A presentation on management of dementias

1. Management of DEMENTIAS
Guided by – Dr. A Paliwal sir
Associate Professor
Department of Psychiatry
Presented by – Dr. Priyash Jain

2. .
 Introduction
 Etiology
 Classifications
 Clinical features
 Diagnosis
 Subtypes
 Management
 Conclusion
Content

3. Introduction
Dementia is usually progressive and largely
irreversible clinical syndrome that is characterized
by global deterioration in intellectual function,
behavior and personality in the presence of
normal consciousness and perception.

4. Etiology of Dementia
Neurodegenerative Alzheimer’s ds
Lewy Body
Pick’s ds
Parkinson’s ds
Huntington’s ds
Vascular Infarction
Binswanger’s ds
Hemodynamic insufficiency
Neurological Multiple sclerosis
Brain tumor (primary Or metastatic)

5. Etiology of Dementia
Endocrine Hypothyroidism
Hypercalcemia
Hypoglycemia
Nutritional Vit B12, B6,B3 def.
Infections HIV, CJD, Neurosyphilis
Metabolic Wilson’s ds
Hepatic insufficiency
Renal insufficiency
Traumatic Subdural hematoma
Dementia pugilistica
Exposure Alcohol, heavy metals, radiation,
Anticholinergic med, co2

7. Classification
In ICD-10 dementias are further classified in 4 subtypes
 1. F00 - dementia in alzheimer’s ds
 2. F01 - vascular dementia
 3. F02 - dementia in other diseases
 4. F03 - unspecified dementia

8.  The F02 is further classified into
 1. F02.0 - dementia in Pick’s ds
 2. F02.1 - dementia in Creutzfeldt-Jacob ds
 3. F02.2 - dementia in Huntington’s ds
 4. F02.3 - dementia in parkinson’s ds
 5. F02.4 - dementia in HIV ds
 6. F02.8 - dementia in other specified diseases classified elsewhere.

9. . DSM-V introduces the 2 terms
“mild neurocognitive disorder”, which is similar to MCI (mild cognitive
impairment), and
“major neurocognitive disorder”, which is analogous to dementia.
 Mild neurocognitive disorder represents a cognitive decline which does not
impair daily activities
 DSM-5 does not mention the duration for which symptoms must be
present.

10. Clinical Features
 The symptoms of dementia vary across types and stages
Behavior Cognition Emotion
Communication Memory Apathy
Personal care Learning Unregulated
Safety Praxis functions disorganized
Delusions Language Lability
Hallucination

11. .
 Alzheimer’s ds
 Vascular dementia
 DLB
 Fronto-temporal dementia
 Dementia due to gen medical conditions
Sub types of dementia

12. Diagnosis
 Cognitive testing -
 There are many test, MMSE is the best studied and most commonly
used.
Other cognitive tests include
 MOCA (Montreal Cognitive Assessment)
 Abbreviated mental test score (AMTS),
 Modified Mini-Mental State Examination(3MS),
 Cognitive Abilities Screening Instrument (CASI)

13. Laboratory test
 Routine blood tests are also usually performed to rule
out treatable causes. These tests include vitamin
B12, Niacin, TSH,VDRL,HIV, full blood
count, electrolytes, calcium, renal function, and liver
enzymes.
 Abnormalities may suggest vitamin deficiency, infection,
or other problems that commonly cause confusion or
disorientation in the elderly.

14. Management of dementia
Pharmacological management
Non-pharmacological management

15. PHARMACOLOGIC MANAGEMENT OF
DEMENTIA
Three broad categories of dementia
pharmacotherapy:
Symptomatic treatment of memory
disturbance
Disease-modifying treatments
Symptomatic treatment of behavioral
disturbance

16. Symptomatic Treatment
. The mainstay of symptomatic treatment of
Dementia, 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.

17. DONEPEZIL
In 1996, donepezil, a selective cholinesterase
inhibitor, was approved for use in Alzheimer disease.
marketed under the trade name Aricept by its is a
centrally acting reversible acetylcholinesterase
inhibitor
devoid of peripheral cholinomimetic adverse effects.

