The original version of this consensus statement on mechanical thrombectomy was approved at the European Stroke Organisation (ESO)-Karolinska Stroke Update conference in Stockholm, 16-18 November 2014. The statement has later, during 2015, been updated with new clinical trials data in accordance with a decision made at the conference. Revisions have been made at a face-to-face meeting during the ESO Winter School in Berne in February, through email exchanges and the final version has then been approved by each society. The recommendations are identical to the original version with evidence level upgraded by 20 February 2015 and confirmed by 15 May 2015. The purpose of the ESO-Karolinska Stroke Update meetings is to provide updates on recent stroke therapy research and to discuss how the results may be implemented into clinical routine. Selected topics are discussed at consensus sessions, for which a consensus statement is prepared and discussed by the participants at the meeting. The statements are advisory to the ESO guidelines committee. This consensus statement includes recommendations on mechanical thrombectomy after

Background and Purpose— Dural arteriovenous shunts with cortical venous reflux or drainage may cause neurological symptoms and death with or without intracranial hemorrhage. Present knowledge about the natural history of these lesions is limited, however. We investigated the incidences of intracranial hemorrhage, progressive dementia syndrome, and death in patients diagnosed in our neurovascular center. Methods— We evaluated the records of 85 patients with dural arteriovenous shunts with cortical venous drainage or reflux hospitalized in our institution from 1978 to 2007. The annual incidences of intracranial hemorrhage, progressive dementia syndrome, and death were calculated. Results— Fifty-three patients did not have an intracranial hemorrhage as the presenting event. One of these patients bled after diagnosis. Thirty-two patients had an intracranial hemorrhage as the presenting event. Three patients bled after diagnosis. One of these patients died. Apart from deficits caused by hemorrhage, no patient reported adverse neurological symptoms. In patients presenting with an intracranial hemorrhage the annual risk for hemorrhage is approximately 7.4% and in those not presenting with a hemorrhage it is approximately 1.5%. Conclusion— The risk of intracranial hemorrhage from a dural arteriovenous shunt with cortical venous drainage is most likely smaller than previously proposed. Presentation with hemorrhage is a risk factor for hemorrhage. The risks of developing neurological symptoms not related to hemorrhage are also less than previously reported.

Peripheral hypersensitivity (hyperalgesia and allodynia) are common phenomena both in inflammatory and in neuropathic pain conditions. Several rat models of mononeuropathy (Bennett, Seltzer and Gazelius models) display such symptoms following partial injury to the sciatic nerve. Using immunohistochemistry and behavioral tests, we investigated inflammatory cell and cytokine responses in the sciatic nerve 14 days after injury created in these different models as well as after axotomy. Tactile hypersensitivity ('allodynia') was present in all Gazelius model rats whereas only 38 and 29% of the Bennett and Seltzer models, respectively, displayed this sign of neuropathy. The inflammatory reactions in rats with and without tactile allodynia were compared. Monocytes/macrophages (ED-1), natural killer cells, T lymphocytes, and the pro-inflammatory cytokines tumor necrosis factor-alpha (TNF-alpha) and interleukin-6 (IL-6), were significantly upregulated in all nerve injured rats in comparison to sham-operated controls. Interestingly, ED-1-, TNF-alpha- and IL-6-positive cells increased more markedly in allodynic Bennett and Seltzer rats than in non-allodynic ones. The magnitude of the inflammatory response does not seem to relate to the extent of damage to the nerve fibers because axotomized rats displayed much lower upregulation. Our findings indicate that the considerable increase in monocytes/macrophages induced by a nerve injury results in a very high release of IL-6 and TNF-alpha. This may relate to the generation of tactile allodynia/hyperalgesia, since there was a clear correlation between the number of ED-1 and IL-6-positive cells and the degree of allodynia. It is possible that measures to reduce monocyte/macrophage recruitment and the release of pro-inflammatory interleukins after nerve damage could influence the development of neuropathic pain.