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DEMENTIA everything u need to know


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Published in: Health & Medicine

DEMENTIA everything u need to know

  1. 1. WELCOME
  3. 3. DSM – IV Criteria for Dementia Memory Impairment plus • APHASIA (Deterioration of Language function) • APRAXIA (inability to Execute Motor function) • AGNOSIA (inability to Recognise or Naming of Object) Disturbance in executive functioning with • Impairment in occupational or social functioning
  4. 4. 70% of dementia is Alzheimer’s 10-15% is Vascular dementia 10-15% Lewy Body dementias 5-10% Others Overall Situation: Alzheimer’s disease 70 % Vacular Dementia 15-20% Lewy Body Dementia 10-15 % Others 5 %
  5. 5. Classification : Types : Dementia Classification: Primary (degenerative) dementia Secondary dementia DementiaTypes: Cortical dementia Subcortical dementia
  6. 6. Psudodementia A group of disease due to functional disease rather than organic dementia • Depression • Hysterical Dementia • Psychogenic amnesia
  7. 7. Causes of Dementia Primary Degenerative Dementia: •Alzheimer’s Disease •Frontotemporal dementia •Dementia with Lewy Body
  8. 8. Secondary Dementia: VITAMIN Deficiency ENDOCRINE Chronic Infections Thiamine B1 Hypothyroidism Neurosyphilis B3 Adrenal deficiency HIV B12 Cushing Syndrome Prions Hypoparathyroidism
  9. 9. TOXIC HeadTrauma: Neoplastic DIALYSIS DEMENTIA Chronic Subdural Heatoma Primary Brain Tumor Drug Poisoning Post Encephalatis Secondary Brain Tumor Heavy Poisoing Normal Pressure Hydrocephalitis Paraeoplastic
  10. 10. CORTICAL SUBCORTICAL MIXED Alzheimer’s Parkinson’s Vascular Dementia Frontotemporal Dementia Huntington’s disease Lewy body dementia CJD Normal pressure hydrocaphalus Neurosyphilis
  11. 11. SUBCORTICAL CORTICAL Memory impairment moderate Severe Mathemetical skills Preserved Impaired Mood depressed Normal Motor speed Slowed Normal Movements abnormal Common Rare mutism Absent Present
  12. 12. ( REVERSIBLE DEMENTIA IRREVERSIBLE DEMENTIA D= Drugs, Delirium Alzhemer E= Endocrine disorders Lewy Body dementia M= Metabolic Frontotemporal Dementia (Picks disease) E= Emotional Parkinsons disease N= Nutritional Huntington’s disease T =Toxic,Tumor,Trauma Cruze feltd jakob disease A= Alcohol
  14. 14. Depression Dementia: Little effort on tasks Struggles to complete tasks Don’t know answers Attempts answers, but incorrect Absence of Dyspraxia, Have Dyspraxias, Agnosias, No language problem Language problem
  16. 16. Is it Dementia?? Is it Depression or Dementia Is it Delirium or Dementia Is it Alzheimer’s?? IsThere any Reversable Cause?? If not Alzheimer’s What is it??
  18. 18.  video
  19. 19. Alzeimer’s Disease Loss of cholinergic neurons Senile plaques & neurofibrillary tangels Glutamate transmission dysfunctiion 30% symptoms 70% Symptoms
  20. 20. Alzheimer’s Staging:
  21. 21. Alzheimer’s Pathology (Gross) :  Every part of cerebral cortex is involved with relative sparing of occipital pole  Marked Atrophy.  Widened Sulci  Shrinkage of Gyri  Ventricular Dilatation
  22. 22. AD: a progressive CNS disorder) Brain Atrophy **Senile Plaque **Neurofibrillary Tangles Pathology (HALLMARK)
  23. 23. Pathology of AD (Microscopic)
  24. 24. Pathology of AD (Microscopic)
  25. 25. Pathology of AD (Microscopic)
  26. 26.  video2
  27. 27. Cholinergic deficit – progressive loss of cholinergic neurones – progressive decrease in available ACh – impairment in ADL, behaviour and cognition Hippocampus Cortex N. basalis Meynert Pathophysiology of AD (Biochemical)
  28. 28. ALZHEIMER’S VASCULAR Onset Incidious Sudden Risk factors Family history CVD risks Mental status Recent Memory Psychomotor slowing Neuro exam No Focal neuro deficit Behavioral Delusion, Poor insight Apathy, Depression MRI Diffuse / Temporal atrophy Stroke
  29. 29. ALZHEIMER’S VASCULAR LBD FTD Short term Memory Loss Personality change Parkinsonism Prominent Behavior change Dysphasia Dyspraxia Labile Mood Fluctuating Alertness Expressive Dysphasia Wandering Preserved Insight Visual Hallucination Early loss of insight
  30. 30. DEMENTIA: Common diagnostic strategies:  Clinical :  History (from patient, family)  Bedside Examination (e.g. MMSE)  Physical Examination  Neuropsychological Assessment.  Imaging.  Lab Screening for other causes.
  31. 31. History :  Nature of the problem  Memory?  Behavioral  Emotional  Who perceives the problem?  Patient?  Family?  Tempo of the illness  Gradual  Fast  Stepwise  Family history  Other medical problems  Neurological (e.g. movement disorder)  Systemic (e.g. thyroid disease, vascular disease)
  32. 32. Examination of Higher Functions BEDSIDETESTS : •MMSE •CLOCK DRAWING •ADAS cog (Alzeimer’d disease assesment scale cognitive) •Detailed Psychometry
