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Overview Brief psychotic disorder is a period of psychosis that lasts anywhere from one day to one month.

Essentially, it is a brief break from reality. One distinction between this disorder versus other psychotic disorders is that the person suffering from the brief psychotic episode eventually returns to a baseline, or "normal," level of functioning. After returning to the baseline level of functioning, most people recover. More rarely, some people will have recurring episodes. This disorder is not common in the United States, but does occur more frequently in women than in men. It typically occurs in early adulthood (between twenty and thirty years old) in both men and women. Causes The psychosis generally occurs without forewarning, though is more likely to occur in people with a pre-existing condition, such as a personality disorder. However, severe stress factors, such as the death of a loved one, severe illness, employment or financial problems, family conflicts, or accidents, can lead to brief reactive psychosis. This means the psychotic episode is in reaction to some traumatic event. It can also occur approximately four weeks postpartum as brief reactive psychosis. Symptoms As mentioned, the symptoms of this psychotic disorder will come on without forewarning. The common symptoms include hallucinations, delusions, disorganized speech, disorganized behavior, and sometimes, catatonic behavior. While these are the most common symptoms, they are certainly not the only symptoms that may manifest in brief psychotic disorder. Other symptoms that are often associated with this psychotic disorder are rapid mood changes, disorientation, homicidal or suicidal thoughts or behaviors, and impaired attention. People may also exhibit emotional volatility, screaming or muteness, loss of memory for recent events, and outlandish dress or behavior. Brief psychotic disorder does not apply if the symptoms can be explained by schizophrenia, a mood disorder with psychotic features, schizoaffective disorder, and is not caused by a substance such as drug abuse or medication. Diagnosis If the symptoms of brief psychosis disorder are present, a complete medical history and examination will be given, which rules out possible physical causes for the symptoms. If no physical cause for the symptoms is found, the person will be given a mental evaluation by a mental health professional. The evaluation will determine whether the person is experiencing a brief psychotic episode, or whether the symptoms can be attributed to another mental or emotional cause, such as a mood disorder. Treatments

The most common treatment for brief psychotic disorder is psychotherapy. Since most people recover after the initial psychotic episode, medication is not needed. Instead, psychotherapy is the most effective treatment. The psychotherapy can be either group therapy or individual therapy, depending on that person's needs and experiences. Depending on the severity of the symptoms of this psychotic disorder, someone who experiences it may need to be hospitalized for a brief time in order to prevent harm to him or herself, or to someone else.

Background In 1913, Karl Jaspers described specific criteria for the diagnosis of reactive psychosis, including the presence of an identifiable and extremely traumatic stressor, a close relation between the stressor and the development of psychosis, and a generally benign course for the psychotic episode. The Diagnostic and Statistical Manual of Mental Disorders, Fourth Edition, Text Revision (DSMIV-TR) describes brief psychotic disorder based primarily on duration of symptoms. DSM-

IV defines brief psychotic disorder as an illness lasting from 1 day to 1 month, with an eventual return to the premorbid level of functioning.[1] The diagnosis has been better appreciated and more completely studied in Scandinavia and other western European countries than in the United States. Pathophysiology Some data suggest increased incidence of mood disorders in families of patients with brief psychotic disorder. Psychodynamic theories suggest that the psychotic symptoms occur because of inadequate coping mechanisms, as a defense against prohibited fantasy, or as an escape from a specific psychological situation or an overwhelming stressful circumstance. It must be understood that the individual perceives the stress as totally overwhelming. Neither biological nor psychological theories have been validated by carefully controlled clinical studies. Epidemiology Frequency United States Brief psychotic disorder is not common. According to one follow-up study of 221 first-admission patients with affective and nonaffective psychoses, only 20 (9%) of the 221 experienced brief psychoses, and only 7 (3%) experienced acute brief psychoses. International According to an international epidemiologic study, in contrast to schizophrenia, incidence of nonaffective acute remitting psychoses was 10-fold higher in developing countries than in industrialized countries.[2] Some clinicians believe that the disorder may most frequently occur in patients from low socioeconomic classes, patients with preexisting personality disorders, and immigrants. In nonindustrialized countries, such terms as yak, latah, koro, amok, and whitiligo have been used to describe psychotic states precipitated by stressful events. These and several similar cultural terms are now considered to be culture-bound syndromes. Mortality/Morbidity As with any other psychotic episode, the risk of harm to self and/or others increases with an acute episode of brief psychotic disorder.[3] Sex According to an international epidemiologic study, incidence of the disorder was 2-fold higher in women than in men.[2] Study reports in the United States indicate even higher incidence in women than in men. Age The disorder is more common in patients late in the third to early in the fourth decade of life. Cases have also been recognized later in life.

