Visuospatial working memory in schizotypal personality disorder patients

BACKGROUND: Cognitive processing deficits have been identified as an abnormality that schizotypal personality disorder (SPD) individuals share with schizophrenic patients. It has been hypothesized that impaired working memory may be a critical component of several of the more complex cognitive deficits found in schizophrenia spectrum patients. METHOD: 18 DSM-III-R SPD patients, and 17 normal comparison subjects were compared on a pen and paper visuospatial working memory task. Moreover, we identified a second psychiatric comparison group comprised of nine patients with other, non-odd cluster personality disorder diagnoses who met no more than one of the SPD criteria and were also tested on the same task. Each person was given 14 immediate recall trials and 10 trials using a 10 s delay. RESULTS: SPD patients performed significantly worse than normal control subjects on the working memory task. SPD patients also performed significantly worse compared to the non-schizophrenia-related personality disorder psychiatric comparison group. CONCLUSIONS: Like schizophrenic patients, SPD patients demonstrate working memory impairment compared to normal controls. This impairment may be specific to the schizophrenia-related personality disorders.     

Cerebellar functional abnormalities in schizophrenia are suggested by classical eyeblink conditioning.

BACKGROUND: Previous research suggests that schizophrenia may result from disruptions in a cortico-cerebellar-thalamic-cortical circuit (CCTCC) producing a mental incoordination or "cognitive dysmetria." To further evaluate the cerebellar contribution to this disrupted circuitry, medication-free patients with schizophrenia completed classical eyeblink conditioning, a cerebellar-mediated learning task. METHODS: For classical eyeblink conditioning, 70 trials with a tone conditioned stimulus (CS) and air puff unconditioned stimulus (US) were presented to 15 patients with schizophrenia and 15 healthy control subjects. Acquisition rate for the conditioned response (CR) and response timing were compared between the two groups. RESULTS: Patients with schizophrenia displayed facilitated conditioning compared to control subjects based on a greater number of CRs during the session and a faster acquisition of the learned response. CONCLUSIONS: Facilitated conditioning suggests that an enhanced excitability in the cerebellum occurs as part of a disrupted CCTCC in schizophrenia. The enhanced cerebellar-mediated associative learning may be maladaptive in the context of normal cerebro-cerebellar interactions, leading to the characteristic motor and mental incoordination of the disorder. Classical eyeblink conditioning may provide a useful model system for studying cerebellar involvement in the pathogenesis and treatment of schizophrenia.     

Endophenotyping schizotypy: a prelude to genetic studies within the schizophrenia spectrum

Schizophrenia is a complex genetic disease with a prevalence rate of 1% in the general population. Schizotypal personality disorder (SPD) occurs in up to 3% of the population, and these subjects are phenomenologically and perhaps genotypically related to schizophrenia. The diagnosis of SPD was empirically derived based on the symptoms of individuals with a genetic relationship to schizophrenia patients and SPD may be a more common phenotypic expression of a schizophrenia-related diathesis than is schizophrenia itself. Family-genetic studies have determined that (1) relatives of schizophrenic patients have an increased risk of SPD and (2) relatives of SPD subjects have increased the rates of both schizophrenia and SPD. Because SPD subjects do not typically have the confounding effects of a chronic illness, long-term hospitalization or chronic neuroleptic treatment, they are ideal for the study of the proposed trait-related vulnerability markers in schizophrenia spectrum individuals. The study of vulnerability markers in SPD subjects has become increasingly important because it provides a means of assessing phenotypic traits that may not be evident clinically. By combining multiple inhibitory/gating information processing measures, it may be possible to identify a subgroup of SPD subjects with multiple inhibitory deficits who are phenotypically most similar to patients with schizophrenia. Composite phenotypes can also be developed, which increase the probability of identifying the complex genetic architecture of schizophrenia spectrum disorders, which interact with nongenetic protective and exacerbating factors.     

