Updated: May 15, 2009
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 (DSM-IV-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.
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.
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.
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.
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
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.
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.
DSM-IV-TR diagnostic criteria require presence of one or more of the following: delusions, hallucinations, disorganized speech, or grossly disorganized or catatonic behavior. These criteria also require an episodic duration of the disturbance for at least 1 day but less than 1 month, with eventual return to the premorbid level of functioning. According to the DSM-IV-TR, the diagnosis of brief psychotic disorder can be specified as with or without marked stressors or with postpartum onset.4,5 Some clinicians believe that persons with personality disorders (eg, narcissistic, paranoid, borderline, schizotypal) are more prone to develop brief psychotic disorder in stressful situations.6
Causes are largely unknown.
| Delirium | Mental Disorders Secondary to General Medical
Conditions |
| Delusional Disorder | Schizoaffective Disorder |
| Dissociative Disorders | Schizophrenia |
| Factitious Disorder | Schizophreniform Disorder |
| Malingering |
Substance-induced psychotic disorder
Psychotic disorder secondary to general medical condition
Mood disorder with psychotic features
Psychotic disorder not otherwise specified (NOS)
Psychosis associated with personality disorders
Epilepsy
Ganser syndrome
The goals of pharmacotherapy are to reduce morbidity and to prevent complications.
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.
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.
2-5 mg PO/IM qd/bid/tid or 1-2 mg IV bid/tid
Children: Not established
Adolescents: Administer as in adults
Serum plasma levels decreased by rifampin; potentiates effects of CNS depressants (eg, alcohol, opiates, anesthetics); lithium has induced encephalopathic syndrome
Documented hypersensitivity; extrapyramidal symptoms; Parkinson disease
C - Fetal risk revealed in studies in animals but not established or not studied in humans; may use if benefits outweigh risk to fetus
Severe neurotoxicity manifesting as rigidity or inability to walk or talk may occur in patients with thyrotoxicosis also receiving antipsychotics; if administered IV/IM, observe for hypotension; caution in diagnosed CNS depression or cardiac disease; if history of seizures, benefits must outweigh risks; significant increase in body temperature may indicate intolerance to antipsychotics (discontinue if this occurs); ventricular arrhythmias such as torsade de pointes have been reported, especially in patients with cardiac disease and in those administered high doses of IV haloperidol
Blocks postsynaptic blockade of CNS dopamine receptors, inhibiting dopamine-mediated effects. Provides rapid tranquilization in PO and IM forms.
5-20 mg/d PO/IM in single or divided dose
Children: Not established
Adolescents: Administer as in adults
Decreases effects of guanethidine; increases toxicity of CNS depressants, anticholinergics, and alcohol
Documented hypersensitivity; breastfeeding; CNS depression; blood dyscrasias
C - Fetal risk revealed in studies in animals but not established or not studied in humans; may use if benefits outweigh risk to fetus
Caution in narrow-angle glaucoma, severe liver disease, seizures, bone marrow suppression, cardiac disease; extrapyramidal symptoms (eg, muscle rigidity, inability to walk or talk, akathisia, dystonia); opisthotonus and oculogyric crisis; circulatory collapse; coma
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.
2-14 mg/d PO in divided doses
Children: Not established
Adolescents: Administer as in adults
Coadministration with carbamazepine may decrease effects; risperidone may inhibit effects of levodopa; clozapine may increase risperidone levels
Documented hypersensitivity
C - Fetal risk revealed in studies in animals but not established or not studied in humans; may use if benefits outweigh risk to fetus
May cause extrapyramidal reactions, hypotension, tachycardia, and arrhythmias
May inhibit serotonin, muscarinic, and dopamine effects. Efficacy similar to risperidone, fewer dose-dependent adverse effects but more concern about weight gain.
