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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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DISEASES WITH MEMORY LOSS
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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DISEASES WITH MEMORY LOSS
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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DISEASES WITH MEMORY LOSS
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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DISEASES WITH MEMORY LOSS
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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