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• Oh No, Not DaT Again
  Paul Morrish
  Published on: 28 January 2020

• Published on: 28 January 2020

  Oh No, Not DaT Again

  • Paul Morrish, MD na

  It gives more discomfort than pleasure to comment on DaT scanning again but your editorial [1] prompted me to find out that the number of DaTscans carried out in England is increasing yearly, from 4550 in 2012/3 to 8840 in 2018/9. A trip to the dentist might have been wiser, my long-expressed opinion (based on the fundamental principles that let down 18FDopa PET) being that the DaTscan is a waste of time, radiation and money [2]. In brief it is a low resolution, inadequately sensitive, inadequately reproducible test with too many false negatives and little knowledge of confounding influences. The acronym SWEDD has, mercifully, been consigned to the dustbin[3] but we don’t have the neuropathological studies or large and long-term blinded follow-up studies, in patients and healthy individuals, despite the many tests and years since its commercial introduction, that would tell the true false positive and negative rate of the test. We can’t then confidently say how strongly a normal result argues against a clinical diagnosis of PD. Neurology is not the only specialty that uses DaTscan and indication-creep (good for the shareholder, bad for the taxpayer) means that it is also being used to distinguish Lewy Body Dementia from Alzheimer’s Dementia despite limited supportive data (4). It must also be remembered that the test measures biochemistry, not pathology; the statement in the case presentation [5] “a DaTscan was normal, with no evidence of degenerative Parkinsonism” is...

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  It gives more discomfort than pleasure to comment on DaT scanning again but your editorial [1] prompted me to find out that the number of DaTscans carried out in England is increasing yearly, from 4550 in 2012/3 to 8840 in 2018/9. A trip to the dentist might have been wiser, my long-expressed opinion (based on the fundamental principles that let down 18FDopa PET) being that the DaTscan is a waste of time, radiation and money [2]. In brief it is a low resolution, inadequately sensitive, inadequately reproducible test with too many false negatives and little knowledge of confounding influences. The acronym SWEDD has, mercifully, been consigned to the dustbin[3] but we don’t have the neuropathological studies or large and long-term blinded follow-up studies, in patients and healthy individuals, despite the many tests and years since its commercial introduction, that would tell the true false positive and negative rate of the test. We can’t then confidently say how strongly a normal result argues against a clinical diagnosis of PD. Neurology is not the only specialty that uses DaTscan and indication-creep (good for the shareholder, bad for the taxpayer) means that it is also being used to distinguish Lewy Body Dementia from Alzheimer’s Dementia despite limited supportive data (4). It must also be remembered that the test measures biochemistry, not pathology; the statement in the case presentation [5] “a DaTscan was normal, with no evidence of degenerative Parkinsonism” is a common but incorrect oversimplification. For drug-induced parkinsonism, is it my own oversimplification to ask why a drug that is biochemically producing parkinsonism doesn’t change the result of a biochemical test that is used to detect parkinsonism? Small studies with an unreliable test and heavy sales pitch encourage more indication-creep.
  A practical neurologist’s approach is to ask if the outcome of a test will change what one does or advises and if a test can’t be trusted it shouldn’t be requested. I wonder if the £12M or more spent on the test in England in 2018 might have been more usefully used and whether the Scottish, known for their financial prudence, have a neologism for colleagues that request DaTscans?

  References:
  1. Araujo R, van Rumund A, Bloem BR. To scan or not to scan your Parkinson patient: that is the question! Pract Neurol 2019;19:462-4. doi: 10.1136/practneurol-2019-002225
  2. Morrish PK. Controversies in Neuroimaging. in Factor SA and Weiner WJ eds. Parkinson’s disease; Diagnosis and Clinical Management. Demos Publishing (New York). 2008: 317-326

  3. Erro R, Schneider SA, Stamelou M, 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. doi: 10.1136/jnnp-2014-310256

  4. McCleery J, Morgan S, Bradley KM et al. Dopamine transporter imaging for the diagnosis of dementia with Lewy bodies. Cochrane Database of Systematic Reviews 2015, Issue 1. Art. No.: CD010633. doi: 10.1002/14651858.CD010633.pub2

  5. Wiblin I, Mitra D, Naomi W. An unusual cause of treatable parkinsonism. Pract Neurol 2019; 19; 518-20. doi: 10.1136/practneurol-2019-002339

  Acknowledgement: Figures for 2018 DaTscan use kindly provided by Sheila M Dixon, Senior Analytical Manager, Performance Analysis Team, NHS England & NHS Improvement

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  Conflict of Interest:
  None declared.

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