Alzheimer's disease (AD), which is known to be associated with frontal lobe dysfunction, is implicated as a cause of source amnesia. In laboratory conditions, one study found source monitoring to be so poor that the AD participants were correctly performing source memory attributions at approximately chance. This lack of ability to attribute the source of memories is likely related to AD patients' deficits in reality monitoring. Reality monitoring, the process of distinguishing whether information originated from an external or an internal source, relies on judgement processes to examine the qualitative characteristics of the information in order to determine if the information was real or imagined. It appears that it is this process that is experiencing the dysfunction, which causes mild confabulation in some AD patients, as well as being related to the source amnesia experienced in some individuals with AD.

It is normal to have some level of memory distrust, or the lack of trusting in one's own memory. This may occur when speaking with your parents about your childhood, for example. However it seems that everyone has their own level of memory distrust, and memory distrust syndrome seems to be a severe case.

The direct cause is unknown; however, it is possibly a defense or coping mechanism to a preexisting condition that would alter one's memory. This could involve frontal lobe lesions, Alzheimer's disease, amnesia, dementia, or other conditions. Any condition that would alter either existing memories or the formation of new memories could cause a coping scheme such as memory distrust syndrome. Alternatively, an individual may have learned over time to not trust their own memory from conditioning, and as such the individual would develop a defense mechanism to remove themselves from potential embarrassment.

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.

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

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 alcoholism). Additionally confabulation often occurs in people who are suffering from 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. This type of confabulation is commonly seen in Korsakoff's syndrome.

Source amnesia is not a rare phenomenon – everybody experiences it on a near daily basis as, for much of our knowledge, it is important to remember the knowledge itself, rather than its source. However, there are extreme examples of source amnesia caused by a variety of factors.

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.

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.

Normal aging, although not responsible for causing memory disorders, is associated with a decline in cognitive and neural systems including memory (long-term and working memory). Many factors such as genetics and neural degeneration have a part in causing memory disorders. In order to diagnose Alzheimer's disease and dementia early, researchers are trying to find biological markers that can predict these diseases in younger adults. One such marker is a beta-amyloid deposit which is a protein that deposits on the brain as we age. Although 20-33% of healthy elderly adults have these deposits, they are increased in elderly with diagnosed Alzheimer's disease and dementia.

Additionally, traumatic brain injury, TBI, is increasingly being linked as a factor in early-onset Alzheimer's disease.

One study examined dementia severity in elderly schizophrenic patients diagnosed with Alzheimer's disease and dementia versus elderly schizophrenic patients without any neurodegenerative disorders. In most cases, if schizophrenia is diagnosed, Alzheimer's disease or some form of dementia in varying levels of severity is also diagnosed. It was found that increased hippocampal neurofibrillary tangles and higher neuritic plaque density (in the superior temporal gyrus, orbitofrontal gyrus, and the inferior parietal cortex) were associated with increased severity of dementia. Along with these biological factors, when the patient also had the apolipoprotein E (ApoE4) allele (a known genetic risk factor for Alzheimer's disease), the neuritic plaques increased although the hippocampal neurofibrillary tangles did not. It showed an increased genetic susceptibility to more severe dementia with Alzheimer's disease than without the genetic marker.

As seen in the examples above, although memory does degenerate with age, it is not always classified as a memory disorder. The difference in memory between normal aging and a memory disorder is the amount of beta-amyloid deposits, hippocampal neurofibrillary tangles, or neuritic plaques in the cortex. If there is an increased amount, memory connections become blocked, memory functions decrease much more than what is normal for that age and a memory disorder is diagnosed.

The cholinergic hypothesis of geriatric memory dysfunction is an older hypothesis that was considered before beta-amyloid deposits, neurofibrillary tangles, or neuritic plaques. It states that by blocking the cholinergic mechanisms in control subjects you can examine the relationship between cholinergic dysfunction and normal aging and memory disorders because this system when dysfunctional creates memory deficits.

