Old age psychiatry I

Old age psychiatry I



Dementia


The prevalence of dementia rises sharply in old age, with 5% of people over 65 years and 20% of people over 80 years being affected. The commonest causes of dementia in old age in the UK are Alzheimer’s disease (up to 65% of cases), vascular dementia (up to 20%) and Lewy body disease (up to 10%). Alzheimer’s disease is also the commonest form of presenile dementia (dementia presenting before the age of 65), but is usually managed by old age psychiatrists whatever the age of presentation. Pick’s disease is included in this section for the same reason, even though the majority of cases present before the age of 65. Other causes of presenile dementia are described on pages 70–71.



Alzheimer’s disease



Epidemiology and aetiology


Women develop Alzheimer’s disease slightly more often than men. There is a strong genetic component with the risk being three times higher in people with an affected first-degree relative. In the early onset form, there is sometimes an autosomal dominant pattern of inheritance. Abnormalities of the amyloid precursor gene on chromosome 21 have been established in some pedigrees which is not surprising for two reasons – amyloid peptide is found in senile plaques and Alzheimer’s disease develops in up to 50% of patients with Down’s syndrome who survive beyond the age of 40 years. Linkage with a site on chromosome 14 has also been established in other early onset cases and loci on other chromosomes are almost certainly involved. In contrast, late-onset Alzheimer’s disease is familial but does not show a Mendelian pattern of inheritance, which suggests a polygenic aetiology, perhaps in combination with environmental factors. Association with a number of genes has been demonstrated, one example being the E4 allele of apolipoprotein E on chromosome 19 which is found in up to 50% of cases of Alzheimer’s disease but in only 10% of the general population.



Pathology


The characteristic pathology of Alzheimer’s disease consists of progressive atrophy of cortical and subcortical structures. Histologically, there are neurofibrillary tangles and amyloid containing senile plaques throughout the brain. While many neurotransmitters are affected, there is widespread loss of neurones containing acetylcholine which correlates well with the degree of cognitive impairment observed clinically. Both neurofibrillary tangles and senile plaques occur in normal ageing but are more numerous and widespread in Alzheimer’s disease.



Presenting features


In many ways, Alzheimer’s disease is a diagnosis of exclusion, being made when features of other causes of dementia are not present. Any combination of the features of dementia described on page 70 may occur, but many cases present with a characteristic clinical picture which includes:


• poor memory

• disorientation as an early sign which can lead to perplexity, fear and wandering as the illness progresses

• ‘coarsening’ of premorbid personality traits, e.g. a person who has always been stuck in their ways may become much more rigid and inflexible

• gradual deterioration of social skills and behaviour

• non-specific mood changes: depressed, euphoric, flattened or labile

• frontal and parietal lobe signs.


Pick’s disease


Recent claims that Pick’s disease is the cause of up to 20% of cases of presenile dementia are probably exaggerated but it is certainly an important cause of dementia in younger people. It usually presents between the ages of 50 and 60 years. In the small number of cases with a family history, the inheritance appears to be autosomal dominant but in most cases there is no identifiable cause. The characteristic pathology is of cortical atrophy, known as knifeblade atrophy because of the appearance of the atrophic gyri. Within the atrophic areas are silver staining intracellular inclusions known as Pick bodies and swollen neurones known as Pick cells. This atrophy is usually confined to the frontal and temporal lobes and as a result, the clinical picture in the early stages is often dominated by apathy, disinhibition and other changes in personality and social behaviour, with abnormalities of speech developing as the disease progresses.

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Jul 12, 2016 | Posted by in PSYCHIATRY | Comments Off on Old age psychiatry I

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