ObjectiveTo investigate the efficacy of stellate ganglion block (SGB) on postoperative palpebral edema in patients undergoing intracranial aneurysm surgery. MethodsSixty patients who were scheduled to undergo intracranial aneurysm surgery between September 2012 and Novermber 2014 were recruited, and were assigned into 2 groups randomly with 30 in each:SGB group and control group. Patients in SGB group were administered SGB by injecting 0.3% ropivacaine on the operative side under the ultrasound guidance after surgery completed, while patients in the control group received injection of saline on the operative side under the ultrasound guidance. Incidence of postoperative palpebral edema at hour 24, 48, and 72 after surgery were measured. Numerical rating scale (NRS) was used to detect the severity of uncomfortable symptoms for palpebral swelling during rest state. The severity of palpebral edema was evaluated with continuous rating scale (0-5, 0 indicated normal palpebral, and higher score indicated more serious palpebral edema). Complications related with SGB were recorded. ResultsThe overall incidence of palpebral edema at hour 24 after surgery in SGB group was lower than that in the control group (P<0.05). There was no statistically significant difference in the overall incidence of palpebral edema at hour 48 and 72 after surgery between the two groups (P>0.05). The palpebral edema rating scores of the SGB group at hour 24 after surgery were lower than those of the control group (P<0.01).The incidence of palpebral edema which was scored 3 or more at hour 24 and 48 after surgery in SGB group was lower than that in the control group (P<0.05). No statistically significant difference was found in the incidence of palpebral edema which was scored 3 or more at hour 72 after surgery between the two groups (P>0.05). No complication related with SGB was found. ConclusionSGB can safely reduce the incidence of postoperative palpebral edema in patients undergoing intracranial aneurysm surgery, and reduce the severity of palpebral edema.
Neuropathic pain has been redefined by NeuPSIG as “pain arising as a direct consequence of a lesion or disease affecting the somatosensory syste”. However, pharmacological management for neuropathic pain is not effective, which is correlated with the uncertainty of pathogenesis. For a long time, neuron had been considered acting a major role in the development of neuropathic pain. In recent years, a majority of studies revealed that glia cell also involved in the occurrence and development of neuropathic pain, and neuron-glia interaction is one of the key mechanism of neuropathic pain, including complex signaling pathways as purinergic signaling. This review focuses on recent advances on the role of purinergic receptors in neuropathic pain.