What is schizotypal personality disorder?

Introduction

According to the
Diagnostic and Statistical Manual of Mental Disorders: DSM-5 (5th ed., 2013) of the American Psychiatric Association (APA), schizotypal personality disorder (SPD) is characterized by interpersonal deficits, such as suspiciousness and difficulty establishing and maintaining close relationships; cognitive or perceptual distortions; and eccentric behavior, all of which are pervasive throughout much of an individual’s lifetime. Individuals with SPD are not psychotic (out of touch with reality), although others typically perceive them as odd or strange. They often harbor strange ideas, such as magical thinking, which is the belief that merely thinking about an event (such as that their mother will die) can trigger that event. SPD typically begins in early adulthood and is present in about 3 to 5 percent in the general population.

Possible Causes

To help explain the causes of SPD, researchers have attempted to identify genetic markers of the disorder. In the 1960s, University of Minnesota psychologist Paul Meehl introduced the term “schizotaxia” to describe the genetic predisposition to schizophrenia, which he believed to reflect a single gene of large effect. Meehl regarded schizotaxia as a neural deficit that could be expressed as either schizophrenia or what Hungarian psychoanalyst Sandor Rado termed schizotypy—presumably a milder version of schizophrenia—depending on environmental circumstances and other modifying characteristics, such as personality traits and intelligence. Nevertheless, Meehl hypothesized that schizotypy rather than schizophrenia would result from schizotaxia and that only about 10 percent of schizotypes (individuals with schizotypy) develop schizophrenia. In later research, Harvard University psychiatrist Ming Tsuang and his colleagues modified Meehl’s concept of schizotaxia to reflect a condition caused by multiple genes acting in concert rather than a single gene. Although Meehl’s concept of schizotaxia has been refined over the years, his original concept has encouraged researchers to investigate genetic, neurobiological, and clinical similarities between SPD and schizophrenia.

Twin studies suggest that the heritability of clinically assessed schizotypal features is approximately 0.60, meaning that about 60 percent of the differences among people in their levels of these features are caused by differences in their genes. Several other twin studies, including those conducted by Virginia Commonwealth University’s Kenneth Kendler and his colleagues, have demonstrated substantial genetic contributions to SPD.

Diagnosing SPD

Psychiatrists and psychologists added SPD to the third version of the DSM in 1980 to describe individuals who display mild psychotic features and interpersonal deficits, such as social isolation and poor rapport. Certain features of SPD are easily confused with those of other personality disorders. For instance, the psychotic-like features of SPD overlap with the psychotic features of borderline personality disorder (such as brief periods of loss of contact with reality), while the socially inappropriate features of SPD, such as social withdrawal, overlap with those of schizoid personality disorder.

Researchers have raised questions about whether SPD is dimensional or categorical in nature: That is, does SPD differ only in degree from normal functioning (a dimensional model) or in kind (a categorical model)? Studies using sophisticated statistical analyses generally support a categorical view of SPD, in which this condition is underpinned by two core features: oddness of speech and interpersonal dysfunction.

Similarities Between SPD and Schizophrenia

Certain clinical features of SPD are especially related to schizophrenia. In particular, negative schizotypy, that is, such features as odd speech, restricted emotional expression, and aloofness, is closely related to schizophrenia and tends to respond positively to antipsychotic medications. Because certain features of SPD are more related to schizophrenia than others, researchers have investigated whether SPD may contain two or more subtypes. University of Pennsylvania psychologist Adrian Raine hypothesized that two subtypes of schizotypy exist. The first subtype, neurodevelopmental schizotypy, is a condition that is genetically related to schizophrenia and largely influenced by biological factors such as prenatal stress, influenza exposure, and birth complications. The second subtype, pseudoschizotypy, is generally unrelated to schizophrenia, and is largely influenced by environmental adversity such as impaired familial relationships. Although both subtypes share similar clinical features, neurodevelopmental SPD is thought to be more likely to lead to schizophrenia.

Researchers have observed similar neuropsychological problems, such as deficits in attention, memory, and higher-level thought processes, among patients with schizophrenia and SPD. Moreover, they have investigated potential personality similarities between SPD and schizophrenia. Several researchers have applied the influential five-factor model (FFM) of personality, which proposes that personality consists of five major personality traits (extraversion, neuroticism, agreeableness, conscientiousness, and openness to experience) to identify personality characteristics associated with SPD. Researchers using the FFM have found that individuals with SPD and schizophrenia exhibit significantly higher levels of neuroticism and lower levels of extraversion, agreeableness, and conscientiousness than individuals without schizophrenia or SPD. Despite SPD individuals’ high levels of neuroticism, their scores on this dimension tend to be lower than those of individuals with schizophrenia, at least among outpatients.

In the fifth edition of the DSM, SPD was added to the chapter on psychotic disorders as a schizophrenia-spectrum disorder, although it remained cross-listed in the chapter on personality disorders.

Treatment Options

Results from studies on neuropsychology, clinical symptoms, and personality support the hypothesis that SPD is a mild form of schizophrenia. This hypothesis has assisted researchers in formulating pharmacological and psychotherapeutic treatments for this condition. In general, the closer the patient’s symptoms are to those of schizophrenia and related conditions, the more likely that medication will be effective. Small dosages of antipsychotic medications have been effective in ameliorating the symptoms of SPD. In one study, neuropsychological deficits, such as problems with information processing, improved following the administration of guanfacine (Tenex), a medication that works on receptors in the frontal areas of the brain. Another study using olanzapine (Zyprexa; an atypical antipsychotic) with SPD patients found improvements in psychosis, depression, and overall functioning.

In conclusion, SPD shares many clinical, neuropsychological, and personality characteristics with schizophrenia, and may be a mild form of that disorder. SPD is influenced by a host of genetic and environmental factors, most of which remain to be ascertained. Given that SPD may be more than one condition, more research is needed on its causes and effective treatments, both psychotherapeutic and pharmacological.

Bibliography

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