Antisaccade task performance in questionnaire-identified schizotypes1

Schizophrenia Research 35 (1999) 157–166

Antisaccade task performance in questionnaire-identified schizotypes1 Diane C. Gooding * Department of Psychology and Psychiatry, University of Wisconsin-Madison, 1202 W. Johnson Street, Madison, WI 53706-1696, USA Received 8 May 1998; accepted 1 September 1998

Abstract Individuals who scored high on Perceptual Aberration–Magical Ideation Scales (Per–Mag; n=90), the Social Anhedonia Scale (SocAnh; n=39), and control participants (n=89) were administered saccadic refixation (prosaccade) and saccadic suppression (antisaccade) tasks. Eye movements were scored in terms of error rates and latency. None of the groups differed in terms of their performance on the prosaccade task. Both the Per–Mag ( p<0.01) and SocAnh ( p<0.05) groups exceeded the controls in terms of mean antisaccade errors. The high-risk groups did not differ from each other. Eighteen of the Per–Mag individuals and 10 of the SocAnh individuals displayed deviant antisaccade performance. These findings are particularly interesting in light of suggestive evidence that antisaccade task deficits may serve as a marker of susceptibility to schizophrenia. It is hypothesized that the individuals who scored aberrantly on the Chapman scales and displayed antisaccade performance deficits are most likely to be at risk for the development of psychosis. © 1999 Elsevier Science B.V. All rights reserved. Keywords: Antisaccade task; Schizotypy; Schizophrenia; Social anhedonia; Perceptual aberration

1. Introduction The purpose of this investigation is to examine the relationship between psychosis-proneness and antisaccade task performance. In the antisaccade task, subjects are presented with a visual stimulus that moves randomly to the left or right of a central fixation point. In order to perform the task correctly, the subject must inhibit a reflexive saccade and produce a saccade in the opposite direc* Tel: (608) 262-3918; Fax: (608) 262-4029; e-mail: [email protected] 1 Part of these data were presented at the Annual Meeting of the Society for Research in Psychopathology (SRP), Palm Springs, CA, 24 October 1997.

tion. Electrophysiological evidence (cf. Evdokimidis et al., 1996), as well as clinical studies (cf. Guitton et al., 1985; Pierrot-Deseilligny et al., 1991; Gooding et al., 1997), suggests that antisaccade task performance is a measure of dorsolateral prefrontal cortical functioning. Schizophrenia patients ( Fukushima et al., 1988, 1990; Clementz et al., 1994; Katsanis et al., 1997) have displayed significantly poorer performance on the antisaccade task, relative to normal controls. Currently there is equivocal support for the presence of antisaccade deficits in non-schizophrenic psychiatric patients. Patients with schizophrenia produced significantly greater antisaccade errors than non-schizophrenic psychiatric comparison subjects in some investigations (cf. Fukushima

0920-9964/99/$ – see front matter © 1999 Elsevier Science B.V. All rights reserved. PII: S0 9 2 0 -9 9 6 4 ( 9 8 ) 0 0 12 0 - 0

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D.C. Gooding / Schizophrenia Research 35 (1999) 157–166

