Confabulation

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In psychology, confabulation is a memory error consisting of the production of fabricated, distorted, or misinterpreted memories about oneself or the world. It is generally associated with certain types of brain damage (especially aneurysm in the anterior communicating artery) or a specific subset of dementias. [1] While still an area of ongoing research, the basal forebrain is implicated in the phenomenon of confabulation. People who confabulate present with incorrect memories ranging from subtle inaccuracies to surreal fabrications, and may include confusion or distortion in the temporal framing (timing, sequence or duration) of memories. [2] In general, they are very confident about their recollections, even when challenged with contradictory evidence. [3]

Contents

Confabulation occurs when individuals mistakenly recall false information, without intending to deceive. Brain damage, dementia, and anticholinergic toxidrome can cause this distortion. Two types of confabulation exist: provoked and spontaneous, with two distinctions: verbal and behavioral. Verbal statements, false information, and the patient's unawareness of the distortion are all associated with this phenomenon. Personality structure also plays a role in confabulation.

Numerous theories have been developed to explain confabulation. Neuro­psycho­log­i­cal theories suggest that cognitive dysfunction causes the distortion. Self-identity theories posit that people confabulate to preserve themselves. The temporality theory believes that confabulation occurs when an individual cannot place events properly in time. The monitoring and strategic retrieval account theories argue that confabulation arises when individuals cannot recall memories correctly or monitor them after retrieval. The executive control and fuzzy-trace theories also attempt to explain why confabulation happens.

Confabulation can occur with nervous system injuries or illnesses, including Korsakoff's syndrome, Alzheimer's disease, schizophrenia, and traumatic brain injury. It is believed that the right frontal lobe of the brain is damaged, causing false memories. Children are especially susceptible to forced confabulation as they are highly impressionable. Feedback can increase confidence in false memories. In rare cases, confabulation occurs in ordinary individuals.

Different memory tests, including recognition tasks and free recall tasks, can be used to study confabulation. Treatment depends on the underlying cause of the distortion. Ongoing research aims to develop a standard test battery to discern between different types of confabulations, distinguish delusions from confabulations, understand the role of unconscious processes, and identify pathological and nonpathological confabulations.

Description

Confabulation is distinguished from lying as there is no intent to deceive and the person is unaware the information is false. [4] Although individuals can present blatantly false information, confabulation can also seem to be coherent, internally consistent, and relatively normal. [4]

Most known cases of confabulation are symptomatic of brain damage or dementias, such as aneurysm, Alzheimer's disease, or Wernicke–Korsakoff syndrome (a common manifestation of thiamine deficiency caused by alcohol use disorder). [5] Additionally confabulation often occurs in people with anticholinergic toxidrome when interrogated about bizarre or irrational behaviour.

Confabulated memories of all types most often occur in autobiographical memory and are indicative of a complicated and intricate process that can be led astray at any point during encoding, storage, or recall of a memory. [3] This type of confabulation is commonly seen in Korsakoff's syndrome. [6]

Distinctions

Two types of confabulation are often distinguished:

Another distinction is that between: [9]

Signs and symptoms

Confabulation is associated with several characteristics:

  1. Typically verbal statements but can also be non-verbal gestures or actions.
  2. Can include autobiographical and non-personal information, such as historical facts, fairy-tales, or other aspects of semantic memory.
  3. The account can be fantastic or coherent.
  4. Both the premise and the details of the account can be false.
  5. The account is usually drawn from the patient's memory of actual experiences, including past and current thoughts.
  6. The patient is unaware of the accounts' distortions or inappropriateness, and is not concerned when errors are pointed out.
  7. There is no hidden motivation behind the account.
  8. The patient's personality structure may play a role in their readiness to confabulate. [4]

Theories

Theories of confabulation range in emphasis. Some theories propose that confabulations represent a way for memory disabled people to maintain their self-identity. [8] Other theories use neurocognitive links to explain the process of confabulation. [10] Still other theories frame confabulation around the more familiar concept of delusion. [11] Other researchers frame confabulation within the fuzzy-trace theory. [12] Finally, some researchers call for theories that rely less on neurocognitive explanations and more on epistemic accounts. [13]

