Amnestic disorders are syndrome characterized by memory impairment (anterograde and /or retrograde amnesia)which are caused by a general medical condition or substances use and when delirium and dementia have been excluded as causative of the amnesia

1. Amnestic disorders
PRESENTER : DR MEGHA KHARYAL
MODERATOR : DR SRIKANTH
ASSISTANT PROFESSOR
DEPARTMENT OF PSYCHIATRY

2. remove part of the left side of his brain. He
suffered from severe epileptic seizures, and the
doctors hoped that by removing a part of his
brain they'd be able to stop the seizures.
They were right; after the surgery, Molaison no
longer had seizures. But he had another
problem: he also no longer had the ability to
make new memories.
After 14 years, Molaison still could not recall
things that had happened since his surgery.
However, he could still remember things that
had happened prior to the operation.

3. Amnestic disorders are syndrome characterized by memory impairment
(anterograde and /or retrograde amnesia)which are caused by a general
medical condition or substances use and when delirium and dementia have
been excluded as causative of the amnesia
Amnestic disorders may be transient or chronic(<or >1 month)
Amnestic conditions involve neuroanatomical structures:- Frontal cortex,
hippocampus and amygdala, dorsomedial thalamus, mamillary bodies and
periaqueductal grey matter(PAG)
Glutamate transmission at the NMDA receptor is also implicated in
amnesia, mainly due to its role in memory storage to limbic system.

5. ETIOLOGY
EPISODIC AMNESIA
1. Transient global amnesia
2. Pure epileptic amnesia
3. Blackouts
4. Concussion
5. Transient ischemic attacks

6. CHRONIC AMNESIA
1. Korsakoff's syndrome
2. Stroke
3. Tumour
4. Limbic encephalitis
5. Neurodegenerative disorders:-
• Alzheimer's disease
• Frontotemporal lobar degeneration
6. Traumatic brain injury
7. Post hypoxic ischemic
injury
8. Encephalitis
9. Status epilepticus
10.Certain neurosurgical
procedures

7. SYMPTOMS
Memory impairment is the core symptom of all amnestic disorders. It
includes both Anterograde amnesia and Retrograde amnesia.
Short-term memory can also be impaired .
Immediate recall is usually not affected, Attention and implicit learning are
also intact.
 Associated symptoms include confabulations, changes in personality as
well as neurological symptoms corresponding to the underlying illness.
The confabulations are more frequent in diencephalic amnesia
(prototypical Korsakoff syndrome) than in hippocampal amnesia

8. TRANSIENT GLOBAL AMNESIA
It is the prototype of episodic anterograde amnesia.
Onset in the seventh decade of life
Characterized by the appearance of one or more episodes, lasting from
4–18 hours,during which there is a dense anterograde amnesia coupled
with a retrograde amnesia of variable duration, from hours to decades.
During the episode, patients, may repeatedly, and anxiously, ask what is
happening. Recovery is typically complete except for an “island” of
amnesia extending backwards in time from when the episode resolved
an hour or two before the episode began.

9. PURE EPILEPTIC AMNESIA
It represents a partial seizure characterized by a combination of
anterograde and variable retrograde amnesia.
Recurrent episodes of amnesia and disorientation lasting 30mins to
1hr,occurring from sleep or on waking, due to Medial Temporal Lobe
seizures in epilepsy
They are of paroxysmal onset, relatively brief, and not accompanied by
anxious questioning on the patient’s part.
Evidence of either complex partial or grand mal seizures in the history can
be found.

10. BLACKOUTS
Alcoholic blackouts are discrete episodes of memory loss for significant events.
Not to be confused with withdrawal seizures or other ictal phenomena.
Alcoholic blackouts are associated with severe intoxication, patients are generally
not aware anything is amiss
The duration of blackouts ranges from less than an hour up to days
Patients have no memory of what they did while intoxicated, and may anxiously ask
others what happened.
Hypoglycaemia is also a contributory factor, and blackouts are more common where
there is a history of previous head injuries
Blackouts also occur with benzodiazepines, especially those of high potency, such
as triazolam.

