Schizophreniform Disorder DSM-5 295.40 (F20.81)
DSM-5 Category: Schizophrenia Spectrum and Other Psychotic Disorders
Introduction
Schizophreniform disorder is a part of the schizophrenia spectrum in the Diagnostic and Statistical Manual of Mental Disorders, a psychotic condition similar in its symptoms to schizophrenia, but developing rapidly and present for a shorter period of time. Like the other entities in the schizophrenia spectrum, schizophreniform disorder is a serious and often disabling mental illness with both positive and negative thought and behavioral symptoms, demonstrable but nonspecific changes in brain anatomy, impairment of cognitive function evident on neuropsychological testing, suggestion of genetic predisposition and evidence of abnormal brain dopamine neurotransmission and clinical response to dopamine-blocking neuroleptic medications and some types of psychotherapy (Van Os & Kapur, 2009). The fifth edition of the DSM has made no specific changes in diagnostic criteria for schizophreniform disorder but has altered the principal criterion for diagnosis of schizophrenia itself (Criterion A) and eliminated the various subtypes of schizophrenia previously identified (American Psychiatric Association, 2013).
Symptoms and Prognosis of Schizophreniform Disorder
Schizophreniform disorder and schizophrenia share many features and symptoms, but differ in the duration of symptoms and degree of functional impairment. Schizophrenic symptoms must be present for at least 6 months for that condition to be diagnosed, but are by definition present for less than 6 months in schizophreniform disorder. There is usually functional impairment (academic, occupational or social) by the time schizophrenia is diagnosed, such difficulties may not be present at the diagnosis of schizophreniform disorder. Schizophreniform disorder has sometimes been a provisional diagnosis in psychotic individuals, while the condition waits to see if symptoms improve by 6 months of illness or persist or progress to support the impression of schizophrenia (Strakowski, 1994).
The symptoms of both disorders may be positive (hallucinations, delusions, thought disorder and disorganized speech, behavioral disorganization or catatonia) or negative (inability to feel emotions with flattening of affect, inability to experience pleasure or anhedonia), loss of interest in social relationships, lack of motivation and reduction of impairment of speech). About 2/3 of patients initially diagnosed with schizophreniform disorder will go on to be diagnosed with schizophrenia. Several favorable prognostic features have been identified: onset of psychotic symptoms within 4 weeks of first noticed change in behavior or function, confusion or perplexity during these symptoms which suggests insight into their abnormality, good occupational and social functioning before the onset of symptoms and absence of flat affect. Negative symptoms and lack of eye contact are unfavorable prognostic features (Troisi et al., 1991).
Diagnostic Criteria
DSM-5 requires at least 1 of the following symptoms for a significant portion of the time during a 1-month period: delusions, hallucinations or disorganized speech. Grossly disorganized behavior (catatonia) or the negative symptoms described above may also be present. Symptoms may have been present for less than a month, if they resolved after being treated. Symptoms must last more than a month but less than 6 months. There can be no manic, depressive or mixed manic-depressive episodes during these symptoms, and any mood disturbance must have been present during only a minority of this time, thereby excluding schizoaffective disorder or bipolar disorder with psychotic features. These symptoms cannot be due to the effects of a substance (drug of abuse or medication), or to a medical or neurological disorder. Schizophreniform disorder “with good prognostic features” is accompanied by at least 2 of the following: onset of psychotic symptoms within 4 weeks of the first noticeable change in behavior or functioning, good social or occupational function before the onset of symptoms, symptoms accompanied by confusion or perplexity or absence of flat or blunted affect. The disorder is otherwise “without good prognostic features”. Patients “with good prognostic features” may in retrospect be diagnosed with affectrive disorders rather than conditions in the schizophrenic spectrum (Benazzi, Mazzoli , & Rossi, 1993).
No specific DSM-5 changes were made with respect to schizophreniform disorder. The principal criterion by which schizophrenic spectrum disorders are diagnosed (criterion A) was modified by removing the preference (only one such symptom was needed for the diagnosis) for bizarre delusions and what were historically called Schneiderian first-rank auditory hallucinations (those of 2 or more voices conversing). This was done because the Schneider symptoms have over the past century proven diagnostically unreliable, and because the peculiarity of delusions is less important than their specificity for this group of disorders.
Epidemiology
Schizophreniform disorder affects males and females equally, but the peak onset is earlier in men (18-24 years) than women (24-35 years). The incidence of schizophreniform disorder in developed countries is low, about 1/5 that of schizophrenia in the United States. In developing countries, however, schizoaffective disorder is diagnosed more frequently, and may be as common as schizophrenia in some countries. Schizophreniform disorder in these countries is apparently more often associated with good prognostic factors than in developed countries (Sautter, McDermott, & Garver, 1993). It has been suggested that onset and recovery of psychotic illnesses are more rapid in developing countries, which would increase the number of patients meeting criteria for schizophreniform disorder (Jablensky et al., 1992).
