Eye Movement and the Schizophrenia Diagnosis


Researchers from the U.S., Germany and the U.K. found they were able to differentiate 88 persons with schizophrenia diagnoses from 88 controls with almost 100% accuracy on the basis of eye movements. Results were published online in Biological Psychiatry. (See note after the jump).

Abstract → 

Benson, P. Beedle, S. et al; “Simple Viewing Tests Can Detect Eye Movement Abnormalities That Distinguish Schizophrenia Cases from Controls with Exceptional Accuracy.” Biological Psychiatry, online May 21, 2012

Note from Kermit Cole, “In the News” editor

Sara van den Doel from Holland brought this study to my attention. I had seen it when it came online, but passed because I was reluctant to put it up without raising the question of other explanations for eye movement differences between groups. Sara’s message prompted me to do a search on PubMed for “saccade” (eye movement) and “anxiety,” which produced 70 studies from 1976 to 2012, among them:

Cornwell, B. R., S. C. Mueller, et al. (2012). “Anxiety, a benefit and detriment to cognition: behavioral and magnetoencephalographic evidence from a mixed-saccade task.” Brain Cogn 78(3): 257-267.
Abstract: Anxiety is typically considered an impediment to cognition. We propose anxiety-related impairments in cognitive-behavioral performance are the consequences of enhanced stimulus-driven attention. Accordingly, reflexive, habitual behaviors that rely on stimulus-driven mechanisms should be facilitated in an anxious state, while novel, flexible behaviors that compete with the former should be impaired. To test these predictions, healthy adults (N=17) performed a mixed-saccade task, which pits habitual actions (pro-saccades) against atypical ones (anti-saccades), under anxiety-inducing threat of shock and safe conditions. Whole-head magnetoencephalography (MEG) captured oscillatory responses in the preparatory interval preceding target onset and saccade execution. Results showed threat-induced anxiety differentially impacted response times based on the type of saccade initiated, slowing anti-saccades but facilitating erroneous pro-saccades on anti-saccade trials. MEG source analyses revealed that successful suppression of reflexive pro-saccades and correct initiation of anti-saccades during threat was marked by increased theta power in right ventrolateral prefrontal cortical and midbrain regions (superior colliculi) implicated in stimulus-driven attention. Theta activity may delay stimulus-driven processes to enable generation of an anti-saccade. Moreover, compared to safety, threat reduced beta desynchronization in inferior parietal cortices during anti-saccade preparation but increased it during pro-saccade preparation. Differential effects in inferior parietal cortices indicate a greater readiness to execute anti-saccades during safety and to execute pro-saccades during threat. These findings suggest that, in an anxiety state, reduced cognitive-behavioral flexibility may stem from enhanced stimulus-driven attention, which may serve the adaptive function of optimizing threat detection.

Garner, M., A. Attwood, et al. (2011). “Inhalation of 7.5% carbon dioxide increases threat processing in humans.” Neuropsychopharmacology 36(8): 1557-1562.
Abstract: Inhalation of 7.5% CO(2) increases anxiety and autonomic arousal in humans, and elicits fear behavior in animals. However, it is not known whether CO(2) challenge in humans induces dysfunction in neurocognitive processes that characterize generalized anxiety, notably selective attention to environmental threat. Healthy volunteers completed an emotional antisaccade task in which they looked toward or away from (inhibited) negative and neutral stimuli during inhalation of 7.5% CO(2) and air. CO(2) inhalation increased anxiety, autonomic arousal, and erroneous eye movements toward threat on antisaccade trials. Autonomic response to CO(2) correlated with hypervigilance to threat (speed to initiate prosaccades) and reduced threat inhibition (increased orienting toward and slower orienting away from threat on antisaccade trials) independent of change in mood. Findings extend evidence that CO(2) triggers fear behavior in animals via direct innervation of a distributed fear network that mobilizes the detection of and allocation of processing resources toward environmental threat in humans.

Ansari, T. L. and N. Derakshan (2011). “The neural correlates of impaired inhibitory control in anxiety.” Neuropsychologia 49(5): 1146-1153.
Abstract: According to Attentional Control Theory (Eysenck et al., 2007) anxiety impairs the inhibition function of working memory by increasing the influence of stimulus-driven processes over efficient top-down control. We investigated the neural correlates of impaired inhibitory control in anxiety using an antisaccade task. Low- and high-anxious participants performed anti- and prosaccade tasks and electrophysiological activity was recorded. Consistent with previous research high-anxious individuals had longer antisaccade latencies in response to the to-be-inhibited target, compared with low-anxious individuals. Central to our predictions, high-anxious individuals showed lower ERP activity, at frontocentral and central recording sites, than low anxious individuals, in the period immediately prior to onset of the to-be-inhibited target on correct antisaccade trials. Our findings indicate that anxiety interferes with the efficient recruitment of top-down mechanisms required for the suppression of prepotent responses. Implications are discussed within current models of attentional control in anxiety (Bishop, 2009; Eysenck et al., 2007).

