Short term correlates of the Neuro Emotional Technique for cancer-related traumatic stress symptoms: A pilot case series

Introduction As many as one quarter of all cancer survivors report traumatic stress symptoms from cancer-related experiences. While the majority of these patients do not meet the criteria for posttraumatic stress disorder (PTSD), there is growing evidence that subsyndromal symptoms can significantly contribute to functional impairment and negative health outcomes. Treatment options for the hallmark symptoms of traumatic stress—unpleasant, intrusive thoughts and avoidant behaviors—have not been well investigated for the cancer survivorship population. Materials and methods Seven female cancer survivors with traumatic stress symptoms from cancer-related experiences and no other major psychopathology, were enrolled to receive three sessions of Neuro-Emotional Technique (NET), a brief, targeted treatment that combines traditional desensitization principles with complementary modalities. Results Psychological outcome measures (Impact of Event Scale (IES) and Subjective Units of Distress (SUD) and physiological measures (Heart Rate (HR) and Skin Conductance Level (SCL) demonstrated the following changes: 71% on IES, 88% SUD, 74% on HR, and 65% on SCL following the intervention. Statistically significant changes were observed for all four parameters, and effect size g for proportion improved were 0.50 each for IES, SUD, and HR, and 0.20 for SCL. Conclusions These cases suggest feasibility of the NET intervention for cancer-related traumatic stress and the potential for change in symptoms and physiological reactivity. Further investigation is needed to determine the specific and long-term effects of such an approach. Implications for cancer survivors Traumatic stress from cancer-related experiences might represent a constellation of symptoms that are amenable to brief, targeted interventions. This study was supported by the O.N.E. Research Foundation     

Sources of P300 attenuation after head injury: Single-trial amplitude, latency jitter, and EEG power

Single trial amplitude, latency jitter, and electroencephalographic (EEG) power were examined as sources of the group difference in averaged P300 amplitude among 15 traumatically brain injured and 20 control individuals in an auditory oddball paradigm. Mean amplitude of the individual trials was highly correlated with the amplitude of the averaged P300, with little additional unique variance attributable to latency jitter or EEG power. The group difference in P300 amplitude was also explained by the mean amplitude of the single trials. These results support the robustness of the event-related potential averaging technique within the paradigm used.     

颈脊髓压迫模型的建立及意义

目的 :旨在探索、建立颈脊髓压迫损伤的动物模型 ,并观察、研究其病理学改变过程 ,为临床治疗颈脊髓损伤提供理论依据。　方法 :通过在犬C4 、C5椎间孔置入不锈钢螺钉压迫脊髓 ,成功建立起一种新型不完全性颈脊髓压迫损伤的动物模型 ,并通过光镜和电镜研究创伤后不同时间脊髓的病理改变。　结果 :损伤后动物表现为不完全性瘫痪 ,随时间的推移运动功能逐渐恢复。病理改变结果可分三期 :早期脊髓内出血、水肿及神经元和神经纤维变性 ;中期神经元和神经纤维变性达到高峰 ,胶质细胞增生 ;晚期出现机化和修复 ,部分神经元和神经纤维恢复正常形态。　结论 :颈脊髓不完全性压迫损伤后脊髓功能有恢复的可能 ,临床应进行早期治疗。     

Vertebroplasty and Kyphoplasty in Spinal Trauma

Abstract Kyphoplasty and vertebroplasty have become recognized procedures for the treatment of vertebral fractures, especially in patients with osteoporosis. In most cases of osteoporotic spinal vertebral fracture in elderly patients, polymethylmethacrylate (PMMA) cement is used to fill the defect and stabilize the vertebral body. The techniques of vertebroplasty and kyphoplasty differ in the possibility of realignment and reconstruction of the vertebral body and spinal column. Long-term results in terms of integration of the cement and bioreactivity of the vertebral body are still lacking; so, these procedures are still no options in the treatment of younger patients. Vertebroplasty and kyphoplasty show different success in the management of fresh traumatic spine fractures. The acute traumatic vertebral fracture has to be classified sensitively, to find the right indication for cement augmentation. Mild acute compression fractures can be treated by vertebroplasty or kyphoplasty, severe compression and burst fractures by combination of internal fixation and kyphoplasty. The indications for use of biological or osteoinductive cement in spinal fracture management must still be regarded as restricted owing to the lack of basic biomechanical research data. Such cement should not be used except in clinical studies.     

利多卡因治疗外伤性蛛网膜下腔出血疗效分析

目的探讨早期静脉注射利多卡因对外伤性蛛网膜下腔出血（tsAH）继发性脑损伤的治疗作用。方法重度颅脑损伤后SAH患者60例（GCS评分≤8分）。随机分为治疗组（早期静脉注射利多卡因组）和对照组。在治疗前后对患者均进行GCS评分、颅内压（ICP）测定以及头部CT、发射计算机体层摄影（ECT）、经颅多普勒（TCD）检查。结果利多卡因治疗7d后即出现颅内压降低、挫伤脑组织血流供应改善、脑水肿减轻，与对照组比较，有明显差异（P〈0．01）；GCS评分在利多卡因治疗7d、14d后较对照组明显增加（P〈0．01）。结论早期静脉注射利多卡因能明显减轻颅脑损伤后SAH继发性脑组织损伤的程度，有利于神经功能的早期恢复。     

