| ICD-116D72 | AMNESTIC DISORDERAmnestic disorder |
| ICD-10F04 | Organic amnesic syndrome, not induced by alcohol and other psychoactive substances |
| DSM-5-TRF02.8x | Major Neurocognitive Disorder Due to Another Medical Condition (amnestic presentation) |
1. Definition and nosology
Amnestic Disorder (ICD-11: 6D72 Amnestic Disorder; DSM-5-TR: F04 and similar) — significant impairment in learning and recalling new information; other cognitive domains relatively preserved. Due to a medical condition (Wernicke-Korsakoff, brain injury, encephalitis, anoxia), substance effect, or other causes.
2. History
- Korsakoff S. (1887) — description of alcohol-related amnesia.
- Scoville W.B., Milner B. (1957) — H.M. case (amnesia after bilateral medial temporal resection).
3. Epidemiology
- Korsakoff syndrome — in 12–25% of chronic heavy alcohol users.
- Amnesia after traumatic brain injury — in 30–50% of TBI patients.
- Transient global amnesia (TGA) — prevalence in age 65+ 5–25/100,000/year.
4. Aetiology and pathogenesis
- Wernicke-Korsakoff — thiamine (B1) deficiency (alcohol, malnutrition).
- Traumatic brain injury (TBI).
- Hypoxia/anoxia — cardiac arrest, carbon monoxide.
- Herpes simplex encephalitis.
- Autoimmune encephalitis (anti-NMDA, anti-LGI1).
- Transient global amnesia (TGA) — suspected vascular etiology.
- Substance (alcohol blackout, benzodiazepine).
- Stroke (especially bilateral thalamic or hippocampal).
5. Clinical features
- Anterograde amnesia — impairment in learning new information (core feature).
- Retrograde amnesia — memory for the period before the injury (“Ribot's law” — recent memories are lost earlier than remote ones).
- Confabulation — in Korsakoff syndrome — patient fills memory gaps with fabrications.
- Other cognitive domains are relatively preserved (intellect, language, visuospatial).
6. Diagnosis
6.1 Unified diagnostic criteria
A. Impairment in learning new information or impairment in recall of previously learned information.
B. Memory impairment causes significant functional impairment.
C. Does not occur exclusively in the context of delirium or another NCD.
D. Evidence — history, examination, laboratory indicate that memory impairment is due to specific cause (medical condition, substance).
6.2 Source-specific clarifications
- DSM-5-TR — integrated into Major and Mild NCD structure; amnestic subtype.
- ICD-11 — separate category.
6.3 Diagnostic algorithm
- Clinical interview + informant.
- Neuropsychological test — memory (WMS-IV, RAVLT, Wechsler Logical Memory).
- Brain MRI — bilateral hippocampal, medial temporal, thalamic pathology.
- Vitamin B1 level or empirical thiamine (suspected Korsakoff syndrome).
- Toxicology.
- Autoimmune encephalitis panel (in atypical cases).
- EEG.
6.4 Differential diagnosis
| Condition | Distinguishing feature |
|---|---|
| Alzheimer's dementia | Multiple cognitive domains, gradual onset. |
| Delirium (6D70) | Fluctuation of attention. |
| Dissociative amnesia (6B61) | In trauma context; selective past memory; no medical cause. |
| Factitious disorder / malingering | Atypical pattern, secondary gain. |
| TGA | Acute, less than 24 hours; complete recovery. |
7. Examination and assessment
- WMS-IV (Wechsler Memory Scale), RAVLT.
- Brain MRI.
- Thiamine, B12.
- Toxicology.
8. Treatment
- Etiological — thiamine (Wernicke-Korsakoff — 500 mg IV × 3 times/day × 3 days, then 250 mg IM/day × 3–5 days; long-term oral thiamine in alcohol withdrawal).
- Autoimmune encephalitis — immunotherapy (steroids, IVIG, plasmapheresis, rituximab).
- Herpes encephalitis — acyclovir.
- Compensatory strategies (external memory aids, daily structuring).
- Treatment of substance use (alcohol).
- Rehabilitation — cognitive rehabilitation (Wilson B.A.).
Source-specific specifications
- Wernicke-Korsakoff — Royal College of Physicians thiamine protocol.
- Graus F. et al. Lancet Neurol 2016 — autoimmune encephalitis.
Treatment methods
- Wernicke-Korsakoff Prophylaxis and Treatment — High-dose IV/IM thiamine; administration BEFORE glucose is critical (glucose exacerbates Wernicke's in thiamine deficiency).
- Cognitive Rehabilitation — Wilson (Wilson B.A.) — External memory aids (journal, phone reminders), strategy teaching.
- Immunotherapy (Autoimmune Encephalitis) — Graus 2016 protocol.
9. Prognosis
- TGA — full recovery.
- Korsakoff — residual deficit typical; acute intervention with thiamine for Wernicke critical.
- TBI — partial recovery with rehabilitation.
10. Myths and misconceptions
Myth 1: “Amnesia can be ‘recovered’ with hypnosis”
Evidence: hypnosis generates false memory; ineffective in organic amnesia.
Myth 2: “Oral thiamine is sufficient in Wernicke's”
Evidence: Oral absorption insufficient; IV/IM high dose required.
Myth 3: “Glucose ‘cures’ Wernicke's”
Evidence: Glucose given in thiamine deficiency precipitates or worsens Wernicke's encephalopathy; administer thiamine first.
Myth 4: “All amnesia is temporary”
Evidence: Korsakoff, TBI-based amnesia typically chronic; rehabilitation yields improvement, but full recovery rare.
Myth 5: “Confabulation is lying”
Evidence: Confabulation in Korsakoff syndrome is a neurobiological phenomenon, not a conscious lie.
11. Sources
- WHO. ICD-11. 6D72 Amnestic disorder. 2024.
- APA. DSM-5-TR. 2022.
- Royal College of Physicians. Wernicke's encephalopathy and Korsakoff's syndrome. 2014.
- Graus F. et al. A clinical approach to diagnosis of autoimmune encephalitis. Lancet Neurol 2016;15(4):391–404.
- Wilson B.A. Neuropsychological Rehabilitation. Wiley; 2009.