Treatment of OBS varies with the causative disorder or disease. It is important to note that it is not a primary diagnosis and a cause needs to be sought out and treated.

In a confirmed medical diagnosis, therapy is used to isolate and begin treating the cause of the disorder. Thereafter, psychiatric medication is used a secondary step in treatment. Medications include antipsychotic, antidepressant, or sedation-inducing, varying on the patients severity.

Treatment of psychorganic syndrome is directed at the main disease. Nootropics like piracetam, have had positive effects on patients. Vitamin therapy, antioxidants, neurotropic, and cerebroprotective have also found to be effective when put on a repeat course.

An organic brain syndrome (OBS), also known as an organic brain disease/disorder (OBD), an organic mental syndrome (OMS), or an organic mental disorder (OMD), is a syndrome or disorder of mental function whose cause is alleged to be known as organic (physiologic) rather than purely of the mind. These names are older and nearly obsolete general terms from psychiatry, referring to many physical disorders that cause impaired mental function. They are meant to exclude psychiatric disorders (mental disorders). Originally, the term was created to distinguish physical (termed "organic") causes of mental impairment from psychiatric (termed "functional") disorders, but during the era when this distinction was drawn, not enough was known about brain science (including neuroscience, cognitive science, neuropsychology, and mind-brain correlation) for this cause-based classification to be more than educated guesswork labeled with misplaced certainty, which is why it has been deemphasized in current medicine.

"Acute" organic brain syndrome is (by definition) a recently appearing state of mental impairment, as a result of intoxication, drug overdose, infection, pain, and many other physical problems affecting mental status. In medical contexts, "acute" means "of recent onset". As is the case with most acute disease problems, acute organic brain syndrome is often temporary, although this does not guarantee that it will not recur (happen again) or progress to become chronic, that is, long-term. A more specific medical term for the "acute" subset of organic brain syndromes is delirium.

"Chronic" organic brain syndrome is long-term. For example, some forms of chronic drug or alcohol dependence can cause organic brain syndrome due to their long-lasting or permanent toxic effects on brain function. Other common causes of chronic organic brain syndrome sometimes listed are the various types of dementia, which result from permanent brain damage due to strokes, Alzheimer's disease, or other damaging causes which are not reversible.

Though OBS was once a common diagnosis in the elderly, until the understanding of the various types of dementias it is related to a disease process and is not an inevitable part of aging. In some of the older literature, there was an attempt to separate organic brain syndrome from dementia, but this was related to an older world view in which dementia was thought to be a part of normal aging, and thus did not represent a special disease process. The later identification of various dementias as clear pathologies is an example of the types of pathological problems discovered to be associated with mental states, and is one of the areas which led to abandonment of all further attempts to clearly define and use OBS as a term.

Psycho-organic syndrome is typically diagnosed in individuals following 5–10 years of consistent exposure to chemicals like xylene, toluene, and styrene, which are generally found in paint, plastic and degreasing products.

Patients work and environmental history must be evaluated for exposure to organic chemicals. A traumatic brain injury may also lead to POS.

Consistent intoxication (ie excess use of alcohol and drugs) may also cause a lesion in the brain, eventually leading to POS.

Lyme diseae, the great "new imitator", has been known to mimick depression, scizophreania, depersonazlization disorder, and obsessive-complsive disorder.

Although the cause varies by each individual case, localization of the atrophy in the brain can occur due to aging and without external causes, linked to hereditary.

Prevention includes proper and regular use of Preventive Personal Equipment (PPE) in work environments that involve organic chemicals and limiting alcohol and drug substance intake.

Treatment varies according to the type and severity of the encephalopathy. Anticonvulsants may be prescribed to reduce or halt any seizures. Changes to diet and nutritional supplements may help some patients. In severe cases, dialysis or organ replacement surgery may be needed.

Sympathomimetic drugs can increase motivation, cognition, motor performance and alertness in patients with encephalopathy caused by brain injury, chronic infections, strokes, brain tumors.

Treating the underlying cause of the disorder may improve or reverse symptoms. However, in some cases, the encephalopathy may cause permanent structural changes and irreversible damage to the brain. These permanent deficits can be considered a form of stable dementia. Some encephalopathies can be fatal.

Although the brain and spinal cord are surrounded by tough membranes, enclosed in the bones of the skull and spinal vertebrae, and chemically isolated by the blood–brain barrier, they are very susceptible if compromised. Nerves tend to lie deep under the skin but can still become exposed to damage. Individual neurons, and the neural networks and nerves into which they form, are susceptible to electrochemical and structural disruption. Neuroregeneration may occur in the peripheral nervous system and thus overcome or work around injuries to some extent, but it is thought to be rare in the brain and spinal cord.

