R v Wells

[2016] SADC 68

DISTRICT COURT OF SOUTH AUSTRALIA

(Criminal)

R v WELLS

Criminal Trial by Judge Alone

[2016] SADC 68

Reasons for the Verdict of Her Honour Judge Davison

30 June 2016

CRIMINAL LAW - PARTICULAR OFFENCES - DRIVING OFFENCES - CULPABLE OR DANGEROUS DRIVING CAUSING DEATH OR BODILY HARM

Trial by Judge alone - accused charged with aggravated causing serious harm by dangerous driving - whether accused's driving voluntary - accused diagnosed post collision with complex partial seizures - accused had level of about 0.66mg/L of methylamphetamine at time of collision - whether veering off Sturt Highway at 110km/h is dangerous.

Verdict: Guilty.

Criminal Law Consolidation Act 1935 s 19AA, s 21; Evidence Act 1929 s 34, referred to.
Markou v R (2012) NSWCCA 64; R v W (2015) SASCFC 56; R v Radford (1985) 42 SASR 266; R v Falconer (1990) 171 CLR 30; R v Kroon (1991) 55 SASR 476; Ramsay v Watson (1961) 108 CLR 642; McBride v The Queen (1966) 115 CLR 44; R v Greenham (1997) 25 MVR 495, considered.

R v WELLS
[2016] SADC 68

Introduction

1. At about 3.00pm on Saturday 23 March 2013 a silver Holden Barina driven by Martin Wells (“the accused”), collided with the rear of a white Mitsubishi utility that was stationary on the gravel shoulder of the Sturt Highway near Shea-Oak Log. The driver of the white utility, AK, was at the time of the collision, at the rear, or close to the rear of his utility. He was struck and came to rest in the middle of the Sturt Highway. As a result of the collision he suffered significant injuries to his left forearm, right lower leg, left thigh, left lower leg, scalp, torso, left lung and right buttock.

2. The accused was charged with Aggravated Causing Harm by Dangerous Driving and Driving with Prescribed Drug in Oral Fluid or Blood.

   First Count

   Statement of Offence

   Aggravated Causing Harm by Dangerous Driving. (Section 19A(3) of the Criminal Law Consolidation Act, 1935).

   Particulars of Offence

   Martin Wells on the 23^rd day of March 2013 at Shea-Oak Log, drove a motor vehicle in a culpably negligent manner, recklessly, or in a manner which was dangerous to the public and thereby caused serious harm to AK.

   It is further alleged that Martin Wells committed the offence whilst driving a vehicle in contravention of section 47BA of the Road Traffic Act, 1961.

   Second Count

   Statement of Offence

   Driving with Prescribed Drug in Oral Fluid or Blood. (Section 47BA(1) of the Road Traffic Act,1961).

   Particulars of Offence

   Martin Wells on the 23^rd day of March 2013 at Shea-Oak Log, drove a vehicle whilst having a prescribed drug present in his blood, namely methylamphetamine.

3. Upon arraignment, the accused pleaded guilty to Count 2, and not guilty to Count 1. I have heard the trial without a jury on Count 1.

4. There is no dispute that as the accused was driving his car from Nuriootpa to his mother’s house at Para Hills, at a point south of Shea-Oak Log, he left the lane in which he was driving and drifted over the bitumen shoulder, onto the gravel shoulder, and collided with the rear of the utility. There was no evidence of braking, or any other evasive action taken by the accused. There was no evidence about his manner of driving prior to the collision. A sample of his blood taken approximately two hours after the collision disclosed a methylamphetamine level of 0.56mg/L and an amphetamine level of 0.09mg/L.

5. Much of the evidence in this trial related to the effects of this level of methylamphetamine upon a driver of a motor vehicle. In addition to this, there was evidence led by the defence, through the accused and other witnesses, that the accused has been diagnosed, post-impact, with complex partial seizures (“CPS”).

6. The issues to be determined in relation to this matter are:

   1was the accused’s driving a willed or voluntary act at the time of the collision; and

   2if so, was his driving dangerous to the public?

   Reasons

7. The High Court of Australia has stressed that it is necessary for sufficient reasons to be given by trial judges which properly explain the verdict. These reasons must include the principles of law applied by the judge and the facts as found by the judge. A trial judge sitting alone is not obliged to “express all the matters which necessarily have to be stated to a jury unfamiliar with even the basic principles of law.”[1]

   [1]    Markou v R (2012) NSWCCA 64 at [19].

   Legal Directions

8. I set out here some of the fundamental directions which apply in a criminal trial.

9. The accused comes before this court with a presumption of innocence in his favour. The law regards him as innocent unless and until his guilt has been proven by the prosecution beyond reasonable doubt.

10. I must assess each witness as to their truthfulness and their reliability. I must determine whether I can rely upon the evidence that a witness gives. I can reject or accept all or a part of a witness’ evidence.

11. The accused has given evidence. He was not obliged to give evidence but chose to do so. His evidence must be considered along with the other evidence in the case. By giving evidence and presenting a case he has not assumed any burden of proof. That always remains with the prosecution.

12. I must bring an open and unprejudiced mind to the case. I must make my decision without sympathy, without prejudice or fear, and not influenced by public opinion in relation to this matter.

13. In this case, certain persons said to be experts in particular fields, have been called to give evidence. The ordinary rule is that witnesses may speak only to the facts and not express opinions. An exception to that rule is that persons who are qualified in a particular area may express an opinion. That opinion must be relevant to their particular areas of expertise. As I am a sole judge of the facts, I am entitled to accept or reject any opinion evidence as I see fit. Before rejecting that evidence, I must give it consideration, and consider how it fits with any other evidence that I have heard on that topic.

    Elements of the charged offence

14. A person commits the basic form of the charged offence if he drives a motor vehicle in a culpably negligent manner, recklessly, or in a manner which is dangerous to the public, and thereby causes serious harm to another.

