“…It follows that the differences observed between groups in acuity and CS to HSFs are likely attributable to the sustained/parvocellular neural mechanism. The deficit in CS at LSFs in the patient group appears to reflect dysfunction in a distinct (e.g., transient/magnocellular) neural mechanism, and this conclusion supported by the rigorous application of PCA in the current study is consistent with other conclusions based on psychophysical (Green et al, 1994;Jahshan et al, 2017;Schechter et al, 2003), magnetic resonance imaging Martinez et al, 2008), and visual evoked potential (Butler et al, , 2007Martínez, Hillyard, et al, 2012;Schechter et al, 2005) evidence.…”
Section: Contrast Sensitivity In Schizophreniasupporting
Individuals with schizophrenia have problems with visual contrast processing. The current study investigated contrast sensitivity (CS) in schizophrenia/schizoaffective disorder to elucidate the underlying neural mechanisms affected by this disorder and to identify critical testing conditions that distinguish individuals with the disorder from healthy individuals. Principal component analysis was applied to the data (N = 143) to separate responses from distinct visual pathways. Participants were 68 patients and 75 age-similar controls. CS was obtained using a forced-choice psychophysical paradigm with grating patterns of low to high spatial frequency presented at short and long durations. Linear mixed-effects models were used to examine differences in log CS with respect to group, duration, and stimulus condition. Lower CSs were found in patients compared to controls over all stimulus conditions with the magnitude of deficits dependent on both spatial frequency and stimulus duration. Log CSs to low and high spatial frequencies loaded onto separate principal components, supporting the existence of two psychophysical mechanisms, transient and sustained. Critical conditions were identified to tap each mechanism. Visual acuity was correlated moderately with log CS to high, but not low, spatial frequencies, and deficits found for acuity and CS to moderate/high spatial frequencies (4-21 cycles/ degree) appear to reflect dysfunction in the sustained mechanism. CS deficits found at the lowest spatial frequency tested (0.5 cycles/degree) appear to reflect dysfunction in the transient mechanism. Both types of CS deficits may have diagnostic value and implications for social and neurocognitive deficits in this disorder.
“…It follows that the differences observed between groups in acuity and CS to HSFs are likely attributable to the sustained/parvocellular neural mechanism. The deficit in CS at LSFs in the patient group appears to reflect dysfunction in a distinct (e.g., transient/magnocellular) neural mechanism, and this conclusion supported by the rigorous application of PCA in the current study is consistent with other conclusions based on psychophysical (Green et al, 1994;Jahshan et al, 2017;Schechter et al, 2003), magnetic resonance imaging Martinez et al, 2008), and visual evoked potential (Butler et al, , 2007Martínez, Hillyard, et al, 2012;Schechter et al, 2005) evidence.…”
Section: Contrast Sensitivity In Schizophreniasupporting
Individuals with schizophrenia have problems with visual contrast processing. The current study investigated contrast sensitivity (CS) in schizophrenia/schizoaffective disorder to elucidate the underlying neural mechanisms affected by this disorder and to identify critical testing conditions that distinguish individuals with the disorder from healthy individuals. Principal component analysis was applied to the data (N = 143) to separate responses from distinct visual pathways. Participants were 68 patients and 75 age-similar controls. CS was obtained using a forced-choice psychophysical paradigm with grating patterns of low to high spatial frequency presented at short and long durations. Linear mixed-effects models were used to examine differences in log CS with respect to group, duration, and stimulus condition. Lower CSs were found in patients compared to controls over all stimulus conditions with the magnitude of deficits dependent on both spatial frequency and stimulus duration. Log CSs to low and high spatial frequencies loaded onto separate principal components, supporting the existence of two psychophysical mechanisms, transient and sustained. Critical conditions were identified to tap each mechanism. Visual acuity was correlated moderately with log CS to high, but not low, spatial frequencies, and deficits found for acuity and CS to moderate/high spatial frequencies (4-21 cycles/ degree) appear to reflect dysfunction in the sustained mechanism. CS deficits found at the lowest spatial frequency tested (0.5 cycles/degree) appear to reflect dysfunction in the transient mechanism. Both types of CS deficits may have diagnostic value and implications for social and neurocognitive deficits in this disorder.
“…As noted above, results usually suggest that patients with schizophrenia have decreased contrast sensitivity. This deficit is usually more marked when the stimuli are composed of low spatial frequencies ( Butler et al, 2001 ; Jahshan et al, 2017 ). However, studies exploring the perception of spatial frequencies in an incidental way found the opposite result.…”
Section: First Series Of Results: Low Spatial Frequency Processingmentioning
Decades ago, several authors have proposed that disorders in automatic processing lead to intrusive symptoms or abnormal contents in the consciousness of people with schizophrenia. However, since then, studies have mainly highlighted difficulties in patients’ conscious experiencing and processing but rarely explored how unconscious and conscious mechanisms may interact in producing this experience. We report three lines of research, focusing on the processing of spatial frequencies, unpleasant information, and time-event structure that suggest that impairments occur at both the unconscious and conscious level. We argue that focusing on unconscious, physiological and automatic processing of information in patients, while contrasting that processing with conscious processing, is a first required step before understanding how distortions or other impairments emerge at the conscious level. We then indicate that the phenomenological tradition of psychiatry supports a similar claim and provides a theoretical framework helping to understand the relationship between the impairments and clinical symptoms. We base our argument on the presence of disorders in the minimal self in patients with schizophrenia. The minimal self is tacit and non-verbal and refers to the sense of bodily presence. We argue this sense is shaped by unconscious processes, whose alteration may thus affect the feeling of being a unique individual. This justifies a focus on unconscious mechanisms and a distinction from those associated with consciousness.
“…In addition, RNFL thinning is related to the severity of visual hallucinations and functional decline in Parkinson's Disease (Lee et al 2014; Satue et al 2014). Because retinal ganglion cell axons form the optic nerve, leave the retina, and synapse at the lateral geniculate nucleus (LGN), where they provide segregated input to the subcortical magnocellular (M) and parvocellular (P) visual pathways, examination of retinal structure may be especially relevant to schizophrenia, where impairments in both pathways, but especially the M system, have often been reported (Butler et al 2008; Lalor et al 2012; Jahshan et al 2017). Fig.…”
Past reports of retinal thinning may be artifacts of medical comorbidity that is over-represented in schizophrenia, or other confounds. However, optic nerve head abnormalities may hold promise as biomarkers of central nervous system abnormality, including cognitive decline, in schizophrenia.
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