There is no known single cause or causes of schizophrenia, however, it is a heritable disorder.

Several environmental factors, including perinatal complications and prenatal maternal infections could cause schizophrenia. These factors in a greater severity or frequency could result in an earlier onset of schizophrenia. Maybe a genetic predisposition is a important factor too, familial illness reported for childhood-onset schizophrenic patients.

Schizophrenia disorders in children are rare. Boys are twice as likely to be diagnosed with childhood schizophrenia. There is often an disproportionately large number of males with childhood schizophrenia, because the age of onset of the disorder is earlier in males than females by about 5 years. People have been and still are reluctant to diagnose schizophrenia early on, primarily due to the stigma attached to it.

While very early-onset schizophrenia is a rare event, with prevalence of about 1:10,000, early-onset schizophrenia is manifests more often with an estimated prevalence of 0.5 %.

Individuals suffering from Diogenes syndrome generally display signs of collectionism, hoarding, or compulsive disorder. Individuals who have suffered damage to the brain, particularly the frontal lobe, may be at more risk to developing the syndrome. The frontal lobes are of particular interest, because they are known to be involved in higher order cognitive processes, such as reasoning, decision-making and conflict monitoring.

Diogenes Syndrome tends to occur among the elderly. The behavioural patterns that is usually reflected by those living with this disorder are suffering from significant functional problem that is correlated with morbidity and mortality.

Many different causes of aboulia have been suggested. While there is some debate about the validity of aboulia as a separate disease, experts mostly agree that aboulia is the result of frontal lesions and not with cerebellar or brainstem lesions. As a result of more and more evidence showing that the mesolimbic and the mesocortical dopamine system are key to motivation and responsiveness to reward, aboulia may be a dopamine-related dysfunction. Aboulia may also result from a variety of brain injuries which cause personality change, such as dementing illnesses, trauma, or intracerebral hemorrhage (stroke), especially stroke causing diffuse injury to the right hemisphere.

Diogenes syndrome is a disorder that involves hoarding of rubbish and severe self-neglect. In addition, the syndrome is characterized by domestic squalor, syllogomania, social alienation, and refusal of help. It has been shown that the syndrome is caused as a reaction to stress that was experienced by the patient. The time span in which the syndrome develops is undefined, though it is most accurately distinguished as a reaction to stress that occurs late in life.

In most instances, patients were observed to have an abnormal possessiveness and patterns of compilation in a disordered manner. These symptoms suggest damages on the prefrontal areas of the brain, due to its relation to decision making. Although in contrast, there have been some cases where the hoarded objects were arranged in a methodical manner, which may suggest a cause other than brain damage.

Although most patients have been observed to come from homes with poor conditions, and many had been faced with poverty for a long period of time, these similarities are not considered as a definite cause to the syndrome. Research showed that some of the participants with the condition had solid family backgrounds as well successful professional lives. Half of the patients were of higher intelligence level. This indicates the "Diogenes syndrome" does not exclusively affect those experiencing poverty or those who had traumatic childhood experiences.

The severe neglect that they bring on themselves usually results in physical collapse or mental breakdown. Most individuals who suffer from the syndrome do not get identified until they face this stage of collapse, due to their predilection to refuse help from others.

The patients are generally highly intelligent, and the personality traits that can be seen frequently in patients diagnosed with Diogenes syndrome are aggressiveness, stubbornness, suspicion of others, unpredictable mood swings, emotional instability and deformed perception of reality. Secondary DS is related to mental disorders. The direct relation of the patients' personalities to the syndrome is unclear, though the similarities in character suggest potential avenues for investigation.

Reduced affect display, sometimes referred to as emotional blunting, is a condition of reduced emotional reactivity in an individual. It manifests as a failure to express feelings (affect display) either verbally or non-verbally, especially when talking about issues that would normally be expected to engage the emotions. Expressive gestures are rare and there is little animation in facial expression or vocal inflection. Reduced affect can be symptomatic of autism, schizophrenia, depression, posttraumatic stress disorder, depersonalization disorder, schizoid personality disorder or brain damage. It may also be a side effect of certain medications (e.g., antipsychotics and antidepressants). Individuals with blunted or flat affect show different regional brain activity when compared with typical individuals.

