People with catatonia may experience an extreme loss of motor skill or even constant hyperactive motor activity. Catatonic patients will sometimes hold rigid poses for hours and will ignore any external stimuli. People with catatonic excitement can suffer from exhaustion if not treated. Patients may also show stereotyped, repetitive movements.

They may show specific types of movement such as waxy flexibility, in which they maintain positions after being placed in them by someone else. Conversely, they may remain in a fixed position by resisting movement in proportion to the force applied by the examiner. They may repeat meaningless phrases or speak only to repeat what the examiner says.

While catatonia is only identified as a symptom of schizophrenia in present psychiatric classifications, it is increasingly recognized as a syndrome with many faces. It appears as the Kahlbaum syndrome (motionless catatonia), malignant catatonia (neuroleptic malignant syndrome, toxic serotonin syndrome), and excited forms (delirious mania, catatonic excitement, oneirophrenia).

It has also been recognized as grafted on to autism spectrum disorders.

Catatonia is a state of psycho-motor immobility and behavioral abnormality manifested by stupor. It was first described in 1874 by Karl Ludwig Kahlbaum, in ("Catatonia or Tension Insanity").

Though catatonia has historically been related to schizophrenia (catatonic schizophrenia), it is now known that catatonic symptoms are nonspecific and may be observed in other mental disorders and neurological conditions. In the fifth edition of the "Diagnostic and Statistical Manual of Mental Disorders" (DSM), catatonia is not recognized as a separate disorder, but is associated with psychiatric conditions such as schizophrenia (catatonic type), bipolar disorder, post-traumatic stress disorder, depression and other mental disorders, narcolepsy, as well as drug abuse or overdose (or both). It may also be seen in many medical disorders including infections (such as encephalitis), autoimmune disorders, focal neurologic lesions (including strokes), metabolic disturbances, alcohol withdrawal and abrupt or overly rapid benzodiazepine withdrawal. In the fifth edition of the DSM, it is written that a variety of medical conditions may cause catatonia, especially neurological conditions: encephalitis, cerebrovascular disease, neoplasms, head injury. Moreover, metabolic conditions: homocystinuria, diabetic ketoacidosis, hepatic encephalopathy, hypercalcaemia.

It can be an adverse reaction to prescribed medication. It bears similarity to conditions such as encephalitis lethargica and neuroleptic malignant syndrome. There are a variety of treatments available; benzodiazepines are a first-line treatment strategy. Electroconvulsive therapy is also sometimes used. There is growing evidence for the effectiveness of NMDA receptor antagonists for benzodiazepine-resistant catatonia. Antipsychotics are sometimes employed but require caution as they can worsen symptoms and have serious adverse effects.

There is evidence that trauma during childhood increases the risk of developing psychosis. One meta-analysis found that 60-70% of those who experience psychosis have experienced childhood trauma (abuse and neglect). The relationship appears to be causal and cumulative one, meaning the more adverse childhood events experienced the greater the likelihood of developing psychosis of one kind of another.

Waxy flexibility is a psychomotor symptom of catatonia as associated with schizophrenia, bipolar disorder, or other mental disorders which leads to a decreased response to stimuli and a tendency to remain in an immobile posture. Attempts to reposition the patient are met by "slight, even resistance", and after being repositioned the patient will typically remain in the new position. Waxy flexibility rarely occurs in cases of delirium. The presence of waxy flexibility along with at least two other catatonic symptoms such as stupor or negativism are enough to warrant a diagnosis of catatonia.

For instance, if one were to move the arm of someone with waxy flexibility, they would keep their arm where one moved it until it was moved again, as if it were made from wax. Further alteration of an individual's posture is similar to bending a candle. Although waxy flexibility has historically been linked to schizophrenia, there are also other disorders which it may be associated with, for example, mood disorder with catatonic behaviour.

Electroconvulsive therapy is often used as a treatment for catatonia. A study has found that catatonic patients suffering from waxy flexibility responded faster to electroconvulsive therapy, compared to patients with different catatonic symptoms.

Bouffée délirante is a culture-bound syndrome in West Africa and Haiti of a sudden outburst of aggression, confusion and psychomotor excitement, possibly including visual or auditory hallucinations and paranoia.

Approximately three percent of people who are suffering from alcoholism experience psychosis during acute intoxication or withdrawal. Alcohol related psychosis may manifest itself through a kindling mechanism. The mechanism of alcohol-related psychosis is due to the long-term effects of alcohol resulting in distortions to neuronal membranes, gene expression, as well as thiamin deficiency. It is possible in some cases that alcohol abuse via a kindling mechanism can cause the development of a chronic substance induced psychotic disorder, i.e. schizophrenia. The effects of an alcohol-related psychosis include an increased risk of depression and suicide as well as causing psychosocial impairments.

