Overview of Dementia
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Dementia
Importance:
This is the single most important illness in old age not just because it is increasing in numbers due to the increasing number of old people, but because it is a devastating and currently terminal illness which affects not just the person suffering from it, but also carers and puts a great burden on society and services.
Definition:
The progressive, irreversible, impairment of higher cortical functions including memory, and other cognitive functions with other psychiatric symptoms, a change in personality and the loss of functional skills and in the absence of clouding of consciousness.
Epidemiology:
The prevalence rate for dementia (all types) doubles every 5.1 years age. With Alzheimers rising more steeply (doubling every 4.5 years) than vascular dementia (every 5.3 years). Vascular dementia prevalence varies because there is no clear definition of diagnostic criteria and it varies between different countries. Age stratified dementia rates are as follows:
60-64: 0.7
65-69: 1.4
70-74: 2.8
75-79: 5.6
80-84: 11.1
85-89: 23.6
90-94: 33.0
95-99: 44.8
Types of Dementia:
Another classification of dementias involves the neuropsychological picture and substrate involved, e.g. cortical (Alzheimers), subcortical (e.g. vascular or Lewy body) or focal (e.g. fronto-temporal)
ALZHEIMERS DISEASE (AD)
Epidemiology:
Age stratified prevalence rates: (first figure for males, second for females)
60-64: 0.6-0.7
70-74: 1.5-2.3
75-79: 1.8-4.3
80-84: 6.3-8.4
85-89: 8.8-14.2
90-94: 17.6-23.6
The incidence of AD is 0.5% per year up to 75 then increasing to 3% up to 90.
Aetiology:
One of the great scientific endeavours of the last 20 years. Not clearly known but a mixture of genetic and environmental, with the former predominating the earlier the age of onset.
Pathology
The pathological changes are plaques (with a core of beta-amyloid protein) and tangles (hyper-phosphorylated paired helical filaments). How they arise, and what is a cause and what is an effect is still open to debate though current opinion favours defective amyloid / defective processing as a cause with accumulation of an abnormal fraction starting cell death and inflammation. What results is a profound loss of acetylcholine producing cells in the hippocampus initially which then spreads to involve the cortex and then sub-cortical structures. Plaques and tangles can appear without dementia and it is now known that co-existent ischaemic changes in the brain show up clinical changes earlier.
Risk factors
Age is the greatest single risk factor. Genetic factors include excess Chromosome 21 (Downs), and mutations on chromosome 21 (amyloid gene), Chromosome 14 and 1 (presenilin genes). Other risk factors are head injury, cardiovascular risk factors including high cholesterol and being ApOE4 homozygous.
Clinical features:
The progression has been likened to reverse childhood development. It starts gradually and proceeds steadily and slowly, though it may seem to appear and progress quickly because of situational factors (e.g. superimposed medical problem, new situation, death of protective spouse). Progression is steady and death occurs within 10-12 years of earliest signs (though recognition may be quite late).
COGNITIVE DIFFICULTIES
Amnesia: initially failure to learn new information and to retrieve from store. Later memory loss (STM>LTM) leading to repetition of speech, loss of everyday objects, etc. Confabulation may be present as LTM is used to patch up STM holes. In later phases LTM becomes impaired as well. Disorientation is an early sign, first to time then to place.
aphasia: Dysphasia is common. Nominal aphasia (the loss of naming ability) is an early sign (complex words > simple words) with archaic substitutions sometimes being present. Receptive aphasia the inability to understand speech.
Apraxia: the inability to perform co-ordinated learnt motor tasks (e.g. writing, dressing) is a task of the dominant parietal lobe. It may lead to a variety of day-to day difficulties such as initially complex matters (like setting the video) and later to simple tasks (such as eating with a knife or fork).
Agnosia: the inability to recognise peripheral sensory stimuli e.g. prosopagnoisa (inability to recognise faces), visual agnosia (inability to recognise fire), olfactory agnosia (ignoring smell of gas), etc.
PSYCHIATRIC DIFFICULTIES
Mood changes: depression (63% have at least one symptom) to mania (4%)- associated with slower cognitive impairment.
Delusions: (in 16-37% of all patients) of theft, suspicions are isolated and transient compared to functional illnesses.
Perceptual disorders: visual (13%) and auditory (10%) hallucinations -if present this is associated with a faster cognitive decline. Misidentifications may occur in later stages: e.g. inability to recognise reflection, mistaking TV or pictures for real people, imagining people in the house, mistaking people for others. Visual hallucinations may be present as a result of secondary delirium (acute confusional state).
PERSONALITY AND BEHAVIOURAL CHANGES
Personality changes : people change depending on premorbid personality traits, with a reaction to illness initially with some disinhibition when frontal lobes involved.
Disturbance in sleep/wake cycle: this is due to a disorder rather than just disorientation. People sleep during day and wake up at night.
Behavioural changes: reduced decisiveness, initiative, drive, social skills, emotional control (catastrophic reactions to difficulties) leading to irritability, screaming, aggression swearing) .
Functional abilities: reduction in ability to do every day tasks such as cooking, house work, self care, managing money, driving, etc.
OTHER