Amnesia is a global impairment in the ability to acquire new memories regardless of sensory modality, and a loss of some memories, especially recent ones, from the period before amnesia began. [1] During states of amnesia a person will usually retain functional perceptual abilities and short-term memory which can still be used to recall events that recently occurred; this effect is distinct from the memory impairment produced by sedation. [2] 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 [3] . 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. [4] 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. [5]

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 [6] , benzodiazepines [7] , GHB [8] , and zolpidem [9] . 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.


  1. Squire, L. R., & Zola, S. M. (1997). Amnesia, memory and brain systems. Philosophical Transactions of the Royal Society of London B: Biological Sciences, 352(1362), 1663-1673. |
  2. Veselis, R. A., Reinsel, R. A., & Feshchenko, V. A. (2001). Drug-induced Amnesia Is a Separate Phenomenon from Sedation: Electrophysiologic Evidence. Anesthesiology: The Journal of the American Society of Anesthesiologists, 95(4), 896-907. |
  3. 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. |
  4. 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. |
  5. 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. |
  6. Lee, H., Roh, S., & Kim, D. J. (2009). Alcohol-induced blackout. International Journal of Environmental Research and Public Health, 6(11), 2783-2792. |
  7. Mejo, S. L. (1992). Anterograde amnesia linked to benzodiazepines. The Nurse Practitioner, 17(10), 44-49. |
  8. 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. |
  9. Canaday, B. R. (1996). Amnesia possibly associated with zolpidem administration. Pharmacotherapy: The Journal of Human Pharmacology and Drug Therapy, 16(4), 687-689. |




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