Cognitive suppressions

From PsychonautWiki
Jump to navigation Jump to search

Cognitive suppressions are defined as any subjective effect which decreases or lowers the intensity of a facet of a person's cognition in a manner that is generally considered either functional or dysfunctional.

This page lists and describes the various cognitive suppressions which can occur under the influence of certain psychoactive compounds.

Addiction suppression

Main article: Addiction suppression

Addiction suppression is defined as the experience of a total or partial suppression of a psychological addiction to a specific substance and the cravings associated with it. This can occur as an effect which lasts long after the compound which induced it wears off or it can last only while the compound is still active.

Addiction suppression is a rare effect that is most commonly associated with psychedelics,[1] psilocin,[2] LSD,[3] ibogaine[4] and N-acetylcysteine (NAC).[5]

Anxiety suppression

Main article: Anxiety suppression

Anxiety suppression (also known as anxiolysis or minimal sedation)[6] is medically recognized as a partial to complete suppression of a person’s ability to feel anxiety, general unease, and negative feelings of both psychological and physiological tension.[7] The experience of this effect may decrease anxiety-related behaviours such as restlessness, muscular tension,[8] rumination, and panic attacks. Complete anxiety suppression can produce feelings of extreme calmness and relaxation; however, it can also lead to undesirable outcomes when accompanied by other effects such as disinhibition or sedation.

It is most commonly induced under the influence of moderate dosages of anxiolytic compounds which primarily include GABAergic depressants,[9][10] such as benzodiazepines,[11] alcohol,[12] GHB,[13] and gabapentinoids[14]. However, it can also occur to a lesser extent under the influence of a large variety of other pharmacological classes which include but are not limited to cannabinoids,[15] dissociatives,[16] SSRIs, and opioids.

Disinhibition

Main article: Disinhibition

Disinhibition is medically recognized as an orientation towards immediate gratification, leading to impulsive behavior driven by current thoughts, feelings, and external stimuli, without regard for past learning or consideration of future consequences.[17][18][19] This is usually manifested through recklessness, poor risk assessment, and a disregard for social conventions.

At its lower levels of intensity, disinhibition can allow one to overcome emotional apprehension and suppressed social skills in a manner that is moderated and controllable for the average person. This can often prove useful for those who suffer from social anxiety or a general lack of self-confidence.

However, at higher levels of intensity, the disinhibited individual may be completely unable to maintain any semblance of self-restraint, at the expense of politeness, sensitivity, social appropriateness, or local laws and regulations. This lack of constraint can be negative, neutral, or positive depending on the individual and their current environment. The negative consequences of disinhibited behaviour range from relatively benign consequences (such as embarrassing oneself) to destructive and damaging ones (such as driving under the influence or committing criminal acts).

Disinhibition is often accompanied by other coinciding effects such as amnesia and anxiety suppression in a manner which can further decrease the person's observance of and regard for social norms. It is most commonly induced under the influence of moderate dosages of GABAergic depressants, such as alcohol,[20] benzodiazepines,[21] phenibut, and GHB. However, it may also occur under the influence of certain stimulants,[22] entactogens,[23] and dissociatives[24].

Dream suppression

Main article: Dream suppression

Dream suppression is defined as a decrease in the vividness, intensity, frequency, and recollection of a person's dreams. At its lower levels, this can be a partial suppression which results in the person having dreams of a lesser intensity and a lower rate of frequency. However, at its higher levels, this can be a complete suppression which results in the person not experiencing any dreams at all.

Dream suppression is most commonly induced under the influence of moderate dosages of cannabinoids[25] and most types of antidepressants[26][27][28]. This is due to the way in which they increase REM latency, decrease REM sleep, reduce total sleep time and efficiency, and increase wakefulness.[25][26][27][29] REM sleep is where the majority of dreams occur.[30]

Emotion suppression

Main article: Emotion suppression

Emotion suppression (also known as flat affect, apathy, or emotional blunting) is medically recognized as a flattening or decrease in the intensity of one's current emotional state below normal levels.[31][32][33] This dulls or suppresses the genuine emotions that a person was already feeling prior to ingesting the drug. For example, an individual who is currently feeling somewhat anxious or emotionally unstable may begin to feel very apathetic, neutral, uncaring, and emotionally blank. This also impacts the degree to which the person will express their emotional state through body language, tone of voice, and facial expressions.

It is worth noting that although a reduction in the intensity of one's emotions may be beneficial at times (e.g., the blunting of an anger response in a volatile patient), it may be detrimental at other times (e.g., emotional indifference at the funeral of a close family member).[34]

Emotion suppression is often accompanied by other coinciding effects such as motivation suppression, thought deceleration, and analysis suppression. It is most commonly induced under the influence of moderate dosages of antipsychotic compounds, such as quetiapine, haloperidol, and risperidone.[31][35] However, it can also occur in less consistent form under the influence of heavy dosages of dissociatives,[36][37] SSRI's,[34][38] and GABAergic depressants[39].

