Glucocorticoid medications have been known to be associated with significant side effects involving behavior and mood, regardless of previous psychiatric or cognitive condition, since the early 1950s. But cognitive side effects of steroid medications involving memory and attention are not as widely publicized and may be misdiagnosed as separate conditions, such as attention deficit disorder (ADHD or ADD) in children or early Alzheimer's disease in elderly patients.

Regions of the brain with a high density of glucocorticoid receptors (GRs) including the hippocampus, hypothalamus, and prefrontal cortex are particularly sensitive to elevated circulating levels of glucocorticoids even in the absence of stress. Scientific studies have mainly focused on the impact of glucocorticoids on the hippocampus because of its role in memory processes and on the prefrontal cortex for its role in attention and executive function.

Elevated glucocorticoid activity is associated with down-regulation of GRs (known as "glucocorticoid cascade hypothesis"), which diminishes neuroreparative activity and attenuates neurogenesis that can result in decreased hippocampal volume with prolonged glucocorticoid exposure.

Variations in individual sensitivity to glucocorticoid medications may be due to either GR hypofunction or hyperfunction. Similarly, variations in individual hypothalamic-pituitary-adrenal (HPA) axis responsiveness can modulate the type and number of side effects.

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.

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.

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.

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).

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.

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.

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.

It is thought that with the development of plaques and tangles associated with Alzheimer's disease there might be a disruption within the suprachiasmatic nucleus (SCN). The suprachiasmatic nucleus is associated with regulating sleep patterns by maintaining circadian rhythms, which are strongly associated with external light and dark cues. A disruption within the suprachiasmatic nucleus would seem to be an area that could cause the types of confusion that are seen in sundowning. However, finding evidence for this is difficult, as an autopsy is needed to definitively diagnose Alzheimer's in a patient. Once an Alzheimer's patient has died, they have usually surpassed the level of dementia and brain damage that would be associated with sundowning. This hypothesis is, however, supported by the effectiveness of melatonin, a natural hormone, to decrease behavioral symptoms associated with sundowning.

Another cause can be oral problems, like tooth decay with pain. When the time a meal is served comes close, a patient can show symptoms of sundowning. This cause is not widely recognized, however anticipation of food can increase dopamine levels, and dopamine and melatonin have an antagonistic relationship.

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.

Pseudodementia is a phenotype approximated by a wide variety of underlying disorders (1). Data indicate that some of the disorders that can convert to a pseudodementia-like presentation include depression (mood), schizophrenia, mania, dissociative disorders, Ganser syndrome, conversion reaction, and psychoactive drugs (2). Although the frequency distribution of disorders presenting as pseudodementia remains unclear, what is clear is that depressive pseudodementia, synonymously referred to as depressive dementia(3) or major depression with depressive dementia (4), represents a major subclass of the overarching category of pseudodementia (4).

It has long been observed that in the differential diagnosis between dementia and pseudodementia, depressive pseudodementia appears to be the single most difficult disorder to distinguish from nosologically established "organic" categories of dementia(5), especially degenerative dementia of the Alzheimer type (6).

Depressive Pseudodementia is a syndrome seen in older people in which they exhibit symptoms consistent with dementia but the cause is actually depression.

Older people with predominant cognitive symptoms such as loss of memory, and vagueness, as well as prominent slowing of movement and reduced or slowed speech, were sometimes misdiagnosed as having dementia when further investigation showed they were suffering from a major depressive episode. This was an important distinction as the former was untreatable and progressive and the latter treatable with antidepressant therapy or electroconvulsive therapy or both. In contrast to major depression, dementia is a progressive neurodegenerative syndrome involving a pervasive impairment of higher cortical functions resulting from widespread brain pathology.

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).

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.

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.

