced funding to enable us to achieve these objectives within a 5 and 10 year time frame.
004 ACCESS TO CARE IN DEMENTIA AND IMPACT ON CARERS
S. Banerjee.HSRD, The Institute of Psychiatry, King’s College London, UK
Dementia is one of the most common and serious disorders of later life. There are profound impacts on the person with dementia, their family and carers, and also on health, social, and voluntary services. Despite this only 10–15% of people with dementia are referred to specialist services, with particularly low rates of referral from minority ethnic groups. Large numbers of people with dementia and their carers may therefore not have access to specialist assessment, advice, and management (drug and non-drug) that they might benefit from. Current policy requires effective and early identification, care, and treatment of dementia. Therefore current services can be said to be failing the majority of people of dementia.
In order to address this there is a need to understand how patients and carers make decisions concerning attribution of illness, presentation, and help-seeking, and how primary care see their role in the management of dementia. There is then the need to generate and test models of service delivery that can deliver timely, effective, acceptable, and efficient care.
This presentation has three elements. The first will consider the impacts of dementia on people with dementia themselves and their family carers using data from longitudinal and cross-sectional studies. In the second the focus will be on barriers and facilitators to care from a patient and carer viewpoint as well as those of primary and secondary care. Novel data from a recently completed qualitative study will be presented. Finally data on service configurations to meet the needs of people with dementia will be considered.
005 DEMENTIA IN DEVELOPING COUNTRIES
M. Prince, for and on behalf of the 10/66 Dementia Research Group.Institute of Psychiatry, London, UK
Background: There is a need for more research into dementia in developing countries where up to 66% of those with dementia live, but only 10% of research is conducted. The 10/66 Dementia Research group was founded in 1998 as a network of researchers, mainly from developing countries, wishing to redress this imbalance, and to provide evidence of use to advocacy groups and policymakers.
Objectives: To give an overview of the 10/66 Dementia Research Group’s programme of pilot and population-based research in developing countries.
Methods and Results: ADI’s 10/66 Dementia Research Group has now completed pilot studies of dementia diagnosis and care arrangements for people with dementia in 26 centres in 16 mainly developing countries in Latin America, the Caribbean, Africa, India, China, and south east Asia. We have demonstrated the feasibility of diagnosing dementia in a simple one-stage research interview. We also showed that caregivers in developing countries experience considerable psychological, economic, and practical strain. Although larger households were associated with lower carer strain, strain was as marked as in the developed world. Many carers had cutback on paid work to care. Those in the poorest countries were most likely to use expensive private medical services, and to spend more in relative terms on health. Lack of awareness was a major problem sometimes leading to stigma and blame attaching to the caregiver.
Conclusions: ADI’s 10/66 Dementia Research Group is now working on population-based studies in Cuba, Brazil, Dominican Republic, Venezuela, Peru, Argentina, Mexico, India, and China. The aims and designs of these studies shall be described, including preliminary descriptions of risk factor profiles between continents, and early data on the workings of the new DSMIV one phase computerised diagnostic algorithm. We will also outline the new 10/66 caregiver education and training intervention, which we implement and evaluate in the course of our field work. The descriptive studies will provide much needed data for policymakers in prioritising service development. The intervention may suggest new and generalisable models of care for health care systems with limited specialist resources.
006 MANAGEMENT OF PSYCHIATRIC SYMPTOMS AND BEHAVIOURAL DISTURBANCES IN DEMENTIA
A. Burns.Wythenshawe Hospital, Manchester, UK
Psychiatric symptoms and behavioural disturbances are a core feature of the dementia syndrome. A wide variety of management strategies are available for their control.
Non-pharmacological approaches include simple advice on behaviour and education for carers as to the significance and implications of the symptoms. This general advice seems to be effective whether it is provided for professional care staff in nursing and residential home, or for informal carers of patients in their own homes. The exact nature of the advice is of secondary importance but it is important to involve patients as far as possible in the techniques, as well as raising staff morale in homes. The information can attenuate the care givers’ reaction to behaviours.
Two novel types of management include bright light therapy and aromatherapy. There is good randomised controlled trial evidence for both of these interventions that they are effective in reducing agitation in people with dementia.
A wide variety of drugs have been tried with moderate degrees of success to control behavioural problems, usually agitation. The atypical antipsychotics and the cholinesterase inhibitors are the two for which there is emerging evidence. The recent Committee on Safety of Medicines warning on the use of risperidone and olanzapine for the management of agitation in people with dementia has increased interest in alternative ways of managing these symptoms. It is beginning to emerge that use of the cholinesterase inhibitors is an emerging force, in some circumstances as first line treatment, for the management of these symptoms even though their primary purpose is deemed improvement of cognitive function.
A combined behavioural, psychosocial, and pharmacological approach is probably best for the management of psychiatric symptoms and behavioural disturbances in dementia.
007 IMPACT OF BRAIN DAMAGE ON FUNCTIONING IN THE REAL WORLD
D. T. Stuss.The Rotman Research Institute, Baycrest Centre, University of Toronto, Canada
The ultimate objective of evaluation in neurological and neuropsychiatric patients is to understand how brain changes impact on functioning in the “real world”. There are several steps necessary to achieve this goal.
An appropriate approach to research in this area is required. In the first part of this presentation an overview of the general approach being undertaken at Baycrest Centre for Geriatric Care (through The Rotman Research Institute and the Kunin Lunenfeld Applied Research Unit) is presented. The research must be interdisciplinary: theoretical, structural and functional imaging, clinical, and functional. The focus will be on the functions of the frontal lobes.
Using the example of attention the importance of precise delineation of deficits through cognitive neuropsychology will be demonstrated. There are at least three different attentional processes within the frontal regions, related to three different anatomical regions. This knowledge provides the impetus for developing focused rehabilitation procedures, from both a cognitive (top-down) and a functional (bottom-up) approach.