Focus suppression

Main article: Focus suppression

Focus suppression (also known as distractability[40]) is medically recognized as a decreased ability to selectively concentrate on an aspect of the environment while ignoring other things.[41][42] It can be best characterized by feelings of intense distractability which can prevent one from focusing on and performing basic tasks that would usually be relatively easy to not get distracted from.[43] This effect will often synergize with other coinciding effects such as motivation suppression, thought deceleration, and sedation.[44]

Focus suppression is often accompanied by other coinciding effects such as sedation, motivation suppression, and creativity suppression. It is most commonly induced under the influence of moderate or heavy dosages of antipsychotics,[45] benzodiazepines, cannabinoids,[44] and hallucinogens. However, it is worth noting that stimulant compounds which primarily induce focus enhancement at light to moderate dosages will also often lead into focus suppression at their heavier dosages.[46]

Memory suppression

Main article: Memory suppression

Memory suppression (also known as ego suppression, ego dissolution, ego loss or ego death) is defined as an inhibition of a person's ability to maintain a functional short and long-term memory.[47][48][49] This occurs in a manner that is directly proportional to the dosage consumed, and often begins with the degradation of one's short-term memory.

Memory suppression is a process which may be broken down into the 4 basic levels described below:

  1. Partial short-term memory suppression - At the lowest level, this effect is a partial and potentially inconsistent failure of a person's short-term memory. It can cause effects such as a general difficulty staying focused, an increase in distractibility, and a general tendency to forget what one is thinking or saying.
  2. Complete short-term memory suppression - At this level, this effect is the complete failure of a person's short-term memory. It can be described as the experience of being completely incapable of remembering any specific details regarding the present situation and the events leading up to it for more than a few seconds. This state of mind can often result in thought loops, confusion, disorientation, and a loss of control, especially for the inexperienced. At this level, it can also become impossible to follow both conversations and the plot of most forms of media.
  3. Partial long-term memory suppression - At this level, this effect is the partial, often intermittent failure of a person's long-term memory in addition to the complete failure of their short-term memory. It can be described as the experience of an increased difficulty recalling basic concepts and autobiographical information from one's long-term memory. Compounded with the complete suppression of short term memory, it creates an altered state where even basic tasks become challenging or impossible as one cannot mentally access past memories of how to complete them.

    For example, one may take a longer time to recall the identity of close friends or temporarily forget how to perform basic tasks. This state may create the sensation of experiencing something for the first time. At this stage, a reduction of certain learned personality traits, awareness of cultural norms, and linguistic recall may accompany the suppression of long-term memory.

  4. Complete long-term memory suppression - At the highest level, this effect is the complete and persistent failure of both a person's long and short-term memory. It can be described as the experience of becoming completely incapable of remembering even the most basic fundamental concepts stored within the person's long-term memory. This includes everything from their name, hometown, past memories, the awareness of being on drugs, what drugs even are, what human beings are, what life is, that time exists, what anything is, or that anything exists.

    Memory suppression of this level blocks all mental associations, attached meaning, acquired preferences, and value judgements one may have towards the external world. Sufficiently intense memory loss is also associated with the loss of a sense of self, in which one is no longer aware of their own existence. In this state, the user is unable to recall all learned conceptual knowledge about themselves and the external world, and no longer experiences the sensation of being a separate observer in an external world. This experience is commonly referred to as "ego death".

Memory suppression is often accompanied by other coinciding effects such as thought loops, personal bias suppression, amnesia, and delusions. It is most commonly induced under the influence of moderate dosages of hallucinogenic compounds, such as psychedelics, dissociatives, and deliriants.[50]

It is worth noting that although memory suppression is vaguely similar in its effects to amnesia, it differs in that it directly suppresses one's usage of their long or short term memory without inhibiting the person's ability to recall what happened during this experience afterward. In contrast, amnesia does not directly affect the usage of one's short or long-term memory during its experience but instead renders a person incapable of recalling events after it has worn off. A person experiencing memory suppression cannot access their existing memory, while a person with drug-induced amnesia cannot properly store new memories. 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 is not the case with memory suppression.

Personal bias suppression

Main article: Personal bias suppression

Personal bias suppression (also called cultural filter suppression) is defined as a decrease in the personal or cultural biases, preferences, and associations which a person knowingly or unknowingly filters and interprets their perception of the world through.[51]

Analyzing one's beliefs, preferences, or associations while experiencing personal bias suppression can lead to new perspectives that one could not reach while sober. The suppression of this innate tendency often induces the realization that certain aspects of a person's personality, world view and culture are not reflective of objective truths about reality, but are in fact subjective or even delusional opinions.[51] This realization often leads to or accompanies deep states of insight and critical introspection which can create significant alterations in a person's perspective that last anywhere from days, weeks, months, or even years after the experience itself.

Personal bias suppression is often accompanied by other coinciding effects such as conceptual thinking, analysis enhancement, and especially memory suppression. It is most commonly induced under the influence of heavy dosages of hallucinogens such as dissociatives and psychedelics. However, it can also occur to a much lesser extent under the influence of very heavy dosages entactogens and cannabinoids.

