2006PubMedOpen access

Dynamic CT perfusion imaging in subarachnoid hemorrhage-related vasospasm.

A.M. Laslo, James D. Eastwood, F.-X. Chen, T-Y Lee

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Abstract

BACKGROUND AND PURPOSE: Nimodipine is a therapy that reduces morbidity and mortality in patients with subarachnoid hemorrhage (SAH), though the mechanisms by which it does so are not well understood. In a rabbit model of SAH, we studied the effects of nimodipine by using functional CT imaging. We hypothesized that the nimodipine treatment group would have (1) increased mean basilar artery diameter, (2) less diminished cerebral blood flow (CBF) following vasospasm, and (3) better neurologic outcomes. METHODS: SAH was induced in 26 New Zealand White rabbits randomized to 2 groups: treated (nimodipine) or control (no treatment). CT perfusion and CT angiography were used to measure CBF and basilar artery diameter at baseline, 10, 30, and 60 minutes after SAH, and on days 3, 5, 7, 9, and 16. Neurologic assessments were performed on each day of scanning. RESULTS: Basilar artery diameter in the treated group was greater than in the control group post-SAH (P < .05). When vasospasm was >15%, CBF in the nimodipine group was significantly greater than in the control group in the brain stem, cerebellum, parieto-occipital cerebrum, and deep gray matter (P < .05). Neurologic scores in the nimodipine group were significantly better than in the control group on days 5 and 9 (P < .05). CONCLUSION: Animals treated with nimodipine showed (1) increased mean basilar artery diameter, (2) improved neurologic outcome, and (3) increased mean CBF despite no significant difference in the incidence and severity of delayed vasospasm. These data provide a basis for future studies comparing the efficacy of new treatments for SAH to that of nimodipine.

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BACKGROUND AND PURPOSE: Nimodipine is a therapy that reduces morbidity and mortality in patients with subarachnoid hemorrhage (SAH), though the mechanisms by which it does so are not well understood. In a rabbit model of SAH, we studied the effects of nimodipine by using functional CT imaging. We hypothesized that the nimodipine treatment group would have (1) increased mean basilar artery diameter, (2) less diminished cerebral blood flow (CBF) following vasospasm, and (3) better neurologic outcomes. METHODS: SAH was induced in 26 New Zealand White rabbits randomized to 2 groups: treated (nimodipine) or control (no treatment). CT perfusion and CT angiography were used to measure CBF and basilar artery diameter at baseline, 10, 30, and 60 minutes after SAH, and on days 3, 5, 7, 9, and 16. Neurologic assessments were performed on each day of scanning. RESULTS: Basilar artery diameter in the treated group was greater than in the control group post-SAH (P < .05). When vasospasm was >15%, CBF in the nimodipine group was significantly greater than in the control group in the brain stem, cerebellum, parieto-occipital cerebrum, and deep gray matter (P < .05). Neurologic scores in the nimodipine group were significantly better than in the control group on days 5 and 9 (P < .05). CONCLUSION: Animals treated with nimodipine showed (1) increased mean basilar artery diameter, (2) improved neurologic outcome, and (3) increased mean CBF despite no significant difference in the incidence and severity of delayed vasospasm. These data provide a basis for future studies comparing the efficacy of new treatments for SAH to that of nimodipine.

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Available abstract

BACKGROUND AND PURPOSE: Nimodipine is a therapy that reduces morbidity and mortality in patients with subarachnoid hemorrhage (SAH), though the mechanisms by which it does so are not well understood. In a rabbit model of SAH, we studied the effects of nimodipine by using functional CT imaging. We hypothesized that the nimodipine treatment group would have (1) increased mean basilar artery diameter, (2) less diminished cerebral blood flow (CBF) following vasospasm, and (3) better neurologic outcomes. METHODS: SAH was induced in 26 New Zealand White rabbits randomized to 2 groups: treated (nimodipine) or control (no treatment). CT perfusion and CT angiography were used to measure CBF and basilar artery diameter at baseline, 10, 30, and 60 minutes after SAH, and on days 3, 5, 7, 9, and 16. Neurologic assessments were performed on each day of scanning. RESULTS: Basilar artery diameter in the treated group was greater than in the control group post-SAH (P < .05). When vasospasm was >15%, CBF in the nimodipine group was significantly greater than in the control group in the brain stem, cerebellum, parieto-occipital cerebrum, and deep gray matter (P < .05). Neurologic scores in the nimodipine group were significantly better than in the control group on days 5 and 9 (P < .05). CONCLUSION: Animals treated with nimodipine showed (1) increased mean basilar artery diameter, (2) improved neurologic outcome, and (3) increased mean CBF despite no significant difference in the incidence and severity of delayed vasospasm. These data provide a basis for future studies comparing the efficacy of new treatments for SAH to that of nimodipine.

Key concepts: Nimodipine, Medicine, Basilar artery, Vasospasm, Subarachnoid hemorrhage, Cerebral vasospasm, Anesthesia, Perfusion

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