[123I]-FP/CIT SPECT imaging for distinguishing drug-induced parkinsonism from Parkinson's disease
Parkinsonism in patients taking neuroleptic medications might be induced by dopamine receptor blockade alone or by dopamine blockade with nigrostriatal dysfunction. The differentiation between Parkinson's disease (PD) and drug‐induced parkinsonism (DIP) is difficult to assess on clinical ground...
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Published in | Movement disorders Vol. 21; no. 4; pp. 510 - 514 |
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Main Authors | , , , , , |
Format | Journal Article |
Language | English |
Published |
Hoboken
Wiley Subscription Services, Inc., A Wiley Company
01.04.2006
Wiley |
Subjects | |
Online Access | Get full text |
ISSN | 0885-3185 1531-8257 |
DOI | 10.1002/mds.20748 |
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Abstract | Parkinsonism in patients taking neuroleptic medications might be induced by dopamine receptor blockade alone or by dopamine blockade with nigrostriatal dysfunction. The differentiation between Parkinson's disease (PD) and drug‐induced parkinsonism (DIP) is difficult to assess on clinical grounds alone. In this study, we have evaluated the clinical characteristics and striatal binding of 123I‐FP‐CIT (N‐ω‐fluoropropyl‐2β‐carboxymethoxy‐3β‐{4‐iodophenyl}tropane) in patients who developed DIP. A total of 20 patients (mean age, 62 ± 13 years) who developed parkinsonism while on neuroleptic agents and 10 age‐matched controls were enrolled. [123]‐FP‐CIT single‐photon emission computed tomography (SPECT) was performed in all subjects. Neurological assessment was performed with the Motor part of the Unified Parkinson's Disease Rating Scale. [123]‐FP‐CIT binding of the entire striatum, caudate, and putamen was calculated. Patients were divided into two subgroups according to SPECT results for comparison of clinical characteristics. There were 9 patients who had normal scans and 11 who showed significantly diminished striatal binding, suggesting degeneration of the nigrostriatal system. Subanalyses of abnormal scans revealed significantly diminished binding in the caudate (P < 0.001 for right and left caudate) and putamen (P = 0.002 and P < 0.05 for right and left putamen, respectively). There were no differences in clinical features between patients with normal and abnormal scans. Symptoms included asymmetric tremor, bradykinesia, and rigidity in both groups. Freezing gait was present in two patients with normal scans. These results indicate that DIP is clinically indistinguishable from PD. Brain imaging with FP‐CIT helps to determine whether DIP is entirely drug‐induced or an exacerbation of subclinical PD. © 2005 Movement Disorder Society |
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AbstractList | Parkinsonism in patients taking neuroleptic medications might be induced by dopamine receptor blockade alone or by dopamine blockade with nigrostriatal dysfunction. The differentiation between Parkinson's disease (PD) and drug‐induced parkinsonism (DIP) is difficult to assess on clinical grounds alone. In this study, we have evaluated the clinical characteristics and striatal binding of 123I‐FP‐CIT (N‐ω‐fluoropropyl‐2β‐carboxymethoxy‐3β‐{4‐iodophenyl}tropane) in patients who developed DIP. A total of 20 patients (mean age, 62 ± 13 years) who developed parkinsonism while on neuroleptic agents and 10 age‐matched controls were enrolled. [123]‐FP‐CIT single‐photon emission computed tomography (SPECT) was performed in all subjects. Neurological assessment was performed with the Motor part of the Unified Parkinson's Disease Rating Scale. [123]‐FP‐CIT binding of the entire striatum, caudate, and putamen was calculated. Patients were divided into two subgroups according to SPECT results for comparison of clinical characteristics. There were 9 patients who had normal scans and 11 who showed significantly diminished striatal binding, suggesting