Intraparenchymal blood-fluid levels in traumatic intracerebral haematomas

Summary Blood-fluid levels within the cerebral parenchyma are observed more frequently on CT and MRI in traumatic intracerebral haematomas than in those of other aetiologies. The intraparenchymal blood-fluid interface can be formed without a fluid cavity. It is suggested that the blood-fluid levels represent layering of red blood cells within areas of contusion necrosis as well as extensive contusion oedema. The more extensive the damage to brain tissue, the more often blood-fluid levels formed. A poorer outcome can be therefore predicted when an intraparenchymal blood-fluid interface is seen.     

血乳酸浓度监测与组织氧合相关性的临床观察

目的　寻找能反映严重烧伤后组织氧合状况的简便易行、微创、有效的生化指标。方法　将收治的 34例大面积烧伤患者随机分为两组 ,A组 18例 ,采用改进后的抗休克复苏方案 ,使患者尿量维持在每小时 10 0ml左右 ;B组 16例 ,采用常规补液公式 ,使患者尿量维持在每小时 4 0ml左右。两组同时于复苏前、复苏后 1、8、16、2 4、4 8、72h监测血乳酸浓度 (BL)及常规监测指标 (尿量、血压、心率、神志 )。　结果　 (1)A组患者复苏后 2 4h内 ,血BL浓度平均为 (3.2± 0 .4 )mmol/L ,常规指标均处于正常范围 ;B组患者常规指标基本正常 ,血BL平均值为 (7.4± 1.6 )mmol/L ,持续时间可达 72h以上。 (2 )在常规监测指标指导下 ,B组复苏治疗效果不佳 ,病死率高 (31.2 % ) ;A组通过监测BL指导治疗 ,病死率仅为 5 .5 %。 (3)BL与尿量呈负相关 ,与心率呈正相关。　结论　 (1)严重烧伤休克时组织的乏氧代谢增强 ,监测血BL ,能基本达到快捷、灵敏、简单、有效、微创的要求 ,是反映全身组织器官氧合状况的良好指标。 (2 )建议烧伤抗休克的复苏时间应延长至 72h ,尿量保持在 10 0ml/h ,确保复苏的质量和效果。     

外伤性视神经病变的临床治疗分析

目的　探讨大剂量甲基强的松龙冲击疗法治疗外伤性视神经病变的疗效。方法　 2 0例 (2 0只眼 )外伤性视神经病变患者为治疗组 ,应用大剂量甲基强的松龙冲击治疗 ,另 2 0例 (2 0只眼 )外伤性视神经病变患者为对照组 ,使用常规剂量的地塞米松治疗。两组均同时使用高渗剂、血管扩张剂、神经营养剂及 B族维生素治疗 ,对两组病例药物治疗的结果进行总结分析。结果　治疗组经治疗后视力开始恢复的时间早于对照组 ,治疗组的总有效率为 80 % ,对照组的总有效率为 6 0 % ,治疗组的疗效优于对照组 ,且治疗越早疗效越好。两组比较具有显著的统计学差异 (P <0 .0 5 )。结论　大剂量甲基强的松龙冲击疗法治疗外伤性视神经病变疗效显著 ,治疗方便 ,是较理想的治疗方法     

Memory outcome at 5 years post-childhood traumatic brain injury

Primary objective: This study seeks to extend previous findings by documenting memory performance in a sample of 70 children at 5 years post-injury. It was anticipated that increasing injury severity would be associated with decreased performance on working and complex memory tasks. It was also expected that injury severity would significantly predict memory, but that the time from insult to subsequent testing would be associated with an increased relationship to non-injury factors.

Research design: Participants were assessed at 5 years post-injury, aged between 6-14 years, using measures of immediate, working and complex memory.

Methods and procedures: The sample comprised 18 children who had sustained a severe TBI, 24 with a moderate TBI, 11 with a mild TBI and 17 healthy controls, matched for age, gender and socio-economic-status.

Results: Results indicated that severe TBI was associated with decreased complex auditory-verbal memory performance, although children with TBI did not display impairment on immediate, working or complex visual-spatial memory. While injury severity significantly predicted complex memory outcome, non-injury factors failed to significantly predict either working or complex memory performance.

Conclusions: Future research should be engineered towards further clarifying what influences recovery from childhood TBI in the elongated post-injury period.     

