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Objectives To evaluate the relationship between TGFBR3 rs284875 single nucleotide polymorphism (SNP) state and silent cerebral infarction (SCI) in asymptomatic patients with sickle cell disease (SCD). Methods A cross-sectional study was conducted on 50 children with SCD above 2 y of age followed up at the hematology outpatient clinic of Alexandria University Children's Hospital in Egypt. Twenty-four healthy children were included as a control group. All patients included in the study were subjected to complete history and clinical examination. Real-time polymerase chain reaction was performed on patients and controls for identifcation of SNP rs284875 of the TGFBR3 gene. A magnetic resonance imaging (MRI) of the brain were performed only on patients for detection of SCI. Results Fifty SCD patients were enrolled (26 males and 24 females), with a median age of 10.9 y (2.3–17.8 y), and 24 children as healthy control for the studied SNP. Thirty-fve (70%) patients had homozygous SCD, while 30% had sickle ?-thalassemia. The brain MRI was normal in all the patients except for 2 patients who had features of SCI. The TGFBR3 rs284875 SNP was detected in 15 (30%) patients in the homozygous state (GG) versus only 1 (4.2%) child from the control group (p=0.003). The prevalence of SCI was low in the study population and there was no statistically signifcant relationship between the TGFBR3 rs284875 SNP status and the presence of SCI in the brain MRI (p=0.621). Conclusions This study confrmed a low prevalence of SCI in the SCD patient included in the study. The TGFBR3 rs284875 SNP did not signifcantly increase SCI among those patients.
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Pituitary apoplexy (PA) is a clinical diagnosis comprising a sudden onset of headache, neurological deficits, endocrine disturbances, altered consciousness, visual loss, or ophthalmoplegia. However, clinically, the presentation of PA is extremely variable and occasionally fatal. While meningitis and cerebral infarcts are themselves serious diseases, they are rarely seen as manifestations of PA and are exceedingly rare when present together. We present the case of a 20-year-old male with a rapid progression of symptoms of meningitis, PA and stroke. The present article seeks to emphasize a rare manifestation of PA with an attempt to understand the intricacies of its evaluation and management.
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Humans , Male , Adult , Pituitary Apoplexy/surgery , Pituitary Apoplexy/etiology , Meningitis, Bacterial/complications , Stroke/complications , Spinal Puncture/methods , Pituitary Apoplexy/diagnostic imaging , Cerebral Infarction/complications , Endoscopy/methodsABSTRACT
Objective:To explore the predictive ability of apparent diffusion coefficient (ADC) value in magnetic resonance imaging (MRI) mapping sequences in outcomes of brain tissues in patients with acute ischemic stroke (AIS) who had successful recanalization after endovascular treatment.Methods:A total of 45 patients with AIS who received endovascular treatment and successful recanalization in our hospital from January 2019 to December 2019 were selected. Post-processing software was used to analyze the images of these patients by MRI before surgery and one week after surgery, and the differences of ADC value in the core area of cerebral infarction, lesion reversal area and increased cerebral infarction area displayed by diffusion weighted imaging (DWI) before surgery were measured and compared. Receiver operating characteristic (ROC) curve was used to analyze the predictive ability of preoperative ADC value in the reversal of lesions showed by DWI.Results:Lesion reversal area and increased cerebral infarction area indicated by preoperative DWI existed in all patients after successful recanalization. The preoperative ADC values of the infarct core, lesion reversal area and increased cerebral infarction area were 0.555×10 -3 mm 2/s (0.462, 0.648), 0.637×10 -3 mm 2/s (0.509, 0.765) and 0.948×10 -3 mm 2/s (0.905, 0.991), respectively, with significant differences ( P<0.05). The optimal cut-off point to predict DWI lesion reversal after successful recanalization was 0.57×10 -3mm 2/s, and the accuracy was 87.1% (area under curve=0.871; 95%CI: 0.868-0.875, P=0.000), with sensitivity of 97.2% and specificity of 68.3%. Conclusion:In patients with AIS after successful recanalization, the preoperative ADC values are obviously different in brain tissues with different outcomes, which can be used to predict the final imaging outcomes of the brain tissues.