et al., 1990; Clementz et al., 1994; McDowell and Clementz, 1997), while other findings (Sereno and Holzman, 1995; Tien et al., 1996; Katsanis et al., 1997) suggest that impairment in antisaccade performance is not specific to schizophrenia. Nonetheless, the presence of these performance deficits in unaffected relatives of schizophrenics (Clementz et al., 1994; Katsanis et al., 1997) support the hypothesis that the antisaccade task may be a useful measure for identifying individuals with an increased risk for schizophrenia. There are a plethora of studies indicating that schizotypes, identified on the basis of their responses to the Chapman Psychosis-Proneness Scales, perform abnormally on biobehavioral markers of risk (cf. Miller and Yee, 1994; Gooding and Iacono, 1995). Detailed descriptions of each of the Chapman Psychosis-Proneness Scales can be found elsewhere (cf. Chapman et al., 1995). Briefly, the Chapman scales are based in part on Meehl’s conceptualization of schizotypy (Meehl, 1962, 1964; Golden and Meehl, 1979). Research on these scales suggests that in unselected populations they are relatively free of social desirability biases (Chapman et al., 1995). Most of these investigations have focused on individuals defined as at-risk using the Perceptual Aberration Scale (Chapman et al., 1978). The emphasis on the Perceptual Aberration Scale stems largely from findings that this scale identifies a subgroup of psychosis-prone individuals, some of whom eventually manifest a psychotic disorder (cf. Chapman et al., 1994). Usually, at-risk subjects identified using the Magical Ideation Scale are not assessed using psychophysiological measures. However, it is typical for individuals who score high on the Perceptual Aberration Scale to also score aberrantly high on the Magical Ideation Scale, and vice versa; the scales correlate around 0.70 (Chapman et al., 1982; Lipp et al., 1994; Chapman et al., 1994). There are several indications (cf. Mishlove and Chapman, 1985) that the revised Social Anhedonia Scale is useful as a measure of psychosis-proneness. Kwapil et al. (1997) reported that although high scorers on the Social Anhedonia Scale do not differ markedly from control subjects on crosssectional measures of psychosis-proneness, longitudinal data suggest that these subjects are especially

psychosis-prone at 10-year follow-up. More recently, Kwapil (in press) reported that 24% of high scorers on the revised Social Anhedonia Scale were diagnosed with schizophrenia-spectrum disorders at the follow-up, compared to only 1% of the control group. These findings suggest that the Social Anhedonia Scale, unlike the Perceptual Aberration Scale, may identify individuals at specific risk for the development of schizophreniaspectrum disorders. To date, there has been only one published report of antisaccade performance in hypothetically psychosis-prone individuals. Holzman et al. (1995) examined the antisaccade task performance of 56 undergraduates who had been screened using the Perceptual Aberration Scale. Students with high scores on the Perceptual Aberration Scale (n=31) made significantly more errors than the low scoring students (n=25). It is also noted that the authors of the prior report made no mention of individuals’ performance on a reflexive saccade task; it is beneficial to include such a task in order to demonstrate that the subjects were adequately motivated during their assessment. On the basis of the Holzman et al. (1995) study, subjects with high perceptual aberration scores would be expected to produce significantly more errors on the antisaccade task than controls. This study was undertaken in order to replicate and extend the Holzman et al. (1995) finding. Psychosis-prone individuals identified by their elevated scores on the revised Social Anhedonia Scale might also be expected to produce more antisaccade errors than control subjects. Elevated antisaccade error rates have been found in neurological patients with frontal lobe lesions (cf. Guitton et al., 1985; Gooding et al., 1997) and anhedonia is frequently associated with frontal lobe deficits (Stuss and Benson, 1986). In schizophrenia patients, anhedonia is associated with the ‘deficit’ or ‘negative’ symptoms, and some investigators have proposed that these symptoms are more likely to involve prefrontal neural circuits ( Weinberger, 1987)2. 2 The Physical Anhedonia Scale also measures anhedonia. However, because the Physical Anhedonia Scale has not proven useful in terms of predicting either psychosis or psychosisproneness (cf. Chapman et al., 1994), this scale was not used for subject selection.

D.C. Gooding / Schizophrenia Research 35 (1999) 157–166

The main goal of the present study was to examine the association between psychosis-proneness and antisaccade task performance. This investigation extends the research literature by examining a larger sample of at-risk subjects, including subjects identified on the basis of their scores on the revised Social Anhedonia Scale. Moreover, this investigation compares two main factors of psychosis proneness, namely, cognitive/perceptual distortion and anhedonia ( Kelley and Coursey, 1992; Lipp et al., 1994) in terms of their putative association with inhibitory deficits such as that reflected by poor performance on antisaccade tasks. Examination of the association between schizotypy, as measured by psychosisproneness scales, and antisaccade task performance may further our understanding of the phenotype of the schizophrenia spectrum.

