ABSTRACT
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.
ABSTRACT
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.
Subject(s)
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
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.
ABSTRACT
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.
ABSTRACT
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.
ABSTRACT
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.
Subject(s)
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.
ABSTRACT
<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>
ABSTRACT
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.
ABSTRACT
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.
ABSTRACT
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.
Subject(s)
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.
Subject(s)
Humans , Middle Aged , Angioplasty, Balloon, Coronary , Atrial Fibrillation , Cerebral Infarction , Diagnosis , Drug-Eluting Stents , Embolism , Intracranial Embolism , Middle Cerebral Artery , Myocardial Infarction , StrokeABSTRACT
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.
ABSTRACT
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.
ABSTRACT
Objective To investigate the safety and efficacy of intravenous thrombolytic therapy with recombinant tissue plasminogen activator(rtPA)in patients with isolated penetrating artery territory infarct (IPAI).Methods Data of retrospectively collected clinical,laboratory,and radiological from 75 consecutive patients with acute ischemic stroke treated with intravenous rtPA therapy from June 2009 to April 2011.Etiological classification was carried out according to the Chinese Ischemic Stroke Classification of Subgroups(CISS).The rates of hemorrhagic transformation(HT)and clinical outcomes of patients were compared between IPAI group and non-IPAI group.Results All 75 patients with mean age of 67.4years and 25(33.3％)fenale,were treated with intravenous rtPA.Before treatment,their average score of the National Institutes of Health Stroke Scale(NIHSS)was 12.3 ± 6.4,and mean length of time from onset to treatment was 239.6 ±97.5 minutes.After thrombolytic therapy,the radiological HT was found in 24 patients(32％).Symptomatic intracraneal hemorrhage(ICH)occurred in 4 patients(5.3％).Of 22 (29.3％)patients with IPAI,only one experienced HT.Logistic regression analysis suggested that IPAI wasan individualized predictor used alone for determining the low risk of HT.In the patients with IPAI,82％ of them had an individual clinical outcome(mRS ＜ 2)one month after onset,and the neurological outcomes were better in patients with IPAI than those in patients with non-IPAI(P ＜ 0.01).Conclusions The risk of hemorrhagic complication was low and the clinical outcome was good in patients with isolated penetrating artery territory infarct after intravenous thrombolytic therapy with rtPA.Imaging diagnosis of IPAI might facilitate the treatment with rtPA in this cohort of patients.
ABSTRACT
Pneumococcal meningitis does continue to be an important cause of mortality and morbidity in childhood despite widespread vaccination. It develops thorough invasion of the meninges by the agent via bloodstream. It may manifest typical signs of meningeal irritation and even the symptoms not belonging to the central nervous system, such as diarrhea. The diagnosis is made by microscopic evaluation and culture of cerebrospinal fluid (CSF) obtained by lumbar puncture. Despite the treatment, the risk of occurrence of cerebral and neurologic complications is high. A two-month old baby girl was presented to our outpatients’ clinic because of fever and diarrhea; she was diagnosed with pneumococcal meningitis and developed cerebral infarct during surveillance. The reason why we presented this patient is to highlight that meningitis due to pneumococ, one of the most common causing agents in childhood meningitis, may have clinical presentations other than expected.
ABSTRACT
Objective To investigate the secondary degeneration of corticospinal tracts in cervical spinal cord following a recently cerebral infarct with diffusion tensor imaging(DTI) and its potential impact on neurological recovery.Methods Twenty-six patients with a focal cerebral infract underwent DTI at the first week, the fourth and twelfth week after stroke onset, respectively.The NIH Stroke Scale (NIHSS), the Fugl-Meyer motor scale (FM) and the barthel index (BI) were used to evaluate the neurological function before every DTI.Twenty-six gender and age match healthy volunteers underwent DTI three times at same time points.The DTI parameters of mean diffusivity (MD) and fractional anisotropy (FA value) were measured at the cervical spinal cord and initial lesion.Results Compared to the controls, the FA values of the contralateral side corticospinal tracts in the cervical spinal cord in patients significantly decreased at every observed time point (P<0.01).In patients group, the FA values of the contralateral side corticospinal tracts in the cervical spinal cord decreased progressively from 1~(st) week to 12~(th) week (P<0.01), but MD remained unchange.The absolute value of the percent reduction of FA value of the contralateral side corticospinal tracts in the cervical spinal cord in patients associated negatively with the absolute value of the percent change of NIHSS and FM (P<0.05), but not with the absolute value of the percent change of BI(P>0.05).Conclusions Conclusions: The secondary degeneration of the corticospinal tracts resulted from cerebral infarction may extend to the cervical spinal cord.Which may last at lest three months and thus hamper the process of neurological recovery.