degeneration of the nigrostriatal system. Subanalyses of abnormal scans revealed significantly diminished binding in the caudate (P < 0.001 for right and left caudate) and putamen (P = 0.002 and P < 0.05 for right and left putamen, respectively). There were no differences in clinical features between patients with normal and abnormal scans. Symptoms included asymmetric tremor, bradykinesia, and rigidity in both groups. Freezing gait was present in two patients with normal scans. These results indicate that DIP is clinically indistinguishable from PD. Brain imaging with FP‐CIT helps to determine whether DIP is entirely drug‐induced or an exacerbation of subclinical PD. © 2005 Movement Disorder Society Parkinsonism in patients taking neuroleptic medications might be induced by dopamine receptor blockade alone or by dopamine blockade with nigrostriatal dysfunction. The differentiation between Parkinson's disease (PD) and drug‐induced parkinsonism (DIP) is difficult to assess on clinical grounds alone. In this study, we have evaluated the clinical characteristics and striatal binding of 123 I‐FP‐CIT (N‐ω‐fluoropropyl‐2β‐carboxymethoxy‐3β‐{4‐iodophenyl}tropane) in patients who developed DIP. A total of 20 patients (mean age, 62 ± 13 years) who developed parkinsonism while on neuroleptic agents and 10 age‐matched controls were enrolled. [123]‐FP‐CIT single‐photon emission computed tomography (SPECT) was performed in all subjects. Neurological assessment was performed with the Motor part of the Unified Parkinson's Disease Rating Scale. [123]‐FP‐CIT binding of the entire striatum, caudate, and putamen was calculated. Patients were divided into two subgroups according to SPECT results for comparison of clinical characteristics. There were 9 patients who had normal scans and 11 who showed significantly diminished striatal binding, suggesting degeneration of the nigrostriatal system. Subanalyses of abnormal scans revealed significantly diminished binding in the caudate ( P < 0.001 for right and left caudate) and putamen ( P = 0.002 and P < 0.05 for right and left putamen, respectively). There were no differences in clinical features between patients with normal and abnormal scans. Symptoms included asymmetric tremor, bradykinesia, and rigidity in both groups. Freezing gait was present in two patients with normal scans. These results indicate that DIP is clinically indistinguishable from PD. Brain imaging with FP‐CIT helps to determine whether DIP is entirely drug‐induced or an exacerbation of subclinical PD. © 2005 Movement Disorder Society Parkinsonism in patients taking neuroleptic medications might be induced by dopamine receptor blockade alone or by dopamine blockade with nigrostriatal dysfunction. The differentiation between Parkinson's disease (PD) and drug-induced parkinsonism (DIP) is difficult to assess on clinical grounds alone. In this study, we have evaluated the clinical characteristics and striatal binding of super(123)I-FP-CIT (N- omega -fluoropropyl-2 beta -carboxymethoxy-3 beta -{4-iodophen yl}tropane) in patients who developed DIP. A total of 20 patients (mean age, 62 plus or minus 13 years) who developed parkinsonism while on neuroleptic agents and 10 age-matched controls were enrolled. [123]-FP-CIT single-photon emission computed tomography (SPECT) was performed in all subjects. Neurological assessment was performed with the Motor part of the Unified Parkinson's Disease Rating Scale. [123]-FP-CIT binding of the entire striatum, caudate, and putamen was calculated. Patients were divided into two subgroups according to SPECT results for comparison of clinical characteristics. There were 9 patients who had normal scans and 11 who showed significantly diminished striatal binding, suggesting degeneration of the nigrostriatal system. Subanalyses of abnormal scans revealed significantly diminished binding in the caudate (P < 0.001 for right and left caudate) and putamen (P = 0.002 and P < 0.05 for