The document provides an overview of dementia, including definitions, clinical presentation, causes, functional anatomy, evaluation approach, and treatment. It describes the typical presentation and progression of different types of dementia like Alzheimer's disease, vascular dementia, frontotemporal dementia, and dementia with Lewy bodies. Evaluation involves obtaining a detailed history, physical and neurological examination, and cognitive testing using tools like the Mini-Mental State Examination to assess domains like memory, language, and executive function.

1. DR. POORNA PAVANI
P.G IN MEDICINEAPPROACH TO DEMENTIA
1

2. Over view
• Definition
• Indian scenario
• Clinical presentation
• Functional anatomy of dementias
• Causes of dementia
• Approach to the patient
History
Physical and neurologic examination
Cognitive and neuropsychiatric examination
Laboratory tests
Treatment
• Conclusion
2

3. • Dementia--- Latin origin--- ”devoid of the mind”
• Now called as major neurocognitive disorder.
• It is an acquired deterioration in cognitive abilities
that impairs the successful performance of
activities of daily living.
• Although a number of definitions exist for dementia,
the DSM definition provides a reasonable frame
work in clinical practice.
3

4. Diagnostic and statistical mannual (DSM)—5 :
Criteria for dementia include the following:
 Evidence from the history and clinical assessment that indicates
significant cognitive impairment in at least one of the following
cognitive domains:
Learning and memory
Language
Executive function
complex attention
Perceptual-motor function
Social cognition
 Impairment must be acquired and represent a significant decline
from a previous level of functioning.
4

5. (DSM)—5 :
contd…..
 The cognitive deficits must interfere with independence in
everyday activities.
 In case of neurodegenerative dementias like Alzheimer disease,
the disturbances are of insidious onset and are progressive,
based on evidence from history or serial mental-status
examinations.
 The disturbances are not occurring exclusively during the
course of delirium.
 The disturbances are not accounted for by another mental
disorder(eg : major depressive disorder, schizophrenia).
5

6. Indian scenario
• Increasing population and life-expectancy in India is resulting in
an increase in the individuals at risk for dementia.
• Urbanisation, migration of the youth, and fragmentation of joint
families in India is increasing the cognitive stress and decreasing
the support to the growing number of people at risk for dementia
and, thereby, perhaps increasing its incidence.
• Population-based studies from different parts of the country have
shown that the prevalence of dementia (and AD) in those >60
years of age ranges from 0.8% (and 0.1%) in rural North India to
3.5% (and 1.31%) in urban South India.
6

7. Clinical presentation
 Episodic memory, the ability to recall events specific in time
and place, is the cognitive function most commonly lost;
 In addition to memory, dementia may erode other mental
faculties, including
 Language
 Visuospatial
 Praxis
 Calculation
 Judgment
 problem-solving abilities.
7

8. Clinical presentation
 Neuropsychiatric and social deficits also arise in many dementia
syndromes, manifesting as
 depression
 Apathy
 Anxiety
 Hallucinations
 Delusions
 Agitation
 Insomnia
 sleep disturbances
 Compulsions
 disinhibition
8

9. Clinical presentation
• Patient with dementia may have difficulty with one or more of
the following
 Retaining new information(eg: trouble remembering events)
 Handling complex tasks(eg: balacing a cheque book)
 Reasoning(eg: unable to cope with unexpected events)
 Spatial ability and orientation(eg: getting lost in familiar places)
 Language(eg: word finding)
 Behaviour
9

10. Clinical presentation
• Most patients with dementia do not present with a
complaint of memory loss; it is often a spouse or other
informant who brings the problem to the physicians
attention
• Self reported memory loss does not appear to correlate
with the subsequent development of dementia.
• Informant reported memory loss is a much better
predictor of the current presence and future
development of dementia.
10

11. Clinical presentation
• The clinical course may be
 slowly progressive, as in Alzheimer’s disease (AD)
 static, as in anoxic encephalopathy
 may fluctuate from day to day or minute to minute, as in
dementia with Lewy bodies.
• Most patients with AD, the most prevalent form of dementia,
begin with episodic memory impairment.
• In other dementias, such as frontotemporal dementia,
memory loss is not typically a presenting feature.
11