ABSTRACT
Objective To study the effect of transcranial magnetic stimulation (TMS) on the rehabilitation of rats with cerebral infarction. Methods One hundred Sprague-Dawley rats were randomly divided into a normal group, a sham-operated control group, a model group and a TMS group with 25 rats in each group. A cerebral infarction model was established in the latter two groups by left middle cerebral artery occlusion (MCAO). TMS was started at either 12 or 24 hours after reperfusion, and sham-TMS was given to the first two groups at the same time points. The expression of Bcl-2 mRNA and BDNF mRNA were measured by RT-PCR after 14 days. Results Bcl-2 mRNA and BDNF mRNA were detected in all groups. The expression of Bcl-2 mRNA in the TMS-12 h group, and that of BDNF mRNA in the TMS-24 h group were significantly higher than in the other groups. Conclusions The expression of Bcl-2 mRNA and BDNF mRNA in the brains of rats after cerebral infarction peak when TMS is administered 12 h and 24 h after reperfusion, respectively. TMS might have protective and rehabilitative effects on rats after cere-bral infarct.
ABSTRACT
Objective To evaluate the effect of hyperbaric oxygen (HBO) therapy on pathological and ul-trastructure changes in cortical neurons after model focal cerebral isehemia. Methods Middle cerebral artery occlu-sion (MCAO) using the Zea-Longa method was administered to 48 Sprague-Dawley rats, who were subjected to cere-bral ischemia for 2 hours followed by reperfusion. They were then randomly divided into a treatment group and a con-trol group. HBO was applied to the rats in the treatment group, and any changes in the pathology and uhrastructure of neurons in the cortex were observed at preset time points. Results The infarct volume was significantly smaller inthe treatment group than in the control group, and pathological changes in brain tissue were also milder. Conclu-sions HBO could help protect cortical neurons in acute cerebral ischemia.
ABSTRACT
Spasticity is a determining for functional loss following ischemic stroke. OBJECTIVE: To detect possible predictive factors for its occurrence. METHOD: Demographic, clinical and tomographic data on 146 stroke patients were analyzed. RESULTS: Spasticity was noted more frequently among patients who underwent physiotherapy (p<0.0001; OR=19.4; 95 percent CI: 4.4-84.5), those who underwent such treatment for long periods (p=0.028; OR=4.80; 95 percent CI: 1.1-8.3) and those with manual work (p=0.041; OR=2.2; 95 percent CI: 1.02-4.6), lower income (p=0.038), pain complaints (p<0.0001; OR=107.0; 95 percent CI: 13.5-847.3), appearance of pain at the same time as spasticity (p<0.0001), previous vascular disease (p=0.001; OR=4.2; 95 percent CI: 1.7-10.3), muscle weakness (p<0.0001; OR=91.9; 95 percent CI: 12.0-699.4), extensive lesions as seen on tomography (p=0.01) and lesions affecting more than one cerebral lobe (p=0.018). Manual work had a relative risk of 2.9; previous stroke 3.9, and extensive lesion 3.6. CONCLUSION: Spasticity affected 25 percent of the patients, and was associated with: manual work, previous stroke, extensive lesions, decrease in individual income, underwent physiotherapy, underwent physiotherapy for longer period, pain complaints, the pain started simultaneously with the spasticity, presented changes in strength.
A espasticidade é fator determinante para perda funcional após o acidente vascular cerebral isquêmico (AVCI). OBJETIVO: Detectar possíveis fatores preditivos para a ocorrência da espasticidade. MÉTODO: Foram analisados dados demográficos, clínicos e tomográficos de 146 pacientes pós-AVCI. RESULTADOS: Na análise univariada a espasticidade foi notada com maior freqüência em pacientes que realizaram fisioterapia (p<0,0001; OR=19,4; 95 por cento CI: 4,4-84,5), com maior tempo de duração desse tratamento (p=0,028; OR=4,80; 95 por cento CI: 1,1-8,3) e que realizavam trabalho braçal (p=0,041; OR=2,2; 95 por cento CI: 1,02-4,6), renda menor (p=0,038), referência de dor (p<0,0001; OR=107,0; 95 por cento CI: 13,5-847,3) e seu aparecimento simultâneo à espasticidade (p<0,0001), acidente vascular cerebral (AVC) pregresso (p=0,001; OR=4,2; 95 por cento CI: 1,7-10,3), fraqueza muscular (p<0,0001; OR=91,9; 95 por cento CI: 12,0-699,4), lesão tomográfica extensa (p=0,01) e lesão afetando mais de um lobo cerebral (p=0,018). Na análise de regressão multivariada a atividade braçal apresentou risco relativo de 2,9; acidente vascular cerebral prévio com risco relativo de 3,9 e lesão tomográfica extensa risco relativo de 3,6. CONCLUSÃO: A espasticidade afetou um quarto da população estudada e esteve associada ao trabalho braçal, AVC pregresso, lesões tomográficas extensas, diminuição da renda individual, realização de fisioterapia, realização de fisioterapia por um período maior, presença de dor, surgimento da dor simultânea à espasticidade e alteração da força.