APPROACH TO A

PATIENT WITH
DEMENTIA

DR ROBIN GARG
JUNIOR RESIDENT
DEPTT. OF MEDICINE
DEMENTIA- “OUT OF ONE’S MIND”
 DEMENTIA- the disease with acquired deterioration in cognitive/
intellectual abilities, without impairment of consciousness, that
impairs the successful performance of activities of daily living.

 Cognitive impairment represents a decline from previous level of

functioning.
 Episodic memory, the ability to recall events specific in time &
place, is the cognitive function most commonly lost.
 In addition to memory, dementia may erode language, visuospatial,
praxis, calculation, judgement & problem solving abilities.
MAJOR NEUROCOGNITIVE DISORDER
DSM- V (DIAGNOSTIC AND STATISTICAL MANUAL)
A. Evidence of significant cognitive decline from a previous level of
performance in one or more area of cognitive domains ( complex
attention, executive function, learning and memory, language,
perceptual-motor or social cognition) based on :
1. Concern of the individual , a knowledgeable informant or the
clinician that there has been a significant decline in cognitive
function; and
2. Substantial impairment in cognitive performance, preferably
documented by standardized neuropsychological testing or , in its
absence , another quantified clinical assessment.
B. The cognitive deficits interfere with independence in everyday
activities.
C. The cognitive deficits do not occur exclusively in the context of a
delirium.
D. The cognitive deficits are not better explained by another mental
disorder (e.g., major depressive disorder, schizophrenia).
 EPIDEMIOLOGY
• Alzheimer's disease is most
 ~ 5 to 8 % of persons age 65 common cause of dementia 
to 70 years 50-75%
 ~ 10 % of persons age >70 • Vascular dementia is second
years most frequent cause.
• Dementia with lewy bodies is
 20-40% of persons age>85
years also common in 15- 30% of
patients.
 DEMENTIA

Lewy Body
Dementia Other Dementias
•Metabolic
Vascular
Alzheimer’s (Multi-
•Drugs/toxic
•White matter disease
Disease infarct) Fronto-
•Mass effects
Dementia Temporal •Infections
•Early onset Lobe •Parkinson’s
Dementias
•Normal onset
 ETIOLOGY
NEURO- Alzheimer's Ds ; Parkinson’s Ds dementia & Dementia with Lewy
DEGENERATIVE Bodies, Fronto-temporal dementia
VASCULAR Multi-Infarct; Diffuse white matter ds(Binswanger’s)
NEUROLOGICAL MS, Huntington’s ds, MSA, Hereditary ataxias, Prion Ds
(Creutzfeldt jakob & GSS), ALS-parkinsonism-dementia complex
of Guam, Adult Down’syndrome with Alzheimer ds, Brain tumour
ENDOCRINE Hypothyroidism; Cushing syndrome; Adrenal insufficiency; Hypo
and Hyperparathyroidism
NUTRITIONAL Def. of Vit.B12(SACD),Thiamine(Wernicke’s), Niacin(Pellagra)
INFECTIOUS HIV; Neurosyphilis; JC virus(PMLE), TB, Fungal, protozoal, Whipple
METABOLIC Hepatic/ Renal Insufficiency; Wilson’s Ds
TRAUMATIC & Chronic Subdural Haematoma; Dementia pugilistica(chronic
DIFFUSE BRAIN traumatic encephalopathy),Postencephalitis, Postanoxia,NPH,
DAMAGE Intracranial hypotension
TOXIC AGENTS Alcoholism; Heavy Metals(Pb,Hg,As,Al); Drug/medication
intoxication(Sedatives, tranquilizers & analgesics)
PSYCHIATRIC Depression(Pseudodementia),Schizophrenia,Conversion disorder
MISCELLANEOUS Sarcoidosis,Vasculitis,CADASIL,Acute intermittent porphyria
CORTICAL VS. SUBCORTICAL DEMENTIA
CORTICAL
o Symptoms-major changes in
memory, language & perceptual
deficits, apraxia .Lack of
extrapyramidal features
o Areas affected-temporal cortex
(medial), parietal cortex, and
frontal lobe cortex
o Examples-Alzheimer’s Ds
Dementia with Lewy Bodies
Frontotemporal Dementia
Vascular Dementia
SUBCORTICAL
o Symptoms-behavioral changes,
impaired affect and mood, motor
slowing, executive dysfunction,
less severe changes in
memory.extra pyramidal features
o Areas affected- thalamus,
striatum, midbrain, striatofrontal
projections
o Examples - Parkinson’s disease,
progressive supranuclear palsy,
NPH, Huntington’s disease,
Creutzfeldt-Jakob disease, vit.
Deficiency, thyroid ds, metabolic,
dementia pugilistica
MIXED
 Both cortical and sub-cortical area involved.
 Example: vascular dementia, Dementia with Lewy
bodies, Corticobasal degeneration, Neurosyphilis
REVERSIBLE DEMENTIA