12. Dementia vs delirium
12

13. Mild cognitive impairment
• A measurable cognitive problem that does not seriously disrupt
daily activities is often referred to as mild cognitive impairment
(MCI).
• Factors that predict progression from MCI to an AD dementia
include a
 prominent memory deficit,
 family history of dementia,
 presence of an apolipoprotein ε4 (Apo ε4) allele,
 small hippocampal volumes,
 an AD-like signature of cortical atrophy,
 low cerebrospinal fluid Aβ,
 and elevated tau or evidence of brain amyloid deposition on
(PET) imaging.
13

14. FUNCTIONAL ANATOMY OF THE DEMENTIAS
• Dementia syndromes result from the disruption of specific large-scale
neuronal networks
• The location and severity of synaptic and neuronal loss combine to
produce the clinical features.
• Behaviour, mood, and attention are modulated by ascending
noradrenergic, serotonergic, and dopaminergic pathways.
• cholinergic signalling is critical for attention and memory functions.
• The dementias differ in the relative neurotransmitter deficit profiles;
accordingly, accurate diagnosis guides effective pharmacologic therapy.
14

15. FUNCTIONAL ANATOMY OF THE DEMENTIAS
• AD begins in the entorhinal region of the medial temporal lobe,
spreads to the hippocampus, and then moves to lateral and
posterior temporal and parietal neocortex, eventually causing a
more widespread degeneration.
• So, AD typically presents with episodic memory loss
accompanied later by aphasia or navigational problems.
.
15

16. FUNCTIONAL ANATOMY OF THE DEMENTIAS
• Vascular dementia is associated with focal damage in a
variable patchwork of cortical and subcortical regions or white
matter tracts that disconnect nodes within distributed
networks.
• Dementias that begin in frontal or subcortical regions, such as
frontotemporal dementia (FTD) or Huntington’s disease (HD),
are less likely to begin with memory problems and more likely
to present with difficulties with judgment, mood, executive
control, movement, and behavior.
16

17. FUNCTIONAL ANATOMY OF THE DEMENTIAS
Lesions of frontal-striatal pathways produce specific and
predictable effects on behaviour.
•The dorsolateral prefrontal cortex has connections with a central
band of the caudate nucleus.
•Lesions of either the caudate or dorsolateral prefrontal cortex, or
their connecting white matter pathways, may result in executive
dysfunction, manifesting as poor organization and planning,
decreased cognitive flexibility, and impaired working memory
17

18. FUNCTIONAL ANATOMY OF THE DEMENTIAS
• The lateral orbital frontal cortex connects with the ventromedial
caudate, and lesions of this system cause impulsiveness,
distractibility, and disinhibition.
• The anterior cingulate cortex and adjacent medial prefrontal
cortex project to the nucleus accumbens, and interruption of this
system produces apathy, poverty of speech, emotional blunting,
or even akinetic mutism.
• All corticostriatal systems also include topographically organized
projections through the globus pallidus and thalamus, and
damage to these nodes can likewise reproduce the clinical
syndrome of cortical or striatal injury.
18

19. Causes of Dementia
Most Common Causes of Dementia
Alzheimer’s disease
Vascular dementia
Multi-infarct
Diffuse white matter disease (Binswanger’s)
 Alcoholism
Parkinsons Disease dementia/Lewy Body Disease
spectrum
Drug/medication intoxication
19

20. Less Common Causes of Dementia
 Vitamin deficiencies
• Thiamine (B1): Wernicke’s encephalopathy
• B12 (subacute combined degeneration)
• Nicotinic acid (pellagra)
 Endocrine and other organ failure
• Hypothyroidism
• Adrenal insufficiency and Cushing’s syndrome
• Hypo- and hyperparathyroidism
• Renal failure
• Liver failure
• Pulmonary failure
20

21. Less Common Causes of Dementia
 Chronic infections
• HIV
• Neurosyphilis
• Papovavirus (JC virus) (progressive multifocal leuko encephalopathy)
• Tuberculosis, fungal, and protozoal
• Whipple’s disease
 Head trauma and diffuse brain damage
 Chronic traumatic encephalopathy
 Chronic subdural hematoma
 Post anoxia
 Post encephalitis
 Normal-pressure hydrocephalus
21

22. Less Common Causes of Dementia
 Intracranial hypotension
 Neoplastic
 Primary brain tumor
 Metastatic brain tumor
 Paraneoplastic/autoimmune limbic encephalitis
 Toxic disorders
• Drug, medication, and narcotic poisoning
• Heavy metal intoxication
• Organic toxins
22