Empathic accuracy and cognition in schizotypal personality disorder

Interpersonal dysfunction contributes to significant disability in the schizophrenia spectrum. Schizotypal Personality Disorder (SPD) is a schizophrenia-related personality demonstrating social cognitive impairment in the absence of frank psychosis. Past research indicates that cognitive dysfunction or schizotypy may account for social cognitive dysfunction in this population. We tested SPD subjects and healthy controls on the Empathic Accuracy (EA) paradigm and the Reading of the Mind in the Eyes Test (RMET), assessing the impact of EA on social support. We also explored whether EA differences could be explained by intelligence, working memory, trait empathy, or attachment avoidance. SPD subjects did not differ from controls in RMET, but demonstrated lower EA during negative valence videos, associated with lower social support. Dynamic, multimodal EA paradigms may be more effective at capturing interpersonal dysfunction than static image tasks such as RMET. Schizotypal severity, trait empathy, and cognitive dysfunction did not account for empathic dysfunction in SPD, although attachment avoidance is related to empathic differences. Empathic dysfunction for negative affect contributes to decreased social support in the schizophrenia spectrum. Future research may shed further light on potential links between attachment avoidance, empathic dysfunction, and social support.     

Dopamine regulation in schizotypal personality disorder and psychosis

It has recently been proposed that reduced stimulation of prefrontal cortex DI receptors secondary to hypoactivity of mesocortical dopamine (DA) projections may explain the cognitive impairments experienced by patients with schizophrenia and the schizophrenia spectrum. Findings from studies done during the past two decades suggest that schizotypal personality disorder (SPD), the prototypic disorder of the schizophrenia spectrum, is associated with cognitive deficits and social deterioration that are qualitatively similar, although less severe, to those observed in schizophrenia. It generally is acknowledged that the psychotic symptoms of schizophrenia are associated with hyperactivity of mesolimbic DA projections resulting in excessive stimulation of striatal D2 receptors. In contrast with schizophrenia, dopaminergic interventions improved cognitive function in SPD without worsening psychotic-like symptoms, raising the possibility that patients with SPD are protected against increases in subcortical dopaminergic activity associated with psychosis. However, mounting evidence suggests that alterations in other neurotransmitter systems (eg, glutamate, γ-aminobutyric acid, opioid, serotonergic) may be involved in the pathophysiology of schizophrenia. This over view focuses on common DA-related neurobiological vulnerabilities shared by schizophrenia and the schizophrenia spectrum, in addition to factors that protect SPD from the overt psychotic symptoms and more severe social and cognitive deficits experienced by patients with chronic schizophrenia.     

Schizotypal personality disorder in individuals with and without schizophrenic relatives: similarities and contrasts in neurocognitive and clinical functioning.

Schizophrenia-spectrum disorders may reflect the genotype for schizophrenia. One such disorder, Schizotypal Personality Disorder (SPD), was examined as a function of family history of schizophrenia. Clinical profiles and neurocognitive functioning were evaluated in 25 schizotypal subjects (10 SPD with schizophrenic relatives and 15 SPD without schizophrenic relatives), and in 24 normal controls. The primary finding is that vigilance performance was similarly impaired in both SPD groups. An additional neurocognitive impairment, comprehension of grammatical constructions, was observed only in the SPD group with schizophrenic relatives. Of interest, the clinical profiles of the two SPD groups did not differ significantly. These results suggest that schizotypal personality disorder is associated with a continuum of neurocognitive vulnerability that increases as a function of family history of schizophrenia.     

Schizotypal personality disorder and MRI abnormalities of temporal lobe gray matter.

BACKGROUND: Structural MRI data indicate schizophrenics have reduced left-sided temporal lobe gray matter volumes, especially in the superior temporal gyrus (STG) and medial temporal lobe. Our data further suggest a specificity to schizophrenia spectrum disorders of STG volume reduction. Interpretation of research studies involving schizophrenics may be complicated by the effects of exposure to neuroleptics and chronic illness. Sharing the same genetic diathesis of schizophrenics, subjects with schizotypal personality disorder (SPD) offer a unique opportunity to evaluate commonalities between schizophrenia and SPD, particularly as SPD subjects are characterized by cognitive and perceptual distortions, an inability to tolerate close friendships, and odd behavior, but they are not psychotic and so have generally not been prescribed neuroleptics nor hospitalized. Evaluation of brain structure in SPD may thus offer insight into the "endophenotype" common to both disorders. In addition, differences between groups may suggest which are the brain structures of schizophrenics that contribute to the development of psychosis. METHODS: To test the hypothesis of whether SPD subjects might show similar STG abnormalities, STG and medial temporal lobe regions of interest (ROI) were manually drawn on high resolution coronal MRI 1.5 mm thick slices. Images were derived from 16 right-handed male SPD subjects, without regard to family history, and 14 healthy, right-handed, comparison males who did not differ from the SPD group on parental socio-economic status, age, or verbal IQ. RESULTS: As predicted, SPD subjects showed a reduction in left STG gray matter volume compared with age and gender matched comparison subjects. SPD subjects also showed reduced parahippocampal left/right asymmetry and a high degree of disordered thinking. Comparisons with chronic schizophrenics previously studied by us showed the SPD group had a similarity of left STG gray matter volume reduction, but fewer medial temporal lobe abnormalities. CONCLUSIONS: These abnormalities strengthen the hypothesis of a temporal lobe abnormality in SPD, and the similarity of STG findings in schizophrenia and SPD suggest that STG abnormalities may be part of the spectrum "endophenotype." It is also possible that presence of medial temporal lobe abnormalities may help to differentiate who will develop schizophrenia and who will develop the less severe schizophrenia spectrum disorder, SPD.     

