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Theme: Parkinson’s disease - Review

Imaging cognitive and behavioral symptoms in Parkinson’s disease

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Pages 1827-1838 | Published online: 09 Jan 2014

References

  • Chaudhuri KR, Schapira AH. Non-motor symptoms of Parkinson’s disease: dopaminergic pathophysiology and treatment. Lancet Neurol.8(5), 464–474 (2009).
  • Monchi O, Martinu K, Strafella AP. The contribution of neuroimaging for the study of cognitive deficits in Parkinson’s disease. Clin. EEG Neurosci.41(2), 76–81 (2010).
  • Bowen FP, Kamienny RS, Burns MM, Yahr M. Parkinsonism: effects of levodopa treatment on concept formation. Neurology25(8), 701–704 (1975).
  • Sagar HJ. Clinical similarities and differences between Alzheimer’s disease and Parkinson’s disease. J. Neural Transm. Suppl.24, 87–99 (1987).
  • Cools AR, van den Bercken JH, Horstink MW, van Spaendonck KP, Berger HJ. Cognitive and motor shifting aptitude disorder in Parkinson’s disease. J. Neurol. Neurosurg. Psychiatry47(5), 443–453 (1984).
  • Taylor AE, Saint-Cyr JA, Lang AE. Frontal lobe dysfunction in Parkinson’s disease. The cortical focus of neostriatal outflow. Brain109, 845–883 (1986).
  • Downes JJ, Roberts AC, Sahakian BJ, Evenden JL, Morris RG, Robbins TW. Impaired extra-dimensional shift performance in medicated and unmedicated Parkinson’s disease: evidence for a specific attentional dysfunction. Neuropsychologia27(11–12), 1329–1343 (1989).
  • Morris RG, Downes JJ, Sahakian BJ, Evenden JL, Heald A, Robbins TW. Planning and spatial working memory in Parkinson’s disease. J. Neurol. Neurosurg. Psychiatry51(6), 757–766 (1988).
  • Brown RG, MacCarthy B, Jahanshahi M, Marsden CD. Accuracy of self-reported disability in patients with parkinsonism. Arch. Neurol.46(9), 955–959 (1989).
  • Emre M. What causes mental dysfunction in Parkinson’s disease? Mov. Disord.18(Suppl. 6), S63–S71 (2003).
  • Janvin C, Aarsland D, Larsen JP, Hugdahl K. Neuropsychological profile of patients with Parkinson’s disease without dementia. Dement. Geriatr. Cogn. Disord.15(3), 126–131 (2003).
  • Owen AM, Doyon J, Dagher A, Sadikot A, Evans AC. Abnormal basal ganglia outflow in Parkinson’s disease identified with PET. Implications for higher cortical functions. Brain121, 949–965 (1998).
  • Cools R, Stefanova E, Barker RA, Robbins TW, Owen AM. Dopaminergic modulation of high-level cognition in Parkinson’s disease: the role of the prefrontal cortex revealed by PET. Brain125, 584–594 (2002).
  • Mattay VS, Tessitore A, Callicott JH et al. Dopaminergic modulation of cortical function in patients with Parkinson’s disease. Ann. Neurol.51(2), 156–164 (2002).
  • Brown RG, Marsden CD. Cognitive function in Parkinson’s disease: from description to theory. Trends Neurosci.13(1), 21–29 (1990).
  • Lewis SJ, Dove A, Robbins TW, Barker RA, Owen AM. Cognitive impairments in early Parkinson’s disease are accompanied by reductions in activity in frontostriatal neural circuitry. J. Neurosci.16(23), 6351–6356 (2003).
  • Huang C, Mattis P, Perrine K, Brown N, Dhawan V, Eidelberg D. Metabolic abnormalities associated with mild cognitive impairment in Parkinson disease. Neurology70(16), 1470–1477 (2008).
  • Albin RL, Young AB, Penney JB. The functional anatomy of basal ganglia disorders. Trends Neurosci.12(10), 366–375 (1989).
