IPS Guidelines For Treatment of Dementia
IPS Guidelines For Treatment of Dementia
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of dementia and differentiating it from other cognitive Subjects or informants can be asked if the person is forgetful
disorders is the first task. Other assessments can then about recent events ;especially amnesia for events which
follow. The suggested assessments are best carried out as happened hours or days back. Does the person forget the fact
part of the initial evaluation though it might take a few that he/she had a meal some time after having the meal? Does
sessions to complete. See table -1 . the person tend to ask the same questions repeatedly even
though this was answered many times. Is the person unable
to recall where they’ve placed things and often searching
Table 1: Assessment for dementia
for things? A review of current medication is very important.
1) Look for signs and symptoms of dementia
2) Rule out DELIRIUM, DEPRESSION
Enquire if there is worsening of cognitive symptoms after
3) Look for other Medical Problems initiation of a certain new medication. Details regarding the
4) Assess Cognitive Symptoms use of all medications, including over-the-counter products,
5) Assess Non-Cognitive (Behavioural) and Psychological Symptoms may be collected .See if the person is on medications with
6) Rule out other Mental Health or Substance use disorders anti-cholinergic effects which can worsen cognitive functions.
7) Assess care arrangements and needs of carers
sleep loss, with or without daytime drowsiness, people without pre-existing dementia. The clinician needs
or reversal of the sleep-wake cycle; to differentiate between three possible scenarios namely
(2) nocturnal worsening of symptoms; Delirium with no features suggestive of pre-existing
(3) disturbing dreams and nightmares which may dementia dementia with no features suggestive of delirium
continue as hallucinations or illusions after dementia with superimposed delirium . See table-2 for
awakening. broad guidelines for making this distinction, which by no
means, will be easy in a given clinical setting . When faced
E. Rapid onset and fluctuations of the symptoms over the with uncertainty, it is better to attribute the symptoms to
course of the day. delirium and manage it as delirium.This will allow careful
F. Objective evidence from history, physical and monitoring and detailed evaluation to identify modifiable
neurological examination or laboratory tests of an conditions/factors.
underlying cerebral or systemic disease (other than
psychoactive substance-related) that can be presumed Table-2: Differentiation between Delirium & Dementia
to be responsible for the clinical manifestations in A-D. Delirium Dementia
• Common causes of Delirium include: Onset Usually Abrupt Insidious and progressive
• Infection (e.g. pneumonia, urinary track Comparative features of Delirium and Dementia
infection, etc.) Duration Usually hours to days Months to years
• Drugs (particularly those with anticholinergic Attention Reduced ability to focus, Usually normal except in
side effects e.g. antidepressants, anti- sustain, or shift attention severe dementia
is a hallmark feature that
parkinsonian /anticholinergic drugs, sedatives, occurs early in presentation
etc.) Consciousness (ie, Fluctuating; reduced level Generally intact
• Cardiological (e.g. myocardial infarction, heart awareness of the of consciousness and
failure) environment) impaired orientation
• Metabolic imbalances (e.g. secondary to Speech Often incoherent and Usually coherent, anomia
disorganized or aphasia can be there
dehydration, renal failure) Cause Underlying medical Underlying neurological
• Endocrine and metabolic (e.g. cachexia, condition, substance process (eg, amyloid β
thiamine deficiency, thyroid dysfunction) intoxication, or side-effect plaque accumulation in
• Neurological (e.g. stroke, subdural haematoma, of drugs Alzheimer’s disease)
Epilepsy) Other features Hyperactive, hypoactive, Symptoms vary
and mixed forms, as depending on underlying
• Substance intoxication or withdrawal (e.g. determined by the type of pathology
alcohol) psychomotor disturbance, (eg, fluctuations in
• Respiratory (e.g. pulmonary embolus, hypoxia). are possible; disruption cognition are a feature of
in sleep duration and Lewy body dementia)
architecture; perceptual
Clinician should take care, not to misdiagnose Delirium as
disturbances
Dementia and also not to miss the diagnosis of Delirium
These two syndromes have substantial overlapping in clinical features and
when it is superimposed on dementia. When there is can even coexist in a given patient
clinical suspicion of delirium, the efforts should focus
on identifying the causes. Delirium in older people are Dementia with Psychotic Symptoms and Schizophrenia
most often multifactorial in etiology and identification Presence of BPSD , especially delusions with or without
of the underlying conditions would enable us to provide hallucinations in mild to moderate dementia can resemble
interventions to reverse/modify them. The evaluations need schizophrenia or other psychotic conditions in late life. The
to be comprehensive so that all common causes can be key differentiating features here are history of progressive
ruled out. Prolonged delirium could lead to more neuronal cognitive decline which has onset prior to the development
damage and accelerate cognitive decline by impacting the of psychotic symptoms the presence of clinically significant
cognitive reserve impairment in multiple cognitive domains on clinical
evaluation . This distinction is rather easy when there
The interface between Delirium & Dementia is long duration of illness starting from adulthood. But
Delirium and dementia are two major causes for it could be difficult when psychotic symptoms have onset
cognitive impairment in later years of life. Though these after the age of 60 years and also in situations where it is
two conditions had been conceptualized as distinct , difficult to test cognitive functions due to active psychotic
mutually exclusive entities ,it can be difficult at times to symptoms . One could also come across individuals who
differentiate between them. Delirium in late life is often after many years of illness with onset during adulthood
superimposed on pre-existing dementia and can be the ,either schizophrenia or bipolar disorder , present with
reason for help seeking. Dementia is the leading risk factor cognitive decline and clinical features suggestive of
for delirium in an older person. Occurrence of delirium dementia. In such situations an additional diagnosis of
in turn is a risk factor for subsequent dementia in older dementia can be made apart from the diagnosis of the
pre existing mental health condition. See table-3 for some The diagnostic challenge in MCI here is in the assessment
clinical tips of “significant impairment in functional ability,” which is
required for the diagnosis of dementia. There is also the
controversy about the best way to objectively measure
Table-3: Psychosis of AD compared with Schizophrenia
memory loss. Early recognition of the condition may help
in the elderly
the clinician to monitor the progression of cognitive and
Clinical Features: Psychosis of AD Schizophrenia
other symptoms and the later conversion to dementia.
