AMNESTIC DISORDERS

CHAIR PERSON- Dr.MANJU BHASKAR PRESENTER- Dr.D.ARCHANAA

Introduction
disorder of cognitive function - memory and

learning are out of proportion to components of mentation and behaviour. 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.

FORMS OF MEMORY

Working memory

Long term memory

Recent

Remote

LOSS OF MEMORY

Declarative Memory ( Explicit)

Non-Declarative Memory ( Implicit)

DECLARATIVE MEMORY

Episodic Memory
Memory of specific episodes

Semantic memory

Memory of facts, Principles

& rules
Evolved from episodic memory

AMNESTIC

DISORDER

DSM-IV

A. Memory impairment
-

inability to learn new information, or Inability to recall previously learned information

Memory disturbance significantly impairs

social, occupational function, deterioration from past

 Memory loss not due to delirium, dementia Physiological basis or substance induced
- Distinguish from dissociative disorders,

dissociative amnesia, dissociative identity disorders Specify - Transient less than 1 month - Chronic - more than 1 month

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.

AMNESTIC SYNDROMES

ORGANIC CAUSES

SUBSTANCE INDUCED

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

CLINICAL FEATURES

Memory impairment core symptom

Anterograde {inability to learn new information} Retrograde { inability to recall previously learned information

 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.

Associated symptoms include confabulation, personality changes, neurological symptoms due to underlying illness. Confabulations frequent in diencephalic amnesia than hippocampal.

ORGANIC AMNESTIC SYNDROMES

SEIZURE DISORDER
TRAUMATIC BRAIN INJURY CEREBRAL TUMORS STROKE INFECTIONS METABOLIC TGA ECT

PATTERNS OF MEMORY LOSS

Depends on region affected

Bilateral medial temporal lobe amnesia. Diencephalic amnesia. Frontal lobe amnesia

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.

(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

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.

DISEASES WITH MEMORY LOSS

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

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.

DISEASES WITH MEMORY LOSS

STROKES:

B/L PC infarction:
Supply post. Hippocampus, parahippocampal gurus & connections of hippocampus Bilateral lesion: Global amnesia. Unilateral stroke: Material specific memory loss

Thalamic strokes:
Affecting 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 respond well & early while neuritis & ataxia take longer time, may be permanent

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)

 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.

DISEASES WITH MEMORY LOSS

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 Impairment of all aspects of memory, state

of puzzled bewilderment. Patient can attend personal needs, aware of personal identity. Recurrence rare.

TGA conti
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.

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 (conserved in amnestic disorder) 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: Ask questions about commonly known facts

ASSESSMENT (cont.)
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 (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)

Differential Diagnosis
Dementia & Delirium Normal Aging

Dissociative disorders
Facticious disorders

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

Few would recover(TGA, post ECT) Few would improve(TBI)

THANK U