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

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.

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.

Socioeconomic correlates of health have been well established in the study of heart disease, lung cancer, and diabetes. Many of the explanations for the increased incidence of these conditions in people with lower socioeconomic status (SES) suggest they are the result of poor diet, low levels of exercise, dangerous jobs (exposure to toxins etc.) and increased levels of smoking and alcohol intake in socially deprived populations. Hesdorffer et al. found that low SES, indexed by poor education and lack of home ownership, was a risk factor for epilepsy in adults, but not in children in a population study. Low socioeconomic status may have a cumulative effect for the risk of developing epilepsy over a lifetime.

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.

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.

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.

PCCI affects a subset of cancer survivors, though the overall epidemiology and prevalence is not well known and may depend on many factors.

It generally affects about 10–40% of breast cancer patients, with higher rates among pre-menopausal women and patients who receive high-dose chemotherapy.

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.

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.

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.

Population-based studies of KLS have not been performed. Its prevalence is about 1 case per million people. In France, KLS has a prevalence of 1.5 per million people. It occurs most frequently among Jews in the US and Israel. First-degree relatives of people who have suffered from the syndrome are much more likely than the general population to suffer from it, although only in about one percent of cases do family members contract it. About 70 to 90 percent of patients are male. Patients with the syndrome are more likely than the general population to have genetic disorders, and about a third of people with the syndrome encountered some form of birth difficulty. In a study of 186 older patients, about ten percent had preexisting psychiatric issues. One study found that about ten percent of patients had a neurological condition before KLS developed. The condition does not appear to occur most frequently in one season.

It is not known what causes KLS, but several mechanisms have been proposed. One possible explanation is hypothalamic or circadian dysfunction. The thalamus probably plays a role in the out-of-control sleeping, and patients with diencephalic–hypothalamic dysfunction caused by tumors experience symptoms similar to those of KLS patients. Specifically, the medial temporal regions of the thalamus may be involved, although examinations of KLS patients have not consistently found abnormalities in this area. The temporal lobe also appears to play a role in the condition, possibly causing cognitive difficulties. The apathy and disinhibition found in some KLS sufferers suggest that the condition may include frontal lobe dysfunction as well. The involvement of the thalamus, temporal lobe, and frontal lobe of the brain suggests that there is a multifocal, localized encephalopathy. There are also persistent subclinical abnormalities in KLS sufferers.

Another possible explanation concerns the metabolism of serotonin and dopamine. An imbalance in the neurotransmitter pathways of these chemicals could play a role. Viral infections have also been suggested as a possible cause. Evidence for their role includes lesions found in autopsies. CSF samples from KLS patients indicate that the condition has a different cause than influenza-associated encephalopathy. Triggers of KLS may also affect the blood-brain barrier, which could play a role in the condition. There is limited evidence of what role hypocretin may play, although it often influences hypersomnia.

Androgen might (indirectly) block melatonin receptors, possibly by mean of vasodilation, and cause cholinergic abnormalities in some cases of Kleine–Levin syndrome.

Because KLS occurs at a much higher rate in Jews and in some families, it is likely that there is some genetic component in addition to environmental factors. Genetic studies hold promise for understanding the disease, but they have yielded inconsistent results and few patients are available for testing.

Epilepsy and depression do not appear to cause KLS. The condition's rapid onset after infections indicates that the immune system is not to blame.

There were also observations that hippocampal sclerosis was associated with vascular risk factors. Hippocampal sclerosis cases were more likely than Alzheimer's disease to have had a history of stroke (56% vs. 25%) or hypertension (56% vs. 40%), evidence of small vessel disease (25% vs. 6%), but less likely to have had diabetes mellitus (0% vs. 22%).

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.

In order for dogs to cope with CCD with as little frustration as possible, it is important to make the transition into the progression of the disease easy and stress free. The environment in which the dog lives is prevalent in the coping process. To keep the environment familiar to the dog, consider eliminating clutter around the house to prevent obstacles for the dog, keep commands short as to avoid confusion, immerse the dog in short, friendly play sessions, and develop a feeding and watering schedule that sticks to a routine. Avoid changing decorations or rearranging furniture in the house, as this will avoid confusion and problems with moving around. When these precautions are taken, the dog will have a higher chance of living longer with as little effects of CCD as possible.

Dogs with canine cognitive dysfunction may exhibit many symptoms associated senile behavior and dementia. Dogs will often find themselves confused in familiar places of the home, spending long periods of time in one area of the home, not responding to calls or commands, and experiencing abnormal sleeping patterns. Although some of these symptoms may be attributed to old age itself, when they are exhibited together, there is a higher likelihood of CCD.

While frustrating, the ultimate outcome is very good: symptoms typically disappear in about four years.

