Two types of confabulation are often distinguished:

- Provoked (momentary, or secondary) confabulations represent a normal response to a faulty memory, are common in both amnesia and dementia, and can become apparent during memory tests.

- Spontaneous (or primary) confabulations do not occur in response to a cue and seem to be involuntary. They are relatively rare, more common in cases of dementia, and may result from the interaction between frontal lobe pathology and organic amnesia.

Another distinction is that between:

- Verbal confabulations, spoken false memories are more common, and

- Behavioral confabulations, occur when an individual acts on their false memories.

In psychiatry, confabulation (verb: confabulate) is a disturbance of memory, defined as the production of fabricated, distorted, or misinterpreted memories about oneself or the world, without the conscious intention to deceive. People who confabulate present incorrect memories ranging from "subtle alterations to bizarre fabrications", and are generally very confident about their recollections, despite contradictory evidence.

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 condition is generally considered to be related to source amnesia, which involves the inability to recall the basis for factual knowledge. The main difference between the two is that source amnesia is a lack of knowing the basis of knowledge, whereas memory distrust syndrome is a lack of believing the knowledge that exists. The fact that an individual lacks the trust in their own memory implies that the individual would have a reason or belief that would prevent them from the trust that most of us have in our recollections. Cases concerning memory distrust syndrome have led to documented false confessions in court cases.

The main symptom of memory distrust syndrome is the lack of belief in one's own memory, however this comes with the side effect of using outside sources for information. The individual may have their own memory, but will readily change it depending on chosen outside sources. The memories that they have may be correct, but due to their distrust they will still alter their belief of what is true if contrary information is suggested.

For example, a person has a memory of a house and recalls it to be white. Then, a trusted family member begins talking with them and suggests that it was red instead. The afflicted individual will then believe the house was red despite their recollection of it being white. It is unknown if the person's memory of the house is permanently altered; however, they will say that the house was red regardless of the memory's condition.

Also, this does not necessarily allow for confabulatory memory fabrication. Currently it is not believed that an afflicted individual will readily believe an outside source on a memory of which the person is not involved, such as a randomly shared story. This further suggests that memory distrust syndrome solely alters the individual's currently retrievable memories, and not randomized information.

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 (the fact), but lacks the episodic knowledge to indicate the context in which the knowledge was gained.

Memory representations reflect the encoding processes during acquisition. Different types of acquisition processes (e.g.: reading, thinking, listening) and different types of events (e.g.: newspaper, thoughts, conversation) will produce mental depictions that perceptually differ from one another in the brain, making it harder to retrieve where information was learned when placed in a different context of retrieval. Source monitoring involves a systematic process of slow and deliberate thought of where information was originally learned. Source monitoring can be improved by using more retrieval cues, discovering and noting relations and extended reasoning.

Individuals with frontal lobe damage have deficits in temporal context memory; source memory can also exhibit deficits in those with frontal lobe damage. It appears that those with frontal lobe damage have difficulties with recency and other temporal judgements (e.g., placing events in the order they occurred), and as such they are unable to properly attribute their knowledge to appropriate sources (i.e., suffer source amnesia). Those individuals with frontal lobe damage have normal recall of facts, but they make significantly more errors in source memory than control subjects, with these effects becoming apparent as shortly as 5 minutes after the learning experience. Individuals with frontal lobe damage often mistakenly attribute the knowledge they have to some other source (e.g., they read it somewhere, saw it on TV, etc.) but rarely attribute it to having learned it over the course of the experiment. It appears that frontal lobe damage causes a disconnection between semantic and episodic memory – in that the individuals cannot associate the context in which they acquired the knowledge to the knowledge itself.

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 and, although rare, is most commonly associated with acquired brain injury, particularly simultaneous damage to the right cerebral hemisphere and to both frontal lobes.

Agnosia is the inability to recognize certain objects, persons or sounds. Agnosia is typically caused by damage to the brain (most commonly in the occipital or parietal lobes) or from a neurological disorder. Treatments vary depending on the location and cause of the damage. Recovery is possible depending on the severity of the disorder and the severity of the damage to the brain. Many more specific types of agnosia diagnoses exist, including: associative visual agnosia, astereognosis, auditory agnosia, auditory verbal agnosia, prosopagnosia, simultanagnosia, topographical disorientation, visual agnosia etc.

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.

