Organic Amnesia
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Transcript of Organic Amnesia
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AGENDA
Seminar
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Amnesia Causing Entities
Transient Amnesia Syndromes
Persistent Amnesic Disorders
OADBACKGROUND
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PresenterDr. Anusa A M
Second year MD PG 28th August 2013
Hon. Chairperson
Dr. KUMANAN MD DPM, Professor
Dr. Amudha MD, DCh, Assistant Professor
Prepared by Prof. Rooban T,
Oral & Maxillofacial Pathologist
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What’s Common ?
Finding Nemo
Ghajini
Bourne Identity 50 First dates
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Organic Amnesic Disorders
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Agenda
Memory – Basics
Amnesia
Organic Amnesia
Persistent
Transient
DSM4 vs DSM 5
References
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Memory
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Memory – Long term memory
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HM or Henry Molaison Gustav
“It’s a funny thing—you just live and learn. I ’m living, and you’re learning.”
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Cognitive Disorders – DSM IV TR
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Overlap features
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Core feature of Amnesic Disorder
Memory impairment that is NOT due
to dementia or delirium and
represents a decline from a
previously attained functional level.
Memory impairment is likely to be
restricted to specific kinds of
memory
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Amnesic Disorders
“An abnormal mental state in which
memory and learning are affected out of
all proportion to other cognitive
functions in an otherwise alert and
responsive patient”
Victor et al., 1971
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Amnesic Disorders
Severe memory impairment or deficit, irrespective of the cause
Till 1980s Later
Amnesia is a memory impairment that occurs in the absence of other substantial cognitive impairments, and is restricted to specific disorders - amnesic or amnestic disorders
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Based on proximal cause of impairment
Amnesic disorders
Organic / biological instances
Brain disorders, tumors, Strokes, Temporal lobe surgery, ECT,
Infection, metabolic, trauma, TGA
Functional / Psychogenic
Substance induced
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Organic Amnesic Disorders
SYSTEMIC MEDICALCONDITIONS
Thiamine deficiency(Korsakoff's
syndrome)Hypoglycemia
PRIMARY BRAIN CONDITIONS
Seizures Head trauma - closed and
penetrating Cerebral tumors (especially
thalamic and temporal lobe) Cerebrovascular diseases Surgical procedures on the
brain Encephalitis due to herpes
simplex Hypoxia Electroconvulsive therapy Multiple sclerosis
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Medial Temporal
Diancephalic
Retrograde
AnterogradeEncoding
Site TimeProcess
Declarative
Non-declarative
Transient
Chronic Retrieval
Storage
Content Duration
OAD
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OAD characterized by
Severe impairment of recent or short term memory - inability to learn new material
Impaired remote or long term memory - inability to recall previously learnt material
No impairment of immediate memory - immediate retention and recall.
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OAD – ICD 10 Diagnostic Criteria Recent /remote memory impaired
Antero/retrograde amnesia.
No impairment of Immediate & recall attention, Consciousness Global intellectual functioning.
Historical or objective evidence of brain disease injury
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OAD – ICD 10 Diagnostic CriteriaAssociated features
Confabulations
Emotional changes Apathy Lack of initiative
Lack of insight
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DSM 4 criteria
Part of - “Delirium, Dementia and Amnestic &other Cognitive disorders”
Include Due to General Medicine
Condition Substance induced Persisting Amnestic
disorders Amnestic - NOS
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OAD - Where ?
Any part of the brain Cortex Hypothalamus Hippocampus Thalamus Reticular formation Amygdala Septum
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OAD – Where?
