Cognitive depressions

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Cognitive depressions are defined as any subjective effect which decreases or lowers the intensity of a facet of a person's cognition in a manner that could be generally considered dysfunctional. For a broad overview, consider reading the depression and depression reduction effects.

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

Amnesia

Main article: Amnesia

Amnesia is defined as 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.

Analysis depression

Main article: Analysis depression

Analysis depression is defined as a distinct decrease in a person's overall ability to process information[10][11][12] and logically or creatively analyze concepts, ideas, and scenarios.[13] The experience of this effect leads to significant difficulty contemplating or understanding basic ideas in a manner which can temporarily prevent normal cognitive functioning.

Analysis suppression is often accompanied by other coinciding effects such as sedation, thought deceleration, and emotion suppression. It is most commonly induced under the influence of heavy dosages of antipsychotic compounds,[10][11][13] and is associated with long term use of such drugs[14] like quetiapine, haloperidol, and risperidone. However, it can also occur in a less consistent form under the influence of heavy dosages of dissociatives, cannabinoids,[12] and GABAergic depressants[15].

Cognitive fatigue

Main article: Cognitive fatigue

Cognitive fatigue (also called exhaustion, tiredness, lethargy, languidness, languor, lassitude, and listlessness) is medically recognized as a state usually associated with a weakening or depletion of one's mental resources.[16][17] The intensity and duration of this effect typically depends on the substance consumed and its dosage. It can also be further exacerbated by various factors such as a lack of sleep[18] or food[19]. These feelings of exhaustion involve a wide variety of symptoms which generally include some or all of the following effects:

Cognitive fatigue is most commonly induced under the influence of moderate dosages of antipsychotic compounds,[20][21] such as quetiapine, haloperidol, and risperidone. However, it can also occur during the withdrawal symptoms of many depressants,[22] and during the offset of many stimulants[23].

Confusion

Main article: Confusion

Confusion is defined as an impairment of abstract thinking demonstrated by an inability to think with one’s customary clarity and coherence.[24] Within the context of substance use, it is commonly experienced as a persistent inability to grasp or comprehend concepts and situations which would otherwise be perfectly understandable during sobriety. The intensity of this effect seems to to be further increased with unfamiliarity[25] in either setting or substance ingested.

Confusion is often accompanied by other coinciding effects such as delirium, delusions, and short term memory suppression in a manner which further increases the person's lack of comprehension. It is most commonly induced under the influence of heavy dosages of hallucinogenic compounds, such as psychedelics,[26] dissociatives,[27] synthetic cannabinoids,[28] and deliriants.[29] However, it can also occur to a lesser extent under the influence of heavy dosages of benzodiazepines[30] and antipsychotics[29].

Delirium

Main article: Delirium

Delirium (also known as acute confusion)[31] is medically recognized as a physiological disturbance of awareness that is accompanied by a change in baseline cognition which cannot be better explained by a preexisting or evolving neurocognitive disorder.[32] The disturbance in awareness is manifested by a reduced ability to direct, focus, sustain, and shift attention and the accompanying cognitive change in at least one other area may include memory and learning (particularly recent memory), disorientation (particularly to time and place), alteration in language, or perceptual distortions or a perceptual-motor disturbance. The perceptual disturbances accompanying delirium include misinterpretations, illusions, or hallucinations; these disturbances are typically visual but may occur in other modalities as well, and range from simple and uniform to highly complex. An individual with delirium may also exhibit emotional disturbances, such as anxiety, fear, depression, irritability, anger, euphoria, and apathy with rapid and unpredictable shifts from one emotional state to another.[33]

This disturbance develops over a short period of time, usually hours to a few days, and tends to fluctuate during the course of the day, often with worsening in the evening and night when external orienting stimuli decrease. It has been proposed that a core criterion for delirium is a disturbance in the sleep-wake cycle. Normal attention/arousal, delirium, and coma lie on a continuum, with coma defined as the lack of any response to verbal stimuli.[33]

Delirium may present itself in three distinct forms. These are referred to in the scientific literature as hyperactive, hypoactive, or mixed forms.[34] In its hyperactive form, it is manifested as severe confusion and disorientation, with a sudden onset and a fluctuating intensity. In its hypoactive (i.e. underactive) form, it is manifested by an equally sudden withdrawal from interaction with the outside world accompanied by symptoms such as drowsiness and general inactivity.[35] Delirium may also occur in a mixed type in which one can fluctuate between both hyper and hypoactive periods.

