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The air at high altitude is thin and belongs to the environment of low temperature, low oxygen and low pressure. The human brain is the most sensitive to hypoxia. Hypoxia will cause dysfunction of the central nervous system, resulting in high-altitude hypoxic brain injury, including mild high altitude headache and more destructive high altitude cerebral edema (HACE). Recently, with more and more people work and live in high altitude areas, the development of high-altitude hypoxic brain injury drugs would produce great economic value and social significance. Non clinical pharmacodynamic evaluation is the basic of drug development, which plays a key role in improving the success rate of clinical transformation and reducing the risk of clinical research. This review summarizes the cell models and animal models, and the evaluation indicators usually used to explore the candidates of high-altitude hypoxic brain injury. We aim at establishing a standardized non clinical efficacy evaluation system for high altitude hypoxic encephalopathy, and provide a standardized reference for drug development in hypoxic encephalopathy at high altitude at nonclinical stage.
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The most frequently reported neurological complication of a wasp sting is ischemic stroke. We treated a patient with wasp sting with unusual complications. A 52-year-old man was hospitalized for anaphylactic shock after multiple wasp stings. Although the patient recovered consciousness after 2 days, he had global aphasia and right hemiparesis. Brain magnetic resonance imaging and angiography revealed high-intensity signals in the left basal ganglia and cerebral cortex and stenosis of the left middle cerebral artery. After 2 days, the middle cerebral artery stenosis improved. After 5 days, diffusion-weighted imaging showed an enlarged lesion in the left frontal cortex. The infarct in this case was due to a predominantly unilateral vasoconstrictive hypoxic brain injury from wasp stings.
Subject(s)
Brain InjuriesABSTRACT
Objective To investigate the effect of coenzyme Q10 combined with Shenmai injection on serum enzyme in the treatment of brain hypoxic injury after asphyxia by meconium in newborn.Methods 64 cases with brain hypoxic injury after asphyxia by meconium from Medical University of Tianjin Jinghai Clinical College were selected and randomly divided into 2 groups, 32 cases in each group.The control group received maintained ventilation and circulation function and routine drug therapy adequate, and the experiment group received more with coenzyme Q10 combined with Shenmai injection for 7 days.Serum enzymes and myocardial injury markers, oxidative stress and inflammation related factors and the clinical effect and complications were compared after the treatment.Results Compared with before treatment, levels of CK-MB, AST, LDH, CK and α-HBDH decreased in two groups after the treatment, levels of CT-1, CTnI and Mb decreased, levels of SOD and MDA decreased, contents of GSH-Px, APN, IGF-1 increased, contents of Leptin decreased (P<0.05).Compared with the control group, the levels of CK-MB, AST, LDH, CK and α-HBDH in the experiment group were lower, levels of CT-1, CTnI and Mb were lower, levels of SOD and MDA were lower, contents of GSH-Px, APN, IGF-1 were higher, contents of Leptin were lower(P<0.05).The clinical curative effect rate of control group(65.63%) was lower than the experiment group (87.50%)(P<0.05).Conclusion Coenzyme Q10 combined with Shenmai injection in the treatment of brain hypoxic injury after asphyxia by meconium in newborn is curative effective with high safety, and it can reduce serum enzyme and myocardial injury.
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BACKGROUND: Early prediction of neurologic outcome is important to patients treated with therapeutic hypothermia after hypoxic brain injury. Hypoxic brain injury patients may have poor neurologic prognosis due to increased intracranial pressure. Increased intracranial pressure can be detected by optic nerve sheath diameter (ONSD) measurement in computed tomography (CT) or ultrasound. In this study, we evaluate the relation between neurologic prognosis and optic nerve sheath diameter measured in brain CT of hypoxic brain injury patients. METHODS: We analyzed the patient clinical data by retrospective chart review. We measured the ONSD in initial brain CT. We also measured and calculated the gray white matter ratio (GWR) in CT scan. We split the patients into two groups based on neurologic outcome, and clinical data, ONSD, and GWR were compared in the two groups. RESULTS: Twenty-four patients were included in this study (age: 52.6 +/- 18.3, 18 males). The mean ONSD of the poor neurologic outcome group was larger than that of the good neurologic outcome group (6.07 mm vs. 5.39 mm, p = 0.003). The GWR of the good neurologic outcome group was larger than that of the poor outcome group (1.09 vs. 1.28, p = 0.000). ONSD was a good predictor of neurologic outcome (area under curve: 0.848), and an ONSD cut off > or = 5.575 mm had a sensitivity of 86.7% and a specificity of 77.8%. CONCLUSIONS: ONSD measured on the initial brain CT scan can predict the neurologic prognosis in cardiac arrest and hanging patients treated with therapeutic hypothermia.
Subject(s)
Humans , Brain Injuries , Brain , Heart Arrest , Hypothermia , Intracranial Pressure , Optic Nerve , Prognosis , Retrospective Studies , Sensitivity and Specificity , Tomography, X-Ray Computed , UltrasonographyABSTRACT
Freezing of gait (FOG), which is the most common symptoms in Parkinson's disease, is a unique gait disorder that patients are unable to initiate or continue locomotion. However, the pathophysiology of FOG has been poorly understood. We report two cases, one case is a 26-year old man and the second case is a 65-year old man, who showed FOG following hypoxic brain injuries caused by sudden cardiac arrest and hypovolemic shock, respectively. Brain F-18 FDG-PET images demonstrated the diffuse cortical hypometabolism in case 1 patient, and the decreased metabolism of the subcortical structures in case 2 patient. Two patients showed the typical features of FOG (turning, destination, and tight quarter hesitations combined with kinesia paradoxa) and the abnormal patterns of temporospatial data in kinematic gait analysis. We present two cases of FOG following hypoxic brain injury with reviewing of some literatures.
Subject(s)
Humans , Brain , Brain Injuries , Death, Sudden, Cardiac , Freezing , Gait , Locomotion , Parkinson Disease , Shock , WeatherABSTRACT
Objective:To explore the mechanism of early onset subclinical seizures following hypoxic brain injury. Methods:SD male adult rats were assigned randomly to control rats and rats exposed to global hypoxia by 8% oxygen nitrogen atmosphere. According to electroencephalogram recording seizure discharge,hypoxie rats were divided into subclinical seizures group and non-subclinical seizures group,then the changes in neuropathology and the expression of GFAP in cortex and hippocampus of rat brain were studied by Nissle-staining immunohisochemistry and western-blot. Results:Subclinical seizures occurred in 19.67% rats following hypoxia. Compared with non-subclinical seizure group,neuronal loss of hippocampal CA1 and CA3 region as wel as temporal cortex were distinct in subclinical seizure group(P
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Although carbamazepine is being widely used in treatment of a variety of psychiatric disorders, it has some serious potential risks, including Stevens-johnson syndrome. Authors experienced in consultation a case of Stevens-johnson syndrome due to usage of carbamazepine. The patient was treated with carbamazepine to control for aggressive behavior after a hypoxic brain damage. Authors report a case of Stevens-johnson syndrome due to carbamazepine and also reviews related articles.