Structural and functional neuroimaging in patients with Parkinson's disease and visual hallucinations: A critical review

Lenka, Abhishek; Jhunjhunwala, Ketan; Saini, Jitender; Pal, Pramod Kumar

doi:10.1016/j.parkreldis.2015.04.005

Cited by 88 publications

(65 citation statements)

References 50 publications

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“…A recent case study reported an individual who began having complex visual hallucinations following a stroke that selectively damaged left hemisphere medial VTC (Tombini et al, 2012). Furthermore, structural and functional studies in individuals with Parkinson's disease with visual hallucinations show that the VTC, including medial fusiform, is abnormal (Goldman et al, 2014; Lenka, Jhunjhunwala, Saini, & Pal, 2015; Watanabe et al, 2013). It is notable that in these examples, as well as the results of the current report, the individuals are usually aware that their visual hallucinations are not real.…”

Section: Discussionmentioning

confidence: 99%

Associative hallucinations result from stimulating left ventromedial temporal cortex

Aminoff

Pyles

et al. 2016

Cortex

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Visual recognition requires connecting perceptual information with contextual information and existing knowledge. The ventromedial temporal cortex (VTC), including the medial fusiform, has been linked with object recognition, paired associate learning, contextual processing, and episodic memory, suggesting that this area may be critical in connecting visual processing, context, knowledge and experience. However, evidence for the link between associative processing, episodic memory, and visual recognition in VTC is currently lacking. Using electrocorticography in a single human patient, medial regions of the left VTC were found to be sensitive to the contextual associations of objects. Electrical brain stimulation of this part of the left VTC of the patient, functionally defined as sensitive to associative processing, caused memory related, associative visual hallucinations. This provides evidence of a relationship between visual recognition, associative processing, and episodic memory. These results suggest a potential role for abnormalities of these processes as part of a mechanism that gives rise to some visual hallucinations.

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Section: Discussionmentioning

confidence: 99%

Associative hallucinations result from stimulating left ventromedial temporal cortex

Aminoff

Pyles

et al. 2016

Cortex

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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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“…Three other PD co-morbid syndromes that have been the focus of recent reviews are visual hallucinations (Lenka et al., 2015), impulse control disorders (Jimenez-Urbieta et al, 2015; Vriend et al, 2014a), and dyskinesias (Jimenez-Urbieta et al, 2015). Note that Vriend et al (2014a) reviewed both depression and impulse control disorders in PD, while Jimenez-Urbieta et al (2015) reviewed both impulse control disorders and levodopa induced dyskinesias, as disorders with related neurobiological mechanisms.…”

Section: Neuroimaging Of Pdmentioning

confidence: 99%

Neuroimaging of Parkinson's disease: Expanding views

Weingarten

Sundman

Hickey

et al. 2015

Neuroscience & Biobehavioral Reviews

136

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Advances in molecular and structural and functional neuroimaging are rapidly expanding the complexity of neurobiological understanding of Parkinson’s disease (PD). This review article begins with an introduction to PD neurobiology as a foundation for interpreting neuroimaging findings that may further lead to more integrated and comprehensive understanding of PD. Diverse areas of PD neuroimaging are then reviewed and summarized, including positron emission tomography, single photon emission computed tomography, magnetic resonance spectroscopy and imaging, transcranial sonography, magnetoencephalography, and multimodal imaging, with focus on human studies published over the last five years. These included studies on differential diagnosis, co-morbidity, genetic and prodromal PD, and treatments from L-DOPA to brain stimulation approaches, transplantation and gene therapies. Overall, neuroimaging has shown that PD is a neurodegenerative disorder involving many neurotransmitters, brain regions, structural and functional connections, and neurocognitive systems. A broad neurobiological understanding of PD will be essential for translational efforts to develop better treatments and preventive strategies. Many questions remain and we conclude with some suggestions for future directions of neuroimaging of PD.

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Structural and functional neuroimaging in patients with Parkinson's disease and visual hallucinations: A critical review

Cited by 88 publications

References 50 publications

Associative hallucinations result from stimulating left ventromedial temporal cortex

Associative hallucinations result from stimulating left ventromedial temporal cortex

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

Neuroimaging of Parkinson's disease: Expanding views

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