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 %.

The exact cause of the disorder remains unknown, and relatively few studies have focused exclusively on the etiology of schizophreniform disorder. Like other psychotic disorders, a diathesis–stress model has been proposed, suggesting that some individuals have an underlying multifactorial genetic vulnerability to the disorder that can be triggered by certain environmental factors. Schizophreniform disorder is more likely to occur in people with family members who have schizophrenia or bipolar disorder.

Environmental factors associated with the development of schizophrenia include the living environment, drug use, and prenatal stressors.

Maternal stress has been associated with an increased risk of schizophrenia, possibly in association with reelin. Maternal Stress has been observed to lead to hypermethylation and therefore under-expression of reelin, which in animal models leads to reduction in GABAergic neurons, a common finding in schizophrenia. Maternal nutritional deficiencies, such as those observed during a famine, as well as maternal obesity have also been identified as possible risk factors for schizophrenia. Both maternal stress and infection have been demonstrated to alter fetal neurodevelopment through pro-inflammatory proteins such as IL-8 and TNF.

Parenting style seems to have no major effect, although people with supportive parents do better than those with critical or hostile parents. Childhood trauma, death of a parent, and being bullied or abused increase the risk of psychosis. Living in an urban environment during childhood or as an adult has consistently been found to increase the risk of schizophrenia by a factor of two, even after taking into account drug use, ethnic group, and size of social group. Other factors that play an important role include social isolation and immigration related to social adversity, racial discrimination, family dysfunction, unemployment, and poor housing conditions.

It has been hypothesized that in some people, development of schizophrenia is related to intestinal tract dysfunction such as seen with non-celiac gluten sensitivity or abnormalities in the intestinal flora. A subgroup of persons with schizophrenia present an immune response to gluten different from that found in people with celiac, with elevated levels of certain serum biomarkers of gluten sensitivity such as anti-gliadin IgG or anti-gliadin IgA antibodies.

Schizophreniform disorder is equally prevalent among men and women. The most common ages of onset are 18–24 for men and 18–35 for women. While the symptoms of schizophrenia often develop gradually over a period of years, the diagnostic criteria for schizophreniform disorder require a much more rapid onset.

Available evidence suggests variations in incidence across sociocultural settings. In the United States and other developed countries, the incidence is low, possibly fivefold less than that of schizophrenia. In developing countries, the incidence is substantially higher, especially for the subtype "With Good Prognostic Features". In some of these settings schizophreniform disorder may be as common as schizophrenia.

About half of those with schizophrenia use drugs or alcohol excessively.

Amphetamine, cocaine, and to a lesser extent alcohol, can result in a transient stimulant psychosis or alcohol-related psychosis that presents very similarly to schizophrenia. Although it is not generally believed to be a cause of the illness, people with schizophrenia use nicotine at much higher rates than the general population.

Alcohol abuse can occasionally cause the development of a chronic, substance-induced psychotic disorder via a kindling mechanism. Alcohol use is not associated with an earlier onset of psychosis.

Cannabis can be a contributory factor in schizophrenia, potentially causing the disease in those who are already at risk. The increased risk may require the presence of certain genes within an individual or may be related to preexisting psychopathology. Early exposure is strongly associated with an increased risk. The size of the increased risk is not clear, but appears to be in the range of two to three times greater for psychosis. Higher dosage and greater frequency of use are indicators of increased risk of chronic psychoses.

Other drugs may be used only as coping mechanisms by individuals who have schizophrenia, to deal with depression, anxiety, boredom, and loneliness.

Hypomania (literally "under mania" or "less than mania") is a mood state characterized by persistent disinhibition and elevation (euphoria). It may involve irritation, but less severely than full mania. According to DSM-V criteria, hypomania is distinct from mania in that there is no significant functional impairment; mania, by DSM-V definition, does include significant functional impairment and may have psychotic features.

Characteristic behaviors of persons experiencing hypomania are a notable decrease in the need for sleep, an overall increase in energy, unusual behaviors and actions, and a markedly distinctive increase in talkativeness and confidence, commonly exhibited with a flight of creative ideas. Other symptoms related to this may include feelings of grandiosity, distractibility, and hypersexuality. While hypomanic behavior often generates productivity and excitement, it can become troublesome if the subject engages in risky or otherwise inadvisable behaviors, and/or the symptoms manifest themselves in trouble with everyday life events. When manic episodes are separated into stages of a progression according to symptomatic severity and associated features, hypomania constitutes the first stage of the syndrome, wherein the cardinal features (euphoria or heightened irritability, pressure of speech and activity, increased energy, decreased need for sleep, and flight of ideas) are most plainly evident.