11. CONCUSSION
It occurs after minor head injury or whiplash, accompanied by a dense
anterograde and variable retrograde amnesia.
After recovery, the patient is left with the typical island of amnesia,
extending back from the time of recovery to, generally, either the injury
itself or a short time before that.
Transient ischemic attacks involving either the thalamus or medial aspect of
the temporal lobe is characterized by 15 to 20 minutes of amnesia

12. VASCULAR DISORDERS
Two types of specific vascular lesions affect memory, thalamic
infarction and subarachnoid haemorrhage.
When there is a relatively pure lesion of the anterior thalamus,
anterograde amnesia without an extensive retrograde memory loss
commonly results.
Aneurysms of the Anterior Communicating Artery can result in
amnestic disorder.
Certain neurosurgical procedures may cause amnesia as a
complication, including clipping of anterior communicating artery
aneurysms or temporal lobectomy.

13. TUMOURS
 Cause a progressive amnesia, seen with craniopharyngiomas (which
compress the overlying mamillary bodies), thalamic tumors, and tumors
affecting the columns of the fornix.
LIMBIC ENCEPHALITIS
It results from an autoimmune assault on the limbic system, including
the hippocampus.
Most patients are present with delirium, and it can be preceded by an
amnestic syndrome.

14. NEURODEGENERATIVE DISORDERS
Present with an amnesia that evolves very slowly into a dementia,
and in such cases the amnesia represents, as it were, a “prodrome”
to the dementia.
Most commonly seen with Alzheimer’s disease and frontotemporal
lobar degeneration.

15. TRAUMATIC BRAIN INJURY
Characteristically, may, leave a dementia in its wake; however, at other
times a chronic amnestic disorder will constitute the main sequela.
An open or closed brain injury results in injury to the Anterior Temporal
Poles
Anterograde post traumatic amnesia is prominent with retrograde
amnesia relatively absent

16. POST-HYPOXIC-ISCHEMIC ENCEPHALOPATHY
Occurs with attempted hanging, carbon monoxide intoxication,
cardiorespiratory arrest, or after inhalation anesthesia, characterized by a
chronic amnesia.
Damage of sensitive CA1 and CA3 neurons in the hippocampus
This results in problems with Short Term Memory Storage

17. DISSOCIATIVE AMNESIA
Sudden retrograde autobiographical memory loss.
Ranging from hours to years.
Associated with depersonalization or derealization.

18. HERPES ENCEPHALITIS
Gives rise to a severe form of amnesic syndrome.
Behavioural changes may be seen. Seizures can occur.
Neck rigidity, vomiting, and motor and sensory deficits seen after the first
week.
Some cases commence more insidiously with behavioural change or
psychiatric phenomena, the confusion and neurological features becoming
evident only later.
Diagnosis is by the PCR test or a raised titre of antibodies to the virus in the
cerebrospinal fluid.

19. Neuropathological and neuro-imaging
studies usually show extensive bilateral
temporal lobe damage.
The medial temporal lobe structures are
severely affected, including the
hippocampi, amygdalae, entorhinal, and
perirhinal cortices, and other
parahippocampal structures.
Treatment with IV acyclovir as it may
prevent deficits becoming permanent.

20. WERNICKE’S ENCEPHALOPATHY
Wernicke’s encephalopathy is an acute neuropsychiatric condition
caused by thiamine deficiency with classical’ triad of ophthalmoplegia,
ataxia and altered mental status
In alcohol dependence, thiamine deficiency is secondary to both reduced
dietary intake and reduced absorption.
 If Wernicke’s encephalopathy is suspected, the patient should be
transferred to a medical unit where IV thiamine can be administered.