15. In order to prove this offence, the prosecution must prove three elements beyond reasonable doubt. The first is, that the accused was the driver of the motor vehicle in question. Secondly, the accused drove the motor vehicle in a culpably negligent manner, recklessly, or in a manner dangerous to the public. The third element is that that manner of driving was a substantial cause of serious harm to AK. Serious harm is defined by s19AAB Criminal Law Consolidation Act 1935 (“the Act”) to have the same meaning as in s21 of the Act. That is:-

    serious harm means—

    (a) harm that endangers a person's life; or

    (b) harm that consists of, or results in, serious and protracted impairment of a physical or mental function; or

    (c) harm that consists of, or results in, serious disfigurement.

16. In this case the prosecution relies upon a protracted impairment of a physical function. The third element, insofar as it relates to the serious harm, is not in dispute.

17. If the prosecution proves each of these three elements, then the accused is guilty of the basic offence. In order to prove the circumstance of aggravation, the prosecution must prove beyond reasonable doubt that at the time serious harm was caused to AK, the accused was driving the motor vehicle in contravention of s47BA of the Road Traffic Act 1961, namely that the accused was driving whilst he had methylamphetamine, a prescribed drug, in his blood.[2]

    [2]    See R v W (2015) SASCFC 56.

18. It was not in dispute at this trial that the accused had methylamphetamine in his blood at the time of the collision. This level was 0.56mg/L of blood when the sample was taken from him at about 5.00pm on 23 March 2013. In all likelihood, according to expert evidence given in the trial, his level at the time of the collision, that was at about 3.00pm on the same day, was a little higher, perhaps 0.66mg/L of blood.

    The Evidence

19. Pursuant to s34 of the Evidence Act 1929 a number of matters were agreed. Those matters are as follows:[3]

    [3]    Exhibit P3.

    Matters relating to the collision

    1.   At approximately 3:00pm on Saturday, 23 March 2013 a motor vehicle collision occurred on the Sturt Highway at Shea-Oak Log involving a silver Holden Barina hatchback registration (SA) WIV-876 and a white Mitsubishi utility registration (SA) S831-AFE.

    2.   Martin Wells was the driver and sole occupant of the silver Holden Barina at the time of the collision.

    3.   AK was struck as a result of the collision and came to rest at a position on the road in the middle of the Sturt Highway.

    Medical treatment of AK

    4.   AK was initially treated at the scene by a qualified paramedic from the South Australian Ambulance Service.  He was then conveyed to the Royal Adelaide Hospital by a medical retrieval helicopter.

    5.   Whilst en route to the Royal Adelaide Hospital medical retrieval personnel administered to AK four aliquots of 20mgs of Ketamine over a 45 minute period for pain relief.

    6.   AK was examined at the Royal Adelaide Hospital by Dr Eileen Habashi, who noted the following injuries:

    a)   Left forearm:

    i.Bruising, deformity and 2 lacerations (skin cuts).

    ii.Fracture/break of the radius.

    iii.     Fracture/break of the ulna.

    b)   Right lower leg:

    i.Fracture of the mid shaft of the tibia (shin bone).

    ii.Multiple fractures of the fibula.

    iii.Tension, swelling and reduced sensation in the skin.

    c)   Left thigh:

    i.Laceration.

    d)   Left lower leg:

    i.Fracture of the tibia.

    ii.Fracture of the fibular.

    e)   Scalp:

    i.2cm laceration at the back of the head with surrounding swelling.

    f)   Torso:

    i.Small bruise on the left mid part of the back.

    ii.Tenderness in left upper quadrant of abdomen.

    g)   Left lung:

    i.Area of collapse at base of left lung.

    h)   Right buttock:

    i.Small bruise.

    7.   Details of the treatment administered for the injuries described in paragraph 6 above are contained in the statement of Dr Eileen Habashi dated 16 June 2014.

    8.   Details of rehabilitation treatment undergone by AK at the Hampstead Rehabilitation Centre are set out in the statement of Dr Jessica Stratford dated 3 July 2013.

    9.   The injuries caused to the legs of AK resulted in serious and protracted impairment of a physical function, namely his ability to walk independently of walking aids.

    10.   A sample of blood taken from AK on 23 March 2013 was submitted to the Forensic Science Centre for toxicological analysis. It was labelled G058818.

    Medical treatment of the accused

    11.   Martin Wells was initially treated at the scene by a qualified paramedic from the South Australian Ambulance Service.  He was then conveyed to the Royal Adelaide Hospital by a medical retrieval helicopter.

    12.   Whilst en route to the Royal Adelaide Hospital medical retrieval personnel administered to Martin Wells three aliquots of 20mgs of ketamine over a 45 minute period for pain control.

    13.   Details of the medical examination conducted upon Martin Wells at the Royal Adelaide Hospital are contained in the statement of Dr Claire Michaela Price dated 10 February 2015.

    14.   A sample of blood taken from Martin Wells at about 5:00pm on 23 March 2013 was submitted to the Forensic Science Centre for toxicological analysis. It was labelled G058888.

    Toxicology

    15.   The results of toxicological analyses of the blood samples taken from AK and Martin Wells are set out in the toxicology report attached to the statement of Timothy Lawrence Scott dated 28 October 2013.

    16. Methylamphetamine is a prescribed drug for the purposes of Section 47AB of the Road Traffic Act.

    Vehicle examination

    17.   On 11 February 2014 the silver Holden Barina hatchback registration (SA) WIV-876 was examined by Eliot Cameron McDonald, a senior vehicle examiner attached to the Reconstruction and Technical Examination Unit of the Major Crash Investigation Section of the South Australia Police. As a result of his examination of the vehicle, Mr McDonald formed the opinion that the vehicle had been in reasonable condition prior to the collision and could find nothing mechanically wrong that could have contributed towards or caused the collision. 

