Non-motor symptoms (NMS) in Parkinson’s disease (PD) have gained relevance in recent years due to their impact on patient quality of life and their contribution to institutionalisation at an advanced disease stage.^1,2 NMS are present at disease onset and some, such as psychiatric and sleep disorders, may even precede motor symptoms.^3,4 The pathophysiology of NMS is still poorly understood – dysfunction of both dopaminergic and non-dopaminergic systems contribute to their development.

NMS include cognitive and psychiatric dysfunction, disorders of mood and affect, sensory dysfunction, sleep disturbances and various symptoms of autonomic dysfunction (see Table 1). Dopaminergic therapy can induce non-motor side effects such as orthostatic hypotension, hallucinations, somnolence and insomnia.⁵ Braak and colleagues6 suggested that degeneration in nuclei involving non-motor domains, primarily the lower brainstem and olfactory systems, may occur before pathology begins in th dopamine nigro-striatal system. This hypothesis has inspired studies to determine whether olfactory changes and changes in sleep patterns may serve, in the future, as pre-clinical markers for PD. While the Braak hypothesis is intriguing in terms of our understanding of the pathological course of PD, NMS remain a major factor in determining quality of life, progression of disability and nursing home placement.

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