The emphasis on “real world” urges additional steps. What is the impact of damage on functional neural networks? Can different brain regions compensate to minimise the problems? Evidence from normal aging and Alzheimer’s disease using functional imaging suggests that such compensation does exist. Newer approaches with analysis of networks provide promise of understanding the complexity of human cognition and emotion.
The world is complex; context is continually changing. Yet our assessments are static, not dynamic. In the last part of the presentation, results will be shown to demonstrate that even small changes in task demands, or even in instructions, can alter performance. Moreover, each individual is variable in how they perform, and this variability is influenced by context, task demands, and by location of brain dysfunction.
008 BIOLOGICAL RISK FACTORS FOR DEMENTIA
A. Hofman.Erasmus Medical Centre, Dept of Epidemiology & Biostatistics, PO Box 1738, 3000 DR Rotterdam, The Netherlands
This presentation will discuss the new leads in the aetiology of dementia that have emerged in the past years from clinical and epidemiological research. The evidence for various causes of Alzheimer’s disease, including genetic factors, inflammation, endocrine factors, and vascular factors, will be presented. This presentation also includes evidence for a causal link between vascular factors and dementia. Data obtained in the Rotterdam Study will be shown as an example. Vascular factors to be discussed include blood pressure and smoking. Atherosclerosis and thrombogenesis will be addressed, as well as vascular diseases, diabetes mellitus, and atrial fibrillation. Each of these factors will be assessed for the individual attributable risk for Alzheimer’s disease. In addition, the overall population risk will be estimated. This presentation will, finally, address the burden of Alzheimer’s disease for society and individual, and the potential for prevention of Alzheimer’s disease and associated neurological diseases by intervention of vascular factors and vascular disease.
009 THE NEUROPSYCHOLOGY OF THE FOCAL DEMENTIAS
J. R. Hodges.Cognition and Brain Sciences Unit, Cambridge, UK
Frontotemporal dementia (FTD) is the term currently applied to a range of non-Alzheimer dementia syndromes associated with focal atrophy of the frontal and/or anterior temporal lobe regions. Unlike Alzheimer’s disease, the pathology of FTD is heterogeneous and the clinical syndromes reflect the distribution rather than nature of the pathological changes. In younger patients (<65 years) with dementia FTD is almost as common as Alzheimer’s disease.
My talk will focus on the three main clinical presentations: semantic dementia, progressive non-fluent aphasia, and the frontal or behavioural variant of FTD. I will attempt to relate the predominant symptomatology to current cognitive neuropsychological theories, and findings from structural and functional brain imaging.
In semantic dementia there is progressive breakdown of an “amodal integrative” semantic system, which manifests initially as a deficit in word production and comprehension, although subtle deficits in non-verbal semantics are invariably present and worsen as the disease progresses. Recent structural and functional imaging in semantic dementia point to a key role for the perirhinal and polar temporal regions with the left hemisphere typically more involved than the right. In the rarer right temporal lobe forms of semantic dementia, person-specific knowledge is disproportionately impaired.
Progressive non-fluent aphasic syndrome is more heterogeneous than semantic dementia. Speech output is reduced and laboured. Phonological and/or syntactic processes are disrupted with parallel pathology in the anterior insula and Broca’s region. Patients perform well on verbal and non-verbal tests that are meaning based but fail on phonological tests, especially repetition of complex words and phrases.
In the commonest, frontal or behavioural, variant there is progressive alteration in personality, social conduct, emotional processing, eating, and appetite with a tendency to stereotyped patterns of behaviour. Breakdown of theory of mind and impairment on tests of social and emotional judgement appear to be key defects, and are associated with atrophy of the mesial (para-cingulate) frontal and orbital frontal cortices. Patients may perform normally on standard “frontal executive” tasks.
010 MRI IN DEMENTIA
N. Fox.Institute of Neurology, London, UK
Brain imaging is increasingly accepted as an essential part of the investigation of a patient with cognitive impairment. Recent practice guidelines recommend that structural imaging, either computed tomography (CT) or magnetic resonance imaging (MRI), should be performed at least once in all cases of dementia. Magnetic resonance imaging is the structural imaging modality of choice; giving better resolution and tissue contrast than CT and thereby providing better visualisation of vascular changes and the pattern of atrophy.
Traditionally, CT and MRI were used in a case of cognitive complaints to exclude abnormalities that were potentially amenable to surgical treatment, such as a tumour, haematomata, or hydrocephalus. While this remains an important role of imaging (although remediable lesions are rare), imaging is now being used for its positive predictive diagnostic value rather than simply to exclude other disorders. Imaging can provide strong evidence of cerebrovascular disease and may be particularly helpful in differentiating small vessel vascular dementia from Alzheimer’s disease (AD). Extensive white matter hyperintensities and signal change in the basal ganglia and brain stem (on T2 and fluid attenuated inversion recovery (FLAIR) imaging) suggest vascular damage as the cause of cognitive impairment. Often, however, there is an overlap of pathologies and the distinction between AD, vascular dementia, and mixed disease is difficult. T2-weighted and FLAIR MRI have been proven to have high positive predictive value in the diagnosis of Creutzfeldt-Jakob disease (CJD): pulvinar changes being characteristic of variant CJD and putaminal changes being typical in sporadic disease.
The pattern of atrophy, best seen on coronal T1-weighted MRI, is valuable in the detection and differentiation of the degenerative dementias. Alzheimer’s disease and, to a lesser extent, dementia with Lewy bodies, is characterised by bilateral and symmetrical medial temporal lobe atrophy. Even in mild AD, the hippocampus is typically reduced by 15–20%. Nonetheless, the variability between individuals means there is considerable overlap between normal aging and early AD. As is implied by the name, focal frontal and temporal lobe atrophy is characteristic of the frontotemporal lobar degenerations (FTLD) with limited correspondence between particular patterns of atrophy and the underlying histology in these conditions. In a number of other conditions, the pattern of atrophy may point towards a particular diagnosis—for example, caudate atrophy in Huntington’s, midbrain atrophy in progressive supranuclear palsy (PSP), and cerebellar and pontine atrophy in multiple system atrophy (MSA).
