1. WELCOME

2. DEMENTIA
PRESENTED BY
DR. AHMED TANJIMUL ISLAM
GHORAR DIM, SOMCH

12. 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

13. 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 %

14. Classification :
Types :
Dementia Classification:
Primary (degenerative) dementia
Secondary dementia
DementiaTypes:
Cortical dementia
Subcortical dementia

15. Psudodementia
A group of disease due to functional disease
rather than organic dementia
• Depression
• Hysterical Dementia
• Psychogenic amnesia

16. Causes of Dementia
Primary Degenerative Dementia:
•Alzheimer’s Disease
•Frontotemporal dementia
•Dementia with Lewy Body

17. Secondary Dementia:
VITAMIN
Deficiency
ENDOCRINE Chronic
Infections
Thiamine B1 Hypothyroidism Neurosyphilis
B3 Adrenal deficiency HIV
B12 Cushing Syndrome Prions
Hypoparathyroidism

18. TOXIC HeadTrauma: Neoplastic
DIALYSIS
DEMENTIA
Chronic Subdural
Heatoma
Primary Brain
Tumor
Drug Poisoning Post Encephalatis Secondary Brain
Tumor
Heavy Poisoing Normal Pressure
Hydrocephalitis
Paraeoplastic

19. CORTICAL SUBCORTICAL MIXED
Alzheimer’s Parkinson’s Vascular Dementia
Frontotemporal
Dementia
Huntington’s
disease
Lewy body
dementia
CJD Normal pressure
hydrocaphalus
Neurosyphilis

20. SUBCORTICAL CORTICAL
Memory
impairment
moderate Severe
Mathemetical skills Preserved Impaired
Mood depressed Normal
Motor speed Slowed Normal
Movements
abnormal
Common Rare
mutism Absent Present

21. (
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

22. IS IT
DEPRESSION OR
DEMENTIA??
VS

23. 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

25. IS IT
DELIRIUM or
DEMENTIA ??

27. 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??

28. ALZHEIMER’S DISEASE :

34.  video

40. Alzeimer’s Disease
Loss of
cholinergic
neurons
Senile plaques &
neurofibrillary
tangels
Glutamate
transmission
dysfunctiion
30%
symptoms
70%
Symptoms

41. Alzheimer’s Staging:

42. 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

43. AD: a progressive CNS disorder)
Brain
Atrophy
**Senile Plaque
**Neurofibrillary Tangles
Pathology (HALLMARK)

44. Pathology of AD (Microscopic)

45. Pathology of AD (Microscopic)

46. Pathology of AD (Microscopic)

48.  video2

49. 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)

52. 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

58. 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

59. DEMENTIA:
Common diagnostic strategies:
 Clinical :
 History (from patient, family)
 Bedside Examination (e.g. MMSE)
 Physical Examination
 Neuropsychological Assessment.
 Imaging.
 Lab Screening for other causes.

60. 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)

61. Examination of Higher Functions
BEDSIDETESTS :
•MMSE
•CLOCK DRAWING
•ADAS cog
(Alzeimer’d disease assesment scale cognitive)
•Detailed Psychometry

63. 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

64. 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

67. 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

70. Imaging :
 Structural imaging (CT or MRI )
 Exclusion of structural abnormalities
 Volumetric studies
 Functional imaging
 PET
 SPECT

73. 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

78. 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

80. Diagnosis Flow Chart:
History
Memory =
Activity in
Daily Living
Cognitive
ScreeningTest
MMSE +
CLOCK Drawing
Exclede Reversable causes
by BaselineTests
Neuroimaging

85. MANAGEMENT OF
DEMENTIA

86. Management :Dementia
Reduce Cognitive Symptoms
Reduce Behaviour Symptoms
Slow disease progression
Delay the Onset of Disease

87. Behavioral Strategy
 Scheduled toileting, prompted voiding
for incontinence.
 Graded assistance, & positive
reinforcement to increase functional
independence
 Music, esp. during meals, bathing
 Walking , Light Exercise

88. Management of Dementia
 Supportive treatment
 Non-pharmacological
 Pharmacological
 Treatment of complications &
co-morbidities

90. 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.

91. 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

93. MEMANTINE
 NMDA receptor
antagonist
 Severe AD
 Also useful in
Vascular Dementia
 Improves cognitive
function
 Improves the daily
activity of life.

96. DELAY OF PROGRESSION: Duration
Memantine alone 2-3 years
Memantine + Ch E inhibitors 5-6 years
Ch E Inhibitors alone 1.5 years

97. 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

99. 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

100. Rivastigmine Cautions
 Renal impairment
 Hepatic impairment
 Sick sinus syndrome
 Conduction abnormalities.
 H/O Asthma or COPD
 Pregnancy .

101. 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

102. Exelon Transdermal
9.5 mg/24 h Patch

103. 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

104. 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)

105. 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

108. When to Refer to SPECIALIST:
•Early Onset
•Presentation Atypical
•Severe Parkinsonism
•Focal Finding
•Behaviors seeming to be Untreatable

111. ThankYou