Cerebral amyloid angiopathy-related infarcts imitating high-grade differentiation of a benign meningioma.

To cite: Talarczyk P, Kanodia AK, Ironside J, et al. BMJ Case Rep Published online: [please include Day Month Year] doi:10.1136/bcr-2015211262 DESCRIPTION Meningiomas are divided, by the WHO, into three groups: benign (grade I), atypical (grade II) and malignant (grade III). Although some overlapping features can occur, atypical meningiomas are more likely to exhibit heterogeneous density or intensity, heterogeneous contrast enhancement and relatively large perifocal oedema on CT scan and MRI. Meningiomas typically receive their blood supply from dural arteries, although larger meningiomas can also have a blood supply from leptomeningeal or parenchymal branches. Cerebral amyloid angiopathy (CAA) results from β-amyloid deposition in the walls of leptomeningeal and cortical arteries. It usually causes lobar intracerebral haemorrhage and often occurs in association with Alzheimer’s disease. Rarely, CAA has been documented to be associated with inflammatory changes, sometimes thought to be co-existent primary central nervous system vasculitis or giant cell arteritis, although most literature has focused on probable inflammatory changes secondary to β-amyloid deposition, sometimes described as amyloid β-related angiitis. We could not find any specific association of CAA with Wegener’s granulomatosis in the literature. We present serial brain imaging findings describing the evolution of changes from a stable benign meningioma to a lesion imitating an atypical meningioma, which was surgically removed and subsequently shown to be affected by amyloid angiopathy. A 59-year-old woman presented with a short history of right-sided tinnitus, hearing loss and sinusitis. Her other significant known condition was Wegener’s granulomatosis involving the lungs, diagnosed in another institution. Brain MRI in January 2011 (figure 1) was negative for vestibular schwannoma, but demonstrated an incidental 14 mm parafalcine meningioma in the left frontal region on the background of small vessel cerebrovascular disease. MRI performed in March 2013 (figure 2), due to acute neurological symptoms, demonstrated extensive abnormalities in the right parieto-occipital lobe with further haemorrhage in the left frontal lobe; these were assumed to be due to the patient’s known Wegener’s granulomatosis, rather than from potential CAA. There was some increase in the size of the meningioma, which continued to show homogenous enhancement. A follow-up MRI in April 2014 (figure 3) showed further increase in size of the meningioma to 28 mm, still with homogenous enhancement and without any significant surrounding brain changes. Figure 1 MRI in January 2011. T2 axial (A) and postcontrast T1 axial (B) images showing small left parafalcine meningioma (white arrow).