Pathophysiology
The cause(s) of the disorders in the schizophrenia spectrum are unknown, but there is much evidence to support a disturbance in dopamine neurotransmission. Increasing experience with the second generation or atypical neuroleptic drugs suggests that serotonin may be involved as well (Richland et al., 2007). Patients with schizophrenia and schizophreniform disorder also have evidence of cerebral cortical dysfunction.
Definite findings on neurological examination are infrequent in schizophrenia or schizophreniform disorder, but “soft” neurological signs involving coordination and involuntary movement are increased in incidence in schizophreniform disorder and first-onset schizophrenic patients, with some evidence of a familial association and right-sided predominance, suggesting genetic predisposition and left cerebral hemisphere dysfunction (Bachmann, Bottmer, & Schröder, 2005). Between 5 and 80 per cent of schizophrenic patients have been reported to have slowing or paroxysmal activity on electroencephalogram (EEG) (Hughes & John, 1999), and paroxysmal EEG activity, not necessarily abnormal or specific, has been reported more frequently in schizophreniform disorder than in schizophrenia itself (Inui et al., 1998). Computer-assisted frequency analysis and topographic mapping (quantitative EEG) has shown increased slow activity and greater interhemispheric differences than in depressed patients or normal controls (Begic, 2011), and no difference has been demonstrated between the disorders in the schizophrenia spectrum (Boutros, Arfken, & Iacono, 2008).
Magnetic resonance imaging (MRI) has consistently supported the view that schizophrenia is a brain disorder with altered structure as well as function, showing in particular ventricular enlargement and volume loss in the temporal lobes, less frequently the frontal lobes as well (McCarley et al., 1999). These changes are prognostically negative in schizophrenia; they are also present in schizophreniform disorder, but it is not clear that ventricular enlargement is a poor prognostic sign there. Functional brain imaging with cerebral blood flow (CBF) measurement, photon emission tomography (SPECT) and positron emission tomography (PET) has shown a number of differences from normal, chiefly decreased frontal lobe perfusion, and lesser and more variable degrees of hypoperfusion in parietal and left temporal lobes in schizophreniform disorder as well as schizophrenia (Zipursky, Meyer & Verhoeff, 2007). Neuropsychological testing has shown similar patterns of deficit in schizophrenia and schizophreniform disorder, and attentional, executive and motor impairment at age 13 in those who developed schizophreniform disorder as adults (Cannon et al., 2006).
Medication Treatment of Schizophreniform Disorder
The increasingly large array of antipsychotic, antidepressant and antimanic medications used in various combinations to treat schizophrenia is also effective in schizophreniform disorder (Leucht et al., 2009). The treatment strategy is the same in both conditions, and focuses on finding the lowest effective dose of neuroleptic medication, usually an atypical antipsychotic, with prevention if possible of extrapyramidal side effects. Symptoms resistant to second-generation neuroleptics are usually addressed with newer antipsychotic medications or the addition of lithium, SSRI or SNRI antidepressants or mood-stabilizing anticonvulsants (Sajatovic et al., 2002). Electroconvulsive therapy is occasionally effective for treatment-resistant symptoms (Stromgren, 1988).
Risperidone (Risperdal), quetiapine (Seroquel), olanzapine (Zyprexa) and ziprasidone (Geodon) are the most commonly-used atypical neuroleptics, so called because they do not work solely by blockade of the D2 dopamine receptors as the first-generation or typical neuroleptics like chlorpromazine or haloperidol do. These are about equal in efficacy for schizophrenia and schizoaffective disorder, but may be more effective and better tolerated in lower doses for first-time psychotic symptoms as in schizophreniform disorder (Sanger et al., 1999). A new generation of neuroleptics is effective for resistant psychotic symptoms: aripiperazole (Abilify), which is a partial agonist rather than blocker of dopamine receptors and can be given by injection; paliperidone (Invega), the active metabolite of risperidone which can be given once daily; asenapine (Saphris), a relative of the antidepressant mirtazapine that must be taken sublingually but may also help mania and depression; iloperidone (Zomaril), which antagonizes serotonin as well as dopamine and my cause fewer problems with weight gain and extrapyramidal side effects; and lurasidone (Latuda), which is helpful for bipolar depression as well as psychosis.
