Current methods in treating early-onset schizophrenia follow a similar approach to the treatment of adult schizophrenia. Although modes of treatment in this population is largely understudied, the use of antipsychotic medication is commonly the first line of treatment in addressing symptoms. Recent literature has failed to determine if typical or atypical antipsychotics are most effective in reducing symptoms and improving outcomes. When weighing treatment options, it is necessary to consider the adverse effects of various medications used to treat schizophrenia and the potential implications of these effects on development. A 2013 systematic review compared the efficacy of atypical antipsychotics versus typical antipsychotics for adolescents:

Madaan et al. wrote that studies report efficacy of typical neuroleptics such as thioridazine, thiothixene, loxapine and haloperidol, high incidence of side effects such as extrapyramidal symptoms, akathisia, dystonias, sedation, elevated prolactin, tardive dyskinesia.

For a number of years, scholars debated amongst themselves whether or not antipsychotic drugs had a tendency to increase depression or simply help the patient manage their mental illness. However, conclusive evidence points to antipsychotic drugs actually helping patients with their depression while simultaneously assisting in the suppression of schizophrenic episodes. Specifically risperidone, olanzapine, quetiapine, fluphenazine, haloperidol, and L-sulpiride have done the best in drug trials pertaining to people with schizophrenia. Along with antipsychotic drugs, post-schizophrenic patients may receive antidepressants to actively treat the depression. Drugs are certainly not the only answer, though. At the base of both depression and schizophrenia, social withdrawal is a shared symptom between the two. People suffering from schizophrenia require a strong support system to be healthy, just as is the case with the rest the human population. The opportunity to become a working citizen is another way to ward off depression in patients with schizophrenia, helping them create social ties and a feeling of accomplishment.

Research suggests that paraphrenics respond well to antipsychotic drug therapy if doctors can successfully achieve sufficient compliance. Herbert found that Stelazine combined with Disipal was an effective treatment. It promoted the discharging of patients and kept discharged patients from being readmitted later. While behavior therapy may help patients reduce their preoccupation with delusions, psychotherapy is not currently of primary value.

The article "Cotard's syndrome: A Review" (2010) reports successful pharmacological treatments (mono-therapeutic and multi-therapeutic) using antidepressant, antipsychotic, and mood stabilizing drugs; likewise, with the depressed patient, electroconvulsive therapy (ECT) is more effective than pharmacotherapy. Cotard syndrome resulting from an adverse drug reaction to valacyclovir is attributed to elevated serum concentration of one of valacyclovir's metabolites, 9-carboxymethoxymethylguanine (CMMG). Successful treatment warrants cessation of the drug, valacyclovir. Hemodialysis was associated with timely clearance of CMMG and resolution of symptoms.

STPD is rarely seen as the primary reason for treatment in a clinical setting, but it often occurs as a comorbid finding with other mental disorders. When patients with STPD are prescribed pharmaceuticals, they are most often prescribed the same drugs used to treat patients suffering from schizophrenia including traditional neuroleptics such as haloperidol and thiothixene. In order to decide which type of medication should be used, Paul Markovitz distinguishes two basic groups of schizotypal patients:

- Schizotypal patients who appear to be almost schizophrenic in their beliefs and behaviors (aberrant perceptions and cognitions) are usually treated with low doses of antipsychotic medications, e.g. thiothixene. However, it must be mentioned that long-term efficacy of neuroleptics is doubtful.

- For schizotypal patients who are more obsessive-compulsive in their beliefs and behaviors, SSRIs like Sertraline appear to be more effective.

Lamotrigine, an anti-convulsant, appears to be helpful in dealing with social isolation.

Research efforts are focusing on prevention in identifying early signs from relatives with associated disorders similar with schizophrenia and those with prenatal and birth complications. Prevention has been an ongoing challenge because early signs of the disorder are similar to those of other disorders. Also, some of the schizophrenic related symptoms are often found in children without schizophrenia or any other diagnosable disorder.