18. Pharmacokinetics
Bioavailability 100 (%) not affected by the time of
day or food intake
Protein binding 96%
Half-life 70 hours
peak plasma concentration is reached in 3 to 5 hours.
It is extensively metabolized by the hepatic
isoenzymes CYP2D6 and CYP3A4.
minimally affected by hepatic or renal disease and no
dose adjustment is necessary for these conditions.

19. CONTRAINDICATIONS ADVERSE EFFECTS
cardiac disease, cardiac
conduction disturbances,
chronic obstructive
pulmonary disease,
asthma, severe cardiac
arrhythmias and sick
sinus syndrome.
gastrointestinal disorders
should use caution because
nausea or vomiting may occur.
predisposition to seizures
should be treated with caution.
Common side effects
include bradycardia
cardiac conduction
disturbances
nausea, diarrhea, anor
exiaabdominal pain
vivid dreams
DONEPEZIL

20. TACRINE
In 1993 first Drug approved for the treatment
of Alzheimer's disease
marketed under the trade name Cognex.
Tacrine was first synthesised by Adrie Albert at
the University of Sydney.
Tacrine is a centrally acting anticholinesterase and
indirect cholinergic agonist (parasympathomimetic).

21. Tacrine Pharmacokinetis
Bioavailability 2.4–36% (oral)
Protein binding 55%
Metabolism Hepatic (CYP1A2)
Half-life 2–4 hours
Excretion Renal

22. Very Common >10%
Increased LFTs
Hepatitis
Nausea
Vomiting
Diarrhea
Headache
Dizziness
Common 1-10% incidence
Indigestion,Belching
Abdominal pain
Myalgia
Confusion
Ataxia
Insomnia
Weight loss
Constipation
Somnolence
Tremor
Anxiety
Tacrine Adverse Effects

23. Mechanism of Action
PHARMACOKINETICS
Reversible
acetylcholinesterase
inhibitor that causes an
increase in
concentrations of
acetylcholine, which in
turn enhances
cholinergic
neurotransmission
Absorption
Bioavailability: 36% (PO)
Duration: 10 hr (PO); 24 hr (patch)
Peak plasma time: 1 hr (PO); 8 hr
(patch)
Distribution
Protein bound: 40%
Vd: 1.8-2.7 L/kg
Metabolism
Metabolized by cholinesterase
Elimination
Half-life: 1.5 hr (PO), 3 hr (patch)
Total body clearance: 1.2-2.4 L/min
Excretion: Urine (97%)
Rivastigmine (Rx) - Exelon

24. common
Nausea
Vomiting
Dizziness
Diarrhea
Headache
Anorexia
Abdominal pain
UNCOMMON
Decreased
weight
Insomnia
Anxiety
Asthenia
Vertigo
Fatigue
Rivastigmine - Adverse effects

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

26. Exelon Transdermal
9.5 mg/24 h Patch

27. Exelon Transdermal Patch:
Smooth Continuous Delivery Through the Skin
Exelon 9.5 mg/24 h patch
Exelon 6 mg BID capsule
* Model-predicted analysis based on actual patient data corrected for body weight.

28. Galantamine (Nivalin, Razadyne,
Razadyne ER, Reminyl,
Lycoremine)
It is an alkaloid that is
obtained synthetically
or from the bulbs and
flowers of Galanthus
caucasicus
(Caucasian snowdrop)
Galantamine
hydrobromide was
approved in 2001 by the
FDA Indicated for the
treatment of mild to
moderate dementia IN
Alzheimer's.

29. Galantamine-MOA
weak competitive
and reversible choline
sterase inhibitor in all
areas of the body.
It increases the
concentration and
thereby action
of acetylcholine in
certain parts of the brain.
It has shown activity in
modulating the nicotinic
cholinergic receptors on
cholinergic neurons to
increase acetylcholine
release.