right and left putamen, respectively). There were no differences in clinical features between patients with normal and abnormal scans. Symptoms included asymmetric tremor, bradykinesia, and rigidity in both groups. Freezing gait was present in two patients with normal scans. These results indicate that DIP is clinically indistinguishable from PD. Brain imaging with FP-CIT helps to determine whether DIP is entirely drug-induced or an exacerbation of subclinical PD. copyright 2005 Movement Disorder Society Parkinsonism in patients taking neuroleptic medications might be induced by dopamine receptor blockade alone or by dopamine blockade with nigrostriatal dysfunction. The differentiation between Parkinson's disease (PD) and drug-induced parkinsonism (DIP) is difficult to assess on clinical grounds alone. In this study, we have evaluated the clinical characteristics and striatal binding of 123I-FP-CIT (N-fluoropropyl-2-carboxymethoxy-3-{4-iodophenyl}tropane) in patients who developed DIP. A total of 20 patients (mean age, 62 ± 13 years) who developed parkinsonism while on neuroleptic agents and 10 age-matched controls were enrolled. [123]-FP-CIT single-photon emission computed tomography (SPECT) was performed in all subjects. Neurological assessment was performed with the Motor part of the Unified Parkinson's Disease Rating Scale. [123]-FP-CIT binding of the entire striatum, caudate, and putamen was calculated. Patients were divided into two subgroups according to SPECT results for comparison of clinical characteristics. There were 9 patients who had normal scans and 11 who showed significantly diminished striatal binding, suggesting degeneration of the nigrostriatal system. Subanalyses of abnormal scans revealed significantly diminished binding in the caudate (P < 0.001 for right and left caudate) and putamen (P = 0.002 and P < 0.05 for right and left putamen, respectively). There were no differences in clinical features between patients with normal and abnormal scans. Symptoms included asymmetric tremor, bradykinesia, and rigidity in both groups. Freezing gait was present in two patients with normal scans. These results indicate that DIP is clinically indistinguishable from PD. Brain imaging with FP-CIT helps to determine whether DIP is entirely drug-induced or an exacerbation of subclinical PD. Parkinsonism in patients taking neuroleptic medications might be induced by dopamine receptor blockade alone or by dopamine blockade with nigrostriatal dysfunction. The differentiation between Parkinson's disease (PD) and drug-induced parkinsonism (DIP) is difficult to assess on clinical grounds alone. In this study, we have evaluated the clinical characteristics and striatal binding of (123)I-FP-CIT (N-omega-fluoropropyl-2beta-carboxymethoxy-3beta-{4-iodophenyl}tropane) in patients who developed DIP. A total of 20 patients (mean age, 62 +/- 13 years) who developed parkinsonism while on neuroleptic agents and 10 age-matched controls were enrolled. [123]-FP-CIT single-photon emission computed tomography (SPECT) was performed in all subjects. Neurological assessment was performed with the Motor part of the Unified Parkinson's Disease Rating Scale. [123]-FP-CIT binding of the entire striatum, caudate, and putamen was calculated. Patients were divided into two subgroups according to SPECT results for comparison of clinical characteristics. There were 9 patients who had normal scans and 11 who showed significantly diminished striatal binding, suggesting degeneration of the nigrostriatal system. Subanalyses of abnormal scans revealed significantly diminished binding in the caudate (P < 0.001 for right and left caudate) and putamen (P = 0.002 and P < 0.05 for right and left putamen, respectively). There were no differences in clinical features between patients with normal and abnormal scans. Symptoms included asymmetric tremor, bradykinesia, and rigidity in both groups. Freezing gait was present in two patients with normal