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DISORDERS
Dr. Manu Sharma
Chairperson: Dr. Aruna
Introduction
Disorder of cognitive function- impairment
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.
FORMS OF MEMORY
Working memory
Recent
Remote
LOSS OF MEMORY
Declarative Memory
( Explicit)
Non-Declarative Memory
( Implicit)
DECLARATIVE MEMORY
Episodic Memory
Semantic memory
Epidemiology
The exact prevalence and incidence of the
Clinical features
Patients with amnestic disorder have impaired
Clinical features
Clinical features
In some instances, disorientation to time and
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.
forgetting.
Retrograde memory loss is
temporarily graded, but limited
Semantic memory is preserved
Normal implicit memory
DIENCEPHALIC
AMNESIA
forgetting.
Retrograde memory loss is
temporarily graded, but extensive
Semantic memory is preserved
Normal implicit memory
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
CAUSES:
Diencephalic:
Wernicke-Korsakoffs
Thalamic
syndrome
infarct
Frontal lobe:
Stroke
cortex.
Severe episodic memory loss
Semantic memory loss, if lateral temporal
cortex is affected.
PARANEOPLASTIC LIMBIC
ENCEPHALITIS
An
ANOXIC ENCEPHALOPATHY
Due
Most
ganglia
STROKES:
PC
infarction:
Supply
strokes:
Wernickes
encephalopathy
CAUSES
CLINICAL FEATURES
acute onset
ocular abnormalities 96%
ataxia
mental symptoms 90%
Memory disturbances quite
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
Korsakoffs Psychosis
Once wernickes clears characteristic
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.
epileptic amnesia
IV contrast infusion
TIA of posterior circulation
SAH
Head trauma
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
Head injury
Some retrograde amnesia
PTA may exist without retrograde amnesia,
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
General criteria
1) Not normal, not demented, but cognitive
decline present.
2) Self/informant report & impairment on
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
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
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