Sleepiness

Main article: Sleepiness

Sleepiness (also known as drowsiness) is medically recognized as a state of near-sleep, or a strong desire for sleep without feeling a decrease in one's physical energy levels.[52][53][54] This state is independent of a circadian rhythm;[52] so, unlike sedation, this effect does not necessarily decrease physical energy levels but instead decreases wakefulness. It results in a propensity for tired, clouded, and sleep-prone behaviour. This can lead into a decreased motivation to perform tasks, as the increase in one's desire to sleep begins to outweigh other considerations. Prolonged exposure to this effect without appropriate rest can lead to cognitive fatigue and a range of other cognitive suppressions.

Sleepiness is most commonly induced under the influence of moderate dosages of a wide variety of compounds such as cannabinoids,[55] GABAergic depressants,[56][57] opioids,[58] antipsychotics,[59][60] some antihistamines,[61] and certain psychedelics. However, it is worth noting that the few compounds which selectively induce this effect without a number of other accompanying effects are referred to as hypnotics.

Suggestibility suppression

Main article: Suggestibility suppression

Suggestibility suppression is defined as a decreased tendency to accept and act on the suggestions of others. A common example of suggestibility suppression in action would be a person being unwilling to believe or trust another person's suggestions without a greater amount of prior discussion than would usually be considered necessary during every day sobriety.

Although this effect can occur as a distinct mindstate, it may also arise due to interactions between a number of other effects. For example, a person who is currently experiencing mild paranoia combined with analysis enhancement may find themselves less trusting and more inclined to think through the suggestions of others before acting upon them, alternatively, a person who is experiencing ego inflation may find that they value their own opinion over others and are therefore equally less likely to follow the suggestions of others.

Alcohol has been shown to decrease suggestibility in a dose-dependent manner,[62][63] while its withdrawals increases suggestibility.[64] A large proportion of individuals who come in contact with law enforcement personnel are under the influence of alcohol, including perpetrators, victims, and witnesses of crimes. This has to be taken into account when investigative interviews are planned and conducted, and when the reliability of the information derived from such interviews is evaluated.[62][63][64]

Suggestibility suppression is often accompanied by other coinciding effects such as irritability[62] and ego inflation. It is most commonly induced under the influence of GABAergic depressants.[62][63][64]

Thought deceleration

Main article: Thought deceleration

Thought deceleration (also known as bradyphrenia)[65] is defined as the process of thought being slowed down significantly in comparison to that of normal sobriety. When experiencing this effect, it will feel as if the time it takes to think a thought and the amount of time which occurs between each thought has been slowed down to the point of greatly impairing cognitive processes. It can manifest itself in delayed recognition, slower reaction times, and fine motor skills deficits.

Thought deceleration is often accompanied by other coinciding effects such as analysis suppression and sedation in a manner which not only decreases the person's speed of thought, but also significantly decreases the sharpness of a person's mental clarity. It is most commonly induced under the influence of heavy dosages of depressant compounds, such as GABAergics,[66][67][68] antipsychotics,[69] and opioids.[70][71][72] However, it can also occur to a lesser extent under the influence of heavy dosages of hallucinogens such as psychedelics,[73] dissociatives,[74] deliriants,[68][75] and cannabinoids.[76][77][78][79]