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Aim To observe the effect of hydroxysafflor yellow A (HSYA) on the COX-2/PGD/DPs pathway in the cortex of mice with cerebral ischemia-reperfusion injury. Methods C57BL/6 male mice were randomly divided into sham group, model group and HSYA group. Right middle cerebral artery occlusion/reperfusion model was established in mice by intraluminal suture method. HYSA (20 mg • kg"1) was injected into the tail vein for five consecutive days before the operation. The sham group and the model group were given the same volume of normal saline. The neurological function score and cerebral infarct volume were measured 24 hours after operation. The histopathological changes of mouse cortex were observed by HE staining. The protein and mRNA expression of COX-2, DP, and DP2 were detected by Western blot and qRT- PCR respectively. The levels of TNF-a, IL-1 (3 and PGD2 were detected by ELISA. Results Compared with sham group, the scores of neurological function, infarct volume, the expression of COX-2, DP, and DP2 protein and mRNA, and the contents of TNF-a, IL-1 (3 and PGD2 in the cortex of model group significantly increased. Compared with model group, the scores of neurological function and the infarct volume significantly decreased in HSYA-treated group, and the damage of cortical cells in ischemic area was significantly improved. The expressions of COX-2, DP, and DP2mRNA and protein were significantly down-regula- ted, and the levels of inflammatory factors such as TNF-a, IL-1 p and PGD2 were markedly down-regula- ted. Conclusions HSYA inhibits the activation of COX-2/PGD2/DPs pathway in mouse brain tissues, which may be involved in the protective mechanism of HSYA in cerebral ischemia-reperfusion injury.
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@#Objective To improve the skills of diagnosis and treatment of Trousseau syndrome in order to reduce misdiagnosis and mistreatment.Methods Twelve cases admitted in our hospital and subsequently proved Trousseau syndrome were retrospectively analyzed,including their clinical characteristics,radiography results,and treatment effect.Results Twelve cases began as acute cerebral infarction,associated with increased D-dimer in ten cases and multiple acute infarction involving multiple arterial innervation region in MR of all cases.Among twelve cases,seven cases of lung cancer,one case of pancreatic cancer,two cases of breast cancer and two cases of ovarian cancer were finally diagnosed.Then,six patients were treated with anticoagulant therapy and six abandoned.Conclusion If the lesions’ distribution of acute cerebral infarction doesn’t conform to the conventional and single arterial innervation region in aged patients,doctors should search causes actively,especially should be vigilant about Trousseau syndrome,in order to treat correctly and prevent recurrent episodes that aggravate the disease.
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@#Objective To investigate neural functional recovery and intracranial vascular disease of acute cerebral infarct (ACI) patients complicated with polyvascular disease (PolyVD).Methods Retrospective analysis was conducted on 83 ACI patients with monovascular disease and 68 ACI patients with polyvascular disease seeking hospitalization in the Neurology Department of the Third Affiliated Hospital of Jinzhou Medical University from January 2019 to September 2019.The changes of intracranial artery disease and neural functional recovery of the monovascular disease group and polyvascular disease group were analyzed,and multiple factors that affect neural function recovery were analyzed.Results (1)Compared with the monovascular disease group,the PolyVD group was found with a higher percentage of poor neural functional recovery,lower recovery rate of neural functions,and a larger number of vessels associated with the intracranial disease.The differences were statistically significan（P<0.05）.(2)The number of vessels associated with the intracranial disease and the number of vascular beds were positively correlated（P<0.05）,while the neural functional recovery rate and the number of vascular beds were negatively correlated（P<0.05）.(3)Age,medical history of diabetes and stroke,and number of vascular beds were all independent risk factors of poor neural functional recovery.Conclusions Polyvascular disease is an independent risk factors of poor neural functional recovery among ACI patients.The higher the number of vascular beds of the disease complicated with carotid atherosclerosis is,the higher the possibility of poor neural functional recovery will be,and the worse the intracranial artery disease will be.