scans. These results indicate that DIP is clinically indistinguishable from PD. Brain imaging with FP-CIT helps to determine whether DIP is entirely drug-induced or an exacerbation of subclinical PD. Parkinsonism in patients taking neuroleptic medications might be induced by dopamine receptor blockade alone or by dopamine blockade with nigrostriatal dysfunction. The differentiation between Parkinson's disease (PD) and drug-induced parkinsonism (DIP) is difficult to assess on clinical grounds alone. In this study, we have evaluated the clinical characteristics and striatal binding of (123)I-FP-CIT (N-omega-fluoropropyl-2beta-carboxymethoxy-3beta-{4-iodophenyl}tropane) in patients who developed DIP. A total of 20 patients (mean age, 62 +/- 13 years) who developed parkinsonism while on neuroleptic agents and 10 age-matched controls were enrolled. [123]-FP-CIT single-photon emission computed tomography (SPECT) was performed in all subjects. Neurological assessment was performed with the Motor part of the Unified Parkinson's Disease Rating Scale. [123]-FP-CIT binding of the entire striatum, caudate, and putamen was calculated. Patients were divided into two subgroups according to SPECT results for comparison of clinical characteristics. There were 9 patients who had normal scans and 11 who showed significantly diminished striatal binding, suggesting degeneration of the nigrostriatal system. Subanalyses of abnormal scans revealed significantly diminished binding in the caudate (P < 0.001 for right and left caudate) and putamen (P = 0.002 and P < 0.05 for right and left putamen, respectively). There were no differences in clinical features between patients with normal and abnormal scans. Symptoms included asymmetric tremor, bradykinesia, and rigidity in both groups. Freezing gait was present in two patients with normal scans. These results indicate that DIP is clinically indistinguishable from PD. Brain imaging with FP-CIT helps to determine whether DIP is entirely drug-induced or an exacerbation of subclinical PD.Copyright 2005 Movement Disorder Society. |
Author | Melamed, Eldad Lampl, Yair Hellmann, Mark Treves, Therese A. Djaldetti, Ruth Lorberboym, Mordechai |
Author_xml | – sequence: 1 givenname: Mordechai surname: Lorberboym fullname: Lorberboym, Mordechai organization: Department of Nuclear Medicine Edith Wolfson Medical Center, Holon, Israel – sequence: 2 givenname: Therese A. surname: Treves fullname: Treves, Therese A. organization: Department of Neurology, Rabin Medical Center, Petah Tiqwa and Sackler Faculty of Medicine, Tel Aviv University, Tel Aviv, Israel – sequence: 3 givenname: Eldad surname: Melamed fullname: Melamed, Eldad organization: Department of Neurology, Rabin Medical Center, Petah Tiqwa and Sackler Faculty of Medicine, Tel Aviv University, Tel Aviv, Israel – sequence: 4 givenname: Yair surname: Lampl fullname: Lampl, Yair organization: Department of Neurology, Edith Wolfson Medical Center, Holon, Israel – sequence: 5 givenname: Mark surname: Hellmann fullname: Hellmann, Mark organization: Department of Neurology, Rabin Medical Center, Petah Tiqwa and Sackler Faculty of Medicine, Tel Aviv University, Tel Aviv, Israel – sequence: 6 givenname: Ruth surname: Djaldetti fullname: Djaldetti, Ruth email: ruthdjal@clalit.org.il organization: Department of Neurology, Rabin Medical Center, Petah Tiqwa and Sackler Faculty of Medicine, Tel Aviv University, Tel Aviv, Israel |
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Keywords | presynaptic degeneration Nervous system diseases Parkinson's disease Parkinson disease Single photon emission tomography [123I]-FP/CIT SPECT Photon drug-induced Parkinsonism Cerebral disorder Parkinsonism Central nervous system disease Degenerative disease Degeneration Extrapyramidal syndrome Presynaptic |
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PublicationTitle | Movement disorders |
