amnestic disorders

7/28/2019 Amnestic Disorders

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CHAIR PERSON- Dr.MANJU BHASKAR

PRESENTER- Dr.D.ARCHANAA

AMNESTIC DISORDERS


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Introduction

disorder of cognitive function - memory andlearning are out of proportion to componentsof mentation and behaviour.

originally defined by Ribot

Involves both anterograde and retrogradememory process

Due to damage or dysfunction in hypothalamicdiencephalic systems and or hippocampalsystems, which subserve memory.


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FORMS OF MEMORY

Working memory Long term memory

Recent Remote


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LOSS OF MEMORY

Declarative Memory

( Explicit)

Non-Declarative Memory

( Implicit)


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DECLARATIVE MEMORY

Episodic Memory Semantic memory

Memory of specific episodes

Memory of facts, Principles& rules

Evolved from episodic memory


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Memory loss not due to delirium, dementia

Physiological basis or substance induced

- Distinguish from dissociative disorders,dissociative amnesia, dissociative identitydisorders

Specify

- Transient less than 1 month

- Chronic - more than 1 month


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Amnestic disorders

Amnestic disorder due to cerebral or systemic

medical condition.

Substance induced amnestic disorder.

Amnestic disorder due to unknown etiology.

Amnestic disorder not otherwise specified.


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AMNESTIC SYNDROMES

ORGANIC CAUSES

SUBSTANCE INDUCED


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Epidemiology

Data regarding over all prevalence lacking.

Alcohol induced amnestic disorder varies from 0.2 -4 %

Incidence of transient global amnesia 5.2/1,00,000


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CLINICAL FEATURES

Memory impairment core symptom

Anterograde {inability to learn new information}

Retrograde { inability to recall previously

learned information


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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.


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Associated symptoms include confabulation,

personality changes, neurological symptoms due to

underlying illness.

Confabulations frequent in diencephalic amnesia than

hippocampal.


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ORGANIC AMNESTIC SYNDROMES

SEIZURE DISORDER

TRAUMATIC BRAIN INJURY

CEREBRAL TUMORS STROKE

INFECTIONS

METABOLIC TGA

ECT


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PATTERNS OF MEMORY LOSS

Depends on region affected

Bilateral medial temporal lobe amnesia.

Diencephalic amnesia.

Frontal lobe amnesia


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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 temporarilygraded, but limited

Semantic memory is preserved

Normal implicit memory


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DIENCEPHALIC AMNESIA

Short term memory is normal.

Severe anterograde memory loss

Once learned there is rapid rate of forgetting.

Retrograde memory loss is temporarilygraded, but extensive

Semantic memory is preserved

Normal implicit memory


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FRONTAL LOBE AMNESIA

No real memory loss

Due to poor attention & executive function.

Fail to recall, but normal recognition.

(Multiple trial list learning task

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


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DISEASES WITH MEMORY LOSS

CAUSES: Medial temporal lobe:

Encephalitis. PCA stroke, Anoxia.

Diencephalic:

Wernicke-Korsakoff ssyndrome

Thalamic infarct

Frontal lobe:

Stroke or tumor affecting basal forebrain.


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HERPES SIMPLEX ENCEPHALITIS Damage to medial & lateral temporal cortex.

Severe episodic memory loss

Semantic memory loss, if lateral temporal cortex isaffected.

PARANEOPLASTIC LIMBIC ENCEPHALITIS

An autoimmune response to cancer

Similar to HSE


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ANOXIC ENCEPHALOPATHY

Due to cardiac arrest, respiratory distress,strangulation or CO poisoning.

Susceptible areas: Hippocampus

Cerebellum

Basal ganglia

Most vulnerable is CA1 segment. Defect may vary from mild to severe

memory loss.


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STROKES:

B/L PC infarction:

Supply post. Hippocampus, parahippocampalgurus & connections of hippocampus

Bilateral lesion:

Global amnesia.

Unilateral stroke:

Material specific memory loss

Thalamic strokes:

Affecting mamillothalamic tract & internal

medullary lamina


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Wernickes encephalopathy

CAUSES

Thiamine deficiency (chronic alcoholism, Ca

stomach, toxemia of pregnancy, vomiting,diarrhea, pernicious anemia, dietarydeficiency)

Association between alcoholism &wernickes explained by certainmechanisms.