Increased rates of atrophy are a characteristic feature of degenerative dementias and this has some diagnostic value in difficult early cases, either of AD or of FTLD. In order to detect and quantify change, serial imaging needs to be acquired, typically with an interval of 6 months or more apart. In AD, whole brain atrophy rates (2–2.5% per year) are several times the rate of atrophy in normal elderly subjects (typically <0.5% per year).
This recognition that MRI may be used to measure rates of brain volume loss with a high level of precision has led to it being proposed as a surrogate marker of disease progression for treatment trials. A number of studies, both in MCI and AD, have incorporated measures of whole brain and/or hippocampal atrophy rates as outcome measures. The proof of these measures as useful surrogate markers of progression awaits their use in a trial with a truly disease-modifying therapy.
011 NON-ALZHEIMER’S DEMENTIA – BIOLOGY, NEUROPSYCHIATRY AND TREATMENT
C. Ballard, P. Francis, S. Sharpe, D. Aarsland, E. Perry.Wolfson Centre for Age Related Diseases, King’s College London, UK
The presentation will predominantly focus upon the associations of neurochemical deficits and key clinical symptoms in parkinsonian dementias (dementia with Lewy bodies (DLB), Parkinson’s disease dementia) and vascular dementia. Behavioural and Psychological Symptoms in Dementia (BPSD), especially psychotic symptoms, are particularly frequent in patients with DLB. Several studies, focusing predominantly upon the cholinergic system, have evaluated the potential neurochemical associations of these symptoms. Visual hallucinations appear to be associated with reduced cortical choline acetyltransferase (ChAT) activity in the temporal cortex, a marker of cholinergic innervation, but not with predominantly postsynaptic muscarinic M1 receptor binding; whereas delusions were significantly associated with elevated M1 receptor binding but not with reductions in ChAT. Visual hallucinations and delusional misidentification (but not delusions) were also associated with lower binding to nicotinic receptors ([(125)I]alpha bungarotoxin binding was reduced in the same area of the temporal cortex). No associations were identified between dopaminergic binding and any of the psychotic symptoms. Whilst there are too few studies to establish a general consensus, the association of visual hallucinations with cholinergic deficits in DLB has been replicated and is consistent with the good response of visual hallucinations to cholinesterase inhibitors in these patients. In PDD, however, the association between cholinergic deficits and visual hallucinations is less clear. In both dementias, attentional deficits are prominent and probably related to cholinergic dysfunction, with placebo controlled double blind clinical trials indicating good response of attentional deficits to cholinesterase therapy. Fluctuating cognition, underpinned by impairments of consciousness, are also prominent in both dementias but are more likely to be related to alterations in nicotinic binding and there is no clear evidence of response to cholinesterase therapy. Fewer studies have examined the associations of serotonergic or noradrenergic deficits, although preliminary evidence suggests a possible association with mood symptoms and L-tryptophan depletion exacerbates cognitive deficits. Further work needs to determine whether key neurochemical deficits impact upon the progression of the underlying disease substrates, and to investigate the potential therapeutic value of therapies targeting other neurochemical systems.
From the studies so far completed in vascular dementia (VaD) it appears that generalised cholinergic deficits are only evident in VaD patients with concurrent Alzheimer pathology, although a preliminary case report indicates the possibility of a specific pattern of cholinergic deficits in the context of severe sub-cortical ischaemic vascular disease. The lack of a clear association between pure vascular dementia and cholinergic deficits probably explains the relative lack of response to cholinesterase inhibitors in these patients. There has been very little work focusing upon specific sub-types of VaD or upon other neurochemical systems. Preliminary work from our own group has begun to indicate a link between serotonergic dysfunction and mood symptoms in VaD, which may have important therapeutic implications given the high frequency of mood disorders in these patients.
012 CURRENT TREATMENT APPROACHES IN DEMENTIA: AN UPDATE
A. Burns.Wythenshawe Hospital, Manchester, UK
The cholinesterase inhibitors and the glutamatergic agent, memantine, are the drugs most widely prescribed for Alzheimer’s disease. The cholinesterase inhibitors are now established in the treatment of the mild to moderate stages of Alzheimer’s disease but there is emerging evidence of their utility in the more advanced stages and their use in primarily managing psychiatric symptoms and behavioural disturbances.
Memantine is licensed for the treatment of more severe Alzheimer’s disease and has been used with benefit in combination with cholinesterase inhibitors. These medications are moderately effective and have a key role to play in the treatment of Alzheimer’s disease. Studies are increasingly challenging their traditional therapeutic area in terms of the cholinesterase inhibitors treating more severe illness and memantine being used in people with mild disease.
Treatment of vascular dementia is largely confined to control and reduction of cerebrovascular risk factors. Recent evidence of the ad-mixture of vascular and Alzheimer pathology in the same patient has led to the prospect of prevention of dementia by rigorous control of these documented risk factors such as high blood pressure, high cholesterol, high homocysteine, atrial fibrillation, obesity, and smoking. Other double treatments traditionally used for the primary and secondary prevention of cerebrovascular disease and myocardial infarction may have an important role to play.
013 CATATONIA’S MANY FACES WARRANT A DSM HOME OF ITS OWN
M. Fink.University of New York, New York, USA
For almost a century, the presence of delusions in a psychiatric examination assured a diagnosis of dementia praecox (schizophrenia). This intimate connection was broken when delusions were identified in patients with affective disorders (mania and depression), infections (neurosyphilis), and toxic states (hallucinogenic and alcoholic psychoses).