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References | Hietala J, Syvalahti E, Vuorio K, et al. Presynaptic dopamine function in striatum of neuroleptic-naive schizophrenic patients. Lancet 1995; 346: 1130-1131. Meyer-Lindenberg A, Miletich RS, Kohn PD, et al. Reduced prefrontal activity predicts exaggerated striatal dopaminergic function in schizophrenia. Nat Neurosci 2002; 5: 267-271. Goetz CG. Drug-induced parkinsonism and idiopathic Parkinson's disease. Arch Neurol 1983; 40: 325-326. Marti-Massó JF, Carrera N, Urtasun M. Drug-induced parkinsonism: a growing list [letter]. Mov Disord 1993; 8: 125. Hausner RS. Neuroleptic-induced parkinsonism and Parkinson's disease: differential diagnosis and treatment. J Clin Psychiatry 1983; 44: 13-16. Hassin-Baer S, Sirota P, Korczyn AD, et al. Clinical characteristics of neuroleptic-induced parkinsonism. J Neural Transm 2001; 108: 1299-1308. Melamed E, Achiron A, Shapira A, Davidovicz S. Persistent and progressive parkinsonism after discontinuation of chronic neuroleptic therapy: an additional tardive syndrome? Clin Neuropharmacol 1991; 14: 273-278. Reith J, Benkelfat C, Sherwin A, et al. Elevated dopa decarboxylase activity in living brain of patients with psychosis. Proc Natl Acad Sci U S A 1994; 91: 11651-11654. Burn DJ, Brooks DJ. Nigral dysfunction in drug-induced parkinsonism: an 18F-dopa PET study. Neurology 1993; 43: 552-556. Chakos MH, Mayerhoff DI, Loebel AD, Alvir JM, Lieberman JA. Incidence and correlates of acute extrapyramidal symptoms in first episode of schizophrenia. Psychopharmacol Bull 1992; 28: 81-86. Dao-Castellana MH, Paillere-Martinot ML, Hantraye P, et al. Presynaptic dopaminergic function in the striatum of schizophrenic patients. Schizophr Res 1997; 23: 167-174. Ayd FJ. A survey of drug-induced extrapyramidal reactions. JAMA 1961; 175: 1054-1060. McCreadie RG. The Nithsdale schizophrenia surveys. An overview. Soc Psychiatry Psychiatr Epidemiol 1992; 27: 40-45. Booij J, Speelman JD, Horstink MW, Wolters EC. The clinical benefit of imaging striatal dopamine transporters with [123I]FP-CIT SPECT in differentiating patients with presynaptic parkinsonism from those with other forms of parkinsonism. Eur J Nucl Med 2001; 28: 266-272. Hardie RJ, Lees AJ. Neuroleptic-induced Parkinson's syndrome: clinical features and results of treatment with levodopa. J Neurol Neurosurg Psychiatry 1988; 51: 850-854. Tolosa E, Coelho M, Gallardo M. DAT imaging in drug-induced and psychogenic parkinsonism. Mov Disord 2003; 18(Suppl. 7): S28-S33. McGowan S, Lawrence AD, Sales T, Quested D, Grasby P. Presynaptic dopaminergic dysfunction in schizophrenia. A positron emission tomographic [18F]fluorodopa study. Arch Gen Psychiatry 2004; 61: 134-142. Miller LG, Jankovic J. Metoclopramide-induced movement disorders. Arch Intern Med 1989; 149: 2486-2492. Lavalaye J, Linszen DH, Booij J, et al. Dopamine transporter density in young patients with schizophrenia assessed with [123]I FP-CIT SPECT. Schizophr Res 2001; 47: 59-67. Hansen TE, Brown WL, Weigel RM, Casey DE. Underrecognition of tardive dyskinesia and drug-induced parkinsonism by psychiatric residents. Gen Hosp Psychiatry 1992; 14: 340-344. Klawans HL, Bergen D, Bruyn GW. Prolonged drug-induced Parkinsonism. Confin Neurol 1973; 35: 368-377. Stephen PJ, Williamson J. Drug-induced parkinsonism in the elderly. Lancet 1984; 2: 1082-1083. Laakso A, Bergman J, Haaparanta M, et al. Decreased striatal dopamine transporter binding in vivo in chronic schizophrenia. Schizophr Res 2001; 52: 115-120. Korczyn AD, Goldberg GJ. Extrapyramidal effects of neuroleptics. J Neurol Neurosurg Psychiatry 1976; 39: 866-869. Rajput AH, Rozdilsky B, Hornykiewicz O, Shannak K, Lee T, Seeman P. Reversible drug-induced parkinsonism. Clinicopathologic study of two cases. Arch Neurol 1982; 39: 644-646. 1993; 8 2004; 61 1982; 39 1991; 14 1973; 35 2002; 5 1993; 43 1997; 23 1992; 14 2003; 18 1988; 51 2001; 28 2001; 108 2001; 47 1961; 175 1989; 149 1984; 2 1992; 28 1983; 40 1995; 346 1992; 27 1994; 91 1976; 39 2001; 52 1983; 44 e_1_2_6_18_2 e_1_2_6_19_2 e_1_2_6_12_2 e_1_2_6_13_2 e_1_2_6_10_2 e_1_2_6_11_2 e_1_2_6_16_2 e_1_2_6_17_2 e_1_2_6_14_2 e_1_2_6_15_2 Marti‐Massó JF (e_1_2_6_2_2) 1993; 8 e_1_2_6_20_2 Hausner RS (e_1_2_6_9_2) 1983; 44 Chakos MH (e_1_2_6_3_2) 1992; 28 e_1_2_6_8_2 e_1_2_6_7_2 e_1_2_6_4_2 e_1_2_6_6_2 e_1_2_6_5_2 e_1_2_6_24_2 e_1_2_6_23_2 e_1_2_6_22_2 e_1_2_6_21_2 e_1_2_6_26_2 e_1_2_6_25_2 |