The specific causes of neurological problems vary, but can include genetic disorders, congenital abnormalities or disorders, infections, lifestyle or environmental health problems including malnutrition, and brain injury, spinal cord injury or nerve injury. The problem may start in another body system that interacts with the nervous system. For example, cerebrovascular disorders involve brain injury due to problems with the blood vessels (cardiovascular system) supplying the brain; autoimmune disorders involve damage caused by the body's own immune system; lysosomal storage diseases such as Niemann-Pick disease can lead to neurological deterioration. The National Institutes of Health recommend considering the evaluation of an underlying celiac disease in people with unexplained neurological symptoms, particularly peripheral neuropathy or ataxia.

In a substantial minority of cases of neurological symptoms, no neural cause can be identified using current testing procedures, and such "idiopathic" conditions can invite different theories about what is occurring.

A widely accepted treatment for the syndrome of subjective doubles has not been developed. Treatment methods for this disease sometimes include the prescription of antipsychotic drugs, however, the type of drug prescribed depends on the presence of other mental disorders. Antipsychotic drugs (also known as neuroleptics) such as risperidone, pimozide, or haloperidol may be prescribed to treat the underlying psychiatric illness.

In addition to drug therapy, interpersonal counseling has also been suggested as a method to ease relations between the patient and his/her suspected doubles. However, the relationship between the patient and his/her double is not always negative.

A neurological disorder is any disorder of the nervous system. Structural, biochemical or electrical abnormalities in the brain, spinal cord or other nerves can result in a range of symptoms. Examples of symptoms include paralysis, muscle weakness, poor coordination, loss of sensation, seizures, confusion, pain and altered levels of consciousness. There are many recognized neurological disorders, some relatively common, but many rare. They may be assessed by neurological examination, and studied and treated within the specialities of neurology and clinical neuropsychology.

Interventions for neurological disorders include preventative measures, lifestyle changes, physiotherapy or other therapy, neurorehabilitation, pain management, medication, or operations performed by neurosurgeons. The World Health Organization estimated in 2006 that neurological disorders and their sequelae (direct consequences) affect as many as one billion people worldwide, and identified health inequalities and social stigma/discrimination as major factors contributing to the associated disability and suffering.

Recovery from this syndrome is situational, as some drug therapies have been effective in some individuals but not others. Patients may live in a variety of settings, including psychiatric hospitals, depending on the success of treatment. With successful treatment, an individual may live at home. In many of the reported cases, remission of symptoms occurred during the follow-up period.

This disorder can be dangerous to the patient and others, as a patient may interrogate or attack a person they believe to be a double. Inappropriate behavior such as stalking and physical or psychological abuse has been documented in some case studies. Consequently, many individuals suffering from this disorder are arrested for the resulting misconduct (see the case of Mr. B in #Presentation).

The treatment of PRES dependent on its cause. Anti-epileptic medication may also be appropriate.

"Early onset schizophrenia" (EOS) is not childhood schizophrenia, because this term is used to identify adolescence patients who develop first episode of psychosis before the age of 18. Childhood schizophrenia manifests before the age of 13, so it's correct names are "childhood-onset schizophrenia" (COS) and "very early-onset schizophrenia" (VEOS).

Adolescents (teenagers) are persons between the ages of 13 and 18. Children are defined as persons under the age of 13, so the term "early onset schizophrenia" (EOS) is not not appropriate in the article about childhood schizophrenia.

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.

Many cases resolve within 1–2 weeks of controlling blood pressure and eliminating the inciting factor. However some cases may persist with permanent neurologic impairment in the form of visual changes and seizures among others. Though uncommon, death may occur with progressive swelling of the brain (cerebral edema), compression of the brainstem, increased intracranial pressure, or a bleed in the brain (intracerebral hemorrhage). PRES may recur in about 5-10% of cases; this occurs more commonly in cases precipitated by hypertension as opposed to other factors (medications, etc.).

New brain-computer interfaces (BCIs) may provide future remedies. One effort in 2002 allowed a fully locked-in patient to answer yes-or-no questions; others reported in 2017 having repeated this result with a larger study. In 2006, researchers created and successfully tested a neural interface which allowed someone with locked-in syndrome to operate a web browser. Some scientists have reported that they have developed a technique that allows locked-in patients to communicate via sniffing.

It is extremely rare for any significant motor function to return. The majority of locked-in syndrome patients do not regain motor control, but devices are available to help patients communicate. However, some people with the condition continue to live much longer, while in exceptional cases, like that of Kerry Pink and Kate Allatt, a full spontaneous recovery may be achieved.