A similar history has unfolded for catatonia. Karl Kahlbaum in 1874 described the motor phenomena of catatonia in patients with diverse illnesses. He was optimistic about their outcome despite the lack of effective therapy. Two decades later, Emil Kraepelin pigeonholed catatonia as a subtype of dementia praecox (schizophrenia) with a poor prognosis. The tie between catatonia and schizophrenia was broken when catatonia was described in manic-depressive and neurotoxic patients between 1973 and 1977. These observations were ignored and official classifications (DSM, ICD) still bind catatonia to schizophrenia.
When studied systematically, however, about 10% of inpatient psychiatric populations exhibit the cluster of motor signs of mutism, negativism, rigidity, posturing, stereotypy, staring, and others. These patients have been labelled as suffering from catatonia, Kahlbaum Syndrome, malignant catatonia, delirious mania, catatonic excitement, Bell’s mania, benign stupor, neuroleptic malignant syndrome, toxic serotonin syndrome, and oneiric states. We believe these syndromes to have a common psychopathology and respond to the common therapy of sedative anticonvulsants (barbiturates, benzodiazepines) and to electroconvulsive therapy. Viewing these syndromes as disorders of similar brain pathophysiology is of immediate clinical merit as it encourages effective treatment. It is also of theoretic interest.
Catatonia can be reliably identified. It is a common syndrome that meets the requirements for a separate designation in psychiatric classification. We propose that psychiatric classifications include a category of “catatonia”, as it does “delirium”, with modifiers that parallel those for delirium.
014 CATATONIA AND THE BRAIN – A CLINICAL PERSPECTIVE
D. Rogers.Frenchay Hospital, Bristol, UK
The German Neuropsychiatrist Kahlbaum described a constellation of motor symptoms 130 years ago, which he called Catatonia and for which he expected an eventual cerebral explanation. The syndrome is still instantly recognisable clinically, but cerebral explanations for it remain primitive. Historical reasons have contributed to this. I reviewed the English and French 20th Century literature in experimental animals and human patients on the structural basis of Catatonia. This was notable by being so limited. I only found 28 papers to review. Catatonia can be associated with neurological, but most commonly with psychiatric disorder. For most of the 20th Century, explanations of psychiatric disorder in cerebral terms were not sought. Neurologists had little interest in psychiatric disorder. They used different nomenclature, such as akinetic mutism, for symptoms identical to those called stupor in psychiatric disorders. A case of stupor associated with a schizophrenic illness, with unrecognised oculogyric crisis is presented. This is compared to the lack of neurological interest in oculogyric crisis after this was first described in encephalitic patients in the 1920s. A plea for hypotheses for cerebral explanations of catatonic motor disorder is made.
015 BASAL GANGLIA FUNCTION: A NEW PERSPECTIVE
P. Plaha, S. S. Gill.Institute of Neurosciences, Frenchay Hospital, Bristol, UK
Introduction: The basal ganglia are a group of subcortical nuclei involved in the planning and execution of behaviour and in procedural learning. Present models attempting to explain the neural mechanism involved in it’s functioning are simple circuit diagram and nuclei are attributed with increased or decreased activity to explain physiological or pathological processes. More recently it has been shown that there is vast axonal collateralisation interconnecting many parts of the basal ganglia and their afferent and efferent structures such that increased activity in one nucleus produce conflicting influences on another and the model breaks down.
Discussion: In the light of recent evidence that information processing is not represented by a change in neuronal firing frequency but includes the degree of temporal and spatial synchronisation and also the degree and duration of bursting activity of neuronal assemblies and not single neurones we discuss the functioning of the basal ganglia. With its role in directing information processing in the frontal cortex we discuss various “hypo” and “hyperkinetic” movement disorders and the role they play in offering an insight into the functioning of the basal ganglia. Lastly, we attempt to understand the functional interactions of the basal ganglia with a number of subcortical nuclei such as the CM/Pf nucleus, midbrain extrapyramidal area, the reticular thalamic nucleus of the thalamus, and the Zona Incerta.
016 HUMOUR, SOCIAL UNDERSTANDING AND THE FRONTAL LOBES
D. T. Stuss.The Rotman Research Institute, Baycrest Centre, University of Toronto, Canada
Disorders of awareness of self, and the social implications of such, have been attributed to different brain regions, from the parietal to the frontal lobes. A common teaching was that such disorders existed on a continuum – from denial, neglect, unawareness, to unconcern. One of our efforts, common in current neuroscience, has been to examine if there are potential dissociations in this continuum, and to see if these relate to different brain regions.
This presentation begins with the end – a proposed model of how the brain relates to the external world to allow awareness of different aspects of the world. It is suggested that there are different types of awareness, and different levels, related to distinct brain regions. Damage to posterior parts of the brain results in disorders of awareness at the level of knowledge. These are domain specific. Two types of disorders have an association with the frontal lobes. Evidence from a case study of Capgras syndrome, known in the neurological evidence as reduplicative paramnesia, suggests that at one level disorders of self are based on difficulties in executive judgement. There is also evidence that a higher disorder of awareness may exist, one that is a true awareness of “self”, of one’s past, and the relation of the past and present to the future. Both of these examples suggest a priority of the right frontal region.
These clinical concepts have been pursued experimentally. Studies of humour demonstrate that this right frontal region is important for both identifying and appreciating higher levels of humour, which imply integration of concepts. Examination of theory of mind in patients with frontal lesions also emphasises an important role of the polar, primarily right, frontal regions. These functions underlie an individual’s ability to interact in a social context.
It is obvious that “self”, social interactions, theory of mind, and appreciation of humour, are multi-faceted concepts. Regardless, the frontal lobes, particularly on the right, appear to play a pre-eminent role, perhaps because of the potential of integration of information from multiple different regions of the brain.