  33. 33. COGNITIVE FUNCTION BEHAVIOUR & PSYCHOLOGICAL FEATURES ACTIVITY OF DAILY LIVING DEPRESSION MMSE Neuropsychiatric inventory Bristol Scale Cornel Scale Clock Drawing Test Behave AD AD functional Assesment scale Geriatric Depression Scale Seven Minute Screen Cohen Mansfield Aggression Inventory Disability Assesment Dementia MentalTest Score
  34. 34. Mini Mental State Examiation :  Staging of Disease by MMSE Normal 27-30 Mild 25-26 Mild- Moderate 10-24 Moderate- Severe 6-9 Very Severe <6
  35. 35. Clock Drawing  “Draw a clock and set the hands to ten minutes to two”  Marked out of ten e.g. Perfect 10 Noticable palcement errors of the hand 8 Numbers & clock face not conected 3 uninterruptable 1
  36. 36. Imaging :  Structural imaging (CT or MRI )  Exclusion of structural abnormalities  Volumetric studies  Functional imaging  PET  SPECT
  37. 37. In A, MRI shows cortical atrophy and ventricular enlargement. In B, PET scan shows reduced glucose metabolism in the parietal lobes bilaterally (blue green) as compared with more normal metabolism in other cortical areas (yellow) Probable Alzheimer’s Disease
  38. 38. BASELINE TESTS: Baseline investigations for Dementia: CBC, ESR S. Electrolytes Calcium, Phosphate Syphilis Chest X ray HIV CT, MRI Thyroid Function test B12, Folate Liver function tests EEG, ECG Renal FunctionTests
  39. 39. Diagnosis Flow Chart: History Memory = Activity in Daily Living Cognitive ScreeningTest MMSE + CLOCK Drawing Exclede Reversable causes by BaselineTests Neuroimaging
  41. 41. Management :Dementia Reduce Cognitive Symptoms Reduce Behaviour Symptoms Slow disease progression Delay the Onset of Disease
  42. 42. Behavioral Strategy  Scheduled toileting, prompted voiding for incontinence.  Graded assistance, & positive reinforcement to increase functional independence  Music, esp. during meals, bathing  Walking , Light Exercise
  43. 43. Management of Dementia  Supportive treatment  Non-pharmacological  Pharmacological  Treatment of complications & co-morbidities
  44. 44. Symptomatic Treatment of AD . The mainstay of symptomatic treatment of AD, so far, is the cholinergic treatment strategies and most widely used, till now, are the Cholinesterase (ChE) inhibitors. . These agents •Reduce the metabolism of acetylcholine •Prolonging its action at cholinergic synapses.
  45. 45. Cholinesterase inhibitors: two classes exist for the treatment of Dementia Class Inhibit Dual ChE inhibitors – Rivastigmine Both AChE – Tacrine and BuChE Single ChE inhibitors – Donepezil AChE – Galantamine Weinstock, 1999
  46. 46. MEMANTINE  NMDA receptor antagonist  Severe AD  Also useful in Vascular Dementia  Improves cognitive function  Improves the daily activity of life.
  47. 47. DELAY OF PROGRESSION: Duration Memantine alone 2-3 years Memantine + Ch E inhibitors 5-6 years Ch E Inhibitors alone 1.5 years
  48. 48. Proposed or unregulated drugs which require further studies Selegeline Vit-E Oestrogen Prednisolone NSAIDs Ginkgo biloba Statins IVIg Glycogen syntehtase kinase 3 (GSK 3) β-secretase inhibitors γ-secretase inhibitors α-secretase enhancers Immunotherapy
  49. 49. ALZEIMER’S VASCULAR FRONTO TEMPORAL LEWY BODY DONEPEZIL ChE Inhibitors No ChE inhibitors ChE inhibitors RIVASTIGMIE HMG CoA SSRI SSRI GALANTAMINE Stroke Prevent Antipsychotics Memantine MEMANTINE Memantine Memantine Levadopa SSRI Antipsychotic
  50. 50. Rivastigmine Cautions  Renal impairment  Hepatic impairment  Sick sinus syndrome  Conduction abnormalities.  H/O Asthma or COPD  Pregnancy .
  51. 51. Transdermal Patch Technology: Reservoir versus Matrix Nitti VW, et al Urology. 2006;67:657–64 Drug contained in adhesive layer along with polymer Smaller and thinner than reservoir patches Reservoir Matrix Drug contained in separate layer, with a rate-controlling membrane Matrix Diffusion Controlled Patch Release Liner Drug + Polymer + Adhesive Backing Rate-Controlled Reservoir/Membrane Patch Dermal Layer Backing Drug Reservoir Release Liner Adhesive Layer
  52. 52. Exelon Transdermal 9.5 mg/24 h Patch
  53. 53. Where to Apply Exelon Patch Apply to:  Upper and lower back  Upper arm  Chest The skin should be clean, dry and hairless before the patch is applied Normal daily activities, such as bathing, are permitted
  54. 54. Exelon Transdermal Patch: Smooth Continuous Delivery Through the Skin Exelon 6 mg BID capsule Exelon 9.5 mg/24 h patch Plasmaconcentration(ng/mL) Exelon 9.5 mg/24 h patch delivered comparable average concentrations (AUC) to those provided by an oral dose of 6 mg BID (12 mg/day)* * Model-predicted analysis based on actual patient data corrected for body weight. 0 5 10 15 20 25 0 6 12 18 24 Time (hours)
  55. 55. Starting transdermal ChEI therapy Rivastigmine 4.6 mg/24 h patch Rivastigmine 9.5 mg/24 h patch Starting dose Target dose 4 weeks One-step dose increase
  56. 56. When to Refer to SPECIALIST: •Early Onset •Presentation Atypical •Severe Parkinsonism •Focal Finding •Behaviors seeming to be Untreatable
  57. 57. ThankYou