RESUMEN
Objective: To retrospectively evaluate the efficacy and security of Willis covered stent (WCS) deployment for complex vascular diseases of the internal carotid (ICA) and vertebral (VA) arteries. Methods: Retrospective analysis was performed on complex vascular disease patients (n=36) treated with WCSs at our center between March 2017 and December 2022, with a 3-36-months follow-up surveillance and digital subtraction angiography (DSA) examination. Results: The WCSs were successfully deployed in all the patients. The 36 included lesions were carotid-cavernous sinus fistulas (CCFs; n=10) (27.8%), complex saccular aneurysms (n=10) (27.8%), traumatic pseudoaneurysms (n=7) (19.4%), blood blister-like aneurysms (BBAs; n=5) (13.9%), and iatrogenic carotid or vertebral artery ruptures (n=4) (11.1%). The WCS was released at the communicating segment (n=2) (5.6%), the ophthalmic segment (n=3) (8.3%), the clinoid and cavernous segment (n=28) (77.8%), the petrous segment (n=2) (5.6%) of ICA and the V3 segment (n=1) (2.8%) of VA. Postoperative DSA showed complete lesion occlusion in 26 patients (72.2%) who were immediately treated with WCSs, and endoleaks occurred in 3 patients (8.3%) (endoleaks resolved postadjustment in 7 patients (19.4%)). In patients (n=3) (8.3%) treated with double stents at the break of the ICA, the endoleak remained in 1 CCF patient (2.8%) during the 3-month follow-up, and the residual shunt disappeared after the second stent system was placed 3 months later. No aneurysm, bleeding or infarct recurrence reported, and only 1 patient (2.8%) had mild asymptomatic in-stent stenosis. Deaths and procedural complications did not occur during follow-up. Conclusion: Treatment with a WCS for intracranial complex vascular diseases resulted in satisfactory clinical outcomes and appeared effective and safe. Controlled, multicenter, large sample sizes and longer follow-up periods studies are necessary.
RESUMEN
PURPOSE: Posttraumatic cerebral infarction (PTCI) is a common and relatively serious complication of traumatic brain injury (TBI) without a clear etiology. Evaluating risk factors in advance is particularly important to predict and avoid the occurrence of PTCI. PATIENTS AND METHODS: We retrospectively analyzed 297 patients with moderate to severe TBI admitted to the Department of Neurosurgery in our hospital from January 2019 to September 2020 and evaluated the effects of various factors such as age, sex, admission Glasgow Coma Scale (GCS), skull base fracture, subarachnoid hemorrhage (SAH), brain herniation, hypotensive shock, and decompressive craniectomy on the incidence of PTCI. We also performed a multivariate logistics regression analysis on the relevant factors identified and evaluated the diagnostic value of each risk factor in advance by receiver operating characteristic (ROC) analyses. RESULTS: Among the patients, 32 (10.77%) suffered PTCI. The incidence rates of PTCI in those with GCS scores of 3-8 and 9-12 were 15.87% (30/189) and 1.85% (2/108), respectively, while the rates were 18.84% (13/69), 15.03% (29/193), 18.57% (13/70), and 20.59% (14/68) in those with skull base fractures, traumatic SAH, brain herniation, and hypotensive shock, respectively, and 14.38% (23/160) in those who underwent decompressive craniectomy. These differences in PTCI incidence were statistically significant. However, the differences in PTCI incidence caused by patient age and sex were not statistically significant. CONCLUSION: Low GCS score, skull base fractures, traumatic SAH, brain herniation, hypotensive shock, and decompressive craniectomy are risk factors for the occurrence of PTCI, while age and sex are not significantly correlated with the occurrence of PTCI.
RESUMEN
Traumatic brain injury can cause loss of neuronal tissue, remote symptomatic epilepsy, and cognitive deficits. However, the mechanisms underlying the effects of traumatic brain injury are not yet clear. Hippocampal excitability is strongly correlated with cognitive dysfunction and remote symptomatic epilepsy. In this study, we examined the relationship between traumatic brain injury-induced neuronal loss and subsequent hippocampal regional excitability. We used hydraulic percussion to generate a rat model of traumatic brain injury. At 7 days after injury, the mean modified neurological severity score was 9.5, suggesting that the neurological function of the rats was remarkably impaired. Electrophysiology and immunocytochemical staining revealed increases in the slope of excitatory postsynaptic potentials and long-term depression (indicating weakened long-term inhibition), and the numbers of cholecystokinin and parvalbumin immunoreactive cells were clearly reduced in the rat hippocampal dentate gyrus. These results indicate that interneuronal loss and changes in excitability occurred in the hippocampal dentate gyrus. Thus, traumatic brain injury-induced loss of interneurons appears to be associated with reduced long-term depression in the hippocampal dentate gyrus.
RESUMEN
Traumatic brain injury induces potent inflammatory responses that can exacerbate secondary blood-brain barrier (BBB) disruption, neuronal injury, and neurological dysfunction. Dexmedetomidine is a novel α2-adrenergic receptor agonist that exert protective effects in various central nervous system diseases. The present study was designed to investigate the neuroprotective action of dexmedetomidine in a mouse traumatic brain injury model, and to explore the possible mechanisms. Adult male C57BL/6J mice were subjected to controlled cortical impact. After injury, animals received 3 days of consecutive dexmedetomidine therapy (25 µg/kg per day). The modified neurological severity score was used to assess neurological deficits. The rotarod test was used to evaluate accurate motor coordination and balance. Immunofluorescence was used to determine expression of ionized calcium binding adapter molecule-1, myeloperoxidase, and zonula occluden-1 at the injury site. An enzyme linked immunosorbent assay was used to measure the concentration of interleukin-1ß (IL-1ß), tumor necrosis factor α, and IL-6. The dry-wet weight method was used to measure brain water content. The Evans blue dye extravasation assay was used to measure BBB disruption. Western blot assay was used to measure protein expression of nucleotide-binding oligomerization domain-like receptor family pyrin domain-containing 3 (NLRP3), caspase-1 p20, IL-1ß, nuclear factor kappa B (NF-κB) p65, occluding, and zonula occluden-1. Flow cytometry was used to measure cellular apoptosis. Results showed that dexmedetomidine treatment attenuated early neurological dysfunction and brain edema. Further, dexmedetomidine attenuated post-traumatic inflammation, up-regulated tight junction protein expression, and reduced secondary BBB damage and apoptosis. These protective effects were accompanied by down-regulation of the NF-κB and NLRP3 inflammasome pathways. These findings suggest that dexmedetomidine exhibits neuroprotective effects against acute (3 days) post-traumatic inflammatory responses, potentially via suppression of NF-κB and NLRP3 inflammasome activation.