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Sulcal Hyperintensity as an Early Imaging Finding in Cerebral Amyloid Angiopathy-Related Inflammation
Larysa Panteleienko1, Gargi Banerjee1, Dermot Henry Mallon1
1From the Stroke Research Centre (L.P., D.J.W.), Department of Brain Repair and Rehabilitation, UCL Queen Square Institute of Neurology, London, United Kingdom; Department of Neurology (L.P.), Bogomolets National Medical University, Kyiv, Ukraine; MRC Prion Unit at UCL (G.B.), Institute of Prion Diseases; National Hospital for Neurology and Neurosurgery (G.B., R.O., G.H., H.R.J.), Queen Square, University College London Hospitals NHS Foundation Trust; Neuroradiological Academic Unit (D.H.M., H.R.J.), UCL Queen Square Institute of Neurology; Lysholm Department of Neuroradiology (D.H.M.), National Hospital for Neurology and Neurosurgery; National Hospital for Neurology and Neurosurgery (V.H.), Queen Square, University College London Hospitals NHS Foundation Trust; Torbay and South Devon NHS Foundation Trust (W.K.); York and Scarborough Teaching Hospitals NHS Foundation Trust (S.D.); Queen Square Institute of Neurology and National Hospital for Neurology and Neurosurgery (M.S.Z.), University College London Hospitals NHS Foundation Trust; and Department of Neuroinflammation (M.S.Z.), UCL Queen Square Institute of Neurology, London, United Kingdom.
Background And Objectives:
Cerebral amyloid angiopathy-related inflammation (CAA-ri) is a subtype of CAA with distinct clinical and radiologic features. Existing diagnostic criteria require the presence of characteristic asymmetrical white matter hyperintensity (WMH), together with classical hemorrhagic neuroimaging markers of CAA. There are limited data for other diagnostic neuroimaging markers of CAA-ri.
Methods:
This is a case series from a specialist hospital intracerebral hemorrhage service.
Results:
We describe 4 patients with CAA-ri who had regions of sulcal hyperintensity, with or without gyral swelling at clinical presentation, but did not fulfill current diagnostic criteria because of the absence of typical asymmetric WMH on brain MRI. All 4 patients were subsequently diagnosed with CAA-ri; three later developed asymmetric WMHs with disease relapse, and 2 had pathologically proven CAA-ri; 1 patient had both.
Discussion:
Regions of sulcal hyperintensity, sometimes with associated gyral swelling, can be an early imaging finding in CAA-ri. These neuroimaging markers could potentially improve the accuracy of existing diagnostic criteria for CAA-ri to allow earlier diagnosis and treatment without biopsy in patients with atypical presentations.
