AMNESTIC

DISORDERS
Dr. Manu Sharma
Chairperson: Dr. Aruna

Introduction
Disorder of cognitive function- impairment

memory and learning are out of proportion

to components of mentation and behavior.
originally defined by Ribot
Involves both anterograde and retrograde
memory process
Due to damage or dysfunction in
hypothalamic diencephalic systems and or
hippocampal systems, which subserve
memory.

AMNESIA
Origin: Greek- to forget/forgetfulness
Loss of memory usually due to brain injury,
illness, shock, repression, fatigue
Gap in ones memory
The selective overlooking or ignoring events
or facts that are not favorable /useful to ones
purpose/position

PARAMNESIA
Origin: Neo-latin
A distortion of memory in which fantasy and
objective experience are confused.

Definition
Overall, DSM-IV-TR provides four diagnostic
entities under this category:
1. Amnestic disorder due to cerebral or
systemic medical condition,
2. Substance-induced amnestic disorder,
3. Amnestic disorder due to unknown etiology,
and
4. Amnestic disorder not otherwise specified.

ICD-10, amnestic disorder is defined as

Organic amnestic syndrome, not induced by

alcohol and other psychoactive substances.
For substance-induced amnestic disorder, ICD10 uses the term Amnestic syndrome.

 Memory impairment manifest by both:

a defect of recent memory (impaired learning of

new material), to a degree sufficient to interfere

with daily living; and
a reduced ability to recall past events
Absence of:
a defect in immediate recall (as tested, for
example, by the digit span)
clouding of consciousness and disturbance of
attention, as defined in Delirium
global intellectual decline (dementia)
Objective evidence (physical and neurological
examination, laboratory tests) and/or history of an
insult to or a disease of the brain (especially involving
bilaterally the diencephalic and medial temporal
structures but other than alcoholic encephalopathy)
that can reasonably be presumed to be responsible for

FORMS OF MEMORY

Working memory

Long term memory

Recent

Remote

LOSS OF MEMORY

Declarative Memory
( Explicit)

Non-Declarative Memory
( Implicit)

DECLARATIVE MEMORY

Episodic Memory

Semantic memory

Memory of specific episodes

Memory of facts,
Principles
& rules
Evolved from episodic
memory

Epidemiology
The exact prevalence and incidence of the

amnestic disorders are unknown (Kaplan et al.

1994 ).
Memory disturbances alcohol abuse and head
trauma appear to be the two most common
causes of amnestic disorders.
In the hospital setting the incidence of alcoholinduced amnestic disorders is decreasing while
that of amnestic disorders secondary to head
trauma is on the rise (Korvath et al. 1989 ).
Alcohol induced amnestic disorder varies from 0.2
-4 %

Clinical features
Patients with amnestic disorder have impaired

ability to learn new information (anterograde

amnesia) or cannot remember material
previously learned (retrograde amnesia).
Memory for the event that produced the
deficit (e.g., a head injury in a motor vehicle
accident) may also be impaired.

Clinical features

Short term memory impaired to variable

degree.
Long term retrograde memory impairment is
temporally graded ( more remote memories
better preserved)
Immediate recall not affected.
Attention & implicit learning intact.

Clinical features
In some instances, disorientation to time and

place may occur, but disorientation to person

is unusual.
Often individuals lack insight into the memory

deficit and vehemently insist that their

inaccurate responses on a MSE are correct.
Associated symptoms include confabulation,
personality changes, neurological symptoms
due to underlying illness.
Confabulations frequent in diencephalic

Areas involved:
the mamillary bodies,
the hippocampus,
the amygdala,
the dorsomedial, and
the midline thalamic nuclei.
Bilateral lesions are considered as the main
culprit, but there are studies reporting unilateral
(left regions being more often involved) damage
as the cause of amnestic disorders.

Frontal lobe involvement may be responsible

for such commonly seen symptoms as apathy

and confabulation.

MEDIAL TEMPORAL LOBE

AMNESIA
Short term memory is normal
Severe anterograde memory loss
Once learned there is rapid rate of

forgetting.
Retrograde memory loss is
temporarily graded, but limited
Semantic memory is preserved
Normal implicit memory

DIENCEPHALIC
AMNESIA

Short term memory is normal.

