“…In addition, a number of recent studies have highlighted pathological impairments in the visual system of individuals with hallucinations, both in the retina [27] and dorsal visual stream [21,22], suggesting that hallucinations are due to a combination of impaired visual input with concomitant exogenous attentional dysfunction [3,28]. This accords with recent investigations into pareidolia-visual misperceptions closely related to hallucinations [29]-which are similarly mediated by topdown attentional control mechanisms [30,31]. This is an exciting avenue for future research, which should seek to determine whether unprovoked hallucinations occur due to a top-down priming from ventral temporal structures or to emergent activity within primary visual cortex.…”
Visual hallucinations occur when our conscious experience does not accurately reflect external reality. However, these dissociations also regularly occur when we imagine the world around us in the absence of visual stimulation. We used two novel behavioural paradigms to objectively measure visual hallucinations and voluntary mental imagery in 19 individuals with Parkinson's disease (ten with visual hallucinations; nine without) and ten healthy, age-matched controls. We then used this behavioural overlap to interrogate the connectivity both within and between the major attentional control networks using restingstate functional magnetic resonance imaging. Patients with visual hallucinations had elevated mental imagery strength compared with patients without hallucinations and controls. Specifically, the sensory strength of imagery predicted the frequency of visual hallucinations. Together, hallucinations and mental imagery predicted multiple abnormalities in functional connectivity both within and between the attentional control networks, as measured with resting-state functional magnetic resonance imaging. However, the two phenomena were also dissociable at the neural level, with both mental imagery and visual misperceptions associated with specific abnormalities in attentional network connectivity. Our results provide the first evidence of both the shared and unique neural correlates of these two similar, yet distinct phenomena.
“…In addition, a number of recent studies have highlighted pathological impairments in the visual system of individuals with hallucinations, both in the retina [27] and dorsal visual stream [21,22], suggesting that hallucinations are due to a combination of impaired visual input with concomitant exogenous attentional dysfunction [3,28]. This accords with recent investigations into pareidolia-visual misperceptions closely related to hallucinations [29]-which are similarly mediated by topdown attentional control mechanisms [30,31]. This is an exciting avenue for future research, which should seek to determine whether unprovoked hallucinations occur due to a top-down priming from ventral temporal structures or to emergent activity within primary visual cortex.…”
Visual hallucinations occur when our conscious experience does not accurately reflect external reality. However, these dissociations also regularly occur when we imagine the world around us in the absence of visual stimulation. We used two novel behavioural paradigms to objectively measure visual hallucinations and voluntary mental imagery in 19 individuals with Parkinson's disease (ten with visual hallucinations; nine without) and ten healthy, age-matched controls. We then used this behavioural overlap to interrogate the connectivity both within and between the major attentional control networks using restingstate functional magnetic resonance imaging. Patients with visual hallucinations had elevated mental imagery strength compared with patients without hallucinations and controls. Specifically, the sensory strength of imagery predicted the frequency of visual hallucinations. Together, hallucinations and mental imagery predicted multiple abnormalities in functional connectivity both within and between the attentional control networks, as measured with resting-state functional magnetic resonance imaging. However, the two phenomena were also dissociable at the neural level, with both mental imagery and visual misperceptions associated with specific abnormalities in attentional network connectivity. Our results provide the first evidence of both the shared and unique neural correlates of these two similar, yet distinct phenomena.
“…The current study aimed to extend the findings of Straughan et al (2016) and Yokoi et al (2014) by assessing differences between patients with and without hallucinations and by adding associative priming to experimentally examine the effects of environmental factors.…”
Section: Introductionmentioning
confidence: 94%
“…Studies have demonstrated considerable overlap in the phenomenology of pareidolia and visual hallucinations (Uchiyama, Nishio, Yokoi, Hosokai, Takeda et al, 2015). Moreover, hallucination severity is positively correlated with experimental pareidolia frequency and both respond to cholinesterase inhibitors (Yokoi, Nishio, Uchiyama, Shimomura, Iizuka et al, 2014). Uchiyama et al (2012) found that the number of illusory perceptions in pareidolia images was able to discriminate between participants with dementia with Lewy bodies and Alzheimer’s disease with 100% sensitivity and a specificity of 88%.Fig.…”
Section: Introductionmentioning
confidence: 99%
“…Yokoi et al (2014) applied signal detection theory to their pareidolia test by varying the absence/presence of real visual objects among ambiguous visual noise. They demonstrated that, compared with participants with Alzheimer’s disease, participants with dementia with Lewy bodies had significantly reduced ability to discriminate visual “signal” from “noise,” and were more prone to report the presence of a visual object when one was not present.…”
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.Electronic supplementary materialThe online version of this article (doi:10.1186/s41235-017-0063-6) contains supplementary material, which is available to authorized users.
“…Cholinergic insufficiency has been suggested to be the common neural background (23). In non-demented PD, pareidolia was reported in all patients with visual hallucinations, and in part of those without (24).…”
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