21 Dr. Perl similarly examined the appellant's ERISP and concluded that his answers were appropriate and responsive, indicating that his cognition was "not significantly impaired" by the alcohol he had consumed. Her evidence is sufficiently encapsulated in the following question and answer:
"Q. Does the demeanour and manner of speaking of the accused during that interview enable you to express any view as to his cognitive ability at the time?
A. I would have said his cognition was almost intact, very little impairment of his memory and certainly full - appeared to have full comprehension of the questions, gave appropriate answers, there didn't seem to be any obvious significant impairment of his coordination, so I would have put him as being slightly impaired."
22 Dr. Strum, a forensic psychiatrist, interviewed the appellant on 5 September 1998. He was unable to detect any sign of disorientation or organic brain damage, but thought that the history of personality traits supplied was suggestive of frontal lobe syndrome. He thought the appellant to be an alcoholic who suffered from a borderline personality disorder with poor judgment and poor impulse control. He saw no reason why he should not have been able to choose to take part in the ERISP, the viewing of which gave no indication of any abnormality or of cognitive impairment on his part. Dr. Strum later added that he could not have pretended to have been functioning normally if in fact he did not have that capacity.
23 His evidence was supplemented by that of a neuro-psychologist, Alexandria Walker, and by a psychologist, Anna Robilliard. The former concluded that the appellant had suffered mild cognitive impairment (particularly in aspects of frontal lobe function) because of his history of alcohol consumption. Ms Robilliard, who conducted the standard psychological tests, expressed the view that while the appellant displayed signs of severe disturbance across most areas of social and interpersonal behaviour, brain damage was not detected on those tests.
24 A certificate was also tendered as to the blood alcohol level of the deceased, which was determined as 0.482 grams per 100 millilitres of blood. The level of alcohol in his occular fluid (0.537 grams per 100ml) and in his urine (0.559 grams per 100 ml) was even higher. Dr Perl said that a reading of 0.482 grams per 100 ml, is likely to result in coma and, most likely in death, except in people who have an extreme tolerance to alcohol as a result of their heavy alcohol intake.
25 Post mortem examination of the deceased, by Dr. Lawrence, revealed that he had suffered fractures to two ribs. Blood was found in his lungs indicating to Dr. Lawrence that he was still alive when his ribs were fractured. Those injuries were consistent with him having been struck by a hammer and with the production of an audible cracking noise. An oblique fracture to the thyroid cartilage was found, along with bruising to the neck of the deceased. The fracture to the cartilage was not itself life threatening, and could have occurred immediately before, at the time of, or just after death, (ie during the peri mortem period).
26 Three factors contributing to death were noted by him, namely the "combined effects of compression of the neck, blunt force chest injury, and acute ethanol intoxication". A fourth significant condition of the deceased was noted, namely that he had a seventy five percent occlusion of a coronary artery, which made him vulnerable to the risk of sudden death, without prior warning signs.
27 The description of the appellant seeing the tongue of the deceased turn blue and his eyes roll back, Dr. Lawrence said, was consistent with the description of a person "being strangled to the point of unconsciousness". The presence of forceful movements, while being strangled, and the absence of breathing, or of a pulse, a short time later, was suggestive to him of a temporal link and causal nexus, between the neck compression and death.
28 A blue tongue, he conceded, could also be indicative of death from a heart attack or from alcohol poisoning, while the rolling back of the eyes could be a sign of a coma due to acute alcoholic intoxication. Although there were no signs of petechial haemorrhages, a common sign in cases of manual strangulation, that, he said, can occur where the compression to the neck is quick and forceful.
29 The normal path towards death from alcohol toxicity, Dr Lawrence said, involved a person becoming progressively more comatose, although that depended on how quickly the alcohol was ingested.
30 Dr. Lawrence agreed that, based purely on the autopsy findings, he could not attribute to any one of the likely causes identified, ie neck compression, acute alcohol toxicity, and cardiac arrest due either to atherosclerosis, or to blunt chest trauma, a higher degree of probability than another.
31 He said, however, that if the deceased had been arguing with the appellant, and had attempted to push him off as he was being strangled, then it would appear that he had not been in a comatose state due to alcoholic intoxication. He also said that sudden compression of the neck and the forceful application of blows to the chest of a person suffering a significant occlusion of a major coronary artery, could contribute to or accelerate a sudden death from that cardiac condition.
32 Dr. Byron Collins, a forensic pathologist, who was called by the defence, said that it was not possible to determine which of the potential causes of death identified by Dr. Lawrence was "the most likely". They may have acted individually or in conjunction. Those observations, however, so it became clear from his evidence, were based solely on the "pathological findings".
33 The thyroid cartilage fracture, which could be associated with a loud crack, he said was unusual in a case of manual strangulation, but not impossible. The absence of petechial haemorrhage, he also agreed, while common in cases of manual strangulation, was not so uncommon as to exclude that possibility. It was also possible, he said, that the neck injuries were due to a fall or were occasioned after death. The rolling of the deceased's eyes and the change in colour of his tongue, he thought, did not indicate anything specific other than that the cerebral, musculature and cardiac functions were compromised. Whether that was due to the cardiac problems or to asphyxia he was unable to say.
34 The toxic effects of alcohol he explained as acting as a depressant for the central nervous system, particularly the respiratory centre, which can cause breathing to stop, leading to death. Additionally, the toxic effects can damage the heart fibres and produce cardiac arrhythmia of sufficient severity to produce death.
35 Another possibility, that emerged in his evidence, related to the circumstance that manual strangulation can lead to sudden death where there is an interference with the carotid sinus and the vagus nerve, a consequence that is more likely in a person predisposed to cardiac arrest. It would in fact help, in the present case, to explain the lack of petechial haemorrhage, as Dr. Collins explained.
36 Passing from the pathological findings to the events described by the appellant, Dr. Collins said:
"Q. If in this case there was evidence from Mr. Moffatt that the man in question was able to talk some short time before death and, indeed, attempted to push off his assailant just prior to death, would that scenario suggest that this was not death by someone slowly lapsing into an alcoholic coma?