Specificity of smooth pursuit eye movement and visual fixation abnormalities in schizophrenia

Amador, Xavier; Sackeïm, Harold A.; Mukherjee, Sukdeb; Halperin, Ronnie; Neeley, Priscilla; Maclin, Edward L.; Schnur, David B.

doi:10.1016/0920-9964(91)90040-x

Cited by 39 publications

(29 citation statements)

References 26 publications

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“…In addition, chronic patients have shown lower acuity in memory-guided saccades (Crawford et al, 1995a; Park et al, 1995; McDowell and Clementz, 1996; Radant et al, 1997; Karoumi et al, 1998; McDowell et al, 2001). Although there is some debate about the usefulness of oculomotor deficits in schizophrenia research (e.g., Calkins and Iacono, 2000; Brownstein et al, 2003; Calkins et al, 2004, 2008; Levy et al, 2004, 2008; Boudet et al, 2005; Heydebrand, 2006), deficits have been identified as schizophrenia spectrum markers (Amador et al, 1991; Sweeney et al, 1994; Faraone et al, 1995; McDowell and Clementz, 1997; Rosenberg et al, 1997; Avila et al, 2002; Kathmann et al, 2003), independent of clinical state (Calkins et al, 2003; Kallimani et al, 2009), or medication (Crawford et al, 1995b; Muller et al, 1999). Furthermore, oculomotor aberrations have been found to fulfill some endophenotypic characteristics (Gottesman and Gould, 2003; Calkins et al, 2008).…”

Section: The Vision Perspective On Schizophreniamentioning

confidence: 99%

“To see or not to see: that is the question.” The “Protection-Against-Schizophrenia” (PaSZ) model: evidence from congenital blindness and visuo-cognitive aberrations

Landgraf¹,

Osterheider²

2013

Front. Psychol.

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The causes of schizophrenia are still unknown. For the last 100 years, though, both “absent” and “perfect” vision have been associated with a lower risk for schizophrenia. Hence, vision itself and aberrations in visual functioning may be fundamental to the development and etiological explanations of the disorder. In this paper, we present the “Protection-Against-Schizophrenia” (PaSZ) model, which grades the risk for developing schizophrenia as a function of an individual's visual capacity. We review two vision perspectives: (1) “Absent” vision or how congenital blindness contributes to PaSZ and (2) “perfect” vision or how aberrations in visual functioning are associated with psychosis. First, we illustrate that, although congenitally blind and sighted individuals acquire similar world representations, blind individuals compensate for behavioral shortcomings through neurofunctional and multisensory reorganization. These reorganizations may indicate etiological explanations for their PaSZ. Second, we demonstrate that visuo-cognitive impairments are fundamental for the development of schizophrenia. Deteriorated visual information acquisition and processing contribute to higher-order cognitive dysfunctions and subsequently to schizophrenic symptoms. Finally, we provide different specific therapeutic recommendations for individuals who suffer from visual impairments (who never developed “normal” vision) and individuals who suffer from visual deterioration (who previously had “normal” visual skills). Rather than categorizing individuals as “normal” and “mentally disordered,” the PaSZ model uses a continuous scale to represent psychiatrically relevant human behavior. This not only provides a scientific basis for more fine-grained diagnostic assessments, earlier detection, and more appropriate therapeutic assignments, but it also outlines a trajectory for unraveling the causes of abnormal psychotic human self- and world-perception.

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Section: The Vision Perspective On Schizophreniamentioning

confidence: 99%

“To see or not to see: that is the question.” The “Protection-Against-Schizophrenia” (PaSZ) model: evidence from congenital blindness and visuo-cognitive aberrations

Landgraf¹,

Osterheider²

2013

Front. Psychol.

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“…Most of the studied used electro-oculography (EOG) to record eye movement, others used infrared reflectometry (IR), or both. A total of 26 articles fulfilled our selection criteria (Acker and Toone, 1978; Allen et al, 1990; Altman et al, 1990; Amador et al, 1991; Blackwood et al, 1991; Boudet et al, 2005; Clementz et al, 1992; Holahan and O’Driscoll, 2005; Holzman et al, 1973; Iacono et al, 1992; Jones and Pivik, 1985; Keefe et al, 1989; Kinney et al, 1998; Levin et al, 1981; Levin et al, 1988; Levy et al, 1992; Levy et al, 2000; Louchart-de la Chapelle et al, 2005; Matthysse et al, 1986; Ross et al, 1998; Saletu et al, 1986; Scarone et al, 1987; Sereno and Holzman, 1995; Siever et al, 1990; Smeraldi et al, 1987; Thaker et al, 1996). Effect sizes and percent abnormal calculations are presented in Table 3.…”