21. If untreated, Wernicke’s encephalopathy progresses to Korsakoff’s
syndrome (permanent memory impairment, confabulation, confusion
and personality changes).
It is associated with pathological lesions in Mamillary bodies, PAG,
Thalamic nuclei and the walls of the Third ventricle

22. PROPHYLACTIC THIAMINE
 Low-risk drinkers without neuropsychiatric complications and with an
adequate diet should be offered oral thiamine: a minimum of 300mg
daily during assisted alcohol withdrawal and periods of continued
alcohol intake.
 Caution: As thiamine is required to utilise glucose, a glucose load in a
thiaminedeficient patient can precipitate Wernicke’s encephalopathy

23. KORSAKOFF SYNDROME.
In 1889, Serghei Korsakoff described a syndrome of polyneuritis,
anterograde amnesia, and confabulations in subjects with chronic alcohol
use.
Emil Kraepelin distinguished between alcohol-related Korsakoff syndrome
and Korsakoff syndrome related to other nonalcoholic processes (e.g.,
neurosyphilis).
 Korsakoff syndrome usually develops secondary to Wernicke
encephalopathy, and frequently they are described together (Wernicke–
Korsakoff syndrome) .

24. Alcohol use induces thiamine deficiency through folate deficiency and
through direct damage of the intestinal mucosa.
Primary thiamine deficiency is caused by general malnutrition and other
conditions like Anorexia nervosa, Acquired immune deficiency syndrome
(AIDS), Hyperemesis gravidarum, Thyrotoxicosis, Metastatic cancer,
Hypomagnesemia, Long-term dialysis, and Congestive heart failure treated
long-term with diuretics.

25. Thiamine is important for normal neurotransmitter function. Acetylcholine,
γ-aminobutyric acid (GABA), glutamate, and aspartate are produced primarily
through the oxidative metabolism of glucose.
Serotonin metabolism also influenced by thiamine deficiency.
CSF levels of 5-hydroxyindoleacetic acid (5-HIAA) reduced in patients with
Wernicke-Korsakoff syndrome.
In Korsakoff syndrome, intelligence is intact, but inability to form new
memories
Immediate recall and implicit learning are preserved.
Individuals with Korsakoff syndrome classically present with confabulation.

26. Three contiguous FLAIR images (5 mm thick with a 2.5 mm skip) of
the acute WE. Note-The hyperintense signal in the mammillary
bodies and colliculi (left), periventricular gray matter (middle), and
fornix and thalamus

27. There has been an extensive literature on the effects of cholinergic
antagonists such as scopolamine upon memory.
Cholinergic blockade produces an effect upon the ‘central executive’
component of working memory.
Benzodiazepines produce a marked anterograde impairment in explicit or
episodic memory.
Forensic psychiatric importance are agents which produce transient but
profound amnesia, and may be implicated in offences such as ‘date
rape’,these include flunitrazepam (Rohypnol) and gammahydroxybutyrate
(GHB).
3,4-methylenedioxymethamphetamine (ecstasy) also produces memory
impairments either by direct or indirect effects.
NEUROPHARMACOLOGY OF MEMORY
DISORDERS

28. MEDICAL HISTORY
The evaluation starts with a detailed medical history.
The type of memory loss and whether it's recent or long term.When the
memory problems started and how they progressed.
Factors that triggered memory problems, such as a head injury, stroke or
surgery.Family history, especially of neurological disease.
Drug and alcohol use,other symptoms such as confusion, language
problems, personality changes or not being able to perform self care.
History of seizures, headaches, depression or cancer. The physical exam
includes a neurological exam to check reflexes, sensory function and
balance.

29. DIAGNOSTIC TEST
A comprehensive evaluation is needed to diagnose amnesia.
It can rule out other possible causes of memory loss such as Alzheimer's
disease, other forms of dementia, depression or a brain tumor.
Imaging tests — including an MRI and CT scan — to check for brain damage
or changes such as shrinkage.
Blood tests to check for infection, nutritional deficiencies or other issues.
An electroencephalogram (EEG) to check for the presence of seizure activity.
ASSESSMENT
Neuropsychological testing usually shows a discrepancy between the
performance on memory scales and the performance on general cognitive
scale

30. COURSE AND PROGNOSIS
 The course of an amnestic disorder depends on its etiology and
treatment.
 The exceptions are the acute amnesias, such as transient global amnesia,
which resolves entirely over hours to days, and the amnestic disorder
associated with head trauma, which improves steadily in the months
after the trauma.
 Amnesia secondary to processes that destroy brain tissue, such as
stroke, tumor, and infection, are irreversible.