017 ATTENTION DEFICIT DISORDER (ADHD) IN CHILDHOOD AND ADULT LIFE
E. Taylor.Institute of Psychiatry, London, UK
The understanding of attention deficit disorder (ADHD) has recently advanced greatly from neurobiological investigation. Structural studies using magnetic resonance imaging (MRI) have agreed that the brain size is often reduced and that some structures (especially right frontal lobes, striatum, and cerebellar vermis) are altered disproportionately. Some of these structures are of particular importance because in normal individuals they are activated during the performance of tests that involve the inhibition of a response. In young people with ADHD these areas are under activated and they have a corresponding difficulty in holding themselves back, delaying gratification, and thinking before they act. Genetic influences are strong and include several DNA variants in genes affecting dopamine systems. Behaviour modification, CNS stimulants, atomoxetine, and other drugs are effective treatments; identification both in children and adults is increasing. It is suggested that wider recognition and treatment in adults would be useful for people currently identified only as showing personality or atypical bipolar features. This talk will therefore present some data from a study in longitudinal epidemiology, which has been in progress for 20 years in London. It examines the adult outcomes for a population sample of boys and girls with ADHD problems, contrasting them with non-hyperactive cases of oppositional/defiant disorder as well as healthy controls.
Methods: The initial survey was carried out on a population consisting of all the boys aged between 6 years and 0 months and 7 years 11 months who were on the rolls of primary schools in the London borough of Newham (n = 2 400). Three years after the completion of the boys’ study, all girls aged between 6 years 0 months and 7 years 11 months at schools in the same area were identified for an identical study.
All children were screened using the Rutter parent and teacher questionnaires and stratified into contrast groups, with and without ADHD symptoms and with and without oppositional/defiant problems. These contrast groups (n = approximately 90 in each) were taken into a second stage of detailed assessment, including parent and teacher rating scales, a standardised teacher interview, intellectual, achievement, and neuropsychological tests (including observations of behaviour), and the Parental Account of Childhood Symptoms (PACS). Neighbourhood indices were taken from census data and social circumstance affecting the family was measured with an index of disadvantage from the parental interview. Follow up was undertaken 10 years later when the young people were on average 17 years and had nearly all left school, and again 20 years later. The absence of treatment resources for ADHD in the UK at the time of the study meant that therapy for ADHD was not given.
Results: The presence of ADHD was a risk factor both for social adjustment and for psychiatric disorders. Separate developmental tracks could be identified. Hyperactivity predicts a pattern of asocial disengagement and accident proneness; inattentiveness one of occupational failure; coexistent learning difficulty tends to persist as an independent trait, uninfluenced by the course of other problems; social rejection predicts an outcome of conduct disorder. Hyperactive girls were qualitatively similar to boys in showing a range of cognitive impairments; indeed, the girls showed a lower performance IQ, a worse. performance on tests of motor coordination, and were more cognitively impulsive than the boys. Outcome differed in females: the presence of hyperactivity removed their normal protection against conduct disorder, and over the course of the study (in contrast to males) they were at enhanced risk for emotional disturbances. Their adverse outcomes were more closely linked to deviant friendship patterns
Implications: Controlled trials in adults with ADHD have shown superiority to placebo for stimulant drugs and atomoxetine. Stimulant actions correlate closely with inhibition of the dopamine transporter (indexed by labelled raclopride in PET). Atomoxetine inhibits noradrenaline transport and increases dopamine levels in frontal regions but not striatal. Doses of stimulants in adult life are quite variable and titration against monitored response is desirable.
018 NEUROPSYCHOLOGICAL DEFICITS IN ADULTS WITH ATTENTION DEFICIT HYPERACTIVITY DISORDER: DO THEY IMPROVE WITH AGE?
J. Bramham, S. Young, R. Morris, P. Asherson, B. Toone.Jessica Bramham Department of Psychology, Institute of Psychiatry, London, UK
Aims: Attention Deficit Hyperactivity Disorder (ADHD) is no longer viewed as a disorder limited to childhood, although many children’s symptoms do diminish with age. Adults with ADHD have been shown to be impaired on various neuropsychological measures, particularly those involving attention, response inhibition, and other executive functioning tasks. However, it is not clear whether these deficits improve with age through adulthood.
Methods: A cross-sectional study design was used. Neuropsychological tests assessing attention, impulsivity, and executive functioning were administered as part of a routine diagnostic assessment. The relationship between age and test performance was examined for 218 diagnosed ADHD patients aged between 16–50 years. Self- and informant-ratings of ADHD, anxiety, and depression symptoms were also analysed for changes in presentation according to age.
Results: There was a significant improvement in response inhibition with increase in age. However, on tests of attention and executive functioning, all age groups exhibited comparable deficits. There was no reduction in either inattention or hyperactive/impulsive symptoms with increasing age but there was a significant increase in both anxiety and depression for older patients.
Conclusions: Response inhibition deficits improve as adults with ADHD grow older. However, many other significant neuropsychological impairments persist into middle adulthood and possibly beyond. Furthermore, there is no decrease in self-reported experience of symptoms and an increase in comorbid disorders. The limitations of the clinical sample will be discussed.
019 DOES METHYLPHENIDATE AMELIORATE ATTENTION DIFFICULTIES IN ADULTS WITH ADHD?
D. Polo, D. Rogers, S. Butler.Burden Neurological Institute, Bristol, UK
Aims: Recent data suggest that the syndrome of Attention Deficit Hyperactivity Disorder (ADHD) persists into adulthood in a significant percentage of childhood onset cases. The purpose of this pilot study is to assess the effect of methylphenidate on attention difficulties shown by adults with ADHD, by means of event related brain potentials (ERPs).
Methods: Neurophysiological, behavioural, and neuropsychological measures of attention obtained from six adults with ADHD were compared on two conditions: when they were free of medication and under the effect of methylphenidate.
Results: Paired t-test comparisons showed an enhanced level of neural activity, as measured by ERPs associated with neural attention mechanisms, when the patients were under the effect of methylphenidate. This effect was accompanied by a higher rate of hits and a lower rate of missing responses on a continuous performance task (CPT).