30. Pharmacokinetics
DOSAGE
Bioavailability - 80 to
100%
Protein binding- 18%
Metabolism-Hepatic
Half-life-7 hours
Excretion -
Renal (95%, of which
32% unchanged), fecal
(5%)
in twice-a-day tablets, in
once-a-day extended-
release capsules, and in
oral solution.
The tablets come in
4 mg, 8 mg, and 12 mg
forms.
The capsules come in
8 mg, 16 mg, and 24 mg
forms.
Galantamine

31. common Rare
Nausea, vomiting,Diarrhea,
abdominal pain, upper
abdominal pain, dyspepsia,
stomach discomfort, abdominal
discomfort
Bradycardia,First degree
atrioventricular block,
palpitations, sinus bradycardia,
supraventricular extrasystoles,
flushing, hypotension
Dizziness, headache, tremor,
syncope, lethargy, somnolence
Blurred vision
confusion
decreased urination
dizziness, faintness, or
lightheadedness
dry mouth
fainting
fast, irregular, pounding, or racing
heartbeat or pulse
feeling of warmth
rapid breathing
redness of the face, neck, arms, and
occasionally, upper chest
sunken eyes,sweating, thirst
Galantamine-Adverse effects

32. Memantine
Memantine is the first in a novel class
of Alzheimer's disease medications acting on
the glutamatergic system by blocking NMDA
receptor.
Memantine is approved by the U.S. F.D.A and the
European Medicines Agency for treatment of
moderate-to-severe Alzheimer's disease

33. Pharmacokinetic
Bioavailability~100%
Metabolism-
Hepatic (<10%)
Half-life- 60–100
hours
Excretion - Renal
MOA
Memantine is a low-affinity
voltage
dependent uncompetitive
antagonist at
glutamatergic NMDA
receptors
non-competitive antagonist
at the 5-HT3 receptor, this
serotonergic activity in the
treatment of Alzheimer's
disease is unknown.
Memantine

34. Common
confusion, dizziness,
drowsiness,
headache, insomnia,
agitation
hallucinations.
Less common
vomiting, anxiety,
hypertonia
cystitis,
increased libido
rare
extrapyramidal side
effects(such as dystonic
reactions etc.) may
occur, in particular, in
the younger population
Memantine -Adverse effects

35. FDA-approved drugs
Drug Target dose Approved for year
Tacrine 40 mg/day Mild to
moderate
1993
Donepezil 10 mg daily All stages 1996
Rivastigmine 6 mg twice
daily or 9.5-mg
patch daily
All stages 2000
Galantamine target dose 24
mg daily,
extended-
release
Mild to
moderate
2001
Memantine 10 mg twice
daily
Moderate to
severe
2003

36. Disease-Modifying Agents
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

37. Disease-Modifying Agents
Vitamin E
 Limits free-radical formation, oxidative stress and lipid
peroxidation
 Promotes survival of cultured neurons exposed to
beta amyloid
 Clinical trials have not be overwhelmingly convincing
Selegiline
 MAO-B inhibitor, increases brain catecholamines
 Also has antioxidant properties
 Clinical trials – alone and in combination with Vit. E not
effective

38. Disease-Modifying Agents
Anti-Inflammatory drugs
 Pathophysiological studies demonstrate a marked
inflammatory reaction induced by amyloid with microglial
activation and cytokine release
 Case-control studies of subjects taking NSAIDs regularly
for arthritis demonstrate a reduced odds-ratio for
developing AD
 Recently developed NSAIDS currently in clinical trials of
AD
Estrogen
 Body of preclinical evidence that estrogen enhances
cerebral blood flow, prevents atrophy of cholinergic
neurons, reduces oxidative stress, and modulates the
effects of nerve growth factors

39. Disease-Modifying Agents
Statins
 Direct association between amyloid processing and
cholesterol in the brain
 An indirect effect via decreasing the risk of stroke, since
even small vascular lesions worsen the severity of
Alzheimer's disease
Ginkgo Biloba
 A single placebo-controlled trial with an extract of ginkgo
biloba showed a very modest improvement on cognitive
testing
 Only 50 percent of the treatment group completed the trial
 Use of ginkgo not recommended due to limited efficacy and
lack of regulation, including variability in the dosing and
contents of herbal extracts

40. Non Pharmacological

41. Nature of Behaviors
•
•
 Until recently, main focus of treatment has been excessive
behaviors, because of the disruption they cause both for the
person with dementia and the carers.
 Disruptive behaviors are taken as an indication of underlying
distress or unmet need.
•
•
For example: UNMET NEED MODEL for AGITATION by Cohen-Mansfield
(2000).
It distinguishes three main functions of behaviors in relation to needs:
1. Behaviors to obtain or meet a need (e.g. pacing to provide stimulation);
2. Behaviors to communicate a need (e.g. repetitive questioning);
3. Behaviors that result from an unmet need (e.g. aggression triggered by
pain or discomfort).