Bizarre or complex delusions Rare Frequent
This might allow potential use of evidence based
Misidentifications of caregivers Frequent Rare
Common form of hallucinations Visual Auditory preventive interventions as and when they become
Schneiderian first-rank symptoms Rare Frequent available.The recognition of MCI as a diagnostic allows
Active suicidal ideation Rare Frequent us to have a better understanding of the nature of mild
Past history of psychosis Rare Frequent memory loss ,which is far more common than dementia
Eventual remission of psychosis Frequent Uncommon
among the older segments of the population.Table-4
Need for long-term treatment with Uncommon Very common
antipsychotics lists out the main differences between the two clinical
conditions
Differentiation between Dementia and Mild Cognitive Table-4: MILD COGNITIVE IMPAIRMENT Vs
Impairment DEMENTIA
MILD COGNITIVE DEMENTIA
The differentiation between early dementia and mild IMPAIRMENT
cognitive impairment can be difficult at times but efforts to Impaired cognition in one or more Significant cognitive decline in one
make that distinction is always warranted. DSM 5 uses the domains, but to a lesser degree or more domains- memory ,speech
term Mild Neurocognitive Disorder to refer to this condition. than in dementia. ,judgement, visuospatial, behaviour
ICD 10 does not have specific criteria. The following DSM Mild impairments in the more Substantial impaired cognition
complex aspects of daily
5 criteria may be used as a guide for clinical diagnosis of functioning,
Mild Cognitive Impairment. No significant impairment on Sufficiently severe to interfere
activities of daily living activities of daily living
DSM 5 criteria for Mild Cognitive Impairment Clinical features: Clinical features:
Difficulty in solving complex Severe memory loss
A. Evidence of modest cognitive decline from a previous
problems Visuospatial dysfunction
level of performance in one or more cognitive domains Difficulty in performing more Language problems, articulating
(complex attention, executive function, learning than one task at a time problem
and memory, language, perceptual motor, or social Personality problem
cognition) based on: Prognosis Prognosis
MCI may represent a prodromal Progressive cognitive decline
1. Concern of the individual, a knowledgeable
state of dementia. However, not
informant, or the clinician that there has been a all individuals with MCI will go
mild decline in cognitive function; and on to develop dementia
2. A modest impairment in cognitive performance,
preferably documented by standardized Assessment of Dementia Syndrome
neuropsychological testing or, in its absence, We need to rule out delirium and mild cognitive disorder
another quantified clinical assessment. before we make a clnical diagnosis of dementia . Then one
should apply and see if the person meets the diagnostic
B. The cognitive deficits do not interfere with capacity criteria for Dementia. If that is met, then there is a need to
for independence in everyday activities (i.e., complex make further evaluations. The next part of evaluation is
instrumental activities of daily living such as paying bills aimed at establishing the cause for the dementia syndrome.
or managing medications are preserved, but greater
effort, compensatory strategies, or accommodation Types and Causes of Dementia
may be required). Dementia is a syndrome which can be caused by many
C. The cognitive deficits do not occur exclusively in the diseases .After the clinical recognition of dementia
context of a delirium. syndrome, the evaluations shall focus on identifying the
D. The cognitive deficits are not better explained by cause of dementia. Causes can be broadly classified as
another mental disorder (e.g., major depressive “reversible causes’ and “Irreversible” causes .Though
disorder, schizophrenia). “Reversible” causes are less frequent, they carry good
prognosis with prompt treatment of the underlying
Behavioral disturbance (e.g., psychotic symptoms, mood condition. Thus the evaluation for all potentially reversible
disturbance, agitation, apathy, or other behavioral conditions which cause dementia syndrome is the first most
symptoms important step in the assessment of dementia syndrome
and this is essential in all cases presenting with features of Vascular dementia, Dementia with Lewy Bodies and Fronto-
dmentia. The type of investigations can be decided based temporal dementia.