  • Liepelt I, Reimold M, Maetzler W et al. Cortical hypometabolism assessed by a metabolic ratio in Parkinson‘s disease primarily reflects cognitive deterioration-[18F]FDG-PET. Mov. Disord.24(10), 1504–1511 (2009).
  • Raichle ME, MacLeod AM, Snyder AZ, Powers WJ, Gusnard DA, Shulman GL. A default mode of brain function. Proc. Natl Acad. Sci. USA98, 676–682 (2001).
  • Raichle ME, Snyder AZ. A default mode of brain function: a brief history of an evolving idea. Neuroimage37(4), 1083–1090 (2007).
  • van Eimeren T, Monchi O, Ballanger B, Strafella AP. Dysfunction of the default mode network in Parkinson disease: a functional magnetic resonance imaging study. Arch. Neurol.66, 877–883 (2009).
  • Nagano-Saito A, Liu J, Doyon J, Dagher A. Dopamine modulates default mode network deactivation in elderly individuals during the Tower of London task. Neurosci. Lett.458, 1–5 (2009).
  • Argyelan M, Carbon M, Ghilardi MF et al. Dopaminergic suppression of brain deactivation responses during sequence learning. J. Neurosci.28, 10687–10695 (2008).
  • Dagher A, Owen AM, Boecker H, Brooks DJ. The role of the striatum and hippocampus in planning: a PET activation study in Parkinson’s disease. Brain124, 1020–1032 (2001).
  • Monchi O, Petrides M, Doyon J, Postuma RB, Worsley K, Dagher A. Neural bases of set-shifting deficits in Parkinson’s disease. J. Neurosci.24, 702–710 (2004).
  • Monchi O, Petrides M, Mejia-Constain B, Strafella AP. Cortical activity in Parkinson’s disease during executive processing depends on striatal involvement. Brain130(1), 233–244 (2007).
  • Samuel M, Ceballos-Baumann AO, Blin J et al. Evidence for lateral premotor and parietal overactivity in Parkinson’s disease during sequential and bimanual movements. A PET study. Brain120(6), 963–976 (1997).
  • Brück A, Aalto S, Nurmi E, Bergman J, Rinne JO. Cortical 6-[18F]fluoro-L-dopa uptake and frontal cognitive functions in early Parkinson’s disease. Neurobiol. Aging26(6), 891–898 (2005).
  • Klein JC, Eggers C, Kalbe E et al. Neurotransmitter changes in dementia with Lewy bodies and Parkinson disease dementia in vivo. Neurology74(11), 885–892 (2010).
  • Rinne JO, Portin R, Ruottinen H et al. Cognitive impairment and the brain dopaminergic system in Parkinson disease: [18F]fluorodopa positron emission tomographic study. Arch. Neurol.57(4), 470–475 (2000).
  • Stoessl AJ. Functional imaging studies of non-motoric manifestations of Parkinson’s disease. Parkinsonism Relat. Disord.15(S3), S13–S16 (2009).
  • Agid Y, Javoy-Agid E, Ruberg M. Biochemistry of neurotransmitters in Parkinson’s disease. In: Movement Disorders. Marsden CD, Fahn S (Eds). 166–230 (1987).
  • Kish SJ, Shannak K, Hornykiewicz O. Uneven pattern of dopamine loss in the striatum of patients with idiopathic Parkinson’s disease. Pathophysiologic and clinical implications. N. Engl. J. Med.318(14), 876–880 (1988).
  • Owen AM Cognitive dysfunction in Parkinson’s disease: the role of frontostriatal circuitry. Neuroscientist10, 525–537 (2004).
  • Marié RM, Barré L, Dupuy B, Viader F, Defer G, Baron JC. Relationships between striatal dopamine denervation and frontal executive tests in Parkinson’s disease. Neurosci. Lett.260(2), 77–80 (1999).
  • Nobili F, Campus C, Arnaldi D et al. Cognitive-nigrostriatal relationships in de novo, drug-naive Parkinson’s disease patients: a [I-123]FP-CIT SPECT study. Mov. Disord.25(1), 35–43 (2010).
  • Sawamoto N, Piccini P, Hotton G, Pavese N, Thielemans K, Brooks DJ. Cognitive deficits and striato–frontal dopamine release in Parkinson’s disease. Brain131, 1294–1302 (2008).