Severe anterograde memory loss
Once learned there is rapid rate of

forgetting.
Retrograde memory loss is
temporarily graded, but extensive
Semantic memory is preserved
Normal implicit memory

FRONTAL LOBE AMNESIA

No real memory loss

Due to poor attention & executive

function.
Fail to recall, but normal recognition.
Certain specific impairment of memory:
Defective recall of temporal order
Defective recall of the context of the
learned items
Defective judges of knowing what they
remember

DISEASES WITH MEMORY

LOSS

CAUSES:

Medial temporal lobe:

Encephalitis.

PCA stroke, Anoxia.

Diencephalic:
Wernicke-Korsakoffs
Thalamic

syndrome

infarct

Frontal lobe:
Stroke

or tumor affecting basal

forebrain.

HERPES SIMPLEX ENCEPHALITIS

Damage

to medial & lateral temporal

cortex.
Severe episodic memory loss
Semantic memory loss, if lateral temporal
cortex is affected.

PARANEOPLASTIC LIMBIC

ENCEPHALITIS
An

autoimmune response to cancer

Similar to HSE

ANOXIC ENCEPHALOPATHY
Due

to cardiac arrest, respiratory

distress, strangulation or CO
poisoning.
Susceptible areas:
Hippocampus
Cerebellum
Basal

Most

ganglia

vulnerable is CA1 segment.

Defect may vary from mild to
severe memory loss.

STROKES:
PC

infarction:

Supply

post. Hippocampus, parahippocampal

gyrus & connections of hippocampus
Bilateral lesion:
Global amnesia.
Unilateral stroke:
Material specific memory loss
Thalamic
Affecting

strokes:

mamillothalamic tract & internal

medullary lamina

Wernickes
encephalopathy
CAUSES

Thiamine deficiency (chronic

alcoholism, Ca stomach, toxemia of
pregnancy, vomiting, diarrhea,
pernicious anemia, dietary deficiency)
Association between alcoholism &
wernickes explained by certain
mechanisms.

CLINICAL FEATURES

acute onset
ocular abnormalities 96%
ataxia
mental symptoms 90%
Memory disturbances quite

prominent when confusion subsides.

Peripheral neuropathy, malnutrition,

frank DT.

Investigation :
raised blood pyruvate level (non specific)
red cell transketolase estimation.
Pathology :
changes in 3rd ventricle, peri aqueductal
region, dorsomedial nuclei of pulvinar,
mamillary bodies, anterior lobe of
cerebellum.
cerebral cortex affected in 27%.

Treatment
correct

Thiamine deficiency by 50mg

thiamine IV followed by im injection of
100mg thiamine daily till
improvement.
magnesium supplementation
correct other nutritional & vitamin
deficiencies
opthalmoplegia responds well & early

while neuritis & ataxia take longer time,

may be permanent

Korsakoffs Psychosis
Once wernickes clears characteristic

memory deficits of Korsakoffs in 84% of

cases.
Different stages of same disease process.
Neurotoxic effects of alcohol also

responsible (cerebral atrophy)

 Clinical features
Memory deficit
Subtle wide spread derangement in other

cognitive function
Defective recent memory, disorientation
in time, impaired new learning,
anterograde amnesia.
If recovery- dense amnestic gap for the
period of illness.

 Confabulation not always found.

Common in early stages

Inability to sustain mental activity,

inflexibility, rigidity of mental set,

perseveration, poor concept formation,
visuo spatial impairments.
Apathy & indifference.

 DD - tumors of 3rd ventricle,

hypothalamic area, SAH, post

trauma, TB meningitis, post anoxic
cases.
Treatment outcome disappointing.
Recovery process continued as
long as two years.

TRANSIENT AMNESIC SYNDROMES

TGA
Migraine
Transient

epileptic amnesia
IV contrast infusion
TIA of posterior circulation
SAH
Head trauma

Transient global amnesia

Described by Fisher and Adams
DD of amnestic syndrome
Memory deficit - most characteristic

feature
Late middle/old age
male>female
Abrupt & sudden onset
Episodic attacks hoursfew days

 complete recovery
Retrograde amnesia recovers before

anterograde amnesia
Impairment of all aspects of memory,
state of puzzled bewilderment
Preceded by headache, vigorous
exercise, stress, medical procedure
Patient can attend personal needs,
aware of personal identity
Recurrence rare

Sometimes permanent deficit in the form

of memory impairment & global cognitive

impairment.
DD Psychomotor seizures, hypoglycemic

attacks, delirium, alcohol & drug

intoxication.
Either seizure activity or result of ischemia

of hippocampal hypothalamic system.