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CLINICAL FEATURES

acute onset

ocular abnormalities 96%ataxia

mental symptoms 90%

Memory disturbances quite prominent whenconfusion subsides.

Peripheral neuropathy, malnutrition, frankDT.


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Investigation :

raised blood pyruvate level(non specific)

red cell transketolase estimation.

Pathology :

changes in 3rd ventricle, periaqueductal

region, dorsomedial nuclei of pulvinar, mamillary

bodies, anterior lobe of cerebellum.cerebral cortex affected in 27%.


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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 respond well & early while

neuritis & ataxia take longer time, may be

permanent


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Korsakoffs Psychosis

Once wernickes clear characteristic memory

deficits of Korsakoffs in 84% of cases.

Different stages of same disease process.

Neurotoxic effects of alcohol also responsible

(cerebral atrophy)


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Clinical features Memory deficit

Subtle wide spread derangement in other cognitivefunction

Defective recent memory, disorientation in time,

impaired new learning, anterograde amnesia.

If recovery dense amnestic gap for the period ofillness.


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Confabulation not always found common in

early stages

Inability to sustain mental activity, inflexibility,

rigidity of mental set, perseveration, poorconcept formation, visuo spatial impairments.

Apathy & indifference.


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DD - tumors of 3rd ventricle, hypothalamicarea, SAH, post trauma, TB meningitis,post anoxic cases.

Treatment outcome disappointing.

Recovery process continued as long as twoyears.


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TRANSIENT AMNESIC SYNDROMES:

TGA

Migraine

Transient epileptic amnesia

IV contrast infusion.

TIA of posterior circulation.

SAH

Head trauma


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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.


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complete recovery

Impairment ofall aspects of memory, stateof puzzled bewilderment.

Patient can attend personal needs, awareof personal identity.

Recurrence rare.


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TGA conti

Sometimes permanent deficit in the form ofmemory impairment & global cognitiveimpairment.

DD Psychomotor seizures, hypoglycemic attacks,

delirium, alcohol & drug intoxication.

Either seizure activity or result ofischemia of

hippocampal hypothalamic system.


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Mild cognitive impairment

Diagnostic category designed to fill the gapbetween cognitive changes associated with ageing

and cognitive impairment suggestive ofdementia.

Further subsided broadly to amnestic & non

amnestic group.

Amnestic MCI related to AD and vascular dementia,non amnestic group related to FTD.


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General criteria

1) Not normal, not demented, but cognitive declinepresent.

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/ minimalimpairment in complex instrumental function.


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Psychogenic amnesia

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

condition.

Amnesia for personal identity (conserved inamnestic disorder) and circumscribed event.

Preserved memory for new events.

Preserved ability oflearning.

Abrupt onset & resolution , no residual impairment


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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 historicalevents

Semantic memory:

Ask questions about commonly known facts


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ASSESSMENT (cont.)

Other diagnostic evaluations may include EEG- Electroencephalogram

CT- Computed tomography

PET- Positron emission tomography

MRI- Magnetic resonance imaging

Lumbar puncture to examine cerebrospinal fluid

(CSF)


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Differential Diagnosis Dementia & Delirium

Normal Aging

Dissociative disorders

Facticious disorders


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Management

Role ofthiamine in ks not established

No controlled studies regarding donepezil,

rivastigmine, memantine in ks

Others managed based on etiology

Once amnestic deficits emerge few options inpharmacotherapy

Psychotherapy and cognitive rehabilitation

programmes can help improve patients function Not much benefits in restoring or improving

memory in impaired domains

i


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Family Management Suggest: planning Care for Pt

Understanding & Accept

Environmental Manipulation

Supportive Group for Fm. Member

Individual Psych. For Fm. Member


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Course and prognosis

25% ks recover

Rest has varying degree of memory impairment

Most amnestic syndrome have a stable course

Few would recover(TGA, post ECT)

Few would improve(TBI)


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THANK U


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amnestic disorders

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