Forensic pathologists are continually being asked in court to provide opinions on the possible causes, mechanisms, manifestations and effects of specific injuries. Although the pathological findings in some cases may not be of legal importance, the interpretation in others may have profound effects on the outcome of a particular trial by significantly influencing the decisions of judges and/or juries. For this reason pathologists must formulate opinions carefully. Unfortunately this may be difficult, as many traumatic conditions are not completely understood, the understanding of mechanisms may be in evolution, and individual pathologists may lack personal experience of particular types of cases [1, 2]. Blunt craniocerebral trauma is a good example of an injury type that may be associated with a wide range of outcomes. Unfortunately, the clinical manifestations may be nonspecific and there is often little experimental data to help with the evaluation of cases [3]. Histories may also be unreliable as they are often formulated in cases of inflicted head trauma to protect the perpetrator, rather than to provide a clear explanation of the events leading to the injury or death. This means that cases such as this are among the most challenging, particularly in terms of determining mechanisms, predisposing factors, time frames and the degree of force [4]. Involvement of forensic pathologists in experimental work in the laboratory may, however, be one way to answer some of these questions. For a variety of reasons, forensic pathologists are not generally involved in laboratory work. This has the unfortunate effect of isolating pathologists from academic activities such as hypothesis testing using experimental methodology. Although standard and new techniques may be used to clarify or focus on certain diagnostic issues, for example with post-mortem toxicology [5–7], the following studies demonstrate how useful direct collaboration between forensic pathology and the laboratory may be in providing answers to other questions that potentially arise in court. Examples that will be discussed include i) the development of an anesthetized sheep model of traumatic brain injury that has enabled the monitoring of intracranial pressure (ICP) and brain oxygenation following closed head injury, and ii) the measurement of cerebral free magnesium concentrations after blunt cranial trauma in alcohol-intoxicated rats. Studies involving biomechanical testing also demonstrate other fruitful areas of laboratory activity [8]. The first study measuring ICP and brain oxygen levels in anesthetized sheep following blunt head trauma revealed that a dramatic increase in ICP occurred within minutes of trauma [9]. Although this was followed by a gradual decrease, and then a steady increase in ICP, at no stage after injury was the ICP ever normal. We propose that this biphasic response resulted from reactive vasodilation in the first instance, followed by developing cerebral edema. The latter was confirmed by positive staining of sections for albumin, which showed that leakage of serum proteins into tissues had occurred, a hallmark of vasogenic edema. The questions asked in court in this area are often centered around how rapidly manifestations of severe blunt head trauma arise and/or appear. In infants and young children this includes debate over the possibility of the child appearing completely normal following injury, i.e., having a ‘‘lucid interval.’’ The R. W. Byard (&) R. Vink Discipline of Anatomy and Pathology, Adelaide Centre for Neuroscience Research, School of Medical Sciences, The University of Adelaide, Level 3 Medical School North Building, Frome Road, Adelaide 5005, Australia e-mail: roger.byard@sa.gov.au; roger.byard@adelaide.edu.au
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Dec 29, 2023
Raghavi M + 1
Open Access
