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Approach to dementia
1. APPROACH TO DEMENTIA
Guide: DR.PARIDHI SHIVDE
Canditate: DR.SARATH MENON .R
DEPARTMENT OF NEUROLOGY,
MGM MEDICAL COLLEGE ,INDORE.
2. DEMENTIA- “OUT OF ONE’S MIND”
DEMENTIA- the disease with acquired
deterioration in cognitive/ intellectual abilities
without impairment of consciousness
Cognitive deficit represent a decline from previous
level of functioning
3. DSM – IV – DIAGNOSTIC CRITERIA
1. Memory impairment
2. At least one of the following:
Aphasia
Apraxia
Agnosia
Disturbance in executive functioning
3. Disturbance in 1 and 2 interferes with daily function
4. Does not occur exclusively during delirium
4. EPIDEMIOLOGY
~ 5 to 8 % at age 65 to 70
~ 15 to 20 % at age 75 to 80
up to 40 to 50 % over age 85
• Alzheimer's disease is most
common dementia 50-75%
• Dementia with Lewy bodies
15 to 35 %
• Vascular dementia 5 – 20 %
6. CORTICAL VS. SUBCORTICAL DEMENTIA
Cortical
Symptoms: major changes in memory, language deficits,
perceptual deficits, praxis disturbances,lack of extrapyramidal
features
Affected brain regions: temporal cortex (medial), parietal cortex,
and frontal lobe cortex
Examples: Alzheimer’s disease, diffuse Lewy body disease,
vascular dementia, frontotemporal dementias
7. Subcortical
Symptoms: behavioral changes, impaired affect and mood,
motor slowing, executive dysfunction, less severe changes in
memory, extra pyramidal findings
Affected brain regions: thalamus, striatum, midbrain,
striatofrontal projections
Examples: Parkinson’s disease, progressive supranuclear
palsy, normal pressure hydrocephalus, Huntington’s disease,
Creutzfeldt-Jakob disease, chronic meningitis
CORTICAL VS. SUBCORTICAL DEMENTIA
8. MIXED
Both cortical and sub-cortical area involved.
Example: vascular dementia, Dementia with
Lewy bodies, Corticobasal degeneration,
Neurosyphilis
9. D = Delirium
E = Emotions (depression)& Endocrine Disease
M= Metabolic Disturbances
E = Eye & Ear Impairments
N = Nutritional Disorders
T = Tumors, Toxicity, Trauma to Head
I = Infectious Disorders
A= Alcohol, Arteriosclerosis
REVERSIBLE DEMENTIA
11. HOW TO DIAGNOSE A CASE OF DEMENTIA IN
NEUROLOGY OPD
Clinical history
Symptoms analysis
Focussed physical examination
Cognitive and neuropsychiatric examination
Laboratory evaluation
13. FOCUSED HISTORY
Chronology of the problem- from loved ones
- mode of onset – abrupt vs gradual
- progression - stepwise vs continous decline
- duration of symptoms
Medical history
Family history
Socio-economic history
Evaluation for toxic agent exposure
17. INVESTIGATIONS
ASSESSMENTS RATIONALE
Labs: Complete blood count, serum electrolytes,
renal and hepatic function, glucose, albumin and
protein, vitamin B12 and folate, rapid plasma reagin
(syphilis), thyroid- stimulating hormone, urinalysis
Rule out correctable or
contributory causes of
dementia
Imaging: Computed tomography without contrast or
magnetic resonance imaging
Rule out infarcts, mass
lesions, tumors, and
hydrocephalus
Neurological examination Correlate imaging findings
with clinical examination
Neuropsychological testing Mini-Mental State
Examination: Screening
test of cognitive function
21. CASE 1
70 yr old female present with progressive memory
loss for past 1 yr.She also complaints of difficulty in
naming objects and driving car and house
keeping.for the past 1 month she has difficulty in
dressing ,eating and gets agitated easily and
wanders around at night.