Striatal amphetamine-induced dopamine release in patients with schizotypal personality disorder studied with single photon emission computed tomography and [123I]iodobenzamide.

BACKGROUND: Previous imaging studies demonstrated that schizophrenia is associated with increased amphetamine-induced dopamine (DA) release in the striatum, most pronounced during episodes of illness exacerbation. Schizotypal personality disorder (SPD) is a schizophrenia spectrum disorder, genetically related to schizophrenia. The goal of this study was to investigate striatal DA function in patients with SPD. METHODS: In our study, 13 SPD patients and 13 matched healthy control subjects underwent single photon emission computed tomography (SPECT) scan during bolus plus constant infusion of the D2/3 radiotracer [123I]iodobenzamide (IBZM). Striatal specific to nonspecific equilibrium partition coefficient (V(3)") was measured at baseline and following amphetamine administration (.3 mg/kg). RESULTS: No significant differences were observed in baseline V(3)" between groups. Amphetamine induced a larger decrease in [123I]IBZM V(3)" in SPD patients (-12 +/- 5%) compared with control subjects (-7 +/- 5%, p =.03). CONCLUSIONS: The reduction in [123I]IBZM V(3)" induced by amphetamine in SPD was similar to that observed in remitted schizophrenia patients (-10 +/- 9%, n = 17), but significantly lower than that observed during illness exacerbation (-24 +/- 13%, n = 17). This suggests that DA dysregulation in schizophrenia spectrum disorders might have a trait component, present in remitted patients with schizophrenia and in SPD, and a state component, associated with psychotic exacerbations but not SPD.     

Single-cue delay and trace classical conditioning in schizophrenia.

BACKGROUND: Classical conditioning provides a means of addressing mechanisms of learning and can therefore help understand the pathophysiology of memory alteration in schizophrenia. METHODS: Single cue delay and trace eyeblink conditioning were used in patients with schizophrenia and matched normal control subjects to explore, respectively, cerebellar and hippocampal integrity during learning. We measured percent of conditioned (CRs) and unconditioned responses (URs), their amplitude, and onset and peak latencies. We also accounted for spontaneous blink rates and stimulus-induced responses before learning. RESULTS: During delay conditioning, patients showed CRs with longer onset and peak latencies and improved efficiency compared to normal volunteers without there being differences between patients and normal control subjects in the percentage of CRs. During trace conditioning, neither group showed an increase in CRs as a function of conditioned stimulus-unconditioned stimulus pairings, in part because the level of spontaneous blink rates exceeded the level of CRs; however, patients with schizophrenia showed increased responding 150-400 msec after the conditioned stimulus and in the last 100-150 msec before the unconditioned stimulus, whereas normal control subjects showed only the latter type of responses. The former type of response was more frequent in patients with schizophrenia even before either trace or delay conditioning. CONCLUSIONS: These results suggest integrity of cerebellar mechanisms underlying conditioning, although the altered timing of CRs in patients may indicate differences in the modulation of such responses. Both the greater CR onset latency during delay and the presence of early nonadaptive responses during trace are compatible with the pattern of responding seen in animals with hippocampal damage.     

Striatal size and relative glucose metabolic rate in schizotypal personality disorder and schizophrenia.

