Letters to the Editor
Using DaTscan to Diagnose Parkinson Disease
Am Fam Physician. 2021 Jun 1;103(11):647-648.
Original Article: Parkinson Disease
Issue Date: December 1, 2020
Available at: https://www.aafp.org/afp/2020/1201/p679.html
To the Editor: The article by Dr. Halli-Tierney and colleagues summarized the diagnosis and treatment of Parkinson disease well. Although the diagnosis is mostly clinical, in more uncertain cases, the addition of a DaTscan (dopamine transport single-photon emission computed tomography scan) can be helpful.1 By confirming normal dopamine activity, the DaTscan can differentiate drug-induced Parkinson-like syndromes from actual Parkinson disease. For atypical presentations that mimic stroke or depression, the finding of diminished dopamine transport can redirect the differential diagnosis and treatment back to Parkinson disease.2 Clinicians should inquire about the closest DaTscan capability in their area. We have sent patients from our tribal health center to a tertiary medical center for their DaTscan because nearby imaging programs do not offer them.
Rasagiline (Azilect), as a highly selective monoamine oxidase-B (MAOB) inhibitor, works only in the central nervous system and does not block amine oxidation in the gut; therefore, it does not provoke malignant hypertension or other excess stimulant adverse effects. Rasagiline has been found by some to slow the progression of Parkinson disease.
Author disclosure: No relevant financial affiliations.
1. Poewe W, Scherfler C. Role of dopamine transporter imaging in investigation of parkinsonian syndromes in routine clinical practice. Mov Disord. 2003;18(suppl 7):S16–S21.
2. Seifert KD, Wiener JI. The impact of DaTscan on the diagnosis and management of movement disorders: a retrospective study. Am J Neurodegener Dis. 2013;2(1):29–34.
In Reply: Thank you for your letter. We agree that DaTscans can help clarify whether Parkinson disease symptoms are associated with loss of dopaminergic neurons and that normal DaTscan findings can rule out symptoms attributed to the lack of dopamine. DaTscan has been approved by the U.S. Food and Drug Administration and is most useful in differentiating between Parkinson disease and atypical essential tremor. However, the DaTscan cannot differentiate between pure Parkinson disease and Parkinson-plus type syndromes (e.g., progressive supranuclear palsy, multiple system atrophy) because all of the syndromes result in dopaminergic loss.
DaTscan findings could point to drug-induced Parkinson disease, but a thorough medication review may also determine the diagnosis. A clinical evaluation from an experienced neurologist can be as accurate as a DaTscan for early Parkinson disease diagnosis.1 DaTscans are not used quantitatively to monitor disease progression, and results can determine whether the dopaminergic activity is normal or impaired but cannot predict disease severity and should not be used before verifying clinical signs of Parkinson disease. Therefore, the DaTscan's role in diagnosing Parkinson disease is secondary to a thorough clinical history, physical evaluation, and medication review. If available locally, DaTscan should be used only when clinicians cannot differentiate between atypical essential tremor, Parkinson disease, or Parkinson-plus syndromes.2
All three MAOB inhibitors (i.e., selegiline [Eldypryl], rasagiline, and safinamide [Xadago]) are selective for MAOB over monoamine oxidase-A inhibitors. We agree that rasagiline is generally well tolerated and does not provoke malignant hypertension or other excess stimulant adverse effects. Two delayed-start trials explored rasagiline's neuroprotective potential.3,4 The first study was relatively small (n = 404) and of short duration (24 weeks or 52 weeks of active treatment); results statistically favored earlier treatment, suggesting possible neuroprotection with rasagiline, but the trial had numerous limitations.3 The second trial was larger (n = 1,176) with a longer duration (36 weeks or 72 weeks of active treatment) but had conflicting results between the 1-mg (significant disease-modifying effect) and 2-mg (no difference between early or delayed start) arms of the trial.4 Based on these results, there is no conclusive evidence that rasagiline is neuroprotective in Parkinson disease. This finding is reflected in existing guidelines.5,6
Referencesshow all references
1. American Parkinson Disease Association. Accessed February 3, 2021. https://www.apdaparkinson.org/...
2. Isaacson SH, Fisher S, Gupta F, et al. Clinical utility of DaTscan imaging in the evaluation of patients with parkinsonism: a US perspective. Expert Rev Neurother. 2017;17(3):219–225.
3. Parkinson Study Group. A controlled, randomized, delayed-start study of rasagiline in early Parkinson disease. Arch Neurol. 2004;61(4):561–566.
4. Olanow CW, Rascol O, Hauser R, et al.; ADAGIO Study Investigators. A double-blind, delayed-start trial of rasagiline in Parkinson's disease [published correction appears in N Engl J Med. 2011;364(19):1882]. N Engl J Med. 2009;361(13):1268–1278.
5. Miyasaki JM, Martin W, Suchowersky O, et al. Practice parameter: initiation of treatment for Parkinson's disease: an evidence-based review: report of the Quality Standards Subcommittee of the American Academy of Neurology. Neurology. 2002;58(1):11–17.
6. Fox SH, Katzenschlager R, Lim SY, et al.; Movement Disorder Society Evidence-Based Medicine Committee. International Parkinson and Movement Disorder Society evidence-based medicine review: update on treatments for the motor symptoms of Parkinson's disease [published correction appears in Mov Disord. 2018;33(12):1992]. Mov Disord. 2018;33(8):1248–1266.
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