Diagnosis of parkinsonism

Dr Thant and colleagues (April 2002 JRSM1) describe ‘a young man with parkinsonism’ with the unusual features of no tremor, a poor response to levodopa, ‘rapid progression of his symptoms and the presence of other neurological signs’ and ‘conduction abnormalities in the anterior visual pathways bilaterally’ on visual evoked responses. They imply that the demonstration of diffusely increased signal from white matter on T2-weighted images, together with low signal in the basal ganglia and dentate nuclei (the latter shown by CT to be due to calcium deposits) clinched the diagnosis in a way the clinical features did not. This is surely erroneous. I would suggest that they have not made a diagnosis, let alone explained, for example, the visual abnormalities. They do not comment, other than in the case report, on the significance of the white-matter disease. More fundamentally, as they point out, a small proportion of patients without intracranial disease or neurological deficits show calcification in the areas they describe. They attribute ‘pyramidal signs, psychiatric symptoms, urinary incontinence, and epilepsy... in some patients’ to a disease process which these changes might reflect, but the evidence that calcification is not simply an incidental finding in patients being investigated for these disparate conditions is largely lacking. There is confusion in the references; however, I believe the authors are mistaken in their view that MRI ‘is especially useful if... parkinsonian features are associated with other neurological features’ (my italics). As regards papers claiming to demonstrate any utility of differentiating clinically similar conditions by imaging, it may be helpful to remind oneself that in parkinsonism the imaging features have been found to be less constant than the clinical characteristics (on which the studies have been predicated), and that imaging may tend to be least helpful when the clinical diagnosis is in doubt. As regards which patients with akinetic rigid syndromes will respond to treatment with levodopa or dopamine agonists—which would seem to be the greatest potential contribution of MRI or, for example, positron emission tomography—a worker with the latter method observed that ‘informed trial and error seems as good a therapeutic approach as... imaging’2.