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, 175 (12), 1243-1254

Impaired Motion Processing in Schizophrenia and the Attenuated Psychosis Syndrome: Etiological and Clinical Implications


Impaired Motion Processing in Schizophrenia and the Attenuated Psychosis Syndrome: Etiological and Clinical Implications

Antígona Martínez et al. Am J Psychiatry.


Objective: The ability to perceive the motion of biological objects, such as faces, is a critical component of daily function and correlates with the ability to successfully navigate social situations (social cognition). Deficits in motion perception in schizophrenia were first demonstrated about 20 years ago but remain understudied, especially in the early, potentially prodromal, stages of the illness. The authors examined the neural bases of visual sensory processing impairments, including motion, in patients with schizophrenia (N=63) and attenuated psychosis (clinical high risk) (N=32) compared with age-matched healthy control subjects (N=67).

Method: Electrophysiological recordings during stimulus and motion processing were analyzed using oscillatory (time frequency) approaches that differentiated motion-onset-evoked activity from stimulus-onset sensory-evoked responses. These were compared with functional MRI (fMRI) measures of motion processing.

Results: Significant deficits in motion processing were observed across the two patient groups, and these deficits predicted impairments in both face-emotion recognition and cognitive function. In contrast to motion processing, sensory-evoked stimulus-onset responses were intact in patients with attenuated psychosis, and, further, the relative deficit in motion-onset responses compared with stimulus-onset responses predicted transition to schizophrenia. In patients with schizophrenia, motion detection deficits mapped to impaired activation in motion-sensitive visual cortex during fMRI. Additional visual impairments in patients with schizophrenia, not present in patients with attenuated psychosis, implicated other visual regions, including the middle occipital gyrus and pulvinar thalamic nucleus.

Conclusions: The study findings emphasize the importance of sensory-level visual dysfunction in the etiology of schizophrenia and in the personal experience of individuals with the disorder and demonstrate that motion-processing deficits may predate illness onset and contribute to impaired function even in patients with attenuated psychosis.

Keywords: Electroencephalography; Neurophysiology; Prodrome; Schizophrenia; Visual Processing.


Figure 1:
Figure 1:. Behavioral, EEG and fMRI paradigms
A. Behavioral motion-discrimination task. On each trial, a proportion of dots moved coherently (left/right) for 1000ms. Following, participants were cued to indicate the direction of coherent motion. B. Stimulus sequence for EEG task. Each trial began with presentation of one of three stimuli which remained static for 400 ms, drifted rightward (14°/s) for 200ms then (after an 800ms delay), counterphase reversed at a rate of 10 Hz for 3000ms, thereby generating an ssVEP. Each subject took part in 420 trials. C. fMRI paradigm. Low-contrast concentric rings presented at fixation alternated between stationary and moving (expanding/contracting) in twenty-second epochs.
Figure 2:
Figure 2:. Behavioral and EEG responses by group
A. Evoked power to stimulus and motion onset. Time-frequency plots (average across stimuli) for healthy (older) controls (HC), schizophrenia patients (SZ), younger control (YC) and attenuated psychosis (APS) subjects. Latency/frequency testing intervals for delta (1–4Hz) and theta (4–7Hz) are indicated by solid and dashed rectangles, respectively. Mean delta/theta power for each group is shown in bar plots. (***p<.00; **p<.01; *p<.05) B. ssVEP responses. Tracings of group-averaged FFT power derived from ssVEP, collapsed across stimulus types. C. Motion Sensitivity. Motion sensitivity measures for each group and its correlation with delta power and face emotion recognition (ER40) scores across clinical (SZ/APS) subjects.
Figure 3:
Figure 3:. fMRI measures of motion perception
A. MT+ activation. ROIs in middle temporal cortex corresponding to MT+ ( RH is on the right) and bar graphs are of mean activation (beta parameter) elicited by the contrast of moving vs. static across hemispheres in SZ and HC groups. Reduced MT+ activation correlated with diminished delta power (low SF low contrast stimuli) to motion onset (scatterplot on right). B. MOG activation. Mean activation of MOG (LH) and correlation with diminished mean theta power in response to stimulus onset. C. Pulvinar activation. Mean pulvinar (RH) activation and correlation with ssVEP power at 10Hz.
Figure 4:
Figure 4:. Correlation of delta power with neurocognitive measures and measure of transition
A. Correlation of delta power to MATRICS. Across clinical groups (SZ, APS) higher delta evoked power to the magnocellular-biased low SF, low contrast stimulus correlated with higher scores (better performance) on the overall (left) and Visual Learning (right) domains of the MATRICS MCCB. Correlation values and regression lines shown are across all subjects. Within-group correlations were: Overall score-SZ: r=.336, p=.015, APS: r=.476,p=.053; Visual Learning-SZ: r=.341,p=.014, APS: r=.542, p=.025. B. delta/theta ratio in APS subjects. Bar plots of the ratio of delta to theta evoked power to low SF, low contrast stimuli for APS subjects who transitioned to schizophrenia (outlined bar) and those who did not.

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