Neuropsychological theories

The most popular theories of confabulation come from the field of neuropsychology or cognitive neuroscience. [10] Research suggests that confabulation is associated with dysfunction of cognitive processes that control the retrieval from long-term memory. Frontal lobe damage often disrupts this process, preventing the retrieval of information and the evaluation of its output. [14] [15] Furthermore, researchers argue that confabulation is a disorder resulting from failed "reality monitoring/source monitoring" (i.e. deciding whether a memory is based on an actual event or whether it is imagined). [16] Some neuropsychologists suggest that errors in retrieval of information from long-term memory that are made by normal subjects involve different components of control processes than errors made by confabulators. [17] Kraepelin distinguished two subtypes of confabulation, one of which he called simple confabulation, caused partly by errors in the temporal ordering of real events. The other variety he called fantastic confabulation, which was bizarre and patently impossible statements not rooted in true memory. Simple confabulation may result from damage to memory systems in the medial temporal lobe. Fantastic confabulations reveal a dysfunction of the Supervisory System, [18] which is believed to be a function of the frontal cortex.

Self-identity theory

Some argue confabulations have a self-serving, emotional component in those with memory deficits that aids to maintain a coherent self-concept. [8] In other words, people who confabulate are motivated to do so, because they have gaps in their memory that they want to fill in and cover up. People with personality disorders and narcissistic traits confabulate in order to preserve their false self-image and distorted world view.[ citation needed ]

Temporality theory

Support for the temporality account suggests that confabulations occur when an individual is unable to place events properly in time. [8] Thus, an individual might correctly state an action they performed, but say they did it yesterday, when they did it weeks ago. In the Memory, Consciousness, and Temporality Theory, confabulation occurs because of a deficit in temporal consciousness or awareness. [19]

Monitoring theory

Along a similar notion are the theories of reality and source monitoring theories. [9] In these theories, confabulation occurs when individuals incorrectly attribute memories as reality, or incorrectly attribute memories to a certain source. Thus, an individual might claim an imagined event happened in reality, or that a friend told him/her about an event he/she actually heard about on television.

Strategic retrieval account theory

Supporters of the strategic retrieval account suggest that confabulations occur when an individual cannot actively monitor a memory for truthfulness after its retrieval. [9] An individual recalls a memory, but there is some deficit after recall that interferes with the person establishing its falseness.

Executive control theory

Still others propose that all types of false memories, including confabulation, fit into a general memory and executive function model. [20] In 2007, a framework for confabulation was proposed that stated confabulation is the result of two things: Problems with executive control and problems with evaluation. In the executive control deficit, the incorrect memory is retrieved from the brain. In the evaluative deficit, the memory will be accepted as a truth due to an inability to distinguish a belief from an actual memory. [8]

In the context of delusion theories

Recent models of confabulation have attempted to build upon the link between delusion and confabulation. [11] More recently, a monitoring account for delusion, applied to confabulation, proposed both the inclusion of conscious and unconscious processing. The claim was that by encompassing the notion of both processes, spontaneous versus provoked confabulations could be better explained. In other words, there are two ways to confabulate. One is the unconscious, spontaneous way in which a memory goes through no logical, explanatory processing. The other is the conscious, provoked way in which a memory is recalled intentionally by the individual to explain something confusing or unusual. [21]

Fuzzy-trace theory

Fuzzy-trace theory, or FTT, is a concept more commonly applied to the explanation of judgement decisions. [12] According to this theory, memories are encoded generally (gist), as well as specifically (verbatim). Thus, a confabulation could result from recalling the incorrect verbatim memory or from being able to recall the gist portion, but not the verbatim portion, of a memory.