BACKGROUND: Schizotypal personality disorder (SPD) shares social deficits and cognitive impairment with schizophrenia, but is not typically characterized by frank psychosis. Because striatal size and functional activity have both been shown to be associated with psychotic symptoms, we carried out the first study of SPD to assess the caudate and putamen for comparison with findings in schizophrenia. METHODS: Patients with SPD (n = 16), schizophrenic patients (n = 42), and age- and sex-matched normal control subjects (n = 47) were assessed with magnetic resonance imaging. All of the patients with SPD and subsamples of the schizophrenic patients (n = 27) and control subjects (n = 32) were also assessed with positron emission tomography using fluorodeoxyglucose F-18. RESULTS: The relative size of the putamen in controls was significantly larger than in patients with SPD and significantly smaller than in schizophrenic patients, while the relative size of the caudate was similar in all 3 groups. Compared with control values, relative glucose metabolic rate in the ventral putamen was significantly elevated in patients with SPD and reduced in schizophrenic patients. When subsamples of schizophrenic patients (n = 10) and patients with SPD (n = 10) both of whom never received medication were compared, this pattern was more marked, with the highest value for the putamen being found in patients with SPD for the ventral slice and the lowest value for the right dorsal putamen. CONCLUSIONS: Patients with SPD showed reduced volume and elevated relative glucose metabolic rate of the putamen compared with both schizophrenic patients and controls. These alterations in volume and activity may be related to the sparing of patients with SPD from frank psychosis.     

Early stage vision in schizophrenia and schizotypal personality disorder

Previous studies of visual perception have reported deficits in contrast sensitivity and dot motion discrimination in schizophrenia. We tested whether these deficits also appear in schizotypal personality disorder (SPD). SPD appears to be genetically and symptomatically related to schizophrenia, but without the marked psychosocial impairment associated with psychotic disorders. The present study investigated contrast sensitivity for moving and static gratings, form discrimination and dot motion discrimination in 24 patients with schizophrenia or schizoaffective disorder (SZ), 16 individuals with SPD, and 40 control subjects. SZ, but not SPD subjects, showed impairments on tests of contrast sensitivity for static and moving gratings, form discrimination in noise, and dot motion discrimination. Visual performance did not differ between medicated SZ patients and patients withdrawn from medication. These results confirm early stage visual deficits in schizophrenia regardless of medication status. SPD subjects, in contrast, show intact early stage visual processing despite the presence of marked schizotypal symptoms.     

Vulnerability markers in the schizophrenia spectrum: implications for phenomenology, genetics, and the identification of the schizophrenia prodrome.

A continuum of symptoms between "normality" and overt psychosis has been documented in relatives of schizophrenia patients, SPD, and individuals who may be in the early stages of a psychotic illness with "subsyndromal" symptoms. The empirically derived criteria for SPD have been refined to define a clinical phenotype that is linked to schizophrenia. The clinical SPD symptoms define a heterogeneous group of individuals who are often comorbid for Axis I and II disorders, may or may not have a family history of schizophrenia, and are at risk for developing schizophrenia themselves. SPD subjects have similar abnormalities to those observed in schizophrenia patients on various psychophysiologic paradigms designed to study central inhibition, including P50 event-related potential suppression, PPI of the startle response, and the antisaccade task. Because SPD subjects do not have many of the confounding variables observed in schizophrenia patients (i.e., medication effects), these paradigms might represent vulnerability markers that are possible endophenotypes for schizophrenia spectrum illness. Questions still remain as to whether SPD is genotypically linked to schizophrenia but has genes of lesser penetrance, fewer affected genes, lack of a second hit, or perhaps protective factors. It is also possible that SPD, like schizophrenia, is a common final pathway that can come about because of several etiologic factors that affect crucial neurodevelopmental periods. Future directions in SPD work might include the use of vulnerability markers to essentially subtype schizophrenia spectrum patients and create simpler endophenotypes to understand the phenomenologic and neurobiologic substrate. The use of vulnerability markers along with clinical symptoms may help to improve the predictive power for identifying individuals at risk for schizophrenia for early intervention. Finally, genetic studies have yet to be performed in SPD.     

