Peer-review started: January 18, 2015
First decision: February 7, 2015
Revised: February 14, 2015
Accepted: March 5, 2015
Article in press: March 9, 2015
Published online: March 28, 2015
Processing time: 72 Days and 4.7 Hours
Mavridis’ atrophy (MA) is called the human nucleus accumbens (NA) atrophy in Parkinson’s disease (PD). MA begins in early-stage PD patients and is correlated with psychiatric symptoms that occur in PD, mainly apathy and impulsive behavior. It is also associated with cognitive PD symptoms. Purpose of this editorial was to discuss the future perspectives of MA as a pathological and imaging finding. MA is obviously part of the degeneration of the dopaminergic nigrostriatal system that occurs in PD and this also explains the fact that MA precedes clinical phenotype. But does the human NA follow the same pattern of degeneration? It would be quite interesting to have a post-mortem pathological study focused on the NA of parkinsonic individuals. Further questions that remain to be answered are whether all parkinsonics suffer MA and whether this phenomenon is also associated with motor PD symptoms. MA as an imaging finding could be a risk factor for the expression and/or severity of specific PD symptoms. It has therefore to be tested whether the presence of MA is related, for example, with the expression and/or severity of motor PD symptoms and whether the severity of MA affects the severity of specific psychiatric symptoms (apathy, compulsive behavior) of parkinsonic individuals. Such clinical studies, that could provide answers to these vital questions, can be easily preformed given the high frequency of PD in modern populations. Future research efforts are mandatory to enrich our knowledge of MA, namely its underlying mechanisms, its pathological features and its clinical consequences.
Core tip: Mavridis’ atrophy (MA) is the nucleus accumbens atrophy in Parkinson’s disease (PD). MA begins in early-stage PD patients and is correlated with psychiatric and cognitive PD symptoms. MA is obviously part of the dopaminergic nigrostriatal degeneration that occurs in PD. It would be interesting to have a post-mortem pathological study focused on the nucleus accumbens of parkinsonic individuals. MA as an imaging finding could be a risk factor for the expression and/or severity of specific symptoms. Thus it has to be tested whether the presence of MA is related, for example, with the expression and/or severity of motor PD symptoms.