CLINICAL EVALUATION OF

DEMENTIAS
 INTRODUCTION
Organic Mental Disorders caused directly by
abnormalities of brain strctures or alterations of
brain neurochemistry or neurophysiology
Functional vs Organic

Hippocrates Phrenitis and Paraphrenitis (delirium)

A C Celsus (Roman) coined delirium

Philippe Pinel detailed description of dementia

Emil Kraepelin Dementia precox

Alois Alzheimer 1906 Alzheimers disease

 DEMENTIA

DEMENTIA refers to a disease process marked by

progressive cognitive impairment in clear
consciousness.
Not related to low intellectual functioning or mental
retardation (developmental and static)
Cognitive deficits in dementia represent a decline
from a previous level of functioning.
Involves multiple cognitive domains with significant
impairment in social and occupational functioning.
 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

 DSM 5 - NEUROCOGNITIVE DISORDERS
Dementia and amnestic disorder are now included
under neurocognitive disorder (NCD).

Rationale: dementia has been associated with the

older population whereas NCD will capture
etiologies occurring in younger adults as well.

Mild NCD is a new diagnosis

The term dementia is not excluded from use in

etiological subtypes.
HOW TO DIAGNOSE A CASE OF DEMENTIA
IN OPD
Clinical history

Symptoms analysis

Focussed physical examination

Cognitive and neuropsychiatric examination

Laboratory evaluation
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

 CLINICAL SYMPTOMS
COGNITIVE IMPAIRMENT
MOOD CHANGES
FUNCTIONAL
IMPAIRMENT ANXIETY

NEURO-PSYCHIATRIC PERSONALITY CHANGES

MANIFESTATIONS
PSYCHOSIS
BEHAVIOURAL
DISTURBANCES
SLEEP DISTURBANCES
PHYSICAL EXAMINATION
Neurological examination-mobidity and
balance assessment
Focal neurological deficits

Extra-pyramidal signs

Vision & hearing screening

Cardiac and pulmonary evaluation

COGNITIVE & NEUROPSYCHIATRIC
EXAMINATION

Folstein Mini-Mental Status Examination

(MMSE)
MMSE

SCORE RANGE

24-30 Normal
18-23 Mild
10-17 Moderate
< 10 Severe
 INVESTIGATIONS

ASSESSMENTS RATIONALE

Labs: Complete blood count, serum Rule out correctable or

electrolytes, renal and hepatic function, contributory causes of
glucose, albumin and protein, vitamin B12 and dementia
folate, rapid plasma reagin (syphilis), thyroid-
stimulating hormone, urinalysis
Imaging: Computed tomography without Rule out infarcts, mass
contrast or magnetic resonance imaging lesions, tumors, and
hydrocephalus
Neurological examination Correlate imaging
findings with clinical
examination
Neuropsychological testing Mini-Mental State
Examination: Screening
test of cognitive function
DIFFERENTIAL DIAGNOSIS
DELIRIUM SCHIZOPHRENIA

MILD COGNITIVE DEPRESSION

IMPAIRMENT (MCI)
FACTITIOUS D/O
AGE-RELATED COGNITIVE
DECLINE
ALCOHOL ABUSE
MENTAL RETARDATION
DIAGNOSTIC APPROACH
COGNITIVE IMPAIRMENT ?
YES
DETERIORATION FROM A NO
MENTAL
PREVIOUSLY HIGHER LEVEL ? RETARDATION
YES

CONSCIOUSNESS ALTERED? YES DELIRIUM

NO

MULTIPLE COGNITIVE FUNCTIONS APHASIA

NO AMNESTIC D/O, etc
INVOLVED ?
YES

DEMENTIA
DEMENTIA SUB TYPES
CASE 1
70 yr old female present with progressive memory
loss for past 1 yr. She also complains 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

MRI FINDINGS- DIAGNOSIS?
 ALZHEIMERS DISEASE (AD)

About 50 - 70% of all dementia pts. 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)
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
CLINICAL MANIFESTATION
Begin with memory impairment language

visuospatial skills
Anosognosia- unaware of difficulties (disease)
Cognitive decline-driving, shopping, house-keeping
Language impaired- naming, comprehension then
- fluency
Apraxia- seq. motor task cant perform

Visuo spatial deficits

Delusions , capgras syndrome late stages
End stage-rigid, mute , incontinent & bed-ridden
 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.
 CASE 2
76 yr old male presented to 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- increased tone in all limbs, power 3+ in RT.UL

&LL. 4+ in LT side, B/L extensor plantar
 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

VASCULAR DEMENTIA
Multi-infarct dementia- recurrent strokes
- step wise progression
- HTN,DM,CAD
MRI- multiple areas of infarction
Binswangers d/s Diffuse white matter disease
- lacunar infarction
C/F:confusion,personality changes,psychosis
pyramidal signs & cerebellar signs +
gait disorder,urinary incontinence,dysarthria
emotional lability
 CASE 3

55 YR old woman presented with 2yr history of

progressive alteration in social behavior. The pt had
h/o social disinhibition, abusive language, euphoria.
There are 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
MRI (FRONTOTEMPORAL DEMENTIA)
FRONTOTEMPORAL DEMENTIAS
Often begins with marked behavioral
disturbances, unlike AD
Classic form Picks 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
 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 occasionally 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?

 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
 Lewi body dementia: normal hippocampus
 PARKINSONS 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
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
MRI- DIAGNOSIS ?

MRI showing
dilatation of
ventricles out of
proportion to sulcal
atrophy in a patient
with normal
pressure
hydrocephalus.
 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
 NORMAL PRESSURE HYDROCEPHALUS
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
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
MRI DIAGNOSIS?

Changes in the neocortex as seen on FLAIR (left) and DWI

(right) Spongiform changes in the cortical and subcortical gray
matter, with loss of neurons and replacement by gliosis.
CRUETZFELDT-JAKOB SYNDROME(CJD)

Normally the upper border of the midbrain is convex.

The atrophy of the midbrain in PSP results in a
concave upper border of the midbrain with the typical
'humming bird sign' (figure).
 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)

PROGRESSIVE SUPRANUCLEAR PALSY

PSP is also one of the atypical parkinsonian syndromes.

In PSP there is pronounced atrophy of the midbrain
(mesencephalon), which accounts for the typical upward gaze
paralysis.
DISORDERS OF MEMORY FUNCTION
(AMNESTIC DISORDERS)

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
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
Head injury
Retrograde amnesia > antegrade amnesia
With time, memories usually return but rarely to
recall events surrounding trauma
Korsakoffs 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
PSEUDO DEMENTIA
Severe depression
Memory & language intact

Vegetative symptoms insomnia,anergy,

- loss of appetite
Abrupt onset
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