ABSTRACT
@#Objective The clinical diagnosis of head and neck tumors with multiple groups of cranial nerve palsy as the first symptom is challenging.Based on the cases,a review of literature was conducted to discussed the etiology of this rare disease.Methods A retrospective summary of 4 patients with multiple cranial nerve palsy as the first symptom admitted to Shaanxi Provincial People's Hospital and Tangdu Hospital of Air Force Military Medical University from January 2018 to December 2021 were analyzed.Results A case of jugular foramen paraganglioma with the 5th,7th,8th,9th and 12th cranial nerve palsy,and one case of glomus jugular tumor involving the 7th and 8th cranial nerves.Case of germinoma affected the 2th,3th,5th,6th,7th and 8th cranial nerves,and nasal skull base adenocarcinoma had the 1th,3th,4th,5th,6th,7th,8th and 12th cranial nerves paralyzed.Conclusion Multiple cranial nerve palsy could be one of the presenting features of underlying benign or malignant tumors of the head and neck.In terms of etiological diagnosis,enough attentions should be paid to tumors.
ABSTRACT
Objective To explore the clinical features of patients with vertebrobasilar dolichoectasia (VBD).Methods Patients diagnosed with posterior circulation ischemia in our hospital from October 2008 to January 2012 were consecutively collected and were divided into the VBD group and the non-VBD (NVBD) group.Clinical manifestations,risk factors,hemodynamic parameters and neuroimaging features were collected.Results (1) Statistical difference was observed in dyslipidemia,hypertension and the history of diabetes in the two groups (P ＜ 0.05).(2) The cerebral hemodynamic features of the VBD patients were as the following:decreased peak systolic velocity of vertebral artery and basilar artery and decreased systolic/diastolic ratio.Statistical difference was showed in the average peak flow velocity(Vm),pulsatility index(PI) and resistance index(RI) (P =0.036,0.032,0.032,respectively).(3) The main clinical manifestations of VBD were ischemic cerebrovascular disease,hemorrhagic cerebrovascular disease,oppression,brain damage symptoms and hydrocephalus.(4) The diagnosis in most of the VBD patients was confirmed by neural imaging and MRI was the first choice.Conclusion The VBD patients have relative unique clinical features.MRI should be the first choice for neuroimaging.
ABSTRACT
Objective To investigate the expression of adiponectin (APN) and the clinical significance in type 2 diabetic rats with cerebral ischemic reperfusion damage.Methods One hundred and four SD rats were randomly divided into two groups,including normal diet group (n=52) and diabetic diet group (n=52); middle cerebral artery occlusion was performed in some of the rats to induce ischemia reperfusion injury models.Normal diet group was then randomly divided into euglycemia group (n=8) and ischemia reperfusion group (I/R,n-44); diabetic diet group was randomly divided into diabetes groups (n=8) and diabetes complicated with ischemia reperfusion group (DM+I/R,n=44).The blood was collected to detect the APN changes from the tail vein of rats from diabetes group (n=4) and DM+I/R group (n=4) before MCAO surgery and at 3,6,24,48 and 72 h,and 7 d after reperfusion.The rest 40 rats were randomly divided into subgroups subjected to 90 min of focal ischemia followed by 3,6,24 and 72 h,and 7 d reperfusion (n=8); the neuroethology assessment was determined by Zea Longa method; morphology of brain tissue was observed by HE staining.APN expression in infarction cores was detected by immunohistochemistry and Western blotting.Results The assessment scores of DM+I/R group (2.79±0.41) were significantly higher than those of I/R group (1.27±0.45,P＜0.05).As compared with that in the I/R group,the serum APN level in the DM+I/R group was significantly decreased 3,6,24,48 and 72 h,and 7 d after reperfusion (P＜0.05).Cerebral tissue damage (cellular degeneration and necrosis) in DM+I/R group was more serious as compared with I/R group at the same reperfusion time.In the ischemic hemisphere,APN expression increased at 3 h,decreased at 6 h,and increased again till 24 h after reperfusion,and then it remained at high level up to 7 days after reperfusion.The expression of APN in DM+I/R group was significantly lower than that in the I/R group (P＜0.05).These findings were consistent with the results of Western blotting.Conclusion APN expression decreases after focal cerebral ischemia-reperfusion injury,indicating that APN plays an important role in aggravating ischemic reperfusion injury by diabetes.
ABSTRACT
Objective To investigate the neuroprotective effect of escitalopram on focal cerebral ischemia/reperfusion in rats and its possible mechanisms.Methods Seventy-five male Sprague-Dawley rats were randomly divided into three groups:sham operation,saline control and escitalopram intervention groups (n =25 in each group).A focal cerebral ischemia reperfusion model in rats was induced by the intraluminal suture method.The modified neurological severity scale was used to evaluate neurological deficit in rats (n =5 in each group).Laser confocal technology was used to observe the microvascular diameter,density,and total area in ischemic region (n =5 in each group).Enzyme-linked immunosorbent assay was used to detect the plasma concentration of vascular endothelial growth factor (VEGF) (n =5 in each group).Immunohistochemical staining (n =5 in each group) and Western blotting (n =5 in each group) were used to detect the expression of VEGF in the ischemic brain tissue.Results At day 14 after modeling,the neurological deficit improved more significantly in the escitalopram intervention group than that in the saline control group (4.39 ±0.92 vs.6.57 ± 1.13; P =0.015).The 3D confocal vascular imaging showed that capillary diameter in the escitalopram intervention group was significantly smaller than that in the saline control group (2.93 ± 0.19 μm vs.3.56 ± 0.22 μm; P ＜0.01); the vascular density was significantly higher than that in the saline control group (232.68 ±12.54/0.002 mm3 vs.176.26 ± 10.87/0.002 mm3; P=0.000); the total microvascular area was significantly greater than that in the saline control group (89 154± 3 298 μm2/0.002 mm3 vs.75 368.14± 3 519 μm2/0.002 mm3; P=0.000).Enzyme-linked immunosorbent assay showed that the plasma VEGF concentration in the escitalopram intervention group was significantly higher than that in the saline control group (50.35 ± 5.44 pg/ml vs.13.75 ± 4.12 pg/ml; P =0.000).Immunohistochemical analysis showed that the VEGF expression in ischemic brain tissue in the escitalopram intervention group was significantly higher than that in the saline control group (P =0.000).Western blotting showed that the VEGF expression in ischemic brain tissue in the escitalopram intervention group was significantly higher than that in the saline control group (0.94 ±0.18 vs.0.62 ±0.22; P =0.006).Conclusions Escitalopram may reduce neurological deficit in cerebral ischemia/reperfusion in rats.Its mechanisms may be associated with VEGF-mediated angiogenesis.