Delirium is most commonly induced under the influence of heavy dosages of deliriant compounds, such as DPH,[36] datura,[37] and benzydamine. However, it can also occur as a result of an extremely wide range of health problems such as urinary tract infections,[38] influenza,[39] and alzheimer’s.[40]

Creativity depression

Main article: Creativity depression

Creativity depression is defined as a decrease in both a person's motivation and capabilities when performing tasks that involve producing artistic output or novel problem-solving.[41] This effect may be particularly frustrating to deal with for artists of any sort as it will induce a temporary creative block.

Although creative subjects paradoxically more often have a history of depression than the average, their creative work is not done during their depressions, but in rebound periods of increased energy between depressions.[41][42]

Creativity suppression is often accompanied by other coinciding effects such as depression,[43] anxiety, and emotion suppression in a manner which further decreases the person's creative abilities.[41] It is most commonly induced under the influence of moderate dosages of antipsychotics.[41][44][45] However, it can also occur due to SSRI's[46] and during the withdrawal symptoms of any dopaminergic compound.[45]

Language depression

Main article: Language depression

Language depression (also known as aphasia) is medically recognized as the decreased ability to use and understand speech.[47] This creates the feeling of finding it difficult or even impossible to vocalize one's own thoughts and to process the speech of others. However, the ability to speak and to process the speech of others doesn't necessarily become suppressed simultaneously; a person may find themselves unable to formulate a coherent sentence while still being able to perfectly understand the speech of others.

Generally, this effect can be divided into four broad categories:[47]

  1. Expressive (also called Broca's aphasia): difficulty in conveying thoughts through speech or writing. The person knows what she/he wants to say, but cannot find the words he needs. For example, a person with Broca's aphasia may say, "Walk dog," meaning, "I will take the dog for a walk," or "book book two table," for "There are two books on the table."
  2. Receptive (Wernicke's aphasia): difficulty understanding spoken or written language. The individual hears the voice or sees the print but cannot make sense of the words. These people may speak in long, complete sentences that have no meaning, adding unnecessary words and even creating made-up words. For example, "You know that smoodle pinkered and that I want to get him round and take care of him like you want before." As a result, it is often difficult to follow what the person is trying to say and the speakers are often unaware of their spoken mistakes.
  3. Global: People lose almost all language function, both comprehension and expression. They cannot speak or understand speech, nor can they read or write. This results from severe and extensive damage to the language areas of the brain. They may be unable to say even a few words or may repeat the same words or phrases over and over again.
  4. Anomic (or amnesiac): the least severe form of aphasia; people have difficulty in using the correct names for particular objects, people, places, or events.

Language suppression is often accompanied by other coinciding effects such as analysis depression and thought disorganization. It is most commonly induced under the influence of heavy dosages of antipsychotic compounds, such as quetiapine,[48] haloperidol,[49] and risperidone.[50] However, it can also occur in a less consistent form under the influence of extremely heavy dosages of hallucinogenic compounds such as psychedelics,[51] dissociatives,[51][52] and deliriants.[53] This is far more likely to occur when the person is inexperienced with that particular hallucinogen.

Motivation depression

Main article: Motivation depression

Motivation depression (also known as avolition or amotivation)[54] is defined as a decreased desire to initiate or persist in goal-directed behavior.[55][56] Motivation depression prevents an individual the ability to sustain the rewarding value of an action into an uncertain future; this includes tasks deemed challenging or unpleasant, such as working, studying, cleaning, and doing general chores. At its higher levels, motivation depression can cause one to lose their desire to engage in any activities, even the ones that would usually be considered entertaining or rewarding to the user. This effect can lead onto severe states of boredom and even mild depression when experienced at a high level of intensity for prolonged periods of time.

