Altered early visual processing components in hallucination-prone individuals
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Of the nonpathological general population, 0.5% experience one or more visual hallucinations on a regular basis without meeting the criteria for clinical psychosis. We investigated the relationship between a proneness to visual hallucinations in 'normal' individuals and early visual event-related potentials during the perception of faces, Mooney faces and scrambled Mooney faces. Findings indicated that individuals prone to visual hallucinations displayed significantly reduced early event-related potential components (P1, P2, but not N170) over parieto-temporal regions. These findings support previous suggestions that individuals who experience visual hallucinations exhibit abnormal early visual processing resulting from degraded visual input, in this case owing to disruption of low level visual processes.Keywords:
Visual processing
Visual hallucinations are a common, distressing, and disabling symptom of Lewy body and other diseases. Current models suggest that interactions in internal cognitive processes generate hallucinations. However, these neglect external factors. Pareidolic illusions are an experimental analogue of hallucinations. They are easily induced in Lewy body disease, have similar content to spontaneous hallucinations, and respond to cholinesterase inhibitors in the same way. We used a primed pareidolia task with hallucinating participants with Lewy body disorders (n = 16), non-hallucinating participants with Lewy body disorders (n = 19), and healthy controls (n = 20). Participants were presented with visual "noise" that sometimes contained degraded visual objects and were required to indicate what they saw. Some perceptions were cued in advance by a visual prime. Results showed that hallucinating participants were impaired in discerning visual signals from noise, with a relaxed criterion threshold for perception compared to both other groups. After the presentation of a visual prime, the criterion was comparable to the other groups. The results suggest that participants with hallucinations compensate for perceptual deficits by relaxing perceptual criteria, at a cost of seeing things that are not there, and that visual cues regularize perception. This latter finding may provide a mechanism for understanding the interaction between environments and hallucinations.
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Introduction Visual hallucinations are often considered to be suggestive of a secondary cause of psychosis, however, this association has never been assessed meta-analytically. We aimed to compare the presence of visual hallucinations in patients with psychosis due to a primary or secondary cause.
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Of the nonpathological general population, 0.5% experience one or more visual hallucinations on a regular basis without meeting the criteria for clinical psychosis. We investigated the relationship between a proneness to visual hallucinations in 'normal' individuals and early visual event-related potentials during the perception of faces, Mooney faces and scrambled Mooney faces. Findings indicated that individuals prone to visual hallucinations displayed significantly reduced early event-related potential components (P1, P2, but not N170) over parieto-temporal regions. These findings support previous suggestions that individuals who experience visual hallucinations exhibit abnormal early visual processing resulting from degraded visual input, in this case owing to disruption of low level visual processes.
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Exploring Bottom-Up Visual Processing and Visual Hallucinations in Parkinson's Disease With Dementia
Visual hallucinations (VH) are a common symptom of Parkinson's disease with dementia (PDD), affecting up to 65% of cases. Integrative models of their etiology posit that a decline in executive control of the visuo-perceptual system is a primary mechanism of VH generation. The role of bottom-up processing in the manifestation of VH in this condition is still not clear although visual evoked potential (VEP) differences have been associated with VH at an earlier stage of PD. Here we compared the amplitude and latency pattern reversal VEPs in healthy controls (n = 21) and PDD patients (n = 34) with a range of VH severities. PDD patients showed increased N2 latency relative to controls, but no significant differences in VEP measures were found for patients reporting complex VH (CVH) (n = 17) compared to those without VH. Our VEP findings support previous reports of declining visual system physiology in PDD and some evidence of visual system differences between patients with and without VH. However, we did not replicate previous findings of a major relationship s between the integrity of the visual pathway and VH.
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Impaired visual processing may play a role in the pathophysiology of visual hallucinations in Parkinson's disease. In order to study involved neuronal circuitry, we assessed cerebral activation patterns both before and during recognition of gradually revealed images in Parkinson's disease patients with visual hallucinations (PDwithVHs), Parkinson's disease patients without visual hallucinations (PDnonVHs) and healthy controls. We hypothesized that, before image recognition, PDwithVHs would show reduced bottom-up visual activation in occipital-temporal areas and increased (pre)frontal activation, reflecting increased top-down demand. Overshoot of the latter has been proposed to play a role in generating visual hallucinations. Nine non-demented PDwithVHs, 14 PDnonVHs and 13 healthy controls were scanned on a 3 Tesla magnetic resonance imaging scanner. Static images of animals and objects gradually appearing out of random visual noise were used in an event-related design paradigm. Analyses were time-locked on the moment of image recognition, indicated by the subjects' button-press. Subjects were asked to press an additional button on a colour-changing fixation dot, to keep attention and motor action constant and to assess reaction times. Data pre-processing and statistical analysis were performed with statistical parametric mapping-5 software. Bilateral activation of the fusiform and lingual gyri was seen during image recognition in all groups (P < 0.001). Several seconds before image recognition, PDwithVHs showed reduced activation of the lateral occipital cortex, compared with both PDnonVHs and healthy controls. In addition, reduced activation of extrastriate temporal visual cortices was seen just before image recognition in PDwithVHs. The association between increased vulnerability for visual hallucinations in Parkinson's disease and impaired visual object processing in occipital and temporal extrastriate visual cortices supported the hypothesis of impaired bottom-up visual processing in PDwithVHs. Support for the hypothesized increased top-down frontal activation was not obtained. The finding of activation reductions in ventral/lateral visual association cortices in PDwithVHs before image recognition further helps to explain functional mechanisms underlying visual hallucinations in Parkinson's disease.
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Psychosis has been associated with neural anomalies across a number of brain regions and cortical networks. Nevertheless, the exact pathophysiology of the disorder remains unclear. Aberrant visual perceptions such as hallucinations are evident in psychosis, while the occurrence of visual distortions is elevated in individuals with genetic liability for psychosis. The overall goals of this project are to: (1) use psychophysical tasks and neuroimaging to characterize deficits in visual perception; (2) acquire a mechanistic understanding of these deficits through development and validation of a computational model; and (3) determine if said mechanisms mark genetic liability for psychosis. Visual tasks tapping both low- and high-level visual processing are being completed as individuals with psychotic disorders (IPD), first-degree biological siblings of IPDs (SibIPDs) and healthy controls (HCs) undergo 248-channel magneto-encephalography (MEG) recordings followed by 7 Tesla functional magnetic resonance imaging (MRI). By deriving cortical source signals from MEG and MRI data, we will characterize the timing, location and coordination of neural processes. We hypothesize that IPDs prone to visual hallucinations will exhibit deviant functions within early visual cortex, and that aberrant contextual influences on visual perception will involve higher-level visual cortical regions and be associated with visual hallucinations. SibIPDs who experience visual distortionsâbut not hallucinationsâare hypothesized to exhibit deficits in higher-order visual processing reflected in abnormal inter-regional neural synchronization. We hope the results lead to the development of targeted interventions for psychotic disorders, as well as identify useful biomarkers for aberrant neural functions that give rise to psychosis.
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