Visual hallucinations (VHs) occur frequently in advanced stages of Parkinson disease (PD). Which brain regions are affected in PD with VH is not well understood.
To characterize the pattern of affected brain regions in PD with VH and to determine whether functional changes in PD with VH occur preferentially in visual association areas, as is suggested by the complex clinical symptomatology.
Positron emission tomography measurements using fluorodeoxyglucose F 18. Between-group statistical analysis, accounting for the variance related to disease stage.
University hospital. Patients Eight patients with PD and VH and 11 patients with PD without VH were analyzed. The presence of VH during the month before positron emission tomography was rated using the Neuropsychiatric Inventory subscale for VH (PD and VH, 4.63; PD without VH, 0.00; P < .002).
Parkinson disease with VH, compared with PD without VH, was characterized by reduction in the regional cerebral metabolic rate for glucose consumption (P < .05, corrected for false discovery rate) in occipitotemporoparietal regions, sparing the occipital pole. No significant increase in regional glucose metabolism was detected in patients with PD and VH.
The pattern of resting-state metabolic changes in regions of the dorsal and ventral visual streams, but not in primary visual cortex, in patients with PD and VH, is compatible with the functional roles of visual association areas in higher-order visual processing. These findings may help to further elucidate the functional mechanisms underlying VH in PD.
"In this situation, frontal dopamine levels are expected to increase in response to dopaminergic treatment (ON state), possibly explaining why visual hallucinations are associated with relative frontal hypermetabolism . Nonetheless, visual hallucinations in PD are also linked to hypometabolism in occipitotemporoparietal regions . "
[Show abstract][Hide abstract] ABSTRACT: Cognitive impairment and behavioural disorders are often encountered in subjects with Parkinson's disease (PD). A simple PD-related frontostriatal cognitive dysfunction (PDFCD) staging is proposed. Executive dysfunction and mental fatigue (stage I), depression/anxiety (stage IIa), apathy/pain (stage IIb), and dementia (stage III) reflect a sequential process of dopamine depletion occurring in different regions of the striatum (stages I and II) and the frontal cortex (stage III). In addition to these nonmotor manifestations present in the unmedicated (OFF) state, the PDFCD model also predicts a number of complications related to dopaminergic treatment (ON state), from impulse control disorders (stages I and IIa) to hallucinations (stage IIb) and psychosis (stage III). Although the model admittedly needs further refinements, it provides a framework for hypothesis testing and may help clinicians optimize therapeutic strategies.
"Also using [123I] IMP SPECT scans, Matsui et al. found reduced perfusion in bilateral inferior parietal lobules, inferior temporal gyrus, precuneus gyrus, and occipital cortex in 31 PD patients with visual hallucinations, compared to 39 without hallucinations . Decreased metabolism in temporal-occipital-parietal regions was found in 8 PD hallucinators compared to 11 nonhallucinators with [18F] FDG-PET . Similar to some fMRI results which indicate disruptions in frontal and posterior activation patterns, Nagano-Saito et al. found greater regional cerebral glucose metabolic rates in frontal regions, especially the left superior frontal gyrus, in 8 nondemented, PD patients with visual hallucinations, compared to nonhallucinating PD and healthy controls, using [18F] FDG-PET . "
[Show abstract][Hide abstract] ABSTRACT: Psychosis is a frequent nonmotor complication in Parkinson's disease (PD), characterized by a broad phenomenology and likely due to a variety of intrinsic (i.e., PD-related) and extrinsic factors. Safe and effective therapies are greatly needed as PD psychosis contributes significantly to morbidity, mortality, nursing home placement, and quality of life. Novel research strategies focused on understanding the pharmacology and pathophysiology of PD psychosis, utilizing translational research including animal models, genetics, and neuroimaging, and even looking beyond the dopamine system may further therapeutic advances. This review discusses new research strategies regarding the neurobiology and treatment of PD psychosis and several associated challenges.
"Joint activations in the basal ganglia and frontal lobes might thus reflect an aspect of internal image generation in these patient groups. In patients with Parkinson's disease , schizophrenia and CBS, increased perfusion or activation of visual association cortices was seen during the occurrence of VHs (Silbersweig et al., 1995; Ffytche et al., 1998; Kataoka et al., 2008), while in other studies reduction of either activation, perfusion or metabolism in visual association cortices was seen during rest or simple visual stimulation (Okada et al., 1999; Stebbins et al., 2004; Matsui et al., 2006a; Boecker et al., 2007). In CBS, the latter probably reflects reduced visual cortical processing due to visual deprivation (Ffytche et al., 1998). "
[Show abstract][Hide abstract] ABSTRACT: 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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