Motivation suppression is often accompanied by other coinciding effects such as sedation and thought deceleration. It is most commonly induced under the influence of an acute dosage of an antipsychotic compound, such as quetiapine, haloperidol, and risperidone.[57][58] However, it is worth noting that chronic treatment with any dose of antipsychotic medication does not cause this effect.[54] It can also occur under the influence of heavy dosages of cannabinoids[59] and benzodiazepines, as a result of long-term SSRI usage,[60] during the offset of stimulants, and during the withdrawal symptoms of almost any compound.

Thought disorganization

Main article: Thought disorganization

Thought disorganization is defined as a state in which one's ability to analyze and categorize conceptual information using a systematic and logical thought process is considerably decreased. It seemingly occurs through an increase in thoughts which are unrelated or irrelevant to the topic at hand, thus decreasing one's capacity for a structured and cohesive thought stream. This effect also seems to allow the user to hold a significantly lower amount of relevant information in their train of thought which can be useful for extended mental calculations, articulating ideas, and analyzing logical arguments.

Thought disorganization is often accompanied by other coinciding effects such as analysis depression and thought acceleration. It is most commonly induced under the influence of heavy dosages of hallucinogenic and depressant compounds, such as dissociatives,[61][62][63][64] psychedelics,[61][65] cannabinoids,[61][66][67] and GABAergics.[68][69] However, it is worth noting that the same stimulant or nootropics compounds which induce thought organization at lower dosages, can also often result in the opposite effect of thought disorganization at their higher dosages.[61][69][70][71]