Reduced affect should be distinguished from apathy, which explicitly refers to a lack of emotion, whereas reduced affect is a lack of emotional expression regardless of whether emotion is actually reduced or not.

A lack of motivation has been reported in 25–50% of patients with Alzheimer's disease. While depression is also common in patients with this disease, aboulia is not a mere symptom of depressions because more than half of the patients with Alzheimer's disease with aboulia do not suffer from depression. Several studies have shown that aboulia is most prevalent in cases of severe dementia which may result from reduced metabolic activity in the prefrontal regions of the brain. Patients with Alzheimer's disease and aboulia are significantly older than patients with Alzheimer's who do not lack motivation. Going along with that, the prevalence of aboulia increased from 14% in patients with a mild case Alzheimer's disease to 61% in patients with a severe case of Alzheimer's disease, which most likely developed over time as the patient got older.

Klüver–Bucy syndrome is a syndrome resulting from bilateral lesions of the medial temporal lobe (including amygdaloid nucleus). Klüver–Bucy syndrome may present with compulsive eating, hypersexuality, insertion of inappropriate objects in the mouth (hyperorality), visual agnosia, and .

People with avolition often want to complete certain tasks but lack the ability to initiate behaviours necessary to complete them. Avolition is most commonly seen as a symptom of some other disorder, but might be considered a primary clinical disturbance of itself (or as a coexisting second disorder) related to disorders of diminished motivation. In 2006, avolition was identified as a negative symptom of schizophrenia by the National Institute of Mental Health (NIMH), and has been observed in patients with bipolar disorder as well as resulting from trauma.

Avolition is sometimes mistaken for other, similar symptoms also affecting motivation, such as aboulia, anhedonia and asociality, or strong general disinterest. For example, aboulia is also a restriction in motivation and initiation, but characterized by an inability to set goals or make decisions and considered a disorder of diminished motivation. In order to provide effective treatment, the underlying cause of avolition (if any) has to be identified and it is important to properly differentiate it from other symptoms, even though they might reflect similar aspects of mental illness.

Neuroleptic-induced deficit syndrome (NIDS) is a psychopathological syndrome that develops in some patients who take high doses of an antipsychotic for an extended time. It is most often caused by high-potency typical antipsychotics, but can also be caused by high doses of many atypicals, especially those closer in profile to typical ones (that have higher D dopamine receptor affinity and relatively low 5-HT serotonin receptor binding affinity), like risperidone and amisulpride.

Neuroleptic induced deficit syndrome is principally characterized by the same symptoms that constitute the negative symptoms of schizophrenia: emotional blunting, apathy, hypobulia, anhedonia, indifference, difficulty in thinking, difficulty or total inability in concentrating, lack of initiative, attention deficits, and desocialization. This can easily lead to misdiagnosis and mistreatment. Instead of decreasing the antipsychotic, the doctor may increase their dose to try to "improve" what they perceive to be negative symptoms of schizophrenia, rather than antipsychotic side effects. The concept of neuroleptic induced deficit syndrome was initially presented for schizophrenia, and it has rarely been associated in other mental disorders. In recent years, atypical neuroleptics are being more often managed to patients with bipolar disorder, so some studies about neuroleptic-induced deficit syndrome in bipolar disorder patients now available.

There are significant difficulties in the differential diagnosis of primary negative symptoms and neuroleptic deficiency syndrome (secondary negative symptoms), as well as depression.

Implications from avolition often result in social deficits. Not being able to initiate and perform purposeful activities can have many implications for a person with avolition. By disrupting interactions with both familiar and unfamiliar people, it jeopardizes the patient's social relations. When part of a severe mental illness, avolition has been reported, in first person accounts, to lead to physical and mental inability to both initiate and maintain relationships, as well as work, eat, drink or even sleep.

Clinically, it may be difficult to engage an individual experiencing avolition in active participation of psychotherapy. Patients are also faced with the stresses of coping with and accepting a mental illness and the stigma that often accompanies such a diagnosis and its symptoms. Regarding schizophrenia, the American Psychiatric Association reported in 2013 that there currently are "no treatments with proven efficacy for primary negative symptoms" (such as avolition). Together with schizophrenia's chronic nature, such facts added to the outlook of never getting well, might further implicate feelings of hopelessness and similar in patients as well as their friends and family.