  • Yeterian EH, Pandya DN. Prefrontostriatal connections in relation to cortical architectonic organization in rhesus monkeys. J. Comp. Neurol.312(1), 43–67 (1991).
  • Rosvold HE. The frontal lobe system: cortical–subcortical interrelationships. Acta Neurobiol. Exp.32, 439–460 (1972).
  • Swainson R, Rogers RD, Sahakian BJ, Summers BA, Polkey CE, Robbins TW. Probabilistic learning and reversal deficits in patients with Parkinson’s disease or frontal or temporal lobe lesions: possible adverse effects of dopaminergic medication. Neuropsychologia38, 596–612 (2000).
  • Cools R, Barker RA, Sahakian BJ, Robbins TW. Enhanced or impaired cognitive function in Parkinson’s disease as a function of dopaminergic medication and task demands. Cereb. Cortex11, 1136–1143 (2001).
  • Owen AM, Evans AC, Petrides M. Evidence for a two-stage model of spatialworking memory processing within the lateral frontal cortex: a positron emission tomography study. Cereb. Cortex6, 31–38 (1996).
  • Alexander GE, DeLong MR, Strick PL. Parallel organization of functionally segregated circuits linking basal ganglia and cortex. Annu. Rev. Neurosci.9, 357–381 (1986)
  • Grahn JA, Parkinson JA, Owen AM. The cognitive functions of the caudate nucleus. Prog. Neurobiol.86, 141–155 (2008).
  • Brooks DJ. Imaging non-dopaminergic function in Parkinson’s disease. Mol. Imaging Biol.9(4), 217–222 (2007).
  • Asahina M, Suhara T, Shinotoh H, Inoue O, Suzuki K, Hattori T. Brain muscarinic receptors in progressive supranuclear palsy and Parkinson’s disease: a positron emission tomographic study. J. Neurol. Neurosurg. Psychiatry65(2), 155–163 (1998).
  • Bohnen NI, Cham R. Postural control, gait, and dopamine functions in parkinsonian movement disorders. Clin. Geriatr. Med.22(4), 797–812 (2006).
  • Dias R, Robbins TW, Roberts AC. Dissociation in prefrontal cortex of affective and attentional shifts. Nature380, 69–72 (1996).
  • Cools R, Barker RA, Sahakian BJ, Robbins TW. L-dopa medication remediates cognitive inflexibility, but increases impulsivity in patients with Parkinson’s disease. Neuropsychologia41(11), 1431–1441 (2003).
  • Jubault T, Monetta L, Strafella AP, Lafontaine AL, Monchi O. L-dopa medication in Parkinson’s disease restores activity in the motor cortico–striatal loop but does not modify the cognitive network. PLoS One4, 6154 (2009).
  • Williams-Gray CH, Hampshire A, Robbins TW, Owen AM, Barker RA. Catechol O-methyltransferase Val158Met genotype influences frontoparietal activity during planning in patients with Parkinson’s disease. J. Neurosci.27, 4832–4838 (2007).
  • Williams-Gray CH, Hampshire A, Barker RA, Owen AM. Attentional control in Parkinson’s disease is dependent on COMT val 158 met genotype. Brain131, 397–408 (2008).
  • Argyelan M, Carbon M, Ghilardi MF et al. Dopaminergic suppression of brain deactivation responses during sequence learning. J. Neurosci.28, 10687–10695 (2008).
  • Bergman H, Wichmann T, DeLong MR. Reversal of experimental parkinsonism by lesions of the subthalamic nucleus. Science249(4975), 1436–1438 (1990).
  • Limousin P, Pollak P, Benazzouz A et al. Effect of parkinsonian signs and symptoms of bilateral subthalamic nucleus stimulation. Lancet345(8942), 91–95 (1995).
  • Limousin P, Greene J, Pollak P, Rothwell J, Benabid AL, Frackowiak R. Changes in cerebral activity pattern due to subthalamic nucleus or internal pallidum stimulation in Parkinson’s disease. Ann. Neurol.42(3), 283–291 (1997).