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Objective: To investigate the possible role of astrocytes after brain infarction in stroke-prone, spontaneously hypertensive (SHR-SP) rats and the association with angiogenesis and the architecture. Methods: We maintained SHR-SP rats on high sodium water starting to accelerate the stroke onset. The 3D quantification of microvasculatures (diameter, branch number) by cofocal microscope after FITC-dextran was injected into the rats via the left femoral vein. Glial fibrillary acidic protein (GFAP) expression and microvessel density (MVD) using counting the number of factor -positive endothelial cells were evaluated by immunofluorescence and immunohistochemistry, respectively. Results: Cerebral infarction occurred at week 7 after high sodium water intake (13 g/L NaCl) in SHR-SP group. When compared with the non-infarcted contralateral hemisphere and SHR-SP on normal sodium intake and WKY rats, GFAP expression and MVD were significantly increased, respectively, and the diameter and the branch number of vessels were decreased, respectively, in cerebral infarcts with boundary zones of SHR-SP rats (P<0.01). Linear correlation analysis showed that GFAP expression was positively correlated with MVD and the diameter and the branch number of vessels in cerebral infarcts in SHR-SP (P<0.01). Conclusion: Astrocytes hyperplasia may be associated with increased regional angiogenesis and the changes of architecture in SHR-SP rats with high sodium water (13 g/L NaCl) that induces focal cerebral infarcts.
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OBJECTIVE: To observe the influence of scalp acupuncture on cerebral infarct size and expression of IL-10, IL-6, and IL-1β in the para-hippocampal gyrus in acute ischemic cerebrovascular disease(AICD) rats, so as to investigate its mechanisms underlying improvement of AICD. METHODS: Forty-eight male SD rats were randomly allocated to normal control (control), AICD model, medication, and scalp acupuncture groups (n＝12 per group). The AICD model was established by occlusion of the middle cerebral artery (MCAO). Rats of the medication group received intraperitoneal injection of Ammonium 1-Pyrrolidinedithiocarbamate (APDC, 100 mg•kg－1•d－1), once daily for 7 days. Scalp acupuncture stimulation was applied to bilateral "Dingnieqianxiexian" (MS6) once daily for 7 days. Before and after intervention, the neurologic deficit score (NDS) and the neurological score (NS) were evaluated according to Longa's and Schäbitz's methods, respectively. At the end of the intervention, the para-hippocampal gyrus and whole brain were collected respectively. The expression levels of IL-10, IL-6 and IL-1β in the para-hippocampal gyrus tissue were detected by immunohistochemistry, and the cerebral infarct volume of the brain was detected by triphenyltetrazollium chloride (TTC) staining after sectioning. RESULTS: Following modeling, the NDS, NS and the expression of IL-10, IL-6 and IL-1β in para-hippocampal gyrus were significantly increased in the model group compared with the control group (P0.05). The effect of scalp acupuncture was obviously superior to that of medication in up-regulating IL-10 expression level (P0.05). CONCLUSION: Scalp acupuncture can improve neurological function and reduce infarct volume in AICD rats, which may be associated with its function in up-regulating the expression of IL-10 and in inhibiting the expression of IL-6 and IL-1β to reduce inflammation reaction.