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.

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.

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.

A restricted or constricted affect is a reduction in an individual's expressive range and the intensity of emotional responses.

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 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.

Apathy is a lack of feeling, emotion, interest, and concern. Apathy is a state of indifference, or the suppression of emotions such as concern, excitement, motivation, or passion. An apathetic individual has an absence of interest in or concern about emotional, social, spiritual, philosophical, or physical life and the world.

The apathetic may lack a sense of purpose, worth, or meaning in their life. An apathetic person may also exhibit insensibility or sluggishness. In positive psychology, apathy is described as a result of the individuals feeling they do not possess the level of skill required to confront a challenge (i.e. "flow"). It may also be a result of perceiving no challenge at all (e.g. the challenge is irrelevant to them, or conversely, they have learned helplessness). Apathy may be a sign of more specific mental problems such as schizophrenia or dementia. However, apathy is something that all people face in some capacity. It is a natural response to disappointment, dejection, and stress. As a response, apathy is a way to forget about these negative feelings. This type of common apathy is usually only felt in the short-term and when it becomes a long-term or even lifelong state is when deeper social and psychological issues are most likely present.

Apathy should be distinguished from reduced affect, which refers to reduced emotional expression but not necessarily reduced emotion.

Klüver–Bucy syndrome was first documented among certain humans who had experienced temporal lobectomy in 1955 by H. Terzian and G.D. Ore. It was first noted in a human with meningoencephalitis in 1975 by Marlowe et al. Klüver–Bucy syndrome can manifest after either of these (lobectomies can be medically required by such reasons as accidents or tumors), but may also appear in humans with acute herpes simplex encephalitis or following a stroke. Other conditions may also contribute to a diagnosis of Klüver–Bucy syndrome, including Pick Disease, Alzheimer's Disease, ischemia, anoxia, progressive subcortical gliosis, Rett syndrome, porphyria and carbon monoxide poisoning, among others.

It is rare for humans to manifest all of the identified symptoms of the syndrome; three or more are required for diagnosis. Among humans, the most common symptoms include placidity, hyperorality and dietary changes. They may also present with an inability to recognize objects or inability to recognize faces or other memory disorders. Social neurosciences research shows that changes in temporal lobe is identified as a cause for aberrant sexual and hyper-sexual behaviors.

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.

As it has already been mentioned, the organic personality disorder is included in a wide group of personality and behavioural disorders. This mental health disorder can be caused by disease, brain damages or dysfunctions in specific brain areas in frontal lobe. The most common reason for this profound change in personality is the traumatic brain injury (TBI). Children, whose brain areas have injured or damaged, may present Attention Deficit Hyperactivity Disorder (ADHD), oppositional defiant disorder (ODD) and organic personality disorder. Moreover, this disorder is characterised as "frontal lobe syndrome". This characteristic name shows that the organic personality disorder can usually be caused by lesions in three brain areas of frontal lobe. Specifically, the symptoms of organic personality disorder can also be caused by traumatic brain injuries in orbitofrontal cortex, anterior cingulate cortex and dorsolateral prefrontal cortex. It is worth to be mentioned that organic personality disorder may also be caused by lesions in other circumscribed brain areas.

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.

Apathy affects nearly 50–70 percent of individuals with Alzheimer's disease. It is a neuropsychiatric symptom of Alzheimer's associated with functional impairment. There are two main causes of apathy that have been recognized in patients with Alzheimer's. First, dysfunction in frontal systems of the brain is thought to be an important neurobiological basis for the onset of apathy. Second, the neuropathological changes associated with dementia, and therefore Alzheimer's, may also result in apathy. Cholinesterase inhibitors, used as the first line of treatment for the cognitive symptoms associated with dementia, have also shown some modest benefit for behavior disturbances such as apathy. Methylphenidate has been the most widely studied drug for the treatment of apathy in dementia. Management of apathetic symptoms using methylphenidate have shown promise in randomized placebo controlled trials of Alzheimer's patients. A phase III multi-centered randomized placebo-controlled trial of methylphenidate for the treatment of apathy is currently underway and planned for completion in August 2020.

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.