Cognitive suppressions - PsychonautWiki

Cognitive suppressions

Cognitive suppressions are defined as any subjective effect which decreases or lowers the intensity of a facet of a person's cognition.

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]


In terms of psychedelics, this effect seems to be primarily triggered by the psychological self-reflection that can manifest through a combination of effects. These primarily include analysis enhancement, personal bias suppression, and introspection. The intensity and effectiveness of this experience occurring under the influence of a psychedelic is unpredictable and depends on a variety of factors such as dosage, setting, state of mind, and a general willingness to change.

In comparison, N-acetylcysteine and a small number of other compounds seem to suppress feelings of addiction in a more direct and consistent manner. This is thought to occur as a result of their action on glutaminergic and dopaminergic pathways which may reverse brain functions that have become disturbed by heavy drug addiction.[5][6][7] This mechanism has been shown to provide relief for those who struggle with compulsive redosing, reward behaviors, and psychological cravings, and has been shown to positively reverse nicotine addiction,[8] cocaine addiction,[9] marijuana dependence,[10] and many other compulsive behaviors.[11] However, it is worth noting that NAC's addiction suppression qualities typically only manifest themselves while the person is still under the influence of the drug and do not seem to last beyond that.


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.[12] 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.[13] 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.[14] 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.[15] 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.[16]

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,[17] benzodiazepines,[18] GHB,[19] and zolpidem[20]. 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 suppression

Main article: Analysis suppression

Analysis suppression is defined as a distinct decrease in a person's overall ability to process information[21][22][23] and logically or creatively analyze concepts, ideas, and scenarios.[24] 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,[21][22][24] and is associated with long term use of such drugs[25] like quetiapine, haloperidol, and risperidone. However, it can also occur in a less consistent form under the influence of heavy dosages of dissociatives, cannabinoids,[23] and GABAergic depressants[26].

Anxiety suppression

Main article: Anxiety suppression

Anxiety suppression (also known as anxiolysis or minimal sedation)[27] 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.[28] The experience of this effect may decrease anxiety-related behaviours such as restlessness, muscular tension,[29] rumination, and panic attacks. This typically results in feelings of extreme calmness and relaxation.

Anxiety suppression is often accompanied by other coinciding effects such as disinhibition and sedation. It is most commonly induced under the influence of moderate dosages of anxiolytic compounds which primarily include GABAergic depressants,[30][31] such as benzodiazepines,[32] alcohol,[33] GHB,[34] and gabapentinoids[35]. 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,[36] dissociatives,[37] SSRIs, and opioids.

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.[38][39] 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[40] or food[41]. 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,[42][43] such as quetiapine, haloperidol, and risperidone. However, it can also occur during the withdrawal symptoms of many depressants,[44] and during the offset of many stimulants[45].


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.[46] 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[47] 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,[48] dissociatives,[49] synthetic cannabinoids,[50] and deliriants.[51] However, it can also occur to a lesser extent under the influence of heavy dosages of benzodiazepines[52] and antipsychotics[51].

Creativity suppression

Creativity suppression 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.[53] 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.[53][54]

Creativity suppression is often accompanied by other coinciding effects such as depression,[55] anxiety, and emotion suppression in a manner which further decreases the person's creative abilities.[53] It is most commonly induced under the influence of moderate dosages of antipsychotics.[53][56][57] However, it can also occur due to SSRI's[58] and during the withdrawal symptoms of any dopaminergic compound.[57]


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.[46] 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[47] 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,[48] dissociatives,[59] synthetic cannabinoids,[50] and deliriants.[51] However, it can also occur to a lesser extent under the influence of heavy dosages of benzodiazepines[52] and antipsychotics[51].


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.[60][61][62] 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,[63] benzodiazepines,[64] phenibut, and GHB. However, it may also occur under the influence of certain stimulants,[65] entactogens,[66] and dissociatives[67].

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[68] and most types of antidepressants[69][70][71]. This is due to the way in which they increase REM latency, decrease REM sleep, reduce total sleep time and efficiency, and increase wakefulness.[68][69][70][72] REM sleep is where the majority of dreams occur.[73]

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.[74][75][76] 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).[77]

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.[74][56] However, it can also occur in less consistent form under the influence of heavy dosages of dissociatives,[78][79] SSRI's,[77][58] and GABAergic depressants[80].