MMSE – 15/30
Neurological exam- normal
Vision & hearing- normal
23. ALZHEIMER’S DISEASE (AD)
About 70% of all cases of dementia in elderly
Incidence increases with age
Occurs in up to 30% of persons >85 years old
Characterized by:
Progressive loss of cortical neurons
Formation of amyloid plaques (beta-amyloid is major component)
and intraneuronal neurofibrillary tangles (hyperphosphorylated tau
proteins is major constituent)
24. DIAGNOSTIC CRITERIA FOR DEMENTIA OF THE
ALZHEIMER TYPE
(DSM-IV, APA, 1994)
A. Development of multiple cognitive deficits
1. Memory impairment
2, other cognitive impairment
B. These impairments cause dysfunction in
In social or occupational activities
C. Course shows gradual onset and decline
D. Deficits are not due to:
1. Other cns conditions
2. Substance induced conditions
F. Do not occur exclusively during delirium
G. Are not due to other psychiatric disorder
25. CLINICAL MANIFESTATION
Begin with memory impairment language
visuospatial skills
Anosognosia- unaware of difficulties
Cognitive decline-driving,shopping,house-keeping
Language impaired- naming,comprehension then
- fluency
Apraxia- seq. motor task can’t perform
Visuo spatial deficits
Delusions ,capgras syndrome – late stages
End stage-rigid,mute ,incontinent & bed-ridden
26. AD DIAGNOSIS
Neurological exam & neuropsychological testing
Brain imaging: brain atrophy due to extensive
neuronal loss and hippocampal atrophy
Diagnosis confirmed by histology of post-mortem
brain
‘Plaques’ & ‘tangles’ in hippocampus & cerebral
cortex.
27. CASE 2
76 yr old male presented in neuro opd with c/o
progressive memory loss,emotional lability,gait
disturbance for past 5 months
h/o of 3 episodes of cerebrovascular accidents +
recent attack 7 months back
h/o HTN,DM,CAD+
O/E- incresed tone in all limbs,power 3+ in RT.UL
&LL. 4+ in LT side, B/L extensor plantar
28. VASCULAR DEMENTIA
Refers to cognitive decline caused by ischemic, hemorrhagic, or
oligemic injury to the brain as a consequence of cerebrovascular or
cardiovascular disease.
Part of a spectrum of vascular disease causing cognitive impairment,
which also includes mild cognitive impairment of vascular origin & mixed
Alzheimer's disease plus cerebrovascular disease.
Kraepelin first described “arteriosclerotic dementia” in 1896
32. CASE 3
55 YR old woman presented with 2yr history of
progressive alteration in social behavior. The pt had
h/o social disinhibation,abusive
language,euphoria.there is complaints of excessive
food intake and weight gain for past 1 yr and pt was
taken to psychiatrist once.
o/e- vitals stable..neurological exam –WNL
MMSE-18/30
34. FRONTOTEMPORAL DEMENTIAS
Often begins with marked behavioral
disturbances, unlike AD
Classic form – Pick’s disease
Patients frequently hot-tempered and socially
disinhibited
memory & visuo spatial skills spared
Impaired planning,judgement and language
Echolalia +
Overlap with PSP,CBD, motor neuron disease
Illness progresses for years, like AD
Inevitable decline
MRI- lobar atrophy of frontal and/or temporal
About 50% of patients have family history
35. CASE 4
82 yr old male came to opd with c/o progressive
decline in memory for the past 6-8 months.He also
complaints of having decreased sleep and
occasional nightmares.He occasional sees his
deceased wife at times.
o/e- vitals stable ,rigidity of limbs+
- gait- slow stepping gait,bradykinesia+
MMSE- 21/30
WHAT IS THE DIAGNOSIS?
