Non-adherence with antidepressant treatment is very common. Increasing adherence to pharmacological treatment may affect response rate.

To review and summarise quantitative evidence on factors associated with adherence and of adherence-enhancing interventions.

A systematic review of computerised databases was carried out to identify quantitative studies of adherence in depression. Papers retained addressed unipolar depression and considered adherence as the primary end-point.

Of studies published between 1973 and 1999, 32 met the review criteria: epidemiological descriptive studies (n=14): non-random comparisons of control and intervention groups (n=3); randomised interventions (n=14); and meta-analysis (n=1). Patient education and medication clinics were the interventions most commonly tested, combined with a variety of other interventions.

The studies did not give consistent indications of which interventions may be effective. Carefully designed clinical trials are needed to clarify the effect of single and combined interventions.

Proposals by the UK Government for preventive detention of people with ‘dangerous severe personality disorders' highlight the unresolved issue of whether personality disorders should be regarded as mental illnesses.

To clarify the issue by examining the concepts of psychopathy and personality disorder, the attitudes of contemporary British psychiatrists to personality disorders, and the meaning of the terms ‘mental illness'and ‘mental disorder’.

The literature on personality disorder is assessed in the context of four contrasting concepts of illness or disease.

Whichever of the four concepts or definitions is chosen, it is impossible to conclude with confidence that personality disorders are, or are not, mental illnesses; there are ambiguities in the definitions and basic information about personality disorders is lacking.

The historical reasons for regarding personality disorders as fundamentally different from mental illnesses are being undermined by both clinical and genetic evidence. Effective treatments for personality disorders would probably have a decisive influence on psychiatrists' attitudes.

Old age psychiatry is no less subject to increasing legal and quasi-legal restraint than other branches of the profession, but the emphases are different. Two themes predominate: first, that of capacity or competence; and second, to what extent formal legal measures should be implemented in cases where incapacitated patients do not dissent from, as opposed to giving active consent to, admission to hospital or receiving treatment.

To discuss the issues of capacity or competence, especially in relation to recent legislation and judgements and to proposed legislation in England and Wales.

Selective review and discussion of recent case law and current and proposed statute law.

The Bournewood case threatened but ultimately failed to upset the status quo. However, the European Convention on Human Rights and the British Human Rights Act 1998 may yet do so.

The high support needs of elderly people with cognitive disability raise questions about the cost-effectiveness of different treatments. Associations between costs and cognitive disability could be influenced by other factors, particularly comorbidities.

To examine the links between costs and cognitive disability in the context of covariates.

Secondary analyses of data from the UK Office of Population Censuses and Surveys disability surveys for over 4500 elderly people living in households were used to examine associations between cost and cognitive disability.

Costs varied considerably, and were associated with severity of disability along a number of dimensions. The cost-raising effects of cognitive disability were smaller when the analyses controlled for levels of disability in other domains.

Cognitive disability is significantly associated with higher costs, but these analyses highlight the need to examine a range of disabilities.

Community-based care at the margin is a substitute for institutional care. Three factors are considered critical: definitions of eligibility, assessment procedures and balance of care.

To examine determinants of the margin between institutional and home-based care, review current practice, identify the implications and contribute to planning of integrated long-term care services.

A selective review was made of findings from research conducted after the community care reforms.

Marked variability and inconsistency in eligibility and assessment processes may contribute to misplacement of frail older people. There remains capacity to shift the balance of care from institutional to home-based care within reasonable cost parameters, particularly with more integrated services.

Greater standardisation of approaches to the determination of eligibility for social care and to assessment of need is required. Providing care at home for some of those currently entering care homes is feasible, but will require different service structures and staff roles, including specialist clinicians.

Patients with Alzheimer's disease show a wide variation in clinical phenotype. Genetic research has been largely concerned with the role of mutations or common variants as risk factors for the disease. Do genetic factors also influence clinical phenotype?

To examine the evidence that genetic factors influence the clinical expression of the disease in addition to influencing risk.

A selective review was made of the key literature.

Mutations in three genes, coding for amyloid precursor protein, presenilin-1 and presenilin-2, and a common variation (ε4) in another gene, APOE, have been shown to lead to an earlier development of the disease. More recently, genetic association and twin studies have suggested a role for genetic factors in the development of other aspects of clinical phenotype, notably the appearance of non-cognitive symptoms.

In Alzheimer's disease genetic variation influences a number of aspects of clinical phenotype.

Alzheimer's disease management involves symptomatic drug treatments passed by the National Institute for Clinical Excellence. Disease modification is now the goal.

To review current and developmental drugs for Alzheimer's disease, their usage, and the clinical context of known facts and proposed specific models.

A brief evidence-based review was made, using literature where available, or evidence from consensus groups where it was absent.

There is good evidence to support the use of cholinesterase inhibitors, and perhaps vitamin E. Oestrogen and anti-inflammatory agents show possibility, but there is not enough evidence to support routine use.

Symptomatic treatments exist for Alzheimer's disease. Observational studies and increasing knowledge of brain biology are leading towards further treatment options. Old age psychiatrists have valuable treatments they now have to learn to use.

Frontotemporal dementia accounts for up to 20% of cases of dementia in the presenium, yet remains poorly recognised. Diagnostic criteria have been devised to aid clinical diagnosis.

To provide an overview of clinical and pathological characteristics of frontotemporal dementia and its nosological status.