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Differential Diagnosis
Dementia
Depressive disorder
Malingering Memory loss
Dissociative amnesia
Amnesia – Substance use
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What is Korsakoff’s Syndrome - KSMemory disorder due to thiamine
deficiency
It affects 1-2% of the population
Causes: Chronic alcoholism Severe malnutrition Medical conditions
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KS – Site of damage
First phase: Wernicke’s encephalopathy Damage in lower parts of the brain
▪ Thalamus▪ Mamillary bodies
Second phase: Korsakoff syndrome Damage to areas
▪ Anterior Thalamus▪ Mamillary body▪ Mamillothalamic tract
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KS - Symptoms
First phase: Wernicke’s encephalopathy
1. Confusion2. Ocular Motor Movement defects3. Ataxia
Second phase: Korsakoff syndrome
1. Amnesia2. Confabulation
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Diagnosis
Difficult to differentiate - alcohol intoxication or withdrawal
Missed -clinical examination in 80% of cases Clinical assessment:
▪ Mental status change▪ Ocular motor movement abnormality▪ Physical assessment for ataxia
Thiamine blood measurement▪ Measure thiamine level directly from the whole blood▪ Measure the activity of transketolase from erythrocytes
Brain imaging (MRI)
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KS The Basal Forebrain:
nuclei of tha basal forebrain
nucleus basalis of Meynert.
The Cerebral Cortex:
Widening of the sulci
↑ size of ventricles - cortical atrophy.
Damage to the frontal cortex.
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Thiamine (Vitamin B1)
Yeast, cereal grains, beans, nuts,
and meat
DDA - 1 mg of thiamine/day
30 mg thiamine in store
Half-life of 9 – 18 days
Signs of encephalopathy - brain
thiamine stores < 20% of normal
levels
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Pathology
Thiamine function: conversion of glucose to
ATP
Thiamine→ Thiamine-pyrophosphate
Thiamine-pyrophosphate: A cofactor for
enzymes involved in glucose metabolism:
• Transketolase
• Pyruvate dehydrogenase
• α-ketoglutarate dehydrogenase
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Overview of
Intracellular
Pathway
Adapted from: Lough, M.E. (2012). Wernicke’s encephalopathy: expanding the diagnostic tool box. Neuropsychol Rev, 22(2), 181-94.
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Transketolase
Adapted from: Martin, P.R., Singleton, C.K., and Sturmhofel, S.H. (2004). The Role of Thiamine Deficiency in Alcoholic Brain Disease. NIAAA.
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Pyruvate Dehydrogenase & α-Ketoglutarate Dehydrogenase
Adapted from: Martin, P.R., Singleton, C.K., and Sturmhofel, S.H. (2004). The Role of Thiamine Deficiency in Alcoholic Brain Disease. NIAAA.
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Thiamine Deficiency & Brain
• Thalamus-major relay for (sensory and motor input)• Mamillary Body-helps processes memories• Cerebellum-movement coordination•Peripheral Nerves-transmission of nerve impulses
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Korsakoff Syndrome
Memory problems
Anterograde
Retrograde
Confabulations:
Falsification of memory
Clear consciousness
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Confabulations
Falsification of memory – clear consciousness Embrassement Fantastic nature
Unaware
Most often – Autobiographic memory
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Management
Thiamine
Replacement
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T2 weighted MRI of patient 4: coronal sections show (especially in the top right—black arrow —and bottom left) involvement of the right sided MS/ndbB complex as well as bilateral lesions of the rectus gyrus together with the clip artefact.