Early and aggressive treatment is important to prevent irreversible neurological damage, hearing loss, or vision loss. Medications used include immunosuppressive agents and corticosteroids such a prednisone, or intravenous immunoglobulins (IVIG). Other drugs that have been used are mycophenolate mofetil (Cellcept), azathioprine (Imuran), cyclophosphamide, rituximab, and anti-TNF therapies.

Hearing aids or cochlear implants may be necessary in the event of hearing loss.

Anumonye reported treatment success with lorazepam; others found benefit with antidepressants and relaxation exercises.

No true psychiatric medications are prescribed for factitious disorder. However, selective serotonin reuptake inhibitors (SSRIs) can help manage underlying problems. Medicines such as SSRIs that are used to treat mood disorders can be used to treat FD, as a mood disorder may be the underlying cause of FD. Some authors (such as Prior and Gordon 1997) also report good responses to antipsychotic drugs such as Pimozide. Family therapy can also help. In such therapy, families are helped to better understand patients (the individual in the family with FD) and that person's need for attention.

In this therapeutic setting, the family is urged not to condone or reward the FD individual's behavior. This form of treatment can be unsuccessful if the family is uncooperative or displays signs of denial and/or antisocial disorder. Psychotherapy is another method used to treat the disorder. These sessions should focus on the psychiatrist's establishing and maintaining a relationship with the patient. Such a relationship may help to contain symptoms of FD. Monitoring is also a form that may be indicated for the FD patient's own good; FD (especially proxy) can be detrimental to an individual's health—if they are, in fact, causing true physiological illnesses. Even faked illnesses/injuries can be dangerous, and might be monitored for fear that unnecessary surgery may subsequently be performed.

It is possible for this disorder to progress over time. A patient suffering from the disorder can improve the condition with treatments. There are several types of therapies that may improve the condition, but depending on a patient’s experience of the disorder or the cause of the disorder, treatments will vary.

- Psychotherapy including behaviour therapy, Gestalt therapy, Adlerian therapy, psychoanalytic therapy and existential therapy.

- Pharmacotherapy through medications including antidepressants.

Individual approaches to treatment are recommended, usually involving a combination of mood stabilizers and atypical antipsychotics. Psychotherapy may be beneficial and should be started early.

Neurodevelopmental disorders are in their multitude associated with widely varying degrees of difficulty, depending on which there are different degrees of mental, emotional, physical, and economic consequences for individuals, and in turn families, groups and society.

Treatment is dependent on the underlying cause, whether it is organic or psychological in origin. If depersonalization is a symptom of neurological disease, then diagnosis and treatment of the specific disease is the first approach. Depersonalization can be a cognitive symptom of such diseases as amyotrophic lateral sclerosis, Alzheimer's, multiple sclerosis (MS), neuroborreliosis (Lyme disease), or any other neurological disease affecting the brain. For those suffering from depersonalization with migraine, tricyclic antidepressants are often prescribed.

If depersonalization is a symptom of psychological causes such as developmental trauma, treatment depends on the diagnosis. In case of dissociative identity disorder or DD-NOS as a developmental disorder, in which extreme developmental trauma interferes with formation of a single cohesive identity, treatment requires proper psychotherapy, and—in the case of additional (co-morbid) disorders such as eating disorders—a team of specialists treating such an individual. It can also be a symptom of borderline personality disorder, which can be treated in the long term with proper psychotherapy and psychopharmacology.

The treatment of chronic depersonalization is considered in depersonalization disorder.

A recently completed study at Columbia University in New York City has shown positive effects from transcranial magnetic stimulation (TMS) to treat depersonalization disorder. Currently, however, the FDA has not approved TMS to treat DP.

A 2001 Russian study showed that naloxone, a drug used to reverse the intoxicating effects of opioid drugs, can successfully treat depersonalization disorder. According to the study: "In three of 14 patients, depersonalization symptoms disappeared entirely and seven patients showed a marked improvement. The therapeutic effect of naloxone provides evidence for the role of the endogenous opioid system in the pathogenesis of depersonalization."

Education, and a "watch and wait" strategy, are the only treatment needed for many, and the majority of individuals with tics do not seek treatment; treatment of tic disorders is similar to treatment of Tourette syndrome.

Brain trauma in the developing human is a common cause (over 400,000 injuries per year in the US alone, without clear information as to how many produce developmental sequellae) of neurodevelopmental syndromes. It may be subdivided into two major categories, congenital injury (including injury resulting from otherwise uncomplicated premature birth) and injury occurring in infancy or childhood. Common causes of congenital injury are asphyxia (obstruction of the trachea), hypoxia (lack of oxygen to the brain) and the mechanical trauma of the birth process itself.