People with WKS often show confabulation, spontaneous confabulation being seen more frequently than provoked confabulation. Spontaneous confabulations refer to incorrect memories that the patient holds to be true, and may act on, arising spontaneously without any provocation. Provoked confabulations can occur when a patient is cued to give a response, this may occur in test settings. The spontaneous confabulations viewed in WKS are thought to be produced by an impairment in source memory, where they are unable to remember the spatial and contextual information for an event, and thus may use irrelevant or old memory traces to fill in for the information that they cannot access. It has also been suggested that this behaviour may be due to executive dysfunction where they are unable to inhibit incorrect memories or because they are unable to shift their attention away from an incorrect response.

Reduplicative paramnesia has been reported in the context of a number of neurological disorders, including stroke, intracerebral hemorrhage, tumor, dementia, encephalopathy and various psychiatric disorders.

Taken from the Benson and colleagues study, the following excerpt illustrates some of the core features of the delusion. The patient had suffered a head injury after a fall in his home. The impact had caused a fractured skull and frontal lobe damage to both sides (although more pronounced on the right) owing to the formation of intracerebral hematomas:

The illusory relocation to a familiar place, such as a home or town the patient knows well, is a common theme, although occasionally the patient believes they are resident in more fantastical or exotic locations (such as, in one case, Timbuktu).

KS is described as an acute onset of severe memory impairment without any dysfunction in intellectual abilities. The DSM IV lists the following criteria for the diagnosis of Korsakoff's Syndrome:

1. anterograde amnesia

2. Variable presentation of retrograde amnesia

One of:

1. Aphasia

2. Apraxia

3. Agnosia

4. A deficit in executive functions

In addition, the DSM-IV indicates that normal activities and function will be impaired by the memory deficits and that the experience of amnesia must occur outside of times where the individual is in a state of delirium, intoxification, or withdrawal. The criteria for diagnosis also maintain that there must be evidence that the amnesia is caused by the use of alcohol.

Despite the assertion that Korsakoff's syndrome must be caused by the use of alcohol, there have been several cases where it has developed from other instances of thiamine deficiency resulting from gross malnutrition due to conditions such as; stomach cancer, anorexia nervosa, and gastrectomy.

There are seven major symptoms of Korsakoff's syndrome (amnestic-confabulatory syndrome):

1. anterograde amnesia, memory loss for events after the onset of the syndrome

2. retrograde amnesia, memory loss extends back for some time before the onset of the syndrome

3. amnesia of fixation, also known as fixation amnesia (loss of immediate memory, a person being unable to remember events of the past few minutes)

4. confabulation, that is, invented memories which are then taken by the patient as true due to gaps in memory, with such gaps sometimes associated with blackouts

5. minimal content in conversation

6. lack of insight

7. apathy – the patients lose interest in things quickly, and generally appear indifferent to change.

Benon R. and LeHuché R. (1920) described the characteristic signs of Korsakoff syndrome with some additional features: confabulation (false memories), fixation amnesia, paragnosia or false recognition of places, mental excitation, euphoria, etc.

Thiamine is essential for the decarboxylation of pyruvate, and deficiency during this metabolic process is thought to cause damage to the medial thalamus and mammillary bodies of the posterior hypothalamus, as well as generalized cerebral atrophy. These brain regions are all parts of the limbic system, which is heavily involved in emotion and memory.

Korsakoff's involves neuronal loss, that is, damage to neurons; gliosis, which is a result of damage to supporting cells of the central nervous system, and hemorrhage or bleeding also occurs in mammillary bodies. Damage to the dorsomedial nucleus or anterior group of the thalamus (limbic-specific nuclei) is also associated with this disorder. Cortical dysfunction may have arisen from thiamine deficiency, alcohol neurotoxicity, and/or structural damage in the diencephalon.

Originally, it was thought that a lack of initiative and a flat affect were important characteristics of emotional presentation in sufferers. Studies have questioned this, proposing that neither is necessarily a symptom of Korsakoff's. Research suggesting that Korsakoff's patients are emotionally unimpaired has made this a controversial topic. It can be argued that apathy, which usually characterizes Korsakoff's patients, reflects a deficit of emotional "expressions", without affecting the "experience" or perception of emotion.

Korsakoff's Syndrome causes deficits in declarative memory in most patients, but leaves implicit spatial, verbal, and procedural memory functioning intact. People who have Korsakoff's syndrome have deficits in the processing of contextual information. Context memories refers to the where and when of experiences, and is an essential part of recollection. The ability to store and retrieve this information, such as spatial location or temporal order information, is impaired.