Individuals in a hypomanic state have a decreased need for sleep, are extremely outgoing and competitive, have a great deal of energy and are otherwise often fully functioning (unlike full mania).

Disorganized schizophrenia, also known as hebephrenia or hebephrenic schizophrenia, is a subtype of schizophrenia, although it is not recognized in the latest version of the "Diagnostic and Statistical Manual of Mental Disorders". It's recognized only in the 10th revision of the International Statistical Classification of Diseases and Related Health Problems (ICD-10).

Disorganized schizophrenia is thought to be an extreme expression of the "disorganization syndrome" that has been hypothesized to be one aspect of a three-factor model of symptoms in schizophrenia, the other factors being "reality distortion" (involving delusions and hallucinations) and "psychomotor poverty" (lack of speech, lack of spontaneous movement and various aspects of blunting of emotion).

Bouffée délirante is a French term that was introduced in 1886 by Valentin Magnan meaning short-lived psychosis. He used it to describe transient psychotic or psychosis reactions. Bouffée délirante reactions are sudden attacks of brief duration with paranoid delusions and often concomitant hallucinations, typically precipitated by an intense fear of magical persecution through sorcery or witchcraft.

The exact incidence and prevalence of brief psychotic disorder is not known, but it is generally considered uncommon. Internationally, it occurs twice as often in women than men, and even more often in women in the United States. It typically occurs in the late 30s and early 40s. The exact cause of brief psychotic disorder is not known. One theory suggests a genetic link, because the disorder is more common in people who have family members with mood disorders, such as depression or bipolar disorder. Another theory suggests that the disorder is caused by poor coping skills, as a defense against or escape from a particularly frightening or stressful situation. These factors may create a vulnerability to develop brief psychotic disorder. In most cases, the disorder is triggered by a major stress or traumatic event. Childbirth may trigger the disorder in some women. Approximately 1 in 10,000 women experience brief psychotic disorder shortly after childbirth. There are general medical causes of brief psychosis that should also be considered when being evaluated. Post-natal depression, HIV and AIDS, malaria, syphilis, Alzheimer's disease, Parkinson's disease, hypoglycaemia (an abnormally low level of glucose in the blood), lupus, multiple sclerosis, brain tumor and PANS.

Oneiroid syndrome, from the Ancient Greek "" ("oneiros", meaning "dream") and "" ("eidos", meaning "form, likeness"), is dream-like fantastic derangement of consciousness with illusions and hallucinations, catatonic symptoms and kaleidoscopic quality of psychopathological experiences. It's an element of the catatonic form of schizophrenia and presents with a dream-like or nightmare-like state as a background of intensive psychopathological experiences.

Oneiroid states were first described by the German physician Wilhelm Mayer-Gross in 1924. Mayer-Gross's 1924 habilitation on "Self-descriptions of Confusional States: the Oneiroid Form of Experience" () is considered the first monograph about oneiroid state. In this monograph the psychopathological method was used (German psychiatrists called that the "phenomenological method" – phänomenologische Methode).

The oneiroid syndrome, known to European and Russian psychiatrists, but all but forgotten in the USA.

Later in 1961 the Bulgarian psychiatrist S.T. Stoyanov studied the dynamics and the course of the oneiroid syndrome in "periodic", or recurrent schizophrenia (ICD-10).

According to this research the syndrome has six stages in its course:

1. initial general-somatic and vegetative disorder

2. delusional mood

3. affective-delusional depersonalisation and derealisation

4. fantastic-delusional and affective depersonalisation and derealisation

5. illusional depersonalisation and derealisation, and

6. catatonic-oneiroid state in the culmination.

In most of the cases of the oneiroid syndrome there were crude pathological changes in the electroencephalography (EEG).

The prognosis of oneiroid catatonia is optimal, in comparison with lucid catatonia.

According to the Mayo Clinic, it is best to start receiving treatment for paranoid schizophrenia as early as possible and to maintain the treatment throughout life. Continuing treatment will help keep the serious symptoms under control and allow the person to lead a more fulfilling life. This illness is typically unpreventable.

It has a strong hereditary component with a first degree parent or sibling. There is some possibility that there are environmental influences including "prenatal exposure to a viral infection, low oxygen levels during birth (from prolonged labor or premature birth), exposure to a virus during infancy, early parental loss or separation, and verbal, physical or sexual abuse in childhood". Eliminating any of these factors could help reduce an individual's future risk of developing paranoid schizophrenia.

