BIG HEALTH PROBLEM The prevalence of dementia is expected to increase dramatically in future years as life expectancy continues to increase
In alert subject
The cumulative incidence of Alzheimer&apos;s disease has been estimated to be as high as 4.7 percent by age 70, 18.2 percent by age 80 and 49.6 percent by age 90.1
AD accounts for 60% of all dementias. Many causes are treatable and can be reversed
Progressive deterioration of intellect,
behavior and personality as a
consequence of diffuse disease of the
brain hemispheres, maximally affecting
the cerebral cortex and hippocampus.
Dementia is a symptom of disease
rather than a single disease entity!!!
• Memory must be impaired to make the diagnosis of
• Loss of memory for recent events is the earlist
feature of dementia.
• Subsequent symptoms include abnormal behavior,
loss of intellect, mood changes, and difficulty
coping with ordinary routes.
• Insight may be retained initially, but is then
• Ultimately, there is loss of self-care, wandering,
incontinence, and often paranoia.
Dementia has to be distinguished from
delirium which is an acute disturbance of
cerebral function with impaired conscious
level, hallucinations and autonomic
overactivity as a consequence of toxic,
metabolic or infective conditions.
Depression can mimic the initial phases of
dementia and it is termed
’pseudodementia’ (which is amenable to
Dementia may occur at any age but is more
common in the elderly, accounting for 40% of
long-term psychiatric in-patients over the age of
The prevalence in persons aged between 50 and
70 years is about 1% and in those approaching 90
years reaches 50%.
An annual incidence rate is 190/100 000 persons.
The rate of progression depends upon
the underlying cause.
The duration of history helps establish the cause of
dementia: Alzheimer‘s disease is slowly progressive over
years, whereas encephalitis may be rapid over weeks.
Dementia due to cerebrovascular disease appears to occur
’stroke by stroke‘.
Dementias – classification
Based on cause
• Alzheimer‘s disease (~60% of all dementias)
• Cerebrovascular (multiinfarct state,
subcortical small vessel, amyloid
• Neurodegenerative (DLB, Pick‘s disease, Huntington‘s
chorea, Parkinson‘s disease)
• Infectious (Creutzfeld-Jakob disease, HIV infection,
progressive multifocal leucoencephalopathy)
• Normal pressure hydrocephalus TREATABLE!
• Nutritional (thiamine deficiency in alcoholics!, B12 deficiency,
• Metabolic (hepatic disease, thyroid d., parathyroid d.,
• Chronic inflammatory (MS, …)
• Trauma (head injury, ’Punch drunk‘ syndrome)
• Tumour (e.g. subfrontal meningioma)
Dementias – history and
• When obtaining a history from a demented
person and relative, establish: rate of intellectual
decline, impairment of social function, general
health and relevant disorders (e.g. stroke, head
injury), nutrition status, drug history, family
history of dementia.
• Tests to assess intellectual function are
designed to check: memory, abstract thought,
judgement, specific focal cortical functions.
The Mini Mental State Examination (MMSE)
• On neurological examination note: focal signs,
involuntary movements, pseudobulbar signs, gait
Dementias – further
• Blood tests (to exclude hypothyroidism, vitamin
B12, thiamine and folate deficiency, Lyme disease,
HIV infection, metabolic disorders and
• Cranial imaging (CT or/and MRI) (tu, NPH)
• PET and SPECT?
• EEG (slowing in AD, normal in pseudodementia,
periodic complexes in CJD)
• Genetic testing (rarely – Huntington mutation,
apolipoprotein E4 mutation in AD)
• Brain biopsy (if treatable cause is suspected)
• The commonest cause of dementia.
• The disorder rarely occurs under the age
of 45 years.
• The incidence increases with age.
• The cause of AD is not known (neurodegenerative d.).
• Up to 30% of cases are familial (the loci
were found on chromosome 21 and 19).
• Pathology – the presence of senile plaques and
neurofibrillary tangles in the brain.
• Diagnosis of AD may be established during
life by early memory failure, slow
progression and exclusion of other causes.
• CT scanning aids diagnosis by excluding
multiple infarction or a mass lesion.
• MRI shows bilateral temporal lobe atrophy.
• SPECT usually shows temporoparietal
Alzheimer's disease -
- Acetylcholinesterase inhibitors (Donepezil [Aricept],
Rivastigmine [Exelon], Galantamine [Reminyl]) have
been shown to enhance cognitive performance in early
disease. Memantine [Ebixa, Axura, Namenda] is
approved for moderate disease. However they do not
- Treat concurrent depression, anxiety and sleep
disorders. Neuroleptic use may be required for
- Mangement of AD requires careful advice and
counseling of the patient and family and shared care
involving the family, caregivers, GPs, hospital specialist,
and community psychiatric services.
- Long-term residential care is ofte required.
Multi-infarct dementia (MID)
• This is an overdiagnosed condition which accounts for less than
10% of cases of dementia.
