Case Notes
History
34 yo male SLE w/ renal failure, presenting with expressive aphasia.Exam
MR-FLAIR sequence
Prior Study
Noncontrast CT Head1. Hyperacute cytogenic edema in the retrosylvian area on the left. No hyperacute arterial or venous intraluminal thrombus is evident.
2. No hemorrhagic conversion is evident
3. Chronic right maxillary sinusitis with chronic bone reaction but no bone dehiscence to suggest aggressive disease.
MRA Neck
Negative MRA of the neck with no evidence of arterial size asymmetry nor atherosclerotic nor arteriopathy (FMD or dissection) changes.
MRA of the head
Patient has known autoimmune disorder (SLE). There are subtle arterial luminal arterial size changes, which could be vasospastic, but are more likely (in the absence of thunderclap headache symptoms), is more likely related to a secondary inflammatory angiitis rather than RCVS.
T1-w pre and post contrast
1. Hyperacute ischemic event in the left retrosylvian region. There is no proximal arterial nor venous cause. There is distal arterial angiitis evident on the head MRA. There is also evidence of multicentric sites of subacute laminar necrosis in other area of the cerebrum. This combination of imaging observations combined with a clinical history of SLE makes this most likely a transcapillary form of stroke in all locations. The basis is secondary angiitis associated in the SLE. These patients often have clotting abnormalities as well. Therefore, screen for APLA (immunebased antiphospholipid antibody syndrome).
MR diffusion sequence
MR diffusion is positve (i.e. hyperacute stroke) in the left retrosylvian area. The diffusion intensity favors the cortex, plus there are multiple other sites of cortical laminar necrosis. This implies the cortex in the left retrosylvian will evolve in the same way. Laminar necrosis indicates an absence of collateral reflow and is therefore consistent with a transcapillary type of ischemic event.