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Eye Tracking Dysfunction in Schizophrenia: Characterization and Pathophysiology

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Part of the book series: Current Topics in Behavioral Neurosciences ((CTBN,volume 4))

Abstract

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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Notes

  1. 1.

    Two studies explicitly followed up the Diefendorf and Dodge report (Couch and Fox 1934; White 1938). Both studies replicated the finding of impaired pursuit in schizophrenic patients, but questioned its specificity and independence from clinical state, especially in manic-depressive patients. Modern psychotropic drugs were not yet in use, but barbiturates were commonly used to control agitation. Impaired pursuit was found during periods of clinical exacerbation, corresponding to periods of barbiturate treatment, whereas pursuit normalized during periods of remission, corresponding to barbiturate discontinuation. Only later were barbiturates discovered to impair pursuit (Rashbass and Russell 1961; Schalen et al. 1988), suggesting that what appeared at the time to be an association between clinical state and pursuit performance was actually a drug-induced epiphenomenon.

  2. 2.

    A discussion of possible reasons for the difference between these results and those of earlier investigators as well as a critical review of the literature on vestibular function in psychopathological conditions can be found elsewhere (Levy et al. 1983). The status of visual−vestibular interaction remains unclear, with some data supporting normal responses in schizophrenic patients (Levy et al. 1978) and other data supporting abnormal responses (Jones and Pivik 1983; Yee et al. 1987; Warren and Ross 1998).

  3. 3.

    This function of gain was discovered by the same Dodge who collaborated with Diefendorf in the first study of oculomotor function in schizophrenia (Dodge 1903).

  4. 4.

    Positive and negative values for effect sizes correspond to whether patients had higher or lower mean scores than controls, respectively.

  5. 5.

    Larger for 10 deg/s targets, no difference for 20 deg/s targets.

  6. 6.

    Differences were found in the last 40 ms of pursuit initiation, but not in the first 60 ms. Other investigators averaged across these epochs.

  7. 7.

    If lesion is unilateral, deficits may be for ipsiversive pursuit only (Morrow and Sharpe 1995) or may affect pursuit in both directions (Lekwuwa and Barnes 1996).

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Acknowledgments

This work was supported in part by NIMH grants R01 MH071523 and MH31340, the Sidney R. Baer, Jr. Foundation, the Essel Foundation, the National Association for Research on Schizophrenia and Depression (NARSAD), an Essel Investigator NARSAD and NSF grant 0924636, a grant from the Canadian Institute of Health Research, a William Dawson Scholar Award, and a Stairs Memorial Foundation grant. The authors thank Dr. Larry Abel for making the original material for Fig. 2 available for adaptation and Joshua Ritz for formatting the figures.

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Levy, D.L., Sereno, A.B., Gooding, D.C., O’Driscoll, G.A. (2010). Eye Tracking Dysfunction in Schizophrenia: Characterization and Pathophysiology. In: Swerdlow, N. (eds) Behavioral Neurobiology of Schizophrenia and Its Treatment. Current Topics in Behavioral Neurosciences, vol 4. Springer, Berlin, Heidelberg. https://doi.org/10.1007/7854_2010_60

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