FTT uses a set of five principles to explain false-memory phenomena. Principle 1 suggests that subjects store verbatim information and gist information parallel to one another. Both forms of storage involve the surface content of an experience. Principle 2 shares factors of retrieval of gist and verbatim traces. Principle 3 is based on dual-opponent processes in false memory. Generally, gist retrieval supports false memory, while verbatim retrieval suppresses it. Developmental variability is the topic of Principle 4. As a child develops into an adult, there is obvious improvement in the acquisition, retention, and retrieval of both verbatim and gist memory. However, during late adulthood, there will be a decline in these abilities. Finally, Principle 5 explains that verbatim and gist processing cause vivid remembering. Fuzzy-trace Theory, governed by these 5 principles, has proved useful in explaining false memory and generating new predictions about it. [22]

Epistemic theory

However, not all accounts are so embedded in the neurocognitive aspects of confabulation. Some attribute confabulation to epistemic accounts. [13] In 2009, theories underlying the causation and mechanisms for confabulation were criticized for their focus on neural processes, which are somewhat unclear, as well as their emphasis on the negativity of false remembering. Researchers proposed that an epistemic account of confabulation would be more encompassing of both the advantages and disadvantages of the process.

Presentation

Associated neurological and psychological conditions

Confabulations are often symptoms of various syndromes and psychopathologies in the adult population, including Korsakoff's syndrome, Alzheimer's disease, schizophrenia, and traumatic brain injury.

Wernicke–Korsakoff syndrome is a neurological disorder typically characterized by years of alcohol use disorder characterized by excessive alcohol consumption and a nutritional thiamine deficiency. [23] Confabulation is one salient symptom of this syndrome. [24] [25] A study on confabulation in Korsakoff's patients found that they are subject to provoked confabulation when prompted with questions pertaining to episodic memory, not semantic memory, and when prompted with questions where the appropriate response would be "I don't know." [26] This suggests that con­fab­u­l­ation in these patients is "domain-specific." Korsakoff's patients who confabulate are more likely than healthy adults to falsely recognize distractor words, suggesting that false recognition is a "confabulatory behavior."

Alzheimer's disease is a condition with both neurological and psychological components. It is a form of dementia associated with severe frontal lobe dys­func­tion. Confabulation in individuals with Alzheimer's is often more spontaneous than it is in other conditions, especially in the advanced stages of the disease. Alzheimer's patients demonstrate comparable abilities to encode information as healthy elderly adults, suggesting that impairments in encoding are not associated with confabulation. [27] However, as seen in Korsakoff's patients, confabulation in Alzheimer's patients is higher when prompted with questions investigating episodic memory. Researchers suggest this is due to damage in the posterior cortical regions of the brain, which is a symptom characteristic of Alzheimer's disease.

Schizophrenia is a psychological disorder in which confabulation is sometimes observed. Although confabulation is usually coherent in its presentation, con­fab­u­l­ationsof schizophrenic patients are often delusional. [28] Researchers have noted that these patients tend to make up delusions on the spot which are often fantastic and become increasingly elaborate with questioning. [29] Unlike patients with Korsakoff's and Alzheimer's, patients with schizophrenia are more likely to confabulate when prompted with questions regarding their semantic memories, as opposed to episodic memory prompting. [30] In addition, confabulation does not appear to be related to any memory deficit in schiz­o­phrenic patients. This is contrary to most forms of confabulation. Also, confabulations made by schizophrenic patients often do not involve the creation of new information, but instead involve an attempt by the patient to reconstruct actual details of a past event.

