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DEMENTIAS Dr SADIK AL-Ghazzawi MRCP, FRCP

DEMENTIAS Dr SADIK AL-Ghazzawi MRCP, FRCP. DEMENTIAS Dementia: -

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DEMENTIAS Dr SADIK AL-Ghazzawi MRCP, FRCP

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  1. DEMENTIAS Dr SADIK AL-Ghazzawi MRCP, FRCP

  2. DEMENTIAS • Dementia:- Progressive deterioration of, 1- intellect, 2- behavior, 3 -personality as a consequence of diffuse disease of the cerebral Hemispheres , maximally affecting the cerebral cortex and hippocampus. Distinguish from ,

  3. delirium:- which is an acute disturbance of cerebral function with impaired conscious level ,hallucinations autonomic over activity as a consequence of toxic, metabolic or infective conditions.

  4. . **Dementia is a symptoms of a disease rather than a single disease entity. Note, When occurring under the age of 65 years it is labeled presenile dementia

  5. Clinical course 1-The rate of progression depends upon the underlying cause. 2-The duration of history helps establish the cause of dementia, e.g. Alzheimer disease is slowly progressive over years, whereas encephalitis may be rapid over weeks.

  6. 3-Dementia due to cerebrovascular disease appears to occur (stroke by stroke) (multi-infarct syndrom). 4-All dementias show a tendency to be accelerated by change in 1-environment, 2- intercurrent infection or 3- surgical procedure.

  7. Development of symptoms Introspective 1-Unsure of self-------------- 2-Difficulty in coping with work and ordinary routine (retained insight)---

  8. 3-Loss of insight,---------- behavioural changes,--------- loss of inhibition.---------- 4-long-term care.----------------------------- Cannot be left unattended.--------------- Mutism, incontinence and------------------------ --- death.

  9. Note:- This initial phase of dementia may be inseparable from the pseudo-dementia of depressive illness DD.

  10. Intellectual function decline • Acute (weeks) (encephalitis) • Sub-acute (months) (Creutzfeldt-Jakob disease, Normal Pressure hydrocephalus) • Chronic (years) (C.J disease ,N.P hydrocephalus, • ,Alzheimer

  11. Classification Based on cause • Alzheimer • Cerebrovascular(multi-infarct dementia, subcortical vascular disease (Branswanger disease)

  12. Neurodegenerative (Pick disease ,Huntington chorea ,Parkinson disease). • Infectious (Creutfeldt- Jakob disease, HIV • infection, Viral encephalitis, • Multifocal leucoencephalitis • Normal pressure hydrocephalus

  13. Nutritional (Wernicke Korsakoff PSYCHOSIS ( Thiamin B1), B12 deficiency , Folate deficiency) • Metabolic • (Hepatic disease, Thyroid disease ,Parathyroid disease, Cushing syndrome)

  14. Chronic inflammatory (Collagen vascular disease and vasculitis ,Multiple sclerosis) • Trauma (Head injury ,Punch drunk syndrome

  15. Tumors (Sub frontal meningioma • Note-1-:- Alzhiemer disease accounts for 60%of all dementias, CVD 20%. Note-2-, It is important to investigate all patients with dementia as many causes are treatable, in practice 10-15% can be reversed.

  16. CLASSIFICATION OF DEMENTIA Based on site, Subdividing dementia depending upon the site of predominant clinical involvement is of questionable diagnostic value. 1-Anterior (frontal pre-motor cortex):- Behavioural changes/loss of inhibition, antisocial behaviour, and irresponsible (normal pressure hydrocephalus, Huntington chorea, Metabolic disease).

  17. 2-Posterior (parietal and temporal lobes):- Disturbance of cognitive function (memory and language) without marked changes in behavior ,(Alzheimer disease)

  18. 3-Sub-cortical Apathetic, forgetful and slow, poor ability to use knowledge ,associated with other neurological signs and movement disorder e.g. (Parkinson Disease ,AIDS dementia complex)

  19. 4-Cortical Higher cortical abnormalities i.e. dysphasia, apraxia, agnosia e.g. Alzheimer disease

  20. History and clinical examination *When obtaining a history from demented person and relative, establish :; • rate of intellectual decline • Impairment of social function

  21. General health and relevant disorders , e.g. stroke,head injury. • Nutritional status • Drug history • Family history of dementia

  22. Tests to assess intellectual are designed to check: 1-Memory 2-Abstract thought 3-Judgment 4-Specific higher cortical functions

  23. A simple bedside battery of tests includes: -Age -Place of birth -Months backwards -Date of birth -Interpretation of proverbs -School -Following three stage commands -Date -Read and obey instructions -Time of day -Name objects -Season of year -Copy design -Serial 7s

  24. On neurological examination note:- -Focal signs. -Involuntary movements . -Pseudobulbar palsy. -Primitive reflexes:- 1-Pout reflex( Tap lips tendon hammer-a* pout response is observed).

