Parkinson disease (PD) is a chronic, progressive neurodegenerative disorder that affects approximately 10 million people worldwide, making it the second most common neurologic disorder after Alzheimer disease.1 The primary pathologies of PD involve neuronal cell inclusions (Lewy bodies) and accumulation of the protein α-synuclein within the basal ganglia (Figure).1 These pathologies lead to degradation of dopaminergic neurons and dopamine depletion in the basal ganglia.2 Further depletion of dopamine, serotonin, and acetylcholine leads to both motor and nonmotor disturbances in PD.1,2

The traditional clinical assessment of PD is focused on the symptoms of motor dysfunction. The 4 cardinal motor symptoms (resting tremor, bradykinesia, rigidity, and postural instability) have been used for decades to support a clinical diagnosis of PD.3 However, PD now is recognized as a complex, diverse neurologic disorder, involving both motor and nonmotor manifestations.3,4 In fact, the nonmotor symptoms of PD often are more disabling and difficult to diagnose and treat in both primary and specialty care settings.3

Nonmotor symptoms of PD include neuropsychiatric dysfunction (depression, anxiety, psychosis, dementia), autonomic dysfunction (orthostatic hypotension, gastrointestinal disorders, sexual dysfunction), sleep disorders, and sensory disturbances of pain and olfaction.3 Nearly all patients with PD will develop nonmotor symptoms, with sensory, sleep, and neuropsychiatric dysfunction being the most frequent and disabling symptoms.3

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Severe neuropsychiatric dysfunction, including psychosis and dementia, is associated with more advanced PD. Neuropsychiatric disorders are associated with more extensive deposition of Lewy bodies and resulting pathologic changes in cortical processing pathways.5 

Parkinson Disease Psychosis

Unlike the prototypical motor symptoms of PD, Parkinson disease psychosis (PDP) can be diagnostically challenging and underreported.3,4,6 However, psychosis has been identified in up to 50% of patients with PD with or without dementia.7 PDP affects both the patient and those involved in the patient’s care; it is correlated with diminished quality of life, high caregiver burden, nursing home placement, and increased patient mortality.8,9

Although PDP can occur in patients with PD at any age, generally it develops in patients with advanced-stage disease.9 Other risk factors for the development of PDP include older age, older age at PD onset, longer duration of PD, higher doses of antiparkinson drugs, comorbid nonmotor symptoms, and severe motor symptoms.5,6

Patients with PDP report hallucinations or delusions as the primary manifestations of psychosis, with visual hallucinations accounting for nearly 40% of these manifestations.10 Nonvisual hallucinations, such as auditory, tactile, or olfactory hallucinations, also may occur, either alone or in conjunction with visual hallucinations.6,10 Visual hallucinations in patients with PDP are complex and commonly include animals, people, objects, “sensations of presence,” or “sensations of movement in the periphery.”10  Delusions usually are persecutory or paranoid in nature, often involving infidelity of a spouse or plots to harm the patient.5,10

Unlike patients with other psychotic disorders, patients with PDP initially maintain insight that their hallucinations or delusions are false, only losing this insight with considerable disease progression.5,10 Nonetheless, even in patients with insight, these hallucinations and delusions negatively affect the ability to perform activities of daily living, distressing both the patient and caregiver.3,8