Traumatic brain injury (TBI) can also result in confabulation. Research has shown that patients with damage to the inferior medial frontal lobe confabulate significantly more than patients with damage to the posterior area and healthy controls. [31] This suggests that this region is key in producing confabulatory responses, and that memory deficit is important but not necessary in con­fab­u­l­ation. Additionally, research suggests that confabulation can be seen in patients with frontal lobe syndrome, which involves an insult to the frontal lobe as a result of disease or traumatic brain injury (TBI). [32] [33] [34] Finally, rupture of the anterior or posterior communicating artery, subarachnoid hemorrhage, and encephalitis are also possible causes of confabulation. [14] [35]

Location of brain lesions

Confabulation is believed to be a result of damage to the right frontal lobe of the brain. [4] In particular, damage can be localized to the ventromedial frontal lobes and other structures fed by the anterior communicating artery (ACoA), including the basal forebrain, septum, fornix, cingulate gyrus, cingulum, anterior hypothalamus, and head of the caudate nucleus. [36] [37]

Developmental differences

While some recent literature has suggested that older adults may be more susceptible than their younger counterparts to have false memories, the majority of research on forced confabulation centers around children. [38] Children are particularly susceptible to forced confabulations based on their high suggestibility. [39] [40] When forced to recall confabulated events, children are less likely to remember that they had previously confabulated these situations, and they are more likely than their adult counterparts to come to remember these confabulations as real events that transpired. [41] Research suggests that this inability to distinguish between past confabulatory and real events is centered on developmental differences in source monitoring. Due to underdeveloped encoding and critical reasoning skills, children's ability to distinguish real memories from false memories may be impaired. It may also be that younger children lack the meta-memory processes required to remember confabulated versus non-confabulated events. [42] Children's meta-memory processes may also be influenced by expectancies or biases, in that they believe that highly plausible false scenarios are not confabulated. [43] However, when knowingly being tested for accuracy, children are more likely to respond, "I don't know" at a rate comparable to adults for unanswerable questions than they are to confabulate. [44] [45] Ultimately, misinformation effects can be minimized by tailoring individual interviews to the specific developmental stage, often based on age, of the participant. [46]

Provoked versus spontaneous confabulations

There is evidence to support different cognitive mechanisms for provoked and spontaneous confabulation. [47] One study suggested that spontaneous confabulation may be a result of an amnesic patient's inability to distinguish the chronological order of events in their memory. In contrast, provoked confabulation may be a compensatory mechanism, in which the patient tries to make up for their memory deficiency by attempting to demonstrate competency in recollection.

Confidence in false memories

Confabulation of events or situations may lead to an eventual acceptance of the confabulated information as true. [48] For instance, people who knowingly lie about a situation may eventually come to believe that their lies are truthful with time. [49] In an interview setting, people are more likely to confabulate in situations in which they are presented false information by another person, as opposed to when they self-generate these falsehoods. [50] Further, people are more likely to accept false information as true when they are interviewed at a later time (after the event in question) than those who are interviewed immediately or soon after the event. [51] Affirmative feedback for confabulated responses is also shown to increase the confabulator's confidence in their response. [52] For instance, in culprit identification, if a witness falsely identifies a member of a line-up, he will be more confident in his identification if the interviewer provides affirmative feedback. This effect of confirmatory feedback appears to last over time, as witnesses will even remember the confabulated information months later. [53]

Among normal subjects

On rare occasions, confabulation can also be seen in normal subjects. [17] It is currently unclear how completely healthy individuals produce confabulations. It is possible that these individuals are in the process of developing some type of organic condition that is causing their confabulation symptoms. It is not uncommon, however, for the general population to display some very mild symptoms of provoked confabulations. Subtle distortions and intrusions in memory are commonly produced by normal subjects when they remember something poorly.

Diagnosis and treatment

Spontaneous confabulations, due to their involuntary nature, cannot be manipulated in a laboratory setting. [9] However, provoked confabulations can be researched in various theoretical contexts. The mechanisms found to underlie provoked confabulations can be applied to spontaneous confabulation mechanisms. The basic premise of researching confabulation comprises finding errors and distortions in memory tests of an individual.

Deese–Roediger–McDermott lists

Confabulations can be detected in the context of the Deese–Roediger–McDermott paradigm by using the Deese–Roediger–McDermott lists. [54] Participants listen to audio recordings of several lists of words centered around a theme, known as the critical word. The participants are later asked to recall the words on their list. If the participant recalls the critical word, which was never explicitly stated in the list, it is considered a confabulation. Participants often have a false memory for the critical word.

