Cognitive depressions

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 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 (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:

• Analysis depression
• Motivation depression
• Thought deceleration
• Short term memory suppression
• Thought disorganization
• Language depression
• Creativity depression

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 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 (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 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 (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 (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 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]}

• Subjective effect index
• Cognitive effects
• Cognitive suppressions