See also

References

</references>

  1. ↑ Nichols, D. E. (2016). "Psychedelics". Pharmacological Reviews. 68 (2): 264–355. doi:10.1124/pr.115.011478. ISSN 1521-0081. 
  2. ↑ Johnson, Matthew W; Garcia-Romeu, Albert; Cosimano, Mary P; Griffiths, Roland R (2014). "Pilot study of the 5-HT2AR agonist psilocybin in the treatment of tobacco addiction". Journal of Psychopharmacology. 28 (11): 983–992. doi:10.1177/0269881114548296. ISSN 0269-8811. 
  3. ↑ Krebs, Teri S; Johansen, Pål-Ørjan (2012). "Lysergic acid diethylamide (LSD) for alcoholism: meta-analysis of randomized controlled trials". Journal of Psychopharmacology. 26 (7): 994–1002. doi:10.1177/0269881112439253. ISSN 0269-8811. 
  4. ↑ Brown, Thomas (2013). "Ibogaine in the Treatment of Substance Dependence". Current Drug Abuse Reviews. 6 (1): 3–16. doi:10.2174/15672050113109990001. ISSN 1874-4737. 
  5. ↑ Moran, M. M. (2005). "Cystine/Glutamate Exchange Regulates Metabotropic Glutamate Receptor Presynaptic Inhibition of Excitatory Transmission and Vulnerability to Cocaine Seeking". Journal of Neuroscience. 25 (27): 6389–6393. doi:10.1523/JNEUROSCI.1007-05.2005. ISSN 0270-6474. 
  6. ↑ anxiolysis, National Cancer Institute 
  7. ↑ Gordon, Joshua A. (2002). "Anxiolytic drug targets: beyond the usual suspects". Journal of Clinical Investigation. 110 (7): 915–917. doi:10.1172/JCI0216846. ISSN 0021-9738. 
  8. ↑ Tyrer, P. (27 February 1988). "Prescribing psychotropic drugs in general practice". BMJ. 296 (6622): 588–589. doi:10.1136/bmj.296.6622.588. 
  9. ↑ Lydiard, R. B. (2003). "The role of GABA in anxiety disorders". The Journal of Clinical Psychiatry. 64 Suppl 3: 21–27. ISSN 0160-6689. 
  10. ↑ Gauthier, Isabelle; Nuss, Philippe (2015). "Anxiety disorders and GABA neurotransmission: a disturbance of modulation". Neuropsychiatric Disease and Treatment: 165. doi:10.2147/NDT.S58841. ISSN 1178-2021. 
  11. ↑ Wood, Alastair J.J.; Shader, Richard I.; Greenblatt, David J. (1993). "Use of Benzodiazepines in Anxiety Disorders". New England Journal of Medicine. 328 (19): 1398–1405. doi:10.1056/NEJM199305133281907. ISSN 0028-4793. 
  12. ↑ Smith, J. P., Randall, C. L. (2012). "Anxiety and alcohol use disorders: comorbidity and treatment considerations". Alcohol Research: Current Reviews. 34 (4): 414–431. ISSN 2168-3492. 
  13. ↑ Schmidt-Mutter, Catherine; Pain, Laure; Sandner, Guy; Gobaille, Serge; Maitre, Michel (1998). "The anxiolytic effect of γ-hydroxybutyrate in the elevated plus maze is reversed by the benzodiazepine receptor antagonist, flumazenil". European Journal of Pharmacology. 342 (1): 21–27. doi:10.1016/S0014-2999(97)01503-3. ISSN 0014-2999. 
  14. ↑ Pollack, Mark H.; Matthews, John; Scott, Erin L. (1998). "Gabapentin as a Potential Treatment for Anxiety Disorders". American Journal of Psychiatry. 155 (7): 992–993. doi:10.1176/ajp.155.7.992. ISSN 0002-953X. 
  15. ↑ Blessing, Esther M.; Steenkamp, Maria M.; Manzanares, Jorge; Marmar, Charles R. (2015). "Cannabidiol as a Potential Treatment for Anxiety Disorders". Neurotherapeutics. 12 (4): 825–836. doi:10.1007/s13311-015-0387-1. ISSN 1933-7213. 
  16. ↑ Irwin, Scott A.; Iglewicz, Alana (2010). "Oral Ketamine for the Rapid Treatment of Depression and Anxiety in Patients Receiving Hospice Care". Journal of Palliative Medicine. 13 (7): 903–908. doi:10.1089/jpm.2010.9808. ISSN 1096-6218. 
  17. ↑ "Glossary of Technical Terms". Diagnostic and statistical manual of mental disorders (5th ed.): 820. 2013. doi:10.1176/appi.books.9780890425596.GlossaryofTechnicalTerms. 
  18. ↑ Zamboni, G.; Huey, E. D.; Krueger, F.; Nichelli, P. F.; Grafman, J. (2008). "Apathy and disinhibition in frontotemporal dementia: Insights into their neural correlates". Neurology. 71 (10): 736–742. doi:10.1212/01.wnl.0000324920.96835.95. ISSN 0028-3878. 
  19. ↑ Källmén, Håkan; Gustafson, Roland (1998). "Alcohol and Disinhibition". European Addiction Research. 4 (4): 150–162. doi:10.1159/000018948. ISSN 1022-6877. 
  20. ↑ Bettinger, Jill C.; Topper, Stephen M.; Aguilar, Sara C.; Topper, Viktoria Y.; Elbel, Erin; Pierce-Shimomura, Jonathan T. (2014). "Alcohol Disinhibition of Behaviors in C. elegans". PLoS ONE. 9 (3): e92965. doi:10.1371/journal.pone.0092965. ISSN 1932-6203. 
