Dementia. Dementia. 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!!!.
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!!!
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 antidepressant medication).
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 65 years.
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‘.
The Mini Mental State Examination (MMSE)
- 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 cure!
= term applied to the triad of:
occuring in conjunction with hydrocephalus and normal CSF pressure.
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.
Diagnosis is based on clinical picture plus CT scan/MRI evidence of ventricular enlargement.
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 shunting.