on the clinical features and context of care. This aspect
is discussed in detail in the 2009 Dementia Supplement of Table 5:Common Subtypes of Irreversible Dementias
Indian Journal of Psychiatry. Dementia Clinical Features Neuropathology Proportion of
subtype dementia cases
Clinical Assessment Alzheimer’s Impaired memory, Cortical amyloid 50-75%
Patients who seek help in clinical settings often do not represent disease (AD) Apathy and Plaques and
cases prevalent in the community. Reversible causes thus may Depression Gradual neurofibrillary
onset tangles
be much more common in clinical settings than in community Vascular Similar to AD, Cerebrovascular 20-30%
settings. Routine investigations should include complete blood dementia (VaD) but Memory less disease Single
count, erythrocyte sedimentation rate, and serum/blood levels affected, and mood Infarcts in
of urea, electrolytes, calcium and phosphate, liver, renal and, fluctuations more Critical regions,
thyroid function tests, urine analysis, VDRL and Serum Bl2 prominent Physical or more diffuse
frailty Stepwise multi-infarct
,and Folate levels. CT scan or MRI scan, at times, can be a very Progression disease
useful investigation in the differential diagnosis of dementia. Dementia with Marked fluctuation Cortical Lewy <5%
Investigations for testing the HIV status, ECG, Chest radiograph, Lewy Bodies in cognitive ability Bodies (alpha-
Electroencephalogram, Neuropsychological assessment etc are (DLB) Visual Hallucinations synuclein)
investigations worth considering. Parkinsonism (tremor
and rigidity)
Fronto-temporal Personality changes No single 5-10%
Common Potentially Reversible Causes dementia (FTD) Mood changes Dis- pathology –
• Depression inhibition Language damage limited
• Medication Induced (Especially drugs with difficulties to Frontal and
anticholinergic activity) temporal lobes in
the initial stages
• Metabolic derangements
• Thyroid disorders (Hyopthyroidism is a common cause)
Please follow the steps described in Figures 1, 2, 3 and 4 for
• Vitamin B12 deficiency
systematic evaluation of a person presenting with cognitive
• Thiamine deficiency
symptoms
• Chronic disease (e.g., renal failure, hepatic failure,
malignancy)
Cognitive assessment can be made as part of detailed
• Gastrointestinal disorders
examination of higher functions. Commonly used
instruments like Mini-Mental State Examination (MMSE)
• Whipple’s disease
can be used. Addenbrooke’s Cognitive Examination (ACE)
• Vitamin E deficiency
is a more detailed test battery for assessing cognitive
• Pellagra
• Infections
• Neurosyphilis
• HIV/AIDS
functions. Assessment of the activities of daily living is G1. Evidence of each of the following:
very important. This information is essential in formulating (1) A decline in memory, which is most evident in the
the individualized plan of intervention. Everyday Activities learning of new information, although in more severe
Scale for India (EASI) developed during the Indo-US cases, the recall of previously learned information may be
Cross-National Dementia Epidemiology Study is useful also affected. The impairment applies to both verbal and
for this purpose, especially in the rural illiterate. Use non-verbal material. The decline should be objectively
verified by obtaining a reliable history from an informant, G2. Preserved awarenenss of the environment (i.e.
supplemented, if possible, by neuropsychological tests absence of clouding of consciousness (as defined in
or quantified cognitive assessments. The severity of F05,criterion A)) during a period of time long enough to
the decline, with mild impairment as the threshold for enable the unequivocal demonstration of G1. When there
diagnosis, should be assessed as follows: are superimposed episodes of delirium the diagnosis of
dementia should be deferred.
Mild: a degree of memory loss sufficient to interfere
with everyday activities, though not so severe as to be G3. A decline in emotional control or motivation, or a change
incompatible with independent living. The main function in social behaviour, manifest as at least one of the following:
affected is the learning of new material. For example, the (1) emotional lability;
individual has difficulty in registering, storing and recalling (2) irritability;
elements in daily living, such as where belongings have been (3) apathy;
put, social arrangements, or information recently imparted (4) coarsening of social behaviour.
by family members.
G4. For a confident clinical diagnosis, G1 should have
Moderate: A degree of memory loss which represents a been present for at least six months; if the period since
serious handicap to independent living. Only highly learned the manifest onset is shorter, the diagnosis can only be
or very familiar material is retained. New information is tentative.
retained only occasionally and very briefly. The individual is
unable to recall basic information about where he lives, what Comments: The diagnosis is further supported by evidence
he has recently been doing, or the names of familiar persons. of damage to other higher cortical functions, such as
aphasia, agnosia, apraxia.
Severe: a degree of memory loss characterized by the
Judgment about independent living or the development
complete inability to retain new information. Only fragments
of dependence (upon others) need to take account of the
of previously learned information remain. The subject fails
cultural expectation and context.
to recognize even close relatives.
Dementia is specified here as having a minimum duration
(2) A decline in other cognitive abilities characterized
of six months to avoid confusion with reversible states with
by deterioration in judgement and thinking, such as
identical behavioural syndromes, such as traumatic subdural
planning and organizing, and in the general processing of
haemorrhage (S06.5), normal pressure hydrocephalus
information. Evidence for this should be obtained when
(G91.2) and diffuse or focal brain injury (S06.2 and S06.3).
possible from interviewing an informant, supplemented, if
possible, by neuropsychological tests or quantified objective ICD 10
assessments. Deterioration from a previously higher level
of performance should be established. The severity of F00 DEMENTIA IN ALZHEIMER’S DISEASE
the decline, with mild impairment as the threshold for A. The general criteria for dementia (G1 to G4) must be
diagnosis, should be assessed as follows: met.
B. There is no evidence from the history, physical
Mild. The decline in cognitive abilities causes impaired examination or special investigations for any other
performance in daily living, but not to a degree making the possible cause of dementia (e.g. cerebrovascular
individual dependent on others. More complicated daily disease, Parkinson’s disease, Huntington’s disease,
tasks or recreational activities cannot be undertaken. normal pressure hydrocephalus), a sysytemic disorder
(e.g. hypothyroidism, vit. B12 or folic acid deficiency,
Moderate. The decline in cognitive abilities makes the hypercalcaemia), or alcohol- or drug-abuse.
individual unable to function without the assistance of
another in daily living, including shopping and handling Comments: The diagnosis is confirmed by post mortem
money. Within the home, only simple chores are preserved. evidence of neurofibrillary tangles and neuritic plaques in
Activities are increasingly restricted and poorly sustained. excess of those found in normal ageing of the brain.