See also

References

  1. ↑ Squire, L. R.; Zola, S. M. (1997). "Amnesia, memory and brain systems". Philosophical Transactions of the Royal Society B: Biological Sciences. 352 (1362): 1663–1673. doi:10.1098/rstb.1997.0148. ISSN 0962-8436. 
  2. ↑ Veselis, R. A., Reinsel, R. A., Feshchenko, V. A. (1 October 2001). "Drug-induced Amnesia Is a Separate Phenomenon from Sedation". Anesthesiology. 95 (4): 896–907. doi:10.1097/00000542-200110000-00018. ISSN 0003-3022. 
  3. ↑ Hartzler, Bryan; Fromme, Kim (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. doi:10.15288/jsa.2003.64.547. ISSN 0096-882X. 
  4. ↑ White, A. M., Signer, M. L., Kraus, C. L., Swartzwelder, H. S. (1 January 2004). "Experiential Aspects of Alcohol‐Induced Blackouts Among College Students". The American Journal of Drug and Alcohol Abuse. 30 (1): 205–224. doi:10.1081/ADA-120029874. 
  5. ↑ Goodwin, Donald W.; Crane, J. Bruce; Guze, Samuel B. (1969). "Alcoholic "Blackouts": A Review and Clinical Study of 100 Alcoholics". American Journal of Psychiatry. 126 (2): 191–198. doi:10.1176/ajp.126.2.191. ISSN 0002-953X. 
  6. ↑ Lee, Hamin; Roh, Sungwon; Kim, Dai Jin (2009). "Alcohol-Induced Blackout". International Journal of Environmental Research and Public Health. 6 (11): 2783–2792. doi:10.3390/ijerph6112783. ISSN 1660-4601. 
  7. ↑ Mejo, S. L. (October 1992). "Anterograde Amnesia Linked to Benzodiazepines:". The Nurse Practitioner. 17 (10): 44–50. doi:10.1097/00006205-199210000-00013. ISSN 0361-1817. 
  8. ↑ Barker, Judith C.; Harris, Shana L.; Dyer, Jo E. (2007). "Experiences of Gamma Hydroxybutyrate (GHB) Ingestion: A Focus Group Study". Journal of Psychoactive Drugs. 39 (2): 115–129. doi:10.1080/02791072.2007.10399870. ISSN 0279-1072. 
  9. ↑ Canaday, B. R. (August 1996). "Amnesia possibly associated with zolpidem administration". Pharmacotherapy. 16 (4): 687–689. ISSN 0277-0008. 
  10. ↑ 10.0 10.1 Knowles, Emma E.M.; David, Anthony S.; Reichenberg, Abraham (2010). "Processing Speed Deficits in Schizophrenia: Reexamining the Evidence". American Journal of Psychiatry. 167 (7): 828–835. doi:10.1176/appi.ajp.2010.09070937. ISSN 0002-953X. 
  11. ↑ 11.0 11.1 Takeuchi, H.; Suzuki, T.; Remington, G.; Bies, R. R.; Abe, T.; Graff-Guerrero, A.; Watanabe, K.; Mimura, M.; Uchida, H. (2013). "Effects of Risperidone and Olanzapine Dose Reduction on Cognitive Function in Stable Patients With Schizophrenia: An Open-Label, Randomized, Controlled, Pilot Study". Schizophrenia Bulletin. 39 (5): 993–998. doi:10.1093/schbul/sbt090. ISSN 0586-7614. 
  12. ↑ 12.0 12.1 Fried, P; Watkinson, B; Gray, R (2005). "Neurocognitive consequences of marihuana—a comparison with pre-drug performance". Neurotoxicology and Teratology. 27 (2): 231–239. doi:10.1016/j.ntt.2004.11.003. ISSN 0892-0362. 
  13. ↑ 13.0 13.1 Kawai, Nobutoshi; Yamakawa, Yuriko; Baba, Atsuomi; Nemoto, Kiyotaka; Tachikawa, Hirokazu; Hori, Takafumi; Asada, Takashi; Iidaka, Tetsuya (2006). "High-dose of multiple antipsychotics and cognitive function in schizophrenia: The effect of dose-reduction". Progress in Neuro-Psychopharmacology and Biological Psychiatry. 30 (6): 1009–1014. doi:10.1016/j.pnpbp.2006.03.013. ISSN 0278-5846. 