Abstract: Ansari, T. L. and N. Derakshan (2011). “The neural correlates of cognitive effort in anxiety: effects on processing efficiency.” Biol Psychol 86(3): 337-348.
We investigated the neural correlates of cognitive effort/pre-target preparation (Contingent Negative Variation activity; CNV) in anxiety using a mixed antisaccade task that manipulated the interval between offset of instructional cue and onset of target (CTI). According to attentional control theory (Eysenck et al., 2007) we predicted that anxiety should result in increased levels of compensatory effort, as indicated by greater frontal CNV, to maintain comparable levels of performance under competing task demands. Our results showed that anxiety resulted in faster antisaccade latencies during medium compared with short and long CTIs. Accordingly, high-anxious individuals compared with low-anxious individuals showed greater levels of CNV activity at frontal sites during medium CTI suggesting that they exerted greater cognitive effort and invested more attentional resources in preparation for the task goal. Our results are the first to demonstrate the neural correlates of processing efficiency and compensatory effort in anxiety and are discussed within the framework of attentional control theory.

Abstract: Wieser, M. J., P. Pauli, et al. (2009). “Probing the attentional control theory in social anxiety: an emotional saccade task.” Cogn Affect Behav Neurosci 9(3): 314-322.
Volitional attentional control has been found to rely on prefrontal neuronal circuits. According to the attentional control theory of anxiety, impairment in the volitional control of attention is a prominent feature in anxiety disorders. The present study investigated this assumption in socially anxious individuals using an emotional saccade task with facial expressions (happy, angry, fearful, sad, neutral). The gaze behavior of participants was recorded during the emotional saccade task, in which participants performed either pro- or antisaccades in response to peripherally presented facial expressions. The results show that socially anxious persons have difficulties in inhibiting themselves to reflexively attend to facial expressions: They made more erratic prosaccades to all facial expressions when an antisaccade was required. Thus, these findings indicate impaired attentional control in social anxiety. Overall, the present study shows a deficit of socially anxious individuals in attentional control-for example, in inhibiting the reflexive orienting to neutral as well as to emotional facial expressions. This result may be due to a dysfunction in the prefrontal areas being involved in attentional control.

Abstract: Derakshan, N., T. L. Ansari, et al. (2009). “Anxiety, inhibition, efficiency, and effectiveness. An investigation using antisaccade task.” Exp Psychol 56(1): 48-55.
Effects of anxiety on the antisaccade task were assessed. Performance effectiveness on this task (indexed by error rate) reflects a conflict between volitional and reflexive responses resolved by inhibitory processes (Hutton, S. B., & Ettinger, U. (2006). The antisaccade task as a research tool in psychopathology: A critical review. Psychophysiology, 43, 302-313). However, latency of the first correct saccade reflects processing efficiency (relationship between performance effectiveness and use of resources). In two experiments, high-anxious participants had longer correct antisaccade latencies than low-anxious participants and this effect was greater with threatening cues than positive or neutral ones. The high- and low-anxious groups did not differ in terms of error rate in the antisaccade task. No group differences were found in terms of latency or error rate in the prosaccade task. These results indicate that anxiety affects performance efficiency but not performance effectiveness. The findings are interpreted within the context of attentional control theory (Eysenck, M. W., Derakshan, N., Santos, R., & Calvo, M. G. (2007). Anxiety and cognitive performance: Attentional control theory. Emotion, 7 (2), 336-353).

Rommelse, N. N., S. Van der Stigchel, et al. (2008). “A review on eye movement studies in childhood and adolescent psychiatry.” Brain Cogn 68(3): 391-414.
Abstract: The neural substrates of eye movement measures are largely known. Therefore, measurement of eye movements in psychiatric disorders may provide insight into the underlying neuropathology of these disorders. Visually guided saccades, antisaccades, memory guided saccades, and smooth pursuit eye movements will be reviewed in various childhood psychiatric disorders. The four aims of this review are (1) to give a thorough overview of eye movement studies in a wide array of psychiatric disorders occurring during childhood and adolescence (attention-deficit/hyperactivity disorder, oppositional deviant disorder and conduct disorder, autism spectrum disorders, reading disorder, childhood-onset schizophrenia, Tourette’s syndrome, obsessive compulsive disorder, and anxiety and depression), (2) to discuss the specificity and overlap of eye movement findings across disorders and paradigms, (3) to discuss the developmental aspects of eye movement abnormalities in childhood and adolescence psychiatric disorders, and (4) to present suggestions for future research. In order to make this review of interest to a broad audience, attention will be given to the clinical manifestation of the disorders and the theoretical background of the eye movement paradigms.


Mad in America hosts blogs by a diverse group of writers. These posts are designed to serve as a public forum for a discussion—broadly speaking—of psychiatry and its treatments. The opinions expressed are the writers’ own.


Mad in America has made some changes to the commenting process. You no longer need to login or create an account on our site to comment. The only information needed is your name, email and comment text. Comments made with an account prior to this change will remain visible on the site.