References_xml | – reference: Hardie RJ, Lees AJ. Neuroleptic-induced Parkinson's syndrome: clinical features and results of treatment with levodopa. J Neurol Neurosurg Psychiatry 1988; 51: 850-854. – reference: Melamed E, Achiron A, Shapira A, Davidovicz S. Persistent and progressive parkinsonism after discontinuation of chronic neuroleptic therapy: an additional tardive syndrome? Clin Neuropharmacol 1991; 14: 273-278. – reference: Hansen TE, Brown WL, Weigel RM, Casey DE. Underrecognition of tardive dyskinesia and drug-induced parkinsonism by psychiatric residents. Gen Hosp Psychiatry 1992; 14: 340-344. – reference: Goetz CG. Drug-induced parkinsonism and idiopathic Parkinson's disease. Arch Neurol 1983; 40: 325-326. – reference: Tolosa E, Coelho M, Gallardo M. DAT imaging in drug-induced and psychogenic parkinsonism. Mov Disord 2003; 18(Suppl. 7): S28-S33. – reference: Klawans HL, Bergen D, Bruyn GW. Prolonged drug-induced Parkinsonism. Confin Neurol 1973; 35: 368-377. – reference: McGowan S, Lawrence AD, Sales T, Quested D, Grasby P. Presynaptic dopaminergic dysfunction in schizophrenia. A positron emission tomographic [18F]fluorodopa study. Arch Gen Psychiatry 2004; 61: 134-142. – reference: Laakso A, Bergman J, Haaparanta M, et al. Decreased striatal dopamine transporter binding in vivo in chronic schizophrenia. Schizophr Res 2001; 52: 115-120. – reference: Meyer-Lindenberg A, Miletich RS, Kohn PD, et al. Reduced prefrontal activity predicts exaggerated striatal dopaminergic function in schizophrenia. Nat Neurosci 2002; 5: 267-271. – reference: Burn DJ, Brooks DJ. Nigral dysfunction in drug-induced parkinsonism: an 18F-dopa PET study. Neurology 1993; 43: 552-556. – reference: Korczyn AD, Goldberg GJ. Extrapyramidal effects of neuroleptics. J Neurol Neurosurg Psychiatry 1976; 39: 866-869. – reference: Hausner RS. Neuroleptic-induced parkinsonism and Parkinson's disease: differential diagnosis and treatment. J Clin Psychiatry 1983; 44: 13-16. – reference: Marti-Massó JF, Carrera N, Urtasun M. Drug-induced parkinsonism: a growing list [letter]. Mov Disord 1993; 8: 125. – reference: Hassin-Baer S, Sirota P, Korczyn AD, et al. Clinical characteristics of neuroleptic-induced parkinsonism. J Neural Transm 2001; 108: 1299-1308. – reference: Booij J, Speelman JD, Horstink MW, Wolters EC. The clinical benefit of imaging striatal dopamine transporters with [123I]FP-CIT SPECT in differentiating patients with presynaptic parkinsonism from those with other forms of parkinsonism. Eur J Nucl Med 2001; 28: 266-272. – reference: Rajput AH, Rozdilsky B, Hornykiewicz O, Shannak K, Lee T, Seeman P. Reversible drug-induced parkinsonism. Clinicopathologic study of two cases. Arch Neurol 1982; 39: 644-646. – reference: McCreadie RG. The Nithsdale schizophrenia surveys. An overview. Soc Psychiatry Psychiatr Epidemiol 1992; 27: 40-45. – reference: Hietala J, Syvalahti E, Vuorio K, et al. Presynaptic dopamine function in striatum of neuroleptic-naive schizophrenic patients. Lancet 1995; 346: 1130-1131. – reference: Stephen PJ, Williamson J. Drug-induced parkinsonism in the elderly. Lancet 1984; 2: 1082-1083. – reference: Reith J, Benkelfat C, Sherwin A, et al. Elevated dopa decarboxylase activity in living brain of patients with psychosis. Proc Natl Acad Sci U S A 1994; 91: 11651-11654. – reference: Chakos MH, Mayerhoff DI, Loebel AD, Alvir JM, Lieberman JA. Incidence and correlates of acute extrapyramidal symptoms in first episode of schizophrenia. Psychopharmacol Bull 1992; 28: 81-86. – reference: Lavalaye J, Linszen DH, Booij