22. European Stroke Conference Vascular surgery and neurosurgery (PO 331-344 ) 331 Vascular surgery and neurosurgery MR-DWI positive microinfarctions and its relationship with symptomatic ischemic complica-tions after coiling of unruptured cerebral aneurysms D.H. Kang1, Y.W. Kim2, Y.H. Hwang3, H.J. Woo4, Y.S. Kim5 Kyungpook National University Hospital, Daegu, SOUTH KOREA1, Kyungpook National University Hospital, Daegu, SOUTH KOREA2, Kyungpook National University Hospital, Daegu, SOUTH KOREA3, Andong General Hospital, Daegu, SOUTH KOREA4, Kyungpook National Uni-versity Hospital, Daegu, SOUTH KOREA5 Purpose: To evaluate the number of MR-DWI positive lesions and its relationship with ischemic complication after coiling of unruptured intracranial aneurysm (UIA). Patients and Methods: Three hundred eighty-two UIAs in 343 patients were treated by coiling and examined by MR-DWI between Mar 2009 and November 2011. The incidence of MR-DWI positive lesion and ischemic complication, and the relationship between the number of MR-DWI positive le-sions and ischemic complication were retrospectively analyzed. Results: The rate of combined TIA and stroke was 3.5%. The incidence of MR-DWI positive was 54.5%. The number of MR-DWI positive lesions significantly differed between the symptomatic and the asymptomatic groups (12.1 ± 10.4 versus 5.0 ± 8.7, p<0.00). In the logistic regression ex-cepting the number of MR-DWI positive lesions, older age was marginally associated with ischemic complication. In the logistic regression including the number of MR-DWI positive lesions, the num-ber of MR-DWI positive lesions was the only independent risk factor for ischemic complication. The cutoff of MR-DWI positive lesions for predicting ischemic complication was>/= 7 (sensitivity 78.6%, specificity 73.6%). After adjusting stent use, aneurysm size, neck size, older age was the only independent risk factor for MR-DWI positive lesions >/= 7 (Odds ratio, 1.024; 95%CI, 1.002 – 1.046). Conclusions: The number of MR-DWI positive lesions was significantly associated with ischemic complication after coiling of UIA. Older age was marginally associated with symptomatic ischemic complication (p=0.054) and was the only independent risk factor for the number of MR-DWI posi-tive lesions >/= cutoff value for predicting symptomatic ischemic complication. 460 © 2013 S. Karger AG, Basel Scientific Programme 332 Vascular surgery and neurosurgery Hoarseness after carotid endarterectomy T. Tamaki1, Y. Node2, M. Kubota3, A. Morita4 Departmrnt of Neurosurgery, Nippon Medical School Tamanagayama Hospital, Tamashi Tokyoto, JAPAN1, Departmrnt of Neurosurgery, Nippon Medical School Tamanagayama Hospi-tal, Tamashi Tokyoto, JAPAN2, Department of Clinical Laboratory, Nippon Medical School, Ta-ma- Nagayama, Tamashi Tokyoto, JAPAN3, Departmrnt of Neurosurgery, Nippon Medical School, Bunkyoku Tokyoto, JAPAN4 Purpose; Hoarseness is a significant complication after carotid endarterectomy (CEA). The causes and mechanisms of hoarseness were examined by performing laryngoscopy and vocal fold electro-myography (EMG) to assess innervation by the vagus nerve (VN). Materials and Methods; In 97 patients, occurrence of hoarseness was monitored over one year after CEA. It was found after CEA in 12 patients (11%). In 6 patients, hoarseness was observed imme-diately after CEA (group A), while the onset was delayed in 6 patients (group B). The larynx, vocal chords, and pharynx were observed by laryngoscopy. We also refolded the vocal fold EMG in 47 patients from 2008. The threshold value of the vocal fold EMG was refolded and compared from the beginning to end of CEA. We also recorded vocal fold EMG before and after preparation VN and coagulation near VN. Results: In group A, laryngoscopy not only showed incomplete vocal fold palsy but also slight palsy of the larynx. In group B, edema and submucosal haemorrhage of the vocal folds were seen, but palsy of the vocal folds, pharynx, or larynx palsy was not observed. The threshold of vocal fold EMG ranged from 0.5 to 1.5 mA. In one patient, we confirmed a threshold change from 1.0 mA to 8 mA during CEA. This patient suffered from hoarseness after CEA with confirmed incomplete vocal fold and laryngeal palsy. Coagulation and preparation of nerve could not so much damage for nerve. Conclusion: There are two causes of hoarseness after CEA. One is submucosal haemorrhage of the vocal fold and pharyngeal compression, while the other cause is incomplete VN palsy. Ipsilateral pharyngeal palsy is caused by damage to the pharyngeal branch of the VN, so the site of injury was near the inferior vagal ganglion. This is at the same level as the upper part of the internal carotid ar-tery during CEA. Refolding of the vocal fold EMG threshold was useful for prediction of hoarseness after CEA.
Karger_ESC London_2013
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