20. The prosecution called Christina Robertson. Ms Robertson had been a passenger in her partner’s car when it approached the collision site from the same direction of travel as the accused. The collision had already occurred when she arrived at the scene. She did not see it occur. She saw an elderly gentleman lying in the middle of the road with a number of people trying to assist him.[4] She went to the Barina that the accused had been driving. He was the only person in the car. The driver’s side door was closed as she approached it. The accused kept saying that he wanted to get out of the car. She tried to convince him to stay in the car because she was not sure about his injuries. Eventually the door was opened and he got out of the car. He had an injury to his head that was bleeding and she applied pressure to it. After he had emerged from the car they sat on the side of the road together talking. She asked him if he wanted her to call anyone and he responded by saying he wanted his mother called. His phone was in the car. They tried to ring his mother but she did not answer. Ms Robertson gave evidence that in the course of the conversation, the accused said that “he did see a gentleman behind the car and, as he was coming up, he seen him coming around the side.”[5] He also said that the sun was in his eyes. Ms Robertson said he was awake after the collision and he appeared to understand what she was saying. Under cross-examination, Mr Jolly put to Ms Robertson that she said to the police at the time she gave a statement on 17 October 2013, “during part of our conversation, the male said he had seen someone at the back of the ute and that he had been walking towards the driver’s door when he hit him.”[6] She agreed that she had said that to the police.

    [4]    TT 41.

    [5]    TT 45.

    [6]    TT 45-46.

21. In addition to the agreed facts and the evidence of Ms Robertson, I was provided with a number of statements of witnesses that were tendered by consent. These statements include a statement of AP who was the passenger in the motor vehicle driven by AK.[7] In his statement he said that: [8]

    [7]    Exhibit P5.

    [8]    Exhibit P5.

    At about 3.00pm we were on the Sturt Highway near SHEA-OAK LOG travelling south when AK, who was driving his ute, wanted a toilet stop. He pulled up to a stop on the side of the Highway, well off the road.

    I got out of the ute from the passenger side, and left the door open. I saw AK making his way to the back of the ute from the driver’s side. As I glanced over at AK, who was near the back driver’s side wheel, I saw a vehicle coming towards the ute. Arthur was facing north, the same direction that the vehicle was coming from, but I don’t know if he saw it.

    The vehicle was a silver Barina driving in the left hand lane of the Highway. I first saw the vehicle from about fifty (50) metres away; it appeared to be driving over the left white lane and heading directly towards the ute, which had been parked on the gravel, completely off the road to the left of the solid white line.

    The speed limit for the area was 110km/hr and the Barina was coming on fast. It didn’t look like it was slowing down.

    The Barina was about twenty five (25) metres away when I yelled out to AK,

    “Look out, look out!”

    I think he had time to look at the Barina, but it all happened so fast. I jumped into the bushes located away from the highway and to the side of the ute. I didn’t see it but I knew that the Barina had hit the ute and I had last seen AK at the back of the ute.

    When I looked out from the bushes I saw both cars had been pushed further up and off the road; the back of the ute was all smashed in. I also saw AK lying in the middle of the road; he wasn’t moving. I don’t know if he was knocked over by the impact between the ute and the Barina, or if he was run over by the Barina.

    I went to the passenger side of the ute to get my mobile to ring 000. As I was on the phone I went out onto the road to try and stop traffic. A couple of cars stopped to help.

    I couldn’t see the other driver at all; I think he was still in his car.

22. AK provided a statement to the police on 7 June 2013.[9] He said he was driving his utility with his friend AP who was in the passenger seat of the vehicle. They decided to stop for a toilet break. He pulled his vehicle over to the left side of the road, “all the way off the road onto the loose gravel.”[10] He got out of the driver’s seat and was walking to the back of the ute when he heard AP yelling something. He has no recollection after that.

    [9]    Exhibit P4.

    [10]  Exhibit P4.

23. Brevet Sergeant Henderson from the Major Crash Investigation Section, who attended on the day of the collision, was called to give evidence. She described the road conditions. She said the road was dry, the weather fine and there was a light breeze and concluded that the driving conditions were generally good. At that time of the day, driving in a south easterly direction, the sun would not have been an impediment. The roadway at the point of the collision was a dual carriageway. There were gauge marks located on the bitumen shoulder close to the gravel shoulder. Brevet Sergeant Henderson concluded that these were gauge marks from the Barina, possibly from the tow ring at the front of the vehicle. The photos that were tendered and the evidence given by Brevet Sergeant Henderson enable a conclusion to be drawn that the front left hand side of the Barina collided with the rear right hand side of the utility.

24. Senior Constable Murch was called to give evidence. He attended at the scene of the collision on 23 March 2013. He then became the assigned Investigating Officer. On 17 April 2013 he received the results of the blood analysis performed on the accused’s blood. He subsequently arranged an interview with the accused. On 9 May 2013 the accused attended at the Gawler Police Station with his partner. A video recorded interview was conducted. The interview was tendered in the trial,[11] the transcript was received.[12] During the course of the interview, the accused says that he recalls the day of the collision. He says that on that day, he was coming back from Nuriootpa where he had just started working and he was heading back to his mum’s at Para Hills. He agrees that he was driving the motor vehicle and he was alone in the car. When asked whether he could recall the collision, he said no. He was told that methylamphetamine had been detected in the blood test. He was asked whether he has any recollection or had he used drugs in the past, or in the week leading up, or on that day. He answered “hm not on that day no.” He was asked whether he knew “of anyone or any other way it might have got into your blood at all, like you know, drinking with others, spiking your drink, or I don’t know?” The accused answered “It could have been, it has been done before.” He said he was not on any current medication at the time of collision, that there was nothing that could affect his vision.

    [11]   Exhibit P19.

    [12]   MFI P20.

    Accused’s Case

25. The accused elected to give evidence. He gave evidence that he is 55 years old, has three children and is currently in a relationship. He described a number of physical ailments he suffers from including osteoarthritis and rheumatoid arthritis, ⅔ movement in his left ankle, two artificial knees, a partially artificial wrist, two torn ligaments; one in each arm, lower back problems and he is asthmatic. He sustained a number of injuries in motorcycle accidents in 1977 and 1996. 