In patients suffering from schizophrenia, grandiose and religious delusions are found to be the least susceptible to cognitive behavioral interventions. Cognitive behavioral intervention is a form of psychological therapy, initially used for depression, but currently used for a variety of different mental disorders, in hope of providing relief from distress and disability. During therapy, grandiose delusions were linked to patients' underlying beliefs by using inference chaining. Some examples of interventions performed to improve the patient's state were focus on specific themes, clarification of neologisms, and thought linkage. During thought linkage, the patient is asked repeatedly by the therapist to explain his/her jumps in thought from one subject to a completely different one.

Patients suffering from mental disorders that experience grandiose delusions have been found to have a lower risk of having suicidal thoughts and attempts.

According to Theodore Millon, the schizotypal is one of the easiest personality disorders to identify but one of the most difficult to treat with psychotherapy. Persons with STPD usually consider themselves to be simply eccentric, productive, or nonconformist. As a rule, they underestimate maladaptiveness of their social isolation and perceptual distortions. It is not so easy to gain rapport with people who suffer from STPD due to the fact that increasing familiarity and intimacy usually increase their level of anxiety and discomfort. In most cases they do not respond to informality and humor.

Group therapy is recommended for persons with STPD only if the group is well structured and supportive. Otherwise, it could lead to loose and tangential ideation. Support is especially important for schizotypal patients with predominant paranoid symptoms, because they will have a lot of difficulties even in highly structured groups.

Individuals who develop paraphrenia have a life expectancy similar to the normal population. Recovery from the psychotic symptoms seems to be rare, and in most cases paraphrenia results in in-patient status for the remainder of the life of the patient. Patients experience a slow deterioration of cognitive functions and the disorder can lead to dementia in some cases, but this development is no greater than the normal population.

There is no clear cause to how certain patients with schizophrenia develop post-schizophrenic depression while others may surpass this stage. However, there are a few theories as to possible causes. Those suffering from post-schizophrenic depression often suffer from social isolation due to their illness, which may increase depression levels. There is strong evidence of stigma-related isolation against those suffering from mental illnesses in a variety of societies, especially those with schizophrenia as they are often viewed as dangerous and unpredictable. Because of this isolation and studies linking social isolation and depression, it is possible that patients under these stigmas eventually develop post-schizophrenic depression. Depression in patients with schizophrenia may also be caused by substance abuse, which is fairly common among those suffering from schizophrenia, as depressants such as alcohol and cannabis can relax the patient. Furthermore, with what little information is currently known about post-schizophrenic depression, the onset may be caused by not giving patients with schizophrenia antipsychotic medications. After being taken off of antipsychotic medication, schizophrenic patients' antidepressant medication had to be increased, while those under antipsychotic medication reported suffering fewer depressive symptoms, further giving reason to believe that a lack of antipsychotic medication in earlier stages of schizophrenia may lead to post-schizophrenic depression. However, some psychology professionals still push for the reduction of neuroleptic drugs, as there is a popular belief that post-schizophrenic depression is caused by neuroleptic treatment. Therapists are also believed to engage the depression in people with schizophrenia, having given too much psychotherapy after the patient had overcome their schizophrenic symptoms. Schizophrenia itself should not be overlooked as a key player in causing post-schizophrenic depression, though. A study done over a two-year time period shadowing patients with schizophrenia and monitoring their depression was unable to locate possible triggers such as the ones previously listed, so it is possible the nature of schizophrenia itself is the primary cause of post-schizophrenic depression.

Cognitive behavioral therapy (CBT) is a newer therapy than exposure therapy, available for those unable or unwilling to undergo exposure therapy. Cognitive therapy has been shown to be useful in reducing intrusive thoughts, but developing a conceptualization of the obsessions and compulsions with the patient is important.

When pseudoneurotic schizophrenia was still being utilized as a diagnostic term, doctors were expected to be able to magically cure patients. Patients usually had very little understanding of themselves and the complexity of their illness. They were willing to employ any process in order to maintain mental stability. Their perception of mental stability, however, was also impaired, which made it much more difficult to make proper, helpful medication prescriptions.