5-20 mg/d PO in divided doses
Children: Not established
Adolescents: Administer as in adults
Fluvoxamine may increase effects of olanzapine; antihypertensives may increase risk of hypotension and orthostatic hypotension; levodopa, pergolide, bromocriptine, charcoal, carbamazepine, omeprazole, rifampin, and cigarette smoking may decrease the effects of olanzapine
Documented hypersensitivity
C - Fetal risk revealed in studies in animals but not established or not studied in humans; may use if benefits outweigh risk to fetus
Caution in narrow-angle glaucoma, cardiovascular disease, cerebrovascular disease, prostatic hypertrophy, seizure disorders, hypovolemia, and dehydration
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.
25 mg PO bid; titrate to 150-750 mg/d PO; not to exceed 800 mg/d
Children: Not established
Adolescents: Administer as in adults
Quetiapine may antagonize levodopa and dopamine agonists; phenytoin, thioridazine, and other liver enzyme inducers may reduce quetiapine levels
Documented hypersensitivity
C - Fetal risk revealed in studies in animals but not established or not studied in humans; may use if benefits outweigh risk to fetus
May induce orthostatic hypotension associated with dizziness, tachycardia, and syncope; the neuroleptic malignant syndrome has been associated with this treatment; cataracts may develop (perform eye examination every 6 mo)
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.
6 mg PO qd initially; if needed, may increase by 3-mg increments after at least 5 d; not to exceed 12 mg/d; some patients respond to lower doses of 3 mg/d
CrCl >50 to <80 mL/min: Do not exceed daily dose of 6 mg
CrCl 10 to <50 mL/min: Do not exceed daily dose of 3 mg
<18 years: Not established
Not substantially metabolized by cytochrome P450 isoenzymes and does not inhibit P-glycoprotein; may increase arrhythmia risk when coadministered with other drugs known to prolong QTc (eg, class IA [quinidine, procainamide] or class III [amiodarone, sotalol] antiarrhythmics, antipsychotics [chlorpromazine, thioridazine], antibiotics [gatifloxacin, moxifloxacin]); coadministration with other CNS depressants, including alcohol, may cause additive effects; coadministration with other drugs causing orthostatic hypotension (eg, alpha-blockers, diuretics) may increase hypotension risk; may antagonize effect of dopamine agonists (eg, levodopa, pramipexole)
Documented hypersensitivity to paliperidone or risperidone
C - Fetal risk revealed in studies in animals but not established or not studied in humans; may use if benefits outweigh risk to fetus
Elderly patients with dementia-related psychosis treated with atypical antipsychotic drugs have increased risk of CVA and TIA (some resulting in death) compared with placebo; decrease dose with renal impairment; causes modest QTc prolongation (caution with other drugs that prolong QTc, congenital long QT syndrome, or history of cardiac arrhythmias); other adverse effects include tachycardia, neuroleptic malignant syndrome, tardive dyskinesia, hyperglycemia (some with associated ketoacidosis, hyperosmolar coma, or death), orthostatic hypotension and syncope, hyperprolactinemia, sedation, priapism, thrombotic thrombocytopenia purpura, disrupted body temperature regulation, and antiemetic effector dysphagia; avoid with preexisting gastrointestinal narrowing (eg, esophageal motility disorders, small bowel inflammatory disease, short gut syndrome, peritonitis, cystic fibrosis, chronic pseudoobstruction, Meckel diverticulum) because tab is nondeformable and does not appreciably change in shape or size through gutand is eliminated intact in feces; swallow tab whole (do not chew or split); suicidality is inherent in psychotic illnesses and close supervision of high-risk patients should accompany therapy
Further inpatient care is unnecessary once the acute attack has ended.
Individual, family, and group psychotherapy may be considered to help cope with stressors and to help resolve conflict.
Both the patient and the family must be educated about the illness and potential adverse effects of the medications. Helpful Web sites include the following:
American Psychiatric Association. Diagnostic and Statistical Manual of Mental Disorders (DSM-IV-TR). 4th ed. Washington DC:. American Psychiatric Press;2000.