1. He described a motor vehicle accident that he was involved in approximately a month prior to the subject collision. He said that he was not 100% sure how the accident occurred but that he hit a guard rail and has no memory of it. He said he came around just as he was right in front of the guardrail.[13]  His memory is very limited, he said that he knew that the sun was in his eyes and he turned his head to evade the sun however he does not have any other memory of the collision.

   [13]   TT 144.

2. On the day of the collision the subject of the charge, the accused was working at Nuriootpa. He was living with his mother in Para Hills at the time and travelled daily from Para Hills to Nuriootpa to work. He had the job for about three weeks prior to the collision and would start work between 8.30am to 9.00am and finish at about 4.30pm to 5.00pm. He said he could not remember anything before, during or after the collision. He had no recollection of the impact with the utility and no recollection of the events immediately after the collision. He accepted that he had methylamphetamine in his blood at the time of the collision, but has no recollection of consuming methylamphetamine at any time on Saturday 23 March 2013. On the evening prior to the collision he gave evidence that he had stopped at a friend’s place to have a BBQ on the way home from work, but denied that he had taken methylamphetamine that night. He gave evidence that he had been a user before 2009 and had consumed two to three points a day at that time. He said that he stopped using methylamphetamine in 2009. He had no explanation for how the methylamphetamine came to be in his system at the time of the collision. Under cross-examination the accused conceded that he has had two relapses since 2009, one in 2011, and the other probably in 2012. He denied that he had taken any methylamphetamine around Christmas 2012, or in the new year 2013. He described the effects of a condition that has been subsequently diagnosed as CPS. I will return to this topic later in the reasons.

   Voluntariness

3. I have concluded that the accused was physically driving the motor vehicle at the time of the collision. The question to be answered at this stage is whether the act of driving was voluntary. A presumption or inference of voluntary driving generally exists in relation to offences of this type. As King CJ observed in Radford:[14]

   It is a basic principle of the criminal law that a person “is not guilty of a crime if the deed which would constitute it was not done in exercise of his will to act”: Ryan v. The Queen, per Barwick C.J. at p. 216. If the actions which would otherwise amount to a crime are performed automatically and are not subject to the control and direction of the will, no crime is committed. The general onus which rests upon the prosecution in a criminal case extends, of course, to establishing that the acts said to constitute the crime were performed in consequence of the exercise of the will. The law recognizes a presumption of mental capacity which is sufficient to establish that an accused person acted pursuant to an exercise of his will unless the presumption is displaced by evidence which leaves the jury in doubt as to whether or not the actions were voluntary. The presumption does not affect the legal burden of proof which remains on the prosecution; it supplies, however, the place of evidence as to voluntariness unless displaced by actual evidence raising a reasonable doubt as to voluntariness: Bratty v. Attorney-General for Northern Ireland, per Viscount Kilmuir L.C. at p. 407 and Lord Denning at p. 413.

   [14]   R v Radford (1985) 42 SASR 266 at 272.

4. In this case, there was evidence called by the accused that may have the effect of displacing such a presumption. In that event, it is for the prosecution to prove that the charged offence was a willed act, or, at common law, was done voluntarily.[15] The law on the area of voluntariness in offences of this kind is well settled.[16]

   It is well established that the question whether a vehicle is driven in a manner dangerous to the public for the purpose of the offences created by s 19a of the Criminal Law Consolidation Act 1935 must be answered by reference to an objective standard and irrespective of whether the accused intended to drive dangerously or appreciated that he was doing so. The character of the driving is tested not by reference to whether the danger to the public involved in the driving was appreciated by the accused but to whether he ought to have appreciated the danger; or, to put it another way, whether a reasonable person in the situation of the accused would have appreciated the danger.

   Although the standard to be applied is objective in the sense defined above, it is applicable only to a voluntary act of driving. It is clear on the authorities, and on principle, that to constitute the offence, there must be a voluntary act of driving. Where the driving or apparent driving is deprived of its voluntary character by, for example, automatism or unconsciousness, the offence is not committed (references omitted).

   [15]   R v Falconer (1990) 171 CLR 30 at 40-41.

   [16]   R v Kroon (1991) 55 SASR 476 at 477

5. There was a significant body of evidence in this case about a medical condition known as CPS, from which it is said that the accused suffers. This condition was diagnosed after the subject charge, but was said to be pre-existing. Evidence was given by the accused, the accused’s son, and the diagnosing doctor, Dr Marantos on this topic. In addition to this, some of the prosecution case may have relevance in assessing the veracity of this evidence and the weight to be given to it.

6. The accused gave evidence of some occasions when his son observed him to black out:[17]

   [17]   TT 145 – 146.

   QHow often would Matthew visit you.                   

   AUsually once a week he would bring my grandson around to see me.  

   QWas there an occasion during that period, so between February 2013 and March 2013, that your son Matthew   became concerned about your health.                 

   AYes.  

   QWhat happened.  

   AI was talking to him and he said I shut me eyes and sort of blacked out, and after a couple of seconds I came around and carried on talking as if nothing happened.     

   QWere you aware that you were doing that.                

   ANo.  

   QDid Matthew bring that to your attention.                

   AYes.  

   QWhat did he say to you.  

   AHe said 'Dad, we've got to get you to the doctors'.      

   QWhat did you say in response.  

   AI said 'Why?  What's going on?'.  

   QDid you have a seizure on that occasion that you're aware of.  

   OBJECTION: MS MATTEO OBJECTS     

   HER HONOUR:    Is he able to answer that question?       

   MR JOLLY:        I will withdraw and rephrase it.         

   HER HONOUR:    I think all he can say at this point is what he physically experienced.  

   MR JOLLY:        Yes.  

   QDo you know if you blacked out on that occasion.        