  21. ↑ Paton, Carol (2018). "Benzodiazepines and disinhibition: a review". Psychiatric Bulletin. 26 (12): 460–462. doi:10.1192/pb.26.12.460. ISSN 0955-6036. 
  22. ↑ Fillmore, M (2003). "Effects of d-amphetamine on behavioral control in stimulant abusers: the role of prepotent response tendencies". Drug and Alcohol Dependence. 71 (2): 143–152. doi:10.1016/S0376-8716(03)00089-9. ISSN 0376-8716. 
  23. ↑ Ando, Romeo D.; Benko, Anita; Ferrington, Linda; Kirilly, Eszter; Kelly, Paul A.T.; Bagdy, Gyorgy (2006). "Partial lesion of the serotonergic system by a single dose of MDMA results in behavioural disinhibition and enhances acute MDMA-induced social behaviour on the social interaction test". Neuropharmacology. 50 (7): 884–896. doi:10.1016/j.neuropharm.2005.12.010. ISSN 0028-3908. 
  24. ↑ Lissek, Silke; Güntürkün, Onur (2003). "Dissociation of Extinction and Behavioral Disinhibition: The Role of NMDA Receptors in the Pigeon Associative Forebrain during Extinction". The Journal of Neuroscience. 23 (22): 8119–8124. doi:10.1523/JNEUROSCI.23-22-08119.2003. ISSN 0270-6474. 
  25. ↑ 25.0 25.1 Schierenbeck, Thomas; Riemann, Dieter; Berger, Mathias; Hornyak, Magdolna (2008). "Effect of illicit recreational drugs upon sleep: Cocaine, ecstasy and marijuana". Sleep Medicine Reviews. 12 (5): 381–389. doi:10.1016/j.smrv.2007.12.004. ISSN 1087-0792. 
  26. ↑ 26.0 26.1 Sharpley, Ann L.; Cowen, Philip J. (1995). "Effect of pharmacologic treatments on the sleep of depressed patients". Biological Psychiatry. 37 (2): 85–98. doi:10.1016/0006-3223(94)00135-P. ISSN 0006-3223. 
  27. ↑ 27.0 27.1 Trivedi, M (1999). "Effects of Fluoxetine on the Polysomnogram in Outpatients with Major Depression". Neuropsychopharmacology. 20 (5): 447–459. doi:10.1016/S0893-133X(98)00131-6. ISSN 0893-133X. 
  28. ↑ Vogel, G.W.; Buffenstein, A.; Minter, K.; Hennessey, Ann (1990). "Drug effects on REM sleep and on endogenous depression". Neuroscience & Biobehavioral Reviews. 14 (1): 49–63. doi:10.1016/S0149-7634(05)80159-9. ISSN 0149-7634. 
  29. ↑ Feinberg, I., Jones, R., Walker, J. M., Cavness, C., March, J. (April 1975). "Effects of high dosage delta-9-tetrahydrocannabinol on sleep patterns in man". Clinical Pharmacology & Therapeutics. 17 (4): 458–466. doi:10.1002/cpt1975174458. ISSN 0009-9236. Retrieved 4 June 2022. 
  30. ↑ Hobson, J. A., Stickgold, R., Pace-Schott, E. F. (February 1998). "The neuropsychology of REM sleep dreaming:". NeuroReport. 9 (3): R1–R14. doi:10.1097/00001756-199802160-00033. ISSN 0959-4965. Retrieved 4 June 2022. 
  31. ↑ 31.0 31.1 Ueda, Satoshi; Sakayori, Takeshi; Omori, Ataru; Fukuta, Hajime; Kobayashi, Takashi; Ishizaka, Kousuke; Saijo, Tomoyuki; Okubo, Yoshiro (2016). "Neuroleptic-induced deficit syndrome in bipolar disorder with psychosis". Neuropsychiatric Disease and Treatment: 265. doi:10.2147/NDT.S99577. ISSN 1178-2021. 
  32. ↑ "Neurocognitive Disorders". Diagnostic and statistical manual of mental disorders (5th ed.): 609. 2013. doi:10.1176/appi.books.9780890425596.dsm17. 
  33. ↑ Gur, R. E; Kohler, C. G; Ragland, J D.; Siegel, S. J; Lesko, K.; Bilker, W. B; Gur, R. C (2006). "Flat Affect in Schizophrenia: Relation to Emotion Processing and Neurocognitive Measures". Schizophrenia Bulletin. 32 (2): 279–287. doi:10.1093/schbul/sbj041. ISSN 0586-7614. 
  34. ↑ 34.0 34.1 Sansone, R. A., Sansone, L. A. (October 2010). "SSRI-Induced Indifference". Psychiatry (Edgmont (Pa.: Township)). 7 (10): 14–18. ISSN 1555-5194. 
  35. ↑ Moncrieff, J.; Cohen, D.; Mason, J. P. (2009). "The subjective experience of taking antipsychotic medication: a content analysis of Internet data". Acta Psychiatrica Scandinavica. 120 (2): 102–111. doi:10.1111/j.1600-0447.2009.01356.x. ISSN 0001-690X. 
  36. ↑ Vollenweider, F. X. (31 December 2001). "Brain mechanisms of hallucinogens and entactogens". Dialogues in Clinical Neuroscience. 3 (4): 265–279. doi:10.31887/DCNS.2001.3.4/fxvollenweider. ISSN 1958-5969. 
  37. ↑ Micallef, J; Tardieu, S; Gentile, S; Fakra, E; Jouve, E; Sambuc, R; Blin, O (2003). "Évaluation psychocomportementale de l'administration de faible dose de kétamine chez le sujet sain". Neurophysiologie Clinique/Clinical Neurophysiology. 33 (3): 138–147. doi:10.1016/S0987-7053(03)00028-5. ISSN 0987-7053. 