Böttger S et al. J Neurol Neurosurg Psychiatry 1998;65:93-102
©1998 by BMJ Publishing Group Ltd
Rupture of Ant. Comm. Artery
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Herpes encephalitis25-year-old woman with herpes simplex virus encephalitis and HIV infection and history of sudden general convulsion and consciousness disorder while talking to friends.A–E, Sequential axial T1-weighted MR image (TR/TE, 435/12) (A), FLAIR image (8,000/105; inversion time, 2,300 (B), diffusion-weighted image (DWI) (4,500/105.2; b = 1,000 s/mm2) (C), apparent diffusion coefficient (ADC) map (D), and contrast-enhanced T1-weighted image (435/12) (E) immediately after onset of neurologic symptoms show T1- and T2-prolonged lesions (arrow, A and B) at left hippocampus and amygdala, left inferior frontal lobe, and insula. High signal intensity (arrow, C) on DWIwith low ADC (arrow, D) also are evident. Abnormal gyral enhancement (arrowheads, E) along left medial temporal lobe occurred after gadopentetate dimeglumine ministration.F–J, Axial T1-weighted MR image (435/12) (F), FLAIR image (8,000/105; inversion time, 2,300 milliseconds (G), DWI (4,500/105.2; b = 1,000 s/mm2) (H), ADC map (I), and contrast-enhanced T1-weighted image (435/12) (J) on day 11 after onset of neurologic symptoms show expansion of affected regions (arrowheads, G–I) in inferior aspect of both frontal lobes, right hippocampus, and amygdala on FLAIR and DWI images and area of T1 shortening (arrows, F) along cortex.K–O, Axial T1-weighted image (528/12 (K), FLAIR image (9,000/108; inversion time, 2,300 milliseconds (L), DWI (4,500/130; b = 1,000 s/mm2) (M), ADC map (N), and contrast-enhanced T1-weighted image (528/12) (O) 34 days after onset of neurologic symptoms show further development of cortical T1 shortening (arrowheads, K), persistence of high signal intensity and atrophic change (arrowheads, L), and disappearance of high signal intensity on DWI and low ADC (N)
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Seizure disorder
Post –Ictal Amnesia
Non purposive wandering
Earlier Autobiographical memory loss
Random in involvement
EEG abnormalities
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Transient Amnesic Syndromes
In a variety of neuropsychiatric disorders
As a normal phenomenon starting in midlife
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TAS
Some short-lived amnesia Transient global amnesia (TGA). Temporal lobe epilepsy/ Transient epileptic
amnesia Transient cerebral ischemia Migraine, Alcohol intoxication (“blackouts”) Drugs (eg, benzodiazepines, barbiturates,
ketamine15) and head injury. Concussion - temporary retrograde and
anterograde
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TGA - OVERVIEW
Benign disorder
Characterized by anterograde and/or retrograde amnesia
Remain oriented to person
No other focal neurologic deficit
Permanent inability to recall TGA episode
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TGA - OVERVIEW
First described by Bender 1956
TGA coined by Fisher and Adams 1964
Annual incidence 8.6 to 10.0 per 100,000 and up to 32 per 100,000 if > 50 years
Usually occur in healthy, middle-aged or elderly patients
Typically no major vascular risk factors
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TGA - Diagnostic Criteria
FEATURES PRESENT:
Anterograde amnesia& also retrograde amnesia
Resolves within 24 hours
Witnessed event
FEATURES ABSENT
Aphasia or apraxia
Clouding of consciousness
Loss of personal identity
Epileptic features
Focal neurologic deficits
Recent hx head trauma
Seizure in preceding 2
years
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Precipitating Events
Emotional stress
Physical exertion
Medical procedures
Valsalva maneuvers
Sexual intercourse
Immersion in cold water
Chronic headaches/migraines
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TGA - Pathogenesis
Controversial
Transient decrease in blood flow to
temporal lobes (seen on SPECT)
Epileptic discharge in the hippocampus
Spreading depression of cortical activity –
short-lasting wave of depolarization –
responsible for auras & migraines
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TGA - Differential Diagnosis
Brain tumor
Stroke
Intracerebral/subarachnoid bleed
Complex partial seizure
Migraine
Toxins/drugs
Acute coronary syndrome
Hepatic encephalopathy
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TGA – work up
EKG, CBC, electrolytes, urine toxicology screen, PT/PTT, cardiac enzymes, liver enzymes, noncontrast head CT
Also consider brain MRI/MRA, EEG, holter monitor, and TTE.