   AFrom what my son said, he said that 'You closed your eyes', so I'm assuming it was a blackout.              

   QWere you aware of that at that time.                   

   ANo.  

7. As I said earlier in these reasons, the accused gave evidence that he had no recollection of the circumstances surrounding the collision, or the events before or after the collision. Matthew Wells, the accused’s son, gave further evidence about the observations of his father:[18]

   [18]   TT 263 – 264.

   QWere there any other instances where you became concerned about his health.  

   ANo, not that I can think of.  

   QAny time when you visited him -  

   AYes.  

   Q- did you make any observations of him that concerned you.  

   AYes, yep.  

   QWhat happened on that occasion.  

   AHe was falling sleep when he was talking to him, so he was sort of nodding off like mid conversation.           

   QWhat did his face look like when that was happening.      

   AWell, sort of sometimes he would just nod off, other times his eyes would roll back a bit, just depended on the time, yeah (INDICATES).  

   QOn the occasions you're describing, did he appear to lose consciousness from what you were seeing.            

   AOn some occasions, yes.  

   QYou said this is while you were talking to him.          

   AYes.  

   QWas he continuing to talk to you when these events were happening.  

   AYes, sometimes he would continue the conversation, so it  was just like he nodded off for a second and then continued talking, whereas other times he is a bit dazed.  

   QWhen you say dazed, what did he look like.             

   AI don't know, kind of like he's just - kind of like he has just woken up, I guess.  

   QDid he appear to be aware of what was going on from what you could see.  

   ANo.  

   QWas that every occasion.  

   AThat he wasn't aware?  

   QYes.  

   AFrom memory, it was a while ago, yeah, I think he wasn't aware that it was happening.  

   QPrior to March 2013, how many of these events did you see.  

   AIt was a few years ago now, I'm trying to think.  It got more regular, so maybe nearly every time I seen it, but I only started to notice it, probably every second time I seen him I would notice it.  

8. The accused gave evidence that he consulted Dr Marantos after the subject collision on the advice of his son and was diagnosed with CPS. These have previously been known as petit mal seizures.

9. Dr Marantos gave evidence.[19] He said that he first saw the accused on 1 May 2013, 6 weeks after the collision. He saw him at the request of his General Practitioner, after a cardiologist had ruled out a cardiac cause for the episodes.

   [19]   TT 281.

10. Dr Marantos is a legally qualified medical practitioner who is a Fellow of the Royal Australian College of Physicians. He has been practicing as a Physician since 1982. Between 1982 and 2012 he was the Senior Visiting Physician at Modbury Hospital, and a consultant in private practice from 1982 to the present time.

11. He gave evidence that general practitioners will refer neurological problems to a general physician first because there is a long waiting time to see a neurologist.

12. The accused attended the first appointment with his son, Matthew Wells. Dr Marantos took a history from both the accused and his son. The accused told Dr Marantos that he had been involved in several accidents but did not go into detail in relation to them. The accused also told Dr Marantos that he had physical ailments as a result of accidents that he had been involved in, in the past. In relation to substance abuse, the accused told Dr Marantos that he had used alcohol and various other recreational drugs. He did not go into details as to what he had used and when his most recent use was, although he did say he had used amphetamines.[20] The accused also gave a history of his current medical conditions. Dr Marantos was also provided with a list of current medications from the referring doctor.

    [20]   TT 286.

13. Dr Marantos said that where there are episodes of lack of awareness, or where people lose consciousness, the witness, if there is a witness to these events, is more valuable than the patient and so he took some history from Matthew Wells. He quoted from his notes and said the son, Matthew Wells said:[21]

    Quite a while talking, suddenly stop talking. Eyes may roll up or close eyes. Duration is a few seconds only and he wakes up spontaneously. After an event he is not aware of the event. He carries on with what he was doing. Son had not noted any change in breathing, colour, vis-a-vis automatic behaviour. The son felt that these episodes had been present since Christmas and increasing frequency.

    [21]   TT 287

14. Dr Marantos then conducted a physical examination of the accused. His conclusion was that everything was normal apart from a soft, low slung palette, which was in keeping with snoring and possibly sleep apnoea. He then made a provisional diagnosis of CPS and thought obstructive sleep apnoea may be contributing. He prescribed Tegretol and organised for a sleep study and a MRI scan. A CT scan had been performed in the past, and although the doctor didn’t specifically say so, I assume that it showed no abnormalities, and it was for that reason that he ordered the MRI scan. He explained it in these terms: [22]

    Complex partial seizures can be associated with temporal lobe abnormalities which you will only see on the MRI scan and, because of the history of previous trauma, I was looking for any scarring in the brain which would not necessarily be picked up by a CT scan.

    [22]   TT 288.

15. The MRI subsequently showed a small area of blood around the surface of the brain and the rest of the MRI was normal. Dr Marantos concluded that there had been a haematoma and that blood was most likely secondary to the accident and post-traumatic. He said a spontaneous bleed around the brain can also make people lose consciousness, but if that was the case, he would have expected a larger amount of blood. The sleep apnoea test showed a mild condition known as periodic limb movement, however, he said that was not significant, and not enough to cause a severe sleep interruption and was otherwise normal.

16. From the results of the sleep study and the MRI, Dr Marantos excluded other pathology that may have contributed to episodes of loss of consciousness or lack of awareness, and confirmed his provisional diagnosis of CPS on 9 May 2013. Dr Marantos increased the dose of Tegretol as the accused reported to him some “gaps in conversations.” A further MRI was also performed to make sure that the visible blood had been reabsorbed. It had been reabsorbed by 17 July. Dr Marantos saw the accused on 11 December 2013 and 11 June 2014, and thereafter for other medical problems that arose, including arthritis.

17. In the first consultation, the accused recounted his memory of the motor vehicle accident that occurred on 25 February 2013. The doctor read from his notes and said that he was told: [23]

    the first episode of loss of consciousness, can recall events up to a certain point, the sun hitting him in the eyes, putting head down and then nothing until he put his head back up again and saw the guard rail coming towards him.

