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Death scene investigation in sudden unexpected deaths in infants and small children Time for a change? Forensic medicine and the media The beginning of a new era?

What is the potential significance of inflicted but non-lethal injuries at autopsy in infancy? Proposal for an International Classification of SUDI: A response to Blair, Byard and Fleming Commentary of Blair et al. Scand J Forens Sci, 2009;15:6-9 Is body position related to the mechanism of death in fatal epilepsy? Findings of amphetamines and ecstasy in drivers in Denmark from 1997 to 2007 Death scene investigation in sudden death in infant and small children

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Struck by a lance through his side Kai Holst – Suicide or Murder? ’The Mysterious Death of Politican Nils Traedal: Accident or Homicide? Conspiracy of one. The assassination of John Fitzgerald Kennedy “How I wish, how I wish you were here” Boganmeldelse

24 28 33 38 44 46

3 4 5 6 7


Dansk Selskab for Retsmedicin Norsk Rettsmedisinsk Forening Svensk Rättsmedicinsk Förening VolumE 16 - No. 1 - 2010 - page 1 - 52

Nordisk rettsmedisin



Scandinavian Journal of

Olav Gunnar Ballo resigned from the position as director of the Institute of Forensic Medicine in Oslo after only nine months in office

Scandinavian Journal of Forensic Science Official journal of the Danish, the Norwegian and the Swedish societies for forensic medicine. The journal will publish original articles, review articles, preliminary communications, letters to the editor and case reports in the different disciplines of forensic sciences: forensic pathology, clinical forensic medicine, forensic genetics, forensic toxicology, forensic anthropology, forensic odontology, forensic psychiatry and forensic science. Submission of articles Manuscripts prepared in accordance with Guide for authors should be sent to the editor-in-chief or to one of the national editors. Editor in chief:

Torleiv Ole Rognum, Oslo

Editorial secretary: Editorial address:

Anne Gunn Winge Rettsmedisinsk institutt, Rikshospitalet, N-0027 Oslo, Norway

National editor, Denmark: Jørgen Lange Thomsen, Odense

National editor, Norway:

Torleiv Ole Rognum, Oslo

National editor, Sweden:

Håkan Sandler, Uppsala

Accountant: Address: Account:

Sigrid I Kvaal Vallegaten 17 A, N-0454 Oslo 7874.06.45012

Clinical forensic medicine:

Markil Gregersen, Århus Kari Ormstad, Oslo Annie Vesterby, Århus

Forensic anthropology:

Per Holck, Oslo

Forensic genetics:

Marie Allen, Uppsala Bertil Lindblom, Linköping Niels Morling, Copenhagen Bjørnar Olaisen, Lovund Antti Sajantilla, Helsinki

Forensic odontology:

Sigrid I Kvaal, Oslo Sven Richter, Reykjavik

Forensic pathology:

Thomas Bajanowski, Münster Roger W Byard, Adelaide Anders Eriksson, Umeå Gunnlaugur Geirsson, Reykjavik Jorma Hirvonen, Oulu Hans Petter Hougen, Copenhagen Pekka Karhunen, Tampereen Inge Morild, Bergen Lennart Rammer, Lindköping Pekka Saukko, Turku Jørn Simonsen, Copenhagen Michael Thali, Bern Ingemar Thiblin, Uppsala

Forensic psychiatry:

Peter Kramp, Copenhagen Randi Rosenqvist, Oslo

Forensic science:

Bjarni Bogason, Reykjavik Frank Jensen, Vanløse Reidar Nilsen, Oslo

Forensic toxicology:

Johan Ahlner, Linköping Jørg Mørland, Oslo

Editorial board

Lay out: Holstad Grafisk, Oslo - Print: prografia, Oslo - ISSN 1503-9552


Death scene investigation in sudden unexpected deaths in infants and small children


ll valid definitions of sudden infant death syndrome (SIDS) require death scene investigation. However, the way the investigation is performed varies from country to country. United Kingdom probably has the most well organised system for death scene investigation. It was introduced after a change in the legislation in April 2008. Professor Peter Fleming and his co-workers have established a multi-agency approach which implies that paediatricians and police officers visit the death scene and talk to the family. In the U.S.A. death scene investigations are partly done by medical examiners or coroners, the police or in some cases a combination of both. In Denmark the death scenes are visited by ordinary police. In Norway the police was withdrawn from the death scene of infants and small children in 1991. This was the result of the SIDS epidemic that caused 150 deaths a year, e.g. almost 0.3 per 1000 live births by the end of the 1980’ties. Unfortunate episodes, in which the police went to the scene with uniformed cars, interrogated the family and finally sent them a letter informing that the criminal case was closed due to lack of evidence, did occur. In 1991 the chief prosecutor instructed the police to stay away from the death scene until they had received the autopsy report. They should also abstain from sending letters to the families. The dead infants should be admitted to the nearest paediatric hospital and the family should be followed up by the hospital and by the community health system. It soon turned out that valuable information was lost in some cases. When the police received the autopsy report it was too late to localize items of interest. Therefore, a research project including death scene investigation by a police expert and the forensic pathologist that performed the autopsy was carried out in Southeast Norway from 2001 to 2004. The results from the project are presented in the present issue of Scand J Forens Sci (page XX). Based on these results and on the report of the Centre for Crisis Psychology which evaluated the impact on the families, it was recommended that death scene investigation by experts should be mandatory. The specialist in crisis psychology concluded in her report that the death scene investigation offered the families a structured approach and qualified information at an early stage in the bereavement process. After five years, debating whether the death scene investigation should be voluntary or mandatory, the Norwegian Government has decided that death scene investigation is to be offered as a voluntary health service to families who experience sudden unexpected death in infants and small children. The Parliament however is requiring a mandatory death scene investigation. The Governmental lawyers claim that a mandatory approach would be against the Norwegian Constitution which says that “house inquisition” can only be allowed in criminal cases, and that a mandatory death scene investigation also interferes with the European Declaration of Human Rights. The Government has delegated the responsibility of the voluntary death scene investigation to the National Institute of Public Health, Section of Psychological Health. This institution has then hired the Institute of Forensic Medicine to perform the investigations. The last move occurred in March 2010. The Parliament unanimously has decided to change the law regulating criminal procedure to allow the police to investigate sudden deaths in infants and children without the requirement of “reasonable grounds for suspicion”. However, until legislative Scand J of FORENSIC SCIENCE - No 1 - 2010 - Page 1-52


changes are made, the death scene investigation will be offered to the families as a voluntary health service. A service with voluntary death scene investigation including all Norway is planned to start November 1, 2010. Two experts with police training and four medical doctors from the Institute of Forensic Medicine, Oslo, as well as experts from four other forensic medical centres of Norway will take part in the service. At the Soria Moria meeting May 19-21, 2011 we hope to be able to share experiences from death scene investigations with participants from all over the world (see announcement for the Soria Moria meeting 2010 on page XX) TOR

Time for a change?


he new director at the Institute of Forensic Medicine has resigned after 9 months in office. This fact reflects the organisational challenges in forensic medicine in Norway. The institute in Oslo was originally organised under the Faculty Division for Laboratory Medicine at the University Hospital. One year ago the Medical Faculty became in charge and in April 2010 the central University administration took over the responsibility. They appointed a board led by former managing director of one of the biggest companies in Norway (Norsk Hydro), Egil Myklebust. It is now time to look at the official report (NOU 2001:12) Expert knowledge in criminal proceedings and the Hareide report from 2006, that both suggest a national body responsible for all branches of forensic medicine. Such an independent institute organizing all medico legal expert knowledge would have the same aim as the different forensic medical institutions. Today the impression may arise that some of the responsible organisations are more interested in the “overhead� than in the quality of the service. Time may have now come for a change! TOR


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Forensic medicine and the media I was recently exposed to the media and wanted to tell a story to cast light on the historical development that should not be forgotten. Jørgen L.Thomsen


ack in the seventies when I was young at the institute in Copenhagen, contact with the press was absolutely prohibited. Nobody should be given access to the sacred halls of forensic medicine. At the time there was only one TV-channel, the appearance on TV meant instant fame. A few weeks ago a book was published on the history of “Rapport” later to be known as “Ugens Rapport”, a magazine that first came out in the mid seventies. The book reminded me of the first dramatic encounter with the press. The deputy state pathologist (Jørgen Voigt) had a view on press con- tact that differed from that of professor Harald Gormsen, state pathologist. So he agreed to contribute to an article in “Rapport” about forensic medicine in Copenhagen He accepted (the horror, the horror) photos from the autopsy room. This was the only time that I can remember, when Harald Gormsen allowed himself to show visible or rather audible criticism of his next in command. It all happened behind closed doors, but we could hear him shout. I remember the chilling feeling when I saw a photo of page one of a death certificate with my name on it. Nobody at the institute really knew the new magazine but we soon found out that the main attraction of “Rapport” were naked women. Since then we have all accepted the right of the media in a democratic society to gain knowledge of our profession. There are of course limitations, and first of all we must keep anonymity of the cases. There are many advantages connected with a strong profile in the media, and it is important to maintain our present, positive status. There are of course also many pitfalls, and in my opinion we have not had enough discussions and teaching on the subject. I therefore suggest that we take it up in the national forensic societies and make it one of the main topics at the Nordic Meeting in 2012 in Aarhus. February 2010 Jørgen L.Thomsen

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The beginning of a new era?


fter > 30 years in forensic medicine although in a remote site of the world (Sweden), the character and premises for the job is really changing. One of the most important contributing factors, apart from new ”brains” within the organisation, is the breakthrough of digital technologies as a complement, or in some instances, replacing the holy autopsy. Until now the forensic expert doctor has been the undisputed proprietor of his case. This situation can be dramatically changed upon. Are we ready for this? Threat or opportunity, or both? At present our department (Uppsala, Sweden) refers its cases to the Department of Clinical Radiology, at our nearby university hospital, for CT or MRI. Eight years with this arrangement has gained some experiences, and raises many questions: - The INDICATIONS for radiology? Crime suspicion only, any trauma, paediatric, SIDS, or any case admitted to, and accepted by the Department? -Facility at your own Department or on a consultant basis? This issue contains to a multitude of subunits; eg. Numbers: At a small department like ours, around 800-900 autopsies are performed annually. Optimized indications, but with the facility” in house”, would subsequently yield around 400-500 digitalized cases. Is this enough to be of pedagogic/educational significance? Expanding indications, sharing information int. and ext. in a scheduled manner could help offsetting this. Competence and skill: This is an individual as well as a team task. Sharing digital information is easier than ever. Interpretation is still very much up to the individual, but the basic process of acquiring knowledge can be much facilitated by maintaining a good relation to a limited number of clinical radiologists, co-projects, and scheduled auscultations within and after our specialist training program at the radiology department. Radiologists must get the same offer. Pro and Contras : As with everything ,there are two sides of the coin. Will the number of performed autopsies further decrease? Paradoxically, the numbers may increase, since being just a digitalized image , the “analogue” autopsy may strengthen its role as “the golden standard”, in the forensic community. Our “customers” will probably also become aware of the combined strength of both procedures. Will there be “perceptual competition” between the two, resulting in a loss of skill in final evaluation of results? As to the digital result, it can be reevaluated in a multitude of ways. By adopting the new technologies, our discipline will probably become more attractive from a recruiting point of view. Also it will bring a lot of new research areas, with offsprings back to the clinic as well. Håkan Sandler national editor Sweden


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What is the potential significance of inflicted but non-lethal injuries at autopsy in infancy? Roger W Byard1, Torleiv O. Rognum2 Discipline of Pathology, The University of Adelaide & Forensic Science SA1, Adelaide, South Australia, Australia; Institute of Forensic Medicine, University of Oslo2, Oslo, Norway.

ABSTRACT Determining a precise cause of death is a difficulty that is often encountered in pediatric autopsies because of subtle or non-diagnostic findings. The issue of classifying a death as being due to sudden infant death syndrome (SIDS) exemplifies this dilemma, as there are no diagnostic pathological or clinical findings. A particular problem arises with the possible significance of inflicted, but non-lethal injuries. Review of infant deaths where inflicted injuries were present was undertaken with formulation of three separate categories: cases where injuries were a) coincidental to the cause of death, i.e. clearly unrelated; b) directly involved in terminal lethal processes, i.e. causative; or c) possibly associated with the terminal lethal condition identified at autopsy: i.e. of unknown significance. Cases in categories a) and b) are relatively straightforward. Cases in category c) present the greatest difficulties in trying to relate injuries to plausible lethal mechanisms. Given that the pathological findings in cases with such injuries are more complex than standard SIDS cases, the use of the term SIDS is not recommended. The following could, therefore, be added to standard SIDS definitions: that ‘the autopsy findings should occur in the absence of evidence of inflicted injury’. Keywords: SIDS, infant death, inflicted injury, abuse, asphyxiation, suffocation

INTRODUCTION A wide range of inflicted injuries involving most tissues and organ systems may be encountered at autopsy in infants. Non-lethal injuries to the skin and subcutaneous tissues include bruises, abrasions and lacerations. There may also be single or multiple bone fractures, some having characteristic features such as bucket handle metaphyseal fractures and spiral fractures of the humerus. Non-lethal injuries include minor subarachnoid hemorrhage, bruising of the mesentery, and healed and healing rib fractures. Usually none of these injuries have caused sufficient organ/tissue disruption or hemorrhage to result in death. PROBLEMS In assigning the manner of death in infant and early childhood deaths it is the practice of some mortality committees to classify deaths in infants who have died of undetermined causes, but who have been found to have inflicted but non-lethal injuries at autopsy, as Address For Correspondence: Prof Roger W. Byard, Discipline of Pathology, Level 3 Medical School North Building, The University of Adelaide, Frome Road, Adelaide 5005, Australia Phone: (618) 8303 5441 Fax: (618) 8303 4408 Email:

homicides. This is done despite the absence of a plausible lethal mechanism, because it is believed that infants who have been abused have a greater risk of suffering a lethal asphyxial event, the features of which may be undetectable at autopsy1. Although this may make intuitive sense, the assumption is often based on minimal evidence in individual cases. Another issue that arises concerns determining the possible contribution that inflicted but non-lethal injuries may have made to the fatal episode. Some pathologists have wondered whether it is possible that an infant with no definite cause of death at autopsy, but with multiple fractures, may have died from a cardiac arrhythmia precipitated by extreme pain. Again, while this may appear to be an intuitive possibility the evidence is lacking. Certain difficulties contributing to these issues involve the infant autopsy. Standard autopsies have varied considerably in scope and quality, with significant omissions being found on review of cases when standard protocols have not been followed2. If critical information is lacking it may be impossible to form a definite conclusion about the cause and manner of death. An additional problem also involves the lack of sensitivity of standard autopsy investigations in detecting certain rare conditions such as metabolic disorders or cardiac rhythm disturbances in the form of prolonged QT syndrome.

In view of these issues it was decided to examine the range of inflicted injuries that may be found in infants at autopsy, from non-lethal to lethal, and to define specific subcategories of cases. CLASSIFICATION Cases may fall into three broad categories when inflicted injuries are found at autopsy: A). Infants with inflicted, non-lethal injuries that are clearly unrelated to death. In these instances the inflicted injuries are purely coincidental to the lethal mechanisms. Examples include a healing torn frenulum from trauma to the mouth in a case of an infant dying in hospital of lethal congenital cardiac malformation, or cigarette burns of the palms of an infant who has died in a vehicle accident. While a meticulous autopsy examination is required to evaluate the presence or absence of other injuries, the deaths are not due to inflicted trauma. Police investigations, reliable witness statements and full autopsy examinations all support this conclusion. B). Infants with inflicted injuries that are clearly the cause of death. Injuries most often result from blunt craniocerebral or abdominal trauma, but may also include chest trauma and burns. Police investigations, reliable Scand J of FORENSIC SCIENCE - No 1 - 2010 - Page 1-52


witness statements and full autopsy examinations all support this conclusion. C). Infants with inflicted, non-lethal injuries that are possibly but not definitely associated with the terminal lethal condition. These cases include those where the cause of death may not be determined at autopsy, even following ancillary microbiologic, toxicologic, radiologic, metabolic and genetic testing. Thus while there is evidence of inflicted injury it cannot be directly associated with the death. Whether the traumatic lesions detected are a marker of occult more significant inflicted injury such as suffocation cannot be determined from the pathology findings. Also included in this group are cases where the cause of death is known, but the issue of adequacy of care is raised. For example, if death was due to a natural disease such as pneumonia or congenital heart disease, was appropriate medical care sought or followed? Also, could inflicted injuries have predisposed to natural disease? For example, did bacterial pneumonia result from reduced respiratory excursion and diminished airway secretion clearance due to the pain from fractured ribs? Did lethal aspiration of gastric contents, with or without superimposed pneumonia, result from an altered conscious state from head trauma or drug effect? Unfortunately many of these issues may remain unresolved even after a full investigation. If an infant with non-lethal inflicted injuries has died of accidental trauma questions may also be raised as to whether this may have been due either to failure to ensure the safety of the infant, or to a reckless indifference to the infant’s welfare. In summary, inflicted injuries in infants that are found at autopsy may be: a. Coincidental to the cause of death: i.e. unrelated; b. Directly involved in terminal lethal processes identified at autopsy: i.e. causative; or c. Possibly but not definitely associated with the terminal lethal condition identified at autopsy: i.e. of unknown significance.


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RELATIONSHIP TO SIDS One of the major difficulties in infancy is in determining whether a death can be attributed to SIDS in the absence of diagnostic features at autopsy3. The National Institute of Human Development and Child Health (NICHHD) defined SIDS as “the sudden death of an infant under one year of age which remains unexplained after a thorough case investigation, including performance of a complete autopsy, examination of the death scene and review of the clinical history” 4. This definition was refined in 2004 by including an apparent association with sleep and an evaluation of the entire circumstances of death, not just the death scene5. Although category IA in the San Diego definition specifies that there is “no evidence of unexplained trauma, abuse, neglect or inflicted injury”, unfortunately no guidance in more general definitions has been provided for cases where inflicted but non-lethal injuries are found; i.e. by definition it could be argued that the death of an infant with completely negative findings except for healed and healing fractures and multiple bruises could be attributed to SIDS, as these are non-lethal (although this would not be usual practice). While it is quite possible for an abused infant to succumb to those mechanisms that cause SIDS, the possibility of an increased risk of other forms of inflicted injury such as smothering has to be considered6. While it is unclear whether the presence of nonlethal inflicted injuries increases the likelihood of such occult homicides, perhaps a qualifier to standard SIDS definitions should be that the autopsy findings occur ‘in the absence of evidence of inflicted injury’. CONCLUSION Inflicted but non-lethal injuries at autopsy in infancy raise considerable diagnostic issues. Rather than attempting to establish a single cause of death, it is probably more useful to indicate in the diagnosis that inflicted injuries are present and to provide an additional comment on the likelihood that these contributed to death.

Infants with inflicted injuries should not be classified as SIDS cases in view of the presence of more complex pathology and the difficulty that exists in excluding a lethal asphyxial episode. Having these cases as a separate subset of SUDI (sudden death in infancy) will flag them as being different to other cases of sudden infant death and will enable further epidemiologic and pathologic studies to be undertaken. REFERENCES 1. Byard RW, Jensen L. Fatal asphyxial episodes in the very young – classification and diagnostic issues. Forensic Sci Med Pathol 2007;3:177-81. 2. Byard RW. Inaccurate classification of infant deaths in Australia: a persistent and pervasive problem. Med J Aust 2001;175:5-7. 3. Byard RW, Krous HF. Sudden infant death syndrome – overview and update. Pediatr Develop Pathol 2003;6:112-27. 4. Willinger M, James LS, Catz C. Defining the sudden infant death syndrome (SIDS): deliberations of an expert panel convened by the National Institute of Child Health and Human Development. Pediatr Pathol 1991;11:677-84. 5. Krous HF, Beckwith JB, Byard RW, Rognum TO, Bajanowski T, Corey T, Cutz E, Hanzlick R, Keens T, Mitchell E. Sudden infant death syndrome (SIDS) and unclassified sudden infant deaths (USID): a definitional and diagnostic approach. Pediatrics 2004;114:234-8. 6. Byard RW, Sawaguchi T. Sudden infant death syndrome or murder? Scand J Forensic Sci 2008;14:14-6.

