title: [123]IBZM binding predicts dopaminergic responsiveness in patients with parkinsonism and previous dopaminomimetic therapy.
abstract: We investigated the cases of 55 patients with parkinsonism and prior dopaminomimetic therapy in whom the response to this treatment was questionable or reported to be negative. None of these patients had shown motor fluctuations prior to this study. We compared the results of imaging of dopamine-D2 receptors by using [123I]iodobenzamide-single-photon-emission computed tomography (IBZM-SPECT) with the improvement in motor signs following a subcutaneous injection of apomorphine and a subsequent increase in oral dopaminomimetic therapy. IBZM-SPECT accurately predicted a positive or negative response to apomorphine in 37 (84%) of 44 patients. The sensitivity/specificity was calculated as 96.3%/ 64.7%. The sensitivity/specificity of IBZM-SPECT for the response to oral treatment with levodopa (L-dopa) was calculated as 100%/75%. After a follow-up period of 2-4 years, 25 patients developed motor fluctuations. All of these patients had normal IBZM binding. Nine developed clinical signs indicating a basal ganglia disorder other than Parkinson's disease. Eight of these nine patients had reduced, and one patient had normal, IBZM binding. We conclude that normal IBZM binding is a useful predictor of a good response to dopaminergic drugs in patients with parkinsonism and a questionable response to previous dopaminomimetic therapy. Reduced IBZM binding seems to exclude a diagnosis of Parkinson's disease, because none of the latter patients clearly benefited from L-dopa and 66.7% developed clinical signs indicating another disorder of the basal ganglia.
authors.affiliation: Department of Neurology, Klinikum Grosshadern, Ludwig-Maximilian University, Germany.
authors.forename: J
authors.initials: J
authors.lastname: Schwarz
authors.forename: K
authors.initials: K
authors.lastname: Tatsch
authors.forename: T
authors.initials: T
authors.lastname: Gasser
authors.forename: G
authors.initials: G
authors.lastname: Arnold
authors.forename: W H
authors.initials: WH
authors.lastname: Oertel
mesh_terms: D000328:Adult; D000368:Aged; D001058:Apomorphine / Q000378:metabolism; D001284:Atrophy / Q000473:pathology; D001549:Benzamides / Q000493:pharmacokinetics*; D001665:Binding Sites; D002540:Cerebral Cortex / Q000473:pathology; D004298:Dopamine / Q000378:metabolism*; D018491:Dopamine Agonists / Q000378:metabolism* / Q000627:therapeutic use*; D018492:Dopamine Antagonists / Q000493:pharmacokinetics*; D005500:Follow-Up Studies; D006801:Humans; D007980:Levodopa / Q000627:therapeutic use*; D008279:Magnetic Resonance Imaging; D008875:Middle Aged; D010300:Parkinson Disease / Q000000981:diagnostic imaging* / Q000188:drug therapy* / Q000473:pathology; D011237:Predictive Value of Tests; D011699:Putamen / Q000473:pathology; D011759:Pyrrolidines / Q000493:pharmacokinetics*; D017448:Receptors, Dopamine D2 / Q000187:drug effects; D015899:Tomography, Emission-Computed, Single-Photon
chemical_list: D001549:Benzamides; D018491:Dopamine Agonists; D018492:Dopamine Antagonists; D011759:Pyrrolidines; D017448:Receptors, Dopamine D2; D007980:Levodopa; C055743:3-iodo-2-hydroxy-6-methoxy-N-((1-ethyl-2-pyrrolidinyl)methyl)benzamide; D001058:Apomorphine; D004298:Dopamine