  • Strafella AP, Paus T, Fraraccio M, Dagher A. Striatal dopamine release induced by repetitive transcranial magnetic stimulation of the human motor cortex. Brain126(12), 2609–2615 (2003).
  • Jahanshahi M, Ardouin CM, Brown RG et al. The impact of deep brain stimulation on executive function in Parkinson’s disease. Brain123(6), 1142–1154 (2000).
  • Schroeder U, Kuehler A, Haslinger B et al. Subthalamic nucleus stimulation affects striato-anterior cingulate cortex circuit in a response conflict task: a PET study. Brain125(9), 1995–2004 (2002).
  • Hershey T, Revilla FJ, Wernle A, Gibson PS, Dowling JL, Perlmutter JS. Stimulation of STN impairs aspects of cognitive control in PD. Neurology62(7), 1110–1114 (2004).
  • Thobois S, Hotton GR, Pinto S et al. STN stimulation alters pallidal–frontal coupling during response selection under competition. Cereb. Blood Flow Metab.27(6), 1173–1184 (2007).
  • Frank MJ, Samanta J, Moustafa AA, Sherman SJ. Hold your horses: impulsivity, deep brain stimulation, and medication in parkinsonism. Science318(5854), 1309–1312 (2007)
  • Ballanger B, van Eimeren T, Moro E et al. Stimulation of the subthalamic nucleus and impulsivity: release your horses. Ann. Neurol.66(6), 817–824 (2009).
  • Campbell MC, Karimi M, Weaver PM et al. Neural correlates of STN DBS-induced cognitive variability in Parkinson disease. Neuropsychologia46(13), 3162–3169 (2008).
  • Kalbe E, Voges J, Weber T et al. Frontal FDG-PET activity correlates with cognitive outcome after STN-DBS in Parkinson disease. Neurology72(1), 42–49 (2009).
  • Meyer JS, Huang J, Chowdhury MH. MRI confirms mild cognitive impairments prodromal for Alzheimer’s, vascular and Parkinson-Lewy body dementias. J. Neurol. Sci.257(1–2), 97–104 (2007).
  • Beyer MK, Janvin CC, Larsen JP, Aarsland D. A magnetic resonance imaging study of patients with Parkinson’s disease with mild cognitive impairment and dementia using voxel-based morphometry. J. Neurol. Neurosurg. Psychiatry78(3), 254–259 (2007).
  • Dalaker TO, Zivadinov R, Larsen JP et al. Gray matter correlations of cognition in incident Parkinson’s disease. Mov. Disord.25(5), 629–633 (2010).
  • Dalaker TO, Larsen JP, Dwyer MG et al. White matter hyperintensities do not impact cognitive function in patients with newly diagnosed Parkinson’s disease. Neuroimage47(4), 2083–2089 (2009).
  • Taylor AE, Saint-Cyr JA, Lang AE. Frontal lobe dysfunction in Parkinson’s disease. The cortical focus of neostriatal outflow. Brain109, 845–883 (1986).
  • Taylor AE, Saint-Cyr JA. Risk of dementia in Parkinson’s disease: a community-based, prospective study. Brain Cogn.28(3), 281–296 (1995).
  • Dubois B, Pillon B. Cognitive deficits in Parkinson’s disease. J. Neurol.244(1), 2–8 (1997).
  • Aarsland D, Andersen K, Larsen JP, Lolk A, Nielsen H, Kragh-Sørensen P. Prevalence and characteristics of dementia in Parkinson disease: an 8-year prospective study. Neurology56(6), 730–736 (2001).
  • Aarsland D, Andersen K, Larsen JP, Lolk A, Kragh-Sørensen P. A 10-year study of the incidence of and factors predicting dementia in Parkinson’s disease. Arch. Neurol.60(3), 387–392 (2003).
  • Hughes TA, Ross HF, Musa S et al. Diagnostic procedures for Parkinson’s disease dementia: recommendations from the movement disorder society task force. Neurology54(8), 1596–1602 (2000).
  • Emre M, Aarsland D, Brown R et al. Clinical diagnostic criteria for dementia associated with Parkinson’s disease. Mov. Disord.22(12), 2007, 1689–1707 (2007).