    [23]   TT 290.

18. When asked about the interplay of light, Dr Marantos said that light may stimulate any seizure.

19. Doctor Marantos gave evidence that when the accused was asked about the collision the subject of the charge on 23 March 2013, he said “cannot recall this in detail. Can recall getting into car after shopping, driving off and then next thing he recalls is waking up in hospital.”[24]

    [24]   TT 290.

20. Dr Marantos went on to explain in general, that a seizure is an abnormal discharge of electricity, or brainwaves in the brain. It may be caused by an underlying injury to the brain or a brain abnormality. However, there are a number of seizures for which no abnormality is located. The most common form of the complex partial seizure is a short-lived lack of awareness, where people may just stop what they are doing, look blank for a few seconds, and then carry on. During that time, the person is unaware of what is happening and does not have any memory of the actual event. These seizures may affect the memory both before and after the event. This depends upon the severity of the turn and is not necessarily consistent. As opposed to tonic-clonic seizures (that were previously known as grand mal seizures) CPS do not have any violent muscle movement associated with them, but are still classified as a form of epilepsy.

21. Dr Marantos said that the signs and symptoms of a complex partial seizure are that occasionally people may have an aura, they may have an awareness that something is wrong, they may have a taste or a funny smell, they may start fidgeting, but that is not always consistent. He said usually, there is no warning at all, and a person will suddenly stop doing what they are doing, look blank, their eyes may shut or roll up, and a few seconds later, they come back. A complex partial seizure will normally be diagnosed through the history of symptoms and that is where a witness is very important. He further explained that all tests that are conducted including MRIs and EEGs, may be normal.

22. Dr Marantos said that he had read the report from Professor White and the paramedics and the police report of the second collision, and nothing that he read caused him to review the diagnosis of CPS. He noted from the police report that there was no evidence of braking, and thought that was in keeping with a brief period of disturbed consciousness.[25] He acknowledged that he has no expertise in relation to the effects of methylamphetamine in relation to individuals.

    [25]   TT 293.

23. He was asked to assume the following facts about the collision, the subject of the charge on 23 March 2013:[26]

    [26]   TT 293-4.

    1That the accused had methylamphetamine in his system at the time of the collision at a level of 0.66mg of methylamphetamine per litre of blood;

    2That he does not regularly consume methylamphetamine;

    3He attended work on the day of the collision;

    4His only memory of work on that day was working on the mud guards of a tanker and has no memory before, during, or immediately after the collision;

    5His next memory is being at his mother’s house some time after discharge from hospital;

    6At a point at which the collision occurred, the highway was two lanes in the same direction of travel, and a straight line;

    7The conditions were clear and dry;

    8The accused’s motor vehicle drifted or veered from the designated lane and crossed on to grass land adjacent to the bitumen;

    9His motor vehicle then struck the rear of a vehicle parked on the grass land well off the bitumen;

    10His vehicle made no attempt to slow down or avoid the vehicle parked on the grass land; and

    11There were no objects, hazards or wildlife in the area that would have caused him to take evasive action.

24. Having made those assumptions, Dr Marantos was asked his opinion as to the possible medical state of the accused just prior to his vehicle leaving the road. Dr Marantos said that it supports the view that the accused may very well have had a brief episode of a loss of consciousness or complex partial seizure at that time.[27]

    [27]   TT 294.

25. In respect of the methylamphetamine being at 0.66mg/L, Dr Marantos said that his understanding of methylamphetamine is that it makes a person erratic and one would have expected witnesses to have seen a driver moving erratically, rather than a car just moving off the road. After providing this opinion, he accepted that he has a limited understanding of the effects of the substance.[28]

    [28]  TT 294-295.

26. Dr Marantos was cross-examined. He said that the figure of 0.66mg/L means nothing to him. He said he would defer to a pharmacologist on the effects of methylamphetamine in the system. He said his experience in relation to methylamphetamine was limited to people seen in an acute setting in a public hospital, who were presenting with the adverse effects of methylamphetamine. He has not dealt with people under the influence of methylamphetamine, other than those in an acute state. He said that he had not ordered any other tests to be conducted, after the initial examination and diagnosis including any blood tests of the accused. Further, he gave evidence that from the history and the observations of the accused’s son, he was fairly confident that the diagnosis was going to be CPS from the first visit.

27. He was cross-examined in greater detail about the history that he had taken from the accused and his son. In relation to the motor vehicle accidents, the accused said that at times he was aware of a gap in concentration, and said it was “only in the last six months these episodes, noticed it when driving, realised something wrong, shakes his head and improves.”[29]

    [29]   TT 299.

1. The doctor was cross-examined about the loss of memory associated with CPS. Dr Marantos agreed that a CPS alone will not cause an individual to subsequently forget a memory that had been previously formed.

2. The relevance of this in relation to this case is that the accused gave evidence in court that he had no memory of the collision. However, there was evidence from Christina Robertson that the accused said that he saw “a gentleman behind the car and, as he was coming up, he seen him coming around the side.”[30] This evidence obviously accords with the evidence of AP.

   [30]   TT 45.

3. Dr Marantos went on to say that the inability of a patient to recall what occurred during a CPS is an important part of the diagnosis.[31] He said that some people may be aware that something has happened, but they cannot be more specific than that. He said that the affect on the memory depends on the severity of the episode, and the connection between the severity of the episode and loss of memory relates to a larger area of the brain being involved. He said that an absence of a matter of seconds would not be classified as being severe, and went on to describe a severe seizure as involving features such as an aura, fidgeting, eyes rolling or blinking, sometimes people make slapping noises, or noises with their mouth, and the duration is always short. By definition, it has to be no more than a minute, and it can last anywhere from a few seconds to 60 seconds.[32] But there is no evidence that the accused suffered from this type of seizure. He said that in the event of a seizure that lasted only a few seconds, a person’s memory would only be affected for the event. He gave evidence that people remember up to the event and after, but not the event if it only lasts a few seconds. He said in the case of a CPS that lasted for some seconds, he would expect the person to have a memory of events leading up to the episode and after the episode.