  14. ↑ Husa, Anja P.; Moilanen, Jani; Murray, Graham K.; Marttila, Riikka; Haapea, Marianne; Rannikko, Irina; Barnett, Jennifer H.; Jones, Peter B.; Isohanni, Matti; Remes, Anne M.; Koponen, Hannu; Miettunen, Jouko; Jääskeläinen, Erika (2017). "Lifetime antipsychotic medication and cognitive performance in schizophrenia at age 43 years in a general population birth cohort". Psychiatry Research. 247: 130–138. doi:10.1016/j.psychres.2016.10.085. ISSN 0165-1781. 
  15. ↑ Paraherakis, Antonios; Charney, Dara A.; Gill, Kathryn (2009). "NEUROPSYCHOLOGICAL FUNCTIONING IN SUBSTANCE-DEPENDENT PATIENTS". Substance Use & Misuse. 36 (3): 257–271. doi:10.1081/JA-100102625. ISSN 1082-6084. 
  16. ↑ "Glossary of Technical Terms". Diagnostic and statistical manual of mental disorders (5th ed.): 821. 2013. doi:10.1176/appi.books.9780890425596.GlossaryofTechnicalTerms. 
  17. ↑ Mizuno, Kei; Tanaka, Masaaki; Yamaguti, Kouzi; Kajimoto, Osami; Kuratsune, Hirohiko; Watanabe, Yasuyoshi (2011). "Mental fatigue caused by prolonged cognitive load associated with sympathetic hyperactivity". Behavioral and Brain Functions. 7 (1): 17. doi:10.1186/1744-9081-7-17. ISSN 1744-9081. 
  18. ↑ Alhola, P., & Polo-Kantola, P. (2007). Sleep deprivation: Impact on cognitive performance. Neuropsychiatric disease and treatment. https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2656292/
  19. ↑ Kim, Jin Young; Kang, Seung Wan (2017). "Relationships between Dietary Intake and Cognitive Function in Healthy Korean Children and Adolescents". Journal of Lifestyle Medicine. 7 (1): 10–17. doi:10.15280/jlm.2017.7.1.10. ISSN 2234-8549. 
  20. ↑ Seo, Rubo J.; MacPherson, Holly; Young, Allan H. (2010). "Atypical Antipsychotics and Other Therapeutic Options for Treatment of Resistant Major Depressive Disorder". Pharmaceuticals. 3 (12): 3522–3542. doi:10.3390/ph3123522. ISSN 1424-8247. 
  21. ↑ Wittkampf, Laura Christina; Arends, Johannes; Timmerman, Leo; Lancel, Marike (2012). "A review of modafinil and armodafinil as add-on therapy in antipsychotic-treated patients with schizophrenia". Therapeutic Advances in Psychopharmacology. 2 (3): 115–125. doi:10.1177/2045125312441815. ISSN 2045-1253. 
  22. ↑ Chaudhuri, Abhijit; Behan, Peter O (2000). "Fatigue and basal ganglia". Journal of the Neurological Sciences. 179 (1-2): 34–42. doi:10.1016/S0022-510X(00)00411-1. ISSN 0022-510X. 
  23. ↑ Lago, Jesus A.; Kosten, Thomas R. (1994). "Stimulant withdrawal". Addiction. 89 (11): 1477–1481. doi:10.1111/j.1360-0443.1994.tb03746.x. ISSN 0965-2140. 
  24. ↑ Burns, A (2004). "Delirium". Journal of Neurology, Neurosurgery & Psychiatry. 75 (3): 362–367. doi:10.1136/jnnp.2003.023366. ISSN 0022-3050. 
  25. ↑ Sheehan, Peter W.; Lewis, Sue-Ellen (2016). "Subjects' Reports of Confusion in Consciousness and the Arousal of Imagery". Perceptual and Motor Skills. 38 (3): 731–734. doi:10.2466/pms.1974.38.3.731. ISSN 0031-5125. 
  26. ↑ Lu, Lin; Krebs, Teri S.; Johansen, Pål-Ørjan (2013). "Psychedelics and Mental Health: A Population Study". PLoS ONE. 8 (8): e63972. doi:10.1371/journal.pone.0063972. ISSN 1932-6203. 
  27. ↑ Mozayani, A. (January 2003). "Phencyclidine - Effects on Human Performance and Behavior". Forensic Science Review. 15 (1): 61–74. ISSN 1042-7201. 