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Objective To investigate the main cell types expressed brain-derived neurotrophic factor (BDNF) in the posterior cortical infarction area in cerebral infarction rats after early vein allograft of bone marrow mesenchymal stem cells (BM-MSCs) and the effect of BM-MSCs transplantation on their ce11 numbers and percentages.Methods (1) Fifteen SD rats were randomly divided into sham-operated group 1,ischemia control group 1,and BM-MSCs transplantation group 1 (n=5);distal middle cerebral artery occlusion (dMCA) models were used in the later two groups;1 × 106 CM-DiI labeled BM-MSCs were intravascularly transplanted into the tail vein of rats from the transplantation group 1 at one h after ischemia;all rats were sacrificed 48 h after ischemia;BM-MSCs with co-existence of CM-Dil and BDNF in the ischemia cortex areas were detected by immunofluorescence staining.(2)Fifteen SD rats were randomly divided into sham-operated group 2,ischemia control group 2,and BM-MSCs transplantation group 2 (n=5);dMCAO models were used in the later two groups;1 ×106 non-labeled BM-MSCs were intravascularly transplanted into the tail vein of rats from the transplantation group 2 at one h after ischemia;48 h after ischemia onset,all rats were sacrificed;the number of BDNF+ and CD68+ microglia cells,BDNF+ and Iba-1+ microglia cells,and BDNF+ and neuron-specific nucleoprotein (NeuN)+ neurons were measured by immunofluorescence staining.Results (1) CM-Dil red fluorescence labeled allogeneic BM-MSCs were only found in BM-MSCs transplantation group 1;the labeled cells scattered in the infarct and peri-infarct cortices;9.70％±3.47％ CM-Dil labeled BM-MSCs expressed BDNF,accounting for 13.32％±4.48％ of all BDNF+ cells in the infarct brain cortex.(2) In the brain tissues of cortex infarct area of BM-MSCs transplantation group 2,38.40％±9.04％ BDNF+ cells were Iba-1+ microglia cells,11.65％±2.76％ BDNF+ cells were CD68+ microglia cells,and 28.96％±6.99％ BDNF+ cells were NeuN+ neurons;the Iba-1+ cell numbers and Iba-1+/BDNF+ double positive cell percentages in the BM-MSCs transplantation group 2 ([92.06±36.52]/mm2 and 79.21％±12.27％) were significantly increased as compared with those in the ischemia control group 2 ([31.13±10.23] mm2 and 60.15％±28.20％,P＜0.05).Conclusion Allogeneic BM-MSCs is capable of migrating into the infarct cortex when intravenous transplantation of BM-MSCs is performed at the early stage after ischemia;the main sources of BDNF in these areas are microglias cells and neurons;these BM-MSCs increase both number and percentage of Iba-1+/BDNF+ double positive cells,which may be one of the underlying mechanisms of therapeutic effects.
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En el mundo hay unos 47 millones de personas que padecen demencia, y cada año se registran cerca de 10 millones de nuevos casos. La demencia es una de las principales causas de discapacidad y dependencia entre las personas mayores de 65 años. La demencia vascular constituye la segunda causa de demencia en adultos mayores y en ocasiones su diagnóstico es poco asertivo por la variedad y similitud de síntomas entre las diferentes enfermedades que originan demencia vascular, incluyendo CADASIL (acrónimo inglés de Cerebral Autosomal Dominant Arteriopathy with Subcortical Infarcts and Leukoencephalopathy); particularmente el déficit cognitivo es de los síntomas más complejos de diagnóstico, teniendo en cuenta que su manifestación clínica depende de la magnitud y localización de la lesión. La enfermedad de CADASIL, aunque se constituye como una infrecuente causa de demencia vascular de naturaleza hereditaria a nivel mundial, representa una patología de gran importancia en el ámbito nacional, dado que en familias colombianas se ha reportado mutaciones que conllevan a dicha patología. Por lo tanto, su diagnóstico y tratamiento constituyen un reto para el personal clínico, sabiendo que la identificación temprana y precisa es la mejor estrategia para evitar la progresión precoz de la enfermedad y el mejoramiento de la calidad de vida del paciente. De acuerdo con lo anterior, se realizó una revisión de la diferenciación clínica del déficit cognitivo del CADASIL con respecto a las demás demencias vasculares, con el fin de generar una herramienta que apoye la diferenciación clínica de dicha patología.