  • Lippa CF, Duda JE, Grossman M et al. DLB and PDD boundary issues: diagnosis, treatment, molecular pathology, and biomarkers. Neurology68(11), 812–819 (2007).
  • Klein JC, Eggers C, Kalbe E et al. Neurotransmitter changes in dementia with Lewy bodies and Parkinson disease dementia in vivo. Neurology74(11), 885–892 (2010).
  • Peppard RF, Martin WR, Carr GD et al. Cerebral glucose metabolism in Parkinson’s disease with and without dementia. Arch. Neurol.49(12), 1262–1268 (1992).
  • Albin RL, Minoshima S, D’Amato CJ, Frey KA, Kuhl DA, Sima AA. Fluoro-deoxyglucose positron emission tomography in diffuse Lewy body disease. Neurology47(2), 462–466 (1996).
  • Vander Borght T, Minoshima S, Giordani B et al. Cerebral metabolic differences in Parkinson’s and Alzheimer’s diseases matched for dementia severity. J. Nucl. Med.38(5), 797–802 (1997).
  • Walker Z, Costa DC et al. Differentiation of dementia with Lewy bodies from Alzheimer’s disease using a dopaminergic presynaptic ligand. J. Neurol. Neurosurg. Psychiatry73(2), 134–140 (2002).
  • Ito K, Nagano-Saito A, Kato T et al. Striatal and extrastriatal dysfunction in Parkinson’s disease with dementia: a 6-[18F]fluoro-L-dopa PET study. Brain125(Pt 6), 1358–1365 (2002).
  • Hilker R, Thomas AV, Klein JC et al. Dementia in Parkinson disease: functional imaging of cholinergic and dopaminergic pathways. Neurology65(11), 1716–1722 (2005).
  • Shimada H, Hirano S, Shinotoh H et al. Mapping of brain acetylcholinesterase alterations in Lewy body disease by PET. Neurology73(4), 273–278 (2009).
  • Brooks DJ. Amyloid β-peptide and the dementia of Parkinson's disease. Mov. Disord.24(S2), S742–S747 (2009).
  • Jendroska K, Lees AJ, Poewe W, Daniel SE. Amyloid β-peptide and the dementia of Parkinson’s disease. Mov. Disord.11(6), 647–653 (1996).
  • Edison P, Rowe CC, Rinne JO et al. Amyloid load in Parkinson’s disease dementia and Lewy body dementia measured with [11C]PIB positron emission tomography. J. Neurol. Neurosurg. Psychiatry79(12), 1331–1338 (2008).
  • Gomperts SN, Rentz DM, Moran E et al. Imaging amyloid deposition in Lewy body diseases. Neurology71(12), 903–910 (2008).
  • Archer HA, Edison P, Brooks DJ et al. Amyloid load and cerebral atrophy in Alzheimer’s disease: an (11)C-PiB positron emission tomography study. Ann. Neurol.60, 145–147 (2006).
  • Fagan AM, Mintun MA, Mach RH et al. Inverse relation between in vivo amyloid imaging load and cerebrospinal fluid Ab42 in humans. Ann. Neurol.59, 512–519 (2006).
  • Price JL, Morris JC. Tangles and plaques in nondemented aging and ‘preclinical’ Alzheimer’s disease. Ann. Neurol.45, 358–368 (1999).
  • Burack MA, Hartlein J, Flores HP et al.In vivo amyloid imaging in autopsy-confirmed Parkinson disease with dementia. Neurology74(1), 77–84 (2010).
  • Weintraub D, Koester J, Potenza MN et al. Impulse control disorders in Parkinson disease: a cross-sectional study of 3090 patients. Arch. Neurol.67(5), 589–595 (2010).
  • Giladi N, Weitzman N, Schreiber S, Shabtai H, Peretz C. New onset heightened interest or drive for gambling, shopping, eating or sexual activity in patients with Parkinson’s disease: the role of dopamine agonist treatment and age at motor symptoms onset. J. Psychopharmacol.21(5), 501–506 (2007).