The review summarises consensus diagnostic criteria for frontotemporal dementia and draws on the authors'clinical experience of 300 frontotemporal dementia cases, and pathological experience of 50 autopsied cases.

Frontotemporal dementia is characterised by pronounced changes in affect and personal and social conduct. Some patients also develop motor neuron disease. Mutations in the tau gene account for some but not all familial cases of frontotemporal dementia.

Frontotemporal dementia is a focal form of dementia, which is clinically and pathologically distinct from other dementias. It represents an important model for understanding the functions of the frontotemporal lobes.

Dementia with Lewy bodies (DLB) is a common dementia subtype that has only been recognised in the past decade and that remains widely underdiagnosed.

To review the pathological and clinical features of DLB, to consider methods of investigation and diagnosis, and to recommend safe and effective management strategies.

A selective review was made of the key literature.

Using operationalised criteria, DLB can be clinically diagnosed with an accuracy similar to that achieved for Alzheimer's disease or Parkinson's disease. Underdetection is largely due to poor definition of the criterion of cognitive fluctuation. Ancillary investigations, particularly neuroimaging, can aid in differential diagnosis. Extreme caution in the use of neuroleptic medication is advised. Cholinesterase inhibitors may be particularly effective in DLB.

Clinicians should be aware of DLB as part of a spectrum of Lewy body disorders. Neuroleptic sensitivity reactions and good response to cholinergic therapies are important aspects of management.

Drawing a distinction between cortical and subcortical dementias seems both useful and justified. Recent research has, however, cast doubt on the clinical, neuropsychological, neuroimaging and neuroanatomical basis of the distinction.

To arrive at a reasoned conclusion about the relationship between the two types of dementia and the validity of distinguishing between them.

The historical and recent clinical and scientific literature on subcortical dementia was reviewed.

The traditional claim that subcortical dementia has distinct clinical manifestations, neuroimaging findings and a neuropathological profile is not altogether borne out by the literature. Some studies show that frontal executive dysfunction and the profile of memory deficits are not significantly different from those seen in Alzheimer's disease. Neuropathological findings also overlap.

The category of subcortical dementia may be clinically useful in highlighting the likelihood that an individual with dementia is more likely to suffer from bradyphrenia and motor difficulties. As neuroscience advances a preoccupation with the distinction may hinder the assessment and treatment of individual cases.

The concept of vascular dementia has a long history but its usefulness as a diagnostic category has been called into question.

To evaluate vascular disease as a risk factor for dementia and the interface between cerebrovascular pathology and Alzheimer's disease.

The literature on this topic was selectively reviewed and synthesised.

Risk factors for cerebrovascular disease are also risk factors for dementia. However, the course of dementia, once it has developed, appears to be frequently determined by Alzheimer's disease.

As a public health measure, modification of vascular risk represents a potentially powerful means to prevent dementia through delaying its onset. However, an effect on progression of dementia, once it has developed, has yet to be established. The traditional view of vascular dementia and Alzheimer's disease as distinguishable conditions is becoming steadily less tenable.

Growing evidence suggests that there may be a subtype of depression arising in later life that is characterised by a distinct clinical presentation and an association with cerebrovascular disease. This has been termed ‘vascular depression’.

To review the evidence for associations between cardiovascular disease and depression and between cerebrovascular disease and depression, and to examine implications for clinical practice and research.

The authors reviewed the medical literature covering the past 5 years.

There is strong evidence for an association between cardiovascular disease and depression, but this is not confined to older people. The causal pathway may be bi-directional. There is also a convergence of evidence suggesting a causal link between cerebrovascular disease and depression, especially that occurring later in life. The major focus has been on neuroradiological findings thought to be due to vascular disease, although the pathology may be heterogeneous.

Although there are gaps in the evidence there is strong support for the concept of vascular depression, characterised by reduced depression ideation, subcortical neurological dysfunction, apathy and psychomotor change. This has implications for both treatment and prevention.

There is a vast array of scales available to assess all aspects of mental and physical health in older people which may be of relevance to the work of old age psychiatrists.

To summarise some of the scales that may be commonly used in clinical and research practice and to give the reader guidelines as to where further information can be obtained.

The scales were selected on the basis of the authors' own clinical and research knowledge and information was gathered from a comprehensive text on assessment scales in old age psychiatry.

The selected scales are described in brief and a table outlines the purposes for which they are most suitable.

Although many scales are available, the choice of the individual scale relies specifically on the question that is to be asked. The ideal scale does not exist.

Social adversity may be a risk factor for depression, by increasing Cortisol secretion, which impairs serotonin (5-HT) neurotransmission.

To examine this causal pathway in a community setting.

Women who were currently ICD–10 depressed (n=94), vulnerable to depression but not depressed (n=166) and non-vulnerable controls (n=177) were recruited. We assessed social adversity and vulnerability (Life Eventsand Difficulties Schedule; Self Evaluation and Social Support Scales) and psychiatric state (Schedules for Clinical Assessment in Neuropsychiatry). Salivary cortisol concentrations were measured at 09.00 and 23.00 h. Serotonin function was assessed using prolactin responses to dexfenfluramine.

Cortisol concentrations were not increased in the depressed or vulnerable. Morning salivary and serum cortisol were reduced in depression. Evening cortisol was increased after recent life events. Life events and depression were associated with increased prolactin responses.

The hypothalamic–pituitary–adrenal axis is sensitive to social stress but does not mediate vulnerability to depression. Exaggerated 5-HT2 receptor responsiveness to stress may play a role in the evolution of depression.