Abstract

This chapter focuses on nonmotor symptoms (NMS), which are considered to be an intrinsic part of the PD process, including smell disturbances, dysautonomia, pain and other sensory symptoms, sleep disturbances, and fatigue. Some less common or disabling NMS such as seborrheic dermatitis or hyperhidrosis, and particularly NMS mostly related to treatment such as skin erosions or skin nodules associated with deep brain stimulation or apomorphine, are presented. Some NMS antedate the classic motor signs of PD, and investigations are presented to define the characteristics of this nonmotor and premotor phase of PD. Most NMS are caused by lesions in the brain involving nondopaminergic structures. Another cause of NMS in PD is drug treatment. Examples of such nondopaminergic NMS—such as dementia, fatigue, smell loss, constipation, and rapid-eye-movement (REM) sleep behavior disorder (RBD)—are discussed. Numerous medications can produce or potentiate PD-related NMS. Examples of NMS induced or aggravated by medications in PD are orthostatic hypotension, hallucinations, excessive daytime sleepiness (EDS), leg edema associated with dopaminergic treatment, and memory problems associated with anticholinergics. Most NMS are thought not to be primarily dopaminergic, but they may be influenced by dopaminergic drugs. Examples of such nonmotor nondopaminergic symptoms that may respond in part to dopaminergic drugs—such as insomnia and other nocturnal problems, urinary urgency, and depression and in general NMS occurring during “off” states—are discussed. Several NMS occur in the premotor phase of PD. The study of symptoms—such as smell loss, constipation, and RBD in the premotor phase—provides important information on where and when PD will start and may allow the use of drugs with potential disease-modifying properties in the earliest stages of disease development.

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