  38. ↑ Bolling, Madelon Y.; Kohlenberg, Robert J. (2004). "Reasons for Quitting Serotonin Reuptake Inhibitor Therapy: Paradoxical Psychological Side Effects and Patient Satisfaction". Psychotherapy and Psychosomatics. 73 (6): 380–385. doi:10.1159/000080392. ISSN 0033-3190. 
  39. ↑ Oscar-Berman, M., Bowirrat, A. (September 2005). "Genetic influences in emotional dysfunction and alcoholism-related brain damage". Neuropsychiatric Disease and Treatment. 1 (3): 211–229. ISSN 1176-6328. 
  40. ↑ "Glossary of Technical Terms". Diagnostic and statistical manual of mental disorders (5th ed.): 820. 2013. doi:10.1176/appi.books.9780890425596.GlossaryofTechnicalTerms. 
  41. ↑ Lleras, Alejandro; Buetti, Simona; Mordkoff, J. Toby (2013). "When Do the Effects of Distractors Provide a Measure of Distractibility?". 59: 261–315. doi:10.1016/B978-0-12-407187-2.00007-1. ISSN 0079-7421. 
  42. ↑ Ahveninen, Jyrki; Jaaskelainen, Iiro P.; Pekkonen, Eero; Hallberg, Anja; Hietanen, Marja; Naatanen, Risto; Schroger, Erich; Sillanaukee, Pekka (2000). "Increased Distractibility by Task-Irrelevant Sound Changes in Abstinent Alcoholics". Alcoholism: Clinical and Experimental Research. 24 (12): 1850–1854. doi:10.1111/j.1530-0277.2000.tb01989.x. ISSN 0145-6008. 
  43. ↑ McCarthy, Danielle E.; Gloria, Rebecca; Curtin, John J. (2009). "Attention bias in nicotine withdrawal and under stress". Psychology of Addictive Behaviors. 23 (1): 77–90. doi:10.1037/a0014288. ISSN 1939-1501. 
  44. ↑ 44.0 44.1 Kowal, Mikael A.; Hazekamp, Arno; Colzato, Lorenza S.; van Steenbergen, Henk; van der Wee, Nic J. A.; Durieux, Jeffrey; Manai, Meriem; Hommel, Bernhard (2014). "Cannabis and creativity: highly potent cannabis impairs divergent thinking in regular cannabis users". Psychopharmacology. 232 (6): 1123–1134. doi:10.1007/s00213-014-3749-1. ISSN 0033-3158. 
  45. ↑ Vigen, Cheryl L.P.; Mack, Wendy J.; Keefe, Richard S.E.; Sano, Mary; Sultzer, David L.; Stroup, T. Scott; Dagerman, Karen S.; Hsiao, John K.; Lebowitz, Barry D.; Lyketsos, Constantine G.; Tariot, Pierre N.; Zheng, Ling; Schneider, Lon S. (2011). "Cognitive Effects of Atypical Antipsychotic Medications in Patients With Alzheimer's Disease: Outcomes From CATIE-AD". American Journal of Psychiatry. 168 (8): 831–839. doi:10.1176/appi.ajp.2011.08121844. ISSN 0002-953X. 
  46. ↑ Salo, Ruth; Nordahl, Thomas E.; Natsuaki, Yutaka; Leamon, Martin H.; Galloway, Gantt P.; Waters, Christy; Moore, Charles D.; Buonocore, Michael H. (2007). "Attentional Control and Brain Metabolite Levels in Methamphetamine Abusers". Biological Psychiatry. 61 (11): 1272–1280. doi:10.1016/j.biopsych.2006.07.031. ISSN 0006-3223. 
  47. ↑ Lebedev, Alexander V.; Lövdén, Martin; Rosenthal, Gidon; Feilding, Amanda; Nutt, David J.; Carhart-Harris, Robin L. (2015). "Finding the self by losing the self: Neural correlates of ego-dissolution under psilocybin". Human Brain Mapping. 36 (8): 3137–3153. doi:10.1002/hbm.22833. ISSN 1065-9471. 
  48. ↑ Carhart-Harris, Robin L.; Muthukumaraswamy, Suresh; Roseman, Leor; Kaelen, Mendel; Droog, Wouter; Murphy, Kevin; Tagliazucchi, Enzo; Schenberg, Eduardo E.; Nest, Timothy; Orban, Csaba; Leech, Robert; Williams, Luke T.; Williams, Tim M.; Bolstridge, Mark; Sessa, Ben; McGonigle, John; Sereno, Martin I.; Nichols, David; Hellyer, Peter J.; Hobden, Peter; Evans, John; Singh, Krish D.; Wise, Richard G.; Curran, H. Valerie; Feilding, Amanda; Nutt, David J. (2016). "Neural correlates of the LSD experience revealed by multimodal neuroimaging". Proceedings of the National Academy of Sciences. 113 (17): 4853–4858. doi:10.1073/pnas.1518377113. ISSN 0027-8424. 
  49. ↑ Carhart-Harris, Robin L.; Leech, Robert; Hellyer, Peter J.; Shanahan, Murray; Feilding, Amanda; Tagliazucchi, Enzo; Chialvo, Dante R.; Nutt, David (2014). "The entropic brain: a theory of conscious states informed by neuroimaging research with psychedelic drugs". Frontiers in Human Neuroscience. 8. doi:10.3389/fnhum.2014.00020. ISSN 1662-5161. 