Patients would often misuse medication in order to receive attention from their families. They would describe the dosage and effects of the medicine in some strange demeanor to demonstrate that their illness was physical rather than psychological. In like manner, taking medication also kept doctors concerned about the possibility of the patient developing substance dependence and/or drug addiction. Patients used this to get attention and sympathy from others.

Antidepressants or antipsychotic medications may be used for more severe cases if intrusive thoughts do not respond to cognitive behavioral or exposure therapy alone. Whether the cause of intrusive thoughts is OCD, depression, or post-traumatic stress disorder, the selective serotonin reuptake inhibitor (SSRI) drugs (a class of antidepressants) are the most commonly prescribed. Intrusive thoughts may occur in persons with Tourette syndrome (TS) who also have OCD; the obsessions in TS-related OCD are thought to respond to SSRI drugs as well.

Antidepressants which have been shown to be effective in treating OCD include fluvoxamine (trade name Luvox), fluoxetine (Prozac), sertraline (Zoloft), paroxetine (Paxil), citalopram (Celexa), and clomipramine (Anafranil). Although SSRIs are known to be effective for OCD in general, there have been fewer studies on their effectiveness for intrusive thoughts. A retrospective chart review of patients with sexual symptoms treated with SSRIs showed the greatest improvement was in those with intrusive sexual obsessions typical of OCD. A study of ten patients with religious or blasphemous obsessions found that most patients responded to treatment with fluoxetine or clomipramine. Women with postpartum depression often have anxiety as well, and may need lower starting doses of SSRIs; they may not respond fully to the medication, and may benefit from adding cognitive behavioral or response prevention therapy.

Patients with intense intrusive thoughts that do not respond to SSRIs or other antidepressants may be prescribed typical and atypical neuroleptics including risperidone (trade name Risperdal), ziprasidone (Geodon), haloperidol (Haldol), and pimozide (Orap).

Studies suggest that therapeutic doses of inositol may be useful in the treatment of obsessive thoughts.

Oneirophrenic patients are resistant to insulin and when injected with glucose, these patients take 30 to 50% longer to return to normal glycemia. The meaning of this finding is not known, but it has been hypothesized that it may be due to an insulin antagonist present in the blood during psychosis. However, There is currently no known treatment for oneiophrenia.

Grandiose delusions (GD), delusions of grandeur, expansive delusions also known as megalomania are a subtype of delusion that occur in patients suffering from a wide range of psychiatric diseases, including two-thirds of patients in manic state of bipolar disorder, half of those with schizophrenia, patients with the grandiose subtype of delusional disorder, and a substantial portion of those with substance abuse disorders. GDs are characterized by fantastical beliefs that one is famous, omnipotent, wealthy, or otherwise very powerful. The delusions are generally fantastic and typically have a religious, science fictional, or supernatural theme. There is a relative lack of research into GD, in contrast to persecutory delusions and auditory hallucinations. About 10% of healthy people experience grandiose thoughts but do not meet full criteria for a diagnosis of GD.

A paranoid reaction may be caused from a decline in brain circulation as a result of high blood pressure or hardening of the arterial walls.

Drug-induced paranoia, associated with amphetamines, methamphetamine and similar stimulants has much in common with schizophrenic paranoia; the relationship has been under investigation since 2012. Drug-induced paranoia has a better prognosis than schizophrenic paranoia once the drug has been removed. For further information, see Stimulant psychosis and Substance-induced psychosis.

Based on data obtained by the Dutch NEMISIS project in 2005, there was an association between impaired hearing and the onset of symptoms of psychosis, which was based on a five-year follow up. Some older studies have actually declared that a state of paranoia can be produced in patients that were under a hypnotic state of deafness. This idea however generated much skepticism during its time.

Pseudoneurotic schizophrenia is a postulated mental disorder categorized by the presence of two or more symptoms of mental illness such as anxiety, hysteria, and phobic or obsessive-compulsive neuroses. It is often acknowledged as a personality disorder. Patients generally display salient anxiety symptoms that disguise an underlying psychotic disorder.

