Spinal cord injury (SCI) provokes an inflammatory response that generates substantial secondary damage within the cord but also may contribute to its repair. Anti-inflammatory treatment of human SCI and its timing must be based on knowledge of the types of cells participating in the inflammatory response, the time after injury when they appear and then decrease in number, and the nature of their actions. Using post-mortem spinal cords, we evaluated the time course and distribution of pathological change, infiltrating neutrophils, monocytes/macrophages and lymphocytes, and microglial activation in injured spinal cords from patients who were 'dead at the scene' or who survived for intervals up to 1 year after SCI. SCI caused zones of pathological change, including areas of inflammation and necrosis in the acute cases, and cystic cavities with longer survival (Zone 1), mantles of less severe change, including axonal swellings, inflammation and Wallerian degeneration (Zone 2) and histologically intact areas (Zone 3). Zone 1 areas increased in size with time after injury whereas the overall injury (size of the Zones 1 and 2 combined) remained relatively constant from the time (1-3 days) when damage was first visible. The distribution of inflammatory cells correlated well with the location of Zone 1, and sometimes of Zone 2. Neutrophils, visualized by their expression of human neutrophil alpha-defensins (defensin), entered the spinal cord by haemorrhage or extravasation, were most numerous 1-3 days after SCI, and were detectable for up to 10 days after SCI. Significant numbers of activated CD68-immunoreactive ramified microglia and a few monocytes/macrophages were in injured tissue within 1-3 days of SCI. Activated microglia, a few monocytes/macrophages and numerous phagocytic macrophages were present for weeks to months after SCI. A few CD8(+) lymphocytes were in the injured cords throughout the sampling intervals. Expression by the inflammatory cells of the oxidative enzymes myeloperoxidase (MPO) and nicotinamide adenine dinucleotide phosphate oxidase (gp91(phox)), and of the pro-inflammatory matrix metalloproteinase (MMP)-9, was analysed to determine their potential to cause oxidative and proteolytic damage. Oxidative activity, inferred from MPO and gp91(phox) immunoreactivity, was primarily associated with neutrophils and activated microglia. Phagocytic macrophages had weak or no expression of MPO or gp91(phox). Only neutrophils expressed MMP-9. These data indicate that potentially destructive neutrophils and activated microglia, replete with oxidative and proteolytic enzymes, appear within the first few days of SCI, suggesting that anti-inflammatory 'neuroprotective' strategies should be directed at preventing early neutrophil influx and modifying microglial activation.

At the Wayne County Medical Examiner Office (WCMEO) in Detroit, Michigan, from 2001 to 2004, thorough scene investigations were performed on 209 sudden and unexpected infant deaths, ages 3 days to 12 months. The 209 cases were reviewed to assess the position of the infant at the time of discovery and identify potential risk factors for asphyxia including bed sharing, witnessed overlay, wedging, strangulation, prone position, obstruction of the nose and mouth, coverage of the head by bedding and sleeping on a couch. Overall, one or more potential risk factors were identified in 178 of 209 cases (85.2%). The increasing awareness of infant positions at death has led to a dramatic reduction in the diagnosis of sudden infant death syndrome at the WCMEO. This study suggests that asphyxia plays a greater role in many sudden infant deaths than has been historically attributed to it.

The use of deadly force during law enforcement is a matter that compels public scrutiny. There were 42 gunshot deaths caused by police over a 4-year period in New York City. The decedents' average age was 31 years and ranged from 17 to 64 years. There were 41 males and one female; and 26 Black, nine Hispanic, and seven White decedents. Ethanol and/or drugs of abuse were detected in 78% (31/40) of the decedents. The vast majority of shootings occurred with the police responding to a crime and 90% of the decedents were armed (26 handguns, six knives, one axe, one metal pipe, and one toy gun). Vehicles were used as weapons in two incidents. A total of 177 bullets struck the 42 decedents. Fourteen decedents sustained single gunshot wounds (GSWs), and the remainder had multiple GSWs ranging from 2 to 21. In the majority of the cases in this study, the number of GSWs of the body was three or fewer. Thirteen decedents had at least one GSW of the back or buttocks, accounting for 25 of the total 177 wounds, and four of the 13 had GSWs of only the back. With the exception of the upper extremities, GSWs of all locations were more likely to penetrate than perforate. Although these deaths may be high profile, the certification is typically straightforward and the cause (i.e., GSW) and manner of death (homicide) are readily apparent. Although police shootings in which the decedent was unarmed and/or sustained numerous GSWs are widely reported by the lay press, these types of shootings were not typical in our study.

Bromethalin is a neurotoxin found in some rodenticides. A delusional 21-year-old male presented to a hospital with altered mental status the day after ingesting a bromethalin-based rodenticide. He died 7 days after his self-reported exposure to c. 17 mg bromethalin (equivalent to 0.33 mg bromethalin/kg). His clinicopathologic course was characterized by altered mental status, obtundation, increased cerebrospinal fluid pressure, cerebral edema, death, and diffuse histologic vacuolization of the white matter in the central nervous system seen on microscopic examination at autopsy. The presence of a demethylated form of bromethalin in the patient's liver and brain was confirmed by gas chromatography with mass spectrometry. Clinical signs and lesions observed in this patient are similar to those seen in animals poisoned with bromethalin. This case illustrates the potential for bromethalin ingestion to result in fatal human poisoning.