POCD is common after cardiac surgery, and recent studies have now verified that POCD also exists after major non-cardiac surgery, although at a lower incidence. The risk of POCD increases with age, and the type of surgery is also important because there is a very low incidence associated with minor surgery. POCD is common in adult patients of all ages at hospital discharge after major noncardiac surgery, but only the elderly (aged 60 years or older) are at significant risk for long-term cognitive problems. Patients with POCD are at an increased risk of death in the first year after surgery. Research interest has increased since early 2000, especially as more elderly patients are able to undergo successful minor and major surgeries.

POCD has been studied through various institutions since the inception of the IPOCDS-I study centred in Eindhoven, Netherlands and Copenhagen, Denmark. This study found no causal relationship between cerebral hypoxia and low blood pressure and POCD. Age, duration of anaesthesia, introperative complications, and postoperative infections were found to be associated with POCD.

- POCD is just as likely to occur after operations under regional anesthesia as under general anesthesia.

- More likely after major operations than minor operations.

- More likely after heart operations than other types of surgery.

- More likely in aged than in younger patients.

- More likely in older patients with high alcohol intake/abuse.

- People with higher preoperative ASA physical status scores are more likely to develop POCD.

- People with lower educational level are more likely to develop POCD than those with a higher educational level.

- People with prior history of a stroke, even though there is complete functional recovery, are more likely to develop POCD.

- More likely in the elderly with pre-existing declining mental functions, termed mild cognitive impairment (MCI). MCI is a transitional zone between normal mental function and evident Alzheimer's disease or other forms of dementia. It is insidious, and seldom recognized, except in retrospect after affected persons are evidently demented.

- Delirium and severe worsening of mental function is very likely in those with clinically evident Alzheimer's disease or other forms of dementia, as well as those with a history of delirium after previous operations.

Recent population-based studies have estimated the prevalence of NPH to be about 0.5% in those over 65 years old, with an incidence of about 5.5 patients per 100,000 of people per year. This is in accordance with comparable findings stating that although normal pressure hydrocephalus can occur in both men and women of any age, it is found more often in the elderly population, with a peak onset generally in the sixth to seventh decades.

The body's inflammatory response to surgery likely plays an important role, at least in elderly patients. Various research initiatives during recent years have evaluated whether actions taken before, during and after surgery can lessen the possible deleterious effects of inflammation. For example, anti-inflammatory agents can be given before surgery. During surgery, inflammation can be modulated by temperature control, use of regional rather than general anesthesia or the use of beta blockers. After surgery, optimal pain management and infection control is important. Several studies have shown variable-significance positive effects when a multidisciplinary, multifactorial approach to elderly patient is followed during pre, peri and post-operative care.

Animal studies indicate that volatile anaesthestics may augment the pathological processes of Alzheimer's Disease by affecting amyloid-beta processing. However, in young healthy mice, the volatile anesthetic isoflurane can also produce long-lasting memory impairment. This adverse effect is preventable by pre-administering the GABA(A)α5 inverse agonist L-655,708.

Chronic traumatic encephalopathy (CTE) is a neurodegenerative disease found in people who have had multiple head injuries. Symptoms may include behavioral problems, mood problems, and problems with thinking. This typically does not begin until years after the injuries. It often gets worse over time and can result in dementia. It is unclear if the risk of suicide is altered.

Most documented cases have occurred in athletes involved in contact sports such as football, wrestling, ice hockey, and soccer. Other risk factors include being in the military, prior domestic violence, and repeated banging of the head. The exact amount of trauma required for the condition to occur is unknown. Definitive diagnosis can only occur at autopsy. It is a form of tauopathy.

As of 2017 there is no specific treatment. Rates of disease have been found to be about 30% among those with a history of multiple head injuries. Population rates, however, are unclear. Research into brain damage as a result of repeated head injuries began in the 1920s, at which time the condition was known as "punch drunk". Changing the rules in some sports has been discussed as a means of prevention.

