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.
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 PDpatients is still sparse. Therefore, we studied PDpatients 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 PDpatients 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.
Authors: J H Meyer; S Krüger; A A Wilson; B K Christensen; V S Goulding; A Schaffer; C Minifie; S Houle; D Hussey; S H Kennedy Journal: Neuroreport Date: 2001-12-21 Impact factor: 1.837
Authors: T Becker; G Becker; J Seufert; E Hofmann; K W Lange; M Naumann; A Lindner; H Reichmann; P Riederer; H Beckmann; K Reiners Journal: J Neurol Neurosurg Psychiatry Date: 1997-11 Impact factor: 10.154
Authors: Daniel Weintraub; Andrew B Newberg; Mark S Cary; Andrew D Siderowf; Paul J Moberg; Galit Kleiner-Fisman; John E Duda; Matthew B Stern; David Mozley; Ira R Katz Journal: J Nucl Med Date: 2005-02 Impact factor: 10.057
Authors: Andre C Felicio; Tais S Moriyama; Clecio Godeiro-Junior; Ming C Shih; Marcelo Q Hoexter; Vanderci Borges; Sonia M A Silva; Edson Amaro-Junior; Luiz A F Andrade; Henrique B Ferraz; Rodrigo A Bressan Journal: Psychopharmacology (Berl) Date: 2010-05-22 Impact factor: 4.530
Authors: Walter Koch; Marcus Unterrainer; Guoming Xiong; Peter Bartenstein; Markus Diemling; Andrea Varrone; John C Dickson; Livia Tossici-Bolt; Terez Sera; Susanne Asenbaum; Jan Booij; Ozlem L Kapucu; Andreas Kluge; Morten Ziebell; Jacques Darcourt; Flavio Nobili; Marco Pagani; Swen Hesse; Thierry Vander Borght; Koen Van Laere; Klaus Tatsch; Christian la Fougère Journal: Eur J Nucl Med Mol Imaging Date: 2014-05-08 Impact factor: 9.236