Thesis (Ph.D.)--University of the Witwatersrand, Faculty of Health Sciences, 2012 / Background and Purposes Suicide by hanging is a relatively common occurrence. The actual cause of death in suicidal hanging is, however, controversial, having been attributed variously to asphyxia, carotid artery compression and vagal nerve stimulation. The aim of this Ph.D thesis was to determine the possible neurovascular cause of death in suicides by hanging by careful study of the anatomy and physiology of the neck region in relation to the ensuing pathology. The study was, therefore, approached from an anatomical, physiological, histological and pathological pespective. It therefore comprised a detailed exploration of the anatomy and physiology of the neck structures to match these with the underlying traumatised neurovascular structures, the latter trauma being brought about by the suicidal hanging process. Methods The methods used in the study included an investigation of the ligature and position of the ligature in relation to the level of the neck and the physical effects of the ligature on the skin and underlying anatomical structures. A careful and detailed dissection of the neck was undertaken and samples of the vessels and nerves were processed for histological study. Fifty consecutive cases of suicidal hanging and five “non-hanging” cases which served as controls were used in the study. In addition, ten cases of suicidal hanging not included in the study were subjected to occlusion studies by means of probe exploration. This technique and procedure was not carried out or applied to the cases included in the study for fear that the probe itself might produce artefactual damage to the delicate endothelium lining the inner layer of the vessel wall. The study was classified into various components such as: 1. Examination of the type and structure of the ligature material; 2. The position of the ligature on the neck, i.e. whether involving upper, middle, or lower third of neck and to correlate this position with the underlying anatomical structures subjected to the accompanying tensile, compressive and haemodynamic forces; 3. The physical effects of the ligature upon the skin and the underlying deeper neurovascular structures of the neck; 4. Meticulous “bloodless” dissection of the neck structures to corroborate any pathology noted with the above three criteria. Currently, all putative causes of death remain speculative; 5. Particular attention was paid to those structures most vulnerable to the compressive forces, tensile forces and haemodynamic forces operative in hanging. These comprise the neurovascular structures contained within the fibrous carotid sheath and the phrenic nerves in the neck, in particular with regard to the anatomical relationship of these structures to the positioning of the ligature. As far as analysing the forces involved, the engineering principles pertaining to these were interpreted in consultation with the Faculty of Engineering at the University of the Witwatersrand. Results The main findings of the study showed damage to vascular, neural (including phrenic nerve), carotid bodies and accessory glomal bodies. The vascular findings emerged following an examination of the total number of arteries in the study, namely, 300, the figure derived as follows: six arteries in each of the fifty hanging subjects, viz., the left common carotid artery, the right common carotid artery, the left internal carotid artery, the right internal carotid artery, the left external carotid artery and the right external carotid artery (6 x 50 = 300). The damage shown was particularly the case with regard to the finding of tears in the various layers of the vessel wall. These extended from the intima through to the adventitia or outermost layer of the vessel wall and these were further subdivided into being either single or multiple. The tears found ranged from those involving the intima alone (single tears being found in 17 (5.6%) of the 300 arteries examined and multiple tears in 37 (12.3%) of the 300 arteries examined., the intima extending to the internal elastic lamina (single tears being found in 20 (6.6%) of the 300 arteries examined and multiple tears in 8 (2.6%) of the 300 arteries examined), tears involving the intima and extending through to involve the media, i.e. intimomedial tears and whether these latter tears involved the inner-, middle-, or outer-thirds of the media (single or multiple). Single intimo-medial tears extending through the intima to involve the inner-third of the media comprised 6 (2.0%) of the arteries examined, those extending from the intima to involve the middle-third of the media comprised 3 (1.0%) of the 300 arteries examined and single intimo-medial tears extending through the intima to involve the outeriv third of the media similarly comprised 3 (1%) of the arteries examined. Multiple intimo-medial tears extending through from intima to inner-, middle-, and outerthirds of the media respectively, comprised 3 (1.0%), 5 (1.6%) and 1 (0.3%) of the arteries examined. Single tears involving the