42. Learning/behavioral models
•
•
•
(Cohen-Mansfield)
Many problem behaviors are learned through reinforcement by
staff members, who provide attention when problem behavior is
displayed.
ABC approach
– A = antecedent or triggering event that precedes the problem behavior
– B= the behavior of concern
– C= the consequence of that behavior
Changing either the antecedent or the consequence may change
the behavior

43. Learning/behavioral models
(Cohen-Mansfield)
1) Identify precisely the problem. The more clearly it is defined,
the easier it is to implement an effective response
2) Gather information about the circumstances surrounding the
problem immediately before and after. There may be several
triggers
3) Set realistic goals, and make plans to achieve them. Seek to
be creative, realistic and tailored to the individual and
caregivers. "Increasing pleasant activity" is more realistic
than "be happy all the time.“
4) Encourage rewards (to all) for small successes. Changing
behavior is hard work for everyone.
5) Continually evaluate and modify plans. Consistency but
flexibility. Strategies may need to change.

44. Environmental
vulnerability/reduced stress-
threshold model (Cohen-Mansfield)
• The dementia process results in greater vulnerability to surroundings and
a greater chance that an event will affect behavior.
• Persons with dementia progressively lose their coping abilities and
therefore perceive their environment as more and more stressful.
• Concurrently, their likelihood of being bothered by the environment
increases, resulting in anxiety and inappropriate behavior when the
environmental stimuli exceed the threshold for tolerating the stress
• An environment of reduced stimulation is supposed to limit the stress
experienced and thereby reduce the level of inappropriate behavior
• Relaxation will reduce the stress and thereby decrease the undesirable
behavior.

45. Reminiscence Therapy
• Reminiscence therapy involves the discussion of past activities, events and
experiences with another person or group of people.
• Uses materials such as old newspapers, photographs, household and other
familiar items from the past to stimulate memories and enable people to share
and value their experiences.
1. Group sessions: to improve interaction
2. Individual sessions: life review sessions, in which the person is guided
chronologically through life experiences and encouraged to evaluate them
• It is seen as a way of increasing levels of well-being and providing pleasure and
cognitive stimulation.
• Studies have suggested that reminiscence work assists in reducing depression in
older people

46. Validation therapy
• It was suggested by its originator, Naomi Feil, that some of the
features associated with dementia such as repetition and
retreating into the past were in fact active strategies on the
part of the affected individual to avoid stress, boredom and
loneliness.
•
•
The idea behind validation therapy is to “validate” or accept
the values, beliefs and “reality” of the person suffering from
dementia.
The key is to “agree” with them, but to also use conversation
to get them to do something else without them realizing they
are actually being redirected.
• Therapists therefore attempt to communicate with individuals
with dementia by empathizing with the feelings and
meanings hidden behind their confused speech and behavior.
• It is the emotional content of what is being said that is more
important than the person’s orientation to the present.

47. Simulated presence therapy
(SPT)
•
•
•
Simulated presence therapy attempts to keep the environment of a patient
with dementia as familiar as possible to reduce anxiety and distress.
It involves making a recording of a familiar person and playing it to the patient.
The recorded voice is usually reassuring but the content can be varied
depending upon the interests of the individual patient concerned.
 Evidences….
•
•
• One systematic review that focused on SPT for the treatment of behavioral
symptoms of dementia.
A meta-analysis found a statistically significant effect of SPT on disruptive,
agitated, or depressed behaviors from pre- to post-intervention, but this
analysis was based on three small experimental studies (ranging from six to
nine subjects in each) and one small RCT (N=30).
Some studies identified which shows increased agitation and challenging
behaviors

48. Reality orientation therapy
• most widely used management strategies for dealing
with people with dementia
• It aims to help people with memory loss and
disorientation by reminding them of facts about
themselves and their environment.
• can be used both with individuals and with groups.
• In either case, can be oriented to their environment
using a range of materials and activities.
• This involves consistent use of orientation devices
such as signposts, notices and other memory aids.

