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DAT-SPECT in old onset Parkinson’s disease: should we trust?

G. Palermo, S. Giannoni, D. Frosini, U. Bonuccelli, R. Ceravolo (Pisa, Italy)

Meeting: MDS Virtual Congress 2021

Abstract Number: 853

Keywords: Aging, Nigrostriatal dopaminergic synapse deficiency, Single-photon emission computed tomography(SPECT)

Category: Parkinson's Disease: Neuroimaging

Objective: .

Background: Scans without evidence of dopaminergic deficit (SWEDD) refers to patients clinically diagnosed with Parkinson’s disease (PD), but show normal findings on dopamine transporter single-photon emission computed tomography (DAT-SPECT). This entity remains highly debate but recent findings suggesting that DAT-SPECT does not reflect either nigral cell bodies or striatal fibers of dopaminergic nigrostriatal neurons could improve our understanding of SWEDD phenomenon. Notably, compensatory downregulation of DAT in the early stages of PD seems to be less efficient in older-onset than in young-onset patients.

Method: We report eight patients with old-age PD diagnosis confirmed during a long-term clinical follow-up and with a positive response to levodopa in which baseline DAT-SPECT was normal both visually and semiquantitatively. Two subjects demonstrated an abnormal scan when repeated later.

Results: .

Conclusion: We suggest that old onset PD SWEDD patients may truly have dopaminergic degeneration despite normal imaging results, simply because of the co-occurrence of an age-related failure of striatal compensatory strategies in the early stages of PD.

References: [1] Erro R, et al What do patients with scans without evidence of dopaminergic deficit (SWEDD) have? New evidence and continuing controversies. J Neurol Neurosurg Psychiatry 2016; 87:319-323. [2] Saari L, et al. Dopamine transporter imaging does not predict the number of nigral neurons in Parkinson disease. Neurology 2017;88:1461–1467. [3] Honkanen EA, et al. No link between striatal dopaminergic axons and dopamine transporter imaging in Parkinson’s disease. Mov Disord. 2019;34:1562-1566. [4] Palermo G, et al. Dopamine Transporter, Age, and Motor Complications in Parkinson’s Disease: A Clinical and Single-Photon Emission Computed Tomography Study. Mov Disord. 2020;35:1028-1036. [5] Marek K, et al. Parkinson Study Group PRECEPT Investigators. Longitudinal follow-up of SWEDD subjects in the PRECEPT Study. Neurology 2014;82:1791-1797. [6] Lee CS, et al. In vivo positron emission tomographic evidence for compensatory changes in presynaptic dopaminergic nerve terminals in Parkinson’s disease. Ann Neurol 2000;47: 493–503. [7] De la Fuente-Fernández R, et al. Age-specific progression of nigrostriatal dysfunction in Parkinson’s disease. Ann Neurol 2011;69:803–810. [8] Nandhagopal R, et al. Longitudinal evolution of compensatory changes in striatal dopamine processing in Parkinson’s disease. Brain. 2011;134:3290-3298. [9] Stoessl AJ. Scans without evidence of dopamine deficiency: the triumph of careful clinical assessment. Mov Disord 2010;25:529–530

To cite this abstract in AMA style:

G. Palermo, S. Giannoni, D. Frosini, U. Bonuccelli, R. Ceravolo. DAT-SPECT in old onset Parkinson’s disease: should we trust? [abstract]. Mov Disord. 2021; 36 (suppl 1). https://www.mdsabstracts.org/abstract/dat-spect-in-old-onset-parkinsons-disease-should-we-trust/. Accessed June 15, 2025.
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