[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 inMovement disorders Vol. 21; no. 4; pp. 510 - 514
Main Authors Lorberboym, Mordechai, Treves, Therese A., Melamed, Eldad, Lampl, Yair, Hellmann, Mark, Djaldetti, Ruth
Format Journal Article
LanguageEnglish
Published Hoboken Wiley Subscription Services, Inc., A Wiley Company 01.04.2006
Wiley
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Online AccessGet full text
ISSN0885-3185
1531-8257
DOI10.1002/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
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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ContentType Journal Article
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Copyright 2005 Movement Disorder Society.
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Issue 4
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
Language English
License http://onlinelibrary.wiley.com/termsAndConditions#vor
CC BY 4.0
Copyright 2005 Movement Disorder Society.
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Notes Tel Aviv University, Tel Aviv, Israel
Amersham Health
Sackler School of Medicine
ArticleID:MDS20748
istex:18A9CB01A41E46195ED24BDD2F997A4CC2256676
National Parkinson Foundation, USA
Alan and Norma Aufzien Chair for Research in Parkinson's Disease
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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.
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– 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.
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  article-title: Dopamine transporter density in young patients with schizophrenia assessed with [ ]I FP‐CIT SPECT
  publication-title: Schizophr Res
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  year: 1997
  end-page: 174
  article-title: Presynaptic dopaminergic function in the striatum of schizophrenic patients
  publication-title: Schizophr Res
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  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
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  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
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  end-page: 1060
  article-title: A survey of drug‐induced extrapyramidal reactions
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  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
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  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
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  publication-title: Mov Disord
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Snippet Parkinsonism in patients taking neuroleptic medications might be induced by dopamine receptor blockade alone or by dopamine blockade with nigrostriatal...
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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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