Schizotypal personality disorder
Although several personality disorders (PDs) may be related to the schizophrenia spectrum, including schizoid, paranoid, and schizotypal personality disorders, we focus on SPD because family studies show its genetic basis more clearly than they do in the other two conditions.25,26
Some general therapeutic issues will be considered, followed by a review of outcome studies. Patients with SPD often chronically view the world as an odd and threatening place, and thus may require extended courses of treatment.27-29
Unfortunately, trust and rapport with the therapist - which are necessary for the success of any psychosocial therapy - are often difficult to establish. The frequent occurrence of paranoia and suspiciousness, together with social aloofness and constricted affect, make exploratory psychotherapeutic approaches less likely to bring about positive changes than approaches that, emphasize supportive and cognitive-behavioral therapies.27,29
In fact, these patients may only seek treatment to alleviate circumscribed problems, like anxiety or somatic complaints. Approaches that emphasize concrete, interim goals, and stipulate explicit, means of attaining them, thus have the best chances of success. Because patients with SPD are vulnerable to decompensation during times of stress and may experience transient episodes of psychosis, they may also benefit, from techniques to facilitate stress reduction (eg, relaxation techniques, exercise, yoga, and meditation). Fortunately, there is evidence that at least some individuals with schizotypal features are likely to seek treatment in times of stress.30
In the short, term, brief courses of antipsychotic treatment may be useful if symptoms of psychosis appear.
Because cognitive problems are also frequently amenable to concrete, goal-oriented approaches to treatment, SPD patients benefit, from an understanding of their cognitive strengths and weaknesses, to help them confront, and cope with long-standing difficulties in their lives. For example, problems in attention, verbal memory, or organizational skills contribute to failures in educational, occupational, and social endeavors, while reinforcing negative selfimages and increasing performance anxiety. Knowledge of circumscribed cognitive problems allows patients to reframe their difficulties in a more positive manner, and facilitate selection of more realistic personal, educational, and occupational goals. Moreover, specific cognitive deficits are often subject, to at least, partial remediation. For example, standard procedures are available to attenuate deficits in the acquisition, organization, and retrieval of new information (eg, writing information down in a notebook, using appointment, books or planners, and rehearsing new information). Distractibility can be reduced by focusing on one task at a time, in contrast, to switching back and forth between activities.
The value of specific treatments for psychiatric symptoms, however, is less clear, owing to a dearth of outcome studies involving psychotherapy, psychosocial, or psych opharmacological treatments for SPD. Published studies show methodological limitations (eg, small samples, subjects with mixed diagnoses, inadequate controls, and problems with internal validity), or provide outcome data on only limited aspects of the disorder. Nevertheless, it. is clear that few treatment gains are evident from recent studies, which serves to reaffirm both the chronicity and the complexity of the disorder. This is particularly true of studies that utilized psych odynamically oriented therapy, either alone or in combination with other treatments (eg, group therapy or art therapy) as the primary treatment modality.
For example, McGlashan31
studied former inpatients approximately 15 years after treatment, who were given retrospective DSM-III diagnoses. The study followed up former patients with a. variety of diagnoses, including, among others, one third with pure SPD (n=10). Multiple outcome measures were employed. Because the main purpose of the study was to examine SPD as a diagnostic entity, there was little emphasis on assessing change in the same measures, which complicates any interpretation. The results showed, however, that most, subjects with pure SPD functioned poorly at follow-up. On one measure of global functioning in which O=continuously disabled and 4=normal, the mean score was 1.6.
Several studies investigated the usefulness of medications in treating SPD, although most investigations employed small numbers of subjects and combined samples of schizotypal and borderline PDs.32,33
For these reasons, conclusions about the effectiveness of treatment must, be conservative. Those studies in which results were reported for SPD separately from other PDs will be emphasized. Typical antipsychotic drugs have been proposed to reduce positive symptoms or depressed mood in times of acute stress, but. the high incidence of adverse side effects has discouraged their widespread use at other times, including the more chronic, stable (ie, noncrisis) phases of the disorder.27,32,34
Other types of medication, including fluoxetine,35
have generally shown nonspecific effects.