2. Methods 2.1. Participants This was a non-clinical university sample. Participants were drawn from a sample of Englishspeaking undergraduates who were enrolled in Introduction to Psychology classes. As part of their ‘Mass Survey Experience’, undergraduates (1662 males, 2240 females) completed a 179-item psychological questionnaire entitled ‘Survey of Attitudes and Experiences’. The ‘Survey of Attitudes and Experiences’ questionnaire was composed of a random mixture of all items from the Chapman Psychosis-Proneness Scales, namely, Perceptual Aberration, Magical Ideation, revised Physical Anhedonia (Chapman et al., 1976; Chapman et al., 1978; Eckblad and Chapman, 1983) and revised Social Anhedonia (unpublished test, M.L. Eckblad, L.J. Chapman, J.P. Chapman and M. Mishlove, 1982) Scales. In order to rule out random responding, a scale composed of infrequent items (the Chapman Infrequency Scale; unpublished test, L.J. Chapman and J.P. Chapman, 1983) was included. Any participants who endorsed three or more items on the Chapman Infrequency Scale were excluded from further study.

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Due to the high correlation between the Perceptual Aberration Scale and the Magical Ideation Scale, individuals scoring high (at least 2 SD beyond the same-sex sample mean) on either of these scales were assigned to the ‘Per–Mag’ group. In addition, the scores on the other Chapman research scales (namely, revised Social Anhedonia and revised Physical Anhedonia) had to be below 0.5 SD of the same-sex sample mean. The criterion for the ‘SocAnh’ group was a social anhedonia score at or beyond 2 SD from the samesex sample mean. Control subjects scored below 0.5 SD of the group mean on each of the four psychosis-proneness scales. The resultant sample included 218 individuals: 90 (36 male, 54 female) subjects in the Per–Mag group; 39 (15 male, 24 female) subjects in the SocAnh group, and 89 (39 male, 50 female) subjects in the control group. Although the groups were not formally matched, chi-square analyses revealed no significant between-group differences in terms of gender [x2(2)=0.43, n.s.]. The mean age of the sample was 19 years; the groups did not differ significantly in terms of age [F(2,215)= 1.37, n.s.]. The means and standard deviations of the psychosis-proneness scores obtained from this study’s screening sample are commensurate with those of previous Chapman samples (Chapman et al., 1980; T.R. Kwapil, 1996, personal communication). The resultant sample of psychosis-prone and control group participants also appears similar to other obtained samples; the means and standard deviations for each psychosis-proneness scale are provided in Table 1. 2.2. Procedures Following the screening procedure using the Chapman Psychosis-Proneness Scales, potential study participants were contacted by telephone and invited to participate in a study of ‘individual differences in brain functioning’. The study was a multiple-session investigation involving neuropsychological, psychophysiological, and clinical assessment. For the remainder of the study, all students were tested individually. Participants either received course credit or monetary remuner-

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Table 1 Age and Chapman Psychosis-Proneness Scale scores Group Per–Mag (n=90)

Age Perceptual aberration Magical ideation Social anhedonia Physical anhedonia

SocAnh (n=39)

Controls (n=89)

Mean

SD

Mean

SD

Mean

SD

18.72 21.76 19.62 8.31 7.69

(1.51) (3.95) (7.88) (4.82) (5.05)

19.13 12.13 9.92 21.08 14.79

(2.21) (6.42) (6.84) (4.63) (7.87)