Focus suppression

Main article: Focus suppression

Focus suppression (also known as distractability[81]) is medically recognized as a decreased ability to selectively concentrate on an aspect of the environment while ignoring other things.[82][83] 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.[84] This effect will often synergize with other coinciding effects such as motivation suppression, thought deceleration, and sedation.[85]

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,[86] benzodiazepines, cannabinoids,[85] 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.[87]

Language suppression

Main article: Language suppression

Language suppression (also known as aphasia) is medically recognized as the decreased ability to use and understand speech.[88] 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:[88]

  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 suppression and thought deceleration. It is most commonly induced under the influence of heavy dosages of antipsychotic compounds, such as quetiapine,[89] haloperidol,[90] and risperidone.[91] However, it can also occur in a less consistent form under the influence of extremely heavy dosages of hallucinogenic compounds such as psychedelics,[92] dissociatives,[92][93] and deliriants.[94] This is far more likely to occur when the person is inexperienced with that particular hallucinogen.

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.[95][96][97] 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.[98]

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.

Ego death

The most significant aspect of complete long-term memory suppression (level 4) is the way in which it suppresses the ability to recall and comprehend conceptual information associated with one's sense of self-hood and identity. The experience of this is colloquially known as ego death and its occurrence is well documented throughout the modern psychonaut subculture. However, it is worth noting that this informal term of "ego death" or "ego dissolution" is also commonly used to refer to states of high level unity and interconnectedness.[95][99]

Complete memory suppression can result in the profound experience that despite remaining fully conscious, there is no longer an “I” experiencing one's sensory input; there is just the sensory input as it is and by itself. This suppresses the otherwise nearly constant sensation in waking life of being a separate observer interacting with an external world. Although ego death does not necessarily shut down awareness of all mental processes, it does remove the feeling of being the thinker or cause of one's mental processes. It often results in the feeling of processing concepts from a neutral perspective completely untainted by past memories, prior experiences, contexts, and biases.

Ego death often synergizes with other coinciding effects such as personal bias suppression, unity and interconnectedness, spirituality enhancement, and delusions.[95][97] These accompanying effects further elevate the subjective intensity and transpersonal significance of ego death experiences.[96]

Motivation suppression

Motivation suppression (also known as avolition or amotivation)[100] is defined as a decreased desire to initiate or persist in goal-directed behavior.[101][102] Motivation suppression 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 suppression 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.[103][104] However, it is worth noting that chronic treatment with any dose of antipsychotic medication does not cause this effect.[100] It can also occur under the influence of heavy dosages of cannabinoids[105] and benzodiazepines, as a result of long-term SSRI usage,[106] during the offset of stimulants, and during the withdrawal symptoms of almost any compound.

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.[107]

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.[107] 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.


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.[108][109][110] This state is independent of a circadian rhythm;[108] 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,[111] GABAergic depressants,[112][113] opioids,[114] antipsychotics,[115][103] some antihistamines,[116] 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

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,[117][118] while its withdrawals increases suggestibility.[119] 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.[117][118][119]

Suggestibility suppression is often accompanied by other coinciding effects such as irritability[117] and ego inflation. It is most commonly induced under the influence of GABAergic depressants.[117][118][119]

Thought deceleration

Main article: Thought deceleration

Thought deceleration (also known as bradyphrenia)[120] 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,[121][122][123] antipsychotics,[124] and opioids.[125][126][127] However, it can also occur to a lesser extent under the influence of heavy dosages of hallucinogens such as psychedelics,[128] dissociatives,[129] deliriants,[123][130] and cannabinoids.[131][132][133][134]

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 suppression and thought acceleration. It is most commonly induced under the influence of heavy dosages of hallucinogenic and depressant compounds, such as dissociatives,[135][136][137][138] psychedelics,[135][139] cannabinoids,[135][140][141] and GABAergics.[142][143] 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.[135][143][144][145]