 D= Delirium
 E= Emotions (Depression) & Endocrine Disease
 M= Metabolic Disturbances
 E= Eye & Ear Impairments
 N= Nutritional Disorders, NPH
 T= Tumors, Toxicity, Trauma to Head(SDH)
 I= Infectious Disorders
 A= Alcohol, Arteriosclerosis
IRREVERSIBLE DEMENTIA
 Alzheimer’s
 Vascular
 Lewy Body Dementia
 Parkinson’s
 Frontotemperal Dementia
 Huntington’s Disease
 Cruzefeldt Jakob Disease
 Leukoencephalopathies
 DIAGNOSTIC APPROACH
COGNITIVE IMPAIRMENT ?
YES

DETERIORATION FROM A MENTAL

NO
PREVIOUSLY HIGHER LEVEL ? RETARDATION
YES
CONSCIOUSNESS ALTERED? YES DELIRIUM
NO

MULTIPLE COGNITIVE FUNCTIONS APHASIA

INVOLVED ? NO AMNESTIC , etc
YES

SERIOUS INTERFERRENCE MILD COGNITIVE

NO
WITH DAILY ACTIVITIES?? IMPAIRMENT(MCI)
YES
DEMENTIA
 HOW TO DIAGNOSE A CASE OF DEMENTIA
 Focussed History

 Symptoms analysis

 Focussed physical examination

 Cognitive and neuropsychiatric examination

 Laboratory evaluation
FOCUSSED HISTORY
 Chronology of the problem
- Mode of onset – acute(Delirium) vs gradual
- Progression -slow (AD)
-stepwise (Vascular dementia)
-rapid (CJD,FTD)
-progression with fluctuations(DLB)
- Duration of symptoms
CLINICAL SYMPTOMS
 COGNITIVE IMPAIRMENT
 ANXIETY
 FUNCTIONAL IMPAIRMENT
 PERSONALITY CHANGES
 NEURO-PSYCHIATRIC
MANIFESTATIONS  PSYCHOSIS

 BEHAVIOURAL  SLEEP DISTURBANCES

DISTURBANCES

 MOOD CHANGES
 COGNITIVE IMPAIREMENT
o Memory impairment
(Episodic; Immediate,recent or
remote; Anterograde vs
retrograde amnesia)
o Aphasia
(impairment of naming,
comprehension or fluency)
o Apraxia
(impaired ability to carry out
learned motor activities despite
intact motor function)
o Agnosia
(failure to recognize or identify
objects despite intact sensory
function)
o Impairment in executive
functioning
(disturbances in planning,
organizing, sequencing, and
abstracting, problem solving)
o Impaired visuo-spatial
functioning
(interference with dressing,
eating or even walking, failure
to solve simple problems or copy
geometric figures or clock
reading)
 FUNCTIONAL IMPAIRMENT
 Each of the cognitive deficits results in a significant impairment in
functioning that represents a decline from a previous level of
functioning.

 Difficulties with job performance if the patient is still working.

 Difficulties in driving, shopping & housekeeping.