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Imaging
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Imaging
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ECT & Amnestic Disorder
Recent memory – Retrograde amnesia
Permanent
Anterograde Amnesia – Retention defect – related to strength & duration of electrical stimulation/ seizures Less after U/L Non dominant ECT
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Post-traumatic Amnesia
Open/ closed injuries of brain
Reflects the intensity of damage to brain
Duration - prognostic factor
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Injury characteristics
Mild TBI Moderate TBI Severe TBI
Loss of consciousness
<30 min 30 min – 24 hrs
> 24 hrs
Posttraumatic amnesia
< 24 hrs 24 hrs – 7 days > 7 days
Disorientation /confusion – Glasgow coma scale
13 – 15 (not below 13 at 30 minutes)
9 - 12 3 - 8
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Alcoholic “Black outs”
Period of Acute intoxications
Prolonged alcohol abuse
Types Fragmentary En-bloc
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Drugs Causing Amnesia
Benzodiazepine Midazolam Flunitrazepam Propofol Scopolamine
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Domoic Acid
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Diagnostic Work Flow
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Tests for intellectual functions
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Is Memory (?) loss Useful
11 Million Bits/Sec of raw data - unconscious mind from all senses
40 bits/sec – conscious
Human retina - brain - 10 million bits/sec
PPT slide - 40 words < 10 sec to read - 1000 bits/sec
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So What ?
May 23rd 2013 DSM 5 was released
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What DSM5 Says ?
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What’s the change?
DSM 4
Delerium, Dementia and Amnestic disorders
DSM 5
Neurocognitive disorders (NCD) Delerium Major/Minor NCD
▪ Alzheimer's associated ▪ Frontotemporal NCD▪ NCD – Lewy Bodies▪ Vascular associated▪ Traumatic Brain injury▪ HIV infection▪ Prion disease▪ Parkinson’s ▪ Huntington’s▪ Another medical conditions▪ Multiple Etiologies▪ Unspecified etiologies
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What change?
Primary deficit is in cognitive function
Acquired
Section Unique - Pathology/etiology known
“AMNESTIC DISORDER” IS REPLACED AS
MAJOR/Mild NCD – DUE TO ANOTHER
MEDICAL CONDITION
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NCD – due to other medical condition
Structural lesions
Brain tumors
Subdural hematoma
Hydrocephalus
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NCD – due to other medical condition
Infectious diseases
Neuro-syphilis
Crytococcosis
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NCD – due to other medical condition
Other neurological
Epilepsy
Multiple sclerosis
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References
1. Markowitch HJ. Staniloiu A. Amnesic Disorders. Lancet 2012;380:1429-402. Bottger S, Prosiegel M< Steiger H, Yassouridis A. Neurobehavioural
disturbances, rehabilitation outcome, and lesion site in patients after rupture and repair of anterior communicating artery aneurysm. J Neurol Neurosurg Psychiatry 1998;65:93–102
3. Levenson JL. Psychiatric Issues in Neurology, Part 4: Amnestic Syndromes and Conversion Disorder. Primary Psychiatry. 2008;15(3):39-42
4. Shimamura, AP, Organic Amnesia, from L. R. Squire (Ed.), Encyclopedia of Learning and Memory, 1992, pp. 30-35, Macmillan: New York
5. Noguchi T et al., CT and MRI Findings of Human Herpesvirus 6–Associated Encephalopathy: Comparison With Findings of Herpes Simplex Virus Encephalitis. AJR 2010;194:754-60
6. Kopelman MD. Disorders of memory. Brain 2002;125:2152-1907. Caixeta L, Ghini BG, Peres JFP. Neuroimaging and Other amnestic disorders.
Neuroimaging for clinicians - combining reseacrh and practice. www.intechopen.com
8. Colchester A et al.,Structural MRI volumetric analysis in patients with organic amnesia, 1: methods and comparative findings across diagnostic groups. J Neurol Neurosurg Psychiatry 2001;71:13–22 13
9. Kopelman MD et al.,Structural MRI volumetric analysis in patients with organic amnesia, 2: correlations with anterograde memory and executive tests in 40 patients. J Neurol Neurosurg Psychiatry 2001;71:23–28 23
10. Madan CR. Organic Amnesia: A Diversity of defects. Eureka;2011:2:37-4211. DANA Foundation. Amnesias. The DANA Guide to Brain Health. Retrieved
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