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Mild affective symptoms in de novo Parkinson's disease patients: relationship with dopaminergic dysfunction


Correspondence: R. Ceravolo, Neurology Unit, Department of Neuroscience, University of Pisa, Via Roma, 67-56126 Pisa, Italy (tel.: +0039 050 993544; fax: +0039 050550562; e-mail:


Background and purpose

The investigation of the relationship between affective symptoms and dopamine transporter (DAT) density provided conflicting data in both Parkinson's disease (PD) and non-PD patients. However, the potential interference of psychoactive as well as anti-parkinsonian drugs on DAT density should be taken into account.


To investigate the relationship between affective symptoms and pre-synaptic dopaminergic function in de novo PD patients.


Forty-four de novo PD consecutive outpatients were recruited, and the severity of anxious symptoms was evaluated with the Hamilton Anxiety Rating Scale (HAM-A), the severity of depressive symptoms with the Hamilton Depression Scale (HAM-D) and the Beck Depression Inventory (BDI). Six patients had a formal diagnosis of depression. All patients performed 123I-FP-CIT SPECT, and semi-quantitative striatal indices were calculated.


Disease severity, as measured by Unified Parkinson's Disease Rating Scale (UPDRSIII), was inversely correlated with bilateral striatal indices. Bilateral striatal uptake was significantly positively correlated with HAM-D (r.329; r.423, respectively, right and left), BDI (r.377; r.360, respectively, right and left) and HAM-A (r.338; r.340, respectively, right and left). After controlling for age, disease duration and severity, and Mini Mental State Examination (MMSE), no significant reduction in r-values was observed (< 0.05).


Our data support the existence of a relationship between depressive and anxious symptoms and the striatal 123I-FP-CIT uptake. The finding of an increased DAT density associated with mild affective symptoms could be due to the lack of compensatory mechanisms usually present in early PD, and/or it might have a pathogenic role in affective symptoms by reducing the dopaminergic tone in the synaptic cleft.