  • Voon V, Hassan K, Zurowski M et al. Prospective prevalence of pathologic gambling and medication association in Parkinson disease. Neurology66(11), 1750–1752 (2006).
  • Shaffer HJ. Strange bedfellows: a critical view of pathological gambling and addiction. Addiction94(10), 1445–1448 (1999).
  • Dodd ML, Klos KJ, Bower JH et al. Pathological gambling caused by drugs used to treat Parkinson disease. Arch. Neurol.62(9), 1377–1381 (2005).
  • Pontone G, Williams JR, Bassett SS, Marsh L. Clinical features associated with impulse control disorders in Parkinson disease. Neurology67(7), 1258–1261 (2006).
  • Potenza MN. The neurobiology of pathological gambling and drug addiction: an overview and new findings. Philos. Trans. R. Soc. Lond. B. Biol. Sci.363(1507), 3181–3189 (2008).
  • Cilia R, Ko JH, Cho SS et al. Reduced dopamine transporter density in the ventral striatum of patients with Parkinson’s disease and pathological gambling. Neurobiol. Dis.39(1), 98–104 (2010).
  • Cools R. Uneven pattern of dopamine loss in the striatum of patients with idiopathic Parkinson’s disease. Pathophysiologic and clinical implications. Neurosci. Biobehav. Rev.30(1), 1–23 (2006).
  • Steeves TD, Miyasaki J, Zurowski M et al. Increased striatal dopamine release in Parkinsonian patients with pathological gambling: a [11C] raclopride PET study. Brain132(5), 1376–1385 (2009).
  • van Eimeren T, Ballanger B, Pellecchia G, Miyasaki JM, Lang AE, Strafella AP. Dopamine agonists diminish value sensitivity of the orbitofrontal cortex: a trigger for pathological gambling in Parkinson‘s disease? Neuropsychopharmacology34(13), 2758–2766 (2009).
  • Abler B, Hahlbrock R, Unrath A, Grön G, Kassubek J. At-risk for pathological gambling: imaging neural reward processing under chronic dopamine agonists. Brain132(9), 2396–2402 (2009).
  • van Eimeren T, Pellecchia G, Cilia R et al. Drug-induced deactivation of inhibitory networks predicts pathological gambling in PD. Neurology DOI: 10.1212/WNL.0b013e3181fc27fa (2010) (Epub ahead of print).
  • Volkow ND, Fowler JS, Wang GJ. Role of dopamine in drug reinforcement and addiction in humans: results from imaging studies. Behav. Pharmacol.13(5–6), 355–366 (2002).
  • Volkow ND, Fowler JS, Wang GJ, Baler R, Telang F. Imaging dopamine‘s role in drug abuse and addiction. Neuropharmacology56(Suppl. 1), 3–8 (2009).
  • Wang GJ, Volkow ND, Thanos PK, Fowler JS. Similarity between obesity and drug addiction as assessed by neurofunctional imaging: a concept review. J. Addict. Dis.23(3), 39–53 (2004).
  • Hamidovic A, Kang UJ, de Wit H. Effects of low to moderate acute doses of pramipexole on impulsivity and cognition in healthy volunteers. J. Clin. Psychopharmacol.28(1), 45–51 (2008).
  • Lee JY, Kim JM, Kim JW et al. Association between the dose of dopaminergic medication and the behavioral disturbances in Parkinson disease. Parkinsonism Relat. Disord.16(3), 202–207 (2010).
  • Brown R, Jahanshahi M. Depression in Parkinson’s disease: a psychosocial viewpoint. Adv. Neurol.65, 61–84 (1999).
  • Cummings JL, Masterman DL. Depression in patients with Parkinson’s disease. Int. J. Geriatr. Psychiatry14(9), 711–718 (1999).
  • American Psychiatric Association. Diagnostic and Statistical Manual of Mental Disorders Forth Edition. American Psychiatric Association, VA, USA (1994).
  • Aarsland D, Marsh L, Schrag A. Neuropsychiatric symptoms in Parkinson’s disease. Mov. Disord.24(15), 2175–2186 (2009).