In the world, there are approximately 47 million people who have dementia, and every year they register near 10 million new cases. The dementia is one of the principal reasons for disability and dependence between people older than 65 years old. Vascular dementia constitutes the second reason of dementia in the elders, and sometimes the diagnosis is slightly assertive because of the variety and similarity of symptoms between the different diseases that originate vascular dementia, including CADASIL (Cerebral Autosomal Dominant Arteriopathy with Subcortical Infarcts and Leukoencephalopathy). Particularly, the cognitive deficit is one of the most complex symptoms of diagnosis, bearing in mind that its clinical manifestation depends on the magnitude and location of the injury. CADASIL disease, though it constituted as an infrequent reason of vascular dementia of hereditary nature worldwide, represents a pathology of great importance in the national area, because, in Colombian families, there have been reported mutations that carry to the above-mentioned pathology. Therefore, its diagnosis and treatment constitute a challenge for the clinical personnel, knowing that the early and precise identification is the best strategy to avoid the rapid progression of the disease and the improvement of the quality of life of the patient. In agreement with the previous information, there was made a review of the clinical differentiation of the cognitive deficit of CADASIL regarding other vascular dementias, to generate a tool that supports the clinical differentiation of the pathology mentioned above.
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Humans , Cognition Disorders/diagnosis , Cognition Disorders/physiopathology , CADASIL/diagnosis , CADASIL/physiopathology , Dementia, Vascular/diagnosis , Dementia, Vascular/physiopathologyABSTRACT
OBJECTIVE: To observe the effect of acupuncture on the expression of silent information regulator factor 2-related enzyme 1 (SIRT 1) and nuclear factor-κB (NF-κB) in rats with acute cerebral ischemia (ACI), so as to explore its mechanisms underlying improvement of ACI. METHODS: One hundred female SD rats were randomly divided into 5 groups: normal control (normal), sham-operation (sham), model, non-acupoint and acupoint, with 20 rats in each. The ACI model was established by occlusion (electric coagulation) of the middle cerebral artery after craniotomy. "Baihui" (GV 20) and "Shuigou" (GV 26) or non-acupoints were punctured with filiform needles which were retained for 30 min after rotating for 1 min. The treatment was conducted once after modeling and 24 h thereafter. The cerebral infarct volume was measured after 2,3,5-triphenyltetrazolium chloride (TTC) staining. The contents of interleukin-1 β (IL-1 β), IL-6 and IL-8 in the serum and ischemic brain tissue were detected by radioimmunoassay, and the expression of protein SIRT 1 and NF-κB p 65 in the ischemic brain tissue was detected by immunoblotting. RESULTS: The brain infarction volume was obvious in the model group in comparison with the normal group (P0.05). CONCLUSION: Acupuncture intervention at acupoints can reduce the ischemic infarction volume in ACI rats, which may be associated with its effects in down-regulating the levels of IL-1 β, IL-6 and IL-8 in the serum and ischemic brain tissue, and in regulating cerebral SIRT 1/NF-κB signaling.
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Objective To investigate effects of mouse nerve growth factor on serum brain-derived neurotrophic factor, Fibulin-5 and intracranial blood flow in patients with acute cerebral infarction.Methods 98 patients with acute cerebral infarction in our hospital from September 2015 to September 2016 were selected as the research object, divided into observation group and control group, 49 cases in each group.The control group was treated with conventional treatment of acute cerebral infarction, patients in the observation group on the basis of conventional treatment combined with mouse nerve growth factor, Enzyme-linked immunosorbent assay was used to detect serum brain-derived neurotrophic factor, Fibulin-5, Intracranial ultrasonography was used to detect intracranial blood flow, the brain-derived neurotrophic factor, Fibulin-5, cerebral blood flow were compared between the two groups before and after treatment.Results Before treatment, two groups of patients with brain-derived neurotrophic factor (BDNF), Fibulin-5 and hemodynamics, the difference was not statistically significant.After treatment, the levels of BDNF and Fibulin-5 in the observation group were (5.63 ±1.34), (156.63 ±12.79), significantly higher than the control group (4.26 ±1.54), (115.52 ±15.66), the difference was statistically significant ( P<0.05 ) , the observation group of patients with cerebral hemodynamics index , average blood flow ( Qmean ) , the average blood flow velocity (Vmean), dynamic impedance (DR), cerebral vascular characteristic impedance (ZCV), cerebral vascular peripheral resistance (R) were significantly better than the control group, the difference was statistically significant (P<0.05), the prognosis of the observation group was better than that of the control group, the difference was statistically significant ( P<0.05 ) .Conclusion Clinical effect of mouse nerve growth factor on acute cerebral infarction is helpful to promote the growth of nerve function inhibition, improve cerebral blood flow, better prognosis.
