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Amnesia can be described as an inability to later recall the events which occurred under the influence of a substance after it has worn off.[1][2][3] During states of amnesia a person will usually retain a functional long and short-term memory which can still recall events that recently occurred despite those same events failing to be retained in a manner which can later be recalled. As such, a person experiencing amnesia may not obviously appear to be doing so, as they can often carry on normal conversations and perform complex tasks.

This state of mind is commonly referred to as a "blackout", an experience that can be divided into 2 formal categories: "fragmentary" blackouts and "en bloc" blackouts.[4] Fragmentary blackouts, sometimes known as "brownouts", are characterized by having the ability to recall specific events from an intoxicated period but remaining unaware that certain memories are missing until reminded of the existence of those gaps in memory. Studies suggest that fragmentary blackouts are far more common than "en bloc" blackouts.[5] In comparison, En bloc blackouts are characterized by a complete inability to later recall any memories from an intoxicated period, even when prompted. It is usually difficult to determine the point at which this type of blackout has ended as sleep typically occurs before this happens.[6]

Amnesia is often accompanied by other coinciding effects such as disinhibition, sedation, and memory suppression. It is most commonly induced under the influence of heavy dosages of GABAergic depressants, such as alcohol,[7] benzodiazepines,[8] GHB,[9] and zolpidem[10]. However, it can also occur to a much lesser extent under the influence of extremely heavy dosages of hallucinogenic compounds such as psychedelics, dissociatives, Salvia divinorum, and deliriants.

Psychoactive substances

Compounds within our psychoactive substance index which may cause this effect include:

See also

External links


  1. Amnesia (mayoclinic) |
  2. Drug-induced memory disturbance (medlink) |
  3. Veselis, R. A., Reinsel, R. A., & Feshchenko, V. A. (2001). Drug-induced Amnesia Is a Separate Phenomenon from SedationElectrophysiologic Evidence. Anesthesiology: The Journal of the American Society of Anesthesiologists, 95(4), 896-907.
  4. Hartzler, B., & Fromme, K. (2003). Fragmentary and en bloc blackouts: similarity and distinction among episodes of alcohol-induced memory loss. Journal of Studies on Alcohol, 64(4), 547-550.
  5. White, A. M., Signer, M. L., Kraus, C. L., & Swartzwelder, H. S. (2004). Experiential aspects of alcohol‐induced blackouts among college students. The American journal of drug and alcohol abuse, 30(1), 205-224.
  6. Goodwin, D. W., Crane, J. B., & Guze, S. B. (1969). Alcoholic" blackouts": A review and clinical study of 100 alcoholics. American Journal of Psychiatry, 126(2), 191-198.
  7. Lee, H., Roh, S., & Kim, D. J. (2009). Alcohol-induced blackout. International Journal of Environmental Research and Public Health, 6(11), 2783-2792.
  8. Mejo, S. L. (1992). Anterograde amnesia linked to benzodiazepines. The Nurse Practitioner, 17(10), 44-49.
  9. Barker, J. C., Harris, S. L., & Dyer, J. E. (2007). Experiences of gamma hydroxybutyrate (GHB) ingestion: a focus group study. Journal of psychoactive drugs, 39(2), 115-129.
  10. Canaday, B. R. (1996). Amnesia possibly associated with zolpidem administration. Pharmacotherapy: The Journal of Human Pharmacology and Drug Therapy, 16(4), 687-689.