Proposal for an International Classification of SUDI: A response to Blair, Byard and Fleming Peter Sidebotham, Thomas Bajanowski, Tom Keens, Thomas Kenner, Reinhold Kerbl, Ronald Kurz, Ed A Mitchell, Rachel Moon, Barry Taylor, Mechtild Vennemann, Jeanine Young, Heinz Zotter

In 2009, Blair, Byard and Fleming, drawing on discussions between SIDS (sudden infant death syndrome) researchers and practitioners, proposed an international classification scheme for SUDI (sudden unexpected death in infancy) (Blair et al., 2009). As indicated in their proposal, the term SUDI incorporates a range of causes of death, both apparent and hidden. Whilst the proportion of SUDI for which a cause is found has risen, at least 50% remain unexplained in all published studies. Blair, Byard and Fleming point out that, although an internationally agreed definition of SIDS exists, use of the term is inconsistent, and both practitioners and researchers often resort to alternative labels for those deaths that remain unexplained. Furthermore, approaches to the investigation of SUDI vary both between and within countries. These inconsistencies complicate research in the field, and potentially hamper our search for understanding of these deaths. Nevertheless they are a reality which will not go away. Blair et al’s proposal is timely. It is essential, as overall numbers of unexpected infant deaths fall, for there to be collaboration within and between countries in continued investigation of the underlying causes and contributory factors for these deaths. Most researchers and practitioners recognise that SIDS is unlikely to be a single entity for which a simple explanation or cure can be found, rather it is likely that those SUDI that currently remain unexplained include deaths from undiagnosed infections, other underlying medical conditions, including various genetic, cardiac or metabolic conditions, and accidents or non-accidental deaths which we are currently unable to identify. The proposed classification allows for this, through the combination of the “Avon” grading through Ia to III, the addition of category 0 to account for incomplete investigations,

and the subgroups of explained deaths within the categories of SUDI. To be useful, any classification system needs to be simple, yet comprehensive, and to be acceptable to both practitioners and researchers. It needs to accommodate differences in practice between individuals and on a wider basis. The proposed system of Blair et al goes a long way to encompassing these elements. Experience in the UK however has shown that the Avon classification can be difficult for practitioners to understand and work with, and a simplified version has now been widely adopted by child death overview panels and teams responding to unexpected child deaths (Sidebotham et al., 2008). This dispenses with the (a) and (b) subclassification and simply uses a 0 – III classification (0 – information not available; I – no factors or noncontributory factors identified; II – factors possibly contributing to death; III – fully explained). Individuals using this system may choose to subdivide categories I and II, but overall it leads to greater uniformity and is more practical for front-line practitioners. There have previous attempts to classify SIDS and SUDI, including the San Diego, GeSID and ESPID classifications (Krous et al., 2004, Kerbl et al., 2003, Findeisen et al., 2004). These classifications acknowledge the variations in presentation of SUDI and the differences in approaches to investigation. Although they do not directly conform to the current proposal, there is sufficient overlap to propose a merger of these systems (Table). It will prove difficult to achieve full consensus on any international system of classification, even amongst researchers, let alone practitioners; nevertheless, this proposal should prompt further debate in the right direction. Thus far, the lack of a generally accepted classification system makes it difficult to reliably compare SIDS

or SUDI figures worldwide, and these figures usually contain incomplete information concerning autopsy rate and the incidence of factors potentially contributing to death in the recorded so-called SIDS cases. A starting point for all epidemiological research should be a description of all infant deaths; the next stage would be to define what is included within any categorisation of SUDI; and finally a clear description of those finally labelled as SIDS, conforming to the internationally agreed definitions (Krous et al., 2004, Willinger et al., 1991), but making clear what parameters have been used within any particular research project. This in itself is not necessarily straightforward, as different areas will include different groups of deaths within their definition of SUDI. Nevertheless, by including all SUDI, within the framework suggested, it is possible to separate out those for which a cause is ultimately found from those that remain unexplained, regardless of the term used to describe this group. In order to fully understand these deaths, we need a system which will allow us to go beyond a simple diagnosis of cause of death, to incorporate the various shades of grey inherent in our approach to investigation and the findings thereof. The proposed system by Blair et al goes some way to achieving this, and we believe, with some modification, could be adopted by researchers and practitioners alike. The proposed classification system could potentially be a starting point for further research and clarification. There remain difficulties in relation to which deaths should be included: for example, in the UK and New Zealand, all sudden unexpected deaths in infancy are referred to the coroner, but this is not necessarily the case elsewhere, and in many places, sudden deaths for which a cause is immediately apparent, including some accidental deaths, or those with an apparent medical cause Scand J of FORENSIC SCIENCE - No 1 - 2010 - Page 1-52


Table: Comparisons of different classification systems for SIDS/SUDI ESPID classification

Unclassified Sudden Infant Unexplained, incomplete Death: investigation. This category may be applied a) deaths that do not meet the criteria for category I in conjunction with other or II SIDS, but for which categories where any part of alternative diagnoses the investigation is of natural or unnatural incomplete. conditions are equivocal (these may be better clasThis category expands on other classifications by incorsified as category II SUDI, with or without a category porating cases with missing 0 to indicate inadequate elements of the investigation, not just noninvestigation) autopsied cases. b) cases for which autopsies were not performed

The GeSID classification was based on pathology findings; being a research based classification, only cases in which a full autopsy had been performed were included.

Non-autopsied SUDI

Unexplained; no contributory factors identified

Category I SIDS a) classic features of SIDS present and completely documented b) classic features of SIDS present but incompletely documented (there is some overlap between this classification and SUDI category 0) There may be some overlap between category I SIDS and SUDI category II, depending on which factors are deemed to be potentially contributory.

Category 1: Without pathological findings from autopsy and additional investigations

Classical SUDI

Category II SIDS Meet category I criteria, except for some features which raise possibilities of an alternative explanation (e.g. outside the typical age range; close family history of SUDI; possibility of mechanical asphyxia; abnormal autopsy findings insufficient to determine a cause of death)

Category 3: Severe findings, but not sufficient to fully explain the death

Borderline SIDS

Category 4: SUDI with clear cause of death found at autopsy.

Explained SUDI

Categories of SUDI



San Diego Classification

GeSID classification

Simplified Blair et al Proposed classification

This classification does not take account of the positive features of a classic SIDS case suggested in the San Diego classification


Unexplained; possible contributory factors identified


Explained: Rapid infection Rapid onset of acute medical condition Unrecognised pre-existing medical condition Accidental death Non-accidental death

may not be included. It is likely that within the spectrum of SUDI, different patterns may emerge at different ages, and some sort of developmental trajectory could be developed to further explore how different infant


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Includes any SUDI for which an autopsy has not been performed; does not account for other missing aspects of an investigation

Category 2: With minor pathological findings in autopsy and investigations

Excludes known unnatural deaths

and environmental factors may be associated with different developmental stages, and different categories of both explained and unexplained sudden infant deaths – an extension of the widely accepted triple risk model of SIDS

(Guntheroth and Spiers, 2002). Further work would be needed also to try to achieve some consensus over which associated factors would be included in category II. There may, for example, be reasonable consensus now to include

prone sleep position, cigarette smoking in pregnancy and necropsy findings of minor infection; whilst other factors, such as the role of co-sleeping may prove more controversial. Finally, there is a continued need to move towards greater standardisation of the processes by which a diagnosis and categorisation of SUDI are achieved. The criteria required for a diagnosis of SIDS have previously been agreed within the international research community (Willinger et al., 1991) and include a complete autopsy and review of the circumstances of death and the clinical history; what specific elements should be incorporated within that, and how the review should be carried out, for example through a multi-disciplinary case review, remain open to interpretation, and will always be dependent on local resources and working practices, but it is hoped that over time greater consistency can be achieved, leading in turn to more robust descriptions of the causes and circumstances of sudden unexpected deaths in infancy.

References BLAIR, P., BYARD, R. & FLEMING, P. (2009) Proposal for an international classification of SUDI. Scandinavian Journal of Forensic Science, 15, 6-9. FINDEISEN, M., VENNEMANN, M., BRINKMANN, B., ORTMANN, C., ROSE, I., KOPCKE, W., JORCH, G. & BAJANOWSKI, T. (2004) German study on sudden infant death (GeSID): design, epidemiological and pathological profile. Int J Legal Med, 118, 163-9. GUNTHEROTH, W. G. & SPIERS, P. S. (2002) The triple risk hypotheses in sudden infant death syndrome. Pediatrics, 110, e64. KERBL, R., ZOTTER, H., EINSPIELER, C., ROLL, P., RATSCHEK, M., KOSTL, G., STRENGER, V., HOFFMANN, E., PERROGON, A., ZOTSCH, W., SCHOBER, P., GRANZ, A., SAUSENG, W., BACHLER, I., KENNER, T., IPSIROGLU, O. & KURZ, R. (2003) Classification of sudden infant death (SID) cases in a multidisciplinary setting. Ten years experience in Styria (Austria). Wien Klin Wochenschr, 115, 887-93. KROUS, H. F., BECKWITH, J. B., BYARD, R. W., ROGNUM, T. O., BAJANOWSKI, T., COREY, T., CUTZ, E., HANZLICK, R., KEENS, T. G. & MITCHELL, E. A. (2004) Sudden infant death syndrome

and unclassified sudden infant deaths: a definitional and diagnostic approach. Pediatrics, 114, 234-8. SIDEBOTHAM, P., FLEMING, P., FOX, J., HORWATH, J., POWELL, C. & WALLACE, K. (2008) Responding when a child dies. London, DCSF. WILLINGER, M., JAMES, L. & CATZ, C. (1991) Defining the sudden infant death syndrome (SIDS): deliberations of an expert panel convened by the National Institute of Child Health and Human Development. Pediatric Pathology, 11, 677-684.

First announcement: Soria Moria meeting 2011 May 19-21 Themes: ● Brain stem research and SIDS ● Genetic risk factors for SIDS ● Domestic violence and effect on early brain development ● Impact of death scene investigation in sudden deaths in infants and small children For more information, please contact: a.g.winge@medisin.uio.n

Contributors: ● Hannah Kinney ● Henry F. Krous ● Roger W. Byard ● Peter Fleming ● Jens Grøgaard ● Magne Raundalen

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Commentary of Blair et al. Scand J Forens Sci, 2009;15 6-9 Proposal for an International Classification of SUDI: Is this Trip Necessary?

David T. Mage, Ph.D. A.I. duPont Hospital for Children, Wilmington, DE, USA

Introduction Blair et al.1 make an interesting suggestion for an International Classification of Sudden Unexpected Deaths in Infancy (SUDI). The authors are “SIDS researchers engaged in identifying different causes of this syndrome.” One of the authors previously wrote: “It is also likely that the aetiology of SIDS is heterogeneous and that the term SIDS is not so much a diagnosis but a term covering a variety of mechanisms which result in a common lethal outcome.”2 More recently, Kinney and Thach wrote: “If all specific causes of infant death are delineated, the designation of SIDS will no longer be needed.”3 This all implies that SIDS may not have a single cause requiring only a single International Classification of Diseases (ICD) rubric and that it is a compendium of other known causes (diseases or conditions) currently undiagnosed by the pathologists and death scene investigators. Blair et al.1 suggest that SIDS needs to be ‘parsed’ into its component parts “to be categorised for research purposes” to aid the discovery of those missing causes. This following discussion shows that rather, SIDS may be a single distinct entity unto itself and that an introspective differential classification system may not be necessary or useful.

SIDS has a characteristic and virtually unique age distribution, the exception being infant botulism onset (IB).4 The SIDS age distribution has not changed since the early 1970s when Raring5 first noted that it appeared to be a 2-parameter lognormal distribution. For example, Pollack6 has shown that the lognormal form of the SIDS age distribution has not changed in the U.S. between 1989 and 1999 in spite of the shift of preferred sleep position from prone to


Scand J of FORENSIC SCIENCE - No 1 - 2010 - Page 1-52

(RI), positional asphyxiation (PA), etc. The authors state “Traditionally all [such] unexplained SUDI deaths have been labeled as sudden infant death syndrome (SIDS).”1 Cramér’s Theorem10 translates as follows: ‘if any finite sum of independent real-valued random variables is normal, then the summands must all be normal.’11 If the SIDS age data set is a summation of undiagnosed NP, RI, PA,... independent age subsets (SIDS = NP + RI + PA + ...) then all NP, RI, PA, etc., must also be 4-parameter lognormally distributed with same xmax and xmin. But as vital statistics show,7,12 the neonatal period (<28 days), and sometimes indeed the very first day of life, are periods of maximal mortality for such conditions as neurological congenital anomalies and other non-SIDS causes of death. This is in direct contrast to SIDS where the above transform (y) of SIDS age (x) has a Gaussian shape, with minimal mortality at birth, maxi-

The 4-parameter Lognormal Age Distribution of 19,949 SIDS from 15 Global Data Sets Combined



supine. Goldberg et al.7 showed how most all other ICD classifications of infant death have a distinctly different age pattern with a maximal rate at birth that decreases with age. This behavior is opposite to SIDS that has a virtually zero rate at birth and increases with age. Mage8 has shown by a metaanalysis of 15 combined independent SIDS age distributions that the SIDS age distribution, shown as Figure 1, was better described by a 4-parameter lognormal distribution, also known as the Johnson SB distribution.9 This transform treats SIDS age x as bounded between a minimum age (xmin) and a maximum age (xmax). The logarithm of the transformed age, y = (x - xmin)/( xmax - x), is then bounded between -∞ and +∞ and is fit well by a Gaussian normal distribution.8 Let SIDS be a summation of subsets of undiagnosed independent causes of death, such as neurological prematurity (NP), respiratory infection

m, month of life

Figure 1. The characteristic lognormal age distribution of SIDS.8,9 Cramér’s Theorem requires any proposed undiagnosed cause of SIDS to have the same Gaussian lognormal distributional form.10,11

mal mortality between 2 and 4 months of life, and mortality decreasing towards zero after one year. Because ages of death for causes such as NP, RI, PA, etc., all suggested to constitute subsets of false-positive SIDS, are not lognormally distributed - that would violate Cramér’s Theorem. Therefore all the putative subsets of cause-of-death claimed to be now masquerading as SIDS (except IB) cannot possibly be true subsets of SIDS. Another way of looking at this impossibility, is that all age distributions of each supposed undiagnosed cause of SIDS would have to be drawn under the envelope bounded by the SIDS age distribution of Figure 1 so that their summation equaled the age distribution of SIDS. Summary SIDS in all developed countries with high medical standards has a consistent lognormal age distribution and a consistent 50% male excess.8,13 Given that these cases come from different societies with different child care practices and are diagnosed by different pathologists with different levels of expertise, the consistency of their global findings in terms of age and gender imply that SIDS is indeed a distinct phenomenon. This suggests that what are now deemed to be potential candidates for undiscovered causes of SIDS are merely risk factors for SIDS and that the appearance of subsets arises where one risk factor happens to be more intense

than the others. A unifying theory for SIDS suggests that it occurs when a status of a potentially terminal cerebral anoxia occurs in neurons of the respiratory control center of the brainstem by several indistinct pathways.14,15 This status can be reached by different combinations of risk factors that are not to be confused with cause of death (e.g., prone sleep position or low-grade respiratory infection). When that status is reached, the infant in possession of an X-linked dominant allele that allows anaerobic oxidation to occur in the anoxic neurons will survive or perhaps present as a non-fatal Apparent Life Threatening Episode (ALTE), but the infant with the corresponding non-protective recessive X-linked allele will die of SIDS.15 This X-linkage mechanism predicts the consistent 50% male excess of SIDS, for which no other explanation appears in the medical literature.16 References 1. Blair PS, Byard RW, Fleming PJ. Proposal for an International Classification of SUDI. Scand J Forensic Sciences 2009;15:6-9. 2. Byard RW. Sudden infant death syndrome a ‘diagnosis’ in search of a disease. J Clin Forensic Med. 1995;2:121-8. 3. Kinney HC, Thach BT. The sudden infant death syndrome. N Engl J Med. 2009;361:795-805. 4. Arnon SS, Breast-feeding and toxigenic intestinal infections: Missing links in SIDS? in Sudden Infant Death Syndrome. Tildon JT, Roeder LM, Stein-

schneider A, eds. New York, Academic Press; 1983: 539-555. 5. Raring RH. Crib Death: Scourge of Infants—Shame of Society. Hicksville, NY: Exposition Press; 1975:93-97. 6. Pollack HA. Changes in the timing of SIDS deaths in 1989 and 1999: indirect evidence of low homicide prevalence among reported cases. Paediatr Perinat Epidemiol. 2006 Jan;20(1):2-13. 7. Goldberg J, Hornung R, Yamashita T, Wehrmacher W. Age at death and risk factors in sudden infant death syndrome. Aust Paediatr J. 1986;22 Suppl 1:21-28. 8. Mage DT. A probability model for the age distribution of SIDS. J. Sudden Infant Death Syndrome and Infant Mortality 1996;1:13-31. 9. Johnson NL. Systems of frequency curves generated by methods of translation. Biometrika 1949;36:297-317. 10. Cramér H. Über eine Eigenschaft der normalen Verteilungsfunktion (in German). Mathematische Zeitschrift 1936;41:405– 414. doi:10.1007/BF01180430 11. Weisstein EW. “Normal Sum Distribution.” From MathWorld--A Wolfram Web Resource. 12. Centers for Disease Control and Prevention, National Center for Health Statistics. Compressed Mortality Files 1979-2005. CDC WONDER On-line Database. Accessed at http://wonder.cdc. gov/, October 15, 2009. 13. Mage DT, Donner EM. A genetic basis for the sudden infant death syndrome sex ratio. Med Hypotheses. 1997;48:137-142. 14. Mage DT, Donner EM. The fifty percent male excess of infant respiratory mortality. Acta Paediatr. 2004;93:1210-1215. 15. Mage DT, Donner EM. A Unifying Theory for SIDS. Int J Pediatr. 2009;2009:368270. 16. Finnström O. A genetic reason for male excess in infant respiratory mortality? Acta Paediatr. 2004;93:1154-1155.

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Is body position related to the mechanism of death in fatal epilepsy? Roger W. Byard1,2, John D Gilbert2, Drew Marshall2 Discipline of Pathology, The University of Adelaide1 & Forensic Science SA2, Adelaide, South Australia, Australia.

ABSTRACT A retrospective study of 81 epileptic deaths of individuals autopsied at Forensic Science SA between January 1994 and August 2005 revealed 47 males and 34 females aged from 1 to 79 years (mean = 37 years). The most common position of the body when found was prone (N = 52; 64%), followed by supine (N = 17; 21%), seated (N = 7; 8.6%) and side (N = 5; 6%). The most common locations of the bodies were in bed (N = 43; 53%), in the home outside the bedroom (N = 19; 23%), the bedroom (N = 10; 12%) and outdoors (N = 8; 10%). Of the 38 victims who were not in bed, 30 were on a floor and 7 were seated. (In one case the location of the body was not stated although the position was documented.) Of the 30 victims found lying on a floor, 19 (63%) were prone. A significantly greater number of epileptic individuals were found dead lying in a prone compared to a supine position (p<0.001), contrasting dramatically with 50 controls who had died suddenly in their beds of whom only 2 (4%) were prone (p<0.001). The preponderance of deaths in the prone position with the face down would certainly be in keeping with suffocation/asphyxia playing a role in the terminal episode. As SUDEP could result from the integration of a number of mechanisms rather than from the effect of one element in isolation, it is possible that compromise of respiration related to body position might also exacerbate a tendency to lethal cardiac arrhythmia. Keywords: epilepsy, sudden death, prone, sleep, SUDEP

INTRODUCTION It is now well-recognized that individuals with epilepsy have higher mortality rates than age-matched controls. Morbidity and mortality may be related to underlying conditions that predispose to epilepsy, such as alcoholism or head injury, or may be associated with accidental immersion or burns occurring during a seizure. Deaths may occur during status epilepticus, or alternatively, fatalities may occur for reasons that are ill-understood but that relate to the intrinsic nature of the condition. There has been a reported 40 times increased risk of sudden unexpected and unexplained death in those with, compared to those without, epilepsy1. This increase in mortality has been documented at all ages2-4. The role of asphyxia/suffocation in the terminal episode has been debated, with suggestions that epileptics may die from asphyxia due to obstruction or compromise of their airways during a seizure, contrasting with assertions that asphyxia is not a significant factor and that the â&#x20AC;&#x2DC;myth of the pillowâ&#x20AC;&#x2122; should be dispelled5,6. However, we

Address For Correspondence: Prof Roger W. Byard, Discipline of Pathology, Level 3 Medical School North Building, The University of Adelaide, Frome Road, Adelaide 5005, Australia Phone: (618) 8303 5441 Fax: (618) 8303 4408 Email:


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have observed that individuals who have died unexpectedly from epilepsy are often found in a face down, prone position. To ascertain whether there is a higher rate of prone positioning in those dying of epilepsy, and to investigate whether this may relate to the mechanism of death, the following study was undertaken. MATERIALS AND METHODS Review was undertaken of all deaths attributed to epilepsy at Forensic Science SA (FSSA) between January 1994 and August 2005. FSSA provides autopsy services to the coroner of South Australia and serves a mixed urban and rural population of approximately 1.5 million people. All cases had full police/coronial investigations and complete autopsies. Cases were included in the study if the victims were found dead and fulfilled the criteria for sudden unexpected and unexplained death in epilepsy (SUDEP)7. Cases were excluded if the deaths involved accidents such as drowning or drug toxicity. Specific information was gathered from both police and pathology reports concerning the location and position of the body when found, prior to any disturbance of the body and scene by observers or ambulance personnel. Body locations were recorded as bed, bedroom, home or outdoors, and body position was recorded as supine (face up), prone (face down), side or seated. Comment on the firmness of the surfaces that the bodies were resting on

was not possible as this information was not usually contained in reports. All brains were examined macroscopically and histologically. No analysis of toxicology results was undertaken. A control group was selected from other FSSA coronial cases of natural deaths where the deceased had been found dead in bed with clear documentation of the position of the body. Statistical analyses were undertaken using SPSS 11 for Macintosh and Chi Square testing. Any association with p<0.01 was considered significant. RESULTS Epileptic group: Eighty-one cases were found of sudden unexpected and unexplained death in epilepsy fulfilling the criteria for SUDEP, consisting of 47 males and 34 females (58% and 42% respectively). The age range was from 1 to 79 years (mean = 37 years). The most common position of the body when found was prone (N = 52; 64%) (p<0.001), followed by supine (N = 17; 21%), seated (N = 7; 8.6%) and side (N = 5; 6%). The most common locations were in bed (N = 43; 53%), in the home outside the bedroom (N = 19; 23%), the bedroom (N = 10; 12%) and outdoors (N = 8; 10%). Of the 38 victims who were not in bed, 30 were on a floor and 7 were seated. In one case the location of the body was not stated although the position was documented. Of the 30 victims found lying on a floor, 19 (63%) were prone.