   [31]   TT 306.

   [32]   TT 308.

4. Dr Marantos was cross-examined about the way a CPS will appear differently to the observer than to a person who falls asleep. He said that people present differently in those two scenarios.[33] If you fall asleep you lose tone in your muscles and your head may slump forward. A person experiencing a complex partial seizure will continue to stare forward and they do not lose tone in their muscles. He said that their eyes may not change, but there are variations.

   [33]   TT 308.

5. Dr Marantos said that if he had received a history of the accused having lost tone, or his head nodding forward when he took the history from Matthew Wells, this would have changed the order of the provisional diagnosis. In that event, sleep apnoea would have been a more likely diagnosis, and CPS second. In relation to this topic, Dr Marantos was asked whether he has any experience with the symptoms of methylamphetamine withdrawal and said that he does not. He went on to say that if he had been given a history by the patient that included regular methylamphetamine use, he may have included investigations in relation to heart conditions, but apart from that, would not have done any other investigations.

   Methylamphetamine

6. A sample of blood was taken from the accused at about 5pm on 23 March 2013. This was submitted to the Forensic Science Centre for analysis. This blood was found to contain 0.56mg of methylamphetamine per L, 0.09mg of amphetamine per L, and approximately 0.2mg of ketamine per L. The accused had been administered ketamine by the Royal Adelaide Hospital Medical Retrieval personnel whilst en route to hospital.

7. As I referred to earlier in these reasons, the accused was unable to provide an explanation as to how he had this level of methylamphetamine and amphetamine in his blood, although he did not dispute the accuracy of these levels.

8. The prosecution called Professor White as to the effects of the drugs methylamphetamine and amphetamine on driving, and the stimulating and withdrawal phases of those drugs. Professor White also gave evidence in relation to the relevance of tolerance.

9. Professor White is the head of the School of Pharmacy and Medical Sciences at the University of South Australia. He obtained a Bachelor of Science with Honours Degree from the University of Adelaide in 1976. He was awarded his phD in Psychology from the University of Adelaide in 1980, and between 1979 and 1981 did post doctoral training in the United States. He studied pharmacology at the Emory University, there he studied the effects of opioid drugs on the brain. This study is a significant part of pharmacology, especially in the area of illicit drugs.

10. Professor White has also worked as a registered psychologist. This work overlapped with his interest in pharmacology. He had the opportunity to work at the Royal Adelaide Hospital and see people who had a range of drug and alcohol problems. He was dealing with the clinical manifestations of people using the same drugs that he was studying in his research.

11. Professor White has written numerous articles, book chapters and has edited books since the late 1970s, and has been continuously involved in research in the area of pharmacology with a special interest in illicit drugs and addiction issues. Part of his research has looked at the stimulant effects of methylamphetamine on the brain, and his research has involved studying people who are using methylamphetamine and similar drugs in a social environment. This research has involved taking various measurements of the effects on the users, and concentrations of the drug. The curriculum vitae of Professor White was tendered.[34] He regularly gives evidence in courts in this state and other states of Australia, in relation to pharmacology issues. He has been involved in a number of studies in relation to the effects of methylamphetamine upon drivers and keeps abreast of the publications in relation to his area of expertise.

    [34]   Exhibit P 14.

12. Professor White gave evidence that methylamphetamine is a stimulant drug and that generally speaking, stimulant drugs act principally in the brain and cause an increase in particular neuro transmitters in the brain, that is, the chemical messengers to communicate between the nerve cells. He said there are three neuro transmitters in particular that are affected by stimulants. The main one is dopamine, secondly, noradrenalin and thirdly, serotonin. Different stimulants affect those three neuro transmitters to varying degrees, but particularly the dopamine and noradrenalin is how they produce their stimulant effects. He said that methylamphetamine can be used for legitimate therapeutic treatment of ADHD, and the typical concentration range for use of this type would be from 0.02 to 0.05mg/L. Even at those low levels, there can be adverse side effects. He explained there have been concerns about appetite suppression and some evidence of an increased risk of psychotic effects occurring. He went on to say that in this jurisdiction, methylamphetamine is generally seen as an illicit drug in the sense there is no legal use for it in Australia, and it is used by people who are abusing the drug. At the present time, it is principally used in the crystalline form that is known as ice. The majority of people smoke the drug by heating the powder and inhale the vapour. Some people use the drug by injection and some orally.[35]

    [35]   TT 74.

13. Professor White described the physiological effects of illicit use of methylamphetamine as increasing the heart rate, increasing blood pressure, increasing body temperature, elevated sweating, an increase in muscle tension and that may be manifest in various ways such as clenching the jaws, grinding of teeth, or a tremor. These are all due to the increase muscle tension. He said that some of the physiological effects would be appreciable to the user who had ingested methylamphetamine, such as the heart rate increasing, and if the person does engage in teeth grinding, claw clenching or have tremor, they would be aware of that. They may be aware that they are sweating, but in all likelihood they would not notice the blood pressure rising, unless they are experiencing a headache from it. In addition to the physiological effects, he said that the drug can produce a euphoria or intense pleasurable feeling. People who consume the drug typically have a lot of confidence, and feel confident in social situations, or have confidence in doing a range of things that they would normally not have much confidence in doing. There can also be a decrease in fatigue, so that if a person had been feeling sleepy, they would not feel sleepy in the same way and it may actually prevent a person sleeping. A person is also likely to have feelings of a lot of energy. These are what he described as being the effects that people enjoy from the drug that are a consequence of the methamphetamine operating in the neuro transmitters in the brain.

