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BNMS President's blog - May 2019

Posted By Caroline Oxley, 12 June 2025

Last month I indulged myself by being somewhat political in what I wrote. What I wrote is still true and we still seem to have a political system which has in modern parlance become “not fit for purpose”. However, this month I will write about something very different.

The use of radioisotopic imaging in brain disease remains a bit if a Cinderella area. It has not received the same level of investment as cancer imaging or the clinical exposure of cardiac disease. Partly this is because brain diseases tend to be chronic and patients die with them and not because of them. If they involve symptoms which distress the patients or their carers it is often not talked about openly. This seems to be much more of a problem with us men and much of this has been highlighted in mental illness awareness week in May.

The other silent disease has been the degenerative diseases of the brain. Here nuclear medicine can have a great input though for many working in nuclear medicine it is not an area of great interest. This was changed with the introduction of ioflupane imaging in Parkinson’s disease and Parkinson plus disorders. Nuclear medicine could offer something unique which could not be offered by other modalities. DAT scanning remains a nice money earner for my department with about 5-10 scans a week mainly for outside providers which have to pay handsomely for the service (mainly due to contracts drawn up before tariffs started).

NHS England will also fund FDG imaging in some cases with suspected Alzheimer’s disease despite the fact the product has not been through a randomised controlled trial which the unfunded amyloid agents have! Though not perfect FDG imaging can provide a diagnosis when MRI has been unhelpful. It is clear that PET agents are most useful in early disease and we often find ourselves scanning patients in their 40s and 50s.

Research using PET is helping us to understand more about dementias develop. Tau proteins seem to signal damage in the brain and recent work has shown that even in young people with brain injuries tau can be seen, though in most patients it resolves in 6-12 months. In early dementia the tau seems to persist and increase in a cycle of inflammation signalling but these seems to result in more inflammation which results in neuronal loss as well as amyloid being laid down. We are also beginning to understand that there is a vascular component to the development of dementia which can be seen by increasing T lymphocyte vascular trapping in the brain which can be visualised using C-11 PK11195. New and more precise probes are being developed to try and understand the mechanism by which dementia develops and why its outcome is so devastating.

Though nuclear medicine techniques are not the only method by which these mechanisms and their effect measured it remains a vital tool as absolute quantification remains possible. At present these diseases have no effective treatment but what we can learn from oncology is that effective treatment depend on understanding why a disease occurs and how it progresses.

Therefore, we should embrace fully the role nuclear medicine has in looking at neurology and hopefully in the future allow us to monitor the effectiveness of disease modifying treatment.

Dr John Buscombe

BNMS President

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