Cerebellar cognitive affective syndrome (CCAS), also called "Schmahmann's syndrome" is a condition that follows from lesions (damage) to the cerebellum of the brain. This syndrome, described by Dr. Jeremy Schmahmann and his colleagues refers to a constellation of deficits in the cognitive domains of executive function, spatial cognition, language, and affect resulting from damage to the cerebellum. Impairments of executive function include problems with planning, set-shifting, abstract reasoning, verbal fluency, and working memory, and there is often perseveration, distractibility and inattention. Language problems include dysprosodia, agrammatism and mild anomia. Deficits in spatial cognition produce visual–spatial disorganization and impaired visual–spatial memory. Personality changes manifest as blunting of affect or disinhibited and inappropriate behavior. These cognitive impairments result in an overall lowering of intellectual function. CCAS challenges the traditional view of the cerebellum being responsible solely for regulation of motor functions. It is now thought that the cerebellum is responsible for monitoring both motor and nonmotor functions. The nonmotor deficits described in CCAS are believed to be caused by dysfunction in cerebellar connections to the cerebral cortex and limbic system.

In psychology and neuroscience, executive dysfunction, or executive function deficit, is a disruption to the efficacy of the executive functions, which is a group of cognitive processes that regulate, control, and manage other cognitive processes. Executive dysfunction can refer to both neurocognitive deficits and behavioural symptoms. It is implicated in numerous psychopathologies and mental disorders, as well as short-term and long-term changes in non-clinical executive control.

Executive dysfunction is not the same as dysexecutive syndrome, a term coined by Alan Baddeley to describe a common pattern of dysfunction in executive functions, such as deficiencies in planning, abstract thinking, flexibility and behavioural control. This group of symptoms, usually resulting from brain damage, tend to occur together. However, the existence of dysexecutive syndrome is controversial.

Symptoms of frontotemporal dementia progress at a rapid, steady rate. Patients suffering from the disease can survive between 2–15 years. Eventually patients will need 24-hour care for daily function.

CSF leaks are a known cause of reversible frontotemporal dementia.

Currently there are no clinically established laboratory investigations available to predict prognosis or therapeutic response.

Tumors in children who develop OMS tend to be more mature, showing favorable histology and absence of n-myc oncogene amplification than similar tumors in children without symptoms of OMS. Involvement of local lymph nodes is common, but these children rarely have distant metastases and their prognosis, in terms of direct morbidity and mortality effects from the tumor, is excellent. The three-year survival rate for children with non-metastatic neuroblastoma and OMS was 100% according to Children’s Cancer Group data (gathered from 675 patients diagnosed between 1980 and 1994); three-year survival in comparable patients with OMS was 77%. Although the symptoms of OMS are typically steroid-responsive and recovery from acute symptoms of OMS can be quite good, children often suffer lifelong neurologic sequelae that impair motor, cognitive, language, and behavioral development.

Most children will experience a relapsing form of OMS, though a minority will have a monophasic course and may be more likely to recover without residual deficits. Viral infection may play a role in the reactivation of disease in some patients who had previously experienced remission, possibly by expanding the memory B cell population. Studies have generally asserted that 70-80% of children with OMS will have long-term neurologic, cognitive, behavioral, developmental, and academic impairment. Since neurologic and developmental difficulties have not been reported as a consequence of neuroblastoma or its treatment, it is thought that these are exclusively due to the immune mechanism underlying OMS.

One study concludes that: ""Patients with OMA and neuroblastoma have excellent survival but a high risk of neurologic sequelae. Favourable disease stage correlates with a higher risk for development of neurologic sequelae. The role of anti-neuronal antibodies in late sequelae of OMA needs further clarification"."

Another study states that: ""Residual behavioral, language, and cognitive problems occurred in the majority"."

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

There is much research that needs to be conducted on CCAS. A necessity for future research is to conduct more longitudinal studies in order to determine the long-term effects of CCAS. One way this can be done is by studying cerebellar hemorrhage that occurs during infancy. This would allow CCAS to be studied over a long period to see how CCAS affects development. It may be of interest to researchers to conduct more research on children with CCAS, as the survival rate of children with tumors in the cerebellum is increasing. Hopefully future research will bring new insights on CCAS and develop better treatments.

The cause of executive dysfunction is heterogeneous, as many neurocognitive processes are involved in the executive system and each may be compromised by a range of genetic and environmental factors. Learning and development of long-term memory play a role in the severity of executive dysfunction through dynamic interaction with neurological characteristics. Studies in cognitive neuroscience suggest that executive functions are widely distributed throughout the brain, though a few areas have been isolated as primary contributors. Executive dysfunction is studied extensively in clinical neuropsychology as well, allowing correlations to be drawn between such dysexecutive symptoms and their neurological correlates.

Executive processes are closely integrated with memory retrieval capabilities for overall cognitive control; in particular, goal/task-information is stored in both short-term and long-term memory, and effective performance requires effective storage and retrieval of this information.

Executive dysfunction characterizes many of the symptoms observed in numerous clinical populations. In the case of acquired brain injury and neurodegenerative diseases there is a clear neurological etiology producing dysexecutive symptoms. Conversely, syndromes and disorders are defined and diagnosed based on their symptomatology rather than etiology. Thus, while Parkinson's disease, a neurodegenerative condition, causes executive dysfunction, a disorder such as attention-deficit/hyperactivity disorder is a classification given to a set of subjectively-determined symptoms implicating executive dysfunction – current models indicate that such clinical symptoms are caused by executive dysfunction.