Introduction

In superficial siderosis (SS), haemosiderin is deposited in the subpial layers of the central nervous system. SS can be diagnosed by the presence of a hypointense rim over the brain surface on gradient recalled echo (GRE) T2 weighted MRI, typically surrounding the brainstem and filling the cerebellar sulci. The classical triad consists of slowly progressive hearing loss, cerebellar ataxia and corticospinal tract signs. SS has classically been attributed to chronic or repeated subarachnoid haemorrhage, which may be otherwise clinically silent. In up to 65% of patients a bleeding source can be detected; the other cases have been labelled idiopathic.1 Recently, Feldman et al presented two patients with SS and histopathology of neuritic plaques and cerebral amyloid angiopathy (CAA).2 A few more patients have been published with both sporadic CAA and SS, without evidence of intraparenchymal amyloid.1 3 In a population based study Vernooij et al found SS in 0.7% of non-demented individuals, all of whom also had intracerebral microbleeds.4

¹¹C-Pittsburgh compound B (PIB) positron emission tomography (PET) marks both vascular and parenchymal β amyloid plaques in vivo. We report ¹¹C-PIB PET findings in two cases with SS. Our findings suggest that SS in the context of β amyloidosis may have a distinct clinical and MRI signature.