In the 1940s, psychiatrists Paul Hoch and Philip Polatin created the term pseudoneurotic schizophrenia. This mental illness, however, is no longer acknowledged as a clinical entity. In 1972 it went on to be called borderline personality disorder, a term coined by Otto Friedmann Kernberg, which referred to an expansive range of issues.

Pseudoneurotic schizophrenia is in the Russian adapted version of the ICD-10 (code F21.3).

Kraepelin had experimented with hypnosis but found it wanting, and disapproved of Freud's and Jung's introduction, based on no evidence, of psychogenic assumptions to the interpretation and treatment of mental illness. He argued that, without knowing the underlying cause of dementia praecox or manic-depressive illness, there could be no disease-specific treatment, and recommended the use of long baths and the occasional use of drugs such as opiates and barbiturates for the amelioration of distress, as well as occupational activities, where suitable, for all institutionalized patients. Based on his theory that dementia praecox is the product of autointoxication emanating from the sex glands, Kraepelin experimented, without success, with injections of thyroid, gonad and other glandular extracts.

Many researchers believe that individuals with paranoia have some sort of cognitive deficit or impairment in reasoning ability or lack social credibility. Studies have shown that there may not be a direct relationship between the impairments and psychotic delusions, but they rather effect other areas of an individual's life, such as social circumstances

can be important factors about delusions. Other researchers have shown that cognitive abilities may be altered, such as when cameras or recordings are involved. This phenomenon appears to be a common theme among those exhibiting psychotic delusions. An investigation involving one hundred delusional patients did indeed reveal that these individuals may have a tendency to jump to conclusions rather than look for other potential information.

Sluggish schizophrenia or slow progressive schizophrenia (, "vyalotekushchaya shizofreniya") was a diagnostic category used in Soviet Union to describe what they claimed was a form of schizophrenia characterized by a slowly progressive course; it was diagnosed even in a patient who showed no symptoms of schizophrenia or other psychotic disorders, on the assumption that these symptoms would appear later. It was developed in the 1960s by Soviet psychiatrist Andrei Snezhnevsky and his colleagues, and was used exclusively in the USSR and several Eastern Bloc countries, until the fall of Communism starting in 1989. The diagnosis has long been discredited because of its scientific inadequacy and its use as a means of confining dissenters. It has never been used or recognized outside of Soviet Union, or by international organizations such as the World Health Organization. It is considered a prime example of the political abuse of psychiatry in the Soviet Union.

Sluggish schizophrenia was the most infamous of diagnoses used by Soviet psychiatrists, due to its usage against political dissidents. After being discharged from a hospital, persons diagnosed with sluggish schizophrenia were deprived of their civic rights, credibility and employability. The usage of this diagnosis has been internationally condemned.

In the Russian version of the 10th revision of the International Statistical Classification of Diseases and Related Health Problems (ICD-10), which has long been used throughout present-day Russia, sluggish schizophrenia is no longer listed as a form of schizophrenia, but it is still included as a schizotypal disorder in section F21 of chapter V.

According to Sergei Jargin, the same Russian term "vyalotekushchaya" for sluggish schizophrenia continues to be used and is now translated in English summaries of articles not as "sluggish" but as "slow progressive".

Dementia praecox (a "premature dementia" or "precocious madness") is a disused psychiatric diagnosis that originally designated a chronic, deteriorating psychotic disorder characterized by rapid cognitive disintegration, usually beginning in the late teens or early adulthood. Over the years, the term "dementia praecox" was gradually replaced by "schizophrenia", which remains in current diagnostic use.

The term "dementia praecox" was first used in 1891 by Arnold Pick (1851–1924), a professor of psychiatry at Charles University in Prague. His brief clinical report described the case of a person with a psychotic disorder resembling hebephrenia. German psychiatrist Emil Kraepelin (1856–1926) popularised it in his first detailed textbook descriptions of a condition that eventually became a different disease concept and relabeled as schizophrenia. Kraepelin reduced the complex psychiatric taxonomies of the nineteenth century by dividing them into two classes: manic-depressive psychosis and dementia praecox. This division, commonly referred to as the Kraepelinian dichotomy, had a fundamental impact on twentieth-century psychiatry, though it has also been questioned.