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Objective To study the effect of low-dose dexamethasone after acute and subacute cerebral infarct.Methods One hundred and forty patients with acute ischemic stroke were randomly divided into acute ischemic stroke group (acute stage group),subacute ischemic stroke group (subacute stage group),placebo and control groups.Subjects in acute stage groups received conventional therapy and 1 mL (5 mg) dexamethasone injection from 1 day to 3 day after admission and in subacute stage group,received the same treatment as acute stage group from 4 day to 6 day after admission.In control and placebo groups,subjects received conventional therapy and conventional therapy + 1 mL normal saline for injection respectively.One week after treatments,complete blood count and erythrocyte sedimentation rate were tested.One month and three month after treatments,neurological function were evaluated by Barthel Index and modified Rankin Scale (mRS).Results The valuate of erythrocyte sedimentation rate in acute stage group were significantly different from it of placebo and control groups (P ＜ 0.05).Moreover,neurological function of subjects in acute stage group was significantly improved than that in placebo and control groups in by Barthel Index and mRS (P ＜ 0.05).However that in subacute stage group was not different from that placebo and control groups (P ＞ 0.05).Conclusion Low-dose dexamethasone plays a neuroprotection role after acutc cerebral ischemia.
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<p><b>OBJECTIVE</b>To explore the effect of electroacupuncture(EA) preconditioning on cerebral infarct volume and the contents of TNF-α, IL-10 in serum of rats with cerebral ischemia-reperfusion injury.</p><p><b>METHODS</b>Thirty-six rats were randomly divided into a sham operation group, a model group and an EA preconditioning group, 12 rats in each group, which were further divided into 12 h and 24 h after reperfusion subgroups, 6 rats in each one. EA was used before model establishment for 2 weeks in the EA preconditioning group. The model of cerebral ischemia-reperfusion injury in rats was established with modified Longa suture method. 12 h and 24 h after reperfusion, the degree of neurological deficit was assessed by the modified behavioral scoring scale; the cerebral infarct volume was measured by TTC method and the contents of TNF-α, IL-10 in serum were detected by ELISA method.</p><p><b>RESULTS</b>Compared with the model group, the neurological severity scores in the EA preconditioning group significantly reduced 12 h and 24 h after reperfusion (both<0.05), the cerebral infarct volume in the EA preconditioning group significantly reduced 12 h and 24 h after reperfusion (both<0.05). Compared with the sham operation group, the serum TNF-α, IL-10 contents in the model group increased 12 h and 24 h after reperfusion (both<0.05). Compared with the model group, the serum TNF-α content reduced, while the serum IL-10 content increased in the EA preconditioning group 12 h after reperfusion (both<0.05). Compared with the model group, the serum TNF-α, IL-10 contents reduced in the EA preconditioning group 24 h after reperfusion (both<0.05).</p><p><b>CONCLUSION</b>EA preconditioning can improve neurological deficit, reduce cerebral infarct volume after cerebral ischemia-reperfusion injury in rats. The mechanism may be related to the regulation of EA on the dynamic balance between pro-inflammatory cytokine TNF-α and anti-inflammatory cytokine IL-10 in peripheral blood of cerebral ischemia-reperfusion injury in acute phase, thus alleviate acute cerebral ischemia-reperfusion inflammatory response.</p>
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Objective To research the recent prognosis of vertebral artery dominance in patients with posterior circula-tion transient ischemic attack. Methods All 120 patients were diagnosed with posterior circulation transient ischemic attack from January 2012 to October 2013 hospitalization, collected the vertebral artery MRA, clinical data ABCD2 score, the incidence of cerebral infarction within 7 days with the patients, and compared the differences. Results The share of vertebral artery dominance was higher than non-vertebral artery dominance in the posterior circulation TIA. According to ABCD2 score stratification, the incidence of cerebral infarction was rising from low-risk group to the risk group to the high-risk group. 7 days after TIA, the incidence of cerebral infarction in group with the vertebral artery dominant compared with the non-vertebral artery dominance had significant difference (P<0.05). If ABCD2 score<4 points, there was no significant difference in incidence of cerebral infarction between the group with vertebral artery dominant and non-vertebral artery dominance (P>0.05). If ABCD2≥ four points, the result was opposite (P<0.05). Conclusion The vertebral artery dominance is one of the risk factors for cerebral infarction to the patient with posterior circulation TIA. ABCD2 score in the high-risk patients'risk of vertebral artery advantage is particularly evident.