Severe. The decline is characterized by an absence, or The following features support the diagnosis, but are not
virtual absence, of intelligible ideation. The overall severity necessary elements: Involvement of cortical functions
of the dementia is best expressed as the level of decline in as evidenced by aphasia, agnosia or apraxia; decrease
memory or other cognitiveabilities, whichever is the more of motivation and drive, leading to apathy and lack of
severe (e.g. mild decline in memory and moderate decline in spontaneity; irritability and disinhibition of social behaviour;
cognitive abilitiesindicate a dementia of moderate severity). evidence from special investigations that there is cerebral
atrophy, particularly if this can be shown to be increasing 5. Perseverative and stereotyped behavior
over time. In severe cases there may be Parkinson-like 6. Utilization behavior
extrapyramidal changes, logoclonia, and epileptic fits.
B. Speech and language
Specification of features for possible subtypes. Because of 1. Altered speech output
the possibility that subtypes exist, it is recommended that a. Aspontaneity and economy of speech
the following characteristics be ascertained as a basis for b. Pressure of speech
a further classification: age at onset; rate of progression; 2. Stereotypy of speech
the configuration of the clinical features, particularly 3. Echolalia
the relative prominence (or lack) of temporal, parietal or 4. Perseveration
frontal lobe signs; any neuropathological or neurochemical 5. Mutism
abnormalities, and their pattern.
C. Physical signs
The division of AD into subtypes can at present be 1. Primitive reflexes
accomplished in two ways: first by taking only the age 2. Incontinence
of onset and labeling AD as either early or late, with an 3. Akinesia, rigidity, and tremor
approximate cut-off point at 65 years 4. Low and labile blood pressure
ICD 10 D. Investigations
1. Neuropsychology: impairment on frontal lobe
F01 VASCULAR DEMENTIA tests without severe amnesia, aphasia, or
G1. The general criteria for dementia (G1 to G4) must be perceptuospatial disorder
met. 2. Electroencephalography: normal on
G2. Unequal distribution of deficits in higher cognitive conventional EEG despite clinically evident
functions, with some affected and others relatively dementia
spared. Thus memory may be quite markedly affected
while thinking, reasoning and information processing Brain imaging (structural and/or functional): predominant
may show only mild decline. frontal and/or anterior temporal abnormality
G3. There is clinical evidence of focal brain damage,
manifest as at least one of the following: Revised criteria for the clinical diagnosis of probable and
(1) unilateral spastic weakness of the limbs; possible dementia with Lewy bodies (DLB)
(2) unilaterally increased tendon reflexes; • Essential for a diagnosis of DLB is dementia, defined as a
(3) an extensor plantar response; progressive cognitive decline of sufficient magnitude to
(4) pseudobulbar palsy. interfere with normal social or occupational functions,
or with usual daily activities. Prominent or persistent
G4. There is evidence from the history, examination, or memory impairment may not necessarily occur in the
tests, of a significant cerebrovascular disease, which early stages but is usually evident with progression.
may reasonably be judged to be etiologically related Deficits on tests of attention, executive function, and
to the dementia (e.g. a history of stroke; evidence of visuoperceptual ability may be especially prominent
cerebral infarction). and occur early.
• Core clinical features (The first 3 typically occur early
Consensus criteria for FRONTOTEMPORAL DEMENTIA and may persist throughout the course.)
o Fluctuating cognition with pronounced variations
I. Core diagnostic features in attention and alertness.
A. Insidious onset and gradual progression o Recurrent visual hallucinations that are typically
B. Early decline in social interpersonal conduct well formed and detailed.
C. Early impairment in regulation of personal conduct o REM sleep behavior disorder, which may precede
D. Early emotional blunting cognitive decline.
E. Early loss of insight o One or more spontaneous cardinal features of
parkinsonism: these are bradykinesia (defined as
II. Supportive diagnostic features slowness of movement and decrement in amplitude
A. Behavioral disorder or speed), rest tremor, or rigidity.
1. Decline in personal hygiene and grooming
2. Mental rigidity and inflexibility • Supportive clinical features
3. Distractibility and impersistence o Severe sensitivity to antipsychotic agents postural
4. Hyperorality and dietary changes instability; repeated falls; syncope or other transient
episodes of unresponsiveness; severe autonomic Lewy body disease are often helpful. In research studies in
dysfunction, e.g., constipation, orthostatic which distinction needs to be made between DLB and PDD,
hypotension, urinary incontinence; hypersomnia; the existing 1-year rule between the onset of dementia and
hyposmia; hallucinations in other modalities; parkinsonism continues to be recommended.
systematized delusions; apathy, anxiety, and
depression. Aassessment of the following will help in planning the
management:
• Indicative biomarkers o Activities of Daily Living ( ADL) .This is essentiality
o Reduced dopamine transporter uptake in basal about the the ablity for feeding, bathing, dressing,
ganglia demonstrated by SPECT or PET. Abnormal mobility, toileting, continence and also the ability to
(low uptake) 123iodine-MIBG myocardial manage finances and medications
scintigraphy. Polysomnographic confirmation of o Assess the Cognitive Status using a reliable and valid
REM sleep without atonia. instrument (e.g. the MMSE, MOCA etc)
o Look for other Medical Conditions,Behavioral Problems
• Supportive biomarkers , Psychotic Symptoms, or Depressive Symptoms
o Relative preservation of medial temporal lobe o Identify the Primary Caregiver: Assess the adequacy of
structures on CT/MRI scan. Generalized low uptake family and other support systems.
on SPECT/PET perfusion/metabolism scan with o Assess Caregiver’s needs and risks ; Re-asses this a
reduced occipital activity 6 the cingulate island sign regular basis
on FDG-PET imaging. Prominent posterior slow- o Assess the patient’s decision-making capacity and
wave activity on EEG with periodic fluctuations in whether a surrogate has been identified
the pre-alpha/ theta range.