Catalepsy is a symptom of certain nervous disorders or conditions such as Parkinson's disease and epilepsy. It is also a characteristic symptom of cocaine withdrawal, as well as one of the features of catatonia. It can be caused by schizophrenia treatment with anti-psychotics, such as haloperidol, and by the anesthetic ketamine. Protein kinase A has been suggested as a mediator of cataleptic behavior.

Treatment consists of high-dose lorazepam or in some cases ECT. The response to the treatment is usually good, especially if detected early

Often, apathy is felt after witnessing horrific acts, such as the killing or maiming of people during a war, e.g. posttraumatic stress disorder. It is also known to be a distinct psychiatric syndrome that is associated with many conditions, some of which are: CADASIL syndrome, depression, Alzheimer's disease, Chagas disease, Creutzfeldt–Jakob disease, dementia (and dementias such as Alzheimer's disease, vascular dementia, and frontotemporal dementia), Korsakoff's syndrome, excessive vitamin D, hypothyroidism, hyperthyroidism, general fatigue, Huntington's disease, Pick's disease, progressive supranuclear palsy (PSP), brain damage, schizophrenia, schizoid personality disorder, bipolar disorder, autism, ADHD, Asperger's syndrome, and others. Some medications and the heavy use of drugs such as opiates or GABA-ergic drugs may bring apathy as a side effect.

Paranoid schizophrenia is an illness that typically requires lifelong treatment with neuroleptics to allow someone to have a relatively stable and normal lifestyle. In order to be successfully treated, a person with schizophrenia should seek help from family or primary care doctors, psychiatrists, psychotherapists, pharmacists, family members, case workers, psychiatric nurses, or social workers, provided he or she is not unable to do so, due to many people with schizophrenia having the inability to accept their condition. Non-compliance with neuroleptics may also occur if the patient considers the side effects (such as extrapyramidal symptoms) to be more debilitating than the condition itself. The main options that are offered for the treatment of paranoid schizophrenia are the following: neuroleptics, psychotherapy, hospitalization, electroconvulsive therapy, and vocational skills training.

There are many different types of disorders that have similar symptoms to paranoid schizophrenia. There are tests that psychiatrists perform to achieve a correct diagnosis. They include "psychiatric evaluation, in which the doctor or psychiatrist will ask a series of questions about the patient's symptoms, psychiatric history, and family history of mental health problems; medical history and exam, in which the doctor will ask about one's personal and family health history and will also perform a complete physical examination to check for medical issues that could be causing or contributing to the problem; laboratory tests in which the doctor will order simple blood and urine tests can rule out other medical causes of symptoms".

There are side effects associated with antipsychotic medication. Neuroleptics can cause high blood pressure and high cholesterol. Many people who take them exhibit weight gain and have a higher risk of developing diabetes.

While apathy and anxiety may appear to be separate, and different, states of being, there are many ways that severe anxiety can cause apathy. First, the emotional fatigue that so often accompanies severe anxiety leads to one's emotions being worn out, thus leading to apathy. Second, the low serotonin levels associated with anxiety often lead to less passion and interest in the activities in one's life which can be seen as apathy. Third, negative thinking and distractions associated with anxiety can ultimately lead to a decrease in one's overall happiness which can then lead to an apathetic outlook about one's life. Finally, the difficulty enjoying activities that individuals with anxiety often face can lead to them doing these activities much less often and can give them a sense of apathy about their lives. Even behavioral apathy may be found in individuals with anxiety in the form of them not wanting to make efforts to treat their anxiety.

The disorder is characterized by a sudden onset of psychotic symptoms, which may include delusions, hallucinations, disorganized speech or behavior, or catatonic behavior. The symptoms must not be caused by schizophrenia, schizoaffective disorder, delusional disorder or mania in bipolar disorder. They must also not be caused by a drug (such as amphetamines) or medical condition (such as a brain tumor). The term bouffée délirante describes an acute nonaffective and nonschizophrenic psychotic disorder, which is largely similar to DSM-III-R and DSM-IV brief psychotic and schizophreniform disorders.

Symptoms generally last at least a day, but not more than a month, and there is an eventual return to full baseline functioning. It may occur in response to a significant stressor in one's life, or in other situations where a stressor is not apparent, including in the weeks following birth. In diagnosis, a careful distinction is considered for culturally appropriate behaviors, such as religious beliefs and activities. It is believed to be connected to or synonymous with a variety of culture-specific phenomena such as latah, koro, and amok.

There are three forms of brief psychotic disorder:

1. Brief psychotic disorder with a stressor, such as a trauma or death in the family.

2. Brief psychotic disorder without a stressor, there is no obvious stressor.

3. Brief psychotic disorder with postpartum onset. Usually occurs about four weeks after giving birth.