Xenon provides short-term neuroprotection in neonatal rats when administered after hypoxia-ischemia. (73/274)

BACKGROUND AND PURPOSE: Brain injury after hypoxic-ischemic insults evolves via an apoptotic/necrotic cascade. Glutamate over release and N-methyl-d-aspartate (NMDA) receptor over activation (excitotoxicity) are believed to trigger this process. Xenon is a nontoxic anesthetic gas that reduces neurotransmitter release and functionally antagonizes NMDA receptors. Administering xenon to hypoxic-ischemic newborns might be clinically effective if the neurotoxic processes continue evolving after delivery. We sought to determine whether xenon administration after the initial hypoxic-ischemic insult was neuroprotective. METHODS: Fifty 7-day-old rats received a 90-minute hypoxic insult after unilateral carotid ligation. They were then randomized to breathe 1 of 2 gas mixtures for 3 hours: 50% Xe/30% O2/20% N2 or 30% O2/70% N2. RESULTS: One week after hypoxic-ischemic survival, significant global protection was seen in the xenon group (80% less injury); cortex/white matter (88% versus 25%), hippocampus (62% versus 0%), basal ganglia (81% versus 25%), and thalamus (50% versus 0%; percentage of global damage score in nonxenon versus xenon groups, respectively). CONCLUSIONS: Three hours of xenon administration commenced after hypoxia-ischemia in neonatal rats provides short-term neuroprotection. This finding suggests that treatment with xenon after perinatal asphyxia would also be neuroprotective. Because xenon does not cause other neurotoxic effects and has demonstrated minimal side effects in extensive anesthesia studies, it would make an ideal candidate for the treatment after human perinatal hypoxia-ischemia.  (+info)

Brief update on animal models of hypoxic-ischemic encephalopathy and neonatal stroke. (74/274)

The discovery of safe and effective therapies for perinatal hypoxia ischemia (HI) and stroke remains an unmet goal of neonatal-perinatal medicine. Because of the many developmental and functional differences between the neonatal brain and the adult brain, the ability to extrapolate adult data to the neonatal condition is very limited. For this reason, it is incumbent on scientists in the field of neonatal brain injury to address the questions of therapeutic efficacy of an array of potential therapies in a developmentally appropriate model. Toward that end, a number of new models of neonatal HI and stroke have been introduced recently. Additionally, some of the established models have been adapted to different species and different ages, giving scientists a greater choice of models for the study of neonatal HI and stroke. Many of these models are now also being used for functional and behavioral testing, an absolute necessity for preclinical therapeutic trials. This review focuses primarily on the newly developed models, recent adaptations to established models, and the studies of functional outcome that have been published since 2000.  (+info)

Relationship between evolving epileptiform activity and delayed loss of mitochondrial activity after asphyxia measured by near-infrared spectroscopy in preterm fetal sheep. (75/274)

Early onset cerebral hypoperfusion after birth is highly correlated with neurological injury in premature infants, but the relationship with the evolution of injury remains unclear. We studied changes in cerebral oxygenation, and cytochrome oxidase (CytOx) using near-infrared spectroscopy in preterm fetal sheep (103-104 days of gestation, term is 147 days) during recovery from a profound asphyxial insult (n= 7) that we have shown produces severe subcortical injury, or sham asphyxia (n= 7). From 1 h after asphyxia there was a significant secondary fall in carotid blood flow (P < 0.001), and total cerebral blood volume, as reflected by total haemoglobin (P < 0.005), which only partially recovered after 72 h. Intracerebral oxygenation (difference between oxygenated and deoxygenated haemoglobin concentrations) fell transiently at 3 and 4 h after asphyxia (P < 0.01), followed by a substantial increase to well over sham control levels (P < 0.001). CytOx levels were normal in the first hour after occlusion, was greater than sham control values at 2-3 h (P < 0.05), but then progressively fell, and became significantly suppressed from 10 h onward (P < 0.01). In the early hours after reperfusion the fetal EEG was highly suppressed, with a superimposed mixture of fast and slow epileptiform transients; overt seizures developed from 8 +/- 0.5 h. These data strongly indicate that severe asphyxia leads to delayed, evolving loss of mitochondrial oxidative metabolism, accompanied by late seizures and relative luxury perfusion. In contrast, the combination of relative cerebral deoxygenation with evolving epileptiform transients in the early recovery phase raises the possibility that these early events accelerate or worsen the subsequent mitochondrial failure.  (+info)

The relation between child death and child maltreatment. (76/274)

The death of a child is a sentinel event in a community, and a defining marker of a society's policies of safety and health. Child death as a result of abuse and neglect is a tragic outcome that occurs in all nations of the world. The true incidence of fatal child abuse and neglect is unknown. The most accurate incidence data of such deaths have been obtained from countries where multi-agency death review teams analyse the causes of child fatalities, as is done in the United States and Australia.  (+info)