Assessment of co-morbidity:
• Probable DLB can be diagnosed if:
o Two or more core clinical features of DLB are Multimorbidity is common in latelife. A clear understanding
present, with or without the presence of indicative of physical aand mental health is important for planning
biomarkers dementia care. Assess for
o Only one core clinical feature is present, but with a. Co-morbidity
one or more indicative biomarkers. • Depression
• Diabetes/HTN/ Vascular diseases
• Probable DLB should not be diagnosed on the basis of • Parkinsonism
biomarkers alone. • Other chronic diseses like COPD/Arthritis
• Possible DLB can be diagnosed if:
o Only one core clinical feature of DLB is present, b. Nutritional Status . Poor nutritional status can be a
with no indicative biomarker evidence consequence of poor self care and poor dietary intake
o One or more indicative biomarkers is present but c. Care arrangements
there are no core clinical features. • Identify the Primary caregiver. This is crucial.
In most instances there will be one person who
• DLB is less likely: generally co-ordinates and provide most of the care
o In the presence of any other physical illness or provision
brain disorder including cerebrovascular disease, • Assess Caregiver support systems
sufficient to account in part or in total for the • Is there a Formal/Paid caregiver
clinical picture, although these do not exclude a • Try to link with local Dementia Society/Palliative
DLB diagnosis and may serve to indicate mixed or Care service
multiple pathologies contributing to the clinical
presentation 2. Formulating a treatment plan (Figure 5-8)
o If parkinsonian features are the only core clinical • Diagnostic Evaluation. Please follow the earlier
feature and appear for the first time at a stage of described format to make assessments when there
severe dementia. is history of cognitive decline. Those steps will help
to identify and differentiate between syndromes
DLB should be diagnosed when dementia occurs before or like delirium, dementia and mild cognitive disorder.
concurrently with parkinsonism. The term Parkinson disease Once the dementia syndrome is identified the
dementia (PDD) should be used to describe dementia that assessments shall be aimed at the following
occurs in the context of well-established Parkinson disease. • Type of Dementia
In a practice setting the term that is most appropriate to the • Presence and nature of cognitive and non-cognitive
clinical situation should be used and generic terms such as symptoms
Table -7: ASSESSMENTS DURING FOLLOW-UP VISITS hastens cognitive decline. Reality orientation and
• Look for Side-effects of Medications reminiscence therapy is of use in this regard.
If on antipsychotics, check for extrapyramidal symptoms .. Stop or • Non-pharmacological interventions for non-cognitive
reduce dose if present. symptoms and challenging behaviour
• Assess for Co-morbid Medical and Mental Health Issues Non-cognitive symptoms and challenging behaviors
• Evaluate Activities of Daily Living: See if there is unmet need for significantly increase the burden of care. They lead
assistance . to caregiver distress and burnout and hence is an
• See if there are Mobility Issues / Risk of Fall
important concern in the management of dementia.
• Assess issues related to Safety/ potential for accidents & trauma ;
considerr appropriate interventions like limit driving/ operating Common non-cognitive symptoms seen in dementia
equipment/, cooking, etc. are delusions, hallucinations, anxiety, agitation and
• Look for emergence of Behavioral Symptoms associated aggressive behavior. Challenging behaviours
• Assess Caregiver Burden / Distress and look for unmet caregiver needs include a range of difficulties experienced by people
with dementia and has a considerable impact on
their caregivers. Common challenging behaviours are
of Alzhiemer’s and Related Disorders Society, Help aggression, agitation, wandering, hoarding, sexual
Age India,Paliative Care Networks, other voluntary disinhibition, apathy and shouting.
agencies engaged in geriatric care and seek support Non-pharmacological interventions for the non-
and guidance cognitive symptoms and challenging behaviours should
• Institutional care: When the hom-based care is not be tailored for each patient with participation from
feasible or unavailable ,the person with dementia may the caregivers.This shall be preceded by assessments
need instituitional care with provision for assisted aimed at identifying factors which may be responsible
living to generate, aggravate or improve such behaviour. Such
• Short-term hospitalization : This is often required when an assessment should be comprehensive and consider
there is a medical or surgical morbidity which often the person’s physical health, possible undetected pain
cannot be handled in ambulatory care settings. Onset or discomfort, side effects of medication, psychosocial
of delirium or sudden worsening of BPSD also could factors, cultural and religious background, and physical
necessitate brief hospitalization. Brief hospitalisations environmental factors. Several modalities of non-
can be used to provide more information and assistance pharmacological interventions like aromatherapy,
to caregivers. This can be an opportunity to identify multisensory stimulation, music/dancing therapy,
unmet care needs as well as needs of the caregivers. massage and animal assisted therapy are available.
• Long-term assisted living. There is a need for this The choice of therapy should be made considering the
facility especially when the home-based care is not able availability along with the person’s preferences, skills
to meet the demands of care.This is a reality in many and abilities. These interventions can be delivered by
household as the family size is dwindling and most health and social care staff and volunteers with proper
young people work outside their homes. training and supervision. The response to each form
of therapy should be monitored and the care plan
Non-pharmacological interventions should be reviewed from time to time as there may be
individual variations in the response to each of these
Non-pharmacological management strategies( Table -8) modalities.
have an important role in the management of dementia
of any type. It is particularly helpful in elderly patients Pharmacological treatment of Dementia
who may not tolerate pharmacological agents due to the General Principles
development of adverse effects even in smaller doses. • The pharmacological treatment of dementia is associated
There are specific non-pharmacological interventions with important challenges such as complexities in the
targeting the cognitive as well as non-cognitive symptoms clinical presentation and diagnosis, non-availability
and challenging behaviours seen in dementia. of therapeutic agents with robust effectiveness and
issues related to tolerability of medications used in the
• Non-pharmacological interventions for cognitive treatment of dementia.
symptoms • Disease modifying drugs to treat Alzheimer’s disease
People with mild to moderate dementia of all types and other related dementias is an important unmet
should be encouraged to participate in structured need in the treatment of chronic medical disorders in
cognitive stimulation programmes. They benefit elderly.
cognition in such patients irrespective of whether any • The currently available options for the pharmacological
drug is prescribed or not. They are also beneficial in treatment of dementia are essentially symptomatic
improving and maintaining their functional capacity. treatments with limited effectiveness.
