Ahead of Print: Minocycline Against Cerebral Hyperperfusion

Screen Shot 2013-11-04 at 12.18.03 PMBackground: Cerebral hyperperfusion (CHP) is a potential complication of superficial temporal artery-middle cerebral artery (STA-MCA) anastomosis for moyamoya disease (MMD), and optimal postoperative management has not yet been established. Minocycline, a neuroprotective antibiotic agent, plays a role in blocking matrix metalloproteinase-9 (MMP-9), which contributes to edema formation and hemorrhagic conversion following cerebral ischemia-reperfusion. Patients with MMD have been shown to have increased serum MMP-9 levels.

Objective: To examine the effect of minocycline on the prevention of postoperative CHP following STA-MCA anastomosis for MMD.

Methods: N-isopropyl-p-[123I]iodoamphetamine single-photon emission computed tomography was performed 1 and 7 days after STA-MCA anastomosis on 109 hemispheres from 86 consecutive patients with MMD (9-69, mean 37 years old). Postoperative systolic blood pressure was strictly controlled under 130 mmHg in all 109 surgeries. The most recent 60 hemispheres were managed by the intra-operative and postoperative intravenous administration of minocycline hydrochloride (200 mg/day). The incidence of focal neurologic deterioration (FND) due to CHP was then compared with 36 patients undergoing 49 surgeries managed without minocycline.

Results: FND due to CHP was observed on 4 operated hemispheres in patients treated without minocycline (4/49, 8.16%), and on none in the minocycline-treated group (0/60) (p=0.00241). Multivariate analysis revealed that minocycline administration (p<0.0001), surgery on the left hemisphere (p=0.0314), and a smaller recipient artery diameter (p=0.0005) significantly correlated with FND due to CHP.

Conclusion: The administration of minocycline with strict blood pressure control may represent secure and effective postoperative management to prevent symptomatic CHP after STA-MCA anastomosis for MMD.

From: Minocycline Prevents Focal Neurologic Deterioration Due to Cerebral Hyperperfusion After Extracranial-Intracranial Bypass for Moyamoya Disease by Fujimura et al.

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