  25. 2-Glabellar reflex. 3-Grasp reflex (Stoking palm of hand, induces *grasp.

  26. Note Primitive reflexes are present in:- 1-infancy 2-aged 3-dementia

  27. Alzheimer’s disease • This is the commonest cause of dementia with an estimated half million sufferers in the UK • The disorder rarely occurs under the age of 45 years. • The incidence increases with age. • Up to 30% of cases are familial.

  28. Pathology;- 1-Neuritic plaque, a complex extra cellular lesion which is aggregates of filaments with central core of amyloid ,found in hippocampus and parietal lobe .

  29. 2-The lesions associated with neuronal loss and granulovascular degeneration. 3-The brain is small with atrophy most evident in the superior and middle temporal gyri .

  30. Neurofibrillary tangle, An intracellular lesion ,a paired helical strand of protein close to nuclei of neurons ,mainly affecting pyramidal cells of cortex.

  31. Diagnosis May be established during life by;- A-the early memory failure. B-slow progression . C-excluding other causes.

  32. D-Recent claims that B amyloid deposition also occurs in skin and intestine raises, Hopes of biopsy as a diagnostic marker. E-CT scanning: aids diagnosis by excluding multiple infarction or a mass lesion.

  33. Treatment *No effective treatment exists *Transmitter augmentation therapy seems unlikely to be effective in view of the Many neurotransmitters involved.

  34. Multi-infarct dementia 1-This is an over diagnosed condition which accounts for less than 10% of cases of dementia. 2-dementia occurs" stroke by stroke", with progressive focal loss of function.

  35. Pick's disease 1-This progressive condition accounts for 5% of all dementia. 2-usually sporadic ,it is more commonly affects women between 40-60years. 3-frontal lobe dysfunction predominate with apathy , lack of initiative and personality changes.

  36. 4-CT scan shows frontal atrophy. 5-blood flow study (SPECT(HMPAO)) reveal anterior hypo perfusion. 6-the disorder is characterized pathologically by argyrophilic inclusion bodies Within the cytoplasm of cells . 7-there is no treatment, death occurring within 2-3 years of the onset.

  37. AIDS dementia complex • Approximately 2/3 of persons with AIDS develop dementia, mostly due to AIDS dementia complex. • In some patients HIV is found in the CNS at postmortem. • In others an immune mechanism .

  38. Dementia is initially of a “sub-cortical” type. • CT shows atrophy ,MRI shows increased T2 signal from white matter. • Imaging excludes other infections and neoplastic causes of intellectual decline.

  39. Metabolic dementia • B12 deficiency may produce dementia , subacut combined degeneration of the spinal cord. • In alcoholic ,consider not only • Wernicke Korsakoff syndrome but also chronic sub-dural haematoma

  40. Normal pressure hydrocephalus dementia Normal pressure hydrocephalus (NPH) is the term applied to the triad of :- • Dementia • Gait disturbance • Urinary incontinence

  41. Occurring in conjunction with hydrocephalus and normal CSF pressure. Two types occur:- -NPH with a preceding cause, 1-subarchnoid haemorrhage. 2-meningitis. 3-truma.

  42. 4-radiation-induceced, (this must be distinguished from hydrocephalus with raised intrcranial pressure associated with these causes. • -NPH with no known preceding cause -idiopathic(50%)

  43. Aetiology:; 1-is unclear. 2-It is presumed that at some preceding period, impedance to normal CSF flow causes raised interventricular pressure and ventricular dilatation . 3-Compensatory mechanism permit a reduction in CSF pressure yet the ventricular dilatation persist and causes symptoms:-

  44. **Dementia -- from (pressure on frontal lobes ,possibly related to decreased cerebral blood flow. **Incontinence -- from (pressure on the cortical center for bladder , bowel

  45. **Gait disturbance and pyramidal signs in the legs : -due to (pressure on the “leg fibers” from the cortex passing around the ventricle toward the internal capsule.-

  46. DIAGNOSIS • -Is based on clinical picture plus CT/MRI scan i.e. ventricular enlargement. • -Normal pressure hydrocephalus must be • differentiated from patients whose • Ventricular enlargement is merely the result of • shrinkage of the surrounding brain tissue, e.g. Alzheimer”s disease.

  47. -These patients don't respond to CSF shunting, • whereas a proportion of patients with NPH • (but not all) show a definitive improvement with shunting

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