This is based on the view that lack of cognitive activity • It would be preferable to plan the pharmacological
treatment of dementia after comprehensive evaluation • There is no clear evidence regarding the benefit of
to understand the possible subtype, associated Cholinesterase inhibitors for the management of
behavioural and psychological symptoms, comorbidity behavioral and psychological symptoms in Alzheimer’s
etc dementia.
• Treatment of dementia needs to be focused on • The efficacy of cholinesterase inhibitors is established
improving the cognitive function, amelioration of clearly in the short term randomized controlled trials
associated behavioral and psychological symptoms and lasting for 3 to 6 months for the cognitive domains and
improvement or stabilization of global functioning in global functioning.
daily activities. • Few studies have indicated continued benefit of
• It would be useful to have clear understanding of the cholinesterase inhibitors in the long term (up to 1 year).
treatment targets and proper monitoring of outcomes But there are limitations in the quality of this evidence.
following treatment to optimize the treatment • The benefit of cholinesterase inhibitors in the long term
appropriately(Figure-9). is suggested through the observation of deterioration
• Behavioral and psychosocial interventions are required of cognitive function and global functioning after the
for all patients with dementia. Pharmacological withdrawal of cholinesterase inhibitors.
treatment needs to be planned in addition to this • The adverse effects that are commonly noted to occur
particularly for behavioral and psychological symptoms with Cholinesterase inhibitors are primarily related
of dementia. to cholinergic effects (nausea, vomiting, diarrhea,
anorexia, weight loss, bradycardia and falls).
Figure-9 • The most common adverse effects with cholinesterase
inhibitors are gastrointestinal side effects. The
cholinergic effects are usually dose related. The
tolerability appears to improve with dose reduction
and slower titration.
• The benefit with cholinesterase inhibitors is difficult
to establish at individual patient level in view of the
progressive nature of the illness and the possibility of
contribution to cognitive decline from multiple factors.
• The assessment of response to treatment is based on the
Pharmacological treatment for cognitive symptoms of effects on cognitive symptoms, activities of daily living
Dementia(Tables 9 & 10) and the clinician judgement about the global change.
• Alzheimer’s disease is the most common cause of • Memantine can be considered as the choice of drug for
dementia and a major contributor for global disease treatment of patients with Alzheimer’s dementia when
burden. Hence there has been very active global cholinesterase inhibitors are contraindicated or could
effort to develop effective disease modifying drug for not be tolerated due to adverse effects.
Alzheimer’s disease in the past decade. • Despite the minor differences in the mechanism of
• However, no new effective drug has been identified action of Donepezil, Rivastigmine and Galantamine,
for improving the cognitive function in patients with there is no clear evidence to support choosing any
dementia due to Alzheimer’s disease in the last decade. specific cholinesterase inhibitor over other drugs.
• Cholinesterase Inhibitors (Donepezil, Rivastigmine and • It would be useful to do Electrocardiogram to rule out
Galantamine) and NMDA antagonist (Memantine) are conduction abnormalities and clarify about pre-existing
the approved pharmacological treatment options for gastrointestinal side effects like nausea and vomiting
the cognitive impairment in Alzheimer’s Dementia prior to initiating cholinesterase inhibitors.
• Donepezil has been approved for all stages of • Patients initiated on medications for dementia requires
Alzheimer’s dementia. Rivastigmine and Galantamine follow up evaluation after 4 to 6 weeks to review the
has been approved for mild to moderate Alzheimer’s adverse effects and adjust the dose as required.
dementia • If a patient is not tolerating one cholinesterase inhibitor
• Memantine has been approved for moderate to severe and it has not improved with dose reduction or slower
Alzheimer’s dementia titration, changeover to another cholinesterase
• Combination of Donepezil and Memantine has been inhibitor can be considered.
approved for moderate to Severe Alzheimer’s dementia • Rivastigmine transdermal patch can be considered if
• Rivastigmine Transdermal patch (4.6mg, 9.5mg or there are significant gastrointestinal side effects with
13,3mg per 24 hours) has been approved for mild to oral cholinesterase inhibitor.
moderate Alzheimer’s dementia. The extent of adverse • High dose (11.5 and 23mg) extended release Donepezil
effects with Rivastigmine is lesser in transdermal patch has been approved for use in moderate to severe dementia
than oral formulation. after 3 months of stabilization with 10mg Donepezil.
• The approval for Donepezil 23mg is based on a single • Low dose atypical antipsychotics (Aripiprazole,
randomized controlled trial which showed that it was Risperidone, Quetiapine etc) can be considered for
significantly better than Donepezil 10mg for improving severe psychotic symptoms and agitation
cognitive function in patients with moderate to severe • Quetiapine and Clozapine can be considered by severe
Alzheimer’s dementia. psychotic symptoms in dementia due to Lewy body
• The clinical utility of Donepezil 23mg is not clear as the disease and Parkinson’s disease
marginal improvement in cognitive function without • Treatment with SSRI and Mirtazapine has not contributed
significant improvement in global functioning may to significant improvement of depression in patients
have limited clinical significance for individuals with with dementia.
moderate to severe dementia.