Internationally, the prevalence rates of WKS are relatively standard, being anywhere between zero and two percent. Despite this, specific sub-populations seem to have higher prevalence rates including people who are homeless, older individuals (especially those living alone or in isolation), and psychiatric inpatients. Additionally, studies show that prevalence is not connected to alcohol consumption per capita. For example, in France, a country that is well known for its consumption and production of wine, prevalence was only 0.4% in 1994, while Australia had a prevalence of 2.8%.

The fact that gastrointestinal surgery can lead to the development of WKS was demonstrated in a study that was completed on three patients who recently undergone a gastrectomy. These patients had developed WKS but were not alcoholics and had never suffered from dietary deprivation. WKS developed between 2 and 20 years after the surgery. There were small dietary changes that contributed to the development of WKS but overall the lack of absorption of thiamine from the gastrointestinal tract was the cause. Therefore, it must be ensured that patients who have undergone gastrectomy have a proper education on dietary habits, and carefully monitor their thiamine intake. Additionally, an early diagnosis of WKS, should it develop, is very important.

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.

The most effective method of preventing Korsakoff's syndrome is to avoid B vitamin/thiamine deficiency. In Western nations, the most common causes of such a deficiency are alcoholism and eating disorders. Because these are behavioral-induced causes, Korsakoff's syndrome is essentially considered a preventable disease. Thus, fortifying foods with thiamine, or requiring companies that sell alcoholic beverages to supplement them with B vitamins in general or thiamine in particular, could avert many cases of Korsakoff's Syndrome.

A number of factors may increase a person's risk to develop Korsakoff’s syndrome. These factors are often related to patients’ general health and their food intake habits.

- Age

- Alcoholism

- Chemotherapy

- Dialysis

- Extreme dieting

- Genetic factors

The prevalence varies from country to country, but is estimated to be around 12.5% of heavy drinkers.

The term "reduplicative paramnesia" was first used in 1903 by psychiatrist Arnold Pick to describe a condition in a patient with suspected Alzheimer's disease who insisted that she had been moved from Pick's city clinic to one she claimed looked identical but was in a familiar suburb. To explain the discrepancy she further claimed that Pick and the medical staff worked at both locations.

In retrospect, however, the phenomenon has been found to have been first reported by the Swiss naturalist Charles Bonnet in 1788, who described a woman who also had what would now be called Cotard delusion. Henry Head and Paterson and Zangwill later reported on soldiers who had the delusional belief that their hospital was located in their home town, although in these cases traumatic brain injury seemed to be the most likely cause.

It wasn't until 1976 that serious consideration was given to the disorder, when three cases were reported by Benson and colleagues. Benson not only described striking reduplication syndromes in his patients, but also attempted to explain the phenomena in terms of the neurocognitive deficits also present in the patients. This was one of the first attempts to give a neuropsychological explanation for the disorder.

The most frequent cause of the syndrome is brain damage to the frontal lobe. Brain damage leading to the dysexecutive pattern of symptoms can result from physical trauma such as a blow to the head or a stroke or other internal trauma.

It is important to note that frontal lobe damage is not the only cause of the syndrome. It has been shown that damage, such as lesions, in other areas of the brain may indirectly affect executive functions and lead to similar symptoms. There is not one specific pattern of damage that leads to DES, as multiple affected brain structures and locations have led to the symptoms. This is one reason why the term frontal lobe syndrome is not preferred.

DES often occurs with other disorders, which is known as comorbidity. Many studies have examined the presence of DES in patients with schizophrenia. Results of schizophrenic patients on the "Behavioural Assessment of the Dysexecutive Syndrome (BADS)" test (discussed below) are comparable to brain injured patients. Further, results of BADS have been shown to correlate with phases of schizophrenia. Patients in the chronic phase of the disorder have significantly lower scores than those who are acute. This is logical due to the similarities in executive disruptions that make everyday life difficult for those with schizophrenia and symptoms that form DES.

