دانلود مقاله ISI انگلیسی شماره 35201
عنوان فارسی مقاله

حرکات چشمپره چشم، اسکیزوتایپی و نقش روان رنجوری

کد مقاله سال انتشار مقاله انگلیسی ترجمه فارسی تعداد کلمات
35201 2005 19 صفحه PDF سفارش دهید محاسبه نشده
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عنوان انگلیسی
Saccadic eye movements, schizotypy, and the role of neuroticism
منبع

Publisher : Elsevier - Science Direct (الزویر - ساینس دایرکت)

Journal : Biological Psychology, Volume 68, Issue 1, January 2005, Pages 61–78

کلمات کلیدی
صفات شخصیتی اسکیزوتایپی - روان رنجوری - عاطفی و منفی - جنون جوانی -
پیش نمایش مقاله
پیش نمایش مقاله حرکات چشمپره چشم، اسکیزوتایپی و نقش روان رنجوری

چکیده انگلیسی

We investigated the relationships of anti- and prosaccades with psychometric schizotypy. One aim was to estimate the role of negative emotionality and general psychopathology (i.e. neuroticism) in this relationship. 115 non-clinical volunteers underwent infrared oculographic assessment of antisaccades and prosaccades. Schizotypy was assessed with the Personality Syndrome Questionnaire (PSQ-80), the Rust Inventory of Schizotypal Cognitions (RISC), and Eysenck Personality Questionnaire-Revised (EPQ-R) Psychoticism. Higher positive schizotypy scores predicted increased antisaccade errors (RISC) and greater prosaccade spatial error (PSQ-80 Unreality). Greater thought disorder (PSQ-80 Activity) predicted shorter prosaccade latencies. EPQ-R Neuroticism was substantially correlated with schizotypy but was not related to saccadic measures and did not account for their relationship with schizotypy. We conclude that saccadic performance patterns in schizotypy are not due to negative emotionality or general psychopathology, but specific to schizophrenia spectrum signs and symptoms.