μ,δ,κ阿片受体在创伤失血性休克大鼠心血管功能抑制中的作用

目的探讨μ，δ和κ阿片受体与创伤失血性休克大鼠心血管功能抑制的关系。方法用大鼠创伤失血性休克模型，观察创伤失血性休克后大鼠心脏和脑μ，δ和κ阿片受体变化及其与血流动力学指标的变化的关系；观察δ和κ阿片受体特异性拮抗剂对创伤失血性休克大鼠血流动力学指标的影响。结果创伤失血性休克后，大鼠心脏和脑δ和κ阿片受体数目明显升高，亲和力无明显变化，心脏和脑的δ和κ阿片受体数目升高与创伤失血性休克后大鼠血流动力学指标下降呈显著负相关。δ和κ阿片受体特异性拮抗剂可明显逆转创伤失血性休克大鼠血流动力学指标的下降。结论δ和κ阿片受体在创伤失血性休克心血管功能抑制中起重要作用，参与了创伤失血性休克的发病过程     

West Nile virus encephalitis with myositis and orchitis

This report documents the hospital course and autopsy findings of a 43-year-old man with a renal allograft who died of West Nile virus (WNV) encephalitis. Central nervous system (CNS) findings were those of severe necrotizing and hemorrhagic encephalitis affecting gray matter regions limited to the diencepahlon, rhombencephalon, spinal cord, and limbic system. The bilateral process exhibited preferential involvement of motor neurons. Brain imaging obtained 6 days before death demonstrated an unusual pattern of involvement corresponding with the autopsy findings, confirming that imaging may be a specific diagnostic guide in WNV encephalitis. Extra-CNS findings include myositis with T-lymphocyte infiltration of nerve fibers, suggesting that the virus may reach the CNS via peripheral nerves. Orchitis with dense T-lymphocyte infiltration and syncytial cell formation thought to be due to WNV were also noted.     

Traumatic Memories: Empirical Foundations, Forensic and Clinical Implications

This article reviews empirical research on memories for negative personal experiences among adults. It examines basic concepts (including neural underpinnings), theoretical models of the affect-memory relationship, and data from three sources: victims or witnesses to crimes and atrocities, "flashbulb memories" for traumatic events, and laboratory simulations of shocking experiences. Evidence suggests that memories for traumatic experiences contain more central than peripheral detail, are reasonably accurate and well-retained for very long periods, but are not completely indelible. Assertions of eyewitness memory's vulnerability to change through suggestion have overstated the evidence. Forensic and clinical implications are discussed and a plea issued for more study of the memory phenomena that characterize posttraumatic stress disorder (PTSD) and are the focus of trauma survivors' treatment.     

Expression of growth associated protein 43 and neural cell adhesion molecule in congenital fibre type disproportion with interstitial myositis

We report on the expression of growth associated protein (GAP)43 and neural cell adhesion molecule (NCAM) in congenital fibre type disproportion (CFTD) with myopathological additional signs of interstitial myositis. We assume that sarcolemmal GAP43 in developmental disordered myocytes plays a role in maintenance of growth morphology. In muscular dystrophy light microscopical evaluation reveals no GAP43 immunoreactivity in regenerating fibres. The expression of GAP43 seems to be a characteristic feature of CFTD. The expression of NCAM, particularly in the sarcolemma of small muscle fibres of CFTD, indicates a functional state of permanent partial denervation. Whether the steroid-responsive interstitial myositis is pathogenetically related to CFTD or a coincidental inflammation is not known. Because of the clinical and myopathological data the differential diagnosis of Emery-Dreifuss muscular dystrophy is considered.     

CD8+T-bet+ cells as a predominant biomarker for inclusion body myositis

Background

Myositis is a heterogeneous group of muscular auto-immune diseases with clinical and pathological criteria that allow the classification of patients into different sub-groups. Inclusion body myositis is the most frequent myositis above fifty years of age. Diagnosing inclusion body myositis requires expertise and is challenging. Little is known concerning the pathogenic mechanisms of this disease in which conventional suppressive-immune therapies are inefficacious.

The prion protein in human neuromuscular diseases

The basis of human prion diseases affecting the nervous system is accumulation of a disease-associated conformer (PrPSc) of the normal cellular prion protein (PrPC). Earlier studies demonstrated increased expression of PrPC in inclusion body myositis (IBM), dermato-, and polymyositis, as well as neurogenic muscle atrophy. To define the spectrum and reliability of PrPC immunoreactivity, its expression was examined systematically in a series of pathologically characterized muscular disorders by means of immunohistochemistry, confocal laser microscopy, and immunogold electron microscopy. Anti-PrPC immunolabelling of rimmed vacuoles was observed in IBM, inclusions of myofibrillary myopathy, targets, regenerating, and atrophic fibres, mononuclear cells, in addition to ragged red fibres in mitochondrial myopathies, and focal sarcolemmal immunostaining in non-diseased controls. Quantitative analysis demonstrated that, in neurogenic muscle lesions, anti-PrPC staining detects a significantly broader spectrum of fibres than anti-vimentin or anti-NCAM. In dystrophic muscle, PrPC expression was mainly restricted to regenerating fibres. In IBM, PrPC expression was not confined to rimmed vacuoles or vacuolated fibres and only a small percentage (7.1%) of rimmed vacuoles were PrPC positive. Ultrastructurally, PrPC was observed in the cytoplasm of lymphocytes, in the myofibrillar network of targets, and in rimmed vacuoles. Knowledge of disease circumstances with altered expression of PrPC is important in the setting of a potentially increased chance for extraneural PrPC-PrPSc conversion. In addition, our observations suggest that PrPC may have a general stress-response effect in various neuromuscular disorders.