Psycho-organic syndrome is typically diagnosed in individuals following 5–10 years of consistent exposure to chemicals like xylene, toluene, and styrene, which are generally found in paint, plastic and degreasing products.

Patients work and environmental history must be evaluated for exposure to organic chemicals. A traumatic brain injury may also lead to POS.

Consistent intoxication (ie excess use of alcohol and drugs) may also cause a lesion in the brain, eventually leading to POS.

Lyme diseae, the great "new imitator", has been known to mimick depression, scizophreania, depersonazlization disorder, and obsessive-complsive disorder.

Although the cause varies by each individual case, localization of the atrophy in the brain can occur due to aging and without external causes, linked to hereditary.

Prevention includes proper and regular use of Preventive Personal Equipment (PPE) in work environments that involve organic chemicals and limiting alcohol and drug substance intake.

Patients with dementia who are confined to a nursing home and may have undiagnosed NPH can possibly become independent again once treated. So far only one study was able to evaluate the prevalence of NPH, both diagnosed and undiagnosed, among residents of assisted-living facilities, showing a prevalence in 9 to 14% of the residents.

NPH may be relieved by surgically implanting a ventriculoperitoneal shunt to drain excess cerebrospinal fluid to the abdomen where it is absorbed. Once the shunt is in place, the ventricles usually diminish in size in 3 to 4 days, regardless of the duration of the hydrocephalus. Even though the ventricular swelling diminishes, only 21% of patients show a marked improvement in symptoms. The most likely patients to show improvement are those that show only gait disturbance, mild or no incontinence, and mild dementia. A more recent study (2004) found better outcomes, concluding that if patients with idiopathic normal pressure hydrocephalus are correctly identified, shunt insertion yielded beneficial outcomes in 86% of patients, in either gait disturbance (81%), improved continence (70%), or both. They also observed that measurements in the diagnostic clinical triad, the cortical sulci size, and periventricular lucencies were related to outcome. However, other factors such as age of the patient, symptom duration, dilation of ventricles, and the degree of presurgical dementia were unrelated to outcome.

Disorders that cause injury or damage to the brain and contribute to OBS include, but are not limited to:

- Alcoholism

- Alzheimer's Disease

- Attention deficit/hyperactivity disorder

- Autism

- Concussion

- Encephalitis

- Epilepsy

- Fetal alcohol syndrome

- Hypoxia

- Parkinson's disease

- Intoxication/overdose caused by drug abuse including alcoholism

- Sedative hypnotic dependence and drug abuse

- Intracranial hemorrhage/trauma

- Korsakoff Syndrome

- Mastocytosis

- Meningitis

- Psychoorganic syndrome

- Stroke/transient ischemic attack (TIA)

- Withdrawal from drugs, especially sedative hypnotics, e.g. alcohol or benzodiazepines

Other conditions that may be related to organic brain syndrome include: clinical depression, neuroses, and psychoses, which may occur simultaneously with the OBS.

Symptoms of CTE, which occur in four stages, generally appear 8 to 10 years after an athlete experiences repetitive mild traumatic brain injury.

First-stage symptoms include attention deficit hyperactivity disorder as well as confusion, disorientation, dizziness, and headaches. Second-stage symptoms include memory loss, social instability, impulsive behavior, and poor judgment. Third and fourth stages include progressive dementia, movement disorders, hypomimia, speech impediments, sensory processing disorder, tremors, vertigo, deafness, depression and suicidality.

Additional symptoms include dysarthria, dysphagia, cognitive disorder such as amnesia, and ocular abnormalities, such as ptosis.

The condition manifests as dementia, or declining mental ability, problems with memory, dizzy spells or lack of balance to the point of not being able to walk under one's own power for a short time and/or Parkinsonism, or tremors and lack of coordination. It can also cause speech problems and an unsteady gait. Patients with DP may be prone to inappropriate or explosive behavior and may display pathological jealousy or paranoia.