Research has also suggested that Korsakoff patients have impaired executive functions, which can lead to behavioral problems and interfere with daily activities. It is unclear, however, which executive functions are affected most. Nonetheless, IQ is usually not affected by the brain damage associated with Korsakoff's syndrome.

At first it was thought that Korsakoff's patients used confabulation to fill in memory gaps. However, it has been found that confabulation and amnesia do not necessarily co-occur. Studies have shown that there is dissociation between provoked confabulation, spontaneous confabulation (which is unprovoked), and false memories. That is, patients could be led to believe certain things had happened which actually had not, but so could people without Korsakoff’s syndrome.

Behavioural symptoms are evident through an individual's actions. People with DES often lose their social skills because their judgments and insights into what others may be thinking are impaired. They may have trouble knowing how to behave in group situations and may not know how to follow social norms. The central executive helps control impulses; therefore when impaired, patients have poor impulse control. This can lead to higher levels of aggression and anger. DES can also cause patients to appear self-centered and stubborn

Utilization behaviour is when a patient automatically uses an object in the appropriate manner, but at an inappropriate time. For example, if a pen and paper are placed in front of an individual with DES they will start to write or if there is a deck of cards they will deal them out. Patients showing this symptom will begin the behaviour in the middle of conversations or during auditory tests. Utilization behaviour is thought to occur because an action is initiated when an object is seen, but patients with DES lack the central executive control to inhibit acting it out at inappropriate times.

Perseveration is also often seen in patients with DES. Perseveration is the repetition of thoughts, behaviours, or actions after they have already been completed. For instance, continually blowing out a match, after it is no longer lit is an example of perseveration behaviour. There are three types of perseveration: continuous perseveration, stuck-in-set perseveration, and recurrent perseveration. Stuck-in-set perseveration is most often seen in dysexecutive syndrome. This type of perseveration refers to when a patient cannot get out of a specific frame of mind, such as when asked to name animals they can only name one. If you ask them to then name colours, they may still give you animals. Perseveration may explain why some patients appear to have obsessive-compulsive disorder.

The emotional symptoms that individuals with DES experience may be quite extreme and can cause extensive problems. They may have difficulty inhibiting many types of emotions such as anger, excitement, sadness, or frustration. Due to multiple impairments of cognitive functioning, there can be much more frustration when expressing certain feelings and understanding how to interpret every day situations. Individuals with DES may have higher levels of aggression or anger because they lack abilities that are related to behavioural control. They can also have difficulty understanding others' points of view, which can lead to anger and frustration.

Anton–Babinski syndrome is mostly seen following a stroke, but may also be seen after head injury. Neurologist Macdonald Critchley describes it thus:

The sudden development of bilateral occipital dysfunction is likely to produce transient physical and psychical effects in which mental confusion may be prominent. It may be some days before the relatives, or the nursing staff, stumble onto the fact that the patient has actually become sightless. This is not only because the patient ordinarily does not volunteer the information that they have become blind, but he furthermore misleads his entourage by behaving and talking as though they were sighted. Attention is aroused however when the patient is found to collide with pieces of furniture, to fall over objects, and to experience difficulty in finding his way around. They may try to walk through a wall or through a closed door on his way from one room to another. Suspicion is still further alerted when they begin to describe people and objects around them which, as a matter of fact, are not there at all.

Thus we have the twin symptoms of anosognosia (or lack of awareness of defect) and confabulation, the latter affecting both speech and behaviour.

Anton–Babinski syndrome may be thought of ideally as the opposite of blindsight, blindsight occurring when part of the visual field is not consciously experienced, but some reliable perception does in fact occur.

Korsakoff's syndrome is an amnestic disorder caused by thiamine deficiency usually associated prolonged ingestion of alcohol. It is rare among other people but some cases have been observed after bariatric surgeries, when deficiency was not prevented by use of nutritional supplements. This neurological disorder is caused by a lack of thiamine (vitamin B) in the brain, and is also often exacerbated by the neurotoxic effects of alcohol. When Wernicke's encephalopathy accompanies Korsakoff's psychosis the combination is called the Wernicke–Korsakoff syndrome; however, a recognized episode of Wernicke's is not always obvious. The syndrome and psychosis are named after Sergei Korsakoff, a Russian neuropsychiatrist who discovered the syndrome during the late 19th century.

Anton–Babinski syndrome, also known as visual anosognosia, is a rare symptom of brain damage occurring in the occipital lobe. Those who suffer from it are "cortically blind", but affirm, often quite adamantly and in the face of clear evidence of their blindness, that they are capable of seeing. Failing to accept being blind, the sufferer dismisses evidence of their condition and employs confabulation to fill in the missing sensory input. It is named after Gabriel Anton and Joseph Babinski.