Section: Neuromotor Abnormalitiesmentioning

confidence: 99%

Endophenotypes in schizophrenia: A selective review

Allen

Griss

Folley

et al. 2009

Schizophrenia Research

185

113

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Background Given the wealth of data in the literature on schizophrenia endophenotypes, it is useful to have one source to reference their frequency data. We reviewed the literature on disease-liability associated variants in structural and functional magnetic resonance images (MRI), sensory processing measures, neuromotor abilities, neuropsychological measures, and physical characteristics in schizophrenia patients (SCZ), their first-degree relatives (REL), and healthy controls (HC). The purpose of this review was to provide a summary of the existing data on the most extensively published endophenotypes for schizophrenia. Methods We searched PubMed and MedLine for all studies on schizophrenia endophenotypes comparing SCZ to HC and/or REL to HC groups. Percent abnormal values, generally defined as > 2 SD from the mean (in the direction of abnormality) and/or associated effect sizes (Cohen’s d) were calculated foreach study. Results Combined, the articles reported an average 39.4% (SD=20.7%; range=2.2-100%) of abnormal values in SCZ, 28.1% (SD=16.6%; range=1.6-67.0%) abnormal values in REL, and 10.2% (SD=6.7%; range=0.0-34.6%) in HC groups. Conclusions These findings are reviewed in the context of emerging hypotheses on schizophrenia endophenotypes, as well as a discussion of clustering trends among the various intermediate phenotypes. In addition, programs for future research are discussed, as instantiated in a few recent large-scale studies on multiple endophenotypes across patients, relatives, and healthy controls.

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“…In addition, several different voluntary saccade paradigms have been used, including saccades to predictable targets (Levin et al 1982; Abel et al 1992; Clementz et al 1994; Crawford et al 1995a, b; Karoumi et al 1998; Hutton et al 2001; Krebs et al 2001; O’Driscoll et al 2005; Spengler et al 2006; Sailer et al 2007) [see also review by (Gooding and Basso 2008); saccades away from targets (antisaccades) (Thaker et al 1989; Fukushima et al 1990; Clementz et al 1994; Sereno and Holzman 1995; Katsanis et al 1997; McDowell and Clementz 1997; Rosenberg et al 1997; Hutton et al 1998; Maruff et al 1998; O’Driscoll et al 1998; Gooding 1999; Castellanos et al 2000; Curtis et al 2001; Gooding and Tallent 2001; Mostofsky et al 2001; Barton et al 2002; Sweeney et al 2002; Brownstein et al 2003; Calkins et al 2003; Munoz et al 2003; Ettinger et al 2004; Levy et al 2004; Radant et al 2007; Barton et al 2008); saccades to remembered or attended targets (Park and Holzman 1992; Ross et al 1994; Park et al 1995; Everling et al 1996; McDowell and Clementz 1996; Sweeney et al 1998a; Muller et al 1999; Larrison-Faucher et al 2002; Winograd-Gurvich et al 2006)]; and saccades to target sequences (Biscaldi et al 1998; LeVasseur et al 2001; Ram-Tsur et al 2006). Fixation (Amador et al 1991; Gooding et al 2000; Munoz et al 2003; Smyrnis et al 2004; Barton et al 2008), the oculocephalic reflex (Lipton et al 1980), and optokinetic and vestibular responses (Levy et al 1978, 1983; Latham et al 1981; Jones and Pivik 1983; Yee et al 1987; Cooper and Pivik 1991; Warren and Ross 1998) have been studied as well.…”

Section: Introductionmentioning

confidence: 99%

Eye Tracking Dysfunction in Schizophrenia: Characterization and Pathophysiology

Levy

Sereno

Gooding

et al. 2010

Current Topics in Behavioral Neurosciences

124

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Eye tracking dysfunction (ETD) is one of the most widely replicated behavioral deficits in schizophrenia and is over-represented in clinically unaffected first-degree relatives of schizophrenia patients. Here, we provide an overview of research relevant to the characterization and pathophysiology of this impairment. Deficits are most robust in the maintenance phase of pursuit, particularly during the tracking of predictable target movement. Impairments are also found in pursuit initiation and correlate with performance on tests of motion processing, implicating early sensory processing of motion signals. Taken together, the evidence suggests that ETD involves higher-order structures, including the frontal eye fields, which adjust the gain of the pursuit response to visual and anticipated target movement, as well as early parts of the pursuit pathway, including motion areas (the middle temporal area and the adjacent medial superior temporal area). Broader application of localizing behavioral paradigms in patient and family studies would be advantageous for refining the eye tracking phenotype for genetic studies.

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Specificity of smooth pursuit eye movement and visual fixation abnormalities in schizophrenia

Cited by 39 publications

References 26 publications

“To see or not to see: that is the question.” The “Protection-Against-Schizophrenia” (PaSZ) model: evidence from congenital blindness and visuo-cognitive aberrations

“To see or not to see: that is the question.” The “Protection-Against-Schizophrenia” (PaSZ) model: evidence from congenital blindness and visuo-cognitive aberrations

Endophenotypes in schizophrenia: A selective review

Eye Tracking Dysfunction in Schizophrenia: Characterization and Pathophysiology

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