Conclusions: Though the results are preliminary and based on a small number of subjects, they suggest methylphenidate helps to counteract brain dysfunction shown by adults with ADHD and results in improvement in sustained attention over time. This finding supports the use of the ERPs as a useful, objective, and non-invasive tool to monitor the effect of drugs on attention processes in adult ADHD.
020 DIVIDED ATTENTION IN AMNESTIC MILD COGNITIVE IMPAIRMENT (AMCI)
T. M. Dannhauser, S. Shergill, Z. Walker, M. Seal, T. Stevens, L. Lee.The Mental Health Unit, St Margaret’s Hospital, Epping, UK
Aims: Recent neuroimaging studies have demonstrated changes in brain function in cognitively normal subjects at increased risk of developing Alzheimer’s disease (AD). Amnestic mild cognitive impairment (AMCI) carries a high risk of developing into AD. In AMCI, altered cortical activation has been demonstrated during memory tasks, using functional magnetic resonance imaging (fMRI). Memory and attention are closely related cognitive functions. We aimed to clarify whether the memory impairment of AMCI is associated with attentional deficits of the sort likely to be revealed by cognitive tasks requiring divided attention (dA).
Methods: Ten elderly adults with AMCI were compared with healthy age matched controls in a dA task using fMRI and behavioural measures. Passive sensory processing tasks were included as a control.
Results: During the dA task both groups activated similar regions of left hemispheric prefrontal and extrastriate visual cortex. However, the AMCI group had attenuated prefrontal activation compared to the controls. Behavioural measures showed that AMCI patients had longer reaction times in the dA task.
Conclusions: We conclude that there are changes in the functional network subserving dA in patients with AMCI as reflected in the attenuation of prefrontal cortical activation and increased reaction time.
021 PHYSIOLOGICAL CORRELATES OF THE EARLY DEGENERATION OF THE LOCUS COERULEUS (LC) IN ALZHEIMER’S DISEASE (AD)
E. Szabadi, C. M. Bradshaw.E. Szabadi Psychopharmacology, Division of Psychiatry, University of Nottingham, UK
Aims: There is evidence that some brain stem nuclei, including the noradrenergic LC, are affected early in the degenerative process of AD. The LC is involved in the maintenance of arousal and regulation of autonomic functions. We examined two autonomic functions known to be controlled by the LC—carbachol evoked sweat gland activation and pupillary reflexes—in three groups of subjects: healthy young people, healthy elderly people, and elderly people suffering from mild AD.
Methods: Carbachol evoked sweating was assessed by the plastic paint impression technique and pupillary reflexes by binocular infrared television pupillometry.
Results: Carbachol evoked sweating, resting pupil diameter, and the amplitude and velocity of the pupillary darkness reflex were reduced in the patients suffering from AD, compared to the age- and sex-matched elderly subjects, whose indices of sweat gland and pupillary activities were attenuated, compared with the healthy young subjects.
Conclusions: These results indicate an age and disease related reduction in sympathetic activity, which is likely to reflect an age and disease dependent reduction in the number of LC neurones. The measurement of sweat gland activation and pupillary reflexes may provide the means for the early recognition of patients developing AD prior to the onset of cognitive symptoms.
022 KNOWLEDGE OF LIVING, NONLIVING, AND “SENSORY QUALITY” CATEGORIES IN SEMANTIC DEMENTIA
E. Carroll, P. Garrard.Institute of Cognitive Neuroscience, 17 Queen Square, London, UK
Aims: To investigate knowledge of novel “sensory quality” items and how they relate to category specific semantic impairments. Differences in performance between both category and modality of item presentation were sought.
Methods: Three patients with semantic dementia and age-matched controls were given items to name from stimulus, match to sample, and name from verbal definition. The items included 33 novel items (liquids, materials, and substances) and 64 pictures from the Snodgrass battery – both living and non-living items.
Results: Group analysis showed that patients performed worse than age-matched controls but that neither group showed any differences in performance across domains. Individual patient analyses, however, showed contrasting profiles between the three patients.
Conclusions: The significance of these results is discussed in terms of the SFT (Warrington & Shallice, 1984) and individual differences (Lambon-Ralph et al, 2003) accounts of category specificity in semantic dementia.
023 EFFICACY OF PSYCHOTROPIC AGENTS IN THE TREATMENT OF AGGRESSION AFTER ACQUIRED BRAIN INJURY
J. Freeland, A. Leonard, A. James, C. Derbyshire, M. Rogish, J. Woods, S. Shaw.John Freeland York House, The Retreat, 107 Heslington Road, York YO10 5BN, UK
Aim: The aim of this research was to assess the differential efficacy of antipsychotics, antidepressants, and anticonvulsants in treating aggression in persons with acquired brain injury.
Methods: In a retrospective research design all of the behavioural and medication records for 92 clients over an 18 month period from two post-acute neurobehavioural rehabilitation units were examined. Seventeen participants were selected who met the inclusion criteria—variation in a psychotropic medication and a threshold level of aggressive behaviours. Forty-four sets of data were examined. Non-parametric correlations were computed as a measure of efficacy.
Results: Fifty percent of the correlations were statistically significant. Seventeen of 44 cases were deemed efficacious (an increase in medication corresponding to a decrease in aggression). The highest percentage of efficacy was measured among the anticonvulsant and antidepressant medication cases with the lowest percentage of efficacy for cases using antipsychotics. Cases with positive correlations would suggest the medications had exacerbated the aggression; the preponderance of such cases were among the antipsychotics.
Conclusions: The findings support the use of antidepressant and anticonvulsant medications in the treatment of aggression in persons with acquired brain injury. They also suggest caution in the use of antipsychotic medications for the treatment of aggression.
