Daniel Kahneman described the important difference between what he called ‘thinking fast’—instantly recognising and understanding a conundrum through years of training and understanding—and ‘thinking slow’ which involves the testing of a sequence of hypotheses until the problem is solved.1

Three case reports in this issue of Practical Neurology 2–4 will remind readers of the rich variety of deficits associated with infarcts in the brainstem, and how many clinical presentations of stroke may not be instantly recognisable but are (eventually) susceptible of rational explanation.

The first report is of Raymond’s syndrome, memorable as much for the eponymous describer’s first name as for the potential of a unilateral pontine lesion to cause an unusual constellation of deficits. The other two, counterintuitively for an area of the brain so anatomically cluttered, describe patients with brainstem infarcts presenting with unilateral cranial nerve palsies—just V in one, just VII in the other—without involving other cranial nerves (nuclei or fascicles), long tracts (pyramidal, parapyramidal or sensory) or the cerebellum and its connections (afferent and efferent).

All these cases were caused by ‘ordinary’ arterial (not venous) ischaemia with no suggestion of vasculitis (deficiency of adenosine deaminase 2 likes the pons), infective or marantic endocarditis, local or adjacent infection, dolichoectasia, meningeal infiltration, remote or local vascular malformations, or endovascular lymphoma. …