The primary disturbance in dementia praecox was seen to be a disruption in cognitive or mental functioning in attention, memory, and goal-directed behaviour. Kraepelin contrasted this with manic-depressive psychosis, now termed bipolar disorder, and also with other forms of mood disorder, including major depressive disorder. He eventually concluded that it was not possible to distinguish his categories on the basis of cross-sectional symptoms.

Kraepelin viewed dementia praecox as a progressively deteriorating disease from which no one recovered. However, by 1913, and more explicitly by 1920, Kraepelin admitted that while there may be a residual cognitive defect in most cases, the prognosis was not as uniformly dire as he had stated in the 1890s. Still, he regarded it as a specific disease concept that implied incurable, inexplicable madness.

Treatment for confabulation is somewhat dependent on the cause or source, if identifiable. For example, treatment of Wernicke–Korsakoff syndrome involves large doses of vitamin B in order to reverse the thiamine deficiency. If there is no known physiological cause, more general cognitive techniques may be used to treat confabulation. A case study published in 2000 showed that Self-Monitoring Training (SMT) reduced delusional confabulations. Furthermore, improvements were maintained at a three-month follow-up and were found to generalize to everyday settings. Although this treatment seems promising, more rigorous research is necessary to determine the efficacy of SMT in the general confabulation population.

There are no evidence-based treatments for the condition; health care providers generally try to help people cope with it by recognizing what the person is experiencing, and by working on coping strategies with the person. Some small studies have been published on the use of sound therapy similar to tinnitus retraining therapy and on cognitive behavioral therapy and particularly exposure therapy, to help people become less aware of the trigger sound. None of these approaches have been sufficiently studied to determine their effectiveness.

Oneirophrenia was studied in the 1950s by the neurologist and psychiatrist Ladislas J. Meduna (1896–1964), also known as the discoverer of one of the forms of shock therapy, using the drug metrazol. Although oneirophrenia was recognized as a specific condition in the 1950's, it was not studied in depth until the 1960s. During its beginning stages oneriophrenia was studied very closely with schizophrenia as an acute form due to the relationship between their symptoms. It wasn't until greater research that oneirophrenia became its own mental disease.

The underlying neurophysiology and psychopathology of Cotard syndrome might be related to problems of delusional misidentification. Neurologically, the Cotard delusion (negation of the Self) is thought to be related to the Capgras delusion (people replaced by impostors); each type of delusion is thought to result from neural misfiring in the fusiform face area of the brain (which recognizes faces) and in the amygdalae (which associate emotions to a recognized face).

The neural disconnection creates in the patient a sense that the face they are observing is not the face of the person to whom it belongs; therefore, that face lacks the familiarity (recognition) normally associated with it. This results in derealization, or a disconnection from the environment. If the observed face is that of a person known to the patient, they experience that face as the face of an impostor (the Capgras delusion). If the patient sees their own face, they might perceive no association between the face and their own sense of Self—which results in the patient believing that they do not exist (the Cotard delusion).

Cotard's syndrome is usually encountered in people afflicted with a psychosis (e.g., schizophrenia ), neurological illness, mental illness, clinical depression, derealization, brain tumor, and with migraine headache. The medical literature indicate that the occurrence of Cotard's delusion is associated with lesions in the parietal lobe. As such, the Cotard-delusion patient presents a greater incidence of brain atrophy—especially of the median frontal lobe—than do the people in the control groups.

The Cotard delusion also has resulted from a patient's adverse physiological response to a drug (e.g., aciclovir) and to its prodrug precursor (e.g., valaciclovir). The occurrence of Cotard delusion symptoms was associated with a high serum-concentration of 9-Carboxymethoxymethylguanine (CMMG), the principal metabolite of the drug aciclovir. As such, the patient with weak kidneys (impaired renal function) continued risking the occurrence of delusional symptoms, despite the reduction of the dose of aciclovir. Hemodialysis resolved the patient's delusions (of negating the Self) within hours of treatment, which suggests that the occurrence of Cotard-delusion symptoms might not always be cause for psychiatric hospitalization of the patient.