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Understanding Dementias - Dr. Sadik Al-Ghazzawi | Symptoms and Classification

Dive into the world of dementias with Dr. Sadik Al-Ghazzawi, exploring the progressive deterioration of intellect, behavior, and personality caused by cerebral diseases. Learn about the different types of dementia, their symptoms, causes, and diagnostic approaches. Discover the complexities of Alzheimer's disease, cerebrovascular dementia, neurodegenerative disorders, and more with this comprehensive guide.

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Understanding Dementias - Dr. Sadik Al-Ghazzawi | Symptoms and Classification

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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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