مقدمه انگلیسی

The antisaccade task requires the initiation of a saccade in the opposite direction to a peripheral target, thereby involving the suppression of a prepotent, or reflexive, response to the target. Performance is primarily measured as the rate of reflexive errors, i.e. glances towards the target, and has been linked to frontal lobe function, in particular the frontal eye fields (FEF), dorsolateral prefrontal cortex (DLPFC), and anterior cingulate, as well as the striatum (Gaymard et al., 1998b, Muri et al., 1998, O’Driscoll et al., 1995 and Sweeney et al., 1996). People with schizophrenia consistently display increased error rates (Crawford et al., 1995a and Crawford et al., 1995b; Curtis et al., 2001 and Fukushima et al., 1988). In contrast to the antisaccade deficit, performance on the prosaccade (or reflexive saccade) task has been argued to be relatively normal in schizophrenia (McDowell and Clementz, 2001). The prosaccade task requires the initiation of a saccade to an abruptly appearing target. Prosaccades share some of the basic saccadic neural circuitry with the antisaccade but do not critically rely on FEF, anterior cingulate, or DLPFC (Gaymard et al., 1998a). The increased antisaccade error rate has been proposed as a schizophrenia endophenotype (Clementz, 1998 and Ettinger and Kumari, 2003). An endophenotype, or intermediate phenotype, is a behavioural or biological marker thought to be a more direct expression of a disease gene than the disease phenotype (Leboyer et al., 1998 and Ott, 1991). A useful endophenotype must meet a number of criteria. In addition to its observation in the patient group under study, the marker should also be found in related, or spectrum, populations. In the field of schizophrenia research, the most important spectrum populations are: (1) clinically unaffected first-degree relatives of schizophrenia patients and (2) schizotypal individuals. These groups have been identified on the basis of an increased frequency of schizophrenia-related genotypes (i.e. first-degree relatives) or phenotypes (i.e. schizotypal individuals). An important methodological advantage of studying these spectrum populations is the relative absence of secondary factors confounding psychological or biological measurement in the patient group, such as antipsychotic treatment, hospitalisation, and variable motivation. Schizotypy refers to temporally stable signs and symptoms (i.e. traits) that are phenomenologically similar to, but of lesser severity than, the full-blown symptoms of schizophrenia. Although the nature of schizotypy has yet to be fully characterised, it is not thought to be a unitary construct; instead, it is believed to consist of a number of dimensions. The most consistent dimensions that have emerged from factor analytic studies of psychometric schizotypy questionnaires are those of positive and negative schizotypal features as well as anxiety-related traits and psychoticism (or nonconformity) ( Vollema and van den Bosch, 1995). Positive features include signs and symptoms resembling, albeit in less severe form, the clinical schizophrenic symptoms of delusions and hallucinations (or reality distortion) on the one hand and thought disorder (or disorganisation) on the other hand. Negative features involve a reduced interest in interpersonal interaction, loss of volition, and anhedonia. Psychoticism, or nonconformity (also termed tough-mindedness by Eysenck, 1992) was initially hypothesised to be a predictor of psychotic illness; however, it is now thought to be more indicative of subclinical psychopathy-related traits ( Corr, 2000). There is thought to be a link between schizotypy and schizophrenia not only at a clinical (or phenomenological) level, but also at genetic and neurocognitive levels. Concerning the hypothesised genetic continuity, individuals with high levels of schizotypy are found with increased frequency amongst the first-degree relatives of schizophrenia patients (Kendler et al., 1995) and have, in turn, an increased prevalence of schizophrenia amongst their first-degree relatives (Kendler and Walsh, 1995). Additionally, levels of schizophrenic symptoms of patients have been shown to be related to levels of schizotypal symptoms of their first-degree relatives (Fanous et al., 2001 and Mata et al., 2003). A longitudinal study showed that schizotypal individuals are at increased risk of developing schizophrenia-related pathology (Chapman et al., 1994). Concerning neurocognitive performance, schizotypal individuals have been shown to display a number of deficits also found in schizophrenia patients (Lenzenweger, 1994). The hypothesised proximity of schizotypy to schizophrenia provides a powerful platform for assessing the validity of a schizophrenia endophenotype. Indeed, there is evidence linking increased antisaccade error rates to elevated levels of both positive and negative schizotypy in non-clinical samples (Gooding, 1999, Larrison et al., 2000 and O’Driscoll et al., 1998; however, see Klein et al., 2000, for a failure to replicate). Increased rates of antisaccade errors were also observed in a subgroup of patients with schizotypal personality disorder (Brenner et al., 2001 and Cadenhead et al., 2002) and in first-degree relatives of schizophrenia patients with schizophrenia spectrum symptoms compared to relatives without such symptoms (Thaker et al., 2000). Concerning the prosaccade task, Gooding (1999) found no association between schizotypy and prosaccade latency. However, Larrison et al. (2000) observed shorter prosaccade latencies in individuals with higher schizotypy levels. Conversely, Iacono and Lykken (1979) observed a relationship between longer latency and higher psychoticism scores. One measure that has, to our knowledge, not been examined