Traumatic brain injury (TBI) is a primary cause of disability and mortality. Ghrelin, a gastrointestinal hormone, has been found to have protective effects for the brain, but the molecular mechanism of these neuroprotective effects of ghrelin remains unclear. In this study, an electronic cortical contusion impactor was used to establish a rat TBI model and we investigated the effect of ghrelin on brain repair by neurological severity score and histological examination. An antibody array was employed to uncover the molecular mechanism of ghrelin's neuroprotective effects by determining the alterations of multiple proteins in the brain cortex. As a result, ghrelin attenuated brain injury and promoted brain functional recovery. After TBI, 13 proteins were up-regulated in the brain cortex, while basic fibroblast growth factor (bFGF) and fibroblast growth factor-binding protein (FGF-BP) were down-regulated after ghrelin treatment. It is known that bFGF can induce angiogenesis in the brain and accelerate wound healing, which can be further enhanced by FGF-BP. Based on the previous studies, it is hypothesized that the exogenous ghrelin curing TBI might cause the closure of bFGF and FGF-BP functions on wound healing, or ghrelin might exert the neuroprotective effects by competitively inhibiting bFGF/FGF-BP-induced neovascularization. Whether the combinational administration of ghrelin and bFGF/FGF-BP can enhance or weaken the therapeutic effect on TBI requires further research.
Objective
To explore the localization and protection of the parapharyngeal segment of the internal carotid artery, and to provide anatomical data for clinical surgery.
Methods
Five adult cranial specimens (10 sides) were dissected by simulating the preauricular sub-temporal fossa approaches under microscope and the endoscopic endonasal transclival approaches, and the relevant data were measured by vernier calipers.
Results
Microscopically, the parapharyngeal internal carotid artery was located between the levator veli palatini anteriorly and the stylopharyngeal muscle posteriorly. The distance between the two muscles was 14.7±0.4 mm (14.2-15.3 mm). From the endoscopic perspective, the parapharyngeal segment of internal carotid artery was located behind the levator veli palatini muscle, and the distance from its attachment to the anterior border of the carotid canal was 5.1±0.2 mm (4.9-5.5 mm). The parapharyngeal internal carotid artery was located in the sheath of the carotid artery with sympathetic nerve attached on its surface. The posterior group nerves descended behind the sheath of the artery. The hypoglossopharyngeal nerve and hypoglossal nerve crossed the internal carotid artery in the posterior part of the styloid muscle groups and moved forward. There was a constant stylopharyngeal fascia on the surface of the carotid sheath, which extended to the fascia on the surface of the long cephalic muscle in front of the carotid sheath. The parapharyngeal internal carotid artery gradually approached the midline from the external orifice of the carotid artery. At the level of the carotid canal, the level of pharyngeal tubercle, and the level of the atlantooccipital junction, the distances from the anterior border of the parapharyngeal segment of the internal artery to the middle line of the clivus were 23.2±2.5 mm (20.6-25.8 mm), 19.3±1.1 mm (17.9-20.7 mm) and 15.5±1.3 mm (14.1-16.9 mm) respectively.
Conclusions
The levator veli palatini muscle could act as the landmark of the parapharyngeal segment of internal carotid artery. The stylopharyngeal fascia and the fascia of the longus capitis major are anatomical barriers to protect parapharyngeal segment of internal carotid artery under the endoscopic endonasal approach.
Key words:
Carotid artery, internal; Neuroanatomy; Natural orifice endoscopic surgery; Levator veli palatini muscle; Stylopharyngeal fascia
Post-traumatic hydrocephalus (PTH) makes recovery from head trauma after decompression more complicated and is associated with high risks of clinical deterioration and poor outcomes. The aim of this study was to verify the predictors associated with the development of PTH in patients with head injury undergoing unilateral decompressive craniectomy (DC).Among traumatic brain injury (TBI) patients who underwent unilateral DC between January 2013 and December 2016, the clinical medical records, radiological information, and changes of patients' conditions in the 3-month after injury were reviewed retrospectively.183 TBI patients after unilateral DC were analyzed, and 50 (27.32%) of them suffered PTH based on head CT scans. Univariate and multivariable analyses revealed that older age (p = 0.002), the Glasgow Coma Scale (GCS) score at admission (p < 0.001), intraventricular hemorrhage (IVH; p = 0.008), post-traumatic cerebral infarction (PCI; p = 0.007), and postoperative meningitis (p = 0.016) were independent predictors for the hydrocephalus after DC. Receiver operating characteristic curves were created and the area under the curve (AUC) were calculated to further assess the accuracy of the variables for predicting PTH. The AUC was 0.836 for the combined all five independent factors (95% confidence interval: 0.775-0.887).TBI patients who undergo unilateral DC with advanced age, lower GCS score at admission, coexisting IVH, PCI, and/or postoperative meningitis should be closely monitored at follow-up assessments for earlier prediction of PTH.
Abstract Hearing impairment is one of the most common chief complaints in newly diagnosed nasopharyngeal carcinoma (NPC) patients, but baseline audiometric assessments are seldom reported. This study aims to investigate the prevalence of hearing impairment in this population through comprehensive audiometric testing and analyse the associated factors. A cohort of 187 newly diagnosed NPC patients were recruited from three hospitals. Pre‐treatment comprehensive audiometric assessments, including pure‐tone audiometry, tympanometry, Eustachian tube function tests and distortion product otoacoustic emissions (DPOAE), were performed to evaluate hearing impairment. Patient characteristics and tumour invasion extent were also recorded. Binary logistic regression was employed to analyse factors associated with hearing impairment. Among the patients, 27.5% of ears showed conductive hearing loss (CHL), 13.6% had sensorineural hearing loss (SNHL), and 10.4% demonstrated mixed hearing loss. Additionally, 43.6% of ears exhibited abnormal tympanograms, 86.1% had Eustachian tube dysfunction, and 77.3% failed the DPOAE test. Multivariable analysis identified subjective hearing symptoms, mastoiditis, and invasion of the tensor veli palatini muscle and Eustachian tube as factors associated with CHL. T stage, mastoiditis, and invasion of the tensor veli palatini muscle and nasal cavity were linked to abnormal tympanograms. T stage, sinusitis, and invasion of the levator veli palatini muscle significantly affected Eustachian tube function, while age influenced both SNHL and DPOAE results. Hearing impairment is prevalent among newly diagnosed NPC patients, with over half exhibiting various forms. Comprehensive baseline audiometric assessment in this population is crucial for developing individualized treatment strategies and enabling early intervention to prevent further hearing deterioration.
'/%3e%3cuse xlink:href='%23a' transform='rotate(23.036 .093 25.536)'/%3e%3cuse xlink:href='%23a' transform='rotate(45.87 1.273 16.18)'/%3e%3cuse xlink:href='%23a' transform='rotate(69.945 .996 12.078)'/%3e%3cuse xlink:href='%23a' transform='rotate(20.66 -19.689 31.932)'/%3e%3c/svg%3e)