• The frequency of cholinergic adverse effects is also Pharmacological Treatment in Non-Alzheimer’s dementia
higher with Donepezil 23mg contributing to poor • Clinical trials on the treatment of dementia has
tolerability and increased risk for discontinuation largely focused on Alzheimer’s dementia due to high
• Other than cholinesterase inhibitors and memantine, prevalence and public health significance
there are no other approved drugs to improve • There is no clear evidence for efficacy of cholinesterase
cognitive function in patients with dementia. Cognitive inhibitors or memantine in Vascular dementia and
enhancers like Ginko Biloba and Piracetam do not have Frontotemporal dementia
clear evidence to be recommended for routine use in • Cholinesterase inhibitors (Particularly Rivastigmine
patients with dementia. and Donepezil) have significant benefits for cognitive
symptoms as well as visual hallucination in dementia
Pharmacological treatment for Behavioural and due to Lewy body disease and Parkinson’s disease
Psychological symptoms of dementia (Table 11) • SSRI and Trazodone are found to be useful in
• Behavioral and Psychological symptoms of dementia Frontotemporal dementia
(BPSD) is very common in patients with dementia. • Lorazepam or Clonazepam and Melatonin are found
Nearly all patients with dementia are likely to develop to be useful for REM sleep behavioural disorder in
BPSD at any point of time during the illness. dementia due to Lewy body disease.
• BPSD is often the most important contributor for the • Patients with Vascular dementia needs treatment with
distress and burden in caregivers. Many patients with medications for risk factors like diabetes, hypertension,
dementia are brought for evaluation and treatment dyslipidemia etc
primarily due to BPSD. • Cholinesterase inhibitors can be tried in patients with
• BPSD is also the important factor that determines the mixed dementia if Alzheimer’s disease is co-existent
risk for institutionalization. with other types of dementia
• Apathy, depression, agitation, aggression, wandering
behavior, sleep disturbance and psychotic symptoms Other Somatic treatments
are the most common BPSD symptoms in dementia. • Electroconvulsive therapy (ECT) can be considered for
• Risperidone is the only treatment approved for the severe depression in patients with dementia.
treatment of agitation and aggression in patients with • ECT can be considered for those with dementia having
dementia. very severe agitation and aggression that are non-
• Use of antipsychotics in elderly with dementia is responsive to other treatments
associated with increased risk for cerebrovascular • Non-invasive brain stimulation like Transcranial
adverse events and mortality direct current stimulation (tDCS) and Transcranial
• Pharmacological treatment for BPSD needs to be Magnetic Stimulation (TMS) have no clear evidence of
considered only if the symptoms are distressing to the effectiveness in patients with dementia.
patient / caregiver or if it is contributing to the risk for
harm to patient / others. Table- 9: Pharmacological Treatment of Dementia
• Recent evidence has suggested the possibility of • Cholinesterase Inhibitors (Donepezil, Rivastigmine and Galantamine )
can be used for all the stages of Dementia due to Alzheimer’s disease
improvement in agitation with Citalopram when it is
• Memantine alone or in combination with Cholinesterase inhibitors is
not severe enough to initiate antipsychotics. useful in moderate to severe Dementia due to Alzheimer’s disease
• Like Citalopram, other Selective Serotonin Reuptake • Donepezil and Rivastigmine can be used in Dementia due to Lewy
Inhibitors (SSRI) are also likely to be effective in controlling Body disease and Parkinson’s Disease
the agitation in patients with dementia. However, there is • Selective Serotonin Reuptake Inhibitors can be used in Frontotemporal
dementia
need for more evidence to support this treatment option.
• Low dose atypical antipsychotics (Risperidone, Aripiprazole,
• Higher dose of Citalopram (used in the study showing Quetiapine) can be considered for severe agitation, aggression and
positive effect on agitation in dementia) is associated psychotic symptoms
with increased risk for QT interval prolongation. Hence • Mood Stabilizers like Divalproex sodium and Carbamazepine may be
it is not recommended. useful in the management of agitation
Table -10: Approved Antidementia drugs Table 11: Psychotropic Agents Useful for the Treatment
Name of the Usual Maximum Side effects Remarks of BPSD
Drug Starting recommended Type and Drug Initial Final Daily Dose Targeted Symptoms
dose in dose (mg/day) Daily (Range)
mg/day Dose
Cholinesterase Inhibitors Atypical antipsychotic
Donepezil 5 10 Nausea, Start with 5mg
vomiting, once daily Risperidone 0.5 mg 1.0 mg Psychosis and
diarrhea, and increase daily (0.75 -1.5 mg daily) agitation
insomnia, to 10mg once
muscle cramps, daily after Olanzapine 2.5 mg 5.0 mg
anorexia, 4 weeks if daily (5-10 mg daily
weight loss, tolerability is Quetiapine 25 mg 200 mg
bradycardia, good daily (50-150 mg twice a day)
syncope Mood stabilizer
Rivastigmine 3 12 Similar side Start with Divalproex 125 mg 500 mg Agitation
effects like 1.5mg twice sodium twice a (250-500 mg twice a day)
Donepezil daily and m day
but slightly increase by Carbamazepine 200 mg 400 mg
more severe 3mg per day twice a (200-500 mg twice a day)
gastrointestinal every 2 weeks day
side effects till 6mg twice Selective serotonin-reuptake inhibitor
daily Citalopram 10 mg 20 mg Depression, anxiety,
Galantamine 8 24 Similar to Start with 4mg daily (20-40 mg daily) psychosis, and
Donepezil and twice daily Escita!opram 5 mg 10 mg agitation
Rivastigmine and increase daily (10-20 mg daily)
by 8mg every Paroxetine 10 mg 20 mg
4 weeks till daily (10-40 mg daily)
12mg twice Sertraline 25 mg 75 mg
daily daily (75-100 mg daily)
Rivastigmine 4.6mg/ 24 9.5mg/24 Occasional Start with
Transdermal hours patch hours patch Skin Irritation 4.6mg/24hours
patch patch and
increase to
• Disease modifying drugs for dementia are expected to
9.5mg/24 be more effective in the stage of MCI compared to the
hours patch stage of dementia.However no effective medication has
after 4 weeks been identified for MCI
if tolerability is
• Acetyl Cholinesterase inhibitorsand Memantine have
good
Donepezil 11.5 23 More severe Titration to not been found to be effective in delaying the conversion
Extended gastrointestinal high dose of MCI to dementia. Routine use of Cholinesterase
Release side effects Donepezil inhibitors or Memantinefor the treatment of MCI is not
needs to be recommended.
