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Dementia- recent updates
1. Dr. Santanu Ghosh, MD
Assistant Professor,
Department of Psychiatry
Tripura medical College
2. What is dementia??
Dementia is defined as a progressive
impairment of cognitive functions
occurring in clear consciousness (that is,
in the absence of delirium)
3. HISTORY
1 2 3
Dementia = Dementatus
Meaning out of one's mind
Celsus
First used the term
dementia
Oribasius,
first attempts to describe
an etiology beyond old
age
4. Epidemiology
>65 years
>85 years
(Outpatient Population)
>85 years
(General Population
Chronic Care Facilities
By 2050
5%
15 - 20 %
20 -40 %
50%
• 14 million :Alzheimer's disease
• >18 million people with dementia
Prevalence
5. Etiologies of Dementia
Degenerative
Alzheimer's disease
Frontotemporal
degeneration
Parkinson's diseaseLewy body deposition
Progressive
supranuclear palsy
Idiopathic cerebral
ferrocalcinosis
11. Infarction (single or multiple or strategic lacunar)
Binswanger's disease
(subcortical arteriosclerotic encephalopathy)
Hemodynamic insufficiency
(e.g., hypoperfusion or hypoxia)
Cardiac,Cardiac,
vascular &vascular &
anoxiaanoxia
Etiology cont….
12. Neuropathology of dementia
Densely packed microfibrils
found in cytoplasm of dead
neuron
Consists of paired helical
filaments of abnormally
phosphorylated tau protein
Primarily affects hippocampal
pyramidal neurons and consists
of group of intra-cytoplasmic
vacuoles about 5 µm in
diameter congaing small
granule
Neurofibrillary
Tangle Senile Plaques Granulovacuolar
Degeneration
Extracellular deposits of 42 –
amino acid amyloid β peptide
derived from amyloid precursor
protein
Grossly: Cortical atrophy particularly involving
anterior frontal & temporo-parietal area
13. Neuropathology of dementia cont..
1= Congophilic angiopathy consisting of amyloid deposit in the wall of small
arteries
2= Generalized loss of neuronal dendrites
3= Loss of choloinergic neurons nucleus basalis of Meynert
4= Loss of noradrenergic neurons in locus coeruleus, loss of serotonergic neurons
of the dorsal raphe nucleus
17. Types of dementia and BPSD
Aspontinity, aggression,
wandering
Incontinence, Paranoid
symptoms
Alzheimer Disease
18. Types of dementia and BPSD cont..
• Visual hallucination
• Auditory hallucination
• Persecutory delusion
• Anxiety
• Depression
• Agitation
• Insomnia
Lewy BodyLewy Body
DementiaDementia
• Changes of character &
social behavior
• Sexual misadventure
• Overeating
• Tendency to touch
Pick’sPick’s
DementiaDementia
• Anxiety
• Depression
• Labile mood
• Judgment and insight
remains intact for
long time
VascularVascular
DementiaDementia
19.
20. Assessment
Other medical
conditions
Behavioral problems,
psychotic symptoms, or
depression
Mini Mental status Examination
• Severe : 0-10
• Moderate : 11-17
• Mild : 18-23
• Normal : 24-30
Daily function
•Feeding
•Bathing
•dressing,
• Mobility
• Manage finances and
medications
23. Alzheimr’s Disease (AD)
• Is the most common cause of dementia.
• > 90% sporadic , age usually >65yrs.
• <10% familial, age usually <60 yrs.
• Clinically: Initially normal- develops ‘Mild Cognitive
Impairment’ – goes on to develop AD.
• Pathology: AD is characterized by senile plaques,
neurofibrillary tangles, decreased synaptic density, neuron
loss and cerebral atrophy.
24. sMRI- Alzehimer’s Disease
Assessment of cerebral atrophy of hemisphere
particularly posterior temporal and parietal lobes & specific
anatomic areas like hippocampus and medial temporal
lobe
1. Visual ranking system: Mild / moderate / severe.
2. Quantitative measurement : Linear / area / volumetric*.
Measurements must be adjusted for age, gender and head
size and then referenced to an appropriate control
population.
25. Among these measurements of hippocampus was most sensitive
marker of pathology of AD early in disease.
Normal ALZHEIMER’S DISEASE
30. • It is characterized by
presence of lewy bodies in the
cortical neurons on histology.
• It is 2nd
/ 3rd
most common
cause of dementia in elderly.
• To date, no MRI features
have been identified that to
characterize DLB.
• “THE ABSENCE OF
SIGNIFICANT MEDIAL
TEMPORAL LOBE
ATROPHY” in a elderly
demented patient suggests
DLB etiology rather than AD
etiology.
32. • Age of onset: 50-65 yrs.
• Genetically linked to chromosome 3 and 17
• FTD is a term used to describe a family of
neurodegenerative disorders characterized by
degeneration of frontal and temporal lobes.
• The three most common HISTOLOGICALLY
classified(Not radiological) FTD syndromes are
Pick's disease.
Frontal-lobe degeneration &
FTD with amyotrophic lateral sclerosis.
33. MRI features of FTD
• MR features:
Severe sharply localized atrophy- bilaterally symmetric-
“knife-blade atrophy.”