  28. ↑ Chase, Peter B.; Hawkins, Jeff; Mosier, Jarrod; Jimenez, Ernest; Boesen, Keith; Logan, Barry K.; Walter, Frank G. (2015). "Differential physiological and behavioral cues observed in individuals smoking botanical marijuana versus synthetic cannabinoid drugs". Clinical Toxicology. 54 (1): 14–19. doi:10.3109/15563650.2015.1101769. ISSN 1556-3650. 
  29. ↑ 29.0 29.1 Kalisch Ellett, Lisa M.; Pratt, Nicole L.; Ramsay, Emmae N.; Barratt, John D.; Roughead, Elizabeth E. (2014). "Multiple Anticholinergic Medication Use and Risk of Hospital Admission for Confusion or Dementia". Journal of the American Geriatrics Society. 62 (10): 1916–1922. doi:10.1111/jgs.13054. ISSN 0002-8614. 
  30. ↑ Nicholson, Katherine L.; Balster, Robert L. (2001). "GHB: a new and novel drug of abuse". Drug and Alcohol Dependence. 63 (1): 1–22. doi:10.1016/S0376-8716(00)00191-5. ISSN 0376-8716. 
  31. ↑ Sendelbach, Sue; Guthrie, Patty Finch; Schoenfelder, Deborah Perry (2009). "Acute Confusion/Delirium". Journal of Gerontological Nursing. 35 (11): 11–18. doi:10.3928/00989134-20090930-01. ISSN 0098-9134. 
  32. ↑ "Delirium". International statistical classification of diseases and related health problems (11th ed.). 2022. Retrieved 20 May 2022. 
  33. ↑ 33.0 33.1 "Neurocognitive Disorders". Diagnostic and statistical manual of mental disorders (5th ed.): 596–602. 2013. doi:10.1176/appi.books.9780890425596.dsm17. 
  34. ↑ Fong, Tamara G.; Tulebaev, Samir R.; Inouye, Sharon K. (2009). "Delirium in elderly adults: diagnosis, prevention and treatment". Nature Reviews Neurology. 5 (4): 210–220. doi:10.1038/nrneurol.2009.24. ISSN 1759-4758. 
  35. ↑ Hosker, Christian; Ward, David (2017). "Hypoactive delirium". BMJ: j2047. doi:10.1136/bmj.j2047. ISSN 0959-8138. 
  36. ↑ Serio, Ryan N (2004). "Acute Delirium Associated with Combined Diphenhydramine and Linezolid Use". Annals of Pharmacotherapy. 38 (1): 62–65. doi:10.1345/aph.1D018. ISSN 1060-0280. 
  37. ↑ Hanna, J. P., Schmidley, J. W., Braselton, W. E. (April 1992). "Datura Delirium:". Clinical Neuropharmacology. 15 (2): 109–113. doi:10.1097/00002826-199204000-00004. ISSN 0362-5664. 
  38. ↑ Balogun, Seki A.; Philbrick, John T. (2014). "Delirium, a Symptom of UTI in the Elderly: Fact or Fable? A Systematic Review*". Canadian Geriatrics Journal. 17 (1). doi:10.5770/cgj.17.90. ISSN 1925-8348. 
  39. ↑ Manjunatha, Narayana; Math, SureshBada; Kulkarni, GirishBaburao; Chaturvedi, SantoshKumar (2011). "The neuropsychiatric aspects of influenza/swine flu: A selective review". Industrial Psychiatry Journal. 20 (2): 83. doi:10.4103/0972-6748.102479. ISSN 0972-6748. 
  40. ↑ Lerner, A. J., Hedera, P., Koss, E., Stuckey, J., Friedland, R. P. (March 1997). "Delirium in Alzheimer Disease:". Alzheimer Disease & Associated Disorders. 11 (1): 16–20. doi:10.1097/00002093-199703000-00004. ISSN 0893-0341. 
  41. ↑ 41.0 41.1 41.2 41.3 Flaherty, Alice W. (2005). "Frontotemporal and dopaminergic control of idea generation and creative drive". The Journal of Comparative Neurology. 493 (1): 147–153. doi:10.1002/cne.20768. ISSN 0021-9967. 
  42. ↑ Jamison, K. R. (1989). Mood disorders and patterns of creativity in British writers and artists. Psychiatry, 52(2), 125-134. https://www.ncbi.nlm.nih.gov/pubmed/2734415/
  43. ↑ von Hecker, Ulrich; Meiser, Thorsten (2005). "Defocused Attention in Depressed Mood: Evidence From Source Monitoring". Emotion. 5 (4): 456–463. doi:10.1037/1528-3542.5.4.456. ISSN 1931-1516. 