Previous articleMindfulness-Based Cognitive Therapy is Effective for Current Depression
Next articleDoctors Concerned by Antipsychotic Prescriptions
Kermit Cole
Kermit Cole, MFT, founding editor of Mad in America, works in Santa Fe, New Mexico as a couples and family therapist. Inspired by Open Dialogue, he works as part of a team and consults with couples and families that have members identified as patients. His work in residential treatment — largely with severely traumatized and/or "psychotic" clients — led to an appreciation of the power and beauty of systemic philosophy and practice, as the alternative to the prevailing focus on individual pathology. A former film-maker, he has undergraduate and master's degrees in psychology from Harvard University, as well as an MFT degree from the Council for Relationships in Philadelphia. He is a doctoral candidate with the Taos Institute and the Free University of Brussels. You can reach him at [email protected].


  1. Emma, not sure which “significance” you are referring to…that all were on Rxs, that anxiety may be a confounding variable, or that they have a test that might correlate 100% of the time with a Dx of Sz. The Rxs confounding variable indicates that maybe the test of eye mvt really is able to differentiate those ‘normals’ from those who take neuroleptic drugs…not those Dx Sz. The anx. confounding variable likewise might indicate that really what the ocular test is picking up on is not a difference of normals and Sz patients, but normals and those with high anxiety…which happen to inculde those Dx Sz. Lastly, the test does seem to be picking up on something…what not sure exactly what yet, as they would need to have a bit more control, higher N’s and more replication. Interesting work though. I may be missing something that Kermit could comment on…as i did not read the study fully.

    Report comment

  2. From the study:
    “Six patients were receiving no antipsychotic medication at time of testing. Others received first-generation antipsychotics only (n = 11), second-generation antipsychotics only (n = 64), or a combination of the two (n = 6). Pharmacology was unavailable for one patient. Median chlorpromazine-equivalent dosage for those receiving antipsychotic medication was 350 mg per day (mean = 455.0, SD = 374.1 mg). A number of patients were also receiving antidepressants (n = 25), hypnotics (n = 6), anxiolytics (n = 12), mood stabilizers (n = 3), and anticholinergic medication (n = 9).”

    “Trait or State Marker?
    The eye-movement abnormalities are unlikely to be secondary to treatment or mental state at the time of testing. No patients were from acute hospital wards or were acutely mentally or behaviorally disturbed at the time of testing. All were reported to be stable or in remission by the clinical teams supervising their psychiatric care. The abnormalities are independent of effects of neuroleptic medication; all medication-free cases scored within the same range of abnormality as the medicated schizophrenia patients, as did the few patients on very small amounts of neuroleptics (see Results). There was no correlation between duration of illness, age of onset or amount of medication and the severity of the abnormalities we observed. Eye-movement abnormalities also showed no correlation with presence or absence of cigarette smoking or daily cigarette consumption. The likelihood of an individual’s eye movements being classified as “schizophrenic” was independent of his or her symptom severity. Finally, our results showed good test–retest reliability when individuals were retested after 9 months. A few patients did show a modest degree of improvement on repeat testing. However, there was no suggestion of different scanning styles at retest even though stimuli were identical in each test. Further repeat testing at yearly intervals are planned.”

    They seem to have attended well to the effects of medication status. The study mentions that “Cases and controls were assessed on a broad spectrum of tests as part of the protocol, and results will be reported elsewhere.” It would be helpful to get those data, of course; without them any discussion about the role of anything other than a schizophrenia diagnosis within the context of this study is merely speculation.

    Report comment

    • If this eye detection test is true, then either someone is 100% schizophrenic or not. Black and white with no shades of grey, which is interesting.
      Secondary question would be what day does schizophrenia occur? The hour after a child is born? Their 15th year after years of school? The legal age of 18? Its black and white.
      The T4 Euthanasia Program could have used this test to help rid the world of my kind (I’m schizophrenic).

      Report comment

  3. Re: Eye Movement

    There is a link on this page for Eye Movement Desensitization and Reprocessing –


    It’s used for trauma, and gets an A-rating from the Veterans Administration. There are other non-drug options on the page as well… Because people heal in different ways…. No two people are alike!

    When is psychiatry going to move beyond labels… ones that dehumanize, and toward helping people fully-recover… and thrive (build careers, families, homes, dreams)?



    Report comment

    • To clarify,

      I don’t like studies that show that people diagnosed with “schizophrenia” have “different” eye movement patterns, any more than any other reader on this site.

      And, IMO, it matters not.
      Here’s why:

      If trauma can cause vitamin depletion, which any prolonged stress can cause, and a study is conducted that shows that people with “schizophrenia” have vitamin B-3 or D-3 defiency, it shouldn’t be taken as anything more than the results of trauma.

      And then the trauma can be treated.
      And if eye-movement desensitization, or vitamin therapy, or neurofeedback, or any other non-drug option helps someone heal, then that’s a good thing!

      That’s what I’m tryin to say.


      Report comment

    • Yes, a fancy research study for something that anybody interacting with someone in prolonged crisis labelled schizohrenic can pick out. A jittery avoidance of eye contact perhaps due to seeing visual hallucinations out of the corner of one’s eye.

      Report comment