Recognition tasks

Confabulations can also be researched by using continuous recognition tasks. [9] These tasks are often used in conjunction with confidence ratings. Generally, in a recognition task, participants are rapidly presented with pictures. Some of these pictures are shown once; others are shown multiple times. Participants press a key if they have seen the picture previously. Following a period of time, participants repeat the task. More errors on the second task, versus the first, are indicative of confusion, representing false memories.

Free recall tasks

Confabulations can also be detected using a free recall task, such as a self-narrative task. [9] Participants are asked to recall stories (semantic or autobiographical) that are highly familiar to them. The stories recalled are encoded for errors that could be classified as distortions in memory. Distortions could include falsifying true story elements or including details from a completely different story. Errors such as these would be indicative of confabulations.

Treatment

Treatment for confabulation is somewhat dependent on the cause or source, if identifiable. For example, treatment of Wernicke–Korsakoff syndrome involves large doses of vitamin B in order to reverse the thiamine deficiency. [55] If there is no known physiological cause, more general cognitive techniques may be used to treat confabulation. A case study published in 2000 showed that Self-Monitoring Training (SMT) [56] reduced delusional confabulations. Furthermore, improvements were maintained at a three-month follow-up and were found to generalize to everyday settings. Although this treatment seems promising, more rigorous research is necessary to determine the efficacy of SMT in the general confabulation population.

Research

Although significant gains have been made in the understanding of confabulation in recent years, there is still much to be learned. One group of researchers in particular has laid out several important questions for future study. They suggest more information is needed regarding the neural systems that support the different cognitive processes necessary for normal source monitoring. They also proposed the idea of developing a standard neuropsychological test battery able to discriminate between the different types of confabulations. And there is a considerable amount of debate regarding the best approach to organizing and combining neuro-imaging, pharmacological, and cognitive/behavioral approaches to understand confabulation. [57]

In a recent review article, another group of researchers contemplate issues concerning the distinctions between delusions and confabulation. They question whether delusions and confabulation should be considered distinct or overlapping disorders and, if overlapping, to what degree? They also discuss the role of unconscious processes in confabulation. Some researchers suggest that unconscious emotional and motivational processes are potentially just as important as cognitive and memory problems. Finally, they raise the question of where to draw the line between the pathological and the nonpathological. Delusion-like beliefs and confabulation-like fabrications are commonly seen in healthy individuals. What are the important differences between patients with similar etiology who do and do not confabulate? Since the line between pathological and nonpathological is likely blurry, should we take a more dimensional approach to confabulation? Research suggests that confabulation occurs along a continuum of implausibility, bizarreness, content, conviction, preoccupation, and distress, and impact on daily life. [58]

See also

Related Research Articles

Source amnesia is the inability to remember where, when or how previously learned information has been acquired, while retaining the factual knowledge. This branch of amnesia is associated with the malfunctioning of one's explicit memory. It is likely that the disconnect between having the knowledge and remembering the context in which the knowledge was acquired is due to a dissociation between semantic and episodic memory – an individual retains the semantic knowledge, but lacks the episodic knowledge to indicate the context in which the knowledge was gained.

Memory distrust syndrome is a condition coined by Gísli Guðjónsson and James MacKeith in 1982, in which an individual doubts the accuracy of their memory concerning the content and context of events of which they have experienced. Since the individual does not trust their own memory, they will commonly depend on outside sources of information rather than using their ability for recollection. Some believe that this may be a defense or coping mechanism to a preexisting faulty memory state such as Alzheimer's disease, amnesia, or possibly dementia.

The Fregoli delusion is a rare disorder in which a person holds a delusional belief that different people are in fact a single person who changes appearance or is in disguise. The syndrome may be related to a brain lesion and is often of a paranoid nature, with the delusional person believing themselves persecuted by the person they believe is in disguise.