Control group The 50 control cases consisted of 35 males and 15 females (70% and 30%, respectively), ranging in age from 12 to 92 years (mean = 64 years). Causes of death included cardiovascular disease (most often ischemic and hypertensive heart disease) (N = 34, 68%), respiratory disease (most often asthma and chronic obstructive airways disease) (N = 8, 16%), neurological disease (cerebrovascular accidents and tumors) (N = 4, 8%), gastrointestinal disease (ruptured esophageal varices and acute peritonitis (N = 3, 6%) and diabetes mellitus (N = 1, 2%). Among the control cases the most common position of the body when found was supine (N = 30; 60%) (p<0.001), followed by side (N = 18; 36%) and finally prone (N = 2; 4%). The positions of bodies in both the epileptic and control groups are shown in Figure 1 demonstrating a significantly greater number of epileptics found in a prone position when compared to controls (p< 0.001). DISCUSSION Sudden unexpected and unexplained death in epilepsy (SUDEP) has been defined as the ‘sudden, unexpected, witnessed or unwitnessed, non-traumatic, and non-drowning death in patients with epilepsy, with or without evidence for a seizure and excluding documented status epilepticus where necropsy examination does not reveal a toxicological or anatomical cause for death’7. Other epileptic deaths were

attributed to airway obstruction, aspiration, trauma or drowning, and those where there was significant underlying cardiorespiratory disease. Criteria for SUDEP were further refined to include the following six features: the victim suffered from epilepsy (defined as recurrent unprovoked seizures), the victim died unexpectedly while in a reasonable state of health, the death occurred ‘suddenly’ (in minutes) when known, the death occurred during normal activities and benign circumstances, an obvious medical cause of death was not found, and the death was not the direct result of the seizure or status epilepticus1. While these authors excluded deaths due to accidents, they did not automatically exclude cases for consideration based on circumstances such as possible drowning. A classification of ‘definite SUDEP’, ‘probable SUDEP’, ‘possible SUDEP’ and ‘not SUDEP’ was proposed based on the availability of information, and the certainty with which diagnoses could be made1. The cause of death in SUDEP remains speculative with sudden death being attributed to suffocation from bedding, asphyxia, pulmonary edema and cardiac arrhythmia. Specific fatal mechanisms have included sympathetic-induced cardiac arrhythmia, parasympathetic-induced bradycardia/ asystole, apnea/respiratory failure, a combination of arrhythmia and apnea, and neurogenic pulmonary edema with cardiac failure8 (Table 1), however evidence is often not strong in support of specific mechanisms.

Figure 1: Position of the body when found in 74 cases of epilepsy and in 50 control cases dying in bed of other types of natural diseases (7 cases of epilepsy who were found seated were not included)

Table: Possible causes of sudden death in epilepsy 1. 2. 3. 4. 5. 6. 7. 8.

Trauma Suffocation Asphyxia Cardiac arrhythmia (sympathetically mediated) Bradycardia/asystole (parasympathetically mediated) Apnea/respiratory failure Arrhythmia/apnea Neurogenic pulmonary edema with cardiac failure

Although one of the standard theories to explain this kind of sudden death involves autonomic nervous system instability with abnormal cardiac rhythms during seizure activity, data on lethal arrhythmic deaths have been contradictory, with few recordings of arrhythmias being taken during lethal episodes9-11. In fact, most reported clinical and experimental cases of arrhythmias associated with cerebral events have not been fatal12,13. In a study of 338 monitored epileptic patients there was no demonstrable increase in cardiac arrhythmias compared to the general population, with only 5% of patients showing high-risk patterns14,15. It is also possible that epilepsy may not be the primary event but is secondary to an underlying cardiac abnormality, with seizures being caused by cerebral hypoxia arising from ventricular tachycardia. In support of this concept there has been an increased incidence of epilepsy reported in patients with hereditary prolongation of the QT interval16. Determining whether anoxia may have played a role in the lethal event is also difficult as some authors have suggested that seizures may be directly responsible for delayed respiratory arrest17, contrasting with others who have asserted that apnea plays only a secondary role during the tonic phase of the seizure8. Given that epileptic individuals may be in a situation where a diminished conscious state precludes them from maintaining or protecting their airway, it would not seem unreasonable to postulate that lethal airway compromise from suffocation due to soft bedding, or from positional asphyxia with angulation of the airway could cause death6. Ascertaining whether or not suffocation may have occurred is, however, often complicated by alteration of scene findings and by the lack of diagnostic findings at autopsy. In the current study a significantly Scand J of FORENSIC SCIENCE - No 1 - 2010 - Page 1-52


greater number of epileptic individuals were found dead lying in a prone compared to a supine position (prone = 52; supine = 17; p<0.001). This contrasted dramatically with the 50 controls who had died suddenly in their beds of whom only 2 (4%) were prone (p<0.001). It is possible that individuals who die suddenly from non-epileptic conditions may be more likely to be sleeping on their backs if they are feeling unwell prior to the terminal episode. They may also have collapsed while trying to get out of bed. This may explain the very low rate of prone sleeping in the controls. It is noted that 40% of the epileptics in the current study involved death in bed or in a bedroom. This is in keeping with other studies where up to 79% of cases of sudden epileptic death have also been found in this situation18, and also with the known association of sudden death in epilepsy with sleep most likely related to reduction in seizure threshold19,20. There are several possibilities for the significantly higher rate of prone position in the epileptic group. If the victims usually slept prone it is possible that a lethal arrhythmia generated by a seizure could result in rapid death before the deceased could roll over. However if this was the case it might be expected that the control cases where lethal arrhythmias complicated ischemic heart disease would also die in the position of sleep and that there should, therefore be a higher number of prone cases than has been recorded. The finding of 19 epileptics (63%) in the prone position out of a total of 30 lying on a floor also suggests that prone is significantly associated with sudden epileptic death whether in bed or not. It may be that epileptics who fit in a supine position are less likely to obstruct their airways, and that loss of consciousness in the prone position causes suffocation when the face pushes into a floor or mattress, or the nose and mouth is obstructed by a pillow. The softness of the underlying bedding could explain the high rate of death in bed. An increased rate of sudden death associated with the prone position has also been shown in infants dying of sudden infant death syndrome (SIDS). While the precise mechanisms responsible for this increase in risk in the face down position are not known, a number of possibilities have been postulated including diaphragmatic splinting/fatigue, rebreathing of carbon


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dioxide, reflex lowering of vasomotor tone with tachycardia, blunting of arousal responses including decreased cardiac response to auditory stimulation, alteration of sleep patterns, compromise of cerebral blood flow, upper airway obstruction from distortion of nasal cartilages, posterior displacement of the mandible and soft bedding21. It is possible that similar effects may be experienced by an unconscious prone individual who has just had an epileptic seizure. Although it is probable that SUDEP results from the integration of a number of mechanisms rather than from the effect of one element in isolation, as in other situations where complex pathophysiological processes are acting, we would not dismiss the possible contribution of suffocation/asphyxia. The preponderance of deaths in the prone position with the face down would certainly be in keeping with this. While the deaths may not be purely asphyxial in nature, compromise of respiration might also exacerbate a tendency to lethal cardiac arrhythmia, producing an additive effect. Pathologists should therefore always obtain a clear account of the circumstances of death in epileptics, including an accurate description of the position of the body when found, the placing of the nose and mouth, the presence of any obstructive materials around the face, the type of bedding and the softness/firmness of the underlying surface. Fixed ventral lividity with congestion, petechiae and ecchymoses and pressure blanching on the anterior chest and abdominal walls may also be used to provide information on position at the time of death. References 1, Annegers JF, Coan SP. SUDEP: overview of definitions and review of incidence data. Seizure 1999;8:347-52. 2. Breningstall GN. Mortality in pediatric epilepsy. Pediatr Neurol 2001;25:9-16. 3. Callenbach PM, Westendorp RG, Geerts AT, Arts WF, Peeters EA, van Donselaar CA, Peters AC, Stroink H, Brouer OF. Mortality risk in children with epilepsy: the Dutch study of epilepsy in childhood. Pediatrics 2001;107:1259-63. 4. Donner EJ, Smith CR, Snead OC. Sudden unexplained death in children with epilepsy. Neurology 2001;57:430-4. 5. Coyle HP, Baker-Brian N, Brown SW. Coronersâ&#x20AC;&#x2122; autopsy reporting of sudden unexplained death in epilepsy (SUDEP) in the UK. Seizure 1994;3:247-54. 6. Nashef L, Garner S, Sander JW, Fish DR, Shorvon SD. Circumstances of death in sudden death in epilepsy: interviews of

Table 2: Checklist of infotmation required from the scene in epileptic deaths 1) 2) 3) 4) 5) 6) 7) 8)

Location of the body Position of the body Position of the mouth and nose Obstructive materials around face Type of bedding Softness of underlying surface Position of lividity Other observations e.g. urinary incontinence, bleeding from the mouth, types of medications etc.

bereaved relatives. J Neurol Neurosurg Psychiatry1998;64:349-52. 7. Nashef L, Brown S. Epilepsy and sudden death. Lancet 1996;348:1324-5. 8. Leestma J. Forensic Neuropathology. New York: Raven Press,1988. 9. Dasheiff RM, Dickinson LJ. Sudden unexpected death of epileptic patient due to cardiac arrhythmia after seizure. Arch Neurol 1986;43: 194-6. 10. Liedholm LJ, Gudjonsson O. Cardiac arrest due to partial epileptic seizures. Neurology 1992;42:824-9. 11. Oppenheimer S. Cardiac dysfunction during seizures and the sudden epileptic death syndrome. J R Soc Med 1990;1346. 12. Dasheiff RM. Sudden unexpected death in epilepsy: a series from an epilepsy surgery program and speculation on the relationship to sudden cardiac death. J Clin Neurophysiol 19918:216-22. 13. Kiok MC, Terrence CF, Fromm GH, Lavine S. Sinus arrest in epilepsy. Neurology 1986;36:115-6. 14. Keilson MJ, Hauser WA, Magrill JP. Electrocardiographic changes during electrographic seizures. Arch Neurol 1989;46:1169-70. 15. Keilson MJ, Hauser WA, Magrill JP, Goldman M. ECG abnormalities in patients with epilepsy. Neurology 1987;37:16246. 16. Bricker JT, Garson AJ, Gillette PC. A family history of seizures associated with sudden cardiac deaths. Am J Dis Child 1984;138:866-8. 17. Earnest MP, Thomas GE, Eden RA, Hossack KF. The sudden unexplained death syndrome in epilepsy: demographic, clinical, and postmortem features. Epilepsia 1992;33:310-16. 18. Schwender LA, Troncoso JC. Evaluation of sudden death in epilepsy. Am J Forensic Med Pathol 1986;7:283-7. 19. Dinner DS. Effect of sleep on epilepsy. J Clin Neurophysiol 2002;19:504-13. 20. Marlow B. Sleep and epilepsy. Neurol Clin 2005;23:1127-47. 21. Byard RW, Krous HF. Sudden infant death syndrome: overview and update. Pediatr Dev Pathol 2003;6:12-27.

Findings of amphetamines and ecstasy in drivers in Denmark from 1997 to 2007 Marie Katrine Klose Nielsen and Sys Stybe Johansen Section of Forensic Chemistry, Department of Forensic Medicine, Faculty of Health Sciences, University of Copenhagen, DK-2100 Copenhagen, Denmark. Abstract There has been a strong public and political interest in Denmark in the abuse of designer amphetamines such as ecstasy (MDMA). In the period from 1997 to 2007, 2461 samples taken from drivers suspected of impaired driving were submitted to the laboratory by the police for toxicological analysis. These investigations have shown a new pattern in drug abuse among drivers and an increase in the number of samples tested positive for designer amphetamines such as MDMA, MDA and MDEA. The first two traffic cases involving designer amphetamines were found in 1997. Four cases were found in 1999. In the last 10 years cases involving designer amphetamine have increased to 13% of all traffic cases requested for toxicological analysis in Denmark. In these 114 designer amphetamines cases involving mainly male drivers the dominating compound was MDMA. A few positive cases of MDEA were also observed, but mostly in mixtures with MDMA and/or MDA. The whole blood concentration of MDMA ranged from 0.02 to 3.7 mg/kg with a mean value of 0.47 mg/kg and a median value of 0.34 mg/kg. The concentration varied from low abuse level to high toxic level. In many of the cases, additional drugs were found in the blood such as benzodiazepines, tetrahydrocannabinol and cocaine metabolites. Keywords Designer amphetamines, MDMA, drivers, blood

Introduction Annually, about 14.000 to 18.000 drives are suspected of drunk driving in Denmark, but until year 2000 a very limited number of drivers have been suspected for driving under the influence of drugs other than alcohol (1,2). Since 2000, the number of cases of driving under the influence of drugs has increased. Benzodiazepines and cannabis are some of the most commonly detected drugs of abuse in the Nordic countries, but also cases with amphetamine have increased in the last years (3,4). Recently, there has been a strong public as well as political interest in Denmark in the abuse of ecstasy (MDMA). MDMA is a ring substituted derivative of methamphetamine abused as a psychedelic substance. Metabolic demethylation of MDMA produces MDA, which is also pharmacological active. MDMA and related drugs such as MDA and MDEA are listed as prohibited drugs in the Danish law (5). These designer amphetamines can cause hallucination, paranoid delirium, seizures, psychosis, coma and even death (6-8). The detection of designer amphetamines in biological fluids is therefore of major concern in forensic toxicology. This corresponding address: Marie Katrine Klose Nielsen Section of Forensic Chemistry, Department of Forensic Medicine, Faculty of Health Sciences, University of Copenhagen, Frederik Vâ&#x20AC;&#x2122;s Vej 11, DK-2100 Copenhagen, Denmark. E-mail:

paper presents some data and statistics on the abuse of amphetamines and designer amphetamines among drivers in Denmark together with a discussion of the development in recent years. Materials and methods Specimens of blood from drivers suspected of impaired driving were submitted to the Department of Forensic Chemistry by the police. From 1997 to 2007 a total of 2461 samples were submitted for toxicological analysis. A broad routine toxicological analysis in blood was applied for common drugs, narcotics and alcohol. Confirmation of amphetamines and designer amphetamines were performed by liquid-liquid extraction of blood and a derivatization followed by gas chromatography-mass spectrometry (GC/MS) analysis (9).

Results The development in positive amphetamines and designer amphetamines cases The development of traffic cases tested positive for amphetamines and designer amphetamines in Denmark since 1997 is shown in Figure 1. Annually, the total numbers of traffic cases for toxicological analysis were between 103 and 345 in this period, while about 14.000 to18.000 blood samples from Danish drivers were investigated for alcohol annually. From 1997 to 2007 at total of 2461 samples were investigated for common drugs and narcotics. In Figure 1, a decrease in the number of positive amphetamine cases is observed from 1998 to 2000 and a simultaneous increase of positive designer amphetamines cases is observed. From 2000 increases of both amphetamines and designer amphetamines cases are observed. The total number of traf-

Figure 1. The development of traffic cases tested positive for amphetamines (amphetamine and methamphetamine) and designer amphetamines (MD MA, MDA and MD EA) against all traffic cases investigated in Denmark since 1997

Scand J of FORENSIC SCIENCE - No 1 - 2010 - Page 1-52


Table 1. Characteristics parameters of designer amphetamines in 114 positive cases in Danish drivers since 1997. Year

Total Total1 Designer2 Designer MDA3 MDMA MDEA Sex Age Traffic Amph. Amph. Amph. Range Range (mg/kg) Range(mg/kg) Range Cases Cases Cases % of total (mg/kg) Mean (Cases) Mean (Cases) Median amph. cases Mean (Cases)





6 (1)

0.05 0.23 (2)

0.23 0.15 (2)


M: 2 F: 0

19-22 21






- -






0.06-0.45 0.19 (4)

M: 4 F: 0

20-30 25






0.22 (1)

0.02-1.1 0.56 (8)

0.03 (1)

M: 10 F: 0

9-30 24






0.15-0.62 0.40 (5)

M: 5 F: 0

19-24 21






0.05 (1)

0.05-1.4 0.38 (15)

M: 15 F: 0

17-27 21






0.03-0.73 0.37 (11)

M: 11 F: 0

19-32 21






0.04-1.5 0.60 (9)

M: 8 F: 1

18-30 23






0.03-0.39 0.16 (5)

0.03-3.7 0.54 (30)

0.05-0.08 0.07 (2)

M: 29 F: 1

18-31 20






0.03 (1)

0.02-1.6 0.46 (13)

M: 12 F: 1

17-30 20






0.02 (1)

0.09-1.1 0.43 (15)

M: 15 F: 0

18-31 20






0.02-0.39 0.11 (10)

0.02-3.7 0.46 (112)

0.03-0.17 0.09 (5)

M: 111 F: 3

17-32 21

- -

Including amphetamine, methamphetamine, MDA, MDMA and MDEA. 2Including MDA, MDMA and MDEA. 3Only cases where the concentration of MDA was higher than 10% of the concentration of MDMA are shown. 1

fic cases involving amphetamines and designer amphetamines has increased from 23 cases in 1997 to 69 cases in 2007 corresponding to 11 and 20% of all traffic cases, respectively. In the whole period (1997-2007), the total number of cases positive for amphetamines and designer amphetamines was 436. The designer amphetamines represented less than 13% of all amphetamines cases until 1999, but in 2000 they were found in 43% of all amphetamines cases (Table 1). Since 2001, the designer amphetamines were found in 22 to 48% of all amphetamines cases. The total number of designer amphetamine cases in the whole period was 114, in 78 cases a mixture of both amphetamines and designer amphetamines were found. In the whole period the designer amphetamines constituted 26% of the 436 cases. Designer amphetamines Characteristic parameters such as sex,


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age and concentrations of designer amphetamines in traffic cases in Denmark from 1997 to 2007 are shown in Table 1. The first two MDMA cases among drivers in Denmark were found in 1997, which corresponds to 0.9% of all 213 traffic samples investigated in 1997. Both cases involved MDMA, MDEA and MDA. In 1999, four cases were positive for MDMA (~1.8%), and in the period from 2000 to 2007 between 5 and 30 cases a year were found positive for designer amphetamines (4 to 13% of all traffic cases). In general, the dominating compound was MDMA. The high incidence of MDA in MDMA cases and the fact that the concentration of MDA was 5-10% of the MDMA concentration in 98% of these cases concur with MDAs nature as a metabolite in MDMA consumption. MDA was only detected alone in one case in 2000. A few cases involved MDEA and always in a mixture with MDA and/or MDMA except for one

case. The dominance of MDMA in the designer amphetamines concurs with the findings in seizures in Denmark. MDMA was the major component in designer drugs tablets in the period (10). The whole blood concentration of MDMA in 114 traffic cases ranged from 0.02 to 3.7 mg/kg with a mean value of 0.46 mg/kg and a median value of 0.34 mg/kg (Table 1). The blood concentrations of MDA and MDEA ranged from 0.02 to 0.39 mg/kg and from 0.03 to 0.17 mg/kg, respectively. The mean values were 0.05 and 0.09 mg/kg, respectively. The MDMA concentrations range from low abuse level to high toxic level. The main part of the cases shown in Table 1 concerned men. Only three cases involved females, which corresponded to 2.6% of the designer amphetamine cases in the whole period. For both genders, the age ranged from 17 to 32 years and the median was 21 years.