Medical Care

Patients with acute psychotic attack may need a brief hospitalization for evaluation and safety concerns. If a patient becomes aggressive and combative, brief seclusion or restraint may be necessary to ensure safety of the patient and/or others. Because of the short duration of brief psychotic disorder, the treatment is brief and focused on being least restrictive. However, since it is rapid in onset and quick in course, it remains clinically imperative to protect the patient from self-injury or harm to others. Hence, a brief hospitalization may be in order. If symptoms are only minimally impairing the patient's function and a specific stressor is identified, removing the stressor should suffice. In the event that symptoms are disabling, an antipsychotic agent should be used for no longer than a month. If adverse effects are intolerable, the use of atypical antipsychotics may be helpful. Unfortunately, not enough information is available in the literature to support the use of atypical antipsychotics for the treatment of brief psychotic disorder. A case series suggests that rapid tranquilization with olanzapine can achieve symptom relief in acute psychosis.[7] A study involving intramuscular ziprasidone showed greater efficacy and tolerability than intramuscular haloperidol in treating acute psychosis.[8] In the authors' experience, intramuscular ziprasidone is the most effective treatment of acute severe psychotic agitation . After the acute episode is resolved, individual, family, and group therapy may be considered to help cope with stressors, resolve conflict, and improve self-esteem and self-confidence.

Medication Antipsychotics Class Summary Are high-potency agents (eg, haloperidol, droperidol) that provide rapid, predictable, and effective sedation in the management of patients who are acutely psychotic. They are less sedating and more easily titrated but are more likely to cause extrapyramidal syndrome (EPS) than lower-potency agents. They are often combined in the same syringe with a benzodiazepine (eg, lorazepam, diazepam) for better sedation and anxiolysis and for less dystonia or akathisia. For prophylaxis of extrapyramidal adverse effects, temporary use of a serotonin-dopamine antagonist may be needed. Administered IM or IV. (In a less emergent setting, administered PO [haloperidol only]). Haloperidol also has a monthly depot form (haloperidol decanoate) that is not useful for brief psychotic disorder because of short duration of the disorder. Depot antipsychotics are not intended for use in the emergent setting.

Haloperidol (Haldol)

Controls psychosis and provides rapid tranquilization. Administer with a benzodiazepine to protect against lowered seizure threshold. In emergencies, select high-potency antipsychotic available in tab, liquid, or IM form. In author's experience, Haldol IV can be used effectively in small doses of 1-2 mg q8h for 2-3 d for acute psychotic agitation, and it can be continued PO for the next several d until symptoms completely subside. Note that IV route is also effective for delirium in case of difficulty differentiating brief psychotic disorder and delirium.

Thiothixene (Navane)

Blocks postsynaptic blockade of CNS dopamine receptors, inhibiting dopamine-mediated effects. Provides rapid tranquilization in PO and IM forms. Risperidone (Risperdal)

Unlike haloperidol, risperidone has serotonergic blocking effects that alleviate negative symptoms of psychosis (eg, anhedonia, avolition, amotivation, flat affect). Well tolerated with fewer extrapyramidal adverse effects than with typical antipsychotics. Doses > 6 mg/d increase risk of extrapyramidal effects. Olanzapine (Zyprexa)

May inhibit serotonin, muscarinic, and dopamine effects. Efficacy similar to risperidone, fewer dose-dependent adverse effects but more concern about weight gain. Quetiapine (Seroquel)

May act by antagonizing dopamine and serotonin effects. Efficacy similar to risperidone and olanzapine. Fewer dose-dependent adverse effects and less concern of weight gain. Paliperidone (Invega)

Major active metabolite of risperidone and first oral agent allowing once-daily dosing. Indicated for treatment of acute schizophrenia. Mechanism of action not completely understood but thought to mediate central receptor antagonism of dopamine type 2 (D2) and serotonin type 2 (5HT2A). Also elicits antagonist activity at adrenergic alpha1 and alpha2 receptors and histamine-1 receptors. Has no affinity for cholinergic, muscarinic, or beta-adrenergic receptors. Available as extended-release drug delivery system via osmotic pressure.