31.  The primary approach to treating amnestic disorders is to treat the
underlying cause.
 Supportive prompts about the date, the time, and the patient’s
location can be helpful and can reduce the patient’s anxiety.
 After the resolution of the amnestic episode, psychotherapy of some
type may help patients incorporate the amnestic experience into their
lives
TREATMENT

32. PSYCHOTHERAPY
 The first phase of recovery, in which patients are incapable of processing
what happened requires clinicians to serve as a supportive auxiliary ego
who explains to a patient what is happening and provides missing ego
functions.
 In the second phase of recovery, as the realization of the injury sets in,
patients may become angry and feel victimized.
 Clinicians can build a therapeutic alliance with patients by explaining
slowly and clearly what happened and by explaining the patient’s internal
experience.

33.  The third phase of recovery is integrative. As a patient accepts what has
happened, a clinician can help the patient form a new identity by
connecting current experiences of the self with past experiences.
Grieving over the lost faculties is an essential feature of the third phase.
 An evaluation of preexisting personality disorders, must be part of the
overall assessment; many patients with personality disorders place
themselves in situations that predispose them to injuries. These
personality features may become a crucial part of the psychodynamic
psychotherapy.
 Centres for cognitive rehabilitation have rehabilitation-oriented
therapeutic milieu designed to promote recovery from brain injury.

34. TECHNOLOGICAL ASSISTANCE
Many people with amnesia find it helpful to use smart technology, such as
a smartphone or a hand-held tablet. With some training and practice, even
people with severe amnesia can use electronic organizers to help with
day-to-day tasks.
 For example, smartphones can be programmed to remind them about
important events or to take medicines.
Low-tech memory aids include notebooks, wall calendars, pill minders,
and photographs of people and places.
No medicines are currently available for treating most types of amnesia.

35.  In contrast to delirium, amnestic disorders evolve on a background of
clear consciousness and intact attention, with no perceptual disturbances
or mood lability
 Amnesia syndrome has no impairment in abstract thinking , judgement ,
or executive functions.
 Cognitive impairment in dementia extends to semantic memory ,
language , and praxis
 Psychogenic amnesia can be differentiated by its presentation and its
course
DIFFERENCE BETWEEN DEMENTIA, DELIRIUM AND AMNESIA

37. AMNESIA FOR OFFENCES
psychiatrists.
 Amnesia is claimed by 25 to 45 per cent of offenders in cases of homicide,
8 per cent of perpetrators of other violent crimes, and small percentage of
non-violent offenders.
 Necessary to exclude underlying neurological or endocrine factors such as
an epileptic automatism, post-ictal confusional state, head injury,
sleepwalking, or hypoglycaemia.
 Underlying medical disorder can be grounds for a so-called ‘insane’
automatism in English law (if the result of an internal brain disease) or a
‘sane’ automatism (if the consequence of an external agent), but otherwise
amnesia per se does not constitute grounds for alleviation of responsibility

38. AMNESIA FOR AN OFFENCE IS MOST COMMONLY ASSOCIATED WITH THE
FOLLOWING:
States of either extreme emotional arousal or peri-traumatic dissociation,
in which the offence is unpremeditated, and the victim usually a lover,
wife, or family member. Seen in homicide cases (‘crimes of passion’).
 Alcohol intoxication , usually involving very high peak levels (‘alcoholic
blackout’), and often a long history of alcohol abuse. The victim is not
necessarily related to the offender, and the offence may vary from criminal
damage, through assault, to homicide.

39. Florid psychotic states or depressed mood. Occasionally offenders
describe a delusional account of what has happened, quite at odds with
what was seen by other observers, and sometimes resulting in
confessions to crimes that the person could not actually have committed
(a paramnesia or delusional memory).
In many other cases, depressed mood is associated with amnesia for an
offence, just as it is a common associate of psychogenic fugue.