Amoxipine, which has antidepressant and neuroleptic effects, was administered to a small group of personalitydisordered patients that included 5 subjects diagnosed with DSM-III
After an average treatment duration of 39 days, significant reductions were evident in total scores on the Brief Psychiatric Rating Scale, and on the Hamilton Rating Scale for Depression. The authors hypothesized that the positive changes in this group were due to the neuroleptic properties of the medication.
Goldberg et al37
administered thiothixene (an antipsychotic medication) to a group of patients that included, among others, DSM-III
SPD (n=6).Thc Global Assessment Scale (GAS) and Hopkins Symptom CheckIist-90 (HSCL-90) were among the measures used to assess treatment effects. At the end of 12 weeks of treatment, little therapeutic change was evident within the schizotypal groups, but. modest improvements were observed in particular areas across groups, such as the psychotic and obsessive-compulsive scales of the HSCL-90.
Hymowitz et al38
administered a low dose of haloperidol to 17 outpatients with DSM-III
diagnoses of SPD, for 6 weeks. The initial dose of 2.0 mg was intended to rise to 12.0 mg, but. side effects prevented administration of such a large increase, and the mean dose was 3.6 mg. Even with lower doses, 50% of the sample withdrew from the study because of side effects. Data analysis was performed on all 17 subjects when they had completed just. 2 weeks of the protocol. Modest improvements were noted in some subscales of the Schedule for Interviewing Borderlines related to schizotypy (ie, ideas of reference, odd communications, and social isolation) and on GAS scores. Taken together, the available literature on treatments for SPD offers few clearly effective treatments. The mechanisms of the few treatments that were somewhat effective are unknown. Interestingly, improvements in types of symptoms (eg, psychoticism) across diagnoses, rather than within them,37
are consistent with the possibility that they may help at least some subgroups of patients. However, more psychopharmacological research is needed in this area, with larger, more homogeneous samples, to test, the latter hypothesis. A review of the medications used in these studies also makes clear a need to find treatments that are well tolerated, and that target negative symptoms and cognitive deficits.
The value of such an approach is considered next, in relation to treatment strategies for schizotaxia.
The general therapeutic considerations discussed above in relation to SPD are relevant to schizotaxia as well. Because schizotaxia. is related biologically to schizophrenia, we considered the possibility that effective treatments for schizophrenia would also be of value in schizotaxia. In particular, we hypothesized that schizotaxic deficits should respond to risperidone, a. medication that improves negative symptoms and neuropsychological dysfunction in schizophrenic patients (see, for example, references 39 and 40). Thus, we completed an open drug trial in a small scries of patients.
The clinical criteria for inclusion in the drug trial are described above.21
Individuals who met. these criteria for schizotaxia and who provided informed consent received low doses of risperidone (0.25-2.0 mg) for 6 weeks. Side effects were temporary and mainly mild. Five out. of 6 individuals showed marked improvements in attention, and mild-to-moderate reductions in negative symptoms. The sixth subject did not. show improvement in either area. This subject, also differed from the other cases in other ways. In particular, her level of overall cognitive ability was below normal (estimated IQ=75), raising the possibility that treatments might be less effective when the ability to utilize them falls below certain levels (the IQs of the other subjects ranged between 92 and 111). The cognitive and clinical improvements in 5 out of 6 individuals are encouraging and provide support, for larger, more controlled trials. These preliminary findings are potentially important for several reasons. First, they suggest that several key clinical and neuropsychological symptoms in schizotaxic, first-degree relatives of patients with schizophrenia, are reversible, at least in part. Moreover, they are reversible by a treatment that is effective against some of the same symptoms in schizophrenia, consistent with the view that these clinical symptoms may reflect, elements that are common to schizophrenia. Second, they show that impairments in such individuals may be ameliorated safely with risperidone. These results are preliminary and require replication in larger, controlled studies before they can be considered as a. basis for treatment. Such studies arc currently in progress.