TRANSIENT EPILEPTIC AMNESIA

Coined by Kapur.
Refers to pts with TGA with epilepsy.
EEG & CT may be normal. Sleep EEG

recordings may be helpful.

Involvement of B/L limbic structures as well as
the mesial diencephalon.

Head injury
Some retrograde amnesia
PTA may exist without retrograde amnesia,

although this is more common with

penetrating lesions
The length of PTA predictive of eventual
cognitive/psychiatric/social outcome
PTA needs to be distinguished from the post
traumatic syndrome

Alcoholic blackouts
Related to the BAC
Common in binge drinkers
Fragmentary blackouts
En bloc blackouts
Hypoglycemia may be contributory
h/o head injuries

Iatrogenic amnesia
ECT
Retrograde memory impairment from the
preceding 1-3 years
A pronounced anterograde memory
impairment on recall & recognition tasks
Accelerated rate of forgetting
Returns to normal within 6-9 months
Verbal memory is particularly sensitive to
disruption

Iatrogenic amnesia
Drugs
BZD- especially triazolam
Barbiturates (thiopental sodium)
Diltiazem
Zalcitabine
Flunitrazepam
GHB

Mild cognitive
impairment
Diagnostic category designed to fill the

gap between cognitive changes associated

with ageing and cognitive impairment
suggestive of dementia.
Further subsided broadly to amnestic &

non amnestic group.

Amnestic MCI related to AD and vascular

dementia, non amnestic group related to

FTD.

General criteria
1) Not normal, not demented, but cognitive

decline present.
2) Self/informant report & impairment on

objective cognitive tasks.

3) And /or evidence of deterioration over time on

objective cognitive tasks.

4) Preserved basic activities of daily living/

minimal impairment in complex instrumental

function.

Psychogenic amnesia
Onset after traumatic event.
No evidence of substance/ general medical

condition.
Amnesia for personal identity and
circumscribed event.
Preserved memory for new events.
Preserved ability of learning.
Abrupt onset & resolution , no residual
impairment

ASSESSMENT OF MEMORY
DISORDERS

Patient has to be alert, attentive &

cooperative
Short term memory digit span.
Long term memory
Multiple trial list learning task.
Recognition- by mixing items from the
learned list with similar items not in the
list
Remote memory:
Naming or describing remote personal
or historical events
Semantic memory:

ASSESSMENT
Diagnostic laboratory evaluations
Include blood and urine to test for

Infections
Renal and liver function tests
Hypoglycemia and diabetes
Electrolyte imbalances
Metabolic and endocrine disorders
Nutritional deficiencies, B12, folate
Presence of toxic substances

ASSESSMENT
Other diagnostic evaluations

may include
EEG
CT
MRI
Lumbar puncture

Differential Diagnosis
Dementia & Delirium
Normal Aging
Dissociative disorders
Facticious disorders
Malingering

Management
Role of thiamine in KS not established
No controlled studies regarding donepezil,

rivastigmine, memantine in KS
Others managed based on etiology
Once amnestic deficits emerge few options
in pharmacotherapy
Psychotherapy and cognitive rehabilitation
programmes can help improve patients
function
Not much benefits in restoring or
improving memory in impaired domains

Family Management

Suggest: planning Care for Pt

Understanding & Accept
Environmental Manipulation

Supportive Group for Fm. Member

Individual Psych. For Fm. Member

Course and prognosis

25% KS recover
Rest has varying degree of memory impairment
Most amnestic syndrome have a stable course
Many would recover(TGA, post ECT)
Few would improve(TBI)

Summary
Diagnostic entities included in DSM-IV-TR. ICD-

10 definition
Structures that are involved
Etiology
Head injury & alcohol abuse are common
causes
Wernicke-Koraskoff syndrome
Differential diagnosis
Treat the cause
Family psychoeducation

THANK YOU