  50. ↑ Vollenweider, Franz X; Geyer, Mark A (2001). "A systems model of altered consciousness: integrating natural and drug-induced psychoses". Brain Research Bulletin. 56 (5): 495–507. doi:10.1016/S0361-9230(01)00646-3. ISSN 0361-9230. 
  51. ↑ 51.0 51.1 Horváth, Lajos; Szummer, Csaba; Szabo, Attila (2017). "Weak phantasy and visionary phantasy: the phenomenological significance of altered states of consciousness". Phenomenology and the Cognitive Sciences. 17 (1): 117–129. doi:10.1007/s11097-016-9497-4. ISSN 1568-7759. 
  52. ↑ 52.0 52.1 "Glossary of Technical Terms". Diagnostic and statistical manual of mental disorders (5th ed.): 829. 2013. doi:10.1176/appi.books.9780890425596.GlossaryofTechnicalTerms. 
  53. ↑ Guilleminault, C. (2001). "Excessive daytime sleepiness: A challenge for the practising neurologist". Brain. 124 (8): 1482–1491. doi:10.1093/brain/124.8.1482. ISSN 1460-2156. 
  54. ↑ Bereshpolova, Y.; Stoelzel, C. R.; Zhuang, J.; Amitai, Y.; Alonso, J.-M.; Swadlow, H. A. (2011). "Getting Drowsy? Alert/Nonalert Transitions and Visual Thalamocortical Network Dynamics". Journal of Neuroscience. 31 (48): 17480–17487. doi:10.1523/JNEUROSCI.2262-11.2011. ISSN 0270-6474. 
  55. ↑ Ware, M. A.; Wang, T.; Shapiro, S.; Robinson, A.; Ducruet, T.; Huynh, T.; Gamsa, A.; Bennett, G. J.; Collet, J.-P. (2010). "Smoked cannabis for chronic neuropathic pain: a randomized controlled trial". Canadian Medical Association Journal. 182 (14): E694–E701. doi:10.1503/cmaj.091414. ISSN 0820-3946. 
  56. ↑ Landauer, Ali A.; Howat, Peter (2007). "Low and moderate alcohol doses, psychomotor performance and perceived drowsiness". Ergonomics. 26 (7): 647–657. doi:10.1080/00140138308963386. ISSN 0014-0139. 
  57. ↑ Koch-Weser, Jan; Greenblatt, David J.; Shader, Richard I.; Abernethy, Darrell R. (1983). "Current Status of Benzodiazepines". New England Journal of Medicine. 309 (7): 410–416. doi:10.1056/NEJM198308183090705. ISSN 0028-4793. 
  58. ↑ Corey, PJ; Heck, Amy M; Weathermon, Ronnie A (2016). "Amphetamines to Counteract Opioid-Induced Sedation". Annals of Pharmacotherapy. 33 (12): 1362–1366. doi:10.1345/aph.19024. ISSN 1060-0280. 
  59. ↑ Van Putten, Theodore (1981). "Subjective Response to Antipsychotic Drugs". Archives of General Psychiatry. 38 (2): 187. doi:10.1001/archpsyc.1981.01780270073010. ISSN 0003-990X. 
  60. ↑ Artaloytia, Juan Francisco; Arango, Celso; Lahti, Adrienne; Sanz, Javier; Pascual, Ana; Cubero, Pedro; Prieto, David; Palomo, Tomás (2006). "Negative Signs and Symptoms Secondary to Antipsychotics: A Double-Blind, Randomized Trial of a Single Dose of Placebo, Haloperidol, and Risperidone in Healthy Volunteers". American Journal of Psychiatry. 163 (3): 488–493. doi:10.1176/appi.ajp.163.3.488. ISSN 0002-953X. 
  61. ↑ Weiler, John M.; Bloomfield, John R.; Woodworth, George G.; Grant, Angela R.; Layton, Teresa A.; Brown, Timothy L.; McKenzie, David R.; Baker, Thomas W.; Watson, Ginger S. (2000). "Effects of Fexofenadine, Diphenhydramine, and Alcohol on Driving Performance". Annals of Internal Medicine. 132 (5): 354. doi:10.7326/0003-4819-132-5-200003070-00004. ISSN 0003-4819. 
  62. ↑ 62.0 62.1 62.2 62.3 Santtila, Pekka; Ekholm, Magnus; Niemi, Pekka (1998). "Factors moderating the effects of alcohol on interrogative suggestibility". Psychology, Crime & Law. 4 (2): 139–152. doi:10.1080/10683169808401754. ISSN 1068-316X. 
  63. ↑ 63.0 63.1 63.2 Santtila, Pekka; Ekholm, Magnus; Niemi, Pekka (1999). "The effects of alcohol on interrogative suggestibility: The role of State-Anxiety and mood states as mediating factors". Legal and Criminological Psychology. 4 (1): 1–13. doi:10.1348/135532599167707. ISSN 1355-3259. 
  64. ↑ 64.0 64.1 64.2 Gudjonsson, Gisli; Hannesdottir, Kristin; Petursson, Hannes; Bjornsson, Gudbjorn (2002). "The effects of alcohol withdrawal on mental state, interrogative suggestibility and compliance: an experimental study". The Journal of Forensic Psychiatry. 13 (1): 53–67. doi:10.1080/09585180210122682. ISSN 0958-5184. 
  65. ↑ Levin, E (1996). "Nicotine-Haloperidol Interactions and Cognitive Performance in Schizophrenics". Neuropsychopharmacology. 15 (5): 429–436. doi:10.1016/S0893-133X(96)00018-8. ISSN 0893-133X. 