Plasma total antioxidant status and cognitive impairments in schizophrenia

Oxidative stress-induced damage to neurons may contribute to cognitive deficits during aging and in neurodegenerative disorders. Schizophrenia has a range of cognitive deficits that may evolve from oxidative stress, and this study examines this association of oxidative stress with cognitive deficits in schizophrenia. We recruited 296 chronic schizophrenia patients and 181 healthy control subjects and examined the Repeatable Battery for the Assessment of Neuropsychological Status (RBANS) and plasma total antioxidant status (TAS) in both groups. Schizophrenia symptoms were assessed using the positive and negative syndrome scale (PANSS). Our results showed that TAS levels were significantly lower in patients than controls (179.6 ± 81.0 U/ml vs. 194.8 ± 46.0 U/ml, p<0.05). Cognitive scores on the RBANS and nearly all of its five subscales (all p<0.001) except for the Visuospatial/Constructional index (p>0.05) were significantly lower in schizophrenia patients than normal controls. For the patients, TAS was inversely associated with some domains of cognitive deficits in schizophrenia, such as Attention and Immediate Memory. Our findings suggest that oxidative stress may be involved in the pathophysiology of schizophrenia, and its associated cognitive impairment.     

Clinical, cognitive, and social characteristics of a sample of neuroleptic-naive persons with schizotypal personality disorder

INTRODUCTION: Schizotypal personality disorder (SPD) shares with schizophrenia many biological features, yet little is known about the clinical characteristics of persons diagnosed with this disorder. This report describes the clinical, cognitive and socio-occupational characteristics of a community sample of subjects diagnosed with SPD. METHOD: Sixty-four male and 40 female neuroleptic-naive DSM-IV SPD subjects and 59 male and 51 female comparison subjects were recruited from the community for a total sample of 214 subjects. Demographic and cognitive differences between groups and, within the SPD group, the effect of gender on clinical features, such as the SPD criteria, SAPS, SANS, Schizotypal Personality Questionnaire, and co-morbidity, were examined using ANOVA and Chi-square distributions. RESULTS: SPD subjects, in contrast to comparison subjects, had significantly lower socio-economic status, poorer social relationships and skills, and lower vocabulary scores. Furthermore, SPD subjects demonstrated more impairment on Vocabulary scores than on Block Design, as measured by the WAIS-R, a pattern not seen in comparison subjects. In the SPD cohort, positive symptoms predominated and nearly half were co-morbid for major depression. With respect to gender, male SPD subjects, compared with female SPD subjects, evinced significantly more negative symptoms, fewer friends, had more odd speech, and were more likely to also suffer from paranoid and narcissistic personality disorders. In contrast to male SPD subjects, female SPD subjects perceived themselves to be more disorganized. CONCLUSIONS: SPD subjects, similar to schizophrenics, are impaired socially, occupationally, and cognitively, particularly in the area of verbal measures. Moreover, male SPD subjects may be more severely affected than female SPD subjects across multiple domains of functioning.     

Ventricular enlargement in schizophrenia spectrum patients with prodromal symptoms of obsessive-compulsive disorder

We hypothesized that male patients with schizophrenia spectrum disorders who have prodromal symptoms of obsessive-compulsive disorder (OCD) have ventricular enlargement compared with non-psychotic OCD patients, and that the difference in the ventricular size would offer a clue to the early detection of schizophrenia spectrum disorders. The ventricle-brain ratios (VBRs) in eight male patients with schizophrenia or schizotypal personality disorder (SPD) who had prodromal symptoms of OCD were compared with eight male patients with non-psychotic OCD and 14 normal male comparison subjects using three-dimensional magnetic resonance imaging (MRI). The VBR of the schizophrenia spectrum group was significantly larger than those of the OCD group or comparison subjects. Even the minimum VBR in the schizophrenia spectrum group was larger than the maximum VBR in the OCD group. These results may suggest the usefulness of three-dimensional MRI for early detection of patients with schizophrenia spectrum disorders who manifest OCD symptoms early in the course of the illness.     

Phosphorus metabolite changes in temporal lobes of subjects with schizotypal personality disorder

Using in vivo (31)P magnetic resonance spectroscopy, phosphorus metabolite levels were measured in the temporal lobes of 11 neuroleptic-free subjects with schizotypal personality disorder (SPD) and 20 age-matched healthy subjects. SPD subjects showed smaller amounts of phosphomonoesters in the left temporal lobe than healthy subjects. Membrane phospholipid abnormalities in the left temporal lobe may be a common pathophysiologic feature in schizophrenia spectrum disorders.     