  • Braak H, Ghebremedhin E, Rub U, Bratzke H, Del Tredici K. Stages in the development of Parkinson’s disease-related pathology. Cell Tissue Res.318, 121–134 (2004).
  • Paulus W, Jellinger K. The neuropathologic basis of different clinical subgroups of Parkinson’s disease. J. Neuropathol. Exp. Neurol.50, 743–755 (1991).
  • Remy P, Doder M, Lees A, Turjanski N, Brooks D. Depression in Parkinson’s disease: loss of dopamine and noradrenaline innervation in the limbic system. Brain128(6), 1314–1322 (2005).
  • Weintraub D, Newberg AB, Cary MS et al. Striatal dopamine transporter imaging correlates with anxiety and depression symptoms in Parkinson’s disease. J. Nucl. Med.46(2), 227–232 (2005).
  • Koerts J, Leenders KL, Koning M, Portman AT, van Beilen M. Striatal dopaminergic activity (FDOPA-PET) associated with cognitive items of a depression scale (MADRS) in Parkinson’s disease. Eur. J. Neurosci.25(10), 3132–3136 (2007).
  • Brooks DJ. Imaging approaches to Parkinson disease. J. Nucl. Med.51(4), 596–609 (2010).
  • Boileau I, Warsh JJ, Guttman M et al. Elevated serotonin transporter binding in depressed patients with Parkinson’s disease: a preliminary PET study with [11C]DASB Mov. Disord.23(12), 1776–1780 (2008).
  • Kim SE, Choi JY, Choe YS, Choi Y, Lee WY. Serotonin transporters in the midbrain of Parkinson’s disease patients: a study with 123I-β-CIT SPECT. J. Nucl. Med.44(6), 870–876 (2003).
  • Bohnen NI, Kaufer DI, Hendrickson R, Constantine GM, Mathis CA, Moore RY. Cortical cholinergic denervation is associated with depressive symptoms in Parkinson’s disease and parkinsonian dementia. J. Neurol. Neurosurg. Psychiatry78(6), 641–643 (2007).
  • Feldmann A, Illes Z, Kosztolanyi P et al. Morphometric changes of gray matter in Parkinson’s disease with depression: a voxel-based morphometry study. Mov. Disord.23(1), 42–46 (2008).
  • Kostic VS, Agosta F et al. Regional patterns of brain tissue loss associated with depression in Parkinson disease. Neurology75(10), 857–863 (2010).
  • Marin RS. Differential diagnosis and classification of apathy. Am. J. Psychiatry147(1), 22–30 (1990).
  • Drapier D, Drapier S, Sauleau P et al. Does subthalamic nucleus stimulation induce apathy in Parkinson’s disease? J. Neurol.253(8), 1083–1091 (2006).
  • Levy R, Dubois B. Apathy and the functional anatomy of the prefrontal cortex-basal ganglia circuits. Cereb. Cortex16(7), 916–928 (2006).
  • Reijnders JS, Scholtissen B, Weber WE, Aalten P, Verhey FR, Leentjens AF. Neuroanatomical correlates of apathy in Parkinson’s disease: a magnetic resonance imaging study using voxel-based morphometry. Mov Disord.25(14), 2318–2325 (2010).
  • Le Jeune F, Drapier D, Bourguignon A et al. Subthalamic nucleus stimulation in Parkinson disease induces apathy: a PET study. Neurology73(21), 1746–1751 (2009).
  • Thobois S, Ardouin C, Lommee E et al. Non-motor dopamine withdrawal syndrome after surgery for Parkinson’s disease: predictors and underlying mesolimbic denervation. Brain133(4), 1111–1127 (2010).
  • Barnes J, David AS. Visual hallucinations in Parkinson’s disease: a review and phenomenological survey. J. Neurol. Neurosurg. Psychiatry70(6), 727–733 (2001).
  • Diederich NJ, Fénelon G, Stebbins G, Goetz CG. Hallucinations in Parkinson disease. Nat. Rev. Neurol.5(6), 331–342 (2009).
  • Banerjee AK, Falkai PG, Savidge M. Visual hallucinations in the elderly associated with the use of levodopa. Postgrad. Med. J.65(764), 358–361 (1989).