23. Less Common Causes of Dementia
 Psychiatric
• Depression (pseudo dementia)
• Schizophrenia
• Conversion disorder
 Degenerative disorders
• Huntington’s disease
• Multisystem atrophy
• Hereditary ataxias (some forms)
• Frontotemporal lobar degeneration spectrum
• Multiple sclerosis
• Adult Down’s syndrome with Alzheimer’s disease
• ALS-parkinsonism-dementia complex of Guam
• Prion (Creutzfeldt-Jakob and Gerstmann-Sträussler-Scheinker diseases)
23

24. Less Common Causes of Dementia
 Miscellaneous
• Sarcoidosis
• Vasculitis
• CADASIL (cerebral autosomal dominant arteriopathy with
subcortical infarcts and leukoencephalopathy)
• Acute intermittent porphyriaa
• Recurrent nonconvulsive seizures
 Additional conditions in children or adolescents
• Pantothenate kinase–associated neurodegeneration
• Subacute sclerosing panencephalitis
• Metabolic disorders (e.g., Wilson’s and Leigh’s diseases,
leukodystrophies, lipid storage diseases, mitochondrial
mutations)
24

25. • The frequency of each condition depends on the age group under
study, access of the group to medical care, country of origin, and
perhaps racial or ethnic background.
• The classification of dementing illnesses into reversible and
irreversible disorders is a useful approach to differential diagnosis.
• When effective treatments for the neurodegenerative conditions
emerge, this dichotomy will become obsolete.
• In a study of 1000 persons attending a memory disorders clinic,
 19% had a potentially reversible cause of the cognitive impairment and
 23% had a potentially reversible concomitant condition that may have
contributed to the patient’s impairment 25

26. • The three most common potentially reversible diagnoses
were
 depression,
 normal pressure hydrocephalus(NPH),
 alcohol dependence;
• medication side effects are also common and should be
considered in every patient
26

27. APPROACH TO THE PATIENT:
Three major issues should be kept at the forefront:
(1) What is the best fit for a clinical diagnosis?
(2) What component of the dementia syndrome is
treatable or reversible?
(3) Can the physician help to alleviate the burden on
caregivers?
27

28. Evaluation of a patient with dementia
28

29. History
• The history should concentrate on the onset, duration, and
tempo of progression.
• An acute or subacute onset of confusion may be due to
delirium and should trigger the search for intoxication,
infection, or metabolic derangement.
• ADelderly person with slowly progressive memory loss over
several years, other early symptoms include difficulty with
managing money, driving, shopping, following instructions,
finding words, or navigating.
29

30. History
• FTD  Personality change, disinhibition, weight gain or
compulsive eating, prominent apathy, compulsivity, loss of
empathy for others, or progressive loss of speech fluency or
single-word comprehension and by a relative sparing of
memory and visuospatial abilities.
• DLB  early visual hallucinations; parkinsonism; proneness
to delirium or sensitivity to psychoactive medications; rapid eye
movement (REM) ; Capgras syndrome, the delusion that a
familiar person has been replaced by an impostor.
30

31. History
• Vascular dementia  history of stroke with irregular
stepwise progression suggests Vascular dementia. It is
also commonly seen in the setting of hypertension,
atrial fibrillation, peripheral vascular disease, and
diabetes.
• CJD  Rapid progression with motor rigidity and
myoclonus
31

32. History
• A history of high-risk sexual behaviours or intravenous drug use
should trigger a search for central nervous system (CNS)
infection, especially HIV or syphilis.
• A history of recurrent head trauma could indicate chronic
subdural hematoma, chronic traumatic encephalopathy (a
progressive dementia best characterized in contact sport
athletes such as boxers and American football players),
intracranial hypotension, or NPH.
• Alcohol abuse creates risk for malnutrition and thiamine
deficiency.
32

33. History
• Veganism, bowel irradiation, an autoimmune diathesis, a remote
history of gastric surgery, and chronic antihistamine therapy for
dyspepsia or gastroesophageal reflux predispose to B12
deficiency.
• A history of mood disorders, the recent death of a loved one, or
depressive signs, such as insomnia or weight loss, raise the
possibility of depression-related cognitive impairments.
• Careful drug history is particularly important; use of the drugs
that impair cognition ( anticholinergics, psychotropic medications
and sedative hypnotics) should be sought.
33