Schizophreniform disorder accompanied by depressive symptoms is usually treated with an SSRI or SNRI antidepressant plus one of the above antipsychotics. If manic symptoms accompany the psychosis, mood stabilizers (lithium carbonate, carbamazepine, valproic acid, lamotrigine or topiramate) can be added. Clozapine, highly effective and free of extrapyramidal complications but attended by agranulocytosis, has been used for refractory psychosis but carries several “black box” warnings and requires regular blood and absolute neutrophil counts.
Psychotherapy for Schizophreniform Disorder
Supportive psychotherapy may help with distress and turmoil often occasioned by the relatively rapid onset and progression of symptoms in this disorder. Insight-oriented therapy is of limited value because of frequent denial and limited insight. Group therapy has been recommended, but may be frightening to C
References
American Psychiatric Association. (2013). Diagnostic and Statistical Manual of Mental Disorders, ed. 5. Washington, DC: APA Press.
Bachmann, S., Bottmer, C., & Schröder, J. (2005). Neurological soft signs in first-episode schizophrenia: A follow-up study. Am J Psychiat, 162(12), 2337-2343.
Begic, D., Popovic-Knapic, V., Grubisin, J., Kosanovic-Rajacic, B., Filipcic, I., Telarovic, J., Jakovlievic, M. (2011). Quantitative electroencephalography in schizophrenia and depression. Psychiatr Danub, 23(4), 355-362.
Benazzi F, Mazzoli M, Rossi E. (1992). A follow-up and family study of DSM-III-R schizophrenifotm disorder with good prognostic features. Eur Arch Psychiatry Clin Neurosci, 242(2-3), 119-121.
Boutros, N.N., Arfken, C., Iacono, W. (2008). The status of spectral EEG abnormality as a diagnostic test for schizophrenia. Schizophrenia Res, 99(1-3), 225-237.
Cannon, M., Moffitt, T., Caspi, A. et al. (2006). Neuropsychological performance at the age of 13 years and adult schizophreniform disorder: Prospective birth cohort study. Br J Psychiat, 189(5), 463-464.
Hughes, J.R., John, E.R. (1999). Conventional and quantitative EEG in psychiatry. J Neuropsychiat Clin Neurosci, 11(2), 190-208.
Inui, K., Motomura, E., Okushima, R., et al. (1998). Electroencephalographic findings in patients with DSM-IV mood disorders, schizophrenia and other psychotic disorders. Biol Psychiat, 43(1), 69-75.
Jablensky, A., Sartorius, N., Ernberg, G. et al. (1992). Schizophrenia: manifestations, incidence and course in different cultures. A World Health Organization ten-country study. Psychol Med Monograph Suppl, 20(1), 1-97.
Leucht, S., Komossa, K., Rummel-Kluge, C., et al. (2009). A meta-analysis of head-to-head comparisons of second-generation antipsychotics in the treatment of schizophrenia. Am J Psychiat, 166(2), 152-163.
McCarley, R.W., Wible, C., Frumin, M., et al. (1999). MRI anatomy of schizophrenia. Bio Psychiat, 45(9), 1099-1119.
Richland, M., Welge, A., Logue, D., et al. (2007). Dopamine and serotonin receptor binding and antipsychotic efficacy. Neuropsychopharmacology, 32(8), 1715-1726.
Sajatovic, M., Mullen, J.M., Sweitzer, D.E. et al. (2002). Efficacy of quetiapine and risperidone against depressive symptoms in outpatients with psychosis. J Clin Psychiat, 63(12), 1156-1163.
Sanger, T.M., Lieberman, J.A., Tohen, M., et al. (1999). Olanzapine versus haloperidol treatment in first-episode psychosis. Am J Psychiat, 156(1), 79-87.
Sautter, F., McDermott, B., & Garver, D. (1993). The course of DSM-III-R schizophreniform disorder. J Clin Psychol, 49(3), 339-344.
Strakowski, S.M. (1994). Diagnostic validity of schizophreniform disorder. Am J Psychiat, 151(6), 815-824.
Stromgren, L.S. (1988). Electroconvulsive therapy in Aarhus, Denmark in 1984: Its application in nondepressive disorders. Convuls Ther, 4(4), 306-313.
Troisi, A., Pasini, A., Bersani, G. et al. (1991). Negative symptoms and visual behavior in DSM-III-R prognostic subtypes of schizophreniform disorder. Acta Psychiatr Scand, 83(5), 391-394.
Van Os, J., & Kapur, S. (2009). Schizophrenia. Lancet, 374 (9690), 635-645.
Zipursky, R.B., Meyer, J.H., Verhoeff, N.P. (2007). PET and SPECT imaging in psychiatric disorders. Can J Psychiat, 52(3), 146-157.
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