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Abstract Purpose: Accumulating evidence suggests that sympathetic noradrenergic system degeneration is associated with the pathophysiology of minor hallucination in patients with Parkinson’s disease (PD). We aimed to elucidate the relationship between visual illusion and the extent and type of cardiovascular sympathetic failure in patients with PD. Methods: The subjects were 133 patients with PD without well-structured visual hallucinations. Visual illusory responses were evaluated using the noise pareidolia test. Cardiac 123I-metaiodobenzylguanidine uptake and neurogenic orthostatic hypotension (nOH) and supine hypertension (nSH) on head-up tilt-table testing were examined in association with the number of illusory responses. Results: Fifty-one (38%) patients had illusory responses. nOH (β = 0.220, p = 0.008), cognitive impairment (β = −0.228, p = 0.028), and longer symptom duration (β = 0.273, p = 0.006) were associated with greater numbers of illusory responses independently of age, sex, motor severity, levodopa equivalent dose, and anticholinergic and cholinesterase inhibitor use; nSH and peripheral sympathetic degeneration reflected by low cardiac 123I-metaiodobenzylguanidine uptake were not. Although nSH and peripheral sympathetic degeneration had no effects on the association between the number of illusory responses and nOH, patients with severe nOH had significantly more illusory responses than those with mild nOH (p = 0.048). Conclusion: nOH was associated with the severity of visual illusion in early PD patients without well-structured visual hallucinations, whereas nSH and peripheral sympathetic degeneration were not. These findings deepen our knowledge of the role of sympathetic noradrenergic degeneration in minor hallucinations and may have prognostic implications in patients with early PD.
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