See also



  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. 5.0 5.1 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. Pettorruso, Mauro; De Risio, Luisa; Martinotti, Giovanni; Di Nicola, Marco; Ruggeri, Filippo; Conte, Gianluigi; Di Giannantonio, Massimo; Janiri, Luigi (2014). "Targeting the Glutamatergic System to Treat Pathological Gambling: Current Evidence and Future Perspectives". BioMed Research International. 2014: 1–11. doi:10.1155/2014/109786. ISSN 2314-6133. 
  7. Reissner, Kathryn J.; Kalivas, Peter W. (2010). "Using glutamate homeostasis as a target for treating addictive disorders". Behavioural Pharmacology. 21 (5-6): 514–522. doi:10.1097/FBP.0b013e32833d41b2. ISSN 0955-8810. 
  8. Knackstedt, Lori A.; LaRowe, Steven; Mardikian, Pascale; Malcolm, Robert; Upadhyaya, Himanshu; Hedden, Sarra; Markou, Athina; Kalivas, Peter W. (2009). "The Role of Cystine-Glutamate Exchange in Nicotine Dependence in Rats and Humans". Biological Psychiatry. 65 (10): 841–845. doi:10.1016/j.biopsych.2008.10.040. ISSN 0006-3223. 
  9. LaRowe, Steven D.; Mardikian, Pascale; Malcolm, Robert; Myrick, Hugh; Kalivas, Peter; McFarland, Krista; Saladin, Michael; McRae, Aimee; Brady, Kathleen (2006). "Safety and Tolerability of N-Acetylcysteine in Cocaine-Dependent Individuals". American Journal on Addictions. 15 (1): 105–110. doi:10.1080/10550490500419169. ISSN 1055-0496. 
  10. Gray, Kevin M.; Watson, Noreen L.; Carpenter, Matthew J.; LaRowe, Steven D. (2010). "N-Acetylcysteine (NAC) in Young Marijuana Users: An Open-Label Pilot Study". The American Journal on Addictions. 19 (2): 187–189. doi:10.1111/j.1521-0391.2009.00027.x. ISSN 1055-0496. 
  11. Kalivas, Peter W.; LaLumiere, Ryan T.; Knackstedt, Lori; Shen, Haowei (2009). "Glutamate transmission in addiction". Neuropharmacology. 56: 169–173. doi:10.1016/j.neuropharm.2008.07.011. ISSN 0028-3908. 
  12. 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. 
  13. 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. 
  14. 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. 
  15. 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. 
  16. 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. 
  17. 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. 
  18. 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. 
  19. 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. 
  20. Canaday, B. R. (August 1996). "Amnesia possibly associated with zolpidem administration". Pharmacotherapy. 16 (4): 687–689. ISSN 0277-0008. 
  21. 21.0 21.1 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. 
  22. 22.0 22.1 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. 
  23. 23.0 23.1 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/ ISSN 0892-0362. 
  24. 24.0 24.1 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. 
  25. 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. 
  26. 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. 
  27. anxiolysis, National Cancer Institute 
  28. 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. 
  29. Tyrer, P. (27 February 1988). "Prescribing psychotropic drugs in general practice". BMJ. 296 (6622): 588–589. doi:10.1136/bmj.296.6622.588. 
  30. Lydiard, R. B. (2003). "The role of GABA in anxiety disorders". The Journal of Clinical Psychiatry. 64 Suppl 3: 21–27. ISSN 0160-6689. 
  31. 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. 
  32. 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. 
  33. 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. 
  34. 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. 
  35. 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. 
  36. 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. 
  37. 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. 
  38. "Glossary of Technical Terms". Diagnostic and statistical manual of mental disorders (5th ed.): 821. 2013. doi:10.1176/appi.books.9780890425596.GlossaryofTechnicalTerms. 
  39. 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. 
  40. Alhola, P., & Polo-Kantola, P. (2007). Sleep deprivation: Impact on cognitive performance. Neuropsychiatric disease and treatment.
  41. 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. 
  42. 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. 
  43. 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. 
  44. 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. 
  45. 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. 
  46. 46.0 46.1 Burns, A (2004). "Delirium". Journal of Neurology, Neurosurgery & Psychiatry. 75 (3): 362–367. doi:10.1136/jnnp.2003.023366. ISSN 0022-3050. 
  47. 47.0 47.1 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. 
  48. 48.0 48.1 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. 
  49. Mozayani, A. (January 2003). "Phencyclidine - Effects on Human Performance and Behavior". Forensic Science Review. 15 (1): 61–74. ISSN 1042-7201. 
  50. 50.0 50.1 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. 
  51. 51.0 51.1 51.2 51.3 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. 
  52. 52.0 52.1 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. 
  53. 53.0 53.1 53.2 53.3 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. 
  54. Jamison, K. R. (1989). Mood disorders and patterns of creativity in British writers and artists. Psychiatry, 52(2), 125-134.
  55. 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. 
  56. 56.0 56.1 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. 
  57. 57.0 57.1 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. 
  58. 58.0 58.1 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. 
  59. Mozayani, A. (January 2003). "Phencyclidine - Effects on Human Performance and Behavior". Forensic Science Review. 15 (1): 61–74. ISSN 1042-7201. 
  60. "Glossary of Technical Terms". Diagnostic and statistical manual of mental disorders (5th ed.): 820. 2013. doi:10.1176/appi.books.9780890425596.GlossaryofTechnicalTerms. 
  61. 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. 
  62. Källmén, Håkan; Gustafson, Roland (1998). "Alcohol and Disinhibition". European Addiction Research. 4 (4): 150–162. doi:10.1159/000018948. ISSN 1022-6877. 
  63. 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. 
