Medullary infarction as a poor prognostic factor after internal coil trapping of a ruptured vertebral artery dissection

Clinical article

Hidenori Endo M.D., Ph.D. 1 , 2 , Yasushi Matsumoto M.D. 1 , Ryushi Kondo M.D., Ph.D. 1 , Kenichi Sato M.D., Ph.D. 1 , 4 , Miki Fujimura M.D., Ph.D. 3 , Takashi Inoue M.D., Ph.D. 2 , Hiroaki Shimizu M.D., Ph.D. 2 , Akira Takahashi M.D., Ph.D. 4 and Teiji Tominaga M.D., Ph.D. 5
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  • 1 Departments of Neuroendovascular Therapy and
  • 2 Neurosurgery, Kohnan Hospital;
  • 3 Department of Neurosurgery, National Hospital Organization Sendai Medical Center; and
  • 4 Departments of Neuroendovascular Therapy and
  • 5 Neurosurgery, Tohoku University Graduate School of Medicine, Sendai, Japan
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Object

Internal coil trapping is a treatment method used to prevent rebleeding from a ruptured intracranial vertebral artery dissection (VAD). Postoperative medullary infarctions have been reported as a complication of this treatment strategy. The aim of this study was to determine the relationship between a postoperative medullary infarction and the clinical outcomes for patients with ruptured VADs treated with internal coil trapping during the acute stage of a subarachnoid hemorrhage (SAH).

Methods

A retrospective study identified 38 patients who presented between 2006 and 2011 with ruptured VADs and underwent internal coil trapping during the acute stage of SAH. The SAH was identified on CT scanning, and the diagnosis for VAD was rendered by cerebral angiography. Under general anesthesia, the dissection was packed with coils, beginning at the distal end and proceeding proximally. When VAD involved the origin of the posterior inferior cerebellar artery (PICA) with a large cerebellar territory, an occipital artery (OA)–PICA anastomosis was created prior to internal coil trapping. The pre- and postoperative radiological findings, clinical course, and outcomes were analyzed.

Results

The internal coil trapping was completed within 24 hours after admission. An OA-PICA anastomosis followed by internal coil trapping was performed in 5 patients. Postoperative rebleeding did not occur in any patient during a mean follow-up period of 16 months. The postoperative MRI studies showed medullary infarctions in 18 patients (47%). The mean length of the trapped VAD for the infarction group (15.7 ± 6.0 mm) was significantly longer than that of the noninfarction group (11.5 ± 4.3 mm) (p = 0.019). Three of the 5 patients treated with OA-PICA anastomosis had postoperative medullary infarction. The clinical outcomes at 6 months were favorable (modified Rankin Scale Scores 0–2) for 23 patients (60.5%) and unfavorable (modified Rankin Scale Scores 3–6) for 15 patients (39.5%). Of the 18 patients with postoperative medullary infarctions, the outcomes were favorable for 6 patients (33.3%) and unfavorable for 12 patients (66.7%). A logistic regression analysis predicted the following independent risk factors for unfavorable outcomes: postoperative medullary infarctions (OR 21.287 [95% CI 2.622–498.242], p = 0.003); preoperative rebleeding episodes (OR 7.450 [95% CI 1.140–71.138], p = 0.036); and a history of diabetes mellitus (OR 45.456 [95% CI 1.993–5287.595], p = 0.013).

Conclusions

A postoperative medullary infarction was associated with unfavorable outcomes after internal coil trapping for ruptured VADs. Coil occlusion of the long segment of the VA led to medullary infarction, and an OA-PICA bypass did not prevent medullary infarction. A VA-sparing procedure, such as flow diversion by stenting, is an alternative treatment in the future, if this approach is demonstrated to effectively prevent rebleeding.

Abbreviations used in this paper:BTO = balloon test occlusion; DSA = digital subtraction angiography; mRS = modified Rankin Scale; OA = occipital artery; PCoA = posterior communicating artery; PICA = posterior inferior cerebellar artery; SAH = subarachnoid hemorrhage; VA = vertebral artery; VAD = VA dissection; WFNS = World Federation of Neurosurgical Societies.

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Contributor Notes

Address correspondence to: Hidenori Endo, M.D., Department of Neuroendovascular Therapy, Kohnan Hospital, 4-20-1 Nagamachiminami, Taihaku-ku, Sendai 982-8523, Japan. email: hideendo@gmail.com.

Please include this information when citing this paper: published online October 5, 2012; DOI: 10.3171/2012.9.JNS12566.

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