 Difficulties in social functioning

 disengagement from usual activities & interests,
 trouble maintaining social relationships & social roles, and
 difficulty performing activities of daily living.
 NEURO-PSYCHIATRIC MANIFESTATIONS
 The Neuropsychiatric Inventory (NPI)  A useful tool
developed to assess psychopathology

 Evaluates 12 neuropsychiatric disturbances:

• Delusions • Euphoria
• Hallucinations • Disinhibition
• Agitation • Aberrant Motor Behaviour
• Dysphoria • Night-time Behaviour
• Anxiety Disturbance
• Apathy • Appetite & Eating Abnormalities
• Irritability
 BEHAVIOURAL DISTURBANCES
 Apathy, disinhibition, compulsivity, loss of empathy for others
& overeating suggests FTD.

 Agitation, aggressive behavior, uncooperative behavior, and

wandering.

 Agitation, particularly worsening in the evening hours, is

common.

 These symptoms account for substantial caregiving burden and

are often the trigger for moves to higher levels of care.
 MOOD CHANGES
 10% Dementia pts in early course have Major Depression.

 50% Alzheimer’s pts have depressive symptoms.

 Depressive symptoms, emotional lability, & irritability may be

related to psychological reactions to the awareness of losing one's
memory & anticipation of increasing functional impairment.

 Suicidal ideation and behavior may also occur – esp in mildly

impaired.
 ANXIETY

 ~ 60% of pts encounter anxiety

 Manifest as fear of being alone, patients will search for their

caregivers so as not to be alone.

 Some patients exhibit “catastrophic reactions” when confronted with

their cognitive limitations or when facing changes in routine or
environment.
 PERSONALITY CHANGES

 Disinhibition  Loss of judgement & reasoning

 Impulsivity  Inappropriate sexual remarks or

behaviors
 Making inappropriate jokes

 Being overly familiar with

strangers

 Disregarding social norms

 PSYCHOSIS

o Delusions are common, usually with common themes of theft,

infidelity or misidentification in late stages of AD.

o In late stages, 10% of AD patients develop Capgras’

syndrome, the delusion that a caregiver has been replaced by
an impostor.

o Visual hallucinations & Capgras’ syndrome are early features

in DLB.
 SLEEP DISTURBANCES

ADVANCING DEMENTIA

ALTERED SLEEP-WAKE
CYCLES

DISRUPTED AND FRAGMENTED SLEEP in ~50%

 REM sleep behavior disorder(RBD) is common in DLB.
OTHER IMPORTANT POINTS IN HISTORY

 H/o movement disorders ( myoclonus in CJD)

 H/o seizures may indicate strokes or neoplasm but can also
occur in AD(particularly early age of onset AD)
 H/o gait disturbance is common in vascular dementia,
PD/DLB & NPH.
 H/o recurrent head trauma could indicate chronic SDH,
chronic traumatic encephalopathy(dementia pugulistica or
punch-drunk syndrome), intracranial hypotension or NPH.
 H/o alcohol abuse causing malnutrition & thiamine
deficiency which causes Wernicke’s encephalopathy
(confusion,ataxia & diplopia) & irreversible Korsakoff ’s
syndrome(unable to recall new information,confabulation).
 H/o veganism, bowel irradiaton, gastric surgery, chronic
antihistamine therapy predispose to B12 deficiency(SACD).
 Past H/o HTN & DM important in vascular dementia.
 H/o high risk sexual behaviors & IV drug abuse can lead to CNS
infection esp HIV or syphilis.
 Occupational History for heavy metal intoxication.
 H/o chronic drug intake esp. sedatives & analgesics.
 Family History for HD & familial forms of AD, FTD, DLB or prion
disorders.
 ALZHEIMER’S DISEASE(AD) – Patients usually begin with memory
symptoms but other early symptoms include difficulty with managing
money, driving, shopping, following instructions, finding words or
navigation.
 FRONTOTEMPORAL DEMENTIA(FTD) – Suggested by personality
change, disinhibition and weight gain or compulsive eating. Other
suggestive points may include prominent apathy, loss of empathy for
others, loss of executive function or progressive abnormalities in
speech. There is relative sparing of memory or visuospatial abilities.
 DEMENTIA WITH LEWY BODIES(DLB) – Suggested by early visual
hallucinations, parkinsonism, proneness to delirium, REM sleep
behaviour disorder(RBD) or Capgras syndrome.
 VASCULAR DEMENTIA – History of sudden stroke with irregular
stepwise progression.
 CREUTZFELDT- JAKOB DISEASE – Rapid progression of dementia in
association with motor rigidity and myoclonus.
PHYSICAL EXAMINATION
 Neurological examination-mobility and balance assessment
 Focal neurological deficits