Accidental asphyxia due to closing of a motor vehicle power window. (77/274)

Injuries and deaths among children left unattended in motor vehicles are frequent and the rates are increasing. Injuries associated with motor vehicle power windows usually affect children, in particular children under 6 years of age. This case report is about a child who was asphyxiated because of a motor vehicle power window closing. She was rapidly resuscitated and recovered fully. A brief review of the literature, epidemiology, and preventive measures to avoid this type of injury is also presented.  (+info)

Suicide in farmers in Scotland. (78/274)

INTRODUCTION: Farmers and farm workers have higher than expected rates of suicide and undetermined deaths in UK studies, and some rural areas of Scotland have higher than average male suicide rates. Firearm access seems to be an influencing factor in England and Wales. Type of farming, and farming social networks may also be important. This article describes suicide and undetermined deaths in male farmers and farm workers in Scotland from 1981-1999 using anonymised, routine data. METHOD: Deaths of men aged 15-74 years from suicide or undetermined cause were identified from anonymised Scottish death records. Farmers and farm workers were identified using occupation codes. Methods of suicide used by farmers were compared with those of the general male population of the same age. A multiple linear regression was used to examine the influence of farm type, and the proportion of farmers in the working population of an area. RESULTS: 307 male farmers or farm workers died by suicide or undetermined cause in the time period. The overall rate was 31.4/100,000 per year (95% CI 28.1-35.1). Deaths using firearms were over-represented (29% of farming deaths compared with 3.6% in the general male population). There was no significant association between the male suicide rate in an area, and the farming suicide rate. Areas with lower proportions of farmers tended to have higher rates of farming suicide and undetermined deaths. This one factor described 85% of the variance among areas. CONCLUSION: Deaths were substantially more likely to involve firearms than suicide and undetermined deaths in the general male population. Less use of other methods did not completely compensate for this, indicating that method availability is likely to contribute to farming suicide rates. Farmers in areas where farming is less common were more likely to die by suicide, and this described most of the differences among areas. Networks and social supports may be important protective factors for farmers.  (+info)

Oro-facial trauma in child abuse fatalities. (79/274)

Many children die as a result of abuse and neglect each year. Early recognition and effective intervention are crucial factors in the fight against this. Child mortality rates increased in South Africa between 1998 and 2004, with child abuse deaths constituting part of these statistics. Autopsies on children who have died of unnatural causes are often not specific as to the possibility of child abuse. This article presents the extra-oral and intra-oral signs of child abuse from a study of the autopsies of child mortality cases seen at Salt River Medico-Legal Laboratory in Cape Town from 1998 to 2004 with reference to the South African child mortality rates.  (+info)

Fatal injuries while under the influence of psychoactive drugs: a cross-sectional exploratory study in England. (80/274)

BACKGROUND: Studies of drug-related mortality rarely describe fatal injuries due to psychoactive drug intoxication (FIUI). The main aim of this study was to determine the nature, extent and pattern of FIUI. METHODS: This observational study covered the period January 1999 to December 2001. Data were provided by members of a study panel of coroners in England using a standard protocol. Sources of data for this study included autopsy protocols, death certificates, hospital records, police reports, toxicology reports and inquest transcripts. Inclusion criteria for this were (i) the mention of one or more psychoactive substances as contributing to fatality; and (ii) the presence of a Controlled Drug at post mortem. RESULTS: A total of 3,803 drug-related deaths of persons aged 16-64 years were reported by the study panel during the three-year period. The study panel accounted for 86% of drug-related deaths in England in this period. There were 147 FIUI cases (119 males, 28 females), giving a proportionate mortality ratio of approximately 4%. The majority of FIUI cases (84%) were aged 16-44 years, with a median age at death of 33 years (Quartile deviation = 7). Fifty-six percent of FIUI occurred in urban areas of England. The population of the study jurisdictions aged 16-64 years contributed 49,545,766 person-years (py) to the study, giving an annual crude rate of 3/1,000,000 person-years (py). Rates for male and females were 4.9 and 1.1/1,000,000 py respectively, giving a male/female rate ratio of 4.5 (95%CI = 2.9-6.8). The rates of intentional and unintentional FIUI were 2 and 1/1,000,000 py respectively. The leading mechanism for intentional FIUI was suffocation while the predominant mechanisms in unintentional FIUI were road traffic accidents and falls. There is a significant difference in the pattern of drug-specific risk between FIUI and fatal poisoning. Risks of intentional FIUI are elevated among Black and Minority Ethnic groups. CONCLUSION: There are differences in the nature, extent and pattern of intentional and unintentional FIUI that should necessitate targeted prevention strategies. Also, there is an opportunity for cross-discipline collaboration between injury prevention specialists and substance abuse/mental health specialists.  (+info)