Susser E, Wanderling J. Epidemiology of nonaffective acute remitting psychosis vs schizophrenia. Sex and sociocultural setting. Arch Gen Psychiatry. Apr 1994;51(4):294-301. [Medline].
Jorgensen P, Mortensen PB. Reactive psychosis and mortality. Acta Psychiatr Scand. Mar 1990;81(3):277-9. [Medline].
Chaudron LH, Pies RW. The relationship between postpartum psychosis and bipolar disorder: a review. J Clin Psychiatry. Nov 2003;64(11):1284-92. [Medline].
[Best Evidence] Valdimarsdottir U, Hultman CM, Harlow B, Cnattingius S, Sparen P. Psychotic illness in first-time mothers with no previous psychiatric hospitalizations: a population-based study. PLoS Med. Feb 10 2009;6(2):e13. [Medline].
Jorgensen P, Bennedsen B, Christensen J, Hyllested A. Acute and transient psychotic disorder: comorbidity with personality disorder. Acta Psychiatr Scand. Dec 1996;94(6):460-4. [Medline].
Karagianis JL, Dawe IC, Thakur A, et al. Rapid tranquilization with olanzapine in acute psychosis: a case series. J Clin Psychiatry. 2001;62 Suppl 2:12-6. [Medline].
Brook S, Lucey JV, Gunn KP. Intramuscular ziprasidone compared with intramuscular haloperidol in the treatment of acute psychosis. Ziprasidone I.M. Study Group. J Clin Psychiatry. Dec 2000;61(12):933-41. [Medline].
Correll CU, Smith CW, Auther AM, McLaughlin D, Shah M, Foley C, et al. Predictors of remission, schizophrenia, and bipolar disorder in adolescents with brief psychotic disorder or psychotic disorder not otherwise specified considered at very high risk for schizophrenia. J Child Adolesc Psychopharmacol. Oct 2008;18(5):475-90. [Medline].
Beighley PS, Brown GR, Thompson JW Jr. DSM-III-R brief reactive psychosis among Air Force recruits. J Clin Psychiatry. Aug 1992;53(8):283-8. [Medline].
Jablensky A, Sartorius N, Ernberg G, et al. Schizophrenia: manifestations, incidence and course in different cultures. A World Health Organization ten-country study. Psychol Med Monogr Suppl. 1992;20:1-97. [Medline].
Jauch DA, Carpenter WT Jr. Reactive psychosis. I. Does the pre-DSM-III concept define a third psychosis?. J Nerv Ment Dis. Feb 1988;176(2):72-81. [Medline].
Jauch DA, Carpenter WT Jr. Reactive psychosis. II. Does DSM-III-R define a third psychosis?. J Nerv Ment Dis. Feb 1988;176(2):82-6. [Medline].
Johnson FA. African perspective on mental disorder. In: Mezzich JE, Honda Y, Kastrup MC, eds. Psychiatric Diagnosis: A World Perspective. New York, NY: Springer Verlag; 1994.
Jorge MR, Mezzich JE. Latin American contributions to psychiatric nosology and classification. In: Mezzich JE, Honda Y, Kastrup MC, eds. Psychiatric Diagnosis: A World Perspective. New York, NY: Springer Verlag; 1994.
Jorgensen P, Jensen J. An attempt to operationalize reactive delusional psychosis. Acta Psychiatr Scand. Nov 1988;78(5):627-31. [Medline].
Karno M, Jenkins JH. Cultural considerations in the diagnosis of schizophrenia and related disorders and psychotic disorders not otherwise classified. In: TA Widiger, ed. DSM-IV Source Book. Washington DC: American Psychiatric Press; 1994.
Lin KM. Cultural influences on the diagnosis of psychotic and organic disorders. In: Mezzich JE, Kleinman A, Horacio F, Parron DL, eds. Culture and Psychiatric Diagnosis: A DSM-IV Perspective. Washington DC: American Psychiatric Press; 1996.
