CT angiography and perfusion CT in cerebral vasospasm after subarachnoid hemorrhage

Abstract

Background and purpose: We investigated the association of multisection CT angiography (MSCTA) and perfusion CT (PCT) for the characterization of vasospasm secondary to aneurysmal subarachnoid hemorrhage.

Materials and methods: Among 27 patients with symptomatic cerebrovascular vasospasm investigated by digital subtraction angiography (DSA), 18 underwent both cerebral PCT and MSCTA. For the remaining 9, only PCT or MSCTA could be performed. MSCTA was compared with DSA for the detection and characterization of vasospasm on 286 intracranial arterial segments. PCT maps were visually reviewed for mean transit time, relative cerebral blood flow, and relative cerebral blood volume abnormalities and were qualitatively compared with the corresponding regional vasospasm detected by DSA.

Results: Vasospasm was grouped into 2 categories: mild-moderate and severe. The depiction of vasospasm by MSCTA showed the best sensitivity, specificity, and accuracy at the level of the A2 and M2 arterial segments (100% for each), in contrast to the carotid siphon (45%, 100%, and 85% respectively). The characterization of vasospasm severity by MSCTA showed a sensitivity, specificity, and accuracy of 86.8%, 96.8%, and 95.2%, respectively, for mild-moderate vasospasm, and 76.5%, 99.5%, and 97.5%, respectively, for severe vasospasm. The PCT abnormalities were related to severe vasospasm in 9 patients and to mild-to-moderate vasospasm in 2. The sensitivity, specificity, and accuracy of PCT in detecting vasospasm were 90%, 100%, and 92.3%, respectively, for severe vasospasm, and 20%, 100%, and 38.5%, respectively, for mild-moderate vasospasm.

Conclusion: MSCTA/PCT can assess the location and severity of cerebrovascular vasospasm and its related perfusion abnormalities. It can identify severe vasospasm with risk of delayed ischemia and can thus guide the invasive treatment.

Figures

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.

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.

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.