In the period from 1997 to 2007, additional drugs or narcotics were detected in 83 cases corresponding to 73% of the cases. The most frequently detected drugs were tetrahydrocannabinol (THC), cocaine and/or its metabolite benzoylecgonine and benzodiazepines, - mainly diazepam. Blood alcohol concentration (BAC) was determined in 18 cases of all designer drug cases (16%) of which eleven cases exceeded the Danish traffic offence limit (0.05%). Amphetamines 322 cases were positive for amphetamine of which seven cases showed amphetamine as a metabolite from methamphetamine consumption. Methamphetamine was detected in 36 cases, but only in eleven cases was methamphetamine detected alone. The whole blood concentration of amphetamine ranged between 0.01 and 2.0 mg/kg and the mean and median were 0.25 and 0.14 mg/kg, respectively. The concentration of methamphetamine ranged from 0.01 to 0.74 mg/kg with mean and median values of 0.13 and 0.06 mg/kg, respectively. Both drugs ranged from low abuse level to toxic level. The cases mostly concerned men, which were also observed for the designer amphetamines cases. Only eleven cases involved females corresponding to 4% of the amphetamines cases. The age of the drivers ranged from 17 to 52 years (median: 24 years) for men and from 17 to 41 years (median: 24 years) for females. Discussion The presented data indicates that abuse of designer amphetamines is occurring and increasing in Denmark. Before 1997 designer drugs did not occur and now they are observed in about 5% of all traffic cases in DK. The increase maybe due to the high attention on these drugs in the public or a high awareness among the police due to early warning program and new traffic act in late 2007. Amphetamine is still the most frequently observed compound of the amphetamines in traffic cases, but designer amphetamines are more common now. MDMA is the most frequently observed designer amphetamine and MDMA is a very toxic substance that affects the psychomo-

tor skills and impairs driving. Studies have shown that the use of MDMA is not consistent with safe driving and that impairment of various types may persist for a considerable time after last use (8). The negative effects include muscle tension, pain, increased sweating, blurred vision, pupillary dilation, ataxia, anxiety, a nervous desire to be in motion, panic attacks etc. (6, 8). All these properties indicate that following the intake of MDMA, a user would suffer effects that would impair the ability to safely operate a motor vehicle. Several cases involved very high concentrations (toxic levels) of MDMA and/or amphetamine that also influence the impairment. Furthermore, the combination of MDMA and alcohol, which was observed in 16% of the investigated cases, induces longer lasting euphoria and well being than intake of MDMA or alcohol alone. MDMA reverse the subjective sedation induced by alcohol without reducing the drunkenness feelings. MDMA do not reverse the actions of alcohol on psychomotor abilities. Subjects may feel euphoric and less sedated and might have the feeling of doing better, but actual performance ability continues to be impaired by the effect of alcohol (11). Multiple drug use are typical in about 60% of the Danish traffic cases as shown in other studies from 1997 to 2000 (1). This indicates that in cases involving amphetamines multiple drugs use is more frequent (73%). Other drugs such as the most frequently one THC will also have a serious negative impact. In future we expect more traffic samples for investigation because of the new Danish traffic act included in late 2007 per se legislation of illegal drugs in DRUID cases. We also expect new designer drugs detected among the traffic samples due to observed changes in designer amphetamines among seizures. The confiscated tablets among seizures from the beginning of 2010 do not contain MDMA anymore (12). Conclusion Abuse of mixtures of amphetamines and designer amphetamines are common and amphetamine users are probably using designer amphetamines such as MDMA as a second step in their abuse pattern. The simultaneous

decrease in amphetamine cases and increase of designer amphetamine cases until 2000 can very well be connected. In 2000, a strong exposure in the media may have influenced amphetamine users and other abusers to experiments with designer amphetamines. Since 2001, the total number of cases involving amphetamines and designer amphetamines among drives in Denmark are increasing (11-31% of all traffic cases), which indicates that the abuse of these substances among drivers in Denmark are common now. References 1.

Steentoft A. Andre stoffer end alcohol i trafikken i Danmark. Nordic conference ”Andre droger an alkohol i trafikken, Norkadt – Nordisk Ratttoksokologisk Kommittee for alkohol, droger and trafiksakerhed, Helsinki, 2001. 2. Behrensdorff I, Steentoft A. Medicinal and illegal drugs among Danish car drivers, Accident Anal Prev, 2003; 35:851-860. 3. Bernhoft IM, Steentoft A, Johansen SS, Klitgaard NA, Larsen LB, Hansen LB, Drugs in injured drivers in Denmark, Forensic Sci Int, 2005; 150:181-189. 4. Christophersen AS, Ceder G, Kristinsson J, Lillsunde P, Steentoft A. Drugged driving in the Nordic countries - a comparative study between five countries. Forensic Sci Int, 1999; 106:173-190. 5. Bekendtgørelse om klassificering af færdselssikkerhedsfarlige stoffer. BEK nr 655 af 19/06/2007. 6. Moore K. Amphetamines/sympathomimietic amines. In Principles of Forensic Toxicology, Levine B, editor, AACC Press, USA, 1999, pp 265-285. 7. Baselt RC. Disposition of Toxic Drugs and Chemicals in Man, 7th ed. Chemical Toxicology Institute, Foster City, CA, 2000. 8. Logan BK, Couper FJ. 3,4-methylenedioxymethamphetamine (MDMA, ecstasy) and Driving Impairment. J Forensic Sci. 2001; 46:1426-1433. 9. Johansen SS, Hansen AC, Muller IB, Lundemose JB, Franzmann MB. Three Fatal cases of PMA and PMMA poisoning in Denmark. J Anal Toxicol. 2003; 27:253-256. 10. Johansen M, Ecstasy i Danmark 2007, http:// Ecstasyrapport2007.pdf 11. Hernandez-Lopez C, Magi F, Roset PN, Menoyo E, Pizarri N, Ortuno J, Torrens M, Cami J, De la Torre R. 3,4-methylenedioxymethamphetamine (ecstasy) and alcohol interactions in humans: psychomotor performance, subjective effects, and pharmacokinetics. J Pharmacol Exp Ther. 2002; 300:236244. 12. SST. Hvad indeholder “ecstasy” pillerne. Overvågning af beslaglagte ”ecstasy” piller i Danmark. Et samarbejdsprojekt mellem Sundhedsstyrelsen, Rigspolitiet og de tre retskemiske afdelinger i København, Odense og Århus. 1. Kvartal 2010.

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Death scene investigation in sudden death in infant and small children The Norwegian experiment Rognum TO, Wille-Sveum L, Arnestad M, Stray-Pedersen A, Vege Å ABSTRACT Due to some unfortunate episodes during the SIDS epidemic in the 1980’ies, the police was withdrawn from the death scene. They were not replaced by other professionals. As SIDS rates dropped during the early nineties and other causes of sudden deaths became relatively more important, it became evident that death scene investigation should be reintroduced. In the period 2001-2004 a research project was carried out in Southeast Norway. The most important findings were disclosure of 7 cases of neglect almost not seen in the years before and after. Furthermore the cases with initial suspicion could immediately be dismissed as non-criminal. Evaluation by a crisis psychologist was very favourable for the project.

Introduction In 1991 the police was instructed not to visit death scenes in cases of sudden infant death. The reason was some unfortunate episodes during the SIDS “epidemic” when as much as 3‰ of all live newborns in Norway died from SIDS (1). Soon after the withdrawel of the police from the death scene it became evident that important information about the circumstances of death was lost. Therefore the Norwegian SIDS Society and the Norwegian Foundation for Health and Rehabilitation sponsored a research project during a period of four years (2,3). The death scenes in cases of sudden death in infants and small children in Southeast Norway were visited by an expert team. Participation in the project was voluntary and dependent on informed consent from the family. The project period was between 2001 and 2004, and this paper presents the results from the project. Method In all cases of sudden unexpected deaths in children between 0 and 3 years of age in Southeast Norway (2.5 million inhabitants), the family was offered a visit by two experts from the Institute of Forensic Medicine, University of Oslo. The expert team consisted of the forensic pathologist who had performed the autopsy and a co-ordinator with education and experience from tactical police investigation at The National Criminal Investigation Service (KRIPOS), Oslo. The police


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expert was employed by the project, not by the police. In most cases infants and small children found lifeless at home are brought with ambulance to the nearest paediatric hospital. These deaths are categorised as unnatural per definition and the police is informed immediately. Request of a forensic autopsy is compulsory. The paediatrician on duty informed the family about the death scene investigation which was voluntary and performed after the family had signed an informed consent form. The dead child was brought to the Institute of Forensic Medicine for a full autopsy including radiology, microbiology, toxicology and genetic investigations and the autopsy was performed within 24 hours. The diagnostic was based on the Nordic criteria for SIDS (4). Shortly after the autopsy two experts visited the death scene. The visit usually lasted for 2 hours and included a structured interview with the parents lead by the police expert. The forensic pathologist informed the parents about the preliminary results of the autopsy (in cases of no criminal nature) and the parents had the opportunity to ask questions. The room in which the baby was found dead was videotaped. By means of a doll with the appropriate size and weight

Figure 1. The dolls and the photo equipment used in the project.

(Fig 1) the parents took part in the reconstruction showing how they put the baby to sleep and the way the baby was found dead. Multi-agency case conferences were held approximately 3 months after the death. In addition to the medical doctors and researchers involved in the project, the paediatrician and nurse on duty on admission of the dead baby/child, as well as other experts such as a radiologist, microbiologist and neuropathologist regularly took part in the case conferences. In some cases representatives from the police also participated. An overview of the case was summarized in a power point presentation containing history of the disease, autopsy results including essential histological features and death scene examination. Subsequent to a thorough discussion the final conclusions were made.

Case control study: Scoring system for risk variables

Table 1. Case control study: Scoring system for risk variables

Score Sliping position Place Head covered Layers of clothing Matress Duvet Room temperature Score range

1-4 1-4 1-2 1-4 1-2 1-2 1-2

Table 2. Modes of death in the project period (n=69)

-4 (prone, face down) -4 (co-sleeping on sofa) -2 (yes) -4 (>2 layers) -2 (soft) -2 (varm/heavy) -2 (varm >22°C)


18 SIDS 9 Borderline SIDS 22 7 7 1 2 3 1

1 (supine) 1 (own bed) 1 (no 1 (one layer) 1 (firm) 1 (light/none 1 (normal)

Score variation


26 unexplained deaths


disease accidents neglect abuse homicide infanticide medical maltreatment

43 explanable deaths

Results During the study period between September 1, 2001 and March 31, 2004, there were totally 69 deaths, 37 boys and 32 girls. Forty-nine (71 %) of the deaths occurred during the first year of life (Fig 2). In 52 cases death scene investigation was offered to the family, and 46 families were visited after having given informed consent. Cases in which crime investigation had been initiated by the police were not visited by the death scene team.. There were 58 case conferences. Causes/modes of death In 27 out of 69 cases (45 %) no cause of death was found. In 18 of these cases there were no pathological findings at all (pure SIDS). In 9 cases pathological findings were documented, but not evaluated sufficient as cause of death (borderline SIDS) (Table 2). In the SIDS/Borderline SIDS group there were 67 % males and 33 % females. Most deaths occurred during the first 4 months after birth (Fig 3). From the remaining 43 cases 22 cases were due to acute disease, there were 7 accidents, 7 cases of neglect and the remaining 7 cases were abuse, homicide, infanticide and medical maltreatment (Table 2).

Figure 2. Age and sex distribution of all victims during the death scene investigation project in Southeast-Norway 2001-2004 (32 females and 37 males)

Figure 3. Age and sex distribution of the unexplained deaths. Note that the typical age peak for SIDS between the 2nd and the 4th month is not more evident.

A network with contact persons in all paediatric hospitals and police districts had been established before the project with death scene investigation started. In all hospitals, a midwife picked out three control cases born at the same time with the same sex, and living in the same type of area as the dead baby. The families of the control cases re-

concerning the baby’s death. The questions contained information about known risk factors for SIDS and scores for risks were given according to the answers. The risk factors and the scoring system are presented in table 1.

Risk factors for SIDS The risk scores for SIDS based on the information from the death scene and the parents who had lost their babies were significantly higher than those of the controls (Fig 4).

ceived a questionnaire containing several of the questions that the families who had lost babies were asked, e.g. they were asked how the baby slept and how the environment looked like during the same night/day as the investigated baby died (5). The bereaved families received identical questionnaires, however also with questions

Impact of the death scene investigation on the diagnosis In the explained deaths the death scene investigation contributed significantly to the diagnosis in 32 % of the cases (Fig 5). Home accidents were seen in 7 cases. In one case an 11 months old boy was suffocated by falling between the mother’s bed and his own cradle (Fig 6). Scand J of FORENSIC SCIENCE - No 1 - 2010 - Page 1-52


Figure 4. Distribution of risk scores for SIDS cases and controls

Signs of neglect were seen in 7 cases. In one case an 11 month old female baby died in a sleigh. She was put in the sleigh only wrapped up in downy coats. The temperature was minus 10°C. She was found dead after a 45 minutes ski race during which she had not been looked after. She was in prone position with the face right down in the downy coat. Cause of death was suffocation, combined with hypothermia. In another case a 3 months old infant was put to sleep with heavy clothing wrapped up in a fleece cover with a duvet on top and a warm water bottle placed in the bed. The parents had forgotten to look after the girl for 18 hours when she was found dead (Fig 7). Maltreatment and homicide were found in three cases. Causes of death were obvious such as scull fractures and knife wounds. There were 3 cases of infanticide.

Figure 5. Significane of death scene investigation for the diagnosis. Cases of explainable deaths, no=28

Figure 6. Reconstruction of the mechanism of death in a 9 months old boy. a) How he was left by the mother b) How he was found lifeless

Medical maltreatment was seen in 1 case. Immediate acquittal of suspicion In 14 cases (30 %) in which the police initially suspected a criminal act, due to e.g. a parent occurring in a criminal register, the death scene investigation led to immediate acquittal from suspicion. Evaluation by crisis psychologist Five weeks after the death scene investigation the 25 first families included in the study were visited by a crisis psychologist who performed a qualitative interview study. The families were asked to rate their impression of the visit on a scale from 1 (very good) to 5 (very bad). 31 answered “very good”, 2 answered “good” and 1 was neutral. None of the asked parents were negative (6). Discussion

Figure 7. Three months old girl found dead after being put to sleep in a warm room, with two layers of clothing, a cap, wrapped in a fleece blanket, under a duvet with a hot water bottle, and left without food for 18 hours.


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The most striking result was a relatively high number of cases of neglect. Seven cases of neglect were found during the 3.5 years project. Interestingly in the 4 years period prior to the death scene project we only disclosed 2 cases of neglect and in the 5 years after the project was finished, only one case has been seen (Fig 8). An equally impor-

References 1. Rognum TO, Lier LA. Police investiga-

Figure 8. Distribution of cases of neglect for Southeast Norway 1997-2009Note the seven cases during the project period.

tant observation was that initial suspicion against 14 families could be dismissed immediately after autopsy and death scene investigation. We thus think that the death scene investigation was important for legal protection of the infants and small children and their families. Six families decided not to take part in the project. We do not know the reasons in all cases. However, our impression is that the way in which they were asked to take part, often was decisive. Paediatricians with a negative stand to the project tended to get more negative answers than those with a positive view. At least one of the families who did not take part felt sorry about the decision and in retrospect contacted the team to be informed about the results of the autopsy. The evaluation performed by crisis psychologist was very positive. The families expressed their thankfulness to the death scene investigation team; the visit offered a structured follow up, it gave the families highly qualified information about cot death in general and about the findings in their child in special. Lastly, in spite of the fact that the death scene investigators were experts and not treating medical staff, the families experienced interest in their child and thus a sort of care. After the project was finished by the end of March 2004, the death scene investigation team at the Institute of Forensic Medicine was asked by the prosecutor general to propose a perma-

nent death scene investigation service. The project report (7) was delivered by September 1, 2004. The report concludes that death scene investigation should be mandatory in all cases of sudden unexpected deaths in infant and small children. It should be performed by experts and not by treating health personnel. The experts should work on behalf of the legal system and report to the police. In the following years the proposal was debated and finally the conclusion was that the Norwegian Institute of Public Health was asked to arrange a voluntary death scene investigation as a health service. However, if criminal conditions were disclosed the death scene visitors should report to the police. The Norwegian Institute of Public Health asked the Institute of Forensic Medicine to perform the investigation, and 2 police experts and 2 medical doctors will be engaged for the task. In March 2010 the parliament unanimously decided that the death scene investigation should be mandatory and the necessary revision of the regulation of criminal procedure will be made, so that the police is allowed to investigate sudden unexpected death in all children independent of suspicion of a criminal act. The voluntary health service project will start in November 2010, and it remains to be seen how soon the mandatory death scene investigation will be put into practice.

tion and SIDS cases. How can health personnel, forensic pathologists and police co-operate? In: Sudden Infant Death Syndrome. New Trends in the Nineties. Ed. TO Rognum. Scandinavian University Press 1995: pp 289-292 2. Vege Å, Arnestad M, Sveum M, Rognum TO. Barnedødsårsaksprosjektet. Bedre undersøkelse ved plutselig uventet død i spedbarns- og barnealder - en forutsetning for å bekjempe dødsfallene. Nordisk Rettsmedisin 2001; 7: 19-22 3. Sveum L, Vege Å, Arnestad M, Heltne U, Rognum TO. Bedre undersøkelse ved plutselig uventet død i spedbarnsog barnealder – en forutsetning for å bekjempe dødsfallene – en oppfølging. Nordisk Rettsmedisin 2002; 8: 61-63 4. Gregersen M, Rajs J, Laursen H, Baandrup U, Fredriksen P, Gidlund E, HelwegLarsen K, HirvonenJ, Isaksen CV, Koch K, Lundemose JB, Løberg EM, Rognum TO, Skullerud K. Pathologic criteria for the Nordic Study of Sudden Infant Death Syndrome. In: Sudden Infant Death Syndrome. New Trends in the Nineties. Ed. TO Rognum. Scandinavian University Press 1995: pp 50-58 5. Arnestad M, Andesen M, Vege Å, Rognum TO. Changes in the epidemiological pattern of SIDS in South-Eastern Norway 1984-1998 — implications for future prevention and research. Arch Dis Child 2001; 85: 108-115 6. Heltne, UM. Foreldres opplevelse av deltakelse i frivillig dødsstedsundersøkelse. Rapport. Senter for Krisepsykologi, Bergen 2003 7. Bedre undersøkelse ved plutselig uventet død i sped- og småbarnsalder. Forskningsprosjekt I helseregion sør og øst. Rapport til Riksadvokaten. Rettsmedisinsk institutt, Universitetet i Oslo, 2004

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Struck by a lance through his side The homicide of King Canute the Saint Peter Mygind Leth and Jesper Lier Boldsen Institute of Forensic Medicine, University of Southern Denmark

Abstract The Danish King Canute the Saint was killed in St Alban church in Odense July 10 1086. According to a legend the king was kneeling in prayers when a lance thrust to his side killed him. Our re-examination of the skeleton presumed to belong to Canute showed a slimly built man with an approximate stature of 165 – 170 cm and an age of 27 – 38 years. There was a peri-mortem lesion on the sacral bone. It was a so-called hinge-fracture that consisted of a horizontal fracture on the ventral surface of the 3rd sacral vertebra, and with a corresponding crack on the dorsal surface of the sacral bone. Computerized tomography showed these two fractures to be connected. We suggest that the fracture was caused by a thrust of a sharp instrument through the abdomen with a direction posterior and to the right.

Political assassinations are not an everyday occurrence in Denmark. An attempt on the Danish prime minister (konseilspræsident) J.B.S.Estrup’s life in 1885 did not succeed because the pistol bullet hit Estrup’s coat button. We have to go back to medieval times to find the last assassination of a Danish political leader, namely the murder of King Erik Klippinge that allegedly took place in a barn in Finnerup in Jutland November 22 1286. At that time such murders were very common. Forty-four percent of the Danish medieval kings met a violent death (1). 12 royal homicides in 350 years give a homicide rate for kings of no less than 3,480 per 100,000 per year. The highest present day national homicide rate is 250 per 100.000 per year (Colombia). This paper concerns the murder of King Canute the Saint. King Canute the Saint was an ambitious Danish king. He was one of King Svend Estridsen’s numerous sons. He was killed in St Alban church in Odense July 10 1086 after a six-year reign. We have had the opportunity to investigate the skeletons believed to belong to King Canute and his brother Benedict, and we would like to communicate some of our findings in this paper, concentrating on the king. It is the first time these skeletons have been investigated by experts in foren-

Corresponding author: Peter Mygind Leth, e-mail: Mobile +45 60 11 30 03. Adress: Institute of Forensic Medicine, J.B.Winsløws Vej 17, 5000 Odense C, Denmark.


