Guided by a theoretical, heuristic model--the """"""""Mendelian latent structure model,"""""""" which postulates a latent trait that can cause schizophrenia or eye tracking dysfunctions (ETD) or both-- we seek to uncover co-familial traits other than ETD that aggregate in the families of schizophrenic patients. The focus of this project is on testing first-degree relatives of schizophrenic, schizo-affective, and bipolar patients. This strategy previously led to the discovery both of familial aggregation of smooth pursuit eye movement abnormalities and of specific qualities of thought disorder. Our search is for other traits that can illuminate the pathophysiology of schizophrenia as well as their qualification as expressions of the latent trait or traits that may interactively affect risk for schizophrenia. The tasks to be studied are: (1) oculomotor delayed response; (2) express saccades; (3) anti-saccades; all of which implicate frontal cortical functioning. In addition, we propose to continue our studies of ETD in an extended investigation of pursuit eye movements, including the use of unpredictable targets such as step-ramps; to quantify effect of tardive dyskinesia on pursuit, and to construct a quantitative algorithm that distinguishes normal from abnormal pursuit. The research also proposes a continued investigation of types of thought disorder among the relatives of schizophrenics and bipolar patients, and issues of the stability of thought disorder among relatives. uncovering such co-familial traits has the advantage of expanding the phenotype of schizophrenia, which both can enhance our understanding of the pathophysiology of schizophrenia and can increase the power of linkage analysis.
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