Ksenija Maravic "Neuropsychology of Visual Hallucinations in Parkinson's Disease"

Idiopathic Parkinson’s disease (PD) is the second most common neurodegenerative disease after Alzheimer’s disease (Schapira 2004). Although the early dominant motor features of PD are related to dopaminergic cell death in the substantia nigra, there are additional foci of neurodegeneration which also begin at an early stage and progress (Schapira 2004). Non-dopaminergic and non-motor symptoms are sometimes present before diagnosis and almost inevitably emerge with disease progression (Chaudhuri, Healy et al. 2006). These include cognitive disturbance (such as executive, visuospatial, attentional, and memory dysfunctions), depression, gait disturbance, autonomic abnormalities (Schapira 2004), neuropsychiatric symptoms (Bodis-Wollner 2003; Chaudhuri, Healy et al. 2006), sleep disorders, gastrointestinal symptoms, sensory symptoms and other symptoms like fatigue, diplopia, blurred vision and weight loss or gain (Chaudhuri, Healy et al. 2006). Indeed, non-motor symptoms dominate the clinical picture of advanced PD and contribute to severe disability, impaired quality of life, and shortened life expectancy (Chaudhuri, Martinez-Martin et al. 2006).

Visual hallucinations (VHs) are one of the most common psychiatric manifestations in PD. Between 8% and 40% of patients with PD will have VHs during the course of their illness (Barnes and David 2001). Multiple risk factors for PD-related VHs have been identified, including cognitive, affective, medication, sensory, and even personality and environmental factors (Aarsland, Andersen et al. 2003; Barnes, Boubert et al. 2003; Schapira 2004; Chaudhuri, Healy et al. 2006), but their role mainly remains controversial.

The two main objectives of the current study are:
(a) to provide a detailed phenomenological analysis of the hallucinations in PD patients and their behavioural coping strategies and
(b) to compare the neuropsychological results of three groups: PD with hallucinations, PD without VHs and an age-matched control group. All patients were controlled for some suggested predisposing factors such as length of illness, age, medication dosage and cognitive decline.

Three main neuropsychological questions will be addressed:
(1)    What is the contribution of the frontal-striatal circuit in the experience of VHs, in particular the role of visual memory and executive functions (as measured by the neuropsychological tests from Cambridge Cognition – CANTAB);
(2)    What is the role of sleep and arousal in the hallucinatory experience (using an objective measure of sleep via actigraphy, in combination with subjective sleep questionnaires);
(3)    How do personality and metacognitive factors contribute to the experience of VHs (as measured by the 16PF and other measures of metacognition, depression and creative experiences).

Results and the following implications will be discussed:
(1)    Can fronto-striatal cognitive deficits have a causal role in the generation of VHs?
(2)    In PD patients with VHs sleep disturbances may shape perceptual organisation and determine the content of the perceptual experience. Specific sleep patterns will be discussed in relation to VHs.
(3)    Is the vulnerability to visually hallucinate accompanied by a relationship between certain metacognitive and other personality factors?

The current research is valuable for understanding the phenomenology of visual experiences in PD populations as well as in healthy general population. Some evidence of similar neuropsychological measures from both PD and healthy general population will be briefly presented. The results correspond with the continuum hypothesis, stating that hallucinations exist on a continuum ranging from very mild expressions in the normal population to the bizarre symptoms characteristic of severe mental illness (Bentall 1990). Aside from the basic scientific interest, the issue of VH has important implications for the phenomenology, analysis, remediation and future applications of brain damage in PD and other neurological disorders.

The studies were supported by the British Academy grant.


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