  64. Paton, Carol (2018). "Benzodiazepines and disinhibition: a review". Psychiatric Bulletin. 26 (12): 460–462. doi:10.1192/pb.26.12.460. ISSN 0955-6036. 
  65. 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. 
  66. 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. 
  67. 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. 
  68. 68.0 68.1 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. 
  69. 69.0 69.1 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. 
  70. 70.0 70.1 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. 
  71. 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. 
  72. 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. 
  73. 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. 
  74. 74.0 74.1 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. 
  75. "Neurocognitive Disorders". Diagnostic and statistical manual of mental disorders (5th ed.): 609. 2013. doi:10.1176/appi.books.9780890425596.dsm17. 
  76. 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. 
  77. 77.0 77.1 Sansone, R. A., Sansone, L. A. (October 2010). "SSRI-Induced Indifference". Psychiatry (Edgmont (Pa.: Township)). 7 (10): 14–18. ISSN 1555-5194. 
  78. 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. 
  79. 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. 
  80. 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. 
  81. "Glossary of Technical Terms". Diagnostic and statistical manual of mental disorders (5th ed.): 820. 2013. doi:10.1176/appi.books.9780890425596.GlossaryofTechnicalTerms. 
  82. 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. 
  83. 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. 
  84. 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. 
  85. 85.0 85.1 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. 
  86. 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. 
  87. 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. 
  88. 88.0 88.1 What Is Aphasia? — Types, Causes and Treatment, National Institute on Deafness and Other Communication Disorders (NIDCD) 
  89. 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. 
  90. 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. 
  91. 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. 
  92. 92.0 92.1 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. 
  93. 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. 
  94. 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. 
  95. 95.0 95.1 95.2 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. 
  96. 96.0 96.1 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. 
  97. 97.0 97.1 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. 
  98. 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. 
  99. Nour, Matthew M.; Evans, Lisa; Nutt, David; Carhart-Harris, Robin L. (2016). "Ego-Dissolution and Psychedelics: Validation of the Ego-Dissolution Inventory (EDI)". Frontiers in Human Neuroscience. 10. doi:10.3389/fnhum.2016.00269. ISSN 1662-5161. 
  100. 100.0 100.1 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. 
  101. 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. 
  102. 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. 
  103. 103.0 103.1 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. 
  104. 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. 
  105. 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. 
  106. 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. 
  107. 107.0 107.1 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. 
  108. 108.0 108.1 "Glossary of Technical Terms". Diagnostic and statistical manual of mental disorders (5th ed.): 829. 2013. doi:10.1176/appi.books.9780890425596.GlossaryofTechnicalTerms. 
  109. 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. 
  110. 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. 
  111. 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. 
  112. 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. 
  113. 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. 
  114. 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. 
  115. 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. 
  116. 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. 
  117. 117.0 117.1 117.2 117.3 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. 
  118. 118.0 118.1 118.2 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. 
  119. 119.0 119.1 119.2 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. 
  120. 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. 
  121. 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. 
  122. 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. 
  123. 123.0 123.1 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. 
  124. 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. 
  125. 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. 
  126. 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. 
  127. 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. 
  128. 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. 
  129. 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. 
  130. 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. 
  131. 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. 
  132. 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. 
  133. 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. 
  134. 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. 
  135. 135.0 135.1 135.2 135.3 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. 
  136. Flohr, H., Glade, U., Motzko, D. (1998). "The neural correlate of consciousness and the mechanisms of general anaesthesia". Toxicology Letters. 100: 23–29. 
  137. 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. 
  138. 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. 
  139. 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. 
  140. 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. 
  141. 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. 
  142. 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. 
  143. 143.0 143.1 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. 
  144. 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. 
  145. 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.