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Although atrial fibrillation is the most frequent cause of embolic stroke, coronary embolism from atrial fibrillation is a very rare cause of acute myocardial infarction. Therefore, simultaneously presented acute ischemic stroke and acute myocardial infarction due to atrial fibrillation in the same patient has not been documented. The present report describes the case of a 58-year-old man with paroxysmal atrial fibrillation who initially presented with a large cerebral infarction due to embolic occlusion of the left middle cerebral artery. Four hours after the diagnosis of cerebral embolism, he was subsequently diagnosed with acute myocardial infarction due to concurrent coronary embolism. He underwent successful coronary revascularization with a drug-eluting stent. The possibility of combined coronary embolism as a rare etiology should be kept in mind when a patient with acute embolic stroke presents, especially when there is evidence of acute myocardial infarction.
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Humans , Middle Aged , Angioplasty, Balloon, Coronary , Atrial Fibrillation , Cerebral Infarction , Diagnosis , Drug-Eluting Stents , Embolism , Intracranial Embolism , Middle Cerebral Artery , Myocardial Infarction , StrokeABSTRACT
Although atrial fibrillation is the most frequent cause of embolic stroke, coronary embolism from atrial fibrillation is a very rare cause of acute myocardial infarction. Therefore, simultaneously presented acute ischemic stroke and acute myocardial infarction due to atrial fibrillation in the same patient has not been documented. The present report describes the case of a 58-year-old man with paroxysmal atrial fibrillation who initially presented with a large cerebral infarction due to embolic occlusion of the left middle cerebral artery. Four hours after the diagnosis of cerebral embolism, he was subsequently diagnosed with acute myocardial infarction due to concurrent coronary embolism. He underwent successful coronary revascularization with a drug-eluting stent. The possibility of combined coronary embolism as a rare etiology should be kept in mind when a patient with acute embolic stroke presents, especially when there is evidence of acute myocardial infarction.
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Humans , Middle Aged , Angioplasty, Balloon, Coronary , Atrial Fibrillation , Cerebral Infarction , Diagnosis , Drug-Eluting Stents , Embolism , Intracranial Embolism , Middle Cerebral Artery , Myocardial Infarction , StrokeABSTRACT
Objective To investigate the effect of vertebral artery (VA) dominance on basilar artery (BA) curvature and pontine or cerebellar infarct occurring around the vertebrobasilar junction of VA. Methods Radiological data (infarct laterality,VA dominance,BA curvature and their directional relationships) were analyzed in 91 patients with acute unilateral pontine or posterior inferior cerebellar artery (PICA) territory infarcts.Multiple regression analysis was performed to predict the moderate to severe BA curvature. Results The dominant VA frequently happened on the left side.Most patients had an opposite directional relationship between the dominant VA and BA curvature. Pontine infarct frequently happened opposite to the side of BA curvature and PICA infarct on the same side as the non-dominant VA side.The VA diameter was the only independent predictor for moderate to severe BA curvature (OR: 2.70; 95％CI: 1.22-5.98). Conclusion VA dominance is an important predictive factor of BA curvature,and BA curvature is usually opposite to the side of BA curvature; VA dominance and BA curvature caused by VA dominance increase the incidence of vertebrobasilar junctional infarcts.