 Extra-pyramidal signs

 Vision & hearing screening

 Cardiac and pulmonary evaluation

 Alzheimer’s Disease – Initially neurological examination is
normal. Motor system involvement occurs later in course.
 Frontotemporal Dementia – Patients develop axial rigidity,
supranuclear gaze palsy or a motor neuron disease.
 Dementia with Lewy bodies – Initial symptoms may include
new onset of a parkinsonian syndrome but it often starts with
visual hallucinations or dementia.
 Progressive supranuclear palsy(PSP) is a/w unexplained falls,
axial rigidity, dysphagia & supranuclear vertical gaze deficits.
 Corticobasal syndrome(CBS) features asymmetric rigidity,
dystonia, myoclonus, apraxia of one limb, alien limb
phenomenon(limb exhibits unintended motor actions such as
grasping, groping, drifting or undoing), pyramidal signs,
nonfluent aphasia, executive dysfunction or a behavioural
disorder.
 Hemiparesis or other focal neurological deficits suggest vascular
dementia or brain tumour.
 Dementia with myelopathy and peripheral neuropathy suggests
Vitamin B12 deficiency.
 Peripheral neuropathy may also indicate another vitamin
deficiency, heavy metal intoxication, thyroid dysfunction, Lyme
ds or vasculitis.
 Dry, cool skin, hair loss and bradycardia suggest
hypothyroidism.
 In the elderly, Hearing impairment or visual loss may produce
confusion and disorientation misinterpreted as dementia.
COGNITIVE & NEUROPSYCHIATRIC EXAMINATION

 Folstein Mini-Mental Status Examination (MMSE)

 Earliest deficits on cognitive testing:-

 AD- Episopic memory loss
 FTD- Deficits in executive control or language function
 PDD/DLB- Deficits in visuospatial function
 Vascular dementia-Mixture of executive comtrol & visuospatial
deficits, with prominent psychomotor slowing
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 contributory causes of
electrolytes, renal and thyroid function dementia
and vitamin B12 level
Imaging: Computed tomography without Rule out infarcts, primary & metastatic neoplasms,
contrast or magnetic resonance subdural hematomas, NPH, diffuse white matter ds
imaging(MRI) or regional pattern of atrophy.
PET and SPECT Temporal-parietal hypoperfusion or hypometabolism
in AD & frontotemporal deficits in FTD.
Amyloid Imaging, Pittsburgh Compound- Radioligands for detecting brain amyloid a/w
B(PiB) & 18F-AV-45(florbetapir) amyloid angiopathy or neuritic plaques of AD
Lumbar Puncture Indicated when CNS infection or inflammation are
possibilities. Presence of low AB42 & mildly elevated
CSF tau is highly suggestive of AD.
EEG Can suggest CJD(repetitive bursts of diffuse high
amplitude sharp waves or periodic complexes) or
underlying nonconvulsive seizure disorder.
Brain Biopsy Only to diagnose vasculitis, potentially treatable
neoplasms or unusual infections.
 TREATMENT
 Major goals are to treat reversible causes. e.g. thyroid replacement for
hypothyroidism, vitamin therapy for thiamine & B12 deficiency,
antimicrobials for infections, ventricular shunting for NPH, appropriate
treatment for CNS neoplasms etc.
 Symptomatic treatment in irreversible causes.
 Drugs used in Alzheimer’s Ds are cholinesterase inhibitors(donepezil,
rivastigmine, galantamine); NMDA receptors blockers(memantine).
 SSRIs are commonly used for depressive symptoms(e.g. escitalopram)
 Seizures can be treated with levetiracetam.
 Antipsychotics such as quetiapine can be used for patients with
agitation, aggression & psychosis but all antipsychotics should be used
with caution due to their untoward side effects.
DEMENTIA
- SUB TYPES
 ALZHEIMER’S DISEASE (AD)
 About 70% of all cases of dementia in elderly
 Incidence increases with age
 Occurs in up to 20-40% of persons >85 years old
 Risk factors include old age, family history, female sex, ApoE4 allele,
HTN,DM,elevated homocysteine & cholesterol levels, decreased folic
acid level, low intake of fruits, vegetables, low levels of exercise.
 Characterized by:
 Progressive loss of cortical neurons
 Formation of neuritic plaques (beta-amyloid is major component)
and intraneuronal neurofibrillary tangles (hyperphosphorylated tau
protein is major constituent)
 Decrease in cortical levels of neurotransmitters esp. Ach & nicotinic
cholinergic receptors.
NORMAL BRAIN CELLS