36. DIFFUSE LEWY BODY DISEASE
Patients have clinical parkinsonism with early and
prominent dementia
Lewy bodies found in brain stem, limbic system, and
cortex
Visual hallucinations and cognitive fluctuations
common, capgras syndrome & REM sleep disorder
Longstanding PD without cognitive decline develop
dementia
Better memory but severe visuospatial deficit
Patients sensitive to adverse effects of neuroleptics
May be second most common cause of dementia
after AD
37.
38. PARKINSON’S DISEASE
About 50% of patients have dementia by 85 years old
Affects executive function disproportionately
Dementia occur in later stage, or as a result of co
morbidities- AD,DLB or side effects of drug
Associated depression & anxiety
Frontal lobe dysfnct- complex tasks,planning,
-memorizing
Language & mathematical skills spared
Predictors- late onset,akinetic-rigid,severe depression
- advanced stage
39. CASE 5
65 YR old male presented to neuro opd with c/o
gait disturbance for past 1 yr. On history taking his
son complained his father is having memory loss
for past 6 months and it is progressing.
The pt also c/o of urinary incontinence+
Neurolog exam- no focal deficits
MMSE- 23/30
41. NORMAL PRESSURE HYDROCEPHALUS
Triad
1. Dementia: typically subcortical
2. Gait instability
3. Urinary incontinence
Walk with “feet stuck to floor”
Symptoms progress over weeks to months
CT shows ventricular enlargement with no
eviddence of cortical atrophy
42. Most important test – therapeutic LP
1. Remove large amount of CSF
2. Examine gait and cognitive function
Ventriculoperitoneal shunt may correct if:
Patients improve within minutes to hours of removal of 30
to 40 mL of spinal fluid
Trauma or subarachnoid hemorrhage
Cause is derangement of CSF hydrodynamics
NORMAL PRESSURE HYDROCEPHALUS
43. CASE 6
50 YR old woman was admitted with c/o
progressive memory loss and gait problem ,slurred
speech within one month; The pt also had
behavioral problem – insomnia,agitation,aggression
duration of 3 weeks.the pt also c/o abnormal jerky
hand movements for past 1 month
o/e- limb & gait ataxia +, reflexes-exagg.
- tone increased all limbs, plantar b/l extensor
- no focal weakness
MMSE- 16/30
45. CRUETZFELDT-JAKOB SYNDROME(CJD)
Rapid progressive dementing prion disorder
Focal cortical signs, rigidity
Onset between 40- 75 years
90% has MYOCLONUS vs 10% in AD
Progressive dementia and personality changes
over weeks to months
Death <1 year from first symptom
EEG- diffuse slowing and periodic sharp waves or
spikes
MRI- basal gangla abnormalities
CSF- detect specific aminoacid sequence (PrPSc)
46. Aging
Mild loss of memory: names and dates
Most sensitive indicator of cognitive change: poor
performance on delayed-recall tasks
Verbal fluency remain intact and vocabulary may
increase
DISORDERS OF MEMORY FUNCTION
(AMNESTIC DISORDERS)
47. Transient global amnesia
Dramatic memory disturbance
Affects patients >50 years
Usually have only one episode, lasting 6 to 12 hrs.
Complete temporal and spatial disorientation
Orientation for person preserved
May be confused with psychogenic amnesia, fugue state, or partial
complex status epilepticus
May be due to vascular insufficiency to hippocampus or midline
thalamic projections
DISORDERS OF MEMORY FUNCTION
48. DISORDERS OF MEMORY FUNCTION
Head injury
Retrograde amnesia > antegrade amnesia
With time, memories usually return but rarely to recall events
surrounding trauma
Korsakoff’s syndrome
Near-total inability to establish new memory
Patients confabulate about recent events
Immediate memory NL,attention NL
Most common cause: thiamine and other nutritional
deficiencies with chronic alcoholism
49. PSEUDO DEMENTIA
Severe depression
Memory & language intact
Vegetative symptoms –insomnia,anergy,
- loss of appetite
Abrupt onset