Specific motion processing pathway deficit during eye tracking in schizophrenia: A performance-matched functional magnetic resonance imaging study

  title={Specific motion processing pathway deficit during eye tracking in schizophrenia: A performance-matched functional magnetic resonance imaging study},
  author={L. Elliot Hong and Malle A. Tagamets and Matthew T. Avila and Ikwunga Wonodi and Henry H. Holcomb and Gunvant K. Thaker},
  journal={Biological Psychiatry},

Response to unexpected target changes during sustained visual tracking in schizophrenic patients

Findings of superior performance by schizophrenic patients are interesting because they circumvent confounds of generalized deficits and provide further evidence of specific deficit in the predictive pursuit mechanism and over-reliance on retinal error signals to maintain pursuit in schizophrenia.

Diminished parietal cortex activity associated with poor motion direction discrimination performance in schizophrenia.

It is suggested that abnormalities in later stages of motion-processing mechanisms, perhaps beyond extrastriate cortex, may account for behavioral deviations among schizophrenia subjects.

Altered Velocity Processing in Schizophrenia during Pursuit Eye Tracking

Altered correlation of target velocity and neural activation in the cortical network supporting SPEM implies impaired transformation of the visual motion signal into an adequate motor command in patients.

Differential activation patterns of occipital and prefrontal cortices during motion processing: Evidence from normal and schizophrenic brains

In patients with schizophrenia, cortical activation was significantly reduced in MT and significantly increased in the inferior convexity of the prefrontal cortex, an area that is normally involved in higher level cognitive processing, evidence that in the context of broadly distributed cortical dysfunction, the usual functional specificity of the cortex becomes modified, even across the domains of sensory and cognitive processing.

Neural mechanisms of smooth pursuit eye movements in schizotypy

These posterior activation differences are compatible with evidence of motion processing deficits from the schizophrenia literature and, therefore, suggest overlap between schizotypy and schizophrenia both on cognitive‐perceptual and neurophysiological levels.

Eye tracking dysfunction in schizophrenia: characterization and pathophysiology.

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 ofThe pursuit pathway, including motion areas (the middle temporal area and the adjacent medial superior temporal area).

Visual and non-visual motion information processing during pursuit eye tracking in schizophrenia and bipolar disorder

Disturbances of eye movement control in psychotic disorders appear to be a consequence of deficits in sensorimotor transformation rather than a pure failure in adding cognitive contributions to pursuit drive in higher-order cortical circuits.



Neurobiology of smooth pursuit eye movement deficits in schizophrenia: an fMRI study.

The observed group differences are consistent with evidence for diminished inhibitory function in the hippocampus as well as for a disturbance in a frontotemporal network subserving smooth pursuit eye movements in schizophrenia.

Smooth pursuit eye movements to extraretinal motion signals: deficits in relatives of patients with schizophrenia.

These results suggest that relatives of patients with schizophrenia, particularly those with SSP, have specific deficits in predictive pursuit based on only extraretinal motion signals, which is likely due to compensation based on retinal motion information.

Neural correlates of eye tracking deficits in first-degree relatives of schizophrenic patients: a positron emission tomography study.

Subtle frontal dysfunction seems to be a pathophysiological substrate of ETD in relatives of schizophrenic patients, and may be one aspect of genetically mediated differences in brain function relevant to schizophrenia.

A model of smooth pursuit eye movement deficit associated with the schizophrenia phenotype.

It is suggested that schizophrenia SPEM deficits involve reduced ability to maintain or integrate extraretinal signals, and that retinal error may be used to compensate.

Functional anatomy of pursuit eye movements in humans as revealed by fMRI.

The current findings provide the first functional imaging evidence for a distinction between two parallel cortical systems that subserve pursuit and saccadic eye movements in humans.

Brain Activation during Smooth-Pursuit Eye Movements

Smooth-pursuit eye movements elicited activation consistently in dorsal cortical eye fields and cerebellum and session-dependent changes in activation were greater in some regions than others and may indicate areas of brain that are sensitive to attentional modulation of eye movements.

Effects of ketamine on leading saccades during smooth-pursuit eye movements may implicate cerebellar dysfunction in schizophrenia.

Results suggest that neurotransmission mediated by N-methyl-D-aspartate (NMDA) is involved in eye-tracking abnormalities, and evidence that the locus of this and other ketamine-induced smooth-pursuit eye-movement deficits involves NMDA receptor functioning in the cerebellum is suggested.

Saccades to moving targets in schizophrenia: evidence for normal posterior cortex functioning.

Results suggest that schizophrenia patients' smooth pursuit abnormalities are not associated with neuropathology of posterior cortical areas, and that the schizophrenia patients did not have general difficulty with motion perception.