Currently, an estimated 60 to 75% of diagnosed dementias are of the Alzheimer's and mixed (Alzheimer's and vascular dementia) type, 10 to 15% are Lewy body type, with the remaining types being of an entire spectrum of dementias, including frontotemporal lobar degeneration (Pick's disease), alcoholic dementia, pure vascular dementia, etc. Dementia with Lewy bodies tends to be under-recognized. Dementia with Lewy bodies is slightly more prevalent in men than women. DLB increases in prevalence with age; the mean age at presentation is 75 years.

Dementia with Lewy bodies affects about one million individuals in the United States.

There are four main causes of easily reversible dementia: hypothyroidism, vitamin B12 deficiency, Lyme disease, and neurosyphillis. All people with memory difficulty should be checked for hypothyroidism and B12 deficiency. For Lyme disease and neurosyphilis, testing should be done if there are risk factors for those diseases in the person. Because risk factors are often difficult to determine, testing for neurosyphillis and Lyme disease as well as the other mentioned factors may be undertaken as a matter of course in cases where dementia is suspected.

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.

Chronic inflammatory conditions that may affect the brain and cognition include Behçet's disease, multiple sclerosis, sarcoidosis, Sjögren's syndrome, systemic lupus erythematosus, celiac disease, and non-celiac gluten sensitivity. This type of dementias can rapidly progress, but usually have a good response to early treatment. This consists of immunomodulators or steroid administration, or in certain cases, the elimination of the causative agent.

Alcohol has a direct effect on brain cells in the front part of the brain, resulting in poor judgment, difficulty making decisions, and lack of insight. Long-time alcohol abuse can often lead to poor nutrition problems causing parts of the brain to be damaged by vitamin deficiencies. These problems could also cause personality changes in some people.

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

Vascular dementia can be caused by ischemic or hemorrhagic infarcts affecting multiple brain areas, including the anterior cerebral artery territory, the parietal lobes, or the cingulate gyrus. On rare occasion, infarcts in the hippocampus or thalamus are the cause of dementia.

Brain vascular lesions can also be the result of diffuse cerebrovascular disease, such as small vessel disease.

Risk factors for vascular dementia include age, hypertension, smoking, hypercholesterolemia, diabetes mellitus, cardiovascular disease, and cerebrovascular disease.

Other risk factors include geographic origin, genetic predisposition, and prior strokes.

Vascular dementia can sometimes be triggered by cerebral amyloid angiopathy, which involves accumulation of beta amyloid plaques in the walls of the cerebral arteries, leading to breakdown and rupture of the vessels. Since amyloid plaques are a characteristic feature of Alzheimer's Disease, vascular dementia may occur as a consequence. Cerebral amyloid angiopathy can, however, appear in people with no prior dementia condition. Some beta amyloid plaques are often present in cognitively normal elderly persons.

Typically, females and older patients with organic brain changes are more likely to develop Pisa syndrome. Organic brain changes are physical changes in the brain which lead to neurological dysfunction, including dementia and frontal lobe syndrome. This includes the presence of neurodegenerative illnesses such as Alzheimer's Disease and Parkinson's Disease.

Pisa syndrome is predominantly caused by a prolonged administration or an overly dosed administration of antipsychotic drugs. Although antipsychotic drugs are known to be the main drugs that are concerned with this syndrome, several other drugs are reported to have caused the syndrome as well. Certain antidepressants, psychoactive drugs, and antiemetics have also been found to cause Pisa syndrome in patients.

Drugs found to have caused Pisa Syndrome:

- Atypical antipsychotic drugs- ex. clozapine, aripiprazole

- Tricyclic antidepressants- ex. clomipramine

- Psychoactive drugs

- Antiemetic drugs

- Cholinesterase inhibitors

- Galantamine

Based on the drugs that caused Pisa syndrome, it has been implicated that the syndrome may be due to a dopaminergic-cholinergic imbalance or a serotonergic or noradrenergic dysfunction. For the development of Pisa syndrome that cannot be alleviated by anticholinergic drugs, it has been considered that asymmetric brain functions or neural transmission may be the underlying mechanism. How these drugs interact with the biochemistry of the brain to cause the syndrome is unknown and a topic of current research.

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