DEMETIA MEMORY IS THE - PowerPoint Presentation

Slide1

DEMETIA

MEMORY IS THE

RECORDING,

RETENTION &RETRIEVAL OF KNOWLEDGE

Slide2

DISORDER OF MEMORY

DEMENTIA:

acquired and

persistent compromise

in multiple cognitive domains that

is severe

enough to interfere with everyday

functioning

IN ADDITION TO

MEMORY

IMPAIRMENT AT LEAST

ONE

OF FOLLOWING MUST OCCURE:

APHASIA

AGNOSIA

DIORDER OF EXECUTIVE FUNCTION

.

Slide3

DEMENTIA

COGNITIVE DEFICIT MUST BE SUFFICIENTLY SEVERE TO CAUSE IMPAIRMENT IN

OCCUPATIONAL OR

SOCIAL ACTIVITY OF DAILY LIVING

.

Slide4

2-DEMENTIA

Slide5

CLINICAL SYNDROME OF MEMORY DISFUNCTION

DEMENTIA

:

1-LOSS OF MULTIPLE

ACQUIRED

COGNITIVE &EMOTIONAL ABILITY SUFFICIENT TO INTERFER WITH DAILY ACTIVITY.

2-

INCIDIOUS

IN ONSET ,PROGRESSIVE

3-

AGE ASSOCIATED

1% IN 60

and doubles every

5

years

30-50%

in

85 years

Slide6

HX

Few definitive tests are available for diagnosing dementing

disorders,

so

reliable historical information regarding the

:

onset,

course

,

and

associated features

of cognitive dysfunction

is the

cornerstone of differential diagnosis.

Slide7

Historical Components of the Dementia Evaluation

INITIAL MANIFESTATIONS

Impaired recent memory

(repeats self, forgets what was heard

or read

, misplaces things)

Poor decision-making, judgment, or problem-solving

;

decreased organizational

skills

Difficulty learning new tasks or performing routine tasks

Problems managing money

(balancing checkbook, forgetting to

pay bills) or household

Difficulties expressing self

(word finding) or participating in

conversation

Getting lost in familiar areas

, forgetting known routes while driving

Change in personality

(apathetic, disinhibited), mood (sad,

irritable), or behavior (odd or bizarre)

Slide8

Historical Components of the Dementia Evaluation

TEMPORAL FACTORS

Mode of onset

(acute ,

subacute

, insidious)

Course

(static progressive, improvement over time, fluctuating)

INDIVIDUAL FACTORS

Cultural background

Educational level

Social/occupational demands

(and changes incurred by

symptoms)

Life circumstances

(social, financial, occupational,

living arrangements

)

Premorbid personality characteristics

Slide9

Historical Components of the Dementia Evaluation

HEREDITARY FACTORS

Familial risk factors

(stroke, hypertension, diabetes mellitus)

Genetic

: family history suggesting autosomal

dominant inheritance

or multiple cases in family suggesting

non-mutation associated

familial

disease (e.g.,

apolipoprotein

E4-associated Alzheimer's

disease)

Slide10

Historical Components of the Dementia Evaluation

MEDICAUNEUROLOGICAL CONDITIONS

General medical conditions

(hypothyroidism,

hypertension, diabetes

mellitus , heart disease)

Neurological conditions

(transient ischemic attacks,

strokes, seizures

, syncope, head trauma)

Associated motor features

(tremor, gait

difficulties, speech/swallowing

disturbance, ataxia)

Sleep disturbances

(sleep apnea, insomnia,

sleep-associated movement

disorder)

Slide11

Evaluation

Cognitive

Assessment

Neuropsychiatric

Assessment

Laboratory

Evaluation

Neuroimaging

Slide12

EXAMINATION OF AMEMORY

MINI MENTAL STATUS EXAMINATION(

MMSE

)

Detection of IMMEDIATE , LONG TERM , REMOTE

Memory

GENERAL &NEUROLOGIC EXAM

Slide13

EVALUATION OF MEMORY

Problem in

IMMEDIATE MEMORY:

Attention ororintation

cause immediate memory deficit

IMMEDIATE: repeat aseries of random digit.

Spared in SEVER

AMNESIA

& mild DEMENTIA

Slide14

EXAM OF MEMORY

LONG TERM MEMORY(

SHORT TERM MEMORY): remember and recall after

3 MINUTES

Remote MEMORY(LONG TERM MEMORY):

RECALL OF PAST PERSONAL , GEOGRAPHICAL OR HISTORICAL TEST.