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sic medicine, and it is also the first time that computerized tomography has been used on these old bones. Historical background King Canute’s reign was marked by vigorous attempts to increase royal power in Denmark, and he was also a devoted champion of the Church. He tried to enforce the collection of tithes, and these policies led to discontent among his subjects who were unaccustomed to

a king who claimed such powers and who interfered in their daily lives. As the grandnephew of Canute the Great he considered the crown of England to be rightfully his and regarded William the conqueror as an usurper. In 1085 he planned an invasion of England and assembled a fleet at Limfjorden, but it never set sail. Possibly Canute was afraid of intervention by the German king and Holy Roman Emperor Heinrich IV. Some consider Canute’s abortive invasion of England as the end of

Figure 1: The murder of King Canute the Saint. Painting by Christian von Benzon (1816 – 1843).

the Viking Age as it was the last time a Viking army was to assemble against Western Europe. In reality King Canute was also very much a man of the new age in his attempts to strengthen the monarchy and in his support of the Church (2). In 1086 a revolt broke out in Jutland. A main historical source for these events stems from the legend written by the clergyman Elnoth of Canterbury 20 years after the incident: â&#x20AC;&#x153;Passio Gloriosissimi Canuti Regis et Martyrisâ&#x20AC;? (3). According to the legend the king, his brother Benedict and 17 of his men sought refuge from the rebels in the Church of St Alban in Odense, but the sanctity of the church was not respected. The rebels stormed the church and slew Canute in front of the high alter, as illustrated in this 19th century painting (fig. 1). According to Elnoth the king did not try to defend himself. He was kneeling in prayers and was killed by a lance thrust to his side. His brother Benedict and most of his entourage were killed as well. This legend is of course not an objective account of what actually happened. The canonizing of King Canute was a political act instituted by his brother King Eric I. Elnoths narrative had a foregone conclusion, and his task was to make the known facts fit reasonably well with the conclusion: that the king was fit to be a saint. Not an easy task considering that the king was killed by compatriots who rebelled against an oppressive and brutal reign. However, the account was written down at a time when some people still remembered the king so the basic facts: that the king was killed by rebels in Odense in 1086 are probably correct. Buried, enshrined, walled in and finally displayed in a glass case Part of King Canuteâ&#x20AC;&#x2122;s strong assertion to power was based on his devoted support of the Church so it was only natural that his body was buried in front of the high alter in the church of St Alban. His bones were exhumed in 1095 and laid in a stone sarcophagus with an account of the incident written on a copper plate (Tabula Othiniensis). In 1100 he was canonized, and after his elevation to saint his bones were enshrined and displayed on the altar of

Figure 2: Photograph of the lesion on the ventral surface of the sacral bone believed to belong to King Canute the Saint.

Figure 3: 3 DM reconstruction of a CT-scanning of the lesion on the ventral surface of the sacral bone.

Figure 4: Photograph of the lesion on the dorsal surface of the sacral bone believed to belong to King Canute the Saint.

Figure 5: Transversal section through a CT-image of the sacral bone believed to belong to King Canute the Saint. The ventral and dorsal fractures are connected.

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the then newly erected stone church of St Canute that was build close to the old church of St Alban. The bones of his half-brother Benedict were also enshrined. There are references to these shrines from various medieval sources, but then they disappear from view. In 1582 St Canute’s shrine was brought to light, presumably from a hiding place in the choir. The shrine held an inscription denoting it as the shrine of St Canute. Benedict’s shrine is not mentioned. During the reformation most relics had been discarded, but these were royal bones and could obviously not be treated in this way. At an uncertain time the shrine was walled up again, and around 1694, while the church was under repair, two shrines were discovered in a bricked-up cavity in the eastern wall. The shrines had been robbed of their costly stones, most of the furnishing had been torn out, one had lost its lid completely and one had lost part of its lid. Both shrines were placed on ends, and the bones were partly intermingled. The shrines were walled up again in 1696 and were brought to light for the last time in 1833. Since then they have been on public display in the church. A scientific committee distributed the bones between the two shrines in 1874-75. Most of the committee members agreed that St Canute’s shrine was the one without a lid. The correctness of the distribution and the identity of the bones have occasionally been questioned. For many years it was discussed if the bones of the younger individual belonged to St Alban – whose relics had also been kept in the St Alban church – or Benedict, but a C-14 dating ruled St Alban out (3). The shrine without a lid has been dated by dendrochronology. Since sapwood was not preserved, it could only be stated that the shrine had been made after 1074 and probably before 1100 (3). It has not been possible to obtain DNA from the bones (3). The skeletons are now on display in a glass case in the crypt of St Canute’s Church in Odense. The anthropological examination The skeletons have been described in earlier investigations (4,5). Our re-examination of the skeleton presumed to belong to St Canute showed a slimly


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Figure 6: A reconstruction of the proposed injury mechanism. The weapon could have been a sword or a spear.

built man with an approximate stature of 165 – 170 cm and an age of 27 – 38 years. The surface of the bones was smooth with a pale brown colour due to preservation with Italian resin, except for the cranial vault, which had a pale gray colour. A rim of lime scale on the inside of the cranial vault may stem from the period of burial. We did not find any reason to believe that the bones belonged to more than one individual. There was a great similarity between the skeletons of the two presumed brothers. We found one lesion that seemed to be peri-mortem. This lesion was found on the sacral bone. At what more suitable place could a future saint be wounded? It was of course also noticed at the previous investigations, but the present investigation was the first to use computerized tomography. The lesion consisted of a horizontal 2.9 cm long and 3.1 mm broad infraction on the ventral surface of the 3rd sacral vertebra (fig. 2). When viewed in a stereomicroscope it could be seen that it was a so-called hinge-fracture where the fractured area of the lamina compacta was still partially attached to its original bone so that the surfaces met at an unnatural angle – not unlike the opening of a letterbox (fig. 3). On the dorsal surface there was a 15 mm long and 4 mm broad horizontal wedge-shaped crack in the median crest at the 3rd dorsal sacral foramen, with fracture lines running in both directions to these foramina. To the right and below the 3rd sacral foramen was 2 mm long fracture line (fig. 4). The CTscanning showed these two fractures to be connected (fig. 5). The fractures did not show any sign of callus formation or other bone reaction. Hinging of a fracture, such as seen in this case, is considered to indicate peri-mortem

trauma (6). The section of bone is bent away from the direction of the injuring force. Hinging can only occur if the bone is moist and contains organic material. Dry bone will snap off when acted on by a force sufficient to cause a break. There also was a 6.6 cm long vertical crack in the left side of the frontal bone in the cranium with no sign of bone reaction. It is uncertain if this is a peri-mortem or a post-mortem lesion. We did not find any other lesions. There were no defence lesions on the lower arms or hands, and no lesions of the ribs. Proposed injury mechanism What could have caused the lesion on the sacral bone? We suggest that it was caused by a thrust of a sharp instrument through the abdomen with a direction posterior and to the right (fig. 6). This interpretation is in accordance with the interpretation given by Tkocz and Jensen (4), whereas Rasmussen et al (5) consider this lesion to be the result of blunt force trauma coming from behind. There were no other sharp lesions on the pelvis, as could have been the case if the weapon had been a sword entering the pelvic cavity through the belly. The weapon could also have been a spear, which is a likely option since the rebels were peasants who were usually armed with spears. The absence of sharp force lesions on other bones could indicate that the king was wearing a chain mail. The force of the impact must have been substantial. It seems unlikely that the king was standing up when he received this lesion as a lot of the energy in the thrush would have been used to propel him back-

ward. If he on the other hand had been pushed over and received the thrust while he lay on his back, more of the energy would have been transferred to the sacral bone causing it to break. We believe that might be possible to verify the theory experimentally, and plan to do so. The idea is to embed sacral bones in ballistic gel with a thickness that corresponds to the soft tissues of the abdomen and subject these bones to a sharp force injury using copies of contemporary swords and spears. We hope it is possible to disprove or verify our theory, and perhaps even get an idea about the murder weapon – spear or sword.

If we are right, this trauma mechanism is more or less in accordance with the account given on the Tabula Othiniensis and the narrative by Elnoth, who claims that the king was “struck by a lance through his side”. The lesion would have been lethal, although not immediately lethal. It is however likely that the king received many more lesions that did not leave any marks on the skeleton. For all we know his throat may have been cut. The interested readers can view the skeletons for themselves. They are on display in a glass case in the crypt of St Canute’s Church in Odense, nicely laid out so you can se the lesions.

Reference list 1. Leth PM, Boldsen J: Skeletterne i krypten. In: Fynske Årbøger 2009, Historisk Samfund for Fyn. 2. Fenger, O: Knud den Hellige. Gyldendal og Politikens danmarkshistorie bind 4, “Kirker rejses allevegne”, 2.ed., 1993; p. 65 -68. 3. Nyberg T, Bekker-Nielsen H, Oxenvad N (eds.). Knudsbogen – studier over Knud den Hellige, Odense bys Museer, Odense, 1986. 4. Tkocz I, Jensen KR: Antropologiske undersøgelser af skelettet i skrinet med de snoede søjler. In: Knudsbogen – studier over Knud den Hellige, Odense bys Museer, Odense, 1986. 5. Rasmussen KL, Bennike P, Kjær U, Rahbek U: Integrity and characteristics of the bones of the Danish King St Knud (II) the Holy. Journal of Danish Archaeology Vol 13, 1996-97; p. 161 – 170. 6. Byers SN: Perimortem Trauma. In: Forensic Anthropology, Allyn and Bacon, 2002; p. 268 – 270.

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Kai Holst – Suicide or Murder? Per Gunnar Egeland, Sonny Björk and Jovan Rajs* ABSTRACT Active in the Norwegian Resistance Movement during WWII, Kai Holst was found shot to death in Stockholm just seven weeks after the liberation. Had he been liquidated? There were several groups with the resources to stage a suicide. Various fractions in the nations at war were well represented on the intelligence level in Stockholm, and Sweden had its own network of secret service agencies.22

Introduction On the morning of June 27, 1945, the 32-year-old Norwegian Kai Holst was found dead in an apartment complex at Gärdet in Stockholm. The gunshot wound in his right temple and the pistol in his right hand indicated suicide. The police investigation ended with that conclusion. Not everyone was satisfied with that verdict, however. Family members of the deceased and several of his friends were all convinced that he had been liquidated. Newly married and a man with many plans for the future, there was no justification that he should take his own life. A new study of the autopsy report and a reconstruction at the place of death give new insight into the case, even though this mystery from the days of the postwar is far from being solved. Due to Kai Holst’s background in the Norwegian Resistance Movement his sudden mystic death caused big newspaper headlines in Sweden and Norway. During 1942-43 he was a key figure for the leaders of the secret military organization (Milorg) that came into being in occupied Norway during WWII. The years following he worked as secretary in Milorg’s military office in Stockholm that operated under The Norwegian Legation. The organization of their courier service to Norway was his primary task up to the time when he was found dead. In addition, it is

*Per Gunnar Egeland, cooperate with Göran Elgemyr on a book planned for publication in 2011. *Sonny Björk, detective superintendent, Department of Crime Scene Investigation, Stockholm Police. *Jovan Rajs, professor emeritus, Institute of Forensic Medicine, Karolinska Institutet, Stockholm.


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known that he had an active role in the intelligence community in Stockholm.1 After suicide had been “established” in the newspapers, the matter settled down publicly until the Swedish journalist Göran Elgemyr produced a program for Swedish Radio in 1992. Reactions in Norway were expectant. The case exploded first in the Norwegian media when historian Tore Pryser and author Espen Haavardsholm wrote each their own book in 1994 in which they questioned the supposed suicide.2 They suspected foul play and pointed a finger at Sweden’s secret military intelligence agency (C-byrån), possibly in cooperation with their American colleagues. Other murder theories through the years blamed communists, Norwegian authorities, and the Gestapo. Kai Holst died in the wake of a period when there had been liquidations on a large scale in the Scandinavian countries. The German occupational power and their henchman carried out liquidations, and in Norway and Denmark we know about, respectively, 82 and approximately 400, liquidations of dangerous opponents (Nazis) that are attributable to the Resistance Movements during the war.3 Conditions in neutral Sweden were, of course, different. Even so, the warring nations were well represented on the intelligence level in Stockholm, and the Swedes also had a well organized and efficient network of secret intelligence services. That there were such organisations or even private persons who worked for them with the resources to stage Holst’s suicide, is not unthinkable. The chain of events On Wednesday, June 27, at 3:10 A.M., Holst arrived by taxi at Rindögatan 42 at Gärdet where he buzzed a Swedish friend from the intercom. This friend

later gave varying explanations to the police about whether he opened or not, but he made it clear that a meeting had not been arranged beforehand. About this time the closest neighbor to the attic corridor was giving a party that was about to break up. The neighbor then heard a bang, which he believed came from the elevator door that had been banged shut with great force; he could not definitely say if it was a pistol shot he had heard. As he was going to escort his guests out, the elevator was standing on the floor where Holst’s Swedish friend lived. Outside the building lay a rucksack and a travel bag that, as it turned out, belonged to Holst. The corpse is discovered At 9:15 A.M., the woman on gate duty discovered Holst’s body. He was found lying on the floor in the attic corridor with his head in a pool of blood. His rain coat was hanging over the railing, and in his right hand there was a loaded semi-automatic Spanish Llama 9 mm pistol. His index finger was on the trigger. In the record kept by the local Stockholm police it was stated that rigor mortis was not yet present, this was stated by the police constable who removed the pistol from the dead man’s hand. Postmortem investigation The autopsy was performed on June 30 by forensic pathologist Dr. K. G. Kling. Here follow excerpts from his report: “Body length 178 centimeters. … In the right temple just in front of and somewhat above the right ear there is a round wound 11 millimeters in diameter. Around the wound there was a black burn area six millimeters in diameter. The hair in the vicinity was not singed (fig 1a). In the left temple




Figure 1 a-d: Reconstruction of the event. 1a: Entrance wound. 1b: Exit wound 1c: Hit point of the bullet after removal of the paint. 1d: Reconstruction with figurant

region … a wound approximately 7 millimeters in diameter… (fig 1b). The wounds are connected by a channel through the cerebrum. ... The hands diffusely soiled with blackish-red coagulated blood … There were a total of up to ten penny-sized, reddish-brown scaly scrapes on the skin along the left side of the neck. …(fig 1b). No other injuries.” No toxicological analyses were undertaken. Following the autopsy, the pathologist wrote out Kai Holst’s death certificate: Vulnus sclopetarium capitis. Suicidium. In the autopsy report which he delivered to the police on July 20, Dr. Kling wrote that Holst died from gunshot wounds fired from a weapon aimed at the right temple at relatively close range, and that the bullet was directed from right to left, slightly upwards, a bit backwards. The report stated further that Holst had earlier been operated for double sided tuberculosis of the lungs, but that no recent progression of the disease could be observed and that the tuberculosis in the lungs at the time of death appeared to be healed. Any comments regarding the manner of death were not made in the report itself.


Reconstruction of the scene at Rindögatan The investigative reports include little information about the scene of death. A local police report refers only to a distinct mark from a bullet on the door to the elevator machine room, about 180 centimeters above the floor. From there the bullet ricocheted to the ceiling where it made a five centimeter long gash. Both marks had traces of blood on them. No photographs or sketches exist, and the criminal police investigators, who arrived quickly on the scene, made no written report about their technical investigation. Since the death scene is described somewhat differently by the police and

the media, we wanted to reinvestigate the scene of death. With permission from the proprietor of the building, we were ready to do a reconstruction of the death scene on May 18, 2009, nearly 64 years after Holst’s death. An open staircase winds up to a small, semi-dark rectangular attic corridor. Only light from the floor below reaches this part of the attic where there is no electricity. The door to the elevator machinery room is made of heavy metal, and exactly 186 centimeters above the floor there is a patch mark. It was just to scrape away filler and paint after a solvent had done its work for about an hour. Here we uncovered a drop-shaped diagonal indentation in the direction of the ceiling (fig 1c). A caste was made by spreading Scand J of FORENSIC SCIENCE - No 1 - 2010 - Page 1-52


a molding compound (Mikrosil) over the area. The casting that was later studied under a microscope shows that the indentation, without question, was made by a bullet. The bullet that killed Holst is still in the police archives. It was found by the woman on gate duty, on June 28, in the stairs one floor beneath the attic. The bullet is pushed in on one side, characteristic for a bullet that has ricocheted at a low angle. The bullet also has a trace of white paint or plaster, probably from the impact made when striking the ceiling. The bullet’s appearance agrees with observations at Rindögatan. In addition, the Swedish forensic crime laboratory determined already in 1945 that the bullet in question had been fired from Holst’s weapon. The laboratory investigation of the pistol may disclose some indications of the range of the shot. Absence of blood within the barrel indicates that blood and tissue have not been sucked into the barrel. This implies that it has not been a contact wound but rather a distance between muzzle and skin of approximately three centimeters. Back squirt of blood from the entrance wound has very likely happened and such small blood squirts should have been left traces on the pistol and on the hands holding the pistol, though not necessarily on the barrel of the pistol. That the pistol was still in Holst’s hand indicates nothing unusual. This may be the case in approximately one in five such incidents (SB, own observation). Regarding Holst´s position at the shooting, this could be determined on the basis of the wounds described in the autopsy report, the autopsy photographs, and Holst’s height. He probably stood a couple of decimeters out from the wall, with his head or his entire body turned about 20 degrees toward the door to the elevator machinery room at the moment the shot was fired (fig 1d and fig 2). Thus, our reconstruction confirms that Holst died on the spot where he was found. Basis for the official version The reconstruction also by and large confirms the police theory. An important testimony apparently had made it clear to the police that Holst could


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Fig. 2: Professor Jovan Rajs who has the same height as Holst in front of the hit point.

have had a motive for going straight up to the attic to shoot himself. Thus an acquaintance of Holst who worked in the Norwegian Legation, the day before the autopsy, had suggested that Holst could have committed suicide in case he had received new information that his tuberculosis had returned. In our opinion, an old tuberculosis, which the autopsy disclosed not to be active, would not be a motive for committing suicide, not under the given circumstances. Holst’s widow told the police that her husband had gone to his doctors for regular check-ups; as recently as in March or April, a doctor in Stockholm told him that his lungs were fine. If the death was due to a suicide, then it was an impulsive action, not premeditated suicide for which there was no apparent motive Even so, this interpretation has not stopped others from thinking similar thoughts. In 1994, the Norwegian media hoped that the Milorg leader and former Minister of Defense and Minister of Justice Jens Chr. Hauge might be able to shed new light on Holst’s death. They assumed that he was well informed in the matter, not least because Holst had worked closely with Hauge in the period before his escape to Sweden. But Hauge knew little more than what would become public knowledge. He was more open with his biographer. He saw no reason to doubt the official version. Hauge thought his old colleague in a state of psychologi-

cal and physical exhaustion may have believed the tuberculosis was on the return and that that was his motive for suicide.4 The Norwegian driver who brought Holst from Hamar, Norway, to Stockholm on the night in question, painted a rather morbid picture of his passenger. Just after crossing the Swedish border Holst, he said, took out a pistol which made the driver uneasy. During the entire trip he never behaved like a normal person; the driver was convinced that Holst was close to a nervous breakdown. The taxi driver who drove him further in Stockholm described him as behaving as though he were confused. The possibility of an impulsive suicide cannot therefore be put aside, even though Holst may have had no symptoms of tuberculosis. That members of the Resistance Movement later had nerve disorders was not uncommon. Alternative course of events? As pointed out by Pryser and Haavardsholm, the Norwegian driver does not appear totally reliable. During his first police interrogation, he said that Holst seemed tired, in the second he came with information that verged on defamation of character, while during the third interrogation with Norwegian police he again described Holst as being tired. And tired he was. It appears

that he had hardly slept the night before because of a raid against German criminals of war undertaken by British intelligence service. His weariness and lethargic manner can, therefore, with a little stretch of the imagination, be construed as something different. And, we might ask, could he have taken out the pistol because he experienced a feeling of threat? Might the episode with the pistol rather represent preparations for self defense than reflecting thoughts of suicide? The impression is that Holst was fully aware that someone wanted to put him out of the way. Wladimir Mørch Hansson was one of the leaders in Milorg who worked closely with Holst both in Norway and in Sweden. He confided to the author Haavardsholm that Holst had received death threats just prior to the liberation. Retired major general Ole Otto Paus took this a step further when he spoke with the same author. Paus said that prior to an intelligence meeting on the Swedish border in the early 1950s, Holst’s murderer was accidentally pointed out to him by a Swedish fiscal agent (chief constable and prosecutor). The identified man had a common Swedish name. However, this does not mean that the fiscal agent’s assertion is necessarily correct. Just as interesting is whether information indicating possible murder was ever followed up by Swedish police. The officer Paus, at any rate, took the information seriously and reported it to the chief of the military staff, lieutenant general Ole Berg (Norway’s military attaché to Sweden in 1945 and Holst’s closest boss at the time of his death). The officer was then given some ‘friendly advice’ to let the matter rest, that further investigations could be very dangerous. Others, too, were advised against private investigations, including family members of the deceased.5 Apart from the gunshot wounds, the autopsy photos focus only on the scrapes on the left side of the neck (fig 1b). The marks are difficult to interpret and Dr. Kling did not state what caused them in his autopsy report. Nor should we speculate about the omission of toxicology, even though this could have disproved the very first and most fanciful murder theory put forward by an anonymous Norwegian source to Aftonbladet on June 29. This

theory implied that the Gestapo had drugged Holst with something that put him in a hypnotic state, and that it was while he was in this state that he shot himself. All this opens the way for an alternative chain of events. In that case the firing position could not exclude an execution. It is somewhat uncertain what took place from the time Holst entered the front door until he was found dead six hours later. Neither the criminal police investigators nor the doctor who pronounced him dead left any written records concerning the dead body. Furthermore, it should be noted that there is no forensic evidence indicating that Holst had shot himself. Suicide versus homicide From the medico legal point of view Kai Holst’s cause of death is indisputable – craniocerebral injury caused by a projectile fired from a handgun. His manner of death, that is, whether it was an accident, suicide or murder, is more problematic. All forensic pathologists have experienced that a death initially determined to be the result of an accident or suicide may later turn out to have been homicide. Or that a murder may be suspected, without a chance of finding positive proof. The initial assessment is generally based on bona fide reports of varying quality and insight, or it may be built on intentionally misleading or false information concerning the deceased. The same may be true for forensic autopsies and (in particular) toxicological investigations. The problem is not made

any simpler when various networks, government security services and various criminal groups are brought into the picture. Moreover, most forensic experts have inadequate knowledge about the methods and techniques of professional assassins. Thus, it is just as unwise to rely unreservedly on “objective” autopsy findings as it is to underestimate the knowledge and intelligence of the murderer. Holst’s autopsy has been assessed as being professional, correct, and well documented, although there is no photo of the entrance wound with shaved hair in its vicinity. What should a pathologist conclude about a manner of death after finding a gunshot wound on the right temple with a bullet channel directed toward the left, backwards, and upwards? And when he learns that the deceased was right handed, that a pistol was found in his right hand, and that his raincoat was neatly placed over the stair railing when he was being found six floors up? Forensic pathologists do not necessarily care whether there is a suicide note or not. Suicide, concluded Dr. Kling on Kai Holst’s death certificate, which he filled out as soon as he had completed the autopsy. But three weeks later, when the investigations were finished and he wrote the autopsy report, he left out routine formula regarding the manner of death. That he omitted this may indicate that he had some new doubts or that he may have felt some dissatisfaction with the police. He could have realized that the shot injury was not a contact shot, but a “relatively close range shot” as indicated by absence of singed hair and by