34. PHYSICAL AND NEUROLOGIC EXAMINATION
 Document dementia.
 To look for other signs of nervous system involvement.
 To search for clues suggesting a systemic disease that
might be responsible for the cognitive disorder.
34

35. PHYSICAL AND NEUROLOGIC EXAMINATION
• Typical AD spares motor systems until later in the course.
• FTD patients often develop axial rigidity, supranuclear gaze palsy, or a
motor neuron disease reminiscent of amyotrophic lateral sclerosis
• In DLB, the initial symptoms may include the new onset of a parkinsonian
syndrome (resting tremor, cogwheel rigidity, bradykinesia, festinating gait.
• Corticobasal syndrome (CBS) features asymmetric akinesia and rigidity,
dystonia, myoclonus, alien limb phenomena, pyramidal signs, and
prefrontal deficits such as nonfluent aphasia with or without motor speech
impairment, executive dysfunction, apraxia, or a behavioral disorder.
35

36. PHYSICAL AND NEUROLOGIC EXAMINATION
• Progressive supra nuclear palsy (PSP) is associated with
unexplained falls, axial rigidity, dysphagia, and vertical gaze
deficits.
• CJD is suggested by the presence of diffuse rigidity, an akinetic-
mute state, and prominent, often startle-sensitive myoclonus.
• Hemiparesis or other focal neurologic deficits suggest vascular
dementia or brain tumor.
• Dementia with a myelopathy and peripheral neuropathy suggests
vitamin B12 deficiency.
• Peripheral neuropathy could also indicate another vitamin
deficiency, heavy metal intoxication, thyroid dysfunction, Lyme
disease, or vasculitis.
36

37. PHYSICAL AND NEUROLOGIC EXAMINATION
• Dry, cool skin, hair loss, and bradycardia suggest
hypothyroidism.
• Fluctuating confusion associated with repetitive stereotyped
movements may indicate ongoing limbic, temporal, or frontal
seizures.
• In the elderly, hearing impairment or visual loss may produce
confusion and disorientation misinterpreted as dementia.
• Profound bilateral sensorineural hearing loss in a younger
patient with short stature or myopathy, however, should raise
concern for a mitochondrial disorder.
37

38. COGNITIVE AND NEUROPSYCHIATRIC EXAMINATION
COGNITIVE TESTING:
•Patients with cognitive complaints should under go a careful
mental status examination.
•Screening tools include
•1. Mini mental state examination
•2. Montreal cognitive assessment
•3. Clinical dementia rating
•4. Mini-cog
•5. Informant interview
•6. Short portable mental status questionnaire
•7. Clock drawing
38

39. Mini mental state examination
39

40. MMSE
• Maximum score on the MMSE is 30 points
• Score of <24 points is suggestive of dementia or
delirium
• Using a cut of 24 points, the MMSE had a sensitivity of
87% and a specificity of 82%.
• The test is not sensitive for mild dementia ,scores may
be influenced by age & education, as well as language,
motor and visual impairments
40

41. MoCA
MONTREAL COGNITIVE ASSESMENT
• It is a brief screening test to detect cognitive
impairment in older adults
• It is a 30 point test.
• Compared with the MMSE ,the MoCA is more
sensitive for the detection of mild cognitive
impairment
• Scores of 25 and below are considered to be
abnormal.
41

42. 42

43. Clinical Dementia Rating
• The Clinical Dementia Rating or CDR was developed at the Memory and
Aging Project at Washington University School of Medicine in 1979 for
the evaluation of staging severity of dementia.
• It was developed primarily for use in persons with dementia of the
Alzheimer type and it can also be used to stage dementia in other
illnesses as well.
• The Clinical Dementia Rating is a five-point scale in which CDR-0
denotes no cognitive impairment
• The remaining four points are for various stages of dementia:
• CDR-0.5 = very mild dementia
• CDR-1 = mild
• CDR-2 = moderate
• CDR-3 = severe
43

44. Mini-Cog
Consists of a
Clock drawing task(CDT)
Unqued recall of 3 unrelated words
•CDT is normal if all numbers are present in correct sequence and
the hands display the correct time in a readable way.
•Scoring is based on following 3 rules:
Recalling none of the words– demented
Recalling all 3 words--- non demented
Subjects with intermediate– classified based on CDT
(Abnormal=demented, normal=non demented)
44

