123I-FP-CIT semi-quantitative SPECT detects preclinical bilateral dopaminergic deficit in early Parkinson's disease with unilateral symptoms

Background and aim123I-FP-CIT SPECT has been successfully used to detect the loss of dopaminergic nigrostriatal neurons in Parkinson's disease at an early stage. In this study we evaluated the capacity of 123I-FP-CIT SPECT to assess bilateral dopamine transporter (DAT) loss in de-novo hemi-Parkinson's disease (PD) patients with one-sided clinical symptoms. Patients and methodsTwenty-nine de-novo hemi-PD patients at an early stage (Hoehn & Yahr stage 1) and 18 gender and age matched healthy subjects were studied. SPECT imaging was always performed at 4 h post-injection. The ratios of striatal (S) to non-specific occipital (O) binding for the entire striatum (S/O), caudate nuclei (C/O), putamina (Pput/O), and the putamen to caudate nucleus index (Pput/C) were calculated in both the basal ganglia. ResultsIn PD patients S/O, C/O and Pput/O ratio values contralateral to the clinically affected side were significantly lower (P<0.001) than in the control group (−38%, −34% and −42%, respectively). A significant reduction (P<0.001) of the striatal binding ratios was also found ipsilaterally (S/O, −31%; C/O, −28%; Pput/O, −33%). The Pput/C index was also bilaterally significantly reduced (P<0.01). DAT loss was significantly greater (P<0.001) in the contralateral than in the ipsilateral S; and putamen bilaterally presented a higher dopaminergic deficit than did caudate. ConclusionOur results indicate that semi-quantitative 123I-FP-CIT SPECT detects a bilateral dopaminergic deficit in early PD with unilateral symptoms and preclinical DAT loss in the ipsilateral striatal binding, corresponding to the side not yet affected by motor signs. Semi-quantitative analysis may thus be used to diagnose PD at an early stage as well as to identify individuals developing bilateral dopaminergic damage.

[1]  K. Jellinger,et al.  Brain dopamine and the syndromes of Parkinson and Huntington. Clinical, morphological and neurochemical correlations. , 1973, Journal of the neurological sciences.

[2]  Jan Booij,et al.  Iodine-123-N-ω-Fluoropropyl-2β-Carbomethoxy-3β-(4-Iodophenyl)Tropane SPECT in Healthy Controls and Early-Stage, Drug-Naive Parkinson's Disease , 1998 .

[3]  K Van Laere,et al.  Automated stereotactic standardization of brain SPECT receptor data using single-photon transmission images. , 2001, Journal of nuclear medicine : official publication, Society of Nuclear Medicine.

[4]  P J Slomka,et al.  Optimization of automated quantification of 123I-IBZM uptake in the striatum applied to parkinsonism. , 2000, Journal of nuclear medicine : official publication, Society of Nuclear Medicine.

[5]  D. Schaid,et al.  Detection of preclinical Parkinson disease in at-risk family members with use of [123I]beta-CIT and SPECT: an exploratory study. , 1999, Mayo Clinic proceedings.

[6]  S. Gacinovic,et al.  Accurate differentiation of parkinsonism and essential tremor using visual assessment of [123I]‐FP‐CIT SPECT imaging: The [123I]‐FP‐CIT study group , 2000, Movement disorders : official journal of the Movement Disorder Society.

[7]  H. Berendse,et al.  Preclinical (premotor) Parkinson’s disease , 2000, Journal of Neurology.

[8]  J. P. Seibyl,et al.  [sup 123 I] beta-CIT/SPECT imaging demonstrates bilateral loss of dopamine transporters in hemi-Parkinson's disease , 1996, Neurology.

[9]  H. Berendse,et al.  [Presymptomatic detection of Parkinson's disease]. , 2002, Tijdschrift voor gerontologie en geriatrie.

[10]  C Trenkwalder,et al.  Striatal dopamine transporter binding assessed by [I-123]IPT and single photon emission computed tomography in patients with early Parkinson's disease: implications for a preclinical diagnosis. , 2000, Archives of neurology.

[11]  H. Reichmann,et al.  Practical importance of neuroprotection in Parkinson's disease , 2002, Journal of Neurology.

[12]  Haruhiko Akiyama,et al.  Rate of cell death in parkinsonism indicates active neuropathological process , 1988, Annals of neurology.

[13]  J. Booij,et al.  Practical benefit of [123I]FP-CIT SPET in the demonstration of the dopaminergic deficit in Parkinson's disease , 2005, European Journal of Nuclear Medicine.

[14]  R. Mayeux,et al.  Does a long preclinical period occur in Parkinson's disease? , 1991, Neurology.

[15]  Yi-Hsin Weng,et al.  Sensitivity and specificity of 99mTc-TRODAT-1 SPECT imaging in differentiating patients with idiopathic Parkinson's disease from healthy subjects. , 2004, Journal of nuclear medicine : official publication, Society of Nuclear Medicine.

[16]  M. Kaufman,et al.  Severe depletion of cocaine recognition sites associated with the dopamine transporter in Parkinson's‐diseased striatum , 1991, Synapse.

[17]  P Slomka,et al.  Quantification and visualization of defects of the functional dopaminergic system using an automatic algorithm. , 1999, Journal of nuclear medicine : official publication, Society of Nuclear Medicine.

[18]  J B Habraken,et al.  Imaging of dopamine transporters with iodine-123-FP-CIT SPECT in healthy controls and patients with Parkinson's disease. , 1998, Journal of nuclear medicine : official publication, Society of Nuclear Medicine.

[19]  P. Riederer,et al.  Is there neuroprotection in Parkinson syndrome? , 2000, Journal of Neurology.

[20]  J. C. Stoof,et al.  Evaluation of [123I] beta-CIT binding with SPECT in controls, early and late Parkinson's disease. , 1995, Nuclear medicine and biology.

[21]  G. Lucignani,et al.  Neurochemical Imaging with Emission Tomography: Clinical Applications , 2006 .

[22]  Nicolaas I Bohnen,et al.  The role of positron emission tomography imaging in movement disorders. , 2003, Neuroimaging clinics of North America.

[23]  Oliver Pogarell,et al.  Prospective study of presynaptic dopaminergic imaging in patients with mild parkinsonism and tremor disorders: Part 1. Baseline and 3‐month observations , 2003, Movement disorders : official journal of the Movement Disorder Society.

[24]  J D Speelman,et al.  [123I]FP-CIT SPECT shows a pronounced decline of striatal dopamine transporter labelling in early and advanced Parkinson's disease. , 1997, Journal of neurology, neurosurgery, and psychiatry.

[25]  S. Kish,et al.  Uneven pattern of dopamine loss in the striatum of patients with idiopathic Parkinson's disease. Pathophysiologic and clinical implications. , 1988, The New England journal of medicine.

[26]  D J Brooks,et al.  Regional changes in [18F]dopa metabolism in the striatum in Parkinson's disease. , 1996, Brain : a journal of neurology.

[27]  J. Seibyl Imaging studies in movement disorders. , 2003, Seminars in nuclear medicine.

[28]  T Jones,et al.  The nigrostriatal dopaminergic system assessed in vivo by positron emission tomography in healthy volunteer subjects and patients with Parkinson's disease. , 1990, Archives of neurology.

[29]  Osama Sabri,et al.  Investigating dopaminergic neurotransmission with 123I-FP-CIT SPECT: comparability of modern SPECT systems. , 2003, Journal of nuclear medicine : official publication, Society of Nuclear Medicine.