The antisaccade task is a classic task of oculomotor control that requires participants to inhibit a saccade to a target and instead make a voluntary saccade to the mirror opposite location. By comparison, the prosaccade task requires participants to make a visually-guided saccade to the target. These tasks have been studied extensively using behavioural oculomotor, electrophysiological and neuroimaging in both non-human primates and humans. In humans, the antisaccade task is under active investigation as a potential endophenotype or biomarker for multiple psychiatric and neurological disorders. A large and growing body of literature has used functional magnetic resonance imaging (fMRI) and positron emission tomography (PET) to study the neural correlates of the antisaccade and prosaccade tasks. We present a quantitative meta-analysis of all published voxel-wise fMRI and PET studies (18) of the antisaccade task and show that consistent activation for antisaccades and prosaccades is obtained in a fronto-subcortical-parietal network encompassing frontal and supplementary eye fields, thalamus, striatum and intraparietal cortex. This network is strongly linked to oculomotor control and was activated to a greater extent for antisaccade than prosaccade trials. Antisaccade but not prosaccade trials additionally activated dorsolateral and ventrolateral prefrontal cortices. We also found that a number of additional regions not classically linked to oculomotor control were activated to a greater extent for antisaccade versus prosaccade trials; these regions are often reported in antisaccade studies but rarely commented upon. While the number of studies eligible to be included in this meta-analysis was small, the results of this systematic review reveal that antisaccade and prosaccade trials consistently activate a distributed network of regions both within and outside the classic definition of the oculomotor network.

Fragile X Mental Retardation 1(FMR1) premutation carriers (PM‐carriers) have a defective trinucleotide expansion on theFMR1gene that is associated with continuum of neuropsychological and mental disorders. Currently, little is known about the distinct subcomponents of executive function potentially impaired in female PM‐carriers, and there have been no investigations into associations between executive function and incidences of mental disorders. A total of 35 female PM‐carriers confirmed by Asuragen triple primed PCR DNA testing and 35 age‐ and intelligence‐matched controls completed tests of executive function (i.e., response inhibition and working memory) and self‐reported on social anxiety, depression, and ADHD predominantly inattentive (ADHD‐PI) symptoms. Compared to controls, PM‐carriers were significantly elevated on self‐reported social anxiety and ADHD‐PI symptoms. Irrespective of mental symptoms, female PM‐carries performed significantly worse than controls on a response inhibition test, and further investigations revealed significant correlations between executive function performance and self‐reported symptoms of anxiety, depression and ADHD‐PI. Critically, among PM‐carriers with good executive function performance, no women exceeded threshold markers for probable caseness of mental disorder. However, rates of probable caseness were elevated in those with average performance (response inhibition: social anxiety: 41.7%; depression: 20%; ADHD: 44.4%; working memory: social anxiety: 27.3%; depression: 9.1%; ADHD: 18.2%) and highly elevated for those with poor executive function performance (response inhibition: social anxiety: 58.3%; depression: 80%; ADHD: 55.6%; working memory: social anxiety: 100%; depression: 50%; ADHD: 83.3%). These data suggest that subtle executive dysfunction may be a useful neuropsychological indicator for a range of mental disorders previously reported in female PM‐carriers.

Objective: To characterise the psychiatric symptoms of visual snow syndrome (VSS), and determine their relationship to quality of life and severity of visual symptoms.Methods: One hundred twenty-five patients with VSS completed a battery of questionnaires assessing depression/anxiety, dissociative experiences (depersonalisation), sleep quality, fatigue, and quality of life, as well as a structured clinical interview about their visual and sensory symptoms.Results: VSS patients showed high rates of anxiety and depression, depersonalisation, fatigue, and poor sleep, which significantly impacted quality of life. Further, psychiatric symptoms, particularly depersonalisation, were related to increased severity of visual symptoms. The severity/frequency of psychiatric symptoms did not differ significantly due to the presence of migraine, patient sex, or timing of VSS onset (lifelong vs. later onset).Conclusion: Psychiatric symptoms are highly prevalent in patients with VSS and are associated with increased visual symptom severity and reduced quality of life. Importantly, patients with lifelong VSS reported lower levels of distress and milder self-ratings of visual symptoms compared to patients with a later onset, while being equally likely to experience psychiatric symptoms. This suggests that the psychiatric symptoms of VSS are not solely due to distress caused by visual symptoms. While no consistently effective treatments are available for the visual symptomology of VSS, psychiatric symptoms offer an avenue of treatment that is likely to significantly improve patient quality of life and ability to cope with visual symptoms.

Motor impairments have been found to be a significant clinical feature associated with autism and Asperger’s disorder (AD) in addition to core symptoms of communication and social cognition deficits. Motor deficits in high-functioning autism (HFA) and AD may differentiate these disorders, particularly with respect to the role of the cerebellum in motor functioning. Current neuroimaging and behavioral evidence suggests greater disruption of the cerebellum in HFA than AD. Investigations of ocular motor functioning have previously been used in clinical populations to assess the integrity of the cerebellar networks, through examination of saccade accuracy and the integrity of saccade dynamics. Previous investigations of visually guided saccades in HFA and AD have only assessed basic saccade metrics, such as latency, amplitude, and gain, as well as peak velocity. We used a simple visually guided saccade paradigm to further characterize the profile of visually guided saccade metrics and dynamics in HFA and AD. It was found that children with HFA, but not AD, were more inaccurate across both small (5°) and large (10°) target amplitudes, and final eye position was hypometric at 10°. These findings suggest greater functional disturbance of the cerebellum in HFA than AD, and suggest fundamental difficulties with visual error monitoring in HFA.