18.67 7.60 4.42 4.58 8.75

(0.96) (3.94) (3.95) (3.16) (4.36)

ation for their participation. All study staff were naive to a potential participant’s group membership throughout recruitment, testing, and scoring. Sample selection and recruitment occurred over three consecutive semesters. All participants gave their informed consent. All participants were screened for personal or family history of emotional and/or physical conditions using a non-patient version of the Structured Clinical Interview for DSM-IV (SCID) and a medical history questionnaire. Any subjects who had a history of strabismus, epilepsy, multiple sclerosis, or any other condition which might adversely affect ocular motor functioning were excluded from subsequent analyses. In addition, individuals with either a personal history of psychosis or a first-degree relative with a history of psychotic illness were excluded from the control group. It was especially important that the control subjects be free of a family history of psychotic illness, given prior evidence (cf. Gottesman, 1991) that individuals genetically related to a schizophrenia patient are at heightened risk for schizophrenia, as well as recent findings (McDowell and Clementz, 1997) which suggest that first-degree relatives of schizophrenia patients display antisaccade task deficits.

darkened computer screen. In both saccadic tasks, the target stimulus moved ±4°, 8°, or 12° from the center in a non-predictable pattern. For each task, there were eight practice trials, each of which was followed by verbal feedback from the experimenter. Following the practice trials, there were two sets of 24 test trials. The stimuli were presented in an identical pseudorandom order to all subjects, at a rate that was paced by the subject (typically one trial every 2 s). The performance on the 48 test trials was included in subsequent analyses. Subjects were allowed to rest (typically for 2 min) between tasks. All subjects were tested in a dimly illuminated room using the Eyelink System (Reingold and Stampe, 1996). This system has a temporal resolution of 4 ms and a spatial resolution of 0.25° of visual angle. Eye position was recorded by an infrared reflection technique, in which eye cameras mounted on a headband worn by the subjects recorded the differential reflectivity between the iris and the sclera. The subject’s head movements were recorded by the headband’s head camera, which picked up phototransistor signals from four diode strips mounted to the computer. Software for stimulus presentation and data acquisition was developed by Drs Eyal Reingold and David Stampe.

2.3. Stimulus and apparatus 2.4. Saccadic refixation task A 33-cm monitor located 53 cm from the subject’s nasion was used to present the stimuli. The target was a small white circle (approximately 2 mm) of light which was presented against a

The saccadic refixation task (hereafter referred to as the ‘prosaccade task’) served as a control task. The purpose of this task was to ensure that

D.C. Gooding / Schizophrenia Research 35 (1999) 157–166

study participants were motivated and attentive throughout the testing session. In the prosaccade task, subjects were required to produce visuallyguided saccades in response to a laterally displaced target. In each trial, a central fixation point was presented for approximately 600 ms. Subjects were told that the target would move from one location to the next, although the direction of the target (either left or right) was random. Subjects were instructed to look immediately at the new location using only their eyes. After the target appeared in the new location, it remained there for approximately 900 ms. Finally the circle of light returned to the center location for another trial. 2.5. Saccadic suppression task The saccadic suppression task (hereafter referred to as the ‘antisaccade task’) was identical to the prosaccade task, in terms of stimulus presentation and fixation duration. The antisaccade task differed from the prosaccade task in terms of the task requirements; in this task, subjects were instructed to look in the opposite direction from a laterally displaced target (either to the left or right of the center). 2.6. Eye movement analysis The eye movement data were analyzed using a computerized program (the Eyelink system) which plotted both the subject’s eye position and the target position for each millisecond of recorded tracking. Saccades were identified using an interactive pattern recognition program. Both the prosaccade and antisaccade tasks were scored in terms of number of errors and response latency. The minimum latency of a visually guided saccade is approximately 100 ms (Fischer and Ramsperger, 1984); the first saccade of at least 2° in amplitude made 100 ms after the target movement was scored as the response. In the prosaccade task, errors were defined as either a failure to make a saccade within 450 ms after the target movement, or a failure to make a saccade in the same lateral direction as the target following the target movement. In the antisaccade task, if the subject looked in the direction of the target, this constituted an

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error. Subjects typically made a corrective saccade following a misdirected saccade; this indicates that they understood the task and were attempting to perform it. However, these corrective saccades were not included in any of the analyses. Fig. 1 provides an example of a correct antisaccade response (top trace) and an error on the antisaccade task (bottom trace).