Mezzich JE, Lin KM. Acute and transient psychotic disorders and culture-bound syndromes. In: Sadock BJ, Sadock VA, eds. Kaplan and Sadock's Comprehensive Textbook of Psychiatry. 6th ed. Baltimore, Md: Lippincott Williams & Wilkins; 1995:1049.
Pull CB, Chaillet G. The nosological views of French-speaking psychiatry. In: Mezzich JE, Honda Y, Kastrup MC, eds. Psychiatric Diagnosis: A World Perspective. New York, NY: Springer Verlag; 1994.
Vanderhart O, Witztum E, Friedman B. From hysterical psychosis to reactive dissociative psychosis. J Trauma Stress. 1993;6:43.
brief reactive psychosis, hysterical psychosis, reactive schizophrenia, transient psychosis, acute and transient psychotic disorders, ATPD, atypical psychosis, stress psychosis, psychogenic psychosis, cycloid psychosis, good-prognosis schizophrenia, yak, latah, koro, amok, whitiligo, thought disturbances, mood disturbances, mood disorders, substance-induced psychosis, bouffee delirante
Mohammed A Memon, MD, Medical Director of Geriatric Psychiatry, Department of Psychiatry, Spartanburg Regional Hospital System
Mohammed A Memon, MD is a member of the following medical societies: American Association for Geriatric Psychiatry, American Medical Association, and American Psychiatric Association
Disclosure: Nothing to disclose.
Michael Larson, DO, Clinical Instructor, Department of Child and Adolescent Psychiatry, Harvard University
Michael Larson, DO is a member of the following medical societies: American Academy of Addiction Psychiatry and American Academy of Child and Adolescent Psychiatry
Disclosure: Nothing to disclose.
Alan D Schmetzer, MD, Professor, Vice-Chair for Education, and Director of Residency Training in General and Addiction Psychiatry, Department of Psychiatry, Indiana University School of Medicine
Alan D Schmetzer, MD is a member of the following medical societies: American Academy of Addiction Psychiatry, American Academy of Clinical Psychiatrists, American Academy of Psychiatry and the Law, American College of Physician Executives, American Medical Association, American Neuropsychiatric Association, American Psychiatric Association, and Association for Convulsive Therapy
Disclosure: Nothing to disclose.
Francisco Talavera, PharmD, PhD, Senior Pharmacy Editor, eMedicine
Disclosure: Nothing to disclose.
David Bienenfeld, MD, Vice-Chair, Program Director, Professor, Department of Psychiatry, Wright State University School of Medicine
David Bienenfeld, MD is a member of the following medical societies: American Medical Association, American Psychiatric Association, and Association for Academic Psychiatry
Disclosure: Nothing to disclose.
Harold H Harsch, MD, Program Director of Geropsychiatry, Department of Geriatrics/Gerontology, Associate Professor, Department of Psychiatry and Department of Medicine, Froedtert Hospital, Medical College of Wisconsin
Harold H Harsch, MD is a member of the following medical societies: American Psychiatric Association
Disclosure: lilly Honoraria Speaking and teaching; Forest Labs Honoraria Speaking and teaching; AstraZeneca Honoraria Speaking and teaching; Pfizer Grant/research funds Speaking and teaching; Northstar Grant/research funds Research; Novartis Grant/research funds research; Pfizer Speaking and teaching; Sanofi-avetis Grant/research funds research; Otsuke Grant/research funds reseach; GlaxoSmithKline Grant/research funds research
Stephen Soreff, MD, President of Education Initiatives, Nottingham, NH; Faculty, Metropolitan College of Boston University, Boston, MA
Stephen Soreff, MD is a member of the following medical societies: American College of Mental Health Administration and American Psychosomatic Society
Disclosure: Nothing to disclose.
© 1994-
by Medscape.
All Rights Reserved
(http://www.medscape.com/public/copyright)