Patients with Alzheimer's disease have been shown to exhibit impairment in executive functioning as well. The effects of DES symptoms on the executive functions and working memory, such as attentiveness, planning and remembering recently learned things, are some of the earliest indicators of Alzheimer's.

Studies have also indicated that chronic alcoholism (see Korsakoff's syndrome) can lead to a mild form of DES according to results of BADS.

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.

Explaining the causes of delusions continues to be challenging and several theories have been developed. One is the genetic or biological theory, which states that close relatives of people with delusional disorder are at increased risk of delusional traits. Another theory is the dysfunctional cognitive processing, which states that delusions may arise from distorted ways people have of explaining life to themselves. A third theory is called motivated or defensive delusions. This one states that some of those persons who are predisposed might suffer the onset of delusional disorder in those moments when coping with life and maintaining high self-esteem becomes a significant challenge. In this case, the person views others as the cause of their personal difficulties in order to preserve a positive self-view.

This condition is more common among people who have poor hearing or sight. Also, ongoing stressors have been associated with a higher possibility of developing delusions. Examples of such stressors are immigration, low socioeconomic status, and even possibly the accumulation of smaller daily hassles.

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.

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.

Wernicke's encephalopathy has classically been thought of as a disease solely of alcoholics, but it is also found in the chronically undernourished, and in recent years had been discovered post bariatric surgery. Without being exhaustive, the documented causes of Wernicke's encephalopathy have included:

- pancreatitis, liver dysfunction, chronic diarrhea, celiac disease, Crohn's disease, uremia, thyrotoxicosis

- vomiting, hyperemesis gravidarum, malabsorption, gastrointestinal surgery or diseases

- incomplete parenteral nutrition, starvation/fasting

- chemotherapy, renal dialysis, diuretic therapy, stem cell/marrow transplantation

- cancer, AIDS, Creutzfeldt–Jakob disease, febrile infections

- this disease may even occur in some people with normal, or even high blood thiamine levels, are people with deficiencies in intracellular transport of this vitamin. Selected genetic mutations, including presence of the X-linked transketolase-like 1 gene, SLC19A2 thiamine transporter protein mutations, and the aldehyde dehydrogenase-2 gene, which may predispose to alcoholism. The APOE epsilon-4 allele, involved in Alzheimer's disease, may increase the chance of developing neurological symptoms.

There are hospital protocols for prevention, supplementing with thiamine in the presence of: history of alcohol misuse or related seizures, requirement for IV glucose, signs of malnutrition, poor diet, recent diarrhea or vomiting, peripheral neuropathy, intercurrent illness, delirium tremens or treatment for DTs, and others. Some experts advise parenteral thiamine should be given to all at-risk patients in the emergency room.

In the clinical diagnosis should be remembered that early symptoms are nonspecific, and it has been stated that WE may present nonspecific findings. There is consensus to provide water-soluble vitamins and minerals after gastric operations.

In some countries certain foods have been supplemented with thiamine, and have reduced WE cases. Improvement is difficult to quantify because they applied several different actions. Avoiding alcohol and having adequate nutrition reduces one of the main risk factors in developing Wernicke-Korsakoff syndrome.

Prognosis is poor, however, current analysis suggests that those associated with thymoma, benign or malignant, show a less favorable prognosis (CASPR2 Ab positive).

Most common cause of autoimmune encephalitis after acute demyelinating encephalitis in England. More than 500 cases have been reported in literature till 2013. In California Encephalitis Project it was found >4 times as frequently as herpes simplex virus type 1 (HSV-1), varicella-zoster virus (VZV), and West Nile virus (WNV). Among patients with first-onset schizophrenia incidence varies between 6–10%.

- Age – frequently 5–76 years, Median age of patients was 23 years

- Sex – 80% Female