Fig. 3: Execution of a Vietcong prisoner. The revolver is directed to the right temple, left-back-up, typically for suicide. The shot distance is estimated to 15 cm (facsimile of Eddie Adams’ photo from 1968: Richard Lacayo and George Russell “Eyewitness: 150 years of photojournalism” (1995)). Scand J of FORENSIC SCIENCE - No 1 - 2010 - Page 1-52


the fact that the entrance wound was small and quite round, which suggests the gun could have been fired from a distance longer than about three centimeters. Having in mind the absence of gun powder and singed hair in the wound´s vicinity, the “black burn area six millimeters in diameter” could just have been a black abrasion collar of an entrance shot wound. Also, that the finding of the pistol in Holst´s right hand could not easily be understood as a genuine cadaver spasm with a firm grip on the pistol, and that neither the police report nor Holst’s history of illness revealed a motive for suicide. Quite the contrary the closest of kin adamantly rejected any motive for suicide. Perhaps Kling understood that Holst was involved in sensitive missions for the Norwegian Resistance Movement. When in an intricate case the pathologist feels uncertainty, it is wisest to leave the manner of death out of the autopsy report. If the police officer who is responsible for the investigation is not aware of it, or will not do it, then the pathologist’s honor is still saved. These words are written by one (JR), who at the time of writing has 50 year’s experience as a forensic pathologist in several countries with varying political and legal systems.


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But even if it had been a matter of a contact shot, this is not decisive for being a matter of suicide. It is well known that liquidations, even mass liquidations during the wartime, took place as contact shots. The position of the gunshot wound should be of great interest. Druid (1997) showed that 38 percent of the gunshot wounds resulting from homicides had entered the victims at anatomical regions typical of suicide. The same author pointed out that the direction of the bullet path was more important than its location. Also, when the entrance wound in the right temple indicated suicide, divergent direction than the typical front-to-backdirection suggested that the wound was more likely to be homicidal.6 Holst’s bullet hole met these criteria, with the minimal deviation, if any, that it was pointed just a bit backwards. With incomplete or wrong information, many pathologists would classify one of the twentieth century’s most documented executions as suicide (fig 3). Neither statistics, clichés called “forensic experience” or great personal experience, can be determinative for the differential diagnosis suicide versus homicide, when the circumstances about a death and other background information are shrouded in darkness.

Conclusion In the case of Kai Holst’s death, we are left with three probabilities: in the judgment of the police, Holst committed suicide; the death may have been the result of murder, never disclosed by the police; or the police understood relatively early that they were dealing with a fait accompli with so-called political implications. Translated by Harry T. Cleven

REFERENCES Tore Pryser, Svik og gråsoner (2010) Tore Pryser, Fra varm til kald krig (1994) and Espen Haavardsholm, Ikke søkt av sol (1994) 3 Arnfinn Moland, Over grensen? and Peter Øvig Knudsen, Etter drapet (Norwegian version 2003) 4 Olav Njølstad, Jens Chr. Hauge - Fullt og helt (2008). pp. 566-567 5 Espen Haavardsholm, Taushetens pris. Et essay til frigjøringsjubileet (1995) p. 54 ff 6 H. Druid, ”Site of entrance wound and direction of bullet path in firearm fatalities as indicators of homicide versus suicide” (Forensic Science International 88-1997) 1


The Mysterious Death of Politician Nils Traedal:

Accident or Homicide? By Johan J. Jakobsen, Former MP

On March 10, 1948, The Czechoslovakian foreign minister Jan Masaryk fell from his office window in Prague. Acting president Nils Trædal held the memorial speech in the Norwegian Parliament leaving little doubt that Masaryk died for his convictions. Seven months later Trædal who was advocating a strong national defense and Norwegian membership in NATO, was found seriously injured beneath a window in the apartment building where he lived. For more than sixty years the death of Trædal has been an enigma.

During the early hours of October 12, 1948, the well-known leader of the Agrarian Party, Nils Traedal, was pronounced dead at Ullevål Hospital. Late the previous evening he had been found unconscious with serious injuries in the backyard of his apartment building at Holtegaten 30 in Oslo, where he rented a room on the fourth floor. To all appearances, he had fallen out of a stairway window located 6.6 meters above ground. That evening he had attended a board meeting of the newspaper Nationen. Following the meeting he had dined at a restaurant with the party’s secretary general, Hans Holten. The landlord, Alf Killingmo, who had heard some strange sounds from the staircase and backyard, found Traedal in a state of unconsciousness with blood flowing from his head. He called an ambulance and Traedal was soon receiving medical treatment at Ullevål Hospital. But shortly after being admitted, the well-known politician died without regaining consciousness. The death certificate issued by the Oslo Board of Health, sent to the municipal doctor at Støren, where Nils Traedal was a legal resident, gave the following cause of death: Fraktura Cranii, Contusio Cerebralie (Cerebralis) – in other words, a fractured skull and brain damage.(1) During the decades since, a cloud of mystery has shrouded the events of that evening when the clergyman-politician was found dying at Holtegaten 30. Already at the funeral services held in Støren on October 19, rumors were circulating that Traedal might have been assassinated. People speculated about many things: There were those, for example, who drew a connection

between the death and the evaluation in Parliament of the Investigative Commission’s report(2), the so-called Hviteboken (White Book) on the role played by the Parliament and the Government during the German occupation of Norway. Others believed that Traedal’s death was related to internal conflicts in the Resistance movement during the closing phase of the war, a conflict in which Traedel had also played a part. During the war, Traedal had been a member of the intelligence organization XU. Still others strongly believed that Traedel, who supported a strong national defense and Norwegian membership in NATO, had been liquidated by Communists who had reacted strongly to a confrontation Traedal had had with NATO opponents in Parliament during the spring of 1948. Traedal had probably also contributed to speculations that his death was politically motivated. When foreign minister Jan Masaryk “fell” from his office window in Prague on March 10, 1948, it was Traedal, as acting president of the Parliament, who held the memorial speech. He left little doubt about what lay behind Masaryk’s death: “Such circumstances tell without words more than anything what it sometimes costs to fight for your convictions!” From the late 1970s to the end of the twentieth century, numerous articles and interviews appeared which described the death of the leader of the Agrarian Party as “suspicious” and “curious.” When I began work on Nils Traedal’s biography with his family’s blessing in 2002, my purpose was twofold. First, I wanted to dust off his memory, because I feel he deserves a greater place in our

political history. Second, I wanted to try to find the answer to a nagging question: namely, was Traedal’s death the result of a political assassination or an accident? It is the latter question that I wish to focus on in this article. There were two things in particular that added to the mystery and that fueled the theories that Traedal’s death was political: the assertion that the death of the politician had never been properly investigated by the police and the claim that no autopsy had been performed on Traedal’s corpse. Reliable documentation existed that supported both these assertions. The keeper of national records in Oslo had, on March 22, 1999, responded as follows to a query from historian May-

Nils Traedal.

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Johan J. Jacobsen (author), Bjørn Davan (police superintendent), Torleiv O. Rognum ( prof. of forensic medicine) and Roald Muggerud & Ragnar Thorset who lived in the building in 1948. Brith Ohman Nielsen: “Neither the accident at Holtegaten on October 11, 1948, nor Nils Traedal’s death was ever recorded in the journal of the Oslo police district at that time.”(3) I went to the National Archives on November 24, 2004, to check if any information regarding the accident had been recorded at the Hegdehaugen police station. Several days later I received an interesting, not to say astounding, letter from the National Archives(4) – and keep in mind the reply that had been made to the aforementioned historian. The letter states: “The Oslo Police District was, of course, brought in to the case of Traedal’s death in accordance with regulations concerning cases of accidental death. The death, however, was not recorded in the journal, either centrally, in the homicide division, or at Hegdehaugen police station. Nor was it entered in the ordinary book of police records, since the death was not classified as ‘a mysterious death.’” At the same time I was informed that some investigations had been made and several people questioned, and that all the case documents, twelve in all, including photographs from the “crime scene,” were stored in the National Archives. One of these documents turned out to be the autopsy report from Ullevål Hospital! According to the historian Ohman-Nielsen, the report from Ullevål Hospital states


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that “No medical examinations were performed on him [Traedal] that could clarify what had taken place.” I contacted the information officer at the Oslo Police District, Jørn-Kr. Jørgensen, who advised me to get in touch with Professor Torleiv Ole Rognum at the Institute of Forensic Medicine (Rettsmedisinsk institutt). That proved to be good advice. Only a few days after I had contacted Rognum, I was informed that an autopsy had been carried out on Traedal at Ullevål Hospital and thus, of course, there was an autopsy report. In the course of only a few days I had been informed by two separate sources – the National Archives and Ullevål Hospital – that an autopsy had taken place and that the autopsy report was available, both at Ullevål Hospital and in the National Archives. In addition, it was now clear that the police had investigated the case and had questioned certain individuals, and that twelve documents relating to these interviews were available in the National Archives. These two important sets of records related to the death had been safely stored in these institutions for 56 years. I shall not go into more detail about the significance these facts would have had on the mystery, the creation of a myth, and the speculations in the wake of Nils Traedal’s death in 1948. The question now was how the

available material from the National Archives and Ullevål Hospital could help to shed light on what had taken place on that tragic evening at Holtegaten 30. I should mention that I had also managed to find a living person who had resided in the same building as Traedal in 1948. The information the then 17-year-old Roald Muggerud had given the police during the interrogation on the night of the tragedy in 1948, and his conversations with the undersigned in 2005, shed new light on what happened on the stairway on that fatal evening. Roald Muggerud had lived on the third floor, with his bedroom adjoining the stairway, and so he had heard Traedal when he came up the stairs. He also says that it was common knowledge to the residents whose apartments opened onto that same stairway that Traedal had respiratory problems, and that halfway up the stairs to his living quarters he would pause to rest. That was also the case on the evening in question. Roald heard the familiar footsteps on the way up to the fourth floor. Traedal stopped, as he usually did, and Roald heard the politician putter with something on the other side of the wall and heard the window move. He did not hear the fall, but a few moments later he heard voices down in the backyard. The 17-year-old went to the kitchen and, looking out the window, saw a person lying on the asphalt below. According to the reports from the Oslo police, Roald’s father, Olai Muggerud, called the criminal division at 12:30 A.M. to report that a man had just fallen from a window at Holtegaten 30, and that the emergency ward had been informed. When the police arrived on the scene “the emergency medical crew members were removing the injured man.” The course of events was described thus: “The injured man, as he ascended the stairs, for some reason or another, lost his balance and fell against the window.” It was also pointed out that the window on the left-hand side was open and that the storm hook was not in place. The autopsy report begins with a reference to the patient’s journal, which states that Nils Traedal fell from a window and died just after being admitted to Ward II of Ullevål Hospital. It also refers to the police report in

stating that “the deceased had fallen out of the window in the stairway between the second and third stories into the backyard. This was covered with asphalt.” The report makes it perfectly clear that the impact with the asphalt in the backyard was very forceful. The autopsy revealed “numerous splintered fractures on, practically speaking, the entire skull. The fractures are largest on the frontal area of the skull, and on the left side.” The left thigh bone was broken as well as ten ribs, and, in addition, the pelvic bone was broken in four places. The autopsy report states that “death resulted from these injuries. These injuries resulted, in all likelihood, from a fall from a great height.” The report concludes with the following somewhat surprising passage: “The blood test reveals that the deceased was intoxicated when the accident occurred.” The autopsy report was signed by Dr. Johan Hertzberg on October 20, 1948. The blood sample taken by Dr. Hertzberg at the time of the autopsy was analyzed at the University Pharmacological Institute. The result, according to a letter sent to the Oslo police and dated October 15, revealed “a content of volatile reducing compounds corresponding to 1.79 promille alcohol.” The letter is signed by Jacob Molland, M.D. I asked Director Jørg Mørland at the National Institute of Public Health Division of forensic toxicology whether the result of such tests carried out in 1948 can be compared directly with the results of today’s tests. With regard to the finding of 1.79 promille alcohol, Mørland replied that an analysis using current methods “would most likely have given a result somewhere between 1.6 and 1.9 promille.” But Mørland adds that methods then were relatively unspecific, and that also substances other than alcohol could have influenced the result, in whole or in part. He further states that the formulation that appears in the report, “volatile reducing compounds corresponding to …,” indicates that volatile compounds other than alcohol could have led to the same test result. Mørland notes that acetone or ketone bodies, which are formed in the bodies of people who have diabetes, can be interpreted as alcohol in an analysis that measures the content of “volatile reducing

compounds.” There is, however, no evidence that Nils Traedal was diabetic. Following the publication of my biography in the autumn of 2005, I was contacted by an acquaintance of mine, Professor Emeritus Dr. Torstein Hovig, who had read Mørland’s evaluation of the analytical methods employed in Rognum and the author inspect the window. 1948 as compared with today’s methods with interest and professional insight. Hovig is of the opinion that the time factor must also be taken into consideration – the time, that is, which elapsed from the moment of death until the taking of the blood sample. He states that it is a known fact that a promille level can be too high if there is a long time lapse between The back yard seen from the window. the time of death and the taking of the blood sample. Even though there are few specific references to time in the documents available in the National Archives and the Oslo Police District, there are some good clues: the Criminal Division received the telephone call from Olai Muggerud reporting the accident at 12:30 A.M. As I have pointed out, the elder Muggerud also informed the police at The place were Traedal was found dying. that time that he had aldeath occurred until the blood sample ready summoned an ambulance. When was taken. the police arrived on the scene, the Professor Jørg Mørland, in a new medical people were about to remove statement dated February 5, 2010, says the accident victim. Traedal was taken that the measured level of alcohol may in the ambulance and, according to Johave been somewhat higher than the han Hertzberg, died just after being adconcentration of alcohol Traedal had mitted to Ward II at Ullevål Hospital. in his blood when he fell. Mørland beDr. Jacob Molland of the Pharmacolieves there are two possible reasons for logical Institute states that Dr. Hertzthis: berg took the blood sample in question “The one is that the fall trauma at 11:45 A.M. on October 12. On the caused considerable physical damage basis of this information, a maximum so that the possibility existed for the of 9 to 10 hours elapsed from the time Scand J of FORENSIC SCIENCE - No 1 - 2010 - Page 1-52


transfer of bacteria to the blood to a far greater degree than would normally occur, and that therefore, to a much greater degree than otherwise, alcohol was produced from glucose. Thus, a more pronounced postmortem formation of alcohol than otherwise, which can explain some of the measured alcohol content, even though the time that was available for the formation of alcohol was relatively short. “The other is that he may possibly have had unabsorbed alcohol in his stomach after visiting the restaurant a relatively short time earlier. The alcohol in his stomach, a relatively short time after his death, may have seeped into nearby tissue, and here a considerable trauma may have affected this more than would otherwise be the case. If the blood sample was taken from blood in the heart (or the periphery), it is possible that the resulting concentration of alcohol was too high due to postmortem contamination. “In conclusion, it should be mentioned that there is evidence that in extreme cases postmortem alcohol formation, with levels of alcohol concentration in the blood up to 1.9 promille, and higher may occur in persons who, apparently, had no alcohol in their blood at the time of death”(5,6). It is a known fact that Nils Traedal was not a teetotaller. Secretary General Holten says in his testimony that he and Traedal had drunk “coffee and a glass of beer” at the restaurant before calling it an evening and that Traedal had taken the Briskeby tram home to Holtegaten. We should keep in mind, however, that the expression “to have a glass of beer” is also popularly used to mean more than a single glass. It is possible that in using the singular form, Holten wished to protect his good friend. But it is also an established fact that Traedal was never known to drink much alcohol. Odd Bye, a retired editor who knew Traedal well, says that he never saw him intoxicated. Toward the completion of my biography of Traedal, I had the help of many good assistants to whom I owe a great debt of gratitude. In the winter of 2005 “these good helpers” and the author agreed that they would try to reconstruct the tragic occurrence. Because the “scene of the crime” – including the backyard, stairway and windows – had not changed essentially


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The window frame where Traedal may have sat down to rest.