额叶外伤后早期数字工作记忆的fMRI研究

目的:利用功能磁共振成像技术研究额叶外伤后,执行工作记忆任务时脑结构损伤与脑激活功能区的改变。材料和方法:对10例额叶外伤后早期患者(伤后平均31d,其中男性7例,女性3例;平均年龄30.1年)和12例正常志愿者作为对照组(男性7例,女性5例;平均年龄26.9年)分别进行2位和4位数字的正反序工作记忆的实验,使用single-trial设计方法;GE3.0T磁共振机扫描、采集图像,运用AFNI软件包进行数据分析。结果:①正常对照组反序4位数字任务大于正序4位数字脑区有辅助运动区SMA,双侧背外侧前额叶,左侧顶叶,右侧角回;②患者组反序4位数字任务大于正序4位数字的脑区有左侧枕叶;③正常对照组反序4位数字任务大于患者组的部位有左侧DLPFC,左侧角回;正序4位数字大于患者组的部位有左侧枕叶,右侧角回;④患者组反序4位数字任务时大于对照组的部位有楔状回,右侧Broca区;正序4位数字大于对照组的部位有右侧初级运动区MA,右侧额极区。结论:前额叶在脑工作记忆网络中处于重要节点,大脑右侧半球在工作记忆系统中起到巨大代偿作用的脑资源,fMRI提供认知功能损伤的影像学依据,应在临床上发挥更大作用。     

MMP-3在咬合创伤牙周组织中的表达

目的:探讨基质金属蛋白酶-3(MMP-3)在咬合创伤牙周组织的表达和意义。方法:通过在Wistar大鼠左侧上颌第一磨牙粘结高出咬合面的牙本质固位钉建立咬合创伤动物模型,应用免疫组织化学方法观察咬合创伤后24h、3、7、15和30d MMP-3在牙周组织的表达。结果:咬合创伤后,随着病变程度不断加重,MMP-3在牙周组织的表达逐渐增强,咬合创伤15d时MMP-3的表达达到最强,咬合创伤1个月时,MMP-3的表达有所下降。结论:MMP-3可能在咬合创伤牙周组织的破坏过程中起重要作用。     

颅脑外伤与脑心综合征

急性颅脑外伤后易出现心脏并发症，包括心电图异常、心肌收缩功能减退、心肌酶谱升高以及心肌病理组织学改变等一系列心脏改变，又称脑心综合征。作者就其主要表现、发病机制及临床意义作一综述，以期提高临床对颅脑外伤后脑心综合征的认识。     

Thrombocytopenia after therapeutic hypothermia in severe traumatic brain injury

Objective: To investigate the clinical characteristics and significance of thrombocytopenia after therapeutic hypothermia in severe traumatic brain injury (TBI). Methods:Ninety-six inpatients with severe brain injury were randomized into three groups: SBC (selective brain cooling) group (n=24), MSH (mild systemic hypothermia ) group (n=30), and control (normothermia) group (n=42). The platelet counts and prognosis were retrospectively analyzed. Results: Thrombocytopenia was present in 18 (75%), 23 (77%) and 15 (36%) patients in SBC group, MSH group and control group, respectively (P<0. 01). Thrombocytopenia, in which the minimum platelet count was seen 3 days after hypothermia, showed no significant difference between SBC and MSH group (P>0.05). Most platelet counts (37 cases, 90 %) in hypothermia group were returned to normal level after 1 to 2 days of natural rewarming. The platelet count in SBC group reduced by 16%, 27% and 29% at day 1, 3 and 5 respectively compared with the baseline value. Good recovery ( GOS score 4-5) rate of thrombocytopenia 1 year after injury for hypothermia group (17 cases, 37%) was significantly lower than that of control group (P < 0.01). Conclusions: Therapeutic hypothermia increases the incidence of thrombocytopenia in severe TBI, and patients with thrombocytopenia after therapeutic hypothermia are associated with unfavorable neurological prognosis.     

Post-traumatic brain hypothermia reduces histopathological damage following concussive brain injury in the rat

The purposes of this study were (1) to document the histopathological consequences of moderate traumatic brain injury (TBI) in anesthetized Sprague-Dawley rats, and (2) to determine whether posttraumatic brain hypothermia (30°C) would protect histopathologically. Twenty-four hours prior to TBI, the fluid percussion interface was positioned over the right cerebral cortex. On the 2nd day, fasted rats were anesthetized with 70% nitrous oxide, 1% halothane, and 30% oxygen. Under controlled physiological conditions and normothermic brain temperature (37.5°C), rats were injured with a fluid percussion pulse ranging from 1.7 to 2.2 atmospheres. In one group, brain temperature was maintained at normothermic levels for 3 h after injury. In a second group, brain temperature was reduced to 30°C at 5 min post-trauma and maintained for 3 h. Three days after TBI, brains were perfusion-fixed for routine histopathological analysis. In the normothermic group, damage at the site of impact was seen in only one of nine rats. In contrast, all normothermic animals displayed necrotic neurons within ipsilateral cortical regions lateral and remote from the impact site. Intracerebral hemorrhagic contusions were present in all rats at the gray-white interface underlying the injured cortical areas. Selective neuronal necrosis was also present within the CA3 and CA4 hippocampal subsectors and thalamus. Post-traumatic brain hypothermia significantly reduced the overall sum of necrotic cortical neurons (519±122 vs 952±130, mean ±SE, P=0.03, Kruskal-Wallis test) as well as contusion volume (0.50±0.14 vs 2.14±0.71 mm³, P=0.004). These data document a consistent pattern of histopathological vulnerability following normothermic TBI and demonstrate hypothermic protection in the post-traumatic setting.Supported by USPHS Grants NS30291 and NS27127