  • Holroyd S, Currie L, Wooten GF Prospective study of hallucinations and delusions in Parkinson’s disease. J. Neurol. Neurosurg. Psychiatry70(6), 734–738 (2001).
  • Boecker H, Ceballos-Baumann AO, Volk D, Conrad B, Forstl H, Haussermann P. Metabolic alterations in patients with Parkinson disease and visual hallucinations. Arch. Neurol.64(7), 984–988 (2007).
  • Okada K, Suyama N, Oguro H, Yamaguchi S, Kobayashi S. Medication-induced hallucination and cerebral blood flow in Parkinson’s disease J. Neurol.246(5), 365–368 (1999).
  • Nagano-Saito A, Washimi Y, Arahata Y et al. Visual hallucination in Parkinson’s disease with FDG PET. Mov. Disord.19(7), 801–806 (2004).
  • Ramírez-Ruiz B, Martí MJ, Tolosa E et al. Brain response to complex visual stimuli in Parkinson’s patients with hallucinations: a functional magnetic resonance imaging study. Mov. Disord.23(16), 2335–2343 (2008).
  • Stebbins GT, Goetz CG, Carrillo MC et al. Altered cortical visual processing in PD with hallucinations: an fMRI study. Neurology63(8), 1409–1416 (2004).
  • Allen P, Larøi F, McGuire PK, Aleman A. The hallucinating brain: a review of structural and functional neuroimaging studies of hallucinations. Neurosci. Biobehav. Rev.32(1), 175–191 (2008).
  • Ibarretxe-Bilbao N, Ramirez-Ruiz B, Junque C et al. Differential progression of brain atrophy in Parkinson’s disease with and without visual hallucinations. J. Neurol. Neurosurg. Psychiatry81(6), 650–657 (2010).
  • Ballanger B, Strafella AP, van Eimeren T et al. Serotonin 2A receptors and visual hallucinations in Parkinson disease. Arch. Neurol.67(4), 416–421 (2010).
  • Halldin C, Farde L, Högberg T et al. Carbon-11-FLB 457: a radioligand for extrastriatal D2 dopamine receptors J. Nucl. Med36(7), 1275–1281 (1995).
  • Olsson H, Halldin C, Farde L. Differentiation of extrastriatal dopamine D2 receptor density and affinity in the human brain using PET. Neuroimage22(2), 794–803 (2004).
  • Slifstein M, Hwang DR, Huang Y et al.In vivo affinity of [18F]fallypride for striatal and extrastriatal dopamine D2 receptors in nonhuman primates. Psychopharmacology175(3), 274–286 (2004).
  • Suhara T, Sudo Y, Okauchi T et al. Extrastriatal dopamine D2 receptor density and affinity in the human brain measured by 3D PET. Int. J. Neuropsychopharmacol.2(2), 73–82 (1999).
  • Monchi O, Ko JH, Strafella AP. Striatal dopamine release during performance of executive functions: a [(11)C] raclopride PET study. Neuroimage33(3), 907–912 (2006).
  • Ginovart N, Galineau L, Willeit M et al. Binding characteristics and sensitivity to endogenous dopamine of [11C]-(+)-PHNO, a new agonist radiotracer for imaging the high-affinity state of D2 receptors in vivo using positron emission tomography. J. Neurochem.97(4), 1089–1103 (2006).
  • Narendran R, Slifstein M, Guillin O et al. Dopamine (D2/3) receptor agonist positron emission tomography radiotracer [11C]-(+)-PHNO is a D3 receptor preferring agonist in vivo. Synapse60(7), 485–495 (2006).
  • Narendran R, Frankle WG, Mason NS et al. Positron emission tomography imaging of D(2/3) agonist binding in healthy human subjects with the radiotracer [(11)C]-N-propyl-norapomorphine: preliminary evaluation and reproducibility studies. Synapse63(7), 574–584 (2009).
  • Boileau I, Guttman M, Rusjan P et al.Decreased binding of the D3 dopamine receptor-preferring ligand [11C]-(+)-PHNO in drug-naive Parkinson’s disease. Brain132(5), 1366–1375 (2009).

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