024 CORTICAL LOCALISATION OF NEUROPSYCHOLOGICAL IMPAIRMENT IN AMYOTROPHIC LATERAL SCLEROSIS (ALS): AN [11C] FLUMAZENIL PET STUDY
P. Wicks, M. R. Turner, S. Abrahams, A. Hammers, D. J. Brooks, P. N. Leigh, L. H. Goldstein.Institute of Psychiatry, London, UK
Aims: Motor neurone disease (MND) is a neurodegenerative disorder in which some patients develop a co-morbid frontotemporal dementia; others exhibit milder cognitive deficits on tests of executive function (particularly verbal fluency) and occasionally memory. Previous activation PET and fMRI studies have identified regions of reduced cerebral blood flow associated with impaired performance on tests of verbal fluency. [11C] Flumazenil PET has previously been used in localisation of strokes and epileptic foci and has proven a sensitive measure of neuronal loss. The current study sought to identify potential neuropsychological correlates of cerebral abnormalities in ALS using [11C] Flumazenil PET.
Methods: Twelve patients fulfilling revised El Escorial criteria for probable or definite ALS underwent an extensive neuropsychological battery including tests of executive functions, memory, language, visuoperception, and measures of everyday behaviour, mood, and emotional lability. They also underwent [11C] Flumazenil PET co-registered with MRI. Statistical parametric mapping was used to identify regions where neuropsychological test scores co-varied with ligand uptake.
Results: Statistically significant correlations were found between: reduced [11C] Flumazenil binding and impaired written verbal fluency performance in the right inferior frontal gyrus; reduced confrontation naming and the left middle frontal gyrus including Broca’s area; and raised scores of emotional lability and the middle frontal gyrus and superior frontal gyrus.
Conclusions: Using this technique, [11C] Flumazenil PET can help localise brain regions associated with cognitive and behavioural measures in ALS and may have implications for our understanding of cortical neurodegeneration.
025 A CASE OF BLIND IMAGINATION?
A. Zeman, L. Torrens, S. D. Sala, R. Logie.Department of Clinical Neurosciences, University of Edinburgh, Western General Hospital, Edinburgh, UK
Aims: Clinical and neuropsychological description of a case of selective impairment of visual imagery.
Methods: Clinical report, structural neuroimaging, neuropsychology.
Results: An intelligent 65 year old man—a keen “visualiser”—reported the abrupt loss of visual imagery and visual dreaming. Neurological, ophthalmological, and formal psychiatric examination were normal. Structural MRI revealed minor white matter high intensities and borderline front-temporal atrophy. WAIS-III full-scale IQ was 136, WMS-III general memory index 128, with visual memory relatively impaired at 106 (immediate) and 112 (delayed). He scored 16/80 at floor on the vividness of visual imagery questionnaire but performed normally on the visual object and space perception battery. Executive function, semantic, autobiographical, and working memory were intact. He performed well on a range of tests thought to require visual imagery, but lacked any associated “visual” experience, prompting the term “blind imagination”.
Conclusion: Our subject provides an exceptionally pure example of a “visual imagery generation deficit”, illustrating the distinction between visual representations, which are intact, and visual imagery, which is impaired. We are using functional imaging methods to test the hypothesis that a neurological lesion has impaired his ability to use intact visual memories to drive activity in visual association cortices required to give imagery its “visual” feel. We review similar previous cases and relevant recent results from functional imaging.
026 EMPATHIC ABILITY IN ASPERGER’S SYNDROME (AS)
E. J. Lawrence, P. Shaw, A. S. David.Institute of Psychiatry, London, UK
Aims: The intention was to explore empathic ability in AS using a battery of tasks to tap both of its dimensions—affective and cognitive (or theory of mind).
Methods: Sixteen people with an ICD-10 diagnosis of AS and 16 controls were tested. Cognitive empathy was assessed using standardised measures such as first and second order theory of mind vignettes (Rowe et al, 2001). Affective empathy was measured using a novel paradigm based on diary extracts detailing emotional events.
Results: There were significant group differences between the AS and control group on the cognitive empathy tasks. However, performance on the affective empathy measures was remarkably similar between groups.
Conclusions: The widespread belief that there is a blanket empathy deficit in AS may be misguided. This study suggests that when specifically directed, people with AS may be able to experience affective empathy. Instead it seems the problem may lie in spontaneously attending to, and decoding, emotional stimuli in the environment. As Haddon’s (2003) character Christopher said when shown a picture of a sad face, “I knew that it meant “sad”, which is what I felt when I found the dead dog.”
027 A TANGLED GENIUS
P. Garrard, A. Majumdar.Peter Garrard Institute of Cognitive Neuroscience, 17 Queen Square, London, UK
Aims: To characterise the effects of Alzheimer’s disease on creative writing.
Methods: Lexical concordance and latent semantic analysis (LSA) applied to randomly selected words from a selection of novels spanning the creative career of the author and philosopher Dame Iris Murdoch (IM). Analyses provided were: (i) content to function word ratios; (ii) lexical characteristics; (iii) density of each word’s neighbourhood in semantic space; and (iv) sentence-to-sentence coherence.
Results: Lexical analyses replicated previous findings,1examined more variables, and reflected all the novels composed during IM’s late creative period, during which Alzheimer’s disease developed. The application of selected techniques of LSA to novels from this late period revealed differences between books in sentence-to-sentence coherence, and semantic neighbourhood density in two contrasting spaces.
Conclusions: Lexical analysis and LSA provide complementary, consistent, and coherent methods for analysing large text corpora. Results from the late period are compatible with the known development of progressive cognitive decline in the domain of language. The data provide some evidence for the timing of the onset of Alzheimer’s disease before untoward intellectual change was noticed.