Neurocognitive disorders can have numerous causes: genetics, brain trauma, stroke, and heart issues. The main causes are neurodegenerative diseases such as Alzheimer's disease, Parkinson's disease, and Huntington's disease because they affect or deteriorate brain functions. Other diseases and conditions that cause NDCs include vascular dementia, frontotemporal degeneration, Lewy body disease, prion disease, normal pressure hydrocephalus, and dementia/neurocognitive issues due to HIV infection. They may also include dementia due to substance abuse or exposure to toxins.

Neurocongnitive disorder may also be caused by brain trauma, including concussions and Traumatic Brain Injuries, as well as post-traumatic stress and alcoholism. This is referred to as amnesia, and is characterized by damage to major memory encoding parts of the brain such as the hippocampus. Difficulty creating recent term memories is called anterograde amnesia and is caused by damage to the hippocampus part of the brain, which is a major part of the memory process. Retrograde amnesia is also caused by damage to the hippocampus, but the memories that were encoded or in the process of being encoded in long term memory are erased

The onset of alcohol dementia can occur as early as age thirty, although it is far more common that the dementia will reveal itself anywhere from age fifty to age seventy. The onset and the severity of this type of dementia is directly correlated to the amount of alcohol that a person consumes over his or her lifetime.

Epidemiological studies show an association between long-term alcohol intoxication and dementia. Alcohol can damage the brain directly as a neurotoxin, or it can damage it indirectly by causing malnutrition, primarily a loss of thiamine (vitamin B1). Alcohol abuse is common in older persons, and alcohol-related dementia is under-diagnosed. A discredited French study claimed that moderate alcohol consumption (up to four glasses of wine per week) protected against dementia, whereas higher rates of consumption have conclusively been shown to increase the chances of getting it.

It should be noticed that describing the causation of reversible dementia is extremely difficult due to the complicated biopsychological systems and the hard-to-define collection of factors associated with cognitive decline.

Roughly, the etiological factors that contribute to cognitive decline could be assigned into four categories: chemical, environmental, physical, and psychiatric. Chemical intoxication might be attributed to anesthesia, alcohol, heavy metal and commonly used medications. Jenike (1988) has recorded a certain amount of medications which may induce cognitive change in elder people.

The list is provided below.

Environmental sources include overstimulation, radical changes in lifestyle, and sensory impairment. Physical disorders which are mostly induced by the aging process, consist of thyroid and other endocrine-system deprivation; metabolic disturbance, and vitamin deficiency. Psychiatric disorders, such as chronic schizophrenia and depression could also produce cognitive decline.

In summary, the etiological factors of reversible dementia are various, subtle and frequently interactive. Therefore, in-depth medical and psychosocial evaluations are vital for accurate diagnosis and treatment design. It is important for families and patients to understand the difficulties in determining an correct diagnosis and be prepared for probable frustration and confusion during evaluation and assessment process.

Treatment of OBS varies with the causative disorder or disease. It is important to note that it is not a primary diagnosis and a cause needs to be sought out and treated.

Vascular dementia is the second-most-common form of dementia after Alzheimer's disease (AD) in older adults. The prevalence of the illness is 1.5% in Western countries and approximately 2.2% in Japan. It accounts for 50% of all dementias in Japan, 20% to 40% in Europe and 15% in Latin America. The incidence of dementia is nine times higher in patients who have had a stroke than in controls. 25% of stroke patients develop new-onset dementia within 1 year of their stroke. The relative risk of incident dementia is 5.5% within four years of suffering a stroke.

One study found that in the United States specifically, the prevalence of vascular dementia in all individuals over the age of 71 is 2.43%, and another found that the prevalence of the dementias doubles with every 5.1 years of age.

The incidence peaks between the fourth and the seventh decades of life and 80% of patients have a history of hypertension.

The prevalence of MCI varies by age. The prevalence of MCI among different age groups is as follows: 6.7% for ages 60–64; 8.4% for ages 65–69, 10.1% for ages 70–74, 14.8% for ages 75–79, and 25.2% for ages 80–84. After a two-year follow-up, the cumulative incidence of dementia among individuals who are over 65 years old and were diagnosed with MCI was found to be 14.9%.

