AJDRAJNR - American Journal of Neuroradiology

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CT Angiography and Perfusion CT in Cerebral Vasospasm after Subarachnoid Hemorrhage

S. Binaghia, M.L. Colleonia, P. Maedera, A. Uskéa, L. Reglib, A. R. Dehdashtib, P. Schnydera and R. Meulia

a Departments of Diagnostic and Interventional Radiology, Neuroradiology Unit, University Hospital, Lausanne, Switzerland
b Department of Neurosurgery, University Hospital, Lausanne, Switzerland


Figure 1
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Fig 1. A 44-year-old woman presenting with weakness of the right arm and leg, clinically attributed to cerebrovascular vasospasm 6 days after SAH related to a ruptured saccular aneurysm of the left MCA bifurcation, which was clipped (bold arrow). DSA showed moderate vasospasm on the distal carotid segment and severe vasospasm on the A1 segment of the left ACA and the M1 and proximal M2 segments of the left MCA (A, black arrowheads). Maximum intensity projection (MIP) MSCTA image before (B) and after (C) intra-arterial infusion of nimodipine showing resolution of the vasospasm (white arrowheads), and followed by the resolution of the symptoms. At pretreatment PCT, MTT was increased in the left MCA territory (D), CBF was normal (E), and a slight increase in CBV (F) was observed, representing vasospasm related auto regulation mechanisms.


Figure 2
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Fig 2. A 44-year-old man with right-sided hemiparesis attributed to cerebrovascular vasospasm occurring 9 days after SAH consecutive to a ruptured aneurysm of the anterior communicating artery, treated by surgical clipping. DSA (A) showed moderate vasospasm on M1 segment of left MCA and focal severe vasospasm on the M2 segment (arrowheads). These findings were confirmed by MIP MSCTA reconstruction (B) and volume-rendered MSCTA reconstruction (C). Perfusion CT performed during the same CT session revealed an increase in MTT (D) and a decrease in rCBF (E), with slight increase of rCBV (F). This pattern of perfusion alterations corresponds to a reversible ischemic lesion consecutive to vasospasm. The patient was then treated by a local intra-arterial nimodipine infusion and a balloon angioplasty of the left M1 segment.


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Fig 3. A 52-year-old man with symptoms of cerebrovascular vasospasm 5 days after SAH. He was treated with a surgical clipping of a ruptured aneurysm of the anterior communicating artery (AcomA). A first postoperative angiogram showed no abnormalities. Actual DSA (A) showed an absence of the distal segments of the right AcomA (black arrowheads), interpreted as secondary to a very tight vasospasm. Posteroanterior (B) MIP reconstructions of the AcomA at MSCTA confirmed the lack of enhancement of the right AcomA. A nonenhanced cerebral CT (not shown) disclosed a vague hypoattenuation in the territory of the right AcomA. Perfusion CT results confirmed an irreversible ischemic lesion in the territory of the right AcomA, characterized by an increased MTT (C), a decreased rCBF (D), and a decreased rCBV (E). Thus, no specific endovascular treatment of the right AcomA was undertaken.