Neurotransmitters (ACh)– being sent

– message being communicated to the
next cell
NORMAL BRAIN CELLS

Once the message is sent, then

enzymes lock onto the messenger
chemicals and take them out of
circulation so a new message can be
sent
BRAIN CELLS WITH ALZHEIMER’S

Less
neurotransmitter
Further to go to get to the
plaques next cell
tangles

Enzymes (AChE) – get to

them BEFORE they deliver
their message
WHAT DO ALZHEIMER’S DRUGS DO?
Alzheimer’s drugs provide
FAKE messenger chemicals
that distract the enzymes.
They attach to the Fake ACh
& the message can get thru
(Cholinesterase inhibitors)
CLINICAL MANIFESTATIONS
 Begin with memory impairment language

visuospatial skills
 Anosognosia - unaware of difficulties
 Cognitive decline-driving, shopping, house-keeping, job difficulties
 Language impaired- naming, comprehension then
- fluency
 Apraxia – learned seq. motor task can’t perform
 Visuospatial deficits
 Late stages- Delusions, capgras’ syndrome,loss of judgement & reasoning,
disinhibition, disrupted sleep-wake patterns.
 End stage - rigid, mute, incontinent & bed-ridden, hyperactive DTRs,
myoclonic jerks.
 Death resuls from malnutrition,. Secondary infections, pulmonary emboli,
heart ds or, most commonly, aspiration.
AD DIAGNOSIS
 Neuroimaging- CT/MRI shows posterior predominant cortical
atrophy & atrophy of medial temporal memory structures
(entorhinal cortex & hippocampus).
 PET – Hypometabolism in posterior temporal-parietal cortex. It
can also detect presence of fibrillar amyloid in the brain.
 EEG- Normal or non-specific slowing

 Lumbar Puncture- CSF shows low AB42 & mildly elevated tau.

Treatment- Cholinesterase inhibitors (donepezil, rivastigmine,

galantamine) & NMDA glutamate receptor blockers(memantine).
AD and the Brain
The Changing Brain in
Alzheimer’s Disease

No one knows what causes AD to begin,

but we do know a lot about what happens
in the brain once AD takes hold.