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Objective To investigate the change of adiponectin (AD),tumor necrosis factor-alpha (TNF-α) and S100 levels in serum elderly patients with rheumatoid arthritis and cerebral infarct in order to evaluate the therapeutic effect of dioscornin.Methods One hundred patients with rheumatoid arthritis and cerebral infarct were selected as our subjects,who were hospitalized in the Department of Neurology of Recovery Changzhi Municipal People's Hospital and the Department of Internal Medicine of the Affiliated Hospital of Shaoxing Medical College,between 2006 September and 2010 September.All subjects (male 55,female 45,average age of 57 years old) were randomly divided into regular and dioscomin groups,50 for per group.Patients in regular group were treated with routine therapy and patients in dioscornin groups were treated with dioscornin 80mg,three daily plus regular treatment drug.Meanwhile 40 middle patients with single rheumatoid arthritis subjects were severed as controls.The changes of BMI,fasting plasma glucose,lipid factors,insulin sensitivity index (ISI),serum adiponectin,TNF-α and serum S100B were determined at treatment before and 6 months after treatments.Results The level of TNF-α,serum S100 in ERA patients were significantly higher andAdiponectin significantly lower than that of the control group,(TNF-α:[(89.0 ± 25.3) ng/L,(88.0 ± 24.2)ng/L vs(74.0 ±21.0) ng/L,F =3.292,P ＜0.05],[S100B:(0.102 ±0.051) μg/L,(0.101 ±0.045) μg/L vs(0.092 ± 0.031) μg/L,F =2.792,P ＜ 0.05],and AD and BMI were lower [AD:(7.2 ± 1.4) μg/L,(7.3 ±1.4) μg/L vs (18.1 ± 3.5) μg/L,F =17.057,P ＜ 0.01],[BMI:(18.9 ± 2.4) kg/m2,(19.0 ± 1.9) kg/m2 vs (21.8 ± 1.8) kg/m2,F =6.147,P ＜ 0.01].There was a negative correlation between adiponect and TNF-α,S100B (r =-0.46,-0.52,P ＜ 0.01) and positive correlation between adiponect and BMI (r =0.44,P ＜0.01).The adiponectin level was significantly increased in patients for six months after dioscornin treatment than that of control group.[AD:(12.2±2.9) μg/L,(7.8 ±1.8) μg/L vs (18.0 ±4.3) μg/L,F=6.480,P＜0.01].The level of TNF-α and S100B significantly decreased than that of the control group,TNF-α:[(72.0 ±21.0) ng/L,(82.0±23.0)ng/L vs (68.0 ±20.0) ng/L,F =3.065,P ＜0.05],[S100B:(0.092 ±0.021)μg/L,(0.099 ±0.031) μg/L vs (0.091 ±0.029) μg/L,F=3.030,P＜0.05].Conclusion Dioscornin could ameliorate the prognosis through decreasing the levels of TNF-α and S100B,and increasing adiponectin level in patients with rheumatoid arthritis and cerebral infarct.
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The article reviewed the research progress of ligustilide in recent years and elaborated its pharmacological functions and mechanisms in detail,especially in ischemic brain injury.Its mechanism includes reducing cerebral infarct volumes and improving neurobehavioral deficits,anti-oxidant and anti-apoptosis,antithrombotic activity,calcium channel blockers function,and effect on erythropoietin.Other pharmacological effects of ligustilide including inhibiting vascular smooth muscle cell proliferation,anti-inflammatory and analgesic effects,effects on LPS-induced endotoxic shock,inhibiting constriction effect,suppression of the central nervous system,and ameliorating the memory impairment induced by scopolamine and so on,are also introduced.Ligustilide has potential pharmacological value,which provides a reference for its further research and development.