Globally, approximately 16% of the population over the age of 70 experiences some type of mild cognitive impairment.

MCI does not usually interfere with daily life, but around 50 percent of people diagnosed with it go on to develop the far more severe Alzheimer's disease within five years. However, some instances of MCI may simply remain stable over time or even remit.

Pseudosenility also reversible dementia is a condition where older people are in a state of memory loss, confusion, or disorientation that may have a cause other than the ordinary aging process. Generally, the term "reversible dementia" is used to describe most cases. A more specific term "Pseudodementia" is referring to "behavioral changes that resembler those of the progressive degenerative dementias, but which are attributable to so-called functional causes".

The "New York Times" reports that illnesses such as the flu and hydrocephalus, as well as side-effects to common medications, can produce symptoms in the elderly that are difficult to distinguish from ordinary dementia caused by aging. However, if the real cause of the effects is caught early enough, the effects can be reversed. According to studies cited in Cunha (1990), approximate 10% to 30% of patients who have exhibited symptoms of dementia might have a treatable or reversible pathologic process to some extent.

Studies have shown that PCA may be a variant of Alzheimer's disease (AD), with an emphasis on visual deficits. Although in primarily different, but sometimes overlapping, brain regions, both involve progressive neural degeneration, as shown by the loss of neurons and synapses, and the presence of neurofibrillary tangles and senile plaques in affected brain regions; this eventually leads to dementia in both diseases. PCA patients have more cortical damage and gray matter (cell body) loss in posterior regions, especially in the occipital, parietal, and temporal lobes, whereas Alzheimer’s patients typically experience more damage in the prefrontal cortex and hippocampus. PCA tends to impair working memory and anterograde memory, while leaving episodic memory intact, whereas AD patients typically have damaged episodic memory, suggesting some differences still lie in the primary areas of cortical damage.

Over time, however, atrophy in PCA patients may spread to regions commonly damaged in AD patients, leading to common AD symptoms such as deficits in memory, language, learning, and cognition. Although PCA has an earlier onset, many PCA patients have also been diagnosed with Alzheimer’s, suggesting that the degeneration has simply migrated anteriorly to other cortical brain regions.

There is no standard definition of PCA and no established diagnostic criteria, so it is not possible to know how many people have the condition. Some studies have found that about 5 percent of people diagnosed with Alzheimer’s disease have PCA. However, because PCA often goes unrecognized, the true percentage may be as high as 15 percent. Researchers and physicians are working to establish a standard definition and diagnostic criteria for PCA.

PCA may also be correlated with the diseases of Lewy body, Creutzfeldt–Jakob disease, Bálint's syndrome, and Gerstmann syndrome. In addition, PCA may result in part from mutations in the presenilin 1 gene (PSEN1).

Many studies have been conducted to determine average survival of patients with dementia. The studies were frequently small and limited, which caused contradictory results in the connection of mortality to the type of dementia and the patient's gender. A very large study conducted in Netherlands in 2015 found that the one-year mortality was three to four times higher in patients after their first referral to a day clinic for dementia, when compared to the general population. If the patient was hospitalized for dementia, the mortality was even higher than in patients hospitalized for cardiovascular disease. Vascular dementia was found to have either comparable or worse survival rates when compared to Alzheimer's Disease, however another very large 2014 Swedish study found that prognosis was worse for male and older patients.

Unlike Alzheimer's Disease, which weakens the patient, causing them to succumb to bacterial infections like pneumonia, vascular dementia can be a direct cause of death due to the possibility of a fatal interruption in the brain's blood supply.

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.

Psychoorganic syndrome is a combination of various symptoms that are caused by organic changes in the brain. The exact component of the solvents that causes the neurological disorder is difficult to isolate due to worker generally being exposed to mixtures of various grades, compositions, and purity of solvents.

