In an examination of the history of psychiatric and cognitive research in Parkinson disease (PD), it was noted that in the first year of publication of Movement Disorders (1986), none of the issues contained primary manuscripts that pertained to the psychiatric and cognitive complications of PD.1 The neuropsychiatric symptoms (NPS; defined here as psychiatric and cognitive complications) of PD received scant attention at that time, although there was an appreciation, present since James Parkinson’s legendary quote about the melancholic features of his defining case, that depression was common. In addition, ever since levodopa was introduced as the first dopamine replacement therapy in the 1960s, studies have documented the occurrence of psychotic symptoms in treated PD patients. In general, it was thought that the “senses” were mainly preserved, in part because the shortened life span of PD patients at that time precluded the development of dementia. When dementia (PDD) did occur, it was considered most often to represent the co-occurrence of Alzheimer disease (AD). Other psychiatric and cognitive complications in PD either were not commonly recognized or were not frequent due to the limited prevailing treatment options available. Beyond a very limited understanding of the epidemiology of these disorders, very little research was conducted on assessment, diagnosis, impact, course, neuropathophysiology, or treatment. Fast forwarding 25 years, although PD is still considered a movement disorder and is diagnosed on that basis, the high prevalence of NPS suggests it is more accurately conceptualized as a neurocognitive-psychiatric disorder. In addition to the most commonly studied aforementioned disorders, other relatively common psychiatric complications include impulse control disorders, anxiety symptoms, disorders of sleep and wakefulness, and apathy. The emergent focus on the NMS of PD over the past 25 years is exemplified by the nonlinear increase in the number of published manuscripts devoted to this topic1 and by quality improvement efforts that increasingly stress the nonmotor features of the disease.2,3 The original lack of focus on cognition in PD, particularly early in the disease course, led astute clinicians to recognize patients who presented with concomitant dementia and parkinsonism, giving rise to the new diagnosis of dementia with Lewy bodies (DLB), now considered the second most common dementia diagnosis in the developed world after AD.4 The clinical features of PDD and DLB are very similar (i.e., presence of dementia plus triad of parkinsonism, fluctuating cognition, and visual hallucinations), as is their neuropathology, and it is controversial whether they are distinct illnesses or simply the same disease with different time courses for the presentation of cognitive deficits relative to parkinsonism. When considering the diseases together, the term Lewy body disease (LBD) is typically used, because Lewy bodies and neurites (intraneuronal aggregates of misfolded α-synuclein) are the pathologic hallmarks of both diseases.