Chapter 110 In the 1800s, Morel introduced the term dementia praecox to describe a progressive deterioration of mental functioning and behavior with onset in adolescence to early adult life.1 In 1911, Bleuler detailed the specifics of this disorder, which he termed schizophrenia, or “split-mindedness.”2 Early treatments of schizophrenia included ice water immersion, barbiturates or insulin to induce prolonged narcosis or coma, seizure induction with pentylenetetrazol, electroconvulsive therapy, and frontal leukotomy.3 The effectiveness of these treatments was marginal at best, and until recent times, most schizophrenic patients were relegated to lifelong institutionalization. Modern-era pharmacotherapy for schizophrenia, with chlorpromazine and haloperidol, began in the early 1950s. This treatment proved so successful that by the 1960s, most psychiatrists believed that schizophrenia could be successfully managed in the outpatient setting. In 1965, the Community Mental Health Centers Act initiated the release of medicated schizophrenic patients into the community.4 Unfortunately, inadequate family support, unavailability of jobs and low-cost housing, and lack of funding for social services and outpatient psychiatric care left many of these individuals isolated without the tools needed for resocialization. Currently 20 to 40% of homeless people in the United States have a major mental illness.5 Emergency departments frequently serve as the primary entry point into the mental health care system for many of these individuals.6 The etiology of schizophrenia is currently believed to be heterogeneous from interaction of biologic and environmental factors. Studies involving adopted twins whose biologic parents have schizophrenia demonstrate a strong genetic basis for the disorder. Although the overall incidence of schizophrenia in the general population is roughly 1%, it is approximately 10% in first-degree biologic relatives of individuals with the disorder.7 With regard to the pathophysiologic mechanism of schizophrenia, dopaminergic, serotonergic, cholinergic, and glutamatergic systems have been implicated.8–11 Schizophrenia is also postulated to be a neurodevelopmental disorder resulting from the influence of environmental factors on genetically predisposed individuals. Disruptions in fetal brain development, caused by perinatal hypoxia, poor nutrition, infection, and other insults, may set the stage for subsequent development of schizophrenia.1,12 New imaging techniques have documented structural brain abnormalities, most of which appear to be developmental rather than degenerative in nature.8 Evidence supports the existence of a progressive continuum of psychotic illness, beginning with unipolar depression and progressing to bipolar illness, schizoaffective psychoses, and finally schizophrenia.1,13,14 The development of schizophrenia involves three phases.15 The premorbid phase is characterized by the development of “negative” symptoms with deterioration in personal, social, and intellectual functioning. Patients progressively withdraw from social interactions and neglect personal appearance and hygiene, which negatively affects their work, school, and home life. The diagnostic criteria for schizophrenia (Box 110-1) are outlined in the Diagnostic and Statistical Manual of Mental Disorders, fourth edition, text revision (DSM-IV-TR).15 • The patient must exhibit two or more of the following symptoms: delusions, hallucinations, disorganized speech, grossly disorganized or catatonic behavior, and negative symptoms (such as flattening of affect, poverty of speech, or inability to perform goal-directed activities). • There must be a sharp deterioration from the patient’s prior level of functioning (work, school, self-care, or interpersonal relations), and there must be continuous signs of disturbance for at least 6 months. • The diagnoses of schizoaffective and mood disorders with psychotic features must be excluded. • In evaluating these patients, emergency physicians must exclude myriad medical conditions that can mimic or cause psychotic symptoms. The DSM-IV-TR defines delusions as “erroneous beliefs that usually involve a misinterpretation of perceptions or experiences.”15 The delusions seen with schizophrenia are most often persecutory, religious, or somatic. Patients with Known Psychiatric Disorders Patients with previously diagnosed thought disorders who present with mild to moderate exacerbation of their symptoms do not require extensive laboratory evaluation.16 Because some of these patients may have coexisting substance abuse or undiagnosed medical disorders, a thorough history, detailed physical examination, and routine toxicology studies are indicated for most patients.17–19 Patients exhibiting severe exacerbation of symptoms accompanied by marked agitation, violent behavior, or significantly abnormal vital signs should undergo more extensive evaluation. Many toxicologic and medical disorders can mimic schizophrenia. Patients with the apparent new onset of psychosis should receive a medical evaluation to exclude toxicologic and medical disorders.20–23 Both the DSM-IV-TR and review articles on this topic emphasize that most toxicologic and medical causes of altered mental status that simulate acute schizophrenia are best recognized by patterns of presentation combined with focused testing based on one’s index of suspicion for nonpsychiatric disease, rather than the reliance on a broad use of screening tests. Certain medications and medical disorders may affect thought processes, causing patients to exhibit abnormal behavior (Boxes 110-2 and 110-3). This behavior may range from mild personality changes to apparent acute psychosis, even in the absence of an underlying psychiatric disorder.1 Factors that should alert one to a medical disorder include the following: history of substance abuse or a medical disorder requiring medication; patient’s age older than 35 years without previous evidence of psychiatric disease; recent fluctuation in behavioral symptoms; hallucinations that are primarily visual in nature; presence of lethargy; abnormal vital signs; and poor performance on cognitive function testing, particularly orientation to time, place, and person. These and other factors may be helpful in differentiating functional (psychiatric) from organic (medical) causes of abnormal behavior and can be easily recalled with the mnemonic MADFOCS (Table 110-1).24
Thought Disorders
Perspective
Principles of Disease
Clinical Features
Phases of Schizophrenia
Criteria for Schizophrenia
Delusions
Diagnostic Strategies
Patients without Known Psychiatric Disorders
Differential Considerations
Thought Disorders