in relation to psychometric schizotypy is that of spatial accuracy of both antisaccades and prosaccades. On saccade trials one can determine not only the direction and latency of the response but also its spatial accuracy. While prosaccade spatial accuracy is generally thought to be a function of an intact basic saccadic neural circuitry, in particular the cerebellar vermis (Botzel et al., 1993 and Ettinger et al., 2002), spatial accuracy on the antisaccade task has been linked to cognitive processes most likely involving cortical activity. These processes are thought to involve the transformation of visuospatial information into a motor response (Krappmann et al., 1998), possibly relying on fronto-parietal structures (Pierrot-Deseilligny et al., 1995). Given the role of frontal and parietal cortex as well as the cerebellum in the pathophysiology of schizophrenia (Andreasen et al., 1999), saccadic spatial accuracy becomes an important measure to investigate across the schizophrenia spectrum. Some previous studies have demonstrated reduced antisaccade or prosaccade spatial accuracy in patients with schizophrenia (Crawford et al., 1995a and Crawford et al., 1995b; Curtis et al., 2001, Ettinger et al., 2004, Karoumi et al., 1998, McDowell et al., 1999 and Schmid-Burgk et al., 1983) and their first-degree relatives (Ettinger et al., 2004, Karoumi et al., 2001, Ross et al., 1998 and Schreiber et al., 1997). Consequently, it needs to be clarified whether deficits in saccadic spatial accuracy are observed in individuals with high levels of schizotypy. One aim of the present study is to address this issue. A second issue that will be addressed here concerns the relationship between schizotypy and negative emotionality. Negative emotionality, or neuroticism, refers to a trait-like, enhanced emotional response to negative stimuli and includes the subclinical signs and symptoms of extensive worrying, psychosomatic complaints, unstable mood, sadness, and anxiety. Clinically, neuroticism may express itself as major depression or anxiety disorder (Claridge and Davis, 2001 and Eysenck and Eysenck, 1991). Interestingly, a number of studies have observed an association between levels of neuroticism and schizotypal traits amongst healthy individuals (Eysenck and Barrett, 1993 and Lipp et al., 1994) individuals. Additionally, there is evidence of increased levels of neuroticism in people with a diagnosis of schizophrenia (Berenbaum and Fujita, 1994 and Catts et al., 2000). The reasons for this association are not well understood. One possibility is that increased levels of neuroticism are observed as a consequence of distressing psychosis-like symptoms (Claridge and Broks, 1984). Alternatively, neuroticism may be a non-specific predictor of many different types of psychopathology, not specific to psychosis (Claridge and Davis, 2001). Irrespective of the precise causal relationships, Raine and Lencz (1995) have argued for the need to examine neurocognitive and behavioural deficits for specificity to schizotypy and/or schizophrenia. This argument has considerable relevance to putative schizophrenia endophenotypes. Previous studies have not conclusively ruled out the existence of antisaccade deficits in people with affective disorder, suggesting perhaps moderate levels of impairments (Curtis et al., 2001 and Gooding and Tallent, 2001). A relationship between antisaccade error rate and affective symptoms would indicate that this oculomotor deficit might be an endophenotype not specific to schizophrenia but possibly to a wider class of psychiatric disorders. Relatedly, Corr et al. (2002) recently observed a relationship between neuroticism and reduced prepulse inhibition (PPI). PPI is an operational measure of sensorimotor gating which has been argued to represent genetic liability to schizophrenia. Another group (Braunstein-Bercovitz, 2000 and Braunstein-Bercovitz et al., 2002) demonstrated that the relationship between schizotypy and latent inhibition (LI), the phenomenon of impaired learning of a previously exposed irrelevant stimulus compared to a novel stimulus, can be accounted for by measures of trait anxiety. These studies suggest the need to consider measures of negative trait emotionality in schizotypy research. Effects of negative emotionality on the association between saccadic impairments and schizotypy have not been explored systematically. O’Driscoll et al. (1998) observed that participants scoring highly on a positive schizotypy scale also had higher scores on measures of state anxiety and depression. Additionally, there was a correlation between scores on the depression scale and antisaccade errors. Importantly, neither of these measures fully accounted for the relationship between antisaccade dysfunction and positive schizotypy. O’Driscoll et al.’s (1998) choice of state emotionality measures, however, leaves open the question of whether negative trait emotionality impacts on the relationship between antisaccade errors and schizotypy. The aims of this study were, therefore, as follows. First, to replicate the relationship between schizotypy and antisaccade error rate. A selection of schizotypy scales tapping the dimensions of reality distortion, thought disorder, negative symptoms, psychoticism, as well as an overall positive schizotypy scale were employed in order to provide a comprehensive assessment of the various dimensions of this construct. Second, to provide the first investigation, to our knowledge, of the relationship between schizotypy and measures of spatial accuracy of both antisaccades and prosaccades. Third, to investigate whether any relationships observed between schizotypy and saccadic performance can be accounted for by neuroticism.

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