  66. ↑ Vermeeren, A.; Muntjewerff, N. D.; Quint, P. J.; O'Hanlon, J. F.; Jackson, J. L.; Harrison, E. M. (1995). "Comparison of acute alprazolam (0.25, 0.50 and 1.0 mg) effects versus those of lorazepam 2 mg and placebo on memory in healthy volunteers using laboratory and telephone tests". Psychopharmacology. 118 (1): 1–9. doi:10.1007/BF02245243. ISSN 0033-3158. 
  67. ↑ Johannes, Sönke; Wieringa, Bernardina M.; Nager, Wido; Dengler, Reinhard; Münte, Thomas F. (2001). "Oxazepam alters action monitoring". Psychopharmacology. 155 (1): 100–106. doi:10.1007/s002130100680. ISSN 0033-3158. 
  68. ↑ 68.0 68.1 Semlitsch, H.V.; Anderer, P.; Saletu, B. (1995). "Acute effects of the anxiolytics suriclone and alprazolam on cognitive information processing utilizing topographic mapping of event-related brain potentials (P300) in healthy subjects". European Journal of Clinical Pharmacology. 49 (3). doi:10.1007/BF00192378. ISSN 0031-6970. 
  69. ↑ Naber, Dieter (2011). "Subjective effects of antipsychotic drugs and their relevance for compliance and remission". Epidemiologia e Psichiatria Sociale. 17 (03): 174–176. doi:10.1017/S1121189X00001238. ISSN 1121-189X. 
  70. ↑ Kurita, Geana Paula; Lundorff, Lena; Pimenta, Cibele Andrucioli de Mattos; Sjøgren, Per (2008). "The cognitive effects of opioids in cancer: a systematic review". Supportive Care in Cancer. 17 (1): 11–21. doi:10.1007/s00520-008-0497-y. ISSN 0941-4355. 
  71. ↑ Twillman, Robert K; Long, Teresa D; Cathers, Teresa A; Mueller, David W (1999). "Treatment of Painful Skin Ulcers with Topical Opioids". Journal of Pain and Symptom Management. 17 (4): 288–292. doi:10.1016/S0885-3924(98)00140-7. ISSN 0885-3924. 
  72. ↑ Ersek, Mary; Cherrier, Monique M; Overman, Steven S; Irving, Gordon A (2004). "The cognitive effects of opioids". Pain Management Nursing. 5 (2): 75–93. doi:10.1016/j.pmn.2003.11.002. ISSN 1524-9042. 
  73. ↑ Kaelen, Mendel; Giribaldi, Bruna; Raine, Jordan; Evans, Lisa; Timmerman, Christopher; Rodriguez, Natalie; Roseman, Leor; Feilding, Amanda; Nutt, David; Carhart-Harris, Robin (2018). "The hidden therapist: evidence for a central role of music in psychedelic therapy". Psychopharmacology. 235 (2): 505–519. doi:10.1007/s00213-017-4820-5. ISSN 0033-3158. 
  74. ↑ Freyd, Jennifer J.; Martorello, Susan R.; Alvarado, Jessica S.; Hayes, Amy E.; Christman, Jill C. (1998). "Cognitive environments and dissociative tendencies: performance on the standard Stroop task for high versus low dissociators". Applied Cognitive Psychology. 12 (7): S91–S103. doi:10.1002/(SICI)1099-0720(199812)12:7<S91::AID-ACP599>3.0.CO;2-Z. ISSN 0888-4080. 
  75. ↑ Nebes, Robert D.; Pollock, Bruce G.; Halligan, Edythe M.; Houck, Patricia; Saxton, Judith A. (2011). "Cognitive Slowing Associated With Elevated Serum Anticholinergic Activity in Older Individuals is Decreased by Caffeine Use". The American Journal of Geriatric Psychiatry. 19 (2): 169–175. doi:10.1097/JGP.0b013e3181e4490d. ISSN 1064-7481. 
  76. ↑ Crean, Rebecca D.; Crane, Natania A.; Mason, Barbara J. (2011). "An Evidence-Based Review of Acute and Long-Term Effects of Cannabis Use on Executive Cognitive Functions". Journal of Addiction Medicine. 5 (1): 1–8. doi:10.1097/ADM.0b013e31820c23fa. ISSN 1932-0620. 
  77. ↑ Tapert, S., Schweinsburg, A., Brown, S. (1 January 2008). "The Influence of Marijuana Use on Neurocognitive Functioning in Adolescents". Current Drug Abuse Reviewse. 1 (1): 99–111. doi:10.2174/1874473710801010099. ISSN 1874-4737. Retrieved 4 June 2022. 
  78. ↑ Bhattacharyya, Sagnik; Sendt, Kyra-Verena (2012). "Neuroimaging Evidence for Cannabinoid Modulation of Cognition and Affect in Man". Frontiers in Behavioral Neuroscience. 6. doi:10.3389/fnbeh.2012.00022. ISSN 1662-5153. 
  79. ↑ Roberto, Aaron J.; Lorenzo, Aileen; Li, Kevin J.; Young, Jonathan; Mohan, Abhishek; Pinnaka, Subhash; Lapidus, Kyle A. B. (2016). "First-Episode of Synthetic Cannabinoid-Induced Psychosis in a Young Adult, Successfully Managed with Hospitalization and Risperidone". Case Reports in Psychiatry. 2016: 1–4. doi:10.1155/2016/7257489. ISSN 2090-682X. 
Retrieved from ‘https://psychonautwiki.org/w/index.php?title=Cognitive_suppressions&oldid=154018’