ABSTRACT
To evaluate the safety and efficacy of mechanical thrombectomy with stent-retriver for anterior circulation small vessel occlusion in patients with acute ischemic stroke (AIS).Methods:From a prospectively collected thrombectomy database of consecutive patients with AIS between January 2017 and November 2018, 311 angiographic images were analyzed to assess small vessel occlusions (A 2 and M 2 segments). Patients were categorized into alteplase with thrombectomy group and thrombectomy alone group. The primary outcome was a favorable outcome (modified Rankin Scale scores 0-2) at 90 days. Secondary outcomes were successful recanalization (modified thrombolysis in cerebral infarction 2b or 3), symptomatic intracranial hemorrhage, and 90-day mortality. Results:Small vessel occlusions were identified in 19 patients, including 14 M 2occlusions, two A 2occlusions, and three M 2+A 2 occlusions. Six patients were in the alteplase with thrombectomy group and 13 patients in the thrombectomy alone group. Favorable outcome was achieved in eight of 19 patients at 90 days. Successful recanalization was achieved in 18 patients (18/19), symptomatic intracranial hemorrhage was observed in one patient (1/19), and death was recorded in five patients (5/19). No statistically significant difference was detected between the two groups with regard to successful recanalization (6/6 in the alteplase with thrombectomy group vs 12/13 in the thrombectomy alone group), symptomatic intracranial hemorrhage (0/6 vs 1/13), favorable outcome (2/6 vs 6/13) and death (1/6 vs 4/13; all P>0.05). Conclusion:As to anterior circulation small vessel occlusions, the combination-therapy within 4.5 hours or mechanical thrombectomy alone in extended time window with perfusion evaluation may be both safe and effective.
ABSTRACT
Objective To observe the changes on the neurogenic inflammation-related factors in the dura mater of the rat model of migraine and investigate the possible mechanism of the pain of migraine.Methods SD rats were randomly divided into stimulation group ( n = 32 ) and sham group ( n = 32 ).Unilateral trigeminal ganglion was stimulated to induce migraine for rats in the stimulation group. Rats in the sham group were subjected to sham surgery. The levels of calcitonin gene-related peptide (CGRP) in the blood of jugular vein in the stimulation side were measured by radioimmunoassay. The levels of histamine in peripheral blood and prostaglandin E2 (PGE2 ) in the dura mater were determined by enzyme-linked immunosorbent assay (ELISA). The number of mast cells and percentage of their degranulation in the dura mater were determined under a microscope after toluidine blue staining. Cyclooxygenase 2 (COX-2)expression in the dura mater was evaluated by immunohistochemical staining and western blot analysis. Results In the stimulation group, the level of CGRP in the ipsilateral jugular vein was (82. 84 ± 16. 24)pg/ml and in the sham group was (59. 20 ±11.66) pg/ml (t = -3.34, P ＜ 0. 05 ). The level of histamine in the ipsilateral jugular vein was ( 11.59 ± 1.20) ng/ml and in the sham group was (9. 87 ±0. 88) ng/ml (t = - 3. 27, P ＜ 0. 05). The number of mast cells in the dura mater decreased from 15.46 ± 2. 40 in the stimulation group to 11.63 ± 1.67 in the sham group ( t = 3.71, P ＜ 0. 05 ). Degranulation of mast cells in the dura mater significantly increased from 14. 09% ±4. 53% in the sham group to 29. 10% ±9. 39% in the stimulation group (t = - 4. 07, P ＜ 0. 05 ). The level of PGE2 in the stimulation group was ( 382. 30 ±20. 90) pg/ml and in the sham group was (80. 70 ± 10. 60) pg/ml (t = - 16. 674, P ＜0. 05). The number of COX-2 positive cells significantly increased from 42. 00 ± 18.40 in the sham group to 139.00 ±20. 50 in the stimulation group (t = -7. 994, P ＜0. 05). Also the COX-2 protein level was elevated from 19. 50 ±9. 20 in the sham group to 359. 20 ±21.90 in the stimulation group (t = -5. 190, P ＜0. 05). Conclusions Electrical stimulation on the unilateral trigeminal ganglion induces neurogenic inflammation in the dura mater. Changes on the neurogenic inflammation-related factors are probably the essential pathophysiological mechanism underlying the pain in migraine.