J, et al. Dopamine transporter density in young patients with schizophrenia assessed with [123]I FP-CIT SPECT. Schizophr Res 2001; 47: 59-67. – reference: Ayd FJ. A survey of drug-induced extrapyramidal reactions. JAMA 1961; 175: 1054-1060. – reference: Miller LG, Jankovic J. Metoclopramide-induced movement disorders. Arch Intern Med 1989; 149: 2486-2492. – reference: Dao-Castellana MH, Paillere-Martinot ML, Hantraye P, et al. Presynaptic dopaminergic function in the striatum of schizophrenic patients. Schizophr Res 1997; 23: 167-174. – volume: 47 start-page: 59 year: 2001 end-page: 67 article-title: Dopamine transporter density in young patients with schizophrenia assessed with [ ]I FP‐CIT SPECT publication-title: Schizophr Res – volume: 23 start-page: 167 year: 1997 end-page: 174 article-title: Presynaptic dopaminergic function in the striatum of schizophrenic patients publication-title: Schizophr Res – volume: 51 start-page: 850 year: 1988 end-page: 854 article-title: Neuroleptic‐induced Parkinson's syndrome: clinical features and results of treatment with levodopa publication-title: J Neurol Neurosurg Psychiatry – volume: 8 start-page: 125 year: 1993 article-title: Drug‐induced parkinsonism: a growing list publication-title: Mov Disord – volume: 35 start-page: 368 year: 1973 end-page: 377 article-title: Prolonged drug‐induced Parkinsonism publication-title: Confin Neurol – volume: 149 start-page: 2486 year: 1989 end-page: 2492 article-title: Metoclopramide‐induced movement disorders publication-title: Arch Intern Med – volume: 44 start-page: 13 year: 1983 end-page: 16 article-title: Neuroleptic‐induced parkinsonism and Parkinson's disease: differential diagnosis and treatment publication-title: J Clin Psychiatry – volume: 175 start-page: 1054 year: 1961 end-page: 1060 article-title: A survey of drug‐induced extrapyramidal reactions publication-title: JAMA – volume: 39 start-page: 644 year: 1982 end-page: 646 article-title: Reversible drug‐induced parkinsonism. Clinicopathologic study of two cases publication-title: Arch Neurol – volume: 39 start-page: 866 year: 1976 end-page: 869 article-title: Extrapyramidal effects of neuroleptics publication-title: J Neurol Neurosurg Psychiatry – volume: 346 start-page: 1130 year: 1995 end-page: 1131 article-title: Presynaptic dopamine function in striatum of neuroleptic‐naive schizophrenic patients publication-title: Lancet – volume: 28 start-page: 266 year: 2001 end-page: 272 article-title: The clinical benefit of imaging striatal dopamine transporters with [ I]FP‐CIT SPECT in differentiating patients with presynaptic parkinsonism from those with other forms of parkinsonism publication-title: Eur J Nucl Med – volume: 14 start-page: 340 year: 1992 end-page: 344 article-title: Underrecognition of tardive dyskinesia and drug‐induced parkinsonism by psychiatric residents publication-title: Gen Hosp Psychiatry – volume: 2 start-page: 1082 year: 1984 end-page: 1083 article-title: Drug‐induced parkinsonism in the elderly publication-title: Lancet – volume: 28 start-page: 81 year: 1992 end-page: 86 article-title: Incidence and correlates of acute extrapyramidal symptoms in first episode of schizophrenia publication-title: Psychopharmacol Bull – volume: 43 start-page: 552 year: 1993 end-page: 556 article-title: Nigral dysfunction in drug‐induced parkinsonism: an F‐dopa PET study publication-title: Neurology – volume: 40 start-page: 325 year: 1983 end-page: 326 article-title: Drug‐induced parkinsonism and idiopathic Parkinson's disease publication-title: Arch Neurol – volume: 5 start-page: 267 year: 2002 end-page: 271 article-title: Reduced prefrontal activity predicts exaggerated striatal dopaminergic function in schizophrenia publication-title: Nat Neurosci – volume: 27 start-page: 40 year: 1992 end-page: 45 article-title: The Nithsdale schizophrenia surveys. An overview publication-title: Soc Psychiatry Psychiatr Epidemiol – volume: 18 start-page: S28 issue: Suppl. 