Although non-specific concepts of madness have been around for several thousand years, the psychiatrist and philosopher Karl Jaspers was the first to define the three main criteria for a belief to be considered delusional in his 1913 book "General Psychopathology". These criteria are:

- certainty (held with absolute conviction)

- incorrigibility (not changeable by compelling counterargument or proof to the contrary)

- impossibility or falsity of content (implausible, bizarre, or patently untrue)

Furthermore, when a false belief involves a value judgment, it is only considered a delusion if it is so extreme that it cannot be, or never can be proven true. For example: a man claiming that he flew into the sun and flew back home. This would be considered a delusion, unless he were speaking figuratively, or if the belief had a cultural or religious source.

A delusion is a mistaken belief that is held with strong conviction even when presented with superior evidence to the contrary. As a pathology, it is distinct from a belief based on false or incomplete information, confabulation, dogma, illusion, or some other misleading effects of perception.

Delusions typically occur in the context of neurological or psychiatric disease, although they are not tied to any particular disorder and have been found to occur in the context of many pathological states (both physical and mental). However, they are of particular diagnostic importance in psychotic disorders including schizophrenia, paraphrenia, manic episodes of bipolar disorder, and psychotic depression.

Korsakoff's syndrome, characterised by memory impairment, confabulation, confusion and personality changes, has a strong and recognised link with WE. A very high percentage of patients with Wernicke-Korsakoff syndrome also have peripheral neuropathy, and many alcoholics have this neuropathy without other neurologic signs or symptoms. Korsakoff´s occurs much more frequently in WE due to chronic alcoholism. It is uncommon among those who do not consume alcohol abusively. Up to 80% of WE patients who abuse alcohol develop Korsakoff's syndrome. In Korsakoff's, is usually observed atrophy of the thalamus and the mammillary bodies, and frontal lobe involvement. In a study, half of Wernicke-Korsakoff cases had good recovery from the amnesic state, which may take from 2 months to 10 years.

Depending on the location of the brain lesion different symptoms are more frequent:

- Brainstem tegmentum. - Ocular: pupillary changes. Extraocular muscle palsy; gaze palsy: nystagmus.

- Hypothalamus. Medulla: dorsal nuc. of vagus. - Autonomic dysfunct.: temperature; cardiocirculatory; respiratory.

- Medulla: vestibular region. Cerebellum. - Ataxia.

- Dorsomedial nuc. of thalamus. Mammillary bodies. - Amnestic syndrome for recent memory.

Mamillary lesion are characteristic-small petechial hemorrhages are found.

- Diffuse cerebral dysfunction.- Altered cognition: global confusional state.

- Brainstem: periaqueductal gray.- Reduction of consciousness

- Hypothalamic lesions may also affect the immune system, which is known in alcohol abusers, causing dysplasias and infections.

MRI: medial temporal lobe signal change bilateral hippocampal lesions, with signals that were hypointense in IR sequences and hyperintense in FLAIR.

Age: Children, Young Adult, Elderly

Sex: Both

Onset: Subacute

Clinical features NMDA Ab related patients in adult shows;

- Early features of higher cognitive dysfunction, confusion, behavioural changes, amnesia, dysphasia. Psychiatric: hallucinations, psychotic, agitation, depressive, anxiety, obsessive. Seizures: generalized, complex partial, simple partial.

- Late features: Spontaneous reduction in conscious level, Movement disorder: choreoathetoid (orofacial, upper limbs, lower limbs), parkinsonian, rigidity, myoclonus, oculogyric crises, opisthotonus, startle. Dysautonomia : tachy/brady-cardia, hyperhidrosis, persistent pyrexia, central hypoventilation, labile/high blood pressure, hypersalivation, pseudoobstruction, cardiac asystole.

NMDA Ab related patients in children and adolescent.

Commonly

- Behavioral or personality change, sometimes associated with

- Seizures and

- Sleep dysfunction;

- Severe speech deficits on admission

- Stereotyped movements,

- Autonomic instability

- Hypoventilation

Rarely

- Dyskinesias or dystonia;

Other Cases have similar presentation

- Disorientation,

- Hallucinations

- Confusion

- Memory loss

- Seizures: Partial temporal lobe. Pilomotor Status epilepticus

- Relative absence of cerebellar and brainstem sings

- Post partum psychosis

- Dyskinesias