At the initial stage, asthenia is prevalent and the progress of the disorder is slow. Acute onset can be diagnosed when a large amount of psychological symptoms surface. The final stage of the disorder is made up of numerous disorders, including demntia, Korsakov's syndrome, and includes severe personality change such as depression, anxiety, memory loss, and drastic change in intellect. Level of kindness, happiness, and insight are greatly affect in the final stage.

The disorder stems from a defect in brain tissue, usually atrophy from another neurological disorder." In pathological findings, focal or diffuse signs of atrophy without inflammation or severe vascular insufficiency are present. Basic clinical picture depends on the localization of atrophy in brain."Although the exact mechanism that solvents have on the nervous system are not fully understood, the metabolism of the solvents in the body that turn them into toxic intermediates are important. Some evidence shows that genetic polymorphisms affect the activity of metabolic enzymes that metabolize foreign chemicals.

While the specific causes of sundowning have not been empirically proven, some evidence suggests that circadian rhythm disruption increases sundowning behaviors. In humans, sunset triggers a biochemical cascade that involves a reduction of dopamine levels and a shift towards melatonin production as the body prepares for sleep. In individuals with dementia, melatonin production may be decreased, which may interrupt other neurotransmitter systems.

Sundowning should be distinguished from delirium, and should be presumed to be delirium when it appears as a new behavioral pattern until a causal link between sunset and behavioral disturbance is established. Patients with established sundowning and no obvious medical illness may be suffering from impaired circadian regulation, or may be affected by nocturnal aspects of their institutional environment such as shift changes, increased noise, or reduced staffing (which leads to fewer opportunities for social interaction).

Delirium can be caused by the worsening of previous medical conditions, substance abuse or withdrawal, mental illness, severe pain, immobilization, sleep deprivation and hypnosis.

Other common causes that may increase the risk of delirium include infections of urinary tract, skin and stomach, pneumonia, old age, and poor nutrition.

Sundowning, or sundown syndrome, is a neurological phenomenon associated with increased confusion and restlessness in patients with delirium or some form of dementia. Most commonly associated with Alzheimer's disease, but also found in those with other forms of dementia, the term "sundowning" was coined due to the timing of the patient's confusion. For patients with sundowning syndrome, a multitude of behavioral problems begin to occur in the evening or while the sun is setting. Sundowning seems to occur more frequently during the middle stages of Alzheimer's disease and mixed dementia. Patients are generally able to understand that this behavioral pattern is abnormal. Sundowning seems to subside with the progression of a patient's dementia. Research shows that 20–45% of Alzheimer's patients will experience some sort of sundowning confusion.

Anosodiaphoria is a condition in which a person who suffers disability due to brain injury seems indifferent to the existence of their handicap. Anosodiaphoria is specifically used in association with indifference to paralysis. It is a somatosensory agnosia, or a sign of neglect syndrome. It might be specifically associated with defective functioning of the frontal lobe of the right hemisphere.

Joseph Babinski first used the term anosodiaphoria in 1914 to describe a disorder of the body schema in which patients verbally acknowledge a clinical problem (such as hemiparesis) but fail to be concerned about it. Anosodiaphoria follows a stage of anosognosia, in which there may be verbal, explicit denial of the illness, and after several days to weeks, develop the lack of emotional response. Indifference is different from denial because it implies a lack of caring on the part of the patient whom otherwise acknowledges his or her deficit.

Binswanger's disease, also known as subcortical leukoencephalopathy, is a form of small vessel vascular dementia caused by damage to the white brain matter. White matter atrophy can be caused by many circumstances including chronic hypertension as well as old age. This disease is characterized by loss of memory and intellectual function and by changes in mood. These changes encompass what are known as executive functions of the brain. It usually presents between 54 and 66 years of age, and the first symptoms are usually mental deterioration or stroke.

It was described by Otto Binswanger in 1894, and Alois Alzheimer first used the phrase "Binswanger's disease" in 1902. However, Olszewski is credited with much of the modern-day investigation of this disease which began in 1962.