7 year: 2003 end-page: S33 article-title: DAT imaging in drug‐induced and psychogenic parkinsonism publication-title: Mov Disord – volume: 14 start-page: 273 year: 1991 end-page: 278 article-title: Persistent and progressive parkinsonism after discontinuation of chronic neuroleptic therapy: an additional tardive syndrome? publication-title: Clin Neuropharmacol – volume: 108 start-page: 1299 year: 2001 end-page: 1308 article-title: Clinical characteristics of neuroleptic‐induced parkinsonism publication-title: J Neural Transm – volume: 91 start-page: 11651 year: 1994 end-page: 11654 article-title: Elevated dopa decarboxylase activity in living brain of patients with psychosis publication-title: Proc Natl Acad Sci U S A – volume: 52 start-page: 115 year: 2001 end-page: 120 article-title: Decreased striatal dopamine transporter binding in vivo in chronic schizophrenia publication-title: Schizophr Res – volume: 61 start-page: 134 year: 2004 end-page: 142 article-title: Presynaptic dopaminergic dysfunction in schizophrenia. A positron emission tomographic [18F]fluorodopa study publication-title: Arch Gen Psychiatry – ident: e_1_2_6_11_2 doi: 10.1002/mds.10575 – ident: e_1_2_6_12_2 doi: 10.1007/s002590000460 – ident: e_1_2_6_5_2 doi: 10.1001/jama.1961.03040120016004 – ident: e_1_2_6_14_2 doi: 10.1016/S0920-9964(96)00102-8 – ident: e_1_2_6_16_2 doi: 10.1016/S0140-6736(95)91801-9 – ident: e_1_2_6_17_2 doi: 10.1038/nn804 – ident: e_1_2_6_18_2 doi: 10.1001/archpsyc.61.2.134 – ident: e_1_2_6_19_2 doi: 10.1016/S0920-9964(00)00095-5 – ident: e_1_2_6_21_2 doi: 10.1136/jnnp.39.9.866 – ident: e_1_2_6_26_2 doi: 10.1001/archneur.1982.00510220042009 – ident: e_1_2_6_24_2 doi: 10.1136/jnnp.51.6.850 – ident: e_1_2_6_22_2 doi: 10.1159/000102857 – volume: 28 start-page: 81 year: 1992 ident: e_1_2_6_3_2 article-title: Incidence and correlates of acute extrapyramidal symptoms in first episode of schizophrenia publication-title: Psychopharmacol Bull – ident: e_1_2_6_8_2 doi: 10.1016/0163-8343(92)90069-M – ident: e_1_2_6_23_2 doi: 10.1097/00002826-199106000-00013 – ident: e_1_2_6_20_2 doi: 10.1212/WNL.43.3_Part_1.552 – ident: e_1_2_6_25_2 doi: 10.1001/archneur.1983.04050050093019 – ident: e_1_2_6_10_2 doi: 10.1007/s007020100006 – ident: e_1_2_6_15_2 doi: 10.1073/pnas.91.24.11651 – ident: e_1_2_6_7_2 doi: 10.1001/archinte.1989.00390110070015 – ident: e_1_2_6_6_2 doi: 10.1016/S0140-6736(84)91516-2 – volume: 44 start-page: 13 year: 1983 ident: e_1_2_6_9_2 article-title: Neuroleptic‐induced parkinsonism and Parkinson's disease: differential diagnosis and treatment publication-title: J Clin Psychiatry – ident: e_1_2_6_4_2 doi: 10.1007/BF00788955 – volume: 8 start-page: 125 year: 1993 ident: e_1_2_6_2_2 article-title: Drug‐induced parkinsonism: a growing list publication-title: Mov Disord – ident: e_1_2_6_13_2 doi: 10.1016/S0920-9964(00)00023-2 |
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SubjectTerms | [123I]-FP/CIT SPECT Aged Aged, 80 and over Biological and medical sciences Case-Control Studies Degenerative and inherited degenerative diseases of the nervous system. Leukodystrophies. Prion diseases Drug toxicity and drugs side effects treatment drug-induced Parkinsonism Female Humans Image Processing, Computer-Assisted - methods Iodine Radioisotopes Iodine Radioisotopes: diagnostic use Male Medical sciences Middle Aged Neurology Parkinson Disease - diagnostic imaging Parkinson Disease: radionuclide imaging Parkinson's disease Parkinsonian Disorders - chemically induced Parkinsonian Disorders - diagnostic imaging Parkinsonian Disorders: radionuclide imaging Pharmacology. Drug treatments presynaptic degeneration Severity of Illness Index Statistics, Nonparametric Tomography, Emission-Computed, Single-Photon Toxicity: nervous system and muscle Tropanes Tropanes: diagnostic use |
Title | [123I]-FP/CIT SPECT imaging for distinguishing drug-induced parkinsonism from Parkinson's disease |
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