40. SUMMARY
 AMNESTIC DISORDERS are syndrome characterized by memory impairment caused by a
general medical condition or substances use and when delirium and dementia have been
excluded as causative of the amnesia.It may be transient or chronic(<or >1 month)
Amnestic conditions involve neuroanatomical structures:- Frontal cortex, hippocampus and
amygdala, dorsomedial thalamus, mamillary bodies and periaqueductal grey matter(PAG)
 ETIOLOGY – Episodic amnesia- Transient global amnesia Pure epileptic
amnesia,Blackouts,Concussion,Transient ischemic Chronic Amnesia-Korsakoff's
syndrome,Stroke,Tumour,Limbic encephalitis,Neurodegenerative disorders(Alzheimer's
disease,Frontotemporal lobar degeneration) Traumatic brain injury,Post hypoxic ischemic
injury,Encephalitis,Status epilepticus,Certain neurosurgical procedures

41.  TRANSIENT GLOBAL AMNESIA-Characterized by the appearance of one or more episodes,
lasting from 4–18 hours, seen with anterograde amnesia coupled with a retrograde amnesia
of variable duration, from hours to decades.
 PURE EPILEPTIC AMNESIA-Recurrent episodes of amnesia and disorientation lasting 30mins
to 1hr often occurring from sleep or on waking, due to Medial Temporal Lobe seizures in
epilepsy
 BLACKOUTS-The duration of blackouts ranges from less than an hour up to days,patients
have no memory of what they did while intoxicated, and may anxiously ask others what
happened
CONCUSSION--It occurs after minor head injury or whiplash, may be accompanied by a
dense anterograde and variable retrograde amnesia.
VASCULAR DISORDER- Aneurysms of the Anterior Communicating Artery can result in
amnestic disorder.
TUMPORS- They cause progressive amnesia, seen with craniopharyngiomas

42. TRAUMATIC BRAIN INJURY -Anterograde post traumatic amnesia is prominent with
retrograde amnesia relatively absent in TBI.
POST-HYPOXIC-ISCHEMIC ENCEPHALOPATHY-Damage of sensitive CA1 and CA3 neurons in
the hippocampus and can result in Short Term Memory Storage
HERPES ENCEPHALITIS- Gives rise to a severe form of amnesic syndrome, with behavioural
change or psychiatric phenomena, neuropathological and neuro-imaging studies show
extensive bilateral temporal lobe damage.
KORSAKOFF SYNDROME- If untreated, Wernicke’s encephalopathy progresses to Korsakoff’s
syndrome (permanent memory impairment, confabulation, confusion and personality
changes),Alcohol use induces thiamine deficiency through folate deficiency

43. In Korsakoff syndrome, intelligence is intact, inability to form new memories,immediate
recall and implicit learning are preserved, and individuals classically present with
confabulation.
Hyperintense signal in the Mammillary Bodies and Colliculi , Periventricular Gray Matter, and
Fornix and Thalamus in FLAIR images seen in WE
DIAGNOSTIC TEST FOR AMENSTIC SYNDROME-Imaging tests like MRI and CT scan to check
for brain damage Blood tests to check for infection, nutritional deficiencies or other issues,
(EEG) to check for the presence of seizure activity.
TREATMENT-Treating amnestic disorders is to treat the underlying cause,supportive
prompts about the date, the time, and the patient’s location is helpful and reduces the
patient’s anxiety.Psychotherapy of some type helps patients incorporate the amnestic
experience into their lives

44. REFERENCES
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textbook of psychiatry. Philadelphia: Wolters Kluwer; 2017:84-96.
Semple D, Smyth R. Oxford handbook of psychiatry. Oxford university
press; 2019 Jul 30.
David A. Lishman’s organic psychiatry : a textbook of neuropsychiatry.
Chichester: Wiley-Blackwell; 2012.
Tasman A. Psychiatry. Tasman A, Kay J, Lieberman JA, editors. Wiley;
2015

45. Kaplan and Sadocks Synopsis of Psychiatry. La Vergne, TN: Cram101; 2022
Taylor DM, Barnes TR, Young AH. The Maudsley prescribing guidelines in
psychiatry. John Wiley & Sons; 14th ed. 2021.
https://www.alz.org/alzheimers-dementia/what-is-dementia/types-of-
dementia/korsakoff-
syndrome#:~:text=Abstaining%20from%20alcohol%20and%20maintaining,f
urther%20alcohol%2Drelated%20health%20problems