The ESDQ: A New Method of Assessing Emotional and Social Dysfunction in Patients Following Brain Surgery

Abstract

The study investigated patterns of intellectual deficit in 13 patients with recently diagnosed Huntington's disease (mean duration of 2.3 years) and 46 offspring “at risk” for the illness using the Wechsler Adult Intelligence Scale (WAIS). The results support the idea that certain cognitive skills remain relatively intact at early stages of the disease while other skills are impaired. A consistent pattern of impairment was observed in the patient group which included the Arithmetic, Digit Span, Digit Symbol, and Picture Arrangement subtests. The most striking result was a demonstration of significantly increased variability among the “at risk” population on the Digit Span and Picture Arrangement subtests. These findings suggest that the WAIS may be a useful adjunct to neurological diagnosis for longitudinal monitoring of intellectual changes even at very early stages of the illness.     

Biological markers in schizotypal personality disorder

The establishment of the new diagnostic category, Schizotypal Personality Disorder (SPD), has stimulated biological studies of patients with this disorder. Such studies offer the potential of better understanding the diagnosis and treatment of SPD as well as more clearly defining the boundaries of the schizophrenic disorders. SPD has been studied in the clinical setting, in family studies of schizophrenia, and in the biological high-risk paradigm. In most cases, biological variables associated with schizophrenia have been evaluated. Decreased activities of plasma amine oxidase and platelet monoamine oxidase have been associated with SPD in the families of schizophrenics and in "biological high-risk" studies. Smooth pursuit eye movement (SPEM) impairment has also been associated with SPD in a "biological high-risk" study of college students. Inferior backward masking performance has been demonstrated in SPD patients in the clinical setting. Other studies using psychophysiological measures have been applied to subjects with psychological characteristics similar to DSM-III SPD and found biological abnormalities similar to those reported in schizophrenia. These studies are consistent with the possibility that some individuals with SPD may share common psychobiological abnormalities with schizophrenic individuals and may sharpen our understanding of SPD and its relationship to schizophrenia.     

Schizotypal disorder: at the crossroads of genetics and nosology

The aim of this paper is to review the available evidence in support of the correctness of including the DSM-III/III-R schizotypal personality disorder (SPD) in the schizophrenia spectrum, to discuss the components that may account for the familial segregation of SPD, and to consider the implications for research and clinical use of this diagnostic category. The majority of the available data from genetic epidemiology studies, starting from probands with schizophrenia or with SPD, suggest that SPD is one of several phenotypes of liability for the schizophrenia spectrum. Recent twin studies suggest that the affect-constricted and eccentric aspects of SPD are the features that truly belong to the spectrum of schizophrenia, sharing important genetic influences. However, other components are more useful for the identification of SPD in clinical settings, and these may be the specific focus of treatment. The present categorization appears to be a reasonable trade-off for the purposes of both the investigator and the clinician, even though different components within SPD may have different origins and can be selectively emphasized according to the different aims involved.     

Reduction of caudate nucleus volumes in neuroleptic-na?ve female subjects with schizotypal personality disorder.

BACKGROUND: The caudate nucleus might contribute to the psychopathological and cognitive deficits observed in schizotypal personality disorder (SPD), a schizophrenia spectrum disorder. Here we focused on female patients, because this group is underrepresented in studies of SPD and schizophrenia, and we might learn more about the caudate and clinical and cognitive impairments that are unique to female patients diagnosed with SPD. METHODS: Magnetic resonance imaging scans, obtained on a 1.5-T magnet with 1.5-mm contiguous slices, were used to measure the caudate in 32 neuroleptic-na?ve women with SPD and in 29 female normal comparison subjects. Subjects were group-matched for age, parental socioeconomic status, and intelligence quotient. RESULTS: We found significantly reduced left and right caudate relative volume (8.3%, 7.7%) in female SPD subjects compared with normal comparison subjects. In female SPD subjects, we found significant correlations between smaller total caudate relative volume and worse performance on the Wisconsin Card Sorting test (nonperseverative errors) and on the California Verbal Learning Test (verbal memory and learning), and significant correlations between smaller total caudate relative volume and both positive and negative symptoms on the Structured Interview for Schizotypy. CONCLUSIONS: These findings demonstrate that, for female SPD subjects, smaller caudate volume is associated with poorer cognitive performance and more schizotypal symptomatology.