45. Mini-Cog
Advantages:
•High sensitivity for predicting dementia status
•Short testing time relative to MMSE
•Ease of administration
•Diagnostic value not limited by subject’s education
or language
45

46. Informant interview
• Brief 8 item questionare for informants
Scoring
• The final score is a sum of the number items
marked “Yes, A change”.
• Interpretation of Results
• 0-1: Normal cognition:
• 2 or greater: Impairment in cognition
46

47. Informant interview questionnaire
47

48. • When the etiology for the dementia syndrome remains
in doubt, a specially tailored evaluation should be
performed that includes tasks of working and episodic
memory, executive function, language, and visuospatial
and perceptual abilities.
48

49. NEUROPSYCHIATRIC EXAMINATION
• Neuropsychiatric assessment is important for
diagnosis, prognosis, and treatment.
• In the early stages of AD, mild depressive features,
social withdrawal, and irritability or anxiety are the most
prominent psychiatric changes, but patients often
maintain core social graces into the middle or late
stages, when delusions, agitation, and sleep
disturbance may emerge
49

50. • In FTD, dramatic personality change with apathy,
overeating, compulsions, disinhibition, euphoria, and
loss of empathy are early and common.
• DLB is associated with visual hallucinations, delusions
related to person or place identity, RBD(REM sleep
behaviour disorder) , and excessive daytime sleepiness.
• Vascular dementia can present with psychiatric
symptoms such as depression, anxiety, delusions,
disinhibition, or apathy.
50

51. LABORATORY TESTS
• The choice of laboratory tests in the evaluation of
dementia is complex and should be tailored to the
individual patient.
• The physician must take measures to avoid missing a
reversible or treatable cause, yet no single treatable
etiology is common; thus, a screen must use multiple
tests, each of which has a low yield.
51

52. LABORATORY TESTS
• The American Academy of Neurology recommends
the routine measurement of
 complete blood count,
 Electrolytes
 renal and thyroid function
 vitamin B12 level
 neuroimaging study
52

53. LABORATORY TESTS
MRI
• help to rule out primary and metastatic neoplasms,
• locate areas of infarction or inflammation,
• detect subdural hematomas,
• suggest NPH or diffuse white matter disease.
• help to establish a regional pattern of atrophy.
• AD----hippocampal atrophy in addition to posterior-predominant
cortical atrophy
• FTD ----Focal frontal, insular, and/or anterior temporal atrophy
53

54. LABORATORY TESTS
MRI
• DLB ------less prominent atrophy, with greater involvement of
amygdala than hippocampus.
• CJD----magnetic resonance (MR) diffusion-weighted imaging
reveals restricted diffusion within the cortical ribbon and basal
ganglia in most patients
• NPH--- Communicating hydrocephalus with vertex effacement
(crowding of dorsal convexity gyri/sulci), gaping Sylvian fissures
despite minimal cortical atrophy.
• Vascular etiology----Extensive white matter abnormalities.
54

55. LABORATORY TESTS
• Reduction in medial temporal
lobe volume in the patient with
AD.
• Fluorodeoxyglucose positron
emission tomography
demonstrate reduced glucose
metabolism in the posterior
temporoparietal regions
bilaterally in AD
55

56. • Axial fluid-attenuated inversion
recovery (FLAIR) magnetic resonance
image through the lateral ventricles
reveals multiple areas of
hyperintensity involving the
periventricular white matter as well as
the corona radiata and striatum.
• this appearance is more pronounced
in patients with dementia of a vascular
etiology
Diffuse white matter disease /(Binswanger’s) 56

57. A---Sagittal
•T1-weighted (MRI) demonstrates
dilation of the lateral ventricle and
stretching of the corpus callosum
•depression of the floor of the third
ventricle
•enlargement of the aqueduct
•Diffuse dilation of the lateral, third,
and fourth ventricles with a patent
aqueduct, typical of communicating
hydrocephalus.
B----Axial T2-weighted MRIs
demonstrate dilation of the lateral
ventricles.
57

58. • CORTICAL RIBBON
SIGN IN CJD
58

59. The major degenerative dementias can usually be distinguished by the
initial symptoms; neuropsychological, neuropsychiatric, and neurologic
findings; and neuroimaging features
59

60. Treatment
Major goals of dementia management
to treat reversible causes
to provide comfort and support to the patient and
caregivers
60