inner-third of the media alone comrised 6 (2.0%) of the 300 arteries examined, single tears involving the middle-third of the media comprised 9 (3.0%) of the arteries examined and single tears involving the outer-third of the media alone comprised 8 (2.6%) of the arteries examined. Multiple tears involving the inner-, middle and outer-thirds of the media respectively comprised 6 (2.0%), 13 (4.3%) and 16 (5.3%) of the arteries examined. Single tears involving both adventitia and media, i.e. adventitio-medial tears extending through the inner-, middle-, or outer-thirds of the media to involve the adventitia comprised 1 (0.3%), 2 (0.6%) and 6 (2.0%) respectively of the 300 arteries examined. Multiple adventitio-medial tears of the inner-, middle-, and outer-thirds of the media, respectively, comprised 0 (0.0%), 3 (1.0%) and 2 (0.6%) of the 300 arteries examined. Single tears of the adventitia alone comprised 21 (7.0%) of the arteries examined while multiple tears comprised 7 (2.3%). Complete circumferential transverse rupture of the vessel wall was found in 3 (1.0%) of the arteries examined while adventitial haemorrhage was found in 103 (34.3%) of the 300 arteries examined. The vascular findings were represented numerically in tabular form in the 50 hanging subjects in Table III and were further analysed and compared with regard to either unilateral or bilateral vessel involvement in the fifty (50) suicidal hanging subjects and the findings represented in Tables IIIa (unilateral involvement) and IIIb (bilateral involvement). Additional vascular findings comprised endothelial elevation/avulsion, internal elastic lamina dehiscence, subendothelial clefts, multiple medial fenestrations, adventitio-medial separation, vascular congestion and a vascular plane of cleavage. These were similarly represented in Table IV and analysed with regard to unilateral or bilateral involvement in Tables IVa and IVb. Endothelial elevation/avulsion was found in 295 (98.3%) of the 300 arteries examined, internal elastic lamina dehiscence in 290 (96.6%) of the arteries examined, subendothelial clefts in 289 (96.3%) of the arteries examined, multiple medial fenestrations in 17 (5.6%) of the arteries examined, adventitiomedial separation in 273 (91.0%) of the arteries examined, vascular congestion in 224 (74.6%) of the arteries examined and a vascular plane of cleavage in 98 (32.6%) of the arteries examined. These findings, unexpected, showed the extreme fragility and vulnerability of the intima and adventitia to the compressive and tensile forces acting on the vessel wall during hanging, being explicable not only on the basis of the various complex forces interacting simultaneously during hanging but on the magnitude of forces applied. A mathematical analysis, found at the end of the Discussion chapter, conducted in order to estimate the minimum peak pressure applied and exerted on the vessel wall during hanging, in collaboration with the School of Mechanical, Industrial and Aeronautical Engineering at the University of the Witwatersrand, confirmed the magnitude of these forces. The neural findings (Table V) were divided into neural congestion, neural haemorrhage, neural internal dehiscence, neural tearing and perineural separation and these were similarly analysed with regard to either unilateral or bilateral involvement in the fifty hanging subjects (Tables Va and Vb). Neural congestion was found in association with 20 (6.6%) of the 300 arteries examined, neural haemorrhage in14 (4.6%), neural internal dehiscence in 54 (18.0%), neural tearing in 35 (11.6%) and perineural separation in 112 (37.3%). Neural ganglionic findings were similarly divided into ganglionic congestion, ganglionic haemorrhage, ganglionic internal dehiscence and ganglionic tearing. Ganglionic congestion, in association with the 300 arteries examined, was found in 20 (6.6%), ganglionic haemorrhage in 8 (2.6%), ganglionic internal dehiscence in 15 (5.0%) and ganglionic tearing in 6 (2.0%). The findings in the carotid bodies were divided into carotid body congestion, carotid body haemorrhage, carotid body internal dehiscence and carotid body tearing. Carotid body congestion, in association with the 300 arteries examined, was found in 8 (2.6%), carotid body haemorrhage in 2 (0.6%), carotid body internal dehiscence in 4 (1.3%) and carotid body tearing in 2 (0.6%). Accessory glomal body findings were, once again, divided into accessory glomal congestion, accessory glomal haemorrhage, accessory glomal internal dehiscence and accessory glomal tearing. However, in view of the close anatomical association between the accessory glomal bodies and the adventitia of the arterial walls, an additional pathological finding of accessory glomal adventitial separation emerged. Accessory glomal congestion, in association with the 300 arteries examined, was found in 20 (6.6%), accessory glomal haemorrhage in 7 (2.3%), accessory glomal internal dehiscence in 50 (16.6%), accessory glomal tearing in 18 (6.0%) and accessory glomal adventitial separation in 124 (41.3%). This latter finding once again