028 ASPERGER’S SYNDROME IN ADULT LIFE
D. Tantam.University of Sheffield, Sheffield, UK
When I first came across autism, as a medical student at Stanford University, the image was of a child, curled in a ball, and unresponsive to others. I now know that this image corresponded only to the most severely affected, and often the most severely institutionalised and mentally retarded person with autism. Increasing awareness of the autistic spectrum has paralleled the increased ability of researchers and clinicians to identify the common core of the autistic impairment or impairments. Children with this common core are now known to be less rare, quite often less severely affected, and to have a better prognosis than my teachers at Stanford ever thought. Other assumptions about autism have also been tested and found not to be true, but still linger: that people with an autistic spectrum disorder cannot make friends, or that gaze avoidances is a universal feature.
However, there is one assumption that persists, untested, which is that children with an autistic spectrum disorder become adults with an autistic spectrum disorder. That this assumption is untested is surprising since, whilst every consultant in child and adolescent psychiatry or in paediatrics is likely to see a child with an autistic spectrum disorder at least every year or so, there are many consultants in general psychiatry who believe that they have no patients, and possibly have never had, a patient with this disorder. In my talk I will consider this conundrum in more detail, basing it on my own clinical practice and on a recent survey of Sheffield adults and adolescents looking for undiagnosed individuals with an autistic spectrum disorder. I shall consider the following possible explanation of the vanishing adult with autism. That:
autism does in fact remit
childhood is more stressful than adult life for people with an autistic spectrum disorder or, conversely, that adulthood is less stressful
people with an autistic spectrum disorder are negatively valued in childhood, but positively valued in adulthood
adults with autism do not benefit and have no need of psychiatric services
autistic spectrum disorder is called something else in adulthood
people with autism are barred from accessing adult services
people with autism are lost: in backrooms, in prisons, on the streets, in hostels, or as recluses
I hope that my talk will contribute to further widening the medical perspective on autistic spectrum disorder to take in the adult and not just the child.
029 THE MACHINE IN THE GHOST: SCIENCE IN SEARCH OF THE SELF
P. Broks.University of Plymouth, Plymouth, UK
How do brains create selves? Like the related problem of consciousness, the question was, until recently, largely avoided by science. Neuroscientists were inclined to view “self” as a secular cousin of “soul” – and to consider it just as illusory as the ghost in the machine. But the intellectual climate is changing. V.S. Ramachandran declares the emergence of self from brain to be the greatest scientific and philosophical riddle of all. Influential theorists such as Antonio Damasio and Joseph Le Doux contend that not only is the self a proper subject for scientific scrutiny but that neuroscience is sufficiently advanced, technically and conceptually, to start the business of charting its biological basis. They are, as it were, looking for the machine in the ghost. An alternative view is that selfhood is a sociolinguistic construct, a product of culture rather than nature, and that the search for selves in neural circuitry is futile. There may be modularised systems of perception, learning and action, but it makes no sense to imagine that their activities converge on some specialised circuitry of the self. Current discussion in neuroscience finds echoes in the old philosophical debate between “ego theorists” (as represented in the work of Descartes) and “bundle theorists” (as represented in the work of Hume). Ego theory is the intuitive, common sense position. We tend to think of ourselves as singular, conscious beings, inhabiting a particular body – the same thing, in essence, from one moment to the next, one day to the next, across a lifetime. Bundle theory, by contrast, rejects the idea that actions and experiences are owned by some inner essence, ego, or “I”. There are just sequences of actions and experiences—nothing more. Each life is a long series, or bundle, of causally related mental states and events.
The fractionations and discontinuities wrought by brain injury seem consistent with bundle theory. But the concept of the disordered self (implying the existence of some central core, or ego) has a long history in psychiatry and still endures. The interpersonal deficits of autism and the intrapersonal disorganisation of schizophrenia are often construed as pathologies of the self. The investigation of such conditions—explorations of the neural architecture of Theory of Mind in autism and of self-monitoring in schizophrenia—may yet show “the self” to be a viable neurobiological construct. But, arguably, rather than opening up new territories for research, the construct of self sets tantalizing limits to the reach of neuroscience. In the words of the critic, Arnold Weinstein, neurology itself can be understood as the war between “I” and “It,” between “Self” and “Soma”. Objective, scientific, observation can only ever give a partial account of the battle. Some features of self will always be more clearly viewed through the subjective lens of literature and the arts.
030 WHEN YOU CAN’T KISS IT BETTER
C. Moore. Journalist and Author, UK
Every parent assumes that an important part of their role is to provide their children with comfort and solace for both physical and emotional ailments. But what happens when a child rejects or ignores the proffered comfort? What happens when the child seems detached, operating on a different emotional plane? What happens, in short, if the child is autistic?
It’s widely known, I hope, that autism covers the entire IQ range. It is more useful to see it as a social handicap than an intellectual one. In a neurotypical child, the imitative bonding with the parent that forms the basis of future social and therefore moral behaviour begins at birth. The child is immediately responsive to the adult’s overtures—emotionally, they talk the same language. The child quickly learns to turn to its parent for entertainment, comfort, and companionship. In an autistic child, this reciprocity is deficient or absent.
It was once believed that autists were cold and robotic. This isn’t so. Both my sons have strong emotions; they form attachments to people; they are not truly ‘aloof’. But they do so on their own terms. Their emotional responses are unpredictable, and their lack of “theory of mind” means they have little empathy with the joys or sorrows of others.
The difference is clear when they watch Disney films. The Disney corporation churns out stories to a failsafe recipe. Disney knows how to provoke tears, fears, and laughter in people the world over. George and Sam love Disney, but they are immune to the emotional string-pulling. They respond intensely to the colours, movements, and sounds, even to some of the characters, but they watch Dumbo’s separation from his mother or Pinocchio’s reunion with Gepetto with calm indifference.
With children like these, does it make sense to talk about “good” or “bad” behaviour? Is it possible to teach them the social and emotional responses that are innate in my youngest, nonautistic son Jake? In my talk I will discuss these issues, and the re-evaluation of what parental love means that takes place when one’s children are autistic.
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