The window seen from the back yard.

since 1948, Torleiv Ole Rognum suggested that we carry out an investigation of the scene. It was a sizeable group that gathered on February 15 at Holtegaten 30 to do this: Professor Torleiv Ole Rognum was there from the Institute of Forensic Medicine, as were the crime technician Bjørn Davan and the information officer Jørn-Kr. Jørgensen, both of the Oslo police. In addition, two persons who had lived in the same building in 1948, retirees named Ragnar Thorsen and Roald Muggerud, the latter of whom had been an engineer, joined the group, as did the undersigned. The purpose of the investigation, as Professor Rognum put it, was “to reconstruct the chain of events in light of the autopsy report and investigations carried out at the scene.” Following the inspection of the scene, Rognum wrote a four-page report. The autopsy had revealed that the injuries Traedal had received were the result of the fall from the window between the second and third floors. That he ascended the stairs and that he stopped, possibly in order to catch his breath, are confirmed both by the landlord Alf Killingmo and Roald Muggerud. Those present at the investigation of the scene were in agreement that the wide windowsill would be inviting to a tired and dizzy person who might wish to sit down in order to “catch his

wind.” Crime technician Bjørn Davan, who “test sat” the windowsill, felt that he acquired quite a comfortable sitting position with his legs placed on a step approximately 40 centimeters lower than the windowsill (see photos). The window between the second and third floors was not latched with a storm hook. Normally, it would have been shut, but Thorsen explained that it sometimes was kept open in order to air out the stairwell. In the church register for Støren parish, Nils Traedal’s widow, Gunda, wrote the following: “The storm hooks had apparently not been fastened, as I often saw was the case when I was there on visits.” It may also be that Traedal himself had opened the window in order to breathe fresh air. Professor Rognum writes as follows in his crime scene report: “The window was normally closed, it seems, but it is thinkable that the storm hooks were unlatched from time to time so that the window could yield to pressure against it. Because he felt that he needed air, it is not inconceivable that Traedal himself could have opened the window. The temperature that night was relatively mild for that time of year (7 - 8 degrees Celsius), and thus it would not be unnatural to open the window in the stairway.” In his report, Rognum writes that the autopsy report shows that there was a severe injury on the left side of Traedal’s forehead, numerous cra-

nial fractures (also on the left side), a fracture on the left thigh bone, several broken ribs, and a number of other fractures, including several fractures of the pelvic bone. Regarding the connection between the fall and the injuries, Professor Rognum writes as follows: “If Traedal sat down to rest, with his left side toward the open window, he could very well have fallen out of the window even though the height of the window is only 120 centimeters. A combination of dizziness, shortness of breath, and some degree of intoxication could have resulted in him losing his balance. If Traedal fell from this position down into the yard, the point of impact could very well have been the left side of his forehead/temple, chest and pelvis. The injuries described in the autopsy report are consistent with a fall such as that described above.” In a report prepared after the inspection of the scene, crime technician Bjørn Davan writes that the placement of the window in relation to the stairs “increases the possibility that a person quite easily could fall out if the window is open and the person either sits in the opening, leans against the opening, or falls against it in an unguarded moment, or loses his balance.” The investigation of the scene and input from experts in both forensic science and crime technology have helped to clarify the succession of events which led to the death of Nils Traedal at the height of his political career. A number of allegations and theories which for close to 60 years had fueled rumors and astounding conclusions have proven to be incorrect. The new information and testimony place the ”Traedal case” in a new light that can be summarized as follows:

• Traedal’s death was investigated by the police “in accordance with the procedures set down in the case of death caused by accidents,” to quote the letter in the National Archives • The police requested that an autopsy be performed on Traedal, and an autopsy report does exist • A new witness, living today, was able to assure the police on the very night that Nils Traedal died that he had heard Traedal ascend the stairs, that Traedal had been alone, and that due to breathing difficulties he had stopped to rest between the second and third floors. Further, there are statements from two of Traedal’s colleagues in the Parliament, Elisæus Vatnaland and Amund R. Skarholt, testifying that Traedal suffered from dizzy spells • It must also be taken into consideration, on the basis of the autopsy report, that Nils Traedal had quite a high level of alcohol in his blood (1.79 promille) • Professor of forensic medicine Torleiv Ole Rognum concludes in his report that a new look at the evidence weakens the theories that Nils Traedal was murdered Unexplainable deaths may often be the result of suicide. Those who knew Nils Traedal well dismiss categorically speculations about a possible suicide. Not only because of his Christian convictions, but also because a leap from a height of six to seven meters would be a rather dubious way of committing suicide. On the basis of new evidence that came to light through close cooperation among persons with broad expertise in criminal technology and fo-

rensic science as well as through new testimony, my conclusion is that Nils Traedal, beyond doubt, died as the result of a tragic accident. One of Norway’s leading criminal technicians, police superintendent Bjørn Davan of the Oslo Police District, who has examined the evidence and who participated in the investigation of the crime scene, has drawn the same conclusion. Davan, who has more than 20 years’ experience as a criminal technician, concludes his report as follows: “There is no evidence in the case which, in my opinion, indicates anything criminal.” Translated by Harry T. Cleven Notes 1) Jakobsen, Johan J., Makten og æren (The Power and the Glory). Biography of Nils Trædal, Gyldendal, 2005. 2) Stortinget (Norwegian Parliament). Regjeringen og hjemmefronten under krigen (The Government and Resistance Movement During the War), Aschehoug & Co, 1948. 3) May-Brith Ohman Nielsen, Senterpartiets historie 1920-1959 (History of the Agrarian Party 1920-1959), Bondekamp om markedsmakt (Agrarian Struggle and Market Power), Det norske samlaget, 2001. 4) National Archives. Twelve documents related to the death of Nils Traedal, including the autopsy report from Ullevål Hospital dated October 20, l948 and miscellaneous police reports and photographs. 5) Høyset G et al. Int j Legal Med (2000) 122: 63-66. 6) Kugelberg FC, AW Jones. Forensic Sci Int (2007) 165: 10-29. 7) Professor Torleiv Ole Rognum, Åstedsbefaring i Holtegaten 30 (Investigating the Crime Scene at Holtegaten 30), 15/2 2005. 8) Forensic technician Bjørn Davan, Rapport / vurdering (Report / Evaluation), April 6, 2005.

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Conspiracy of one The assassination of John Fitzgerald Kennedy. Olav Gunnar Ballo, MD

Managing director Institute of Forensic Medicine Oslo, Norway

The 35th President of USA, John F. Kennedy, was assassinated on 22nd of November 1963 in Dallas, Texas. Although the murder has been thoroughly examined by American authorities, starting with the investigation of a commission led by the Chief Justice of American High Court; Earl Warren, rumours of a conspiracy with an involvement of many conspirators has lived on for nearly 50 years. Does the evidence, including the result of the autopsy, support that view?

On the 21st and 22nd of November 1963 Kennedy and his wife Jacqueline made a visit to Texas as a preparation for the upcoming Presidential Elections the following year. From November 22nd the Presidential couple stayed overnight in Forth Worth. Before noon on the 22nd they were transported by the Presidential airplane Air Force One to the airport in Dallas. The plane landed at Love Field at 11:40 a.m. c.s.t. For the visit in Dallas a motorcade route had been planned from the airport through downtown Dallas to The Trade Mart, where Kennedy was to hold a speech at a luncheon at 12.30. The total length of the route was 16 kilometres, and the planned time for the drive was 45 minutes. The route was presented in the Dallas Times-Herald on November 15th, with new details the following day. On November 19th the Times-Herald afternoon paper detailed the precise route. The Morning News reported corresponding details on the same date. The motorcade followed the route presented by the two newspapers, and made it possible for a sniper to plan for an assassination on the President along this route. (1) The motorcade through Dallas On arrival at the airport the Presidential couple were, among others, met by Vice president Lyndon Baines Johnsen and Texas Governor John Connally and their wives. For the motorcade the couples Kennedy and Connally were seated in the Presidential Limousine, a specially designed Ford Lincoln Continental with two collapsible jump seats


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between the front and rear seats. The President sat on the right rear seat, and his wife in the seat to his left. Connally was placed in the jump seat directly in front of the President, and his wife on the left jump seat, directly in front of Mrs Kennedy. The car was outfitted with a clear plastic bubbletop. It was neither bulletproof nor bullet resistant. There had been rain showers before the President arrived, but because the skies had cleared the bubbletop was not mounted on the car. This corresponded with the wish of the President to be seen by as many as possible while travelling in the motorcade. (2) The cars left Love Field shortly after 11:50 a.m., and drove at speeds between 40 and 50 km/hour in the thinly populated areas on the outskirts of Dallas. Following wishes from the President, the car stopped twice. By both stops Secret Service agents ran up front from running boards on the Follow up car to protect Kennedy from any intimidation from the crowd, but during the two brief stops no incidents did occur. The shots At 12:30 p.m. the Presidentâ&#x20AC;&#x2DC;s open limousine reached Elm Street through a curve from Houston Street, passed The Texas School Book Depository on the cars Figure 1. Exit wound obliterated by the tracheotomy-incision: Kennedy on autopsy table at Bethesda Hospital.

right side and was heading towards a triple underpass when shots were fired towards the motorcade. Connally, who was a trained rifle shooter, heard the first shot. In his testimony to the Warren Commission he told that he immediately thought that what he heard was a rifle shot, that it was an assassination attempt, and that the shot came from behind the Presidential limousine he was sitting in. He turned to his right to look behind his shoulder, but without seeing the President, he started turning back to the left when he felt a strong pain in his back. (3) The shot that hit him, had, according to the Warren Commission Report, at first hit Kennedy in the back of his neck, bruised his right lung, ripped his windpipe, and exited at his throat, nicking the not of his tie (figure 1). Then it continued through Connallys back, chest, right wrist and left thigh, were the bullet stopped right under the skin. (4) (Figure 2) Connally witnessed to the Commission that he was sure the first shot missed him, and that the second shot hit him. He did not hear the second

Figure 2. Connallys wounds as marked on a sketch by the doctors at Parkland Hospital.

shot, which corresponded with his testimony, since a high velocity bullet travels above the speed of sound, and will hit its target before the sound wave from the shot will reach the same target. (5) Jacqueline Kennedy looked to her left while waving to the crowd when she heard what she thought was a backfire from a motorcycle. Shortly afterwards she heard an outcry from governor Connally, which made her turn to her right. She then saw a quizzical look on her husbands face as he raised his left hand to his throat. (6) While looking at her husband she heard another shot and saw parts of the Presidentâ&#x20AC;&#x2122;s skull explode by the impact of the bullet. Fractures of bone, blood and brain matter were blown towards her and stained her dress. (Figure 3) Witnesses to the shooting The passengers in the first cars in the motorcade later witnessed to the Warren Commission that the shots came from the rear and from the right, the general direction of The Texas School Book Depository Building. None of the passengers saw the shots being fired. But different other witnesses saw the gunman before, during, and directly after the shooting.

Howard L. Brennan, 45 years old, watched the motorcade standing on a concrete wall at the southeast corner of Elm and Houston, with a clear view to the Depository Building. Before the motorcade arrived he noticed a man at the southeast corner window of the sixth floor. Soon after the Presidentâ&#x20AC;&#x2122;s car had passed the curve where Brennan stood he heard an explosion. He looked up, and saw a man in the window aiming with a gun, and shooting down Elm Street towards the Underpass. He then saw the man draw the gun back from the window and disappear. Amos Lee Euins faced the Depository Building as the motorcade turned the corner at Elm and Houston. When he heard the first shot he looked around, then up, and saw the gunman fire his next shot. (7) Other witnesses made the same description, and picked the same window as the point from were the shots came. Based on the witnesses the police could send out a description of the man. (8) Two men watched the motorcade from the fifth floor of the depository, directly underneath the southeast corner window. During the shooting, they heard the shots from directly above their heads. Afterwards they described to the police the sounds of the ejected bullet

shells falling to the floor above them. (9) The Warren Commission later made a test from the same standing position, while a gunman fired a rifle from the sixth floor window. The witnesses then could hear the same sound, from the spent shells falling to the wooden floor above their heads. (10) Parkland Hospital The hospital had been alarmed through radio reports from the motorcade, and trauma rooms 1 and 2 were prepared before the arrival. Connally had lost consciousness during the short trip, but woke up as he was lifted out of the car onto a stretcher, describing severe pain. Kennedy was brought in from the car to Trauma Room 1 on a stretcher, transported on his back, where he was examined by Dr. Charles J. Carrico, a resident in general surgery. Carrico found that Kennedy was in a deep coma, with no vital signs of life other than a slow spasmodic, agonal respiration without any coordination and no voluntary movements, eyes open with dilated pupils without any reaction to light, no palpable pulsation, but a few chest sounds thought to be heart beats.

Figure 3. Stills from the Zapruder film showing the impact of the bullet hitting Kennedy in the head.

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On the basis of the findings Carrico concluded that Kennedy was still alive. (11) He noted two wounds; a small bullet wound in the front lower neck, and an extensive wound in the right part of the President‘s head above the ear, where a sizeable portion of the skull was missing. Inside the wound most of the right part of the brain was missing. Carrico felt the back of the President‘s head, without finding any signs of large wounds at this part of the body. To secure free airways he put an endotracheal tube down Kennedy’s throat past the neck injury, inflated the cuff and connected it to a Bennett machine for assisted respiration. (12) Because of the connecting medical equipment and the necessary lifesaving treatment, Kennedy was kept on his back on the stretcher, and was never turned around as long as his body stayed at Parkland Hospital. (13) Other members of the medical staff came into Trauma Room 1 and started assisting Dr Carrico with first aid treatment of the President. Dr Malcolm O. Perry, a trained surgeon, played a major role in the treatment. To achieve free airways Perry performed a tracheotomy through the gunshot wound on the front of the neck. The operation took 3 to 5 minutes to fulfil. (14) The doctors Carrico and Ronald Jones made incisions in Kennedy’s right leg and left arm, after which blood type 0 Rh minus and a Ringerlactat infusion were given simultaneously. 300mg Solu Cortef was administrated by Kennedy’s private physician George Burkley, who knew the President had Addison’s disease, and therefore now was in urgent need of corticosteroids as a substitution for lack of adrenal production through the suprarenal capsules. (15) Although the treatment for a short time made it possible to feel a peripheral pulse on the carotid and radial arteries, the massive head wound, inconsistent with further life, made all lifesaving measures fruitless. After last rites were administered to the President, John F. Kennedy was pronounced dead at close to 1 o‘clock, under half an hour after the shots had been fired. (16)


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a false name, photos in his wife‘s possession showed Oswald with the gun, and his palm print was found on the rifle barrel. (22) (Figure 4) The bullets used in the Tippit slaying matched the revolver he carried, and five witnesses identified Oswald as the gunman of the Tippit murder in the same night. (23) Oswald was arrested only 1 hour and 15 minutes after Kennedy and Connally were shot; at 1:45 p.m.

The travel back to Washington Figure 5. The shot that hit Kennedy in the neck.

The hunt and arrest of the presumed assassin The Dallas Police officer J.D. Tippit stopped his car and went outside to talk to a person he had spotted at 1.16 p.m. The man then shot several shots towards Tippit with a revolver, and killed him on the spot. He then ran away, but brought the pistol with him. (17) At least twelve people saw the man shoot or leave the shooting scene, and gave the police a precise description of the gunman. (18) Shortly afterwards the shoe salesman Johnny Calvin Brewer heard police sirens and then saw a person who seemed to cover himself from the police, behaving suspiciously. This person then went into Texas Theatre without buying a ticket. Brewer had heard about the assassination of Kennedy and, directly before leaving the shoe store, also about the killing of Tippit on the radio. By phone he alarmed the police, who arrived very soon afterwards. Armed police went into the cinema. There Brewer picked out the man, and the police took hold of him. (19) The suspect had a revolver, and tried to fire it against one of the policemen. He was brought into custody, denying presenting his identity to the police. He was identified as Lee Harvey Oswald. (20) During the night both the rifle found at the sixth floor of Texas School Book Depository and the revolver he carried could be identified as his own. (21) Though ordered under

A presidential assassination was to be treated as a local crime in 1963 (American law was later changed to consider it a federal crime) (24), and the whole investigation, including the autopsy, was to take place through orders of the Dallas Police. But Secret Service, under support of Lyndon B. Johnson, insisted on the transport of the body back to Washington, to have the autopsy performed there. (25) A coffin was obtained, and although officials from Dallas County strongly opposed, by the help of Secret Service the coffin was transported to Love Field where it was loaded aboard Air Force One at 2.15. p.m. (26) The new President was sworn in at 2.38 p.m. 9 minutes later the airplane left for Washington. Aboard the plane were Jacqueline Kennedy, the new Presidential couple, and members of

Figure 6. The shot that killed Kennedy.

staff for the late and the new President. So was Kennedy’s personal physician, Admiral George Burkley. While travelling back to Washington Mrs Kennedy was explained by Burkley that an autopsy was needed. (27) The widow was still in her blooded clothes, which she insisted on not taking off, and all people around her where strongly affected by the tragic events they had lived through. She was given a choice between the Naval Medical Center at Bethesda Hospital in Maryland and the Army‘s Walter Reed Hospital in Washington DC. Since Kennedy had served the navy as an officer, Mrs Kennedy chose Bethesda Hospital for the autopsy. (28) None among the party made any second thoughts about the choice, although the autopsies at Bethesda were medical autopsies, with the intention of finding the cause of death to patients dying in the hospital, and not autopsies made for the court in order to solve murder cases. This distinction, although important for the quality and result of the autopsy, seemed to have been lost to all participants involved in the decision, not through evil will, but through absent and distressed minds. The autopsy The autopsy at Bethesda Naval Hospital was led by pathologist James J. Humes, under assistance of Thornton Boswell and Pierre A. Finck. Only Finck had any experience with gunshot wounds, none of the three pathologists were forensic experts. (29) During the autopsy both the diseased Presidents´ brother; Robert F. Kennedy, and Jacqueline Kennedy, waited in the hospital for the autopsy to finish. While they waited RFK repeatedly asked when it would end, so they could bring the corpse to the White House as planned. This made a stress on the doctors who performed the autopsy. RFK also asked them to find the reason for death, but not to do more than what was needed for these findings. Such demands made further restrictions for the pathologists that were to have consequences for the result of the autopsy. (30) By the autopsy a 7 x 4 millimetre oval wound was found on the upper right posterior thorax just above the upper border of the scapula. The

Figure 7. The view from the sixth floor window of the Texas School Book Depository as seen through the telescopic sight of Oswald’s rifle.

wound was measured to be 14 cm from the tip of the right acromion process and 14 cm below the tip of the right mastoid process. In the low anterior neck at approximately the level of the third and fourth tracheal rings a 6.5 cm transverse wound with widely gaping irregular edges was found. (31) In the night the pathologists concluded that the cause of death was a gunshot to the head from behind and above, with a small entrance wound, in the lower, right occipital region, and a massive, gaping exit wound above the right ear, with approximately 70% of the right part of the brain missing as a consequence of the gunshot. Several pieces of the scull were missing, and the exit opening measured appr. 13 centimetres in diameter at its widest, with rugged edges from loose bony parts, only kept together by the overlaying skin. (32) The tracheotomy incision was described as such, but the exit wound caused by the bullet entering through the back of the neck was not identified during the autopsy (figure 5). The bullet path through the soft tissue was not explored and thereby not identified. (33) Because the pathologists could not find any exit wound for the bullet shot in the back neck, they speculated that the bullet could have stopped a short way under the skin, and then fallen off on the stretcher, after the President was placed on his back for life saving treatment. They had heard beforehand from Parkland Hospital that at a bullet had been found on one of the stretchers, without knowing that it was on Connallys stretcher, not Kennedys, that the bullet was found. (34) Notes were made, and Dr Humes wrote a first draft for the autopsy re-

port based on the assumption that one of the shots had no exit wound. In the morning on the 23rd of November, when Humes spoke with the doctors at Parkland Hospital, he was told about the exit wound at the front of the neck, obliterated by the tracheotomy incision. He then had to rewrite parts of the autopsy report. (35) Dr Humes told The Warren Commission that the reason for rewriting the report was that the paper on which the report was written had got blood from the dead president on it. Although this may have been true, the main reason (overseeing the exit wound in the first report) was not mentioned in the Warren Commission. (36) This caused a lot of speculation among sceptics to the Commission Report and especially among the growing numbers of conspiracy seekers in the years to come. Although the autopsy report has been strongly criticised for being incorrect, incomplete and inaccurate, the main conclusions have stood the age of time. It was supplied by the autopsy x-rays, which showed bullet particles along the remaining part of the brain corresponding between the small wound in the back of the head and the gaping wound on the side. (37) Scand J of FORENSIC SCIENCE - No 1 - 2010 - Page 1-52


The Zapruder film At the scene of the crime a man named Abraham Zapruder filmed the motorcade with his camera, and the film both shows Kennedy having been hit in the neck, and shows the impact of the bullet hitting the head. (Figure 6) The film made it possible for the investigators to make an estimated time frame for the shots that were fired, which made it totally plausible, also for an average shooter, to fire, reload and refire twice in the estimated time available between a first and a third shot, on the assumption that the first shot hit Kennedy in the back of the neck, the second shot missed, and the third hit him in the head. Based on Zapruders film such a time frame would indicate 4, 8- 5, 6 seconds to shoot, reload, shoot, reload and shoot. (38) Through later analyses, and especially through thorough examinations made by Gerald Posner, described in his book Case Closed, it is made plausible that the first, and not the second shot missed. That would make the time span even longer, with 4, 8 - 5, 6 seconds not between all three, but only between the two last shots. (39) The conspiracy industry Many hundred books have been written about the assassination of John F. Kennedy, and most have their own theories. Since only one theory can be correct, nearly all of this literature makes myth out of matters. Some saw smoke, and even a gunman on a grassy knoll in front of the President. Some described a gunman shooting from the bridge over the triple underpass. Some even thought that people shot from cars in the motorcade. When all books are put together, there seemed to be guns all over Dealey Plaza on the 22nd of November, and shots seemed to come from everywhere, only not from where a weapon was found, and from where witnesses saw Oswald shoot. A strong belief is needed to come up with explanations excluding hundreds of witnesses, pictures and films from the shooting scene, and pictures and x- rays from the autopsy. Some believe that USAs president was killed in a cover up involving hundreds of people, including their own government. The Warren Commission may


Scand J of FORENSIC SCIENCE - No 1 - 2010 - Page 1-52

Figure 4. Picture taken by wife Marina Oswald showing L. H. Oswald’s possession of murder weapons before killing of Kennedy and Tippit.

have its flaws and weaknesses, but compared to the ever-growing alternative literature of a possible conspiracy the report stands it time over 45 years after it was written. Best evidence What remains as best evidence, all witnesses aside, are the wounds on the corpse of the dead president, and the wounds on Connally, who survived. These wounds showed that two shots hit, both hit from behind, and both from above. The one bullet found on the stretcher at Parkland in Dallas corresponded with small particles found in the right underarm of governor Connally, who was hit in the back, sitting directly in front of president Kennedy. This nearly pristine bullet, sarcastically called “the magic bullet” by critics of the Warren Report, may very well have caused both the wounds in the neck of Kennedy, and the wounds in the thorax, right underarm and left thigh of Connally, as showed through later test shooting under similar circumstances. The bullet, a Mannlicher Carcano 6.5mm corresponded with the weapon the accused assassin Lee Harvey Oswald knowingly had in his possession prior to the killing, and which was found at the Sixth Floor of the Texas School Book depository shortly thereafter. The distance to the target was appr. 60 meters for the shot that hit both Kennedy and Connally, and less than 90 meters for the last shot to Kennedy’s head. Through the telescopic lens the target would look close and sharp, with the car moving slowly along the bullet’s path (figure 7). Every step Oswald made during his last hour as a free man was that of a guilty person trying to escape the consequences of his own actions. These

actions were to cause him his own life less than two days later, when he was shot at point blank by the nightclub owner Jack Ruby. The killing had the same effect to the conspiracy rumours that petrol has to a fire. But no one could come up with any corresponding relations between Ruby and Oswald before Oswald’s murder, or between Ruby and any collaborators. Too hard to handle The explanation for the never ending rumours of a conspiracy connected with the assassination of John F. Kennedy seems tightly connected to the fact that it is nearly impossible to accept the immense consequences the actions of a single, failed human being may have on historical events. On a scale weight Oswald does not seem to fit on the one side when you put John F. Kennedy, the Presidency and the American Constitution on the other. It seems human to try to make the two sides balance, by constructing a conspiracy in Oswald’s place. But when it comes to the evidence there is no other proof left than those found along Oswald’s miserable route. Kennedy’s misfortune was that he came to cross it.