<span class="mw-page-title-main">Wernicke–Korsakoff syndrome</span> Combined presence of Wernickes encephalopathy (WE) and Korsakoffs syndrome

Wernicke-Korsakoff syndrome (WKS) is the combined presence of Wernicke encephalopathy (WE) and alcoholic Korsakoff syndrome. Due to the close relationship between these two disorders, people with either are usually diagnosed with WKS as a single syndrome. It mainly causes vision changes, ataxia and impaired memory.

<span class="mw-page-title-main">Korsakoff syndrome</span> Mental illness caused by a lack of thiamine in the brain

Korsakoff syndrome (KS) is a disorder of the central nervous system characterized by amnesia, deficits in explicit memory, and confabulation. This neurological disorder is caused by a deficiency of thiamine (vitamin B1) in the brain, and it is typically associated with and exacerbated by the prolonged, excessive ingestion of alcohol. Korsakoff syndrome is often accompanied by Wernicke encephalopathy; this combination is called Wernicke–Korsakoff syndrome.

<span class="mw-page-title-main">Frontal lobe</span> Part of the brain

The frontal lobe is the largest of the four major lobes of the brain in mammals, and is located at the front of each cerebral hemisphere. It is parted from the parietal lobe by a groove between tissues called the central sulcus and from the temporal lobe by a deeper groove called the lateral sulcus. The most anterior rounded part of the frontal lobe is known as the frontal pole, one of the three poles of the cerebrum.

In neurology, anterograde amnesia is the inability to create new memories after an event that caused amnesia, leading to a partial or complete inability to recall the recent past, while long-term memories from before the event remain intact. This is in contrast to retrograde amnesia, where memories created prior to the event are lost while new memories can still be created. Both can occur together in the same patient. To a large degree, anterograde amnesia remains a mysterious ailment because the precise mechanism of storing memories is not yet well understood, although it is known that the regions of the brain involved are certain sites in the temporal cortex, especially in the hippocampus and nearby subcortical regions.

In neurology, retrograde amnesia (RA) is the inability to access memories or information from before an injury or disease occurred. RA differs from a similar condition called anterograde amnesia (AA), which is the inability to form new memories following injury or disease onset. Although an individual can have both RA and AA at the same time, RA can also occur on its own; this 'pure' form of RA can be further divided into three types: focal, isolated, and pure RA. RA negatively affects an individual's episodic, autobiographical, and declarative memory, but they can still form new memories because RA leaves procedural memory intact. Depending on its severity, RA can result in either temporally graded or more permanent memory loss. However, memory loss usually follows Ribot's law, which states that individuals are more likely to lose recent memories than older memories. Diagnosing RA generally requires using an Autobiographical Memory Interview (AMI) and observing brain structure through magnetic resonance imaging (MRI), a computed tomography scan (CT), or electroencephalography (EEG).

Reduplicative paramnesia is the delusional belief that a place or location has been duplicated, existing in two or more places simultaneously, or that it has been 'relocated' to another site. It is one of the delusional misidentification syndromes; although rare, it is most commonly associated with acquired brain injury, particularly simultaneous damage to the right cerebral hemisphere and to both frontal lobes.

Mirrored-self misidentification is the delusional belief that one's reflection in the mirror is another person – typically a younger or second version of one's self, a stranger, or a relative. This delusion occurs most frequently in patients with dementia and an affected patient maintains the ability to recognize others' reflections in the mirror. It is caused by right hemisphere cranial dysfunction that results from traumatic brain injury, stroke, or general neurological illness. It is an example of a monothematic delusion, a condition in which all abnormal beliefs have one common theme, as opposed to a polythematic delusion, in which a variety of unrelated delusional beliefs exist. This delusion is also classified as one of the delusional misidentification syndromes (DMS). A patient with a DMS condition consistently misidentifies places, objects, persons, or events. DMS patients are not aware of their psychological condition, are resistant to correction and their conditions are associated with brain disease – particularly right hemisphere brain damage and dysfunction.