3. Results Due to the extreme skewedness of the saccadic error rates, these percentage data were transformed using the arc-sine transformation ( Winer, 1971). The latency data were not skewed, and therefore were not transformed. Table 2 provides the error rates and latencies for each group’s performance on the saccadic tasks. There was no significant difference between the Per–Mag, SocAnh, and control groups in terms of their accuracy on the prosaccade task [F(2,215)=0.11, n.s.]. As expected, all subjects were more likely to produce errors on the antisaccade task than the prosaccade task. However, this finding does not indicate a differential deficit, because the prosaccade and antisaccade tasks are not equivalent in terms of true-score variance. There was a significant group difference in terms of the mean number of antisaccade errors [F(2,215)=6.28, p<0.01]. Glass’ effect size measure, namely, the difference between the two group means (at-risk versus controls) divided by the standard deviation of the control group, was calculated in order to assess the measure’s ability to discriminate between the groups, independent of sample size ( Kraemer and Thiemann, 1987). The effect size is 0.75, a ‘large’ effect size. The subjects who scored high on the Perceptual Aberration and/or Magical Ideation Scales produced significantly more errors on the antisaccade task than the control subjects [t(145)=3.41, p<0.01]. The SocAnh subjects also made significantly more reflexive saccades than controls [t(43)=2.29, p<0.05]. However, the two experimental groups did not differ significantly from each other in terms of their antisaccade task performance [t(53)=0.60, n.s.].

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Fig. 1. Two examples of antisaccade task performance; the red trace is the target movement, the blue trace is the subject’s eye movement. The green bar denotes that a saccade has occurred. The top trace provides an example of correct performance. In the bottom trace, the subject initially makes an antisaccade error (a prosaccade) and subsequently self-corrects by making a second saccade in the opposite direction.

Most (84%) of the subjects in this investigation performed the antisaccade task at a level consistent with other non-patient samples. Fig. 2 (‘Percent of Subjects with Abnormal Antisaccade Task Performance’) provides a graph of the percentage of subjects who displayed deviant performance in

each subject group. A comparison between highrisk and control subjects revealed a significant association between group membership and antisaccade task deficits [x2(2)=8.96, p<0.01]. Overall, subjects’ mean latencies for generating saccades on the antisaccade task were greater for

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D.C. Gooding / Schizophrenia Research 35 (1999) 157–166 Table 2 Performance on saccadic tasks Group Per–Mag (n=90) Variable Prosaccade task Error ratea Latency (ms) Correct response Antisaccade task Error ratea Latency (ms) Error response Correct response

Mean

SocAnh (n=39) SD

Mean

Control (n=89) SD

Mean

SD

0.01

0.03

0.01

0.03

0.01

0.03

168.17

19.86

167.93

21.46

165.97

23.26

0.17

0.13

0.19

0.20

0.12

0.08

168.07 248.58

41.32 37.38

165.29 252.31

50.53 51.84

169.73 243.67

40.17 41.61

aDue to the extreme skewedness of the data, the error rates were transformed using the arc-sine transformation.

correct responses compared to their mean latencies for incorrect responses. Although some of the error responses appeared to have latencies in the range of so-called express saccades (Fischer and Ramsperger, 1984), most of the responses could be classified as regular saccades (cf. Fischer et al., 1997). The subject groups showed no significant group differences in response latency, either for correct saccades or errors (prosaccades) on the antisaccade task [F (2,215)=0.65 and 0.15, n.s., respectively].