Sources A) Report of the Presidentâ&#x20AC;&#x2DC;s Commission on the Assassination of President John F. Kennedy. United States Government Printing Office, Washington, D.C., USA, 1964 B) William Manchester: The Death of a President, Harper & Row, New York, USA, 1967 C) Gerald Posner: Case Closed. Random House, New York, USA, 1993 D) Texas State Journal of Medicine, January 1964. 1) A, p. 38- 39. 2) A, p. 43-45. 3) A, p. 49-50. 4) A, p. 97-109. 5) C, p. 331-332. 6) B, p. 155-158.

7) 8) 9) 10) 11) 12) 13) 14) 15) 16) 17) 18) 19) 20) 21) 22) 23) 24) 25) 26)

A, p. 63- 68. A, p. 143-149. A, p. 68-70. A, p. 71. A, p. 53-54. A, p. 54. C, p. 292. A, p. 54. A, p. 183, D, p. 61. A, p. 55. A, p. 165. A, p. 166-171. A, p. 176-180. A, p. 180. A, p. 180-181. A, p.122-124. A, p. 143-149. B, p. 296-305. B, p. 236-237. A, p. 58.

27) 28) 29) 30) 31) 32) 33) 34) 35) 36) 37) 38)

C, p. 299. C, p. 299. C, p. 300. C, p. 303. A, p. 540. A, p. 541. C, p. 304-305. A, p. 88-89. C, p. 308. A, p. 88-89. C, p. 315-316. A, p. 117. Because the presidential car at that time was partly covered by a road sign the Zapruder film does not show when the first bullet hit Kennedy and Connally, which explains why the time span diverges. 39) C, p. 319, 474-479.

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Olav Gunnar Ballo – First Executive Director of the Institute of Forensic Medicine in Oslo

“How I wish, how I wish you were here” Text and photos: Jørn-Kr. Jørgensen Does it make any sense to appoint a politician as the executive director of the Institute of Forensic Medicine (RMI) in Oslo? Is the question purely rhetorical or does it have a deeper meaning? Who should be responsible for security under the law within the important fields in which RMI is involved – who should make the decisions and who should be responsible for prorities?

There are many questions, but the fact is that Olav Gunnar Ballo, who for twelve years held a seat in Parliament representing the Socialist Left Party (Sosialistisk Venstreparti, SV), took over at the 1. of October 2009 as the institute’s first executive director. In the past, there has been an elected leader, but now everything is changed, and with many more tasks that often are difficult to carry out, an executive director – a professional and administrative leader – has been hired. The idea is that this will strengthen solidarity and that the Institute of Forensic Medicine will secure its position within the University, the National Hospital, the police, and in society at large. There is no doubt that growth and expansion require leadership, and Gunnar Olav Ballo has been chosen for the job. Olav Gunnar Ballo is in fact not only a politician but a medical doctor who was the chief municipal medical officer in Alta before his election to the Storting in 1997. From 1994 to 1997, he was also advisory head physician for the County Health Insurance Office in Finnmark. To keep himself professionally up to date, he has, for the past nine years, worked as a company doc-

tor in addition to serving as an MP. He continues to work on specific days as a company doctor in his home municipality of Alta. As a politician he has proposed many new initiatives and experienced both ups and downs. In his private life, two years ago he experienced the worst thing any parent can imagine. He writes about what happened in the book Kaja (2009). His daughter of that name took her own life while studying in Nice, France, on the same day as she had, for the one and only time in her life, visited the Scientology Church. In his book he describes his relationship with Kaja, which, caused by her eating disorder, had not always been an easy one. It is both enriching and helpful to read the book Kaja, as it reveals aspects of the life of the new director of the Institute for Forensic Medicine. Ballo has written a gripping book about his daughter’s struggle with a serious illness, about how she got better, and about how her death came as a shock to the whole family. One can only imagine how deeply her loss has affected Ballo and his family. Ballo has clearly thought about his new position. It is important for me that I create my own role at the institute, that I am accessible and that I am not authoritarian. I want everyone to have a sense of security all the way into the courtroom with regard to the cases with which we are involved, and it is my wish that the relatives of the deceased and other affected individuals with whom we Olav Gunnar Ballo is a guardian of the law as executive director of the Institute of Forensic Medicine.


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are involved be treated with respect. It is important to remember that in our work it is quality that counts – and that the consequences can be fatal if we make any mistakes. As a physician have you participated in many autopsies? No, only as part of my medical studies. But there have been occasions when I have taken more detailed tests from the deceased in cases of unnatural death. In one case we had to have blood sugar from one of the deceased. So I took a syringe and stuck a needle into the eye of the deceased and withdrew the liquid. The blood sugar count later revealed itself to be central in the investigation of the case. In another case I tapped blood from the groin of a young woman who had been killed in a traffic accident. Such cases are no autopsies, but this is the closest I have come to it, since you raise the question. I am not an expert on forensic medicine, but a general practitioner. Since coming to RMI, I have participated in several autopsies, but I have no experiences with autopsies as such. So I have much to learn and at the institute we have worldclass experts in forensic medicine. But Ballo adds: I learned something from my grandfather who was a telegraph manager and very down-toearth, when it came to dealing with people: Take your time. Give people praise. Be there, close to your employees. I also think about the sudden, unexpected deaths of children. I can never be reconciled to the death of children. The realization that small infants and children die without any good explanation is terrible. That they die is incomprehensible, and even though one day we may manage to learn from research why it happens purely biologically, physically, and physiologically,

the fact that children die will be just as incomprehensible as a phenomenon. There is no meaning to it. Therefore – therefore also – it is important that we continue to do research about it. What is your leadership philosophy? I don’t know that I have any actual leadership philosophy. It is perhaps a bit pretentious to say this after being in the position of executive director for such a short time, but if I were to mention one thing it would have to be: Be present, be attentive, listen, learn, and then make decisions, even though they may be unpopular. But who has said that it should be easy? Leadership is not easy. Many people have great difficulty in managing their own lives, so to lead others is always difficult. But I believe it is important to listen. To listen has also another aspect. I’m not sure it’s wisest to listen to those who talk loudest. I will try to listen to everyone, not least to those who are silent in group gatherings. My experience is that there is a lot of wisdom there, so we’ll see … I have been sitting behind the desk at the institute for less than six months. Do you have any visions for RMI and your work – you must necessarily have thought through this when you stepped into one of the most important jobs in a society based on law and order? Yes, I have reflected over this – and I’ll give it to you point by point. This is important to me – as it must be for my colleagues on all levels in the institute: • We must be able to defend what we do in every context • Everything we do must be professionally rooted in knowledge • What we do must be future-oriented. We have to deal actively with new developments. For example, we have DNA technology. Next comes RNA. We must be ready to change along with society. RMI has to be top-quality and we must achieve this in cooperation with other countries and new technology • RMI must be inclusive and open in relation to the client (which, for the most part, is the police). People should be able to experience contact with us as a positive thing

Olav Gunnar Ballo claims he has much to learn regarding forensic medicine and willingly consults Jon Lundeval’s classic work on the subject. The book was reprinted many times and became the forerunner of later works by Professor Torleiv O. Rognum.

• We must be open – and what an expert on forensic medicine says in court must be put in comprehensible language • We should be grateful when people contact us. In that way we can establish our legitimacy • We must give people time – whether they are colleagues or others. No matter how busy one is, it pays off in the long run to take the time needed to do the job I’m sure there is much more that I could add to the list in time, but this is what I have reflected over and wish to emphasize at the beginning. What do you think about forensic medicine as a separate discipline? It seems reasonable to me that forensic medicine should be a separate discipline. Even though we have few forensic medical experts in Norway, this is not in itself an argument against the identification of forensic pathology and clinical forensic medicine as a distinct discipline. The recognition of this area of expertise as a discipline on its own would probably also contribute to increased recruitment and the strengthening of forensic medicine as a discipline, which in my opinion there is a need for. Olav Gunnar Ballo speaks quickly, to the point, and with precision. In his

spare time he is leader of the Norwegian Tibet Committee. He has met the Dalai Lama on several occasions. He is an enthusiastic amateur photographer. Can he ever stop being the politician? Twelve years as an elected member of the Storting have, of course, left their mark. This may explain his enthusiasm for intense discussions about his profession and about administration, about finances and priorities. I have many interests, says Ballo. When I wake up, I need to have a book within reach, and I like to write. I have dreamed about writing a book with the title Murder as a Method, about politically motivated murders and assassinations of politicians through history. I have thought of starting with Socrates, and concluding with the assassinations of John F. Kennedy, Martin Luther King, Jr., and Robert Kennedy. These three can be taken together, considering the epoch in which they were killed, a U.S.A. full of hatred. What about music, Ballo? Many physicians have a strong interest in music. I have been a fan especially of The Beatles and Pink Floyd – and have been working on a book project about Pink Floyd under the title “Shine on you crazy diamond”. Pink Floyd made some 120 texts to their songs, and I have tried to rewrite these texts in Norwegian. We’ll see if it becomes a book. That was very popular music for many members of my generation, and the music I listened to during my youth isn’t so easy to let go of. There is a line from Pink Floyd that goes, ‘So you think you can tell heaven from hell, blue skies from pain. Can you tell a green field from a cold steel rail?’ For me there is something deep in these words, something that speaks about my relationship to Kaja. How I wish, how I wish you were here. Translated by Harry T. Cleven

Scand J of FORENSIC SCIENCE - No 1 - 2010 - Page 1-52


Boganmeldelse af

”biologisk antropologi med human osteologi” Red. Niels Lynnerup, Pia Bennike og Elisabeth Iregren. Forlag Gyldendal 2008. Vi har i Norden længe savnet en samlet og moderne fremstilling af biologisk antropologi set fra en skandinavisk synsvinkel. Den nye lærebog i biologisk antropologi opfylder dette behov. Den er skrevet af førende forskere fra de skandinaviske lande samt enkelte andre. Bogens opbygning er logisk og overskuelig, og den er sat op med en indbydende grafik og mange interessante illustrationer. Kapitlerne er skrevet i et letforståeligt sprog, og er sat pædagogisk op med mange eksempelbokse. Kapitlerne omfatter både baggrunds kapitler om for eksempel menneskets evolution og mere praktisk orienterede kapitler om for eksempel feltarbejde. Desuden belyses mere teoretiske emner som statistik og etik. Kapitlerne er generelt letlæselige og interessante. Det er lykkedes redaktørerne at fastholde en ensartet stil trods de mange forskellige forfattere. Det er dejligt at se en nordisk lærebog som indeholder kapitler som er skrevet i de skandinaviske originalsprog. Bogen vil være til stor nytte for studerende fra de mange forskellige faggrupper som beskæftiger sig med biologisk antropologi. Den kan også med fordel læses af færdiguddannede fagfolk, som ønsker at opfriske og udvide deres viden om biologisk antropologi, nok især fra tilgrænsende fagområder som arkæologi og lægevidenskab. I øvrigt vil jeg vove den påstand, at bogen vil kunne læses af alle naturvidenskabeligt interesserede. Det er fornøjelig læsning, som sagtens kan konkurrere med kriminalromanen på ferierejsen. Peter Mygind Leth, vicestatsobducent


Scand J of FORENSIC SCIENCE - No 1 - 2010 - Page 1-52

Trafikkulyk etterforsknin gransk

et faglig møte for politi, helsepersonell og and taktiske, tekniske og medis

Dato Sted: Soria Moria, Voksen

Bindende påmelding

Arrangør: Norsk Rettsmedisinsk For

kker – ng og kning

dre som er involvert i sinske undersøkelser

o: 20. oktober 2010 nkollveien 60, Oslo

Kursavgift: kr 1.400,g til Frist 1. oktober 2010 rening og Gjensidigestiftelsen

08.30-09.00 Registrering og kaffe 09.00-09.10 Åpning 09.10-09.30 Politiets arbeid med etterforskning av trafikkulykker - et overordnet perspektiv Jan Guttormsen, Politidirektoratet 09.30-09.50 Hvordan foregår trafikkulykker? Harald Ståle Jansen, Statens Vegvesen UAG, Region ØST 09.50- 10.10 Kan politiet stoppe ”villmannskjøringen” - og redusere trafikkdøden? Roar Skjelbred Larsen, Utrykningspolitiet 10.10-10.30 Kan gjennomgang av alvorlige hendelser forebygge fremtidige dødsulykker? Rolf Mellum, Statens Havarikommisjon. 10.30-10.50 KAFFE 10.50-11.00 Personskader i bilulykker. Bedre sikkerhetsutstyr – færre skader? Arne Stray-Pedersen, Oslo universitetssykehus og Rettsmedisinsk inst 11.00-11.20 Rettsmedisinske undersøkelser. Nye metoder, bl.a. CT/MR – flere svar? Torleiv Ole Rognum, Rettsmedisinsk institutt 11.20-11.40 Kriminaltekniske undersøkelser ved trafikkulykker Trond Sandsbråten, Søndre Buskerud politidistrikt 11.40-12.00 Er dagens biler sikret nok i forhold til utfordringene i trafikken? Om skademekanismer og utvikling av nyere sikkerhetsteknologi Inggard Lereim, NTNU 12.00-13.00 LUNSJ 13.00-13.20 Betydning av rusgivende stoffer ved trafikkulykker? Asbjørg Christoffersen, Folkehelseinstituttet 13.20-13.40 Forekomst av rusgivende stoffer/medikamenter i normal veitrafikk Hallvard Gjerde, Folkehelseinstituttet 13.40-13.55 KAFFE 13.55-14.15 Polititaktisk arbeid på skadestedet - Enkle og vanskelige saker Harald Klemetsen, Oslo politidistrikt 14.15-14.30 Tekniske undersøkelser inne i kjøretøyet – har det noen hensikt? Trond Boye Hansen, Oslo universitetssykehus, Ullevål 14.30-14.45 Prosjekt ”Barn i bil”. Hvordan går det med barna ved alvorlige bilkollisjoner? Marianne Skjerven Martinsen, Rettsmedisinsk institutt 14.45-15.00 Dokumentasjon på skadestedet – er vi gode nok? Trine Staff, Oslo universitetssykehus, Ullevål 15.00-16.00 Paneldebatt: Kan bedre samhandling gi bedre etterforskning og bedre forebygging?

Scand J of FORENSIC SCIENCE - No 1 - 2010 - Page 1-52


First announcement: Soria Moria meeting 2011 May 19-21

Themes: ● Brain stem research and SIDS ● Genetic risk factors for SIDS ● Domestic violence and effect on early brain development ● Impact of death scene investigation in sudden deaths in infants and small children Contributors: ● Hannah Kinney ● Henry F. Krous ● Roger W. Byard ● Peter Fleming ● Jens Grøgaard ● Magne Raundalen For more information, please contact: a.g.winge@medisin.uio.n


Scand J of FORENSIC SCIENCE - No 1 - 2010 - Page 1-52

Scand J of FORENSIC SCIENCE - No 1 - 2010 - Page 1-52



Scand J of FORENSIC SCIENCE - No 1 - 2010 - Page 1-52

Guide for authors Scandinavian Journal of Forensic Sciences is published by the Danish, the Norwegian and the Swedish societies for forensic medicine. It publishes original contributions and review articles in the different disciplines of forensic sciences: forensic pathology, clinical forensic medicine, forensic genetics, forensic toxicology, forensic anthropology, forensic odontology, forensic psychiatry and forensic science. The journal is also open for debate on issues concerning legal medicine and for news from the societies.

Submission of manuscripts Original articles, review articles, preliminary communications, letters to the editor and case reports may be submitted if they are not being considered for publication elsewhere. Papers for consideration should be submitted to Torleiv Ole Rognum (editor in chief), Rettsmedisinsk institutt, Rikshospitalet, N-0027 Oslo, Norway. Tel: +47 23 07 27 18, fax: +47 23 07 13 31, e-mail: or a.g.winge@labmed. Or to the national editors: Jørgen L Thomsen (Denmark), Retsmedicinsk Institut, Winsløwparken 17, DK-5000 Odense C, Denmark. Tel: +45 65 50 30 00, fax +45 65 91 62 27, e-mail: Håkan Sandler (Sweden), Retsmedicinska Avdelningen, Dag Hammarskjöldsväg 17, S-752 37 Uppsala, Sweden. Tel: +46 18 51 57 20 fax: +46 18 55 90 53, e-mail:

Preparation of manuscripts Manuscripts should preferably be written in English (letters to the editor and matters concerning the national societies of forensic medicine may be written in Scandinavian languages). Authors whose native language is not English are strongly advised to have their manuscript checked for style, syntax and grammar prior to submission. Articles should be submitted in triplicate, with each copy being complete in all respects as two copies are sent to referees. The text should be typed in double-spacing on consecutively numbered pages of uniform size, preferably A4. Every page of the manuscript, including the title page, references, tables, etc should be numbered. Manuscripts should be organised in the following order: Title (should be clear, descriptive and not too long) Name(s) of author(s) Complete postal address(es) of affiliation(s) Telephone and fax numbers and e-mail address of the corresponding author Summery, which should be clear, decscriptive and not longer than 250 words Keywords, normally 3-6 items Introduction Materials and methods Results Discussion References

References References should be numbered in the order in which they are cited (using square brackets in the text) and listed in numerical order on a separate sheet. The present journal should be cited as Scand J Forens Sci. References to journals or books should accord with the following examples: 1. Rollmann D, Jarlbæk L. Minimum lethal dose of citalopram. Scand J Forens Sci 2002; 8: 10-11 2. Knight B. Forensic pathology. Sec ed. Arnold, London, 1996 3. Madea B, Henssge C. Eye changes after death. In: Knight B (ed). The estimation of the time since death in the early postmortem period. Edward Arnold, London, 1995

Tables Tables should be typed in double spacing on separate sheets, and numbered according to their sequence in the text. The text should include references to all tables.

Illustrations Illustrations must be accompanied by suitable legends typed in double spacing on a separate sheet. Illustrations must be submitted in a form suitable for direct reproduction. Photographs should be clear, black and white prints on glossy paper. Colour photographs may be accepted. Photographs and figures should, when possible, be submitted as JPG-files.

Proofs One set of proofs will be sent to the corresponding author as given on the title page of the manuscript. Proofs should be returned by fax or express post within 48 hours or receipt. Corrections should be limited to typographical errors only.

Reprints Reprints are not produced. A CD with the article will be offered free of charge to the first author. The first author may also require 5 extra copies of the journal fre of charge.

Advertising information Advertising scientific meetings and courses within the scope of the journal is free of charge.

Commercial advertising and advertising of vacant positions Commercial advertising have the following prices: Back cover page, 1 volume, 4 numbers, Nkr 20,000 (black and white), Nkr 30,000 (colour) Full page, inside the journal, 1 volume, 4 numbers, Nkr 10,000 (black and white) Full page, inside the journal, 1 number, Nkr 4,000 (black and white) Half page, inside the journal, 1 number, Nkr 2,500 (black and white)

Leica FS C - Motorized Forensic Comparison Macroscope The innovative Leica FS C forensic comparison macroscope provides superior optical and motorized performance to forensic scientists. Offering flexibility, convenience, and user comfort, the Leica FS C is the universal instrument for high-precision firearm and toolmark examinations. The highly stable comparison bridge, the ergononmic design and the highest optical performance combined with versatile illumination options makes this system ideal for the simultaneous observation of evidence during training and consultation.

Living up to Life

No. 1, 2010  

Scandinavian Journal of Forensic Science, no.1 2010

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