Epileptiform activity during transient focal neurologic episodes in cerebral amyloid angiopathy

Transient focal neurologic episodes (TFNEs) constitute a paroxysmal clinical manifestation of cerebral amyloid angiopathy (CAA), an age-related small vessel disease characterized by deposition of β-amyloid protein in the walls of cortical and leptomeningeal arteries. Although the most dramatic clinical presentation of CAA is lobar intracerebral hemorrhage, cerebral microbleeds (CMBs), superficial siderosis, and convexity subarachnoid hemorrhages (cSAHs) are relevant neuroimaging markers of CAA.1 The exact nature of TFNE is not yet elucidated: an epileptic origin was suspected but never proved.2,3 A correct pathogenic framing of these disturbances is needed to avoid treatments such as thrombolytic therapy or anticoagulation, which could be highly deleterious in CAA. In differential diagnosis, blood-sensitive MRI sequences are important to obtain because they may reveal signs of silent microbleeds and cortical superficial siderosis that allow a diagnosis of probable CAA.