تهدید و اضطراب خصلتی ثبات تثبیت نگاه را تحت تاثیر قرار می دهد

Threat accelerates early visual information processing, as shown by shorter P100 latencies of pattern Visual Evoked Potentials in subjects with low trait anxiety, but the opposite is true for high anxious subjects. We sought to determine if, and how, threat and trait anxiety interact to affect stability of gaze fixation. We used video oculography to record gaze position in the presence and in the absence of a fixational stimulus, in a safe and a verbal threat condition in subjects characterised for their trait anxiety. Trait anxiety significantly predicted fixational instability in the threat condition. An extreme tertile analysis revealed that fixation was less stable in the high anxiety group, especially under threat or in the absence of a stimulus. The effects of anxiety extend to perceptual and sensorimotor processes. These results have implications for the understanding of individual differences in occulomotor planning and visually guided behavior.

One of the primary roles of the gaze system is to bring and hold visual stimuli of interest onto the fovea, the central area of human retina showing the highest visual acuity, necessary for post-retinal processing. Even during fixation on a stationary stimulus/object (visually guided fixation), constant, small, involuntary “microsaccadic” eye movements prevent the naturally occurring adaptation of post-retinal cortical cellular mechanisms (Movshon and Lennie, 1979 and Webster and De Valois, 1985), which would otherwise lead to depression of sensitivity/salience and even fading of a visual target following prolonged stabilisation of its image on the fovea (Troxler, 1804 and Blakemore and Campbell, 1969). Apart from preventing retinal fading of a visual target, microsaccades also serve to bring the line of sight to visual details that are crucial for finely guided visuomotor tasks that require the highest level of spatial resolution (Steinman et al., 1973 and Ko et al., 2010). Yet, in addition to improve spatial resolution, microsaccades are thought to transform the visual scene into a sequence of discrete views which, one at a time, are processed by attentional resources and guide decision making (Ballard et al., 1997, Ko et al., 2010 and Kowler and Collewijn, 2010). Microsaccades may thus be prompted by cognition and reflect attentional processing and fine strategic visuomotor planning. Initiation of visually triggered microsaccades involves occipital and parietal cortical inputs, including retinal input to “fixation neurons” in the superior colliculus, which then projects to the premotor circuit in the brain stem and cerebellum (Munoz and Istvan, 1998, Munoz and Wurtz, 1993a and Munoz and Wurtz, 1993b). Suppression of reflexive microsaccades is under the tonic control of frontal cortex and basal ganglia, which also project to the superior colliculus and brain stem premotor circuit (Hikosaka et al., 2000, Munoz et al., 2000 and Schall, 1997 for review). Fixation in the absence of a visual stimulus (volitional fixation) is less accurate than stimulus-driven fixation (Smyrnis et al., 2003) and may be driven almost entirely by extra-retinal, prefrontal/basal ganglia input to the SC fixation neurons (Munoz and Wurtz, 1993a, Hikosaka et al., 2000, Munoz et al., 2000 and Schall, 1997 for review). It has been hypothesized (Smyrnis et al., 2004) that these prefrontal regions maintain a “mental” representation of the fixation point and thus may be the same areas mediating spatial memory processing (Goldman-Rakic, 1988). Indeed, it is well-established that a particular region of the frontal lobe neocortex, the frontal eye field (FEF) is prominently involved in control of volitional eye movements, having a distinct sub-region for fixation. The dorsolateral prefrontal cortex in particular, acts as a ≪supervisory≫ area, inhibiting unwanted reflexive saccades when volitional maintenance of fixation is required (Gooding, 1999). Suppression of microsaccades results in stable fixation such as that seen in trained athletes e.g. elite shooters and has been related to their superiority in selective and sustained attention (Di Russo et al., 2003). On the other hand, deficient fixational stability is seen in conditions characterised by attentional and strategic planning deficits due to fronto-striatal pathology, such as schizophrenia (Burton et al., 2008) and attention-deficit hyperactivity disorder (ADHD) (Munoz et al., 2003). Trait anxiety is associated with impoverished recruitment of attentional control mechanisms (Fox, 1993, Eysenck and Calvo, 1992 and Bishop, 2009) and for this reason it is expected to impact on reflexive and volitional saccadic control. Threat commands visual attention through activation of the amygdala and the bed nucleus of stria terminalis (Lang et al., 2000) and is thus preferentially detected in humans (Ohman et al., 2001); it adaptively enhances contrast perception (Phelps et al., 2006) and accelerates the early P100 wave of pattern Visual Evoked Potentials (Laretzaki et al., 2010). The latter effect however, was not observed in high trait anxiety subjects (Laretzaki et al., 2010). This was probably a result of a hyper-responsive pre-attentive, amygdala-centred threat-detection system (Mathews et al., 1997), associated with deficient recruitment of prefrontal cortical mechanisms that are critical in the top–down control of selective attention to threat (Bishop et al., 2004 and Ohman, 2005). In the present study, we sought to determine if, and how, threat and trait anxiety interact to affect fixation of gaze. To this goal, we studied the effects of verbal threat on stimulus driven (a non-emotional target) and volitional (no-target, empty screen) fixation performance, in healthy subjects characterised for their trait anxiety. Subjects were also tested in the absence of threat. Based on available evidence, we predicted generally better fixation performance in the stimulus driven compared to volitional fixation condition. We also predicted that threat would impair fixation performance especially in high trait anxious subjects and this impairment would be more pronounced under volitional fixation since the latter is more critically determined by prefrontal input in the SC. Because of inadequate data in the literature, we made no predictions regarding group differences (high vs. low trait anxious subjects) in fixation performance in the absence of threat.