  44. ↑ 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. 
  45. ↑ 45.0 45.1 Szmulewicz, Alejandro; Samamé, Cecilia; Caravotta, Pablo; Martino, Diego J.; Igoa, Ana; Hidalgo-Mazzei, Diego; Colom, Francesc; Strejilevich, Sergio A. (2016). "Behavioral and emotional adverse events of drugs frequently used in the treatment of bipolar disorders: clinical and theoretical implications". International Journal of Bipolar Disorders. 4 (1). doi:10.1186/s40345-016-0047-3. ISSN 2194-7511. 
  46. ↑ 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. 
  47. ↑ 47.0 47.1 What Is Aphasia? — Types, Causes and Treatment, National Institute on Deafness and Other Communication Disorders (NIDCD) 
  48. ↑ Chien, Ching-Fang; Huang, Poyin; Hsieh, Sun-Wung (2017). "Reversible global aphasia as a side effect of quetiapine: a case report and literature review". Neuropsychiatric Disease and Treatment. Volume 13: 2257–2260. doi:10.2147/NDT.S141273. ISSN 1178-2021. 
  49. ↑ Iqbal, M. M., Aneja, A., Rahman, A., Megna, J., Freemont, W., Shiplo, M., Nihilani, N., Lee, K. (August 2005). "The Potential Risks of Commonly Prescribed Antipsychotics". Psychiatry (Edgmont). 2 (8): 36–44. ISSN 1550-5952. 
  50. ↑ Sinha, Preeti; Vandana, V.P.; Lewis, Nikita Vincent; Jayaram, M.; Enderby, Pamela (2015). "Evaluating the effect of risperidone on speech: A cross-sectional study". Asian Journal of Psychiatry. 15: 51–55. doi:10.1016/j.ajp.2015.05.005. ISSN 1876-2018. 
  51. ↑ 51.0 51.1 Dell'Erba, Sara; Brown, David J.; Proulx, Michael J. (2018). "Synesthetic hallucinations induced by psychedelic drugs in a congenitally blind man". Consciousness and Cognition. 60: 127–132. doi:10.1016/j.concog.2018.02.008. ISSN 1053-8100. 
  52. ↑ Kjellgren, Anette; Jonsson, Kristoffer (2013). "Methoxetamine (MXE) – A Phenomenological Study of Experiences Induced by a "Legal High" from the Internet". Journal of Psychoactive Drugs. 45 (3): 276–286. doi:10.1080/02791072.2013.803647. ISSN 0279-1072. 
  53. ↑ Nguyen, Huy TV; Juurlink, David N (2004). "Recurrent Ibuprofen-Induced Aseptic Meningitis". Annals of Pharmacotherapy. 38 (3): 408–410. doi:10.1345/aph.1D329. ISSN 1060-0280. 
  54. ↑ 54.0 54.1 Fervaha, Gagan; Takeuchi, Hiroyoshi; Lee, Jimmy; Foussias, George; Fletcher, Paul J; Agid, Ofer; Remington, Gary (2015). "Antipsychotics and Amotivation". Neuropsychopharmacology. 40 (6): 1539–1548. doi:10.1038/npp.2015.3. ISSN 0893-133X. 
  55. ↑ Lee, Jung; Jung, Suwon; Park, Il; Kim, Jae-Jin (2015). "Neural Basis of Anhedonia and Amotivation in Patients with Schizophrenia: The Role of Reward System". Current Neuropharmacology. 13 (6): 750–759. doi:10.2174/1570159X13666150612230333. ISSN 1570-159X. 
  56. ↑ Barch, D. M.; Dowd, E. C. (2010). "Goal Representations and Motivational Drive in Schizophrenia: The Role of Prefrontal-Striatal Interactions". Schizophrenia Bulletin. 36 (5): 919–934. doi:10.1093/schbul/sbq068. ISSN 0586-7614. 
  57. ↑ 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. 
  58. ↑ Saeedi, H; Remington, G; Christensen, B (2006). "Impact of haloperidol, a dopamine D2 antagonist, on cognition and mood". Schizophrenia Research. 85 (1-3): 222–231. doi:10.1016/j.schres.2006.03.033. ISSN 0920-9964. 
