Archiv - März 2009
Monoamine transporter availability in Parkinson's disease patients with or without depression.
Swen Hesse1, Philipp M. Meyer1, Karl
Strecker2, Henryk Barthel1,
Florian Wegner2, Christian Oehlwein3, Ioannis
Ugo Isaias2, Johannes Schwarz2 and Osama
1Department of Nuclear Medicine, University of Leipzig, Stephanstraße 11, 04103 Leipzig, Germany
2Department of Neurology, University of Leipzig, Leipzig, Germany
3 Specialized Parkinson’s Disease Outpatient Centre, Gera, Germany
Eur J Nucl Med Mol Imaging. 2009 Mar;36(3):428-35. Epub 2008 Nov 27.
PURPOSE: Depression is a common symptom in patients suffering from Parkinson's disease (PD) and markedly reduces their quality of life. As post-mortem studies have shown, its presence may reflect extensive cell loss in the midbrain and brainstem with imbalances in monoaminergic neurotransmitters. However, in vivo evidence of specific monoaminergic deficits in depressed PD patients is still sparse. Therefore, we studied PD patients with depression (PD+D) and without depression (PD-D) using high-resolution single-photon emission computed tomography (SPECT) and the monoamine transporter marker [(123)I]FP-CIT. METHODS: A magnetic resonance imaging-based region-of-interest analysis was applied to quantify the specific-to-nondisplaceable [(123)I]FP-CIT binding coefficient V(3)'' in the striatum, thalamus and midbrain/brainstem regions. RESULTS: PD+D patients had significantly lower V(3)'' compared with PD-D patients in the striatum (p<0.001), thalamus (p=0.002), and midbrain/brainstem (p=0.025). Only PD+D patients without selective serotonin reuptake inhibitor (SSRI) treatment showed lower thalamic and midbrain V(3)'' than controls (p<0.001, p=0.029). In a small sub-group of SSRI-treated PD+D patients neither thalamic V(3)'' nor midbrain/brainstem V(3)'' differed from those in PD-D patients (p=0.168, p=0.201) or controls (p=0.384, p=0.318). CONCLUSION: Our data indicate that depression in PD is associated with a more pronounced loss of striatal dopamine transporter availability that is most likely secondary to increased dopaminergic degeneration. In addition, depressed PD patients have a lower availability of midbrain/brainstem monoamine transporters than nondepressed PD patients. These findings provide in vivo evidence in support of the known post-mortem data demonstrating more extensive nerve cell loss in PD with depression and indicate that SPECT imaging can help to identify pathophysiological changes underlying nonmotor symptoms in this common movement disorder.