• MID is caused by multiple strokes - SILENT STROKES
• Dementia occurs ’stroke by stroke‘, with progressive focal loss
• Clinical features of stroke profile – hypertension, diabetes, etc.
– are present. More often in males.
• Diagnosis is obtained from the history
and confirmed by CT or MRI scan
(the presence of multiple areas of
• Treatment: Maintain adequate blood
pressure control, anti-platelet
• This progressive condition accounts for 5% of all dementias.
• Usually sporadic, it more commonly affect women between
40 and 60 years.
• Personality and behaviour are initially more affected than
• Frontal lobe dysfunction predominates with apathy, lack of
initiative and personality changes.
• CT or MRI scans show frontal (and/or temporal) atrophy,
• SPECT reveal anterior hypoperfusion, EEG is usually normal.
• The disorder is characterized pathologically by argyrophylic
inclusion bodies within the cytoplasm of cells of the
• There is no treatment, death occuring within 2-3 years of
Primary progressive aphasia
• This condition is one of a group of disorders
characterized by asymmetrical cortical
• Dominant hemisphere perisylvian atrophy is
associated with loss of language, which, after
many years, becomes a more widespread dementia.
• Pathologically non-specific cell loss, Pick’s
pathology or spongiform changes are described.
• MRI and SPECT confirm focal changes.
Dementia with Lewy bodies (DLB)
• One of the most common types of progressive dementia.
• Progressive cognitive decline, combined with three additional
defining features: (1) pronounced “fluctuations” in alertness
and attention; (2) recurrent visual hallucinations, and (3)
parkinsonian motor symptoms, such as rigidity and the loss
of spontaneous movement.
• The symptoms of DLB are caused by the build-up of Lewy
bodies – accumulated bits of alpha-synuclein protein - inside
the nuclei of neurons in areas of the brain that control
particular aspects of memory and motor control. Lewy bodies
are often also found in the brains of people with Parkinson's
and Alzheimer’s diseases.These findings suggest that either
DLB is related to these other causes of dementia or that an
individual can have both diseases at the same time.
• DLB usually occurs sporadically, in people with no known
family history of the disease. However, rare familial cases
have occasionally been reported.
Normal pressure hydrocephalus
= term applied to the triad of:
2. Gait disturbance
3. Urinary incontinence
occuring in conjunction with hydrocephalus and normal CSF
- NPH with a preceding cause (SAH, meningitis,
- NPH with no known preceding cause – idiopathic
Normal pressure hydrocephalus
Aetiology is unclear.
It is presumed that at some preceding period, impedence to
normal SCF flow causes raised intraventricular pressure and
ventricular dilatation. Compensatory mechanisms permit a
reduction in CSF pressure yet the ventricular dilatation persists
and causes symptoms.
Normal pressure hydrocephalus
Diagnosis is based on clinical picture plus CT scan/MRI evidence of
NPH must be differentiated from pts whose ventricular enlargement is
merely the result of shrinkage of the surrounding brain, e.g. AD. These
pts do not respond to CSF shunting, whereas a proportion of NPH pts
(but not all) show a definitive improvement with ventriculo-peritoneal
AIDS dementia complex
• Approximately two-thirds of persons with AIDS
develop dementia, mostly due to AIDS dementia
• In some patients HIV is found in the CNS at
postmortem. In others an immune mechanism or an
unidentified pathogen is blamed.
• Dementia is initially of a "subcortical " type.
• CT - atrophy; MRI - increased T2 signal from
• Treatment with Zidovudine (AZT) halts and
partially revers neuropsychological deficit.
• Reduction of intellectual function is common after
severe head injury.
• Chronic subdural haematoma can also present as
progressive dementia, especially in the elderly.
• Punch-drunk encephalopathy (dementia pugilistica)
is the cumulative result of repeated cerebral
trauma. It occurs in both amateur and professional
boxers and it manifests by dysarthria, ataxia and
expy signs associated with ’subcortical‘ dementia.
There is no treatment for this progressive
• Dementia rarely may be due to intracranial
tumour, especially when tumours occur in certain
• Mental or behavioral changes occur in 50-70% of
all brain tumours as distinct from dementia which
is associated with frontal lobe tumours, III
ventricle tumours and corpus callosum tumours.
• Cognitive impairment also occurs as a non
metastatic complication of systemic malignancy.
Mild cognitive impairment (MCI)
• MCI is a relatively recent term, used to describe
people who have some problems with their
memory but do not actually have dementia.
• Some people (80%?) will be in the early stages of
Alzheimer’s disease or another dementia. Others,
however, will have MCI as a result of stress,
anxiety, depression, physical illness or just an ‘off
• It is estimated that 15% of the population may
be experiencing MCI.
• Currently extensive research on MCI is ongoing.
• At the moment there is not enough evidence to
recommend any specific treatments.