Memory disorders are the result of damage to neuroanatomical structures that hinders the storage, retention and recollection of memories. Memory disorders can be progressive, including Alzheimer's disease, or they can be immediate including disorders resulting from head injury.

Dysexecutive syndrome (DES) consists of a group of symptoms, usually resulting from brain damage, that fall into cognitive, behavioural and emotional categories and tend to occur together. The term was introduced by Alan Baddeley to describe a common pattern of dysfunction in executive functions, such as planning, abstract thinking, flexibility and behavioural control. It is thought to be Baddeley's hypothesized working memory system and the central executive that are the hypothetical systems impaired in DES. The syndrome was once known as frontal lobe syndrome; however 'dysexecutive syndrome' is preferred because it emphasizes the functional pattern of deficits over the location of the syndrome in the frontal lobe, which is often not the only area affected.

Retrospective memory is the memory of people, words, and events encountered or experienced in the past. It includes all other types of memory including episodic, semantic and procedural. It can be either implicit or explicit. In contrast, prospective memory involves remembering something or remembering to do something after a delay, such as buying groceries on the way home from work. However, it is very closely linked to retrospective memory, since certain aspects of retrospective memory are required for prospective memory.

Metamemory or Socratic awareness, a type of metacognition, is both the introspective knowledge of one's own memory capabilities and the processes involved in memory self-monitoring. This self-awareness of memory has important implications for how people learn and use memories. When studying, for example, students make judgments of whether they have successfully learned the assigned material and use these decisions, known as "judgments of learning", to allocate study time.

Recognition memory, a subcategory of explicit memory, is the ability to recognize previously encountered events, objects, or people. When the previously experienced event is reexperienced, this environmental content is matched to stored memory representations, eliciting matching signals. As first established by psychology experiments in the 1970s, recognition memory for pictures is quite remarkable: humans can remember thousands of images at high accuracy after seeing each only once and only for a few seconds.

Amnesia is a deficit in memory caused by brain damage or brain diseases, but it can also be temporarily caused by the use of various sedative and hypnotic drugs. The memory can be either wholly or partially lost due to the extent of damage that is caused.

Memory gaps and errors refer to the incorrect recall, or complete loss, of information in the memory system for a specific detail and/or event. Memory errors may include remembering events that never occurred, or remembering them differently from the way they actually happened. These errors or gaps can occur due to a number of different reasons, including the emotional involvement in the situation, expectations and environmental changes. As the retention interval between encoding and retrieval of the memory lengthens, there is an increase in both the amount that is forgotten, and the likelihood of a memory error occurring.

<span class="mw-page-title-main">Reconstructive memory</span> A theory of memory recall

Reconstructive memory is a theory of memory recall, in which the act of remembering is influenced by various other cognitive processes including perception, imagination, motivation, semantic memory and beliefs, amongst others. People view their memories as being a coherent and truthful account of episodic memory and believe that their perspective is free from an error during recall. However, the reconstructive process of memory recall is subject to distortion by other intervening cognitive functions such as individual perceptions, social influences, and world knowledge, all of which can lead to errors during reconstruction.

Delusional companion syndrome is considered a neuropathology of the self, specifically a delusional misidentification syndrome. Affected individuals believe certain non-living objects possess consciousness and can think independently and feel emotion. The psychosis must coexist with a detectable brain pathology for delusional companion syndrome to be diagnosed. The syndrome is most often identified in patients who suffer from damage to the brain due to physical trauma, neuronal degeneration or developmental abnormalities. Especially in the latter case, patients also tend to present with many other symptoms and are diagnosed as having other established conditions. Comforting objects like cuddly toys are often the focus of delusion.

The false tagging theory (FTT) is a neuroanatomical model of a belief and doubt process that proposes a single, unique function for the prefrontal cortex. The theory was developed by neuroscientist Erik Asp. Evidence indicates that prefrontal-cortex-mediated doubting is at the core of executive functioning and may explain some biases of intuitive judgment.

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