Pet Scan of
Normal Brain

Pet Scan of Alzheimer’s

Disease Brain

Slide 19
 VASCULAR DEMENTIA

 Multi-infarct dementia- recurrent strokes

-step wise progression
-H/o HTN,DM,CAD
MRI- multiple areas of infarction
 Diffuse white matter disease (Binswanger’s ds, leukoaraiosis)

-lacunar infarction, microangiopathy

-dementia may be insidious in onset & progress slowly
-confusion, personality changes, psychosis , emotional lability
-pyramidal signs & cerebellar signs + ,
-gait disorder, urinary incontinence, dysarthria
-MRI- B/L T2 signal hyperintensities in subcortical white matter
 FRONTOTEMPORAL DEMENTIA
 Often begins with marked behavioral disturbances, unlike AD
 Behavioral variant FTD-Apathy,disinhibition,compulsivity,loss of
empathy & overeating, deficits in executive control
 Semantic variant PPA- Inability to decode word,object,person-
specific & emotion meaning.
 Nonfluent/agrammatic variant PPA- Prominent motor speech
impairment.
 Memory & visuo spatial skills spared.
 May be accompanied by motor neuron disease.
 MRI- Focal atrophy of frontal, insular and/or temporal cortex
 Disease is subtyped according to protein composition of neuronal &
glial inclusions, which contain-
 tau,
 TDP-43 or
 FUS
 FTLD spectrum containing tau deposition includes Pick’ s disease,
Progressive supranuclear palsy syndrome(PSP-S) & Corticobasal
Syndrome(CBS).
 PSP-S(Steele-Richardson-Olszewski syndrome)- It involves degeneration
of brainstem,basal ganglia,limbic structures & selected area of cortex. It
is characterized by falls, personality changes, supranuclear vertical
gaze palsy, axial dystonia with hypererect posture,dysarthria,dysphagia
& symmetric axial rigidity.
 Corticobasal syndrome(CBS) is dementia movement disorder a/w
atrophy in perirolandic cortex & basal ganglia. Patients present with
asymmetric rigidity, dystonia, myoclonus, apraxia of one limb, alien limb
phenomenon(limb exhibits unintended motor actions such as grasping,
groping, drifting or undoing), pyramidal signs, nonfluent aphasia,
executive dysfunction or a behavioural disorder.
 Treatment of FTD is symptomatic. SSRIs can be used.
 PARKINSON’S DISEASE DEMENTIA AND
DEMENTIA WITH LEWY BODIES
 When dementia occurs after an established diagnosis of Parkinson’s
Disease, the term used is Parkinson’s Disease Dementia(PDD).
 When dementia precede or co-emerge with parkinsonism, it is referred to
as Dementia with Lewy Bodies(DLB).
 DLB is characterized by visual hallucinations,parkinsonism,fluctuating
alertness, falls, capgras syndrome & REM sleep behavior disorder(RBD).
 Better memory but severe visuospatial deficit.
 Patients sensitive to adverse effects of neuroleptics
 Lewy bodies are found in brainstem, substantia nigra, limbic system and
cortex.
 Lewy bodies are intraneuronal cytoplasmic inclusions containing alpha-
synuclein.
 Cholinesterase inhibitors provide significant benefit.
 NORMAL PRESSURE HYDROCEPHALUS
 Triad
1. Dementia: typically subcortical with executive impairment
2. Gait instability(ataxic or apractic)
3. Urinary incontinence
 Walk with “feet stuck to floor”.
 Symptoms progress over weeks to months.
 It is a communicating hydrocephalus with a patent aqueduct of
sylvius. LP opening pressure falls in high normal range.
 Cause is obstruction to normal CSF flow over cerebral convexities &
delayed resorption into venous system.
 CT shows enlarged lateral ventricles with little or no cortical
atrophy, although sylvian fissures may appear propped open(so
called “boxcarring”), which can be mistaken for perisylvian atrophy.
 CRUETZFELDT-JAKOB DISEASE(CJD)

 Rapidly progressive prion disorder a/w dementia, focal cortical

signs, rigidity & myoclonus.
 90% has myoclonus vs 10% in AD

 Death <1 year after first symptom appear.

 EEG- diffuse slowing and abnormal periodic complexes.

 MRI- Cortical ribboning & basal ganglia hyperintensities on

FLAIR MRI.
 CSF- detect specific amino acid sequence (PrPSc)
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

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
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
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?

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
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
THANK YOU