Antisaccades are thought to involve higher level inputs from neural centers involved in rapid eye movement inhibition and control. Previous work has demonstrated that performance on the antisaccade task can help in the assessment of injury in acute and/or chronic mild traumatic brain injury (mTBI). In this exploratory study, we performed cross-sectional and longitudinal comparisons of rapid eye movement, followed by correlations of antisaccade performance with assessments of symptom burden, diffusion tensor imaging, and a neuropsychological test of response inhibition. Significant deficits in antisaccade median latency, F(2, 31) = 3.65, p = 0.04 and prosaccade error mean duration, F(2, 31) = 3.63, p = 0.04 were found between patient groups and controls: the former was correlated with loss of white matter integrity in the splenium of the corpus callosum in acute mTBI, rho = 0.90, p = 0.0005. Furthermore, increased antisaccade median latency was also correlated with poor performance on an executive functioning task, r2 = 0.439, p = 0.03, and greater symptom burden, r2 = 0.480, p = 0.02 in the acute mTBI patients. Our preliminary research suggests that the antisaccade task could be useful as a neurological marker for mTBI and concussion, but more work is required.

Greater right fronto-temporal grey matter atrophy was observed in MCI or early AD participants with delusions compared to matched patients without delusions. Consistent with our predictions, asymmetric grey matter atrophy in the right hemisphere may contribute to development of delusions through loss of executive inhibition.

Objective We conducted a neuroimaging analysis to understand the neuroanatomical correlates of gray matter loss in a group of mild cognitive impairment and early Alzheimer’s disease patients who developed delusions. Methods With data collected as part of the Alzheimer’s Disease Neuroimaging Initiative, we conducted voxel-based morphometry to determine areas of gray matter change in the same Alzheimer’s Disease Neuroimaging Initiative participants, before and after they developed delusions. Results We identified 14 voxel clusters with significant gray matter decrease in patient scans post-delusional onset, correcting for multiple comparisons (false discovery rate, p < 0.05). Major areas of difference included the right and left insulae, left precuneus, the right and left cerebellar culmen, the left superior temporal gyrus, the right posterior cingulate, the right thalamus, and the left parahippocampal gyrus. Conclusions Although contrary to our initial predictions of enhanced right frontal atrophy, our preliminary work identifies several neuroanatomical areas, including the cerebellum and left posterior hemisphere, which may be involved in delusional development in these patients.

We review the literature to appraise the evidence supporting or disputing the use of eye movement measurement in disorders of consciousness (DOC) with low levels of arousal or awareness, such as minimally conscious state (MCS), vegetative state (VS), and coma for diagnostic and prognostic purposes. We will focus on the effectiveness of each technique in the diagnostic classification of these patients and the gradual trend in research from manual to computerized tracking methods. New tools have become available at clinicians’ disposal to assess eye movements with high spatial and temporal fidelity. The close relationship between eye movement generation and organic dysfunction in the brain allows these tools to be applied to the assessment of severe DOC as a unique supplementary toolset. We posit that eye tracking can improve clinical diagnostic precision for DOC, a key component of assessment that often dictates the course of clinical care in DOC patients. We see the emergence of long-term eye-tracking studies with seamless integration of technology in the future to improve the performance of clinical assessment in DOC.