61. Treatment of underlying causes
• Thyroidreplacement for hypothyroidism.
• Vitamin therapy for thiamine or B12 deficiency or for elevated
serum homocysteine.
• Antimicrobials for opportunistic infections or antiretrovirals for
HIV.
• Ventricular shunting for NPH.
• Appropriate surgical, radiation, and/or chemotherapeutic
treatment for CNS neoplasms. 61

62. Treatment of underlying causes
• Removal of cognition impairing drugs or medications
is frequently useful.
• If the patient’s cognitive complaints stem from a
psychiatric disorder, vigorous treatment of this
condition should seek to eliminate the cognitive
complaint or confirm that it persists despite adequate
resolution of the mood or anxiety symptoms.
62

63. SYMPTOMATIC TREATMENT
Patients with degenerative diseases may also be depressed
or anxious, and those aspects of their condition often
respond to therapy with
Antidepressants, such as selective serotonin reuptake
inhibitors (SSRIs) or serotonin-norepinephrine reuptake
inhibitors (SNRIs) which feature anxiolytic properties but
few cognitive side effects.
Anticonvulsants are used to control seizures.
Levetiracetam may be particularly useful. 63

64. Treatment of behavioural symptoms
• Agitation, hallucinations, delusions, and confusion are difficult to treat
and represent major causes for nursing home placement and
institutionalization.
• Before treating these behaviors with medications, the clinician should
aggressively seek out modifiable environmental or metabolic factors like
 Hunger,
 lack of exercise,
 toothache,
 constipation,
 urinary tract or respiratory infection,
 electrolyte imbalance,
 drug toxicity
all correctable causes that can be remedied without psychoactive drugs
64

65. Treatment of behavioural symptoms
• Drugs such as phenothiazines and benzodiazepines may
ameliorate the behavior problems but have untoward side
effects such as sedation, rigidity, dyskinesia, and
occasionally paradoxical disinhibition (benzodiazepines).
• Despite their unfavourable side effect profile, second
generation antipsychotics such as quetiapine (starting
dose, 12.5–25 mg daily) can be used for patients with
agitation, aggression, and psychosis, although the risk
profile for these compounds is significant.
65

66. Treatment of behavioural symptoms
• It is important to recognize and treat depression;
• Treatment can begin with a low dose of an SSRI (e.g.,
escitalopram, starting dose 5 mg daily, target dose 5–10
mg daily) while monitoring for efficacy and toxicity.
• Sometimes apathy, visual hallucinations, depression, and
other psychiatric symptoms respond to the
cholinesterase inhibitors, especially in DLB, obviating the
need for other more toxic therapies.
66

67. Treatment of AD,PDD
• Cholinesterase inhibitors are being used to treat AD
(donepezil, rivastigmine, galantamine)
• Recent work has focused on developing antibodies
against Aβ42 as a treatment for AD.
• Memantine proves useful when treating some
patients with moderate to severe AD
• PDD is treated with rivastigmine.
67

68. Nondrug behavior therapy
• The primary goals are to make the patient’s life
comfortable, uncomplicated, and safe.
• Preparing lists, schedules, calendars, and labels
can be helpful in the early stages. It is also useful
to stress familiar routines, walks, and simple
physical exercises.
68

69. Treatment of behavioural symptoms
• Demented patients often object to losing control
over familiar tasks such as driving, cooking, and
handling finances.
• Attempts to help or take over may be greeted with
complaints, depression, or anger.
• Hostile responses on the part of the caregiver are
counterproductive and sometimes even harmful.
• Reassurance, distraction, and calm positive
statements are more productive in this setting.
69

70. CARE GIVER BURNOUT
• The clinician must pay special attention to frustration
and depression among family members and caregivers.
Caregiver guilt and burnout are common.
• Caregivers should be encouraged to take advantage of
day-care facilities and respite services.
• Education and counselling about dementia are
important.
• Local and national support groups, such as the
Alzheimer’s Association (www.alz.org), can provide
considerable help.
70

71. CONCLUSION
• Memory is the cognitive function most commonly lost in
dementias.
• Most common causes AD, VD, Alcoholism, PDD/LBD
spectrum, drug or medication intoxication
• Classification of dementias into reversible and
irreversible is a useful approach.
• Major goals of physician in dementia management is
 to treat reversible causes
 to provide comfort and support to the patient and
caregivers
• Education and counseling about dementia are important71

72. Thank you all
72