On visual hallucinations and cortical networks: a trans-diagnostic review

Carter, Rowena; ffytche, Dominic H.

doi:10.1007/s00415-015-7687-6

Cited by 46 publications

(35 citation statements)

References 51 publications

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“…This literature points to cortical abnormalities in PDP, such as reduced gray matter volume in the hippocampus and in frontal, parietal, and occipital cortices (6), and to the presence of Lewy bodies in frontal, cingulate, temporal, and occipital cortices on postmortem examination (9). Psychotic symptoms in PD are often comorbid with dementia and, in some cases, may presage incipient dementia (82).…”

Section: Discussionmentioning

confidence: 99%

Cortical and Striatal Reward Processing in Parkinson’s Disease Psychosis

et al. 2017

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Psychotic symptoms frequently occur in Parkinson’s disease (PD), but their pathophysiology is poorly understood. According to the National Institute of Health RDoc programme, the pathophysiological basis of neuropsychiatric symptoms may be better understood in terms of dysfunction of underlying domains of neurocognition in a trans-diagnostic fashion. Abnormal cortico-striatal reward processing has been proposed as a key domain contributing to the pathogenesis of psychotic symptoms in schizophrenia. This theory has received empirical support in the study of schizophrenia spectrum disorders and preclinical models of psychosis, but has not been tested in the psychosis associated with PD. We, therefore, investigated brain responses associated with reward expectation and prediction error signaling during reinforcement learning in PD-associated psychosis. An instrumental learning task with monetary gains and losses was conducted during an fMRI study in PD patients with (n = 12), or without (n = 17), a history of psychotic symptoms, along with a sample of healthy controls (n = 24). We conducted region of interest analyses in the ventral striatum (VS), ventromedial prefrontal and posterior cingulate cortices, and whole-brain analyses. There was reduced activation in PD patients with a history of psychosis, compared to those without, in the posterior cingulate cortex and the VS during reward anticipation (p < 0.05 small volume corrected). The results suggest that cortical and striatal abnormalities in reward processing, a putative pathophysiological mechanism of psychosis in schizophrenia, may also contribute to the pathogenesis of psychotic symptoms in PD. The finding of posterior cingulate dysfunction is in keeping with prior results highlighting cortical dysfunction in the pathogenesis of PD psychosis.

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Section: Discussionmentioning

confidence: 99%

Cortical and Striatal Reward Processing in Parkinson’s Disease Psychosis

et al. 2017

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“…Despite methodological differences, structural imaging studies of visual hallucinations have yielded a number of consistent findings 98–100 . Several studies have reported atrophy in the visual cortex 101–103 — broadly defined as extending into lateral and ventral occipitotemporal regions including the fusiform gyrus and visual parietal cortex (corresponding to dorsal and ventral visual streams) — although this finding is not univeral 104 .…”

Section: Imaging and Electrophysiologymentioning

confidence: 99%

The psychosis spectrum in Parkinson disease

et al. 2017

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In 2007, the clinical and research profile of illusions, hallucinations, delusions and related symptoms in Parkinson disease (PD) was raised with the publication of a consensus definition of PD psychosis. Symptoms that were previously deemed benign and clinically insignificant were incorporated into a continuum of severity, leading to the rapid expansion of literature focusing on clinical aspects, mechanisms and treatment. Here, we review this literature and the evolving view of PD psychosis. Key topics include the prospective risk of dementia in individuals with PD psychosis, and the causal and modifying effects of PD medication. We discuss recent developments, including recognition of an increase in the prevalence of psychosis with disease duration, addition of new visual symptoms to the psychosis continuum, and identification of frontal executive, visual perceptual and memory dysfunction at different disease stages. In addition, we highlight novel risk factors — for example, autonomic dysfunction — that have emerged from prospective studies, structural MRI evidence of frontal, parietal, occipital and hippocampal involvement, and approval of pimavanserin for the treatment of PD psychosis. The accumulating evidence raises novel questions and directions for future research to explore the clinical management and biomarker potential of PD psychosis.

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“…The lack of prominent deficits in other cognitive domains may reflect the small number of patients with formed hallucinations and differences in tests used in PPMI compared with previous studies of visual hallucinations. The deficits of visual and cognitive function in PD patients with visual hallucinations are thought to relate to volume loss in frontal, parietal, limbic, occipital and hippocampal cortex (see refs [32][33][34] for recent reviews). Here, we found evidence for these structural changes in patients with de novo PD who go on to develop formed hallucinations.…”

Section: Cognition Cortical Changes and Visual Hallucinationsmentioning

confidence: 99%

Risk factors for early psychosis in PD: insights from the Parkinson's Progression Markers Initiative

ffytche

Pereira

Ballard

et al. 2017

J Neurol Neurosurg Psychiatry

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Parkinson's Disease (PD) psychosis refers to the spectrum of illusions, formed hallucinations and delusions that occur in PD. Visual hallucinations and illusions are thought to be caused by specific cognitive and higher visual function deficits and patients who develop such symptoms early in the disease course have greater rates of cognitive decline and progression to dementia. To date, no studies have investigated whether such deficits are found prior to the onset of PD psychosis. Here we compare baseline cognitive, biomarker (structural imaging and cerebrospinal fluid) and other PD psychosis risk factor data in patients who go on to develop illusions or hallucinations within 3-4 years of follow-up in the Parkinson's Progression Markers Initiative cohort of newly diagnosed PD. Of n=423 patients with PD, n=115 (27%) reported predominantly illusions with median onset at 19.5 months follow-up. At study entry these patients had reduced CSF amyloid Aß1-42, lower olfaction scores, higher depression scores and increased REM sleep behaviour disorder symptoms compared to patients without early onset PD psychosis but no differences in cognitive, higher visual or structural imaging measures. A subset of patients with early onset formed hallucinations (n=21) had reduced higher visual function at baseline, cortical thinning in parietal, occipital and frontal cortex and reduced hippocampal volume. The findings suggest early onset illusions and formed hallucinations are linked to amyloid pathology in PD and point to a difference in the underlying pathophysiological mechanism of illusions and formed hallucinations, with implications for their respective links to future cognitive decline.

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On visual hallucinations and cortical networks: a trans-diagnostic review

Cited by 46 publications

References 51 publications

Cortical and Striatal Reward Processing in Parkinson’s Disease Psychosis

Cortical and Striatal Reward Processing in Parkinson’s Disease Psychosis

The psychosis spectrum in Parkinson disease

Risk factors for early psychosis in PD: insights from the Parkinson's Progression Markers Initiative

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