demonstrated the vulnerability of the adventitial layer of the vessel wall to tensile forces, separating it from its associated structures. Damage to the phrenic nerves and surrounding muscles, underlying the site of ligature application, was similarly found, suggesting a role for phrenic nerve stimulation with consequent diaphragmatic paralysis in contributing to death in the hanging process. Discussion and Conclusion In this Ph.D thesis the principles of dimensional analysis i.e., the breaking down of a complex phenomenon into its component parts, have been applied. However, in view of the complexity and proximity of structures to one another in the neck, consisting not only of the rigid hyoid-larynx complex and vertebral column but also the integrated vascular and neural structures, it appears that not one single biological mechanism can be ascribed and attributed to the cause of death in suicidal hanging. Rather, it appears that unconsciousness and death causation appears to be multifactorial. Both the sympathetic and parasympathetic arms of the autonomic nervous system are involved, often with antagonistic and therefore paradoxical effects. In a ddition, pressure to the phrenic nerve, not previously considered in playing a role in death causation in hanging, may, it is suggested, be a major contributory factor in death causation. This nerve, the innervation to the major muscle of respiration, i.e. the diaphragm, in a neural response to the compressive and tensile forces in hanging, fixes the diaphragm in a state of inspiratory paralysis. This latter effect would be further augmented by neural stimulation of the accessory muscles of respiration, i.e. the sternocleidomastoid and scaleni muscles, similarly lying deep to the site of ligature application, contributing to the thoracic cage becoming fixed in a state of inspiratory paralysis. This latter effect, as described in that section of the Discussion chapter dealing with an analysis of the physiological functions at play, is brought about by initiation of the dynamic and static stretch reflexes occurring in these muscles on application of a compressive or tensile stimulus. Compression of the carotid arteries, on the other hand, results, as shown, not only in major damage to these vessels and their accompanying veins, but, in addition, must produce a dramatic element of cerebral ischaemia with ensuing loss of consciousness. It thus appears that loss of consciousness is the critical factor for it is the state when the victim is no longer able to save himself or herself. Without loss of consciousness survival may occur, but with it, death becomes inevitable. The question then arises :- what is the cause of unconsciousness? In physiological terms, carotid artery occlusion induces rapid unconsciousness, i.e. within 11 to 12 seconds, resulting ultimately in death. In other words, the sudden application and unremitting pressure of the ligature must inevitably result in death. On the other hand, the sudden application of a ligature with consequent vagal nerve compression may produce instantaneous cardiac arrest with cessation of blood flow to the brain and resultant loss of consciousness. This event would produce unconsciousness in less than the time period of 11 seconds of carotid artery occlusion (although the brain continues to survive for several minutes thereafter despite cessation of heart beat). If, however, unconsciousness is contributed to by phrenic nerve compression, it would not be instantaneous as shown by the fact that one can normally hold one’s breath for several minutes (as underwater swimmers do) and unconsciousness does not supervene either instantaneously or within 11 seconds. In short, unconsciousness would not occur within 11 seconds in the case of compression of the phrenic nerve unless a more critical factor supervenes.Thus, the rapidity of onset of unconsciousness appears to be the critical factor in determining the progression to ultimate (and inevitable) death. Moreover, as pointed out in the Materials and Methods chapter, the carotid arteries in several tested cases would not allow the passage of a probe through the obstructed arteries beneath a tightly applied ligature. This obstruction would, therefore, appear to be the initiator of the deadly unconsciousness factor, although respiratory arrest would be compounded by neural and muscular factors. While in this thesis the principles of dimensional analysis i.e., the breaking down of a complex phenomenon into its component parts have been applied, the principles of integrated analysis i.e., the combining and synthesis of separate parts into a whole have also been attempted. In essence, while it is suggested that the neural elements play a pivotal role in the hanging process due to the neural effect on both brain and heart as a result of autonomic nervous system stimulation and the function of the phrenic nerve in respiration, it appears that multiple factors, acting in concert, simultaneously or in rapid sequence to one another, all play a role in contributing to death causation in the hanging process.