considered
after at least
(Please see references 12-20 for further reading of
3 months pharmacological treatment)
maintenance Management of different phases of illnesses
with 10mg
Donepezil
The course of Dementia can be divided into three phases;
NMDA
Antagonist mild, moderate and severe, based on the severity of
Memantine 10 20 No significant Start with 5mg cognitive symptoms and functional impirment. Symptoms
adverse effects twice daily like BPSD are more common in the mild to moderate phase
and increase where as the impairments in ADL predominate the severe
by 5mg every
phase.BPSD may not be present in all cases and may not be
week and
titrate to 10mg problematic in some. Mangement of BPSD is particularly
twice daily important during the initial phases of the illness as this
can have direct impact on the quality of life of the affected
individual and the family members involved in care. Refer
Pharmacological Treatment of Mild Cognitive Impairment to the setion on management
• Mild Cognitive Impairment (MCI)is the high-risk state
for dementia with significantly increased risk for Special Issues in the management of Dementia
conversion to dementia compared to those with normal 1. Delirium Superimposed on Dementia
cognition. • When to suspect ?
Older people with dementia have high risk of development 4. Need to Link with Community-based Services
delirium. Both hypoactive and hyperactive delirium can It would help if community outreach services like palliative
occur , but hypoactive delirium is more likely. Any sudden care services or any other similar service can be linked to
deterioration in sensorium ,activity level, behaviour should home-based dementia care
alert the possibility of superimposed delirium. It will be be
associated with disturbance in sleep wake cycle and could 5. Use of diagnostic instruments/tools
also take the form of increased sleepiness. Brief screening tests can be useful ..This can help in eliciting
key information and by making brief cognitive assessment.
• How to manage? The ideal test would be sensitive and specific. It should be
The management should involve attempts to identify short, simple and user friendly. There are large number of
multiple causes which usually contribute to development tests available and that suggests that no one test is the best.
and persistence of delirium .Once identified these factors Shorter tests may confirm a cognitive problem that needs to
may be addressed and the condition be monitored. be evaluated, whereas longer tests contribute more to the
Disappearance of recent onset behavioural symptoms and diagnosis. There are many instruments useful to screen or
improvement in cognitive functions over a period of days find cases of dementia. See http://www.who.int/mental_health/
would usually be indicative of resolution of superimposed mhgap/evidence/dementia/q6/en/index.html for more details of
delirium the review. Details of useful tools are available at the website
of Alzheimer’s Association( https://www.alz.org/documents_
2. Management of Multi-morbidity. custom/141209-CognitiveAssessmentToo-kit-final.pdf)
Dementia is a major neuropsychiatric condition and long-
term medical care. Multimorbidity is common among older CONCLUSIONS
people and people with dementia are no exception. Two
strategies can help here. The first one is to evaluate the Caregiver support and non-pharmacological interventions
person in detail for presence of co-morbidity and sensory to manage symptoms like BPSD are the main ingredients of
impairments.This can be done after making the diagnosis dementia care. Psychosocial management forms the first line
of dementia. Do enquire about the current management of and shall be given to all with BPSD. Psychosocial interventions
each problem. You may include the management of the co- work best when it is contextualized to the socio-cultural
morbid conditions also into the follow-up plan.The second environment and the setting of care. Family and professional
important strategy would be to be on the watch out for caregivers should be considered as key collaborators. Provision
emergence of new problems like delirium or issues related of relevant information , education and seamless support to
falls , infections, cerebrovascular events etc. Prompt caregivers , will be very crucial in dementia care. There is
identification and early interventions can help to prevent unmet need for such help and guidance .The families engaged
or identify major eventsearly. Adherence to interventions in the care of a person affected by dementia will benefit from
is a matter of concern as this would be dependent on such support and this is especially so there are behavioral
the caregivers. Communication with the caregivers will symptoms which are difficult to mange in home setting Some
have to be simple and might need to be repeated. Try to may benefit from pharmacological interventions but this shall
speak to the primary caregivers directly and allow time for be provided under supervision and needs to be monitored.
clarifications if they have doubts. Ask a family member to
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WEBSITES FOR FURTHER INFORMATION How to cite this article: Shaji KS, Sivakumar PT, Rao GP,
Paul N. Clinical Practice Guidelines for Management of
• https://www.alz.org/documents_custom/141209-CognitiveAssessment Dementia. Indian J Psychiatry 2018;60:312-28.
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