Citation

Fornai F, Frati A, Gesi M, Fulceri F, Paparelli S, Falleni A, Ruggieri S. Arch. Ital. Biol. 2013; 151(4): 179-191.

Affiliation

Department of Translational Research and New Technologies in Medicine and Surgery, University of Pisa; I.R.C.C.S. Neuromed, 86077 Pozzilli (IS), Italy. Email: francesco.fornai@med.unipi.it.

Copyright

(Copyright © 2013, Universita Degli Studi Di Pisa)

DOI

unavailable

PMID

24873926

Abstract

The present article aims to review state-of-the-art evidence of altered neurobiology and neuroanatomy underlyingpsychiatric symptoms in parkinsonism. This issue covers a wide range of symptoms encompassing anxiety, mooddisorders, psychosis as well as substance abuse and specific compulsive behaviors. Such a complex nosographymakes it impossible to deal with the neurobiology and neuroanatomy of each psychopathological condition perse, unless offering a trivial list of symptoms joined with brief explanations reporting potential causal mechanisms.This approach would only provide a rough synthesis of what previously reported without adding neither novelconcepts nor evidence to improve our insight into the neurobiology of parkinsonism as a psychiatric condition.Therefore, the analytical description of each psychiatric symptom associated with parkinsonism will be avoided butit will be referenced instead. In contrast, the present article will focus on the mechanisms why such a class of nonmotorsymptoms clusters in parkinsonian patients. In addition, we will seek to establish the relationship betweenthe occurrence of a given psychiatric condition and specific parkinsonian phenotypes. Again, an emphasis will begiven to the occurrence of behavioral fluctuations in parkinsonism where both motor and psychiatric symptomsmay possess a specific timing. The timing of these fluctuations will be related to the timing of dopamine substitutiontherapy and involvement of multiple neurotransmitters and brain regions as well. We provide evidence showingthat specific parkinsonian phenotypes (and genotypes) possess a widespread neuropathology, which in turn associatesto a fairly specific psychopathology. In contrast, other phenotypes (and genotypes) bring to very selectiveneuronal degeneration where the occurrence of psychiatric symptoms is rare if not absent at all. These clinicalpathological phenotypes associate with specific molecular mechanisms in the dynamics of neurobiology of disease.

Language: en