Slide15

EXAM OF MEMORY

CEREBRAL

:cortical

sign other than memory loss.(apraxia, aphasia ,

agnosia

Assesment

of affect , emotional

lability

or poor control over emotional liability)

CRANIAL NERVES

(papilledema, 6

th

nerve palsy,

supraNUCLEAR

PALSY,

homonymus

hemianopia, multiple cranial nerve palsy)

Slide16

EXAM OF MEMORY

motor , reflex, cerebellar, gait

(CHOREA

HUNTINGTON

TREMOR , RIGIDITY, POSTURAL REFLEX IMPAIRMENT

PARKINSON

MYOCLONUS

POST ANOXIC, PRION

PRIMITIVE REFLEX

BILATERAL CORTICAL , SUBCORTICAL AND BRAINSTEM

ATAXIA & CEREBELLAR

WERNIKE

KORSAKOFE

CRANIAL NERVE &HEMIPARASIS

STROKE

Slide17

EXAM OF MEMORY

SENSORY

EXAM IS DIFFICULT

DEFICIT IN HIGH CORTICAL FUNCTION (AGNOSIA, NEGLECT EXTINCTION :

,

CORTICAL LESION

VIBRATION &POSITION SENSE

I

MPAIRMENT

VIT B12 DEFICIENCY

LOSS OF PAIN & TEM. WITH PAIN CRISIS

SYPHILITIC

Slide18

ASSOCIATED MEDICAL FINDING

THYROID

DYSFUNCTION

VIT B12

DEFICIENCY

TOXICITY

OF ANTICHOLINERGIC

WITHDRAWAL

OF ALCHOL&SEDATIVE

HEPATIC

DISEASE

TRAUMA

MENINGITIS, SAH, NPH, INTRACRANIAL MASS

Slide19

EVALUATION OF MEMORY

CT SCAN

MRI

, functional MRI(DETECT SOL,

DIFFUSE ATROPHY ALZHEIMER,

FOCAL ATROPHY PICK,S

PET

(positron emission tomography,

SPECT

(single positron emission computed tomography) asses global

metabolic

patterns

diffuse neuronal loss on degenerative

Slide20

EVALUATION OF MEMORY

ELECTROPHYSIOLOGY

USE FUL TO DETECT :

1-EPILEPSY,

2-SLEEP DISORDER

THAT RESULT TO MEMORY PROBLEM

3-DIFFUSE &NONSPECIFIC SLOWING

4- PERIODIC PATTERN

5-

TRIPHASIC, OR BURST SUPPERATION in

PRION

Slide21

EVALUATION

FLUID &TISSUE ANALYSIS

1-cbcdiff

2-

LFT

3-

TFT,

4-DRUG

ANALYSIS IN TOXICATION,

5-TEST FOR

CHRONIC MEMINGITIS

, CARCINOMA

6

- RECTAL BIOPSY

AMILOIDOSIS

Slide22

EVALUATION

7-BRAIN BIOPSY

(VASCULITIS, PRION, INFECTION

…)

8-CSF

Slide23

EVALUATION OF MEMORY

GENETIC TEST

:

HUNTINGTON , ATYPICAL ALZHEIMER,

Slide24

DEMENTIA

ALZHEIMER

70%

0F DEMENTIA

VASCULAR

10 -20%

OF dementia

ALCHOL DEMENTIA

INTRACRANIAL TUMOR

NORMAL PRESSURE HYDROCEPHALUS

CHRONIC DRUG INTOXICATION , METABOLIC

INFECTION (PRION)

OTHER NEUROLOGIC (PARKINSON, HUNTIONGTON, SUPRANUCLEAR PALSY

PSEUDODEMENTIAI

Slide25

DEMENTIA(r

eversible

)

1-inflammatory

:

sarcoidosis

, SLE,

vasculitis

(primary &secondary)

2- meningitis

due to fungi, TB, listeria

monocytosis

,

lyme

. Syphilis,

whipple

3

-VIT B12 deficiency

4 -

toxics

(drugs)

5- mass lesion

(tumor,

hematom

,communication hydrocephalus

6-coplex partial STATUS

epilepticus

Slide26

DEMENTIA(irreversible)

1- DEGENERATIVE

(Alzeheimer, PICK,S huntington, parkinson, lewy body…)

2-VASCULAR

(multiinfarct dementia, intra vascular coagulation)

3- METABOLIC:

storage disease, leukodystrophy)

4- NEOPLASTIC

( meningeal metastasis ,gliomatosis cerebri)

Slide27

NEUROTRANSMITTER OF MEMORY

CHOLINERGIC SYSTEM

: has a critica l role in longterm memory

SCOPOLAMINE

(cholinergic antagonist) impaire memory

PHYSIOSTIGINE

(cholinergic agonist) faciliate memory performance

CATHECHOLAMINE

: important role in working memory

Slide28

ALZEHEIMER( risk factor)

Age(

Prevalance

):

>60 years 5%

>85years 20-50%

Life time of developing AD is 12-17%

Alzheimer is sporadic , genetics basis 5%

Familial Alzheimer is AD : mutation in the APP ( chromosome 21)

presenilin

1 ( chromosome 14 ) ,

presenilin

2

,

APoe

€

4

Others

:

Limited

education,

depression,gender

,

strogen

replacement, head trauma, history of thyroid disease.