  59. ↑ Lawn, Will; Freeman, Tom P; Pope, Rebecca A; Joye, Alyssa; Harvey, Lisa; Hindocha, Chandni; Mokrysz, Claire; Moss, Abigail; Wall, Matthew B; Bloomfield, Michael AP; Das, Ravi K; Morgan, Celia JA; Nutt, David J; Curran, H Valerie (2016). "Acute and chronic effects of cannabinoids on effort-related decision-making and reward learning: an evaluation of the cannabis 'amotivational' hypotheses". Psychopharmacology. 233 (19-20): 3537–3552. doi:10.1007/s00213-016-4383-x. ISSN 0033-3158. 
  60. ↑ Starcevic, Vladan (2014). "The reappraisal of benzodiazepines in the treatment of anxiety and related disorders". Expert Review of Neurotherapeutics. 14 (11): 1275–1286. doi:10.1586/14737175.2014.963057. ISSN 1473-7175. 
  61. ↑ 61.0 61.1 61.2 61.3 Murray, Robin M.; Morrison, Paul D.; Di Forti, Marta; Paparelli, Alessandra (2011). "Drug-Induced Psychosis: How to Avoid Star Gazing in Schizophrenia Research by Looking at More Obvious Sources of Light". Frontiers in Behavioral Neuroscience. 5. doi:10.3389/fnbeh.2011.00001. ISSN 1662-5153. 
  62. ↑ Flohr, H., Glade, U., Motzko, D. (1998). "The neural correlate of consciousness and the mechanisms of general anaesthesia". Toxicology Letters. 100: 23–29. 
  63. ↑ Flohr, H.; Glade, U.; Motzko, D. (1998). "The role of the NMDA synapse in general anesthesia". Toxicology Letters. 100-101: 23–29. doi:10.1016/S0378-4274(98)00161-1. ISSN 0378-4274. 
  64. ↑ Lahti, A (2001). "Effects of Ketamine in Normal and Schizophrenic Volunteers". Neuropsychopharmacology. 25 (4): 455–467. doi:10.1016/S0893-133X(01)00243-3. ISSN 0893-133X. 
  65. ↑ Winkelman, Michael J. (2017). "The Mechanisms of Psychedelic Visionary Experiences: Hypotheses from Evolutionary Psychology". Frontiers in Neuroscience. 11. doi:10.3389/fnins.2017.00539. ISSN 1662-453X. 
  66. ↑ D’Souza, Deepak Cyril; Sewell, Richard Andrew; Ranganathan, Mohini (2009). "Cannabis and psychosis/schizophrenia: human studies". European Archives of Psychiatry and Clinical Neuroscience. 259 (7): 413–431. doi:10.1007/s00406-009-0024-2. ISSN 0940-1334. 
  67. ↑ Radhakrishnan, Rajiv; Wilkinson, Samuel T.; D’Souza, Deepak Cyril (2014). "Gone to Pot â€" A Review of the Association between Cannabis and Psychosis". Frontiers in Psychiatry. 5. doi:10.3389/fpsyt.2014.00054. ISSN 1664-0640. 
  68. ↑ Bennett, W. R. Murray; Wilson, Lawrence G.; Roy-Byrne, Peter P. (2007). "Gamma-Hydroxybutyric Acid (GHB) Withdrawal: A Case Report". Journal of Psychoactive Drugs. 39 (3): 293–296. doi:10.1080/02791072.2007.10400616. ISSN 0279-1072. 
  69. ↑ 69.0 69.1 Tsuang, Ming T. (1982). "Subtypes of Drug Abuse With Psychosis". Archives of General Psychiatry. 39 (2): 141. doi:10.1001/archpsyc.1982.04290020013003. ISSN 0003-990X. 
  70. ↑ Angrist, Burton; Thompson, Hyacinth; Shopsin, Baron; Gershon, Samuel (1975). "Clinical studies with dopamine-receptor stimulants". Psychopharmacologia. 44 (3): 273–280. doi:10.1007/BF00428906. ISSN 0033-3158. 
  71. ↑ Krystal, John H.; Perry, Edward B.; Gueorguieva, Ralitza; Belger, Aysenil; Madonick, Steven H.; Abi-Dargham, Anissa; Cooper, Thomas B.; MacDougall, Lisa; Abi-Saab, Walid; D’Souza, D. Cyril (2005). "Comparative and Interactive Human Psychopharmacologic Effects of Ketamine and Amphetamine". Archives of General Psychiatry. 62 (9): 985. doi:10.1001/archpsyc.62.9.985. ISSN 0003-990X. 
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