4. Discussion This investigation was undertaken in order to determine whether there is a significant association between antisaccade task deficits and schizotypy. The results support the study’s major hypothesis, namely, that hypothetically schizotypic subjects perform more poorly on antisaccade tasks than control subjects. As such, it is a partial replication of the Holzman et al. (1995) finding. The results also extend prior findings by indicating that compared to normal controls, individuals reporting heightened levels of social anhedonia are also more likely to display elevated error rates on the antisaccade task. Some investigators (cf. Merritt et al., 1993) question the utility of the revised Social

Anhedonia Scale to identify individuals at heightened risk for schizophrenia. However, the observation that individuals with elevated scores on this scale differ from controls on a task that is a putative biobehavioral marker of risk for schizophrenia buttresses support for continued use of the scale. Contrary to expectations, the at-risk individuals reporting high levels of social anhedonia did not produce significantly more errors on the antisaccade task than the at-risk individuals reporting high levels of perceptual aberration and/or magical ideation. These results could be construed as being consistent with the hypothesized notion (cf. Beech et al., 1989) of reduced inhibition being associated with high levels of schizotypy. Another non-mutually exclusive explanation for the association between psychosis-proneness and poor performance on the antisaccade task is that the antisaccade task is a measure of ‘working memory’, the temporary maintenance and processing of information to be used in the guidance of behavior (Baddeley, 1992). Other studies (cf. Park et al., 1995) have suggested an association between working memory deficits and schizotypy, and indeed, in a separate report, Holzman et al. (1995) noted a significant association between antisaccade errors and delayed response task errors. These results, along with those of the current study, provide

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Fig. 2. The percentage of subjects displaying abnormal antisaccade performance, defined as any error score greater than or equal to 2 SDs beyond the control mean.

support for the hypothesized association between schizotypy and frontal lobe dysfunction. On the other hand, it is likely that antisaccade task deficits represent a final common pathway; although both at-risk groups exhibit antisaccade task deficits, their poor performance may reflect different underlying processes. Individuals with higher scores on the Social Anhedonia Scale may have performed poorly on the antisaccade task due to an underlying dysfunction in the neural circuitry involving frontal cortex. As stated earlier, several investigators have suggested that negative symptoms may be attributable to frontal lobe dysfunction. In contrast, the elevated errors displayed by individuals in the Per–Mag group may reflect an attentional problem, one possibly due to interference by competing psychotic-like symptoms. Twenty-two per cent (28 of 129) of the psychosis-prone individuals in this investigation displayed deviant antisaccade performance, operationally defined as any error score greater than or equal to 2 SDs beyond the control mean. These hypothetically schizotypic students were neither medicated nor clinically ill. Their poorer performance on the

antisaccade task suggests that even with an imperfect psychometric measure of schizotypy, it is possible to identify subjects who may have heightened risk for the development of psychosis. The results of the present investigation suggest that the antisaccade task may serve as a useful indicator of individuals who, though not a first-degree relative of a schizophrenia patient, may also be at heightened risk for schizophrenia. Further study is necessary in order to determine whether the presence of antisaccade performance deficits is specific to schizophrenia, as opposed to being a marker of psychosis-proneness in general. It remains to be seen whether the individuals identified as psychosis-prone on the basis of their Chapman scale scores, who also have high antisaccade error rates, are more likely to manifest a psychotic disorder than those individuals who, though identified as being at heightened risk on the basis of their Chapman scale scores, did not exhibit poor antisaccade task performance. A longitudinal, comparative study of both groups of individuals may prove essential to elucidating the developmental events which determine the manifestation of psychosis, particularly schizophrenia

D.C. Gooding / Schizophrenia Research 35 (1999) 157–166

and schizophrenia-spectrum disorders, in vulnerable individuals.

Acknowledgements This research was supported in part by a Wisconsin Alumni Research Foundation ( WARF ) grant. The author wishes to acknowledge the developers of the EyeLink System, Drs Eyal Reingold and Dave Stampe, and Dr Thomas R. Kwapil for invaluable consultation. The author also thanks Kirstie K. Danielson for her assistance in data collection, and Monica C. Remington and David G. Martell for their assistance in data scoring. Finally, the author thanks Loren J. Chapman, Jean P. Chapman, and Richard J. Davidson and anonymous reviewers for their comments on an earlier draft of the manuscript.

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