Slide29

Alzehiemer(clinical features)

1-Memory loss

(recent involved.

2- aphasia (wernike)

3- apraxia

4- agnosia (

a nosognosia, prosopagnosia,

a topoghraphagnosia

)

Slide30

Alzeheimer(clinical symptomes)

5-Psychiatric symptoms

(depression,psychotic symptom

Paranoid delusion , and hallucination.

6-Vegetative

symptoms(sleep disturbance, incontinence)

7-Later bed ridden

Slide31

Alzeiheimer(pathogenesis)

1- CORTICAL ATROPHY

2- NEUROTIC (senile)PLAQUES

, that is amyloid

surroded

by dystrophic neuritis

3- NEUROFIBRILLARY

TANGLE

(paired

hellicalfillaments

.)

Filaments are major constituent of NFT, ,

neuropil

treads,

dystrophic neuritis

.

Slide32

Alzeheimer(pathogenesis)

AD disrupts

cortical input

to

hippcampus

from association and limbic structure

&

DISRUPTS

HIPPOCAMPAL OUT FLOW

FROM

Amomonis

,

subiculum

to association cortex , diencephalon, basal forebrain and amygdala.

Slide33

Alzeheimer( pathogenesis)

ALZEHEIMER disconnect the

hippocampus

from its major

INPUT & OUT PUT

pathways,

BECAUSE

HIPPOCAMAL FORMATION ARE INVOLVED EARLY IN AD

.

Slide34

Alzeheimer (management)

1-MEMORY TONIC

: central

acetylcholinestrase

inhibitor:

TACRIN, EXELON

MILD &MODERATE STAGE OF DISEASE

2

-HALLOPERIDOL FOR DELUSION

3

-SEROTONIN REUPTAKE INHIBITOR FOR DEPRESSION

Slide35

MCI

The most studied form of MCI is that of isolated

recent memory

loss, or amnestic MCI

.

Diagnostic criteria are as follows:

1-a

subjective or objective impairment in recent

memory,

2-relatively

preserved cognitive functions in other

domains,

3- and presence

of normally performed everyday activities of daily living

..

Slide36

MCI

Persons who present with amnestic MCI have an

increased risk

of developing diagnosable AD at rates of

12% to 15%

per year

, in contrast with I% to 2% per year in age-matched

normal subjects.

Increased risk of more rapid transition or "

conversion“ to

AD

includes:

significant

hippocampal atrophy

on MRI,

worsened performance on

recent memory testing

,

Elevated CSF

tau and reduced A~-42 in the CSF

, and

the presence of

an apoE4 allele

Slide37

Slide38

Slide39

Alz PET

Slide40

FTD

onset typically between the ages of

50 and 60 years

and featuring insidious

personality change

,

disinhibition

,

and subsequent

gradual loss of

speech output

. Approximately

50% of

the

cases

were familial

.

Amyloid PLAQUES and NEUROFIBRILLARY TANGLE not seen.

FTD as a

tauopathy

No treatment.

Slide41

NPH

Slide42

NPH

Clinical triad ( gait apraxia , dementia , incontinency )

Ivestigation

:

LP, Imaging

Tretment

: Shunt

Complication of shunt

Slide43

Creutzfeldt-Iakob Disease

clinical

presentation

includes:

rapidly progressive dementia, myoclonus,

Other clinical sign : involvement of cerebral cortex , cerebellum , basal ganglia brainstem and

splinal

cortex

Psychiatric symptom

Pathogenesis :

proteinaceous

infectious

paticle

( prion )

Slide44

CJD

Investigation studies :

EEG

LP ( 14-3-3

pr

)

MRI

Biopsy (

Pr

Psc

)

treatment : no treatment

Slide45

Slide46

DLB

Second most common cause of dementia

Clinical :

cogition

decline without prominent memory impairment

Visual hallucination

Parkinsonism

Note : well respond to

anticholinestrase

but

sensetive

to antipsychotic drugs

Slide47

Dementia with NEUROLOGIC sign

HUNTINGTON

:dominant

inheritence

chore

athetosi

dementia

parkinson

:

tremor

rigidity

bradykinesia

Dementia (10-15%)-

Slide48

Dementia with neurologic sign

Progressive supra nuclear palsy:

falling

Axiall dystonia

pseudobulbar palsy

supra nuclear ophthalmoplegia

Slide49

DEMENTIA WITH NEUROLOGIC SIGN

AIDS DEMENTIA COMPLEX

DEMENTIA

ATAXIA

SACCADIC &PURSUIT MOVEMENT

upper motor sign

Incontinence

NEUROSYPHLIS (GENERAL PARESIS

Slide50

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