Hyperintense signal in the cortex and underlying white
matter of the affected areas.
• Areas involved: frontal lobe, anterior temporal lobes,
extra pyramidal nuclei especially the caudate nucleus,
insular cortex & anterior corpus callosum.
• Areas spared: Posterior two thirds of the superior
temporal gyrus, occipital lobes, parietal lobes &
perirolandic region
• These MR findings in an appropriate clinical setting
may support the diagnosis of FTD.
37. • Dementia due to chronic cerebrovascular disease is
2nd
/ 3rd
most common cause of dementia in elderly(AD
and dementia with Lewy bodies).
• Three main forms are recognized:
Multi infarct dementia.
Sub cortical vascular dementia/ Binswanger’s
disease
Cerebral amyloid angiopathy.
41. • TRIAD: Dementia + gait disturbance + Urinary incontinence.
• AGE: usually after 60 yrs.
• Theories:
Impaired extraventricluar CSF absorption due to prior
subarachnoid hemorrhage / meningitis.
Decrease white matter tensile strength due to deep white
matter infarction / ischemic changes.
• Three primary MR findings have been described in NPH:
Enlargement of the ventricular system out of proportion to the
subarachnoid space
A prominent periventricular halo and
A prominent CSF flow void in the cerebral aqueduct.
42.
43. MRS- Dementia
• NAA loss is consistently seen in Alzheimer's disease.
• NAA loss is also seen in Parkinson’s disease &
Huntington’s disease.
• Significantly elevated myoinositol in grey matter of
Alzheimer's disease.
47. Guidelines for prescribing cholinesterase inhibitors
A. Prescription only for patients-
a) Fulfilling criteria for probable AD
b) Duration of illness being more than 6 months
c) MMSE score more than 10 (i.E., Mild or moderately severe dementia)
B. Three phase evaluation of response-
a) Early (2 weeks) for assessing tolerance and side effects,
b) Later (3 months) for cognitive state,
c) Continued (6 months) for disease state
C. Stop treatment-
a) If early evaluation shows poor tolerance or compliance
b) If deterioration continues at pre-treatment rate after 3-6 months of
treatment
c) If even after reaching maintenance dose accelerating deterioration
continues
48. Anti-amyloid therapy
Vaccines to prevent amyloid plaque formation :
Under experimental stage
Secretase
Inhibitor
Fibrilogenesis
inhibitor
e.g. cliniquinol
Cholesterine
Newer
drugs
49. Other drugs
Quetiapine is
safest
Valproate is
preferable
Sertraline is
preferable
Non
benzodiazepines
are preferable
Sedatives
Antidepressants
Mood
stabilisers
Antipsychotics
50. Non-pharmacological Intervention
I. Environmental modifications
1 2 3
Enhanced Environment
Simulated home environment
with appropriate visual auditory
and olfactory stimuli which
may decrease the chance of
trespassing, exit seeking and
other agitation behaviors
Reduced Stimulation
Environment
Camouflaged doors, neutral
colors and pictures on walls,
no televisions, radios, stereo
players or ringing telephones,
added with a consistent daily
routine, and slow and soft
speech for communication
Natural Environment
Mimic natural surroundings
consisting of recorded
songs of birds, babbling
brooks or small animals,
together with large bright
picture
51. Environment
Calm, non-taxing environments,
good lighting, prominent placement
of frequently required objects
Soft wall colours, non-skid
flooring contrast between the
wall and floor, handrails are
useful
Clear and repetitive instructions,
visual direction to different rooms
through colour lines and pictures
decrease confusion
without frequent change of furniture
minimum change of caregivers or
staff.
Environmental modifications contd..
52. II. Social interactions
““simulated presence therapy,”simulated presence therapy,”““simulated presence therapy,”simulated presence therapy,”
Audio or videos containing a relative’s portion of interaction is
played, and pauses are given that allow the patient to respond to
the relative’s questions. Displaying photos and names of
family and friends in the patient’s living area is helpful.
LanguagePet therapyInteraction
Non-pharmacological Intervention cont.
One to one interaction for 30 min
per day for 10 days to be
effective in decreasing verbally
disruptive behaviour.
Interaction in the mother
tongue and regular
intensive interaction help in
reality orientation.
Spending time with pets or
having a pet at home (pet
therapy) decreases agitation and
verbal aggression
53. III. Minimize the impact of sensory deficits
Provide favourite foods
Devices
Patience
Rapport
Food
Slow and repetitive explanations
reduce confusion and agitation.
Massage and touch, aromatherapy
Minimize the impact of
sensory deficits Corrective
eyeglasses and hearing aids
decrease risk of
disorientation
Non-pharmacological Intervention cont.
54. IV. Medical and nursing interventions
Music
Therapy
Proper
food
Sleep
Hygiene
Light
Therapy
Frequent
outing
Pain
Management
Personal
Hygiene
Non-pharmacological Intervention cont.
57. CARE NACSP ADL
Calming Aggressive
Reactions In Elderly
Nursing Assistant
Communication Skill
Program
Abilities-focused program of
morning care, and training
on activities of daily living
(ADL)
Nonpharmacological Intervention cont.