PMC4596051_01
Initial head computed tomography (a: Axial view) and brain magnetic resonance imaging (b: Axial T1-weighted; c: Axial T2-weighted) show a left thalamic intracerebral hemorrhage with ventricular extension and no discernible flow voids to suggest an arteriovenous malformation
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F1
Head CT, and brain magnetic resonance imaging (MRI) revealed a left thalamic intracerebral hemorrhage with intraventricular extension [Figure 1].
The arteriovenous malformation (AVM) nidus (arrowhead), seen on lateral digital subtraction angiography (a, b and c) and three-dimensional sagittal (d) and coronal (e and f) cone beam computed tomography reconstructions (left carotid injections), is fed by the left anterior choroidal artery (hollow arrow) and a thalamic perforator branch of the left posterior communicating artery (right vertebral injection, not shown), and drained by the left internal cerebral vein (solid arrow). (a) Hematoma obscures the nidus at presentation, (b, d and e) 3 months follow-up reveals the AVM, and (c and f) 7 months follow-up demonstrates complete spontaneous AVM obliteration
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F2
Given the high suspicion for an underlying vascular lesion, DSA was performed, which revealed enlargement of the left anterior choroidal artery and early drainage into the left internal cerebral vein with no discernible nidus, likely due to the concurrent hematoma [Figure 2a]. Diagnostic DSA and CBCT performed 3 months after presentation demonstrated a Spetzler-Martin Grade III left thalamic AVM [Figure 2b, d and e]. SRS planning did not demonstrate the AVM, or the previously seen flow enhancement of the thalamus on MRA. Seven months after initial presentation, DSA and CBCT confirmed the spontaneous angiographic resolution of the AVM [Figure 2c and f] without treatment.