Psychosis in parkinsonism: an unorthodox approach

Abstract

Psychosis in Parkinson's disease (PD) is currently considered as the occurrence of hallucinations and delusions. The historical meaning of the term psychosis was, however, broader, encompassing a disorganization of both consciousness and personality, including behavior abnormalities, such as impulsive overactivity and catatonia, in complete definitions by the International Classification of Diseases-10 (ICD-10) and the Diagnostic and Statistical Manual of Mental Disorders, Fifth Edition (DSM-5). Our review is aimed at reminding that complex psychotic symptoms, including impulsive overactivity and somatoform disorders (the last being a recent controversial entity in PD), were carefully described in postencephalitic parkinsonism (PEP), many decades before dopaminergic treatment era, and are now described in other parkinsonisms than PD. Eminent neuropsychiatrists of the past century speculated that studying psychosis in PEP might highlight its mechanisms in other conditions. Yet, functional assessments were unavailable at the time. Therefore, the second part of our article reviews the studies of neural correlates of psychosis in parkinsonisms, by taking into account both theories on the narrative functions of the default mode network (DMN) and hypotheses on DMN modulation.

Keywords: Parkinson’s disease; atypical parkinsonism; default mode network; postencephalitic parkinsonism; psychosis.

Figure 1

Default mode network (DMN) spatial map obtained from independent component analysis (ICA) on healthy subjects. Note: Yellow-red and green-blue areas indicate positive and negative correlations with the independent component (IC) waveform, respectively. Abbreviations: DLPFC, dorsolateral prefrontal cortex; vmPFC, ventromedial prefrontal cortex; IPL, inferior parietal lobule; IPS, inferior parietal sulcus; PCC, posterior cingulate cortex; MPF, medial prefrontal cortex.

Figure 2

Schematic representation of the structures composing the limbic system and elements of the default mode network embedded in it (ACC and PCC). Abbreviations: ACC, anterior cingulate cortex; PCC, posterior cingulate cortex; A, amygdala; AnTh, Anterior nucleus of thalamus; EC, enhtorinal cortex; F, fornix; Fi, fimbria; H, habenula; Hi, Hippocampus; MB, mammillar body; OfC, orbitofrontal cortex; Th, thalamus; Un, uncus.

Figure 3

Sagittal images of single fluorodeoxy-glucose-photon emission tomography showing in one of our DLB patients, preservation of PCC metabolism, the so called “cingulate island sign”. Abbreviations: DLB, dementia with Lewy bodies; PCC, posterior cingulate cortex; S, sagittal; A, anterior; P, posterior.

Figure 4

Ischemic thalamic lesions in patients with confabulations described in literature (red circles, Onofrj et al, 2016; green circle, Schnider et al, 1996; and blue circles, Markowitsch et al, 1993).

Figure 5

Representative image of the inhibitory input from the anterior cingulate cortex (ACC) on the posterior cingulate cortex (PCC).

Figure 6

Schematic representation of the habenula and its relationship with adjacent structures. Abbreviations: GP, globus pallidus; IN, interpeduncolar nucleus; OfC, orbitofrontal cortex; RN, raphe nucleus; Sp, septum; Str, striatum; Th, thalamus.