49. Snoezelen Multisensory Stimulation Therapy
(primarily used for autism and developmental disabilities)
•
•
•
•
MSS, otherwise known as Snoezelen therapy, is based on the premise
that neuropsychiatric symptoms may result from periods of sensory
deprivation.
It uses multiple stimuli during a treatment session aimed at stimulating
the primary senses of sight, hearing, touch, taste and smell.
It combines the use of such treatments as lights, tactile surfaces, music,
and aroma.
Interventions generally occur in specially designed rooms with a variety
of sensory based materials.
– A typical MSS room provides taped music, aroma, bubble tubes, fiber optic sprays and
moving shapes projected across walls.
– The combination of different materials on a wall may be explored using tactile senses,
and the floor may be adjusted to stimulate the sense of balance.
• MSS has become a popular intervention for behavioral symptoms in
persons with dementia, but the application of MSS varies in form,
procedures, and in frequency of treatment.

50. Snoezelen room

51. Snoezelen room

52. Activity therapy
•
•
Activity therapy involves a rather amorphous group of recreations such as
dance, sport and drama.
It has been shown that these activities can have a number of health
benefits for people with dementia,
for example
•
• reducing the number of falls and
• improving mental health and sleep (King et al, 1997)
• improving their mood and confidence (Young & Dinan, 1994).
• in a small-scale controlled study that daytime exercise helped to reduce
daytime agitation and night-time restlessness. Alessi et al (1999)
An interesting approach to dance therapy is described by Perrin (1998),
who employed a form of dance known as ‘jabadeo’,
– which involves no prescriptive steps or motions
– allows the participants to engage with each other in interactive movements
– This may also fulfill a need for non-sexual physical contact which many people
with dementia find soothing

53. Physical Exercise
 In Early to mild stage of dementia:
•
•
•
•
Gardening
Indoor bowls
Music and dance
Seated exercises
–
–
–
–
–
–
–
–
–
–
marching
turning the body from side to side
raising the heels and toes
bending the arms
bending the legs
clapping under the legs
bicycling the legs
making circles with the arms
raising the opposite arm and leg
Practising moving from sitting to standing.
•
•
•
Swimming
Tai chi/qigong: Tai chi and qigong are gentle forms of Chinese martial arts that combine
simple physical movements and meditation with the aim of improving balance and health
Walking
People who are not
currently active
should be doing about
30 minutes of activity
at least five days a
week
Factsheet: Exercise and physical activity for people with dementia, Alzheimer’s
Society

54. Diet
 Mediterranean diet – a diet rich in fruits, vegetables, legume, olive oil, whole grains
and fishes, mainly sea fishes
 Greater adherence to Mediterranean diet is associated with slower cognitive
decline and lower risk of developing AD. (Lourida et al 2013; Epidemiology)

55. Conclusion
 As there is growing percentage of older population the problems related to geriatric age are on rise,
 specifically dementia and related disorders.
 On the basis of different types ,area involved and comorbidities the sypmtom profile varies from
patient to patient,ex.-
 Managment aims at identifying the reversible causes ,improving functionality ,slowing the detoriation
 Tailor made treatment plan should be used on the basis of symptomatology and type of dementia,
 Should include pharmacological and non pharmacological treatment.
 Future management strategies include early identicfication of illness and drugs for modifying the
course of the illness.

56. REFERENCE
 Sadock B, Sadock V, Ruiz P. Kaplan & Saddocks comprehensive textbook of
psychiatry, volume 1 and 2. 10th ed. Philadelphia: Lippincott Williams and Wilkins;
2009.
 Gelder MG. Oxford textbook of psychiatry. 4th ed. Oxford: Oxford University
Press; 1998.
 The ICD-10 classification of mental and behavioural disorders: clinical descriptions
and diagnostic guidelines. Geneva: World Health Organization; 1992.
 Diagnostic and statistical manual of mental disorders: DSM-5. Washington (D.C.):
American Psychiatric Publishing; 2013.
 Taylor D, Barnes TRE, Young AH. The Maudsley prescribing guidelines in
psychiatry. Hoboken, NJ: Wiley; 2019.