2. ICD-10: Organic Mental Disorder
F00 Dementia in Alzheimer disease
F01 Vascular dementia
F02 Dementia in other diseases classified elsewhere
F03 Unspecified dementia
F04 Organic amnesic syndrome, not induced by
alcohol and other psychoactive substances
F05 Delirium, not induced by alcohol and other
psychoactive substances
F06 Other mental disorders due to brain damage and
dysfunction and physical disease
F07 Personality and behavioral disorders due to brain
disease, damage and dysfunction
F08 Unspecified organic or symptomatic disorder
5. Memory Disturbances
CLINICAL
Time / onset
DISORDER
cause
AMNESIA
loss of memory
AMNESTIC (organic)
DISSOCIATIVE (psychogenic)
anterograde
retrograde
PARAMNESIA
error of memory
CONFABULATION
Unconscious filling
up gaps in memory
DEJA VU
“already seen” in
French
9. What is affected? What is impaired?
Anterograde amnesia, episodic memory:
dramatic inability to learn something new
after the onset of amnesia due to inability to
build up new episodes.
Retrograde amnesia, an inability to
retrieve information that was learned
prior to the onset of amnesia if it was
not purely semantic or implicit memory
Impaired temporal localization of
past experience, as in Korsakoff,
which leads to confabulation
Autobiographic memory also intact,
but amnesic for recent events before
onset of amnesia
10. Confabulation
• ‘‘False statements that are not made to
deceive, are typically more coherent than
thoughts produced during delirium”
• It ranges from small distortions on
laboratory tasks to striking bizarre stories
that patients tell in describing their
personal histories
• Typically occurs in the context of executive
deficits such as perseveration, poor self-
monitoring, and difficulty with self-initiated
processes
12. Transiet Global Amnesia [TGA]
• Characterized by a dense,
transitory inability to learn new
information and a variable inability
to recall events
• Assoc. with cerebrovascular
disease and pathology in
vetebrobasilar system
13. BLACKOUTS
Blackouts are periods of amnesia for
events that occur during heavy
drinking.
Typically, a person awakens the
morning after consumption and does
not remember what happened the
night before.
Blackouts are more a measure of the
amount of alcohol consumed at any
one time.
14. Chronic Amnestic Disorders
Causes - Pathological Process
Damage to specific diencephalic and
mediotemporal lobe structures (e.g.,
mamillary bodies, hippocampus, fornix)
– head trauma
– surgical intervention
– infarction of the distribution of PCA
– hypoxia
– herpes simplex encephalitis
15. • “Persisting” means the memory
disturbances persists long after the
effects of substance intoxication or
withdrawal have ended
• CNS depressants
– Alcohol, sedatives, hypnotics, anxiolytics,
anticonvulsants
• Toxin: lead, mercury, intratheceal
methotrexate, organophosphate
insecticides, and industrial solvents
Substance-Induced Persisting
Amnestic Disorder
16. WERNICKE-KORSAKOFF
SYNDROME [WKS]
Acute WKS: Mammillary bodyAcute WKS: Mammillary body
hemorrhageshemorrhages
Old WKS: mammillary bodyOld WKS: mammillary body
atrophyatrophy
Seen in
Alcoholics
Gastric cancer
Hyperemesis gravidarum
17. Treatment
• The primary goal in the amnestic disorders
is to discover and treat the underlying
cause.
• Some of these causes of amnestic disorder
are associated with dangerous self-
damaging behavior
– e.g., suicide attempts by hanging, carbon
monoxide poisoning, deliberate motor vehicle
accidents, self-inflicted gunshot wounds to the
head and chronic alcohol abuse
Editor's Notes
Anterograde amnesia, episodic memory: dramatic inability to learn something new after the onset of amnesia due to inability to build up new episodes.
Retrograde amnesia, an inability to retrieve information that was learned prior to the onset of amnesia if it was not purely semantic or implicit memory
Contingent upon RA: impaired temporal localization of past experience, as in Korsakoff, which leads to confabulation
Autobiographic memory also intact, but amnesic for recent events before onset of amnesia
Encephalitis: Herpes simplex encephalitis (HSE), a viral infection causing lesions in the limbic regions in the temporal lobe, hippocampus, entorhinal, perirhinal, parahippocampal crtices, amygdala, and polar limbic cortices (O'Connor & Verfaille, 2004)
Anoxia: oxygen deficit due to decreased vascular perfusion or reduced oxygen content in the blood, caused by e.g., cardiac arrest or respiratory distress. Most likely, hippocampal damage is involved, but also basal ganglia, thalamus, white matter projections and diffuse cortical areas. (O'Connor & Verfaille, 2004)
http://www.neuropathologyweb.org/chapter8/chapter8Nutritional.html
The histopathology of WKS is incomplete loss of neurons, damage of axons and myelin which casuses loosening or vacuolization of the neuropil, and punctate hemorrhages. The lesions have a characteristic anatomical distribution which includes the mammillary bodies, the hypothalamus, thalamus, periaqueductal gray matter, colliculi, and the floor of the fourth ventricle. The mammillary bodies are involved in all cases. This is the hallmark of WKS. Lesions of the colliculi and the floor of the fourth ventricle (oculomotor nuclei, vestibular nuclei, dorsal motor nuclei of the vagus) cause the oculomotor and brain stem signs. Involvement of the medial dorsal nucleus of the thalamus is responsible for the memory defect. An identical memory defect (Korsakoff's amnesia) is caused by bilateral hippocampal damage. The hippocampus projects to the mammillary bodies via the fornix but is not affected in the WKS. The MRI shows a hyperintense FLAIR signal in the affected areas. In full-blown WKS, all these structures are involved. In less severe cases, some may be spared. Each successive bout of WKS causes additional loss of neural tissue. Old cases show atrophy of the mammillary bodies and dilatation of the third ventricle. In 30% to 50% of cases, the cerebellum shows degeneration (neuronal loss) of the superior vermis