14. He said that these enjoyable effects occur in the initial phase and then individuals can start to experience more adverse effects, where instead of having feelings of energy, they might feel somewhat agitated, their thinking becomes confused, they might have racing thoughts and they may experience psychotic effects that may range from severe psychotic effects that would be obvious to anyone who saw the individual, to effects that were not obvious at all. Typical psychotic effects can include hallucinations and delusions, accompanied by paranoia, so that the person is very suspicious or may be fearful of things in an irrational way. He also went on to explain that whilst the initial effect of keeping a person awake may be positive, it can move into a negative effect if they then cannot get to sleep for extended periods due to abusing the drug.

15. Professor White said that the effects of the drug occur within a very short time, possibly seconds of ingestion. He said that you reach a peak within minutes of taking the drug, if it is smoked or injected. If it is consumed orally, then it will probably take around 30 minutes for the onset of the effects, and the peak effect may not be for several hours after taking it. Professor White explained that if the drug is smoked or injected, the concentration rises to a peak and then immediately starts dropping, so the peak does not last for any significant length of time. Once the level starts to fall, a person will experience less of the positive effects as these are predominantly the effects occurring as the concentration is rising. He explained that psychotic effects can occur some minutes after ingestion and in some cases, they only develop over an hour or several hours. In the event a person has a concentration level of around 0.3mg/L, they are unlikely to experience psychotic effects, however, in contrast, a person who has 1mg/L will almost certainly have some level of psychotic effect occurring. These features vary however, and one of the factors of the variability is the tolerance of the individual and not all people who consume methylamphetamine become psychotic. However, once the level goes above 0.3mg/L, there starts to be a significant risk of a psychotic episode.  He explained that the level of 1mg/L is the average level for overdose death.

16. When looking at the levels of a very occasional user, Professor White said that they may well be between 0.05mg and 0.1mg/L because the person might only use a relatively small amount of the drug and get a mild stimulation.

17. Professor White gave evidence that if a person consumes methylamphetamine and becomes agitated, these feelings can manifest in their physical presentation. Their speech can become rapid, they sometimes seem quite confused, they have an impairment in their normal cognitive function and they may be experiencing racing thoughts, so that they seem to be quite confused to another person. They can be physically agitated and more active, and they can become more obsessive about certain activities, so they focus to an extreme extent on one particular aspect. In relation to the excessive focus, if a person has a relatively large amount of methylamphetamine in excess of a therapeutic dose, their concentration can become extreme. They seem to focus on particular issues and activity to an abnormal degree, and users can become hyper focused on some particular thing. This is sometimes described like a tunnel vision in relation to their vision but also their focus on one particular narrow thing, and they do not notice other things occurring around them. This can have particular significance if the person is driving a motor vehicle.

18. Professor White said that the factors that are important for this consideration are that concentration of the drug, the degree to which the user is accustomed to using the drug and whether they have built up a tolerance to the drug. The difficulty of the driving may also be a factor as there are some situations which are quite complex for drivers. Professor White explained that the more demanding the situation, “the more a person is likely to be affected by a drug, including methylamphetamine.”[36]

    [36]   TT 83.

19. Professor White gave evidence that the form in which the methylamphetamine has been taken is not as important as knowing the concentration levels. It may be relevant to know when the drug was ingested, as shortly after ingestion, the drug concentration would be changing quite rapidly. He gave evidence that once he has the concentration levels, the amount used is not that significant, nor is the manner in which it was consumed that significant.

20. Professor White then gave evidence in relation to the effect on driving at particular concentration levels. He said at a therapeutic level, that is, between 0.02 and 0.05mg/L, the effect on driving would be minimal. Between 0.05 to 0.01mg/L for a person who is an occasional user, there is evidence from simulator studies that there is impairment at that range. People tested in the study had an average concentration of 0.092mg/L and the impairments exhibited were that they were not as good as keeping appropriate distance from the vehicle in front and made greater numbers of errors in braking and in the use of an indicator.

21. Professor White said he would characterise a medium concentration as between 0.1 to 0.3mg/L, a typical range for people who use the drug illicitly. He said that even tolerant users will have some effects at this leveland the potential effects on driving are increased risk taking, manifested by increased speed, increased risky manoeuvres, not keeping an appropriate distance from the vehicle in front, making more errors in the operation of the vehicle such as braking errors and indicator errors. He said there is also potential for tunnel vision or a high degree of focus on one particular thing, or a particular aspect of the environment to interfere with driving. That is, where a person focuses on something that is not the road ahead of them and then they appear to lose concentration and drive in a manner that may be described as erratic, for example, they may suddenly engage in manoeuvres such as driving off the road or into the wrong lane. In some individuals, they may become psychotic at that range (0.1-0.3mg/L), but this would not necessarily occur in everybody in that range. When asked whether he has seen examples of motor vehicle collisions occurring where a person has driven off the road or into the other lane within that concentration range, Professor White said that this type of driving represents at least 50% of the types of accidents that are seen when people are under the influence of methylamphetamine. He went on to say that he bases this upon his reading of reports done for the police and for third party insurance. He said he personally has done reports in over 100 crashes where methylamphetamine has had a role to play and in over 50% of those, they involve the driver, apparently for no reason, veering in some direction or manner which may be off the road, or maybe into the wrong lane, or on to the wrong side of the road.

22. He then moved to the range of concentrations between 0.3 to 0.5mg/L. In that range he said you would expect a somewhat more intense effect increasing the likelihood of a person becoming agitated and the possibility of psychotic effects. He said he would expect that a person in this range is a tolerant user of methylamphetamine and an occasional user would not normally reach that level unless they had done so accidently, and in that circumstance, they would probably be in a situation where it was producing very strong effects upon them. He gave evidence that if a person had a concentration in this range and was still able to operate a motor vehicle in a basic fashion, then he would assume that they are a tolerant user.

23. In the range of between 0.5 and 1mg/L, he described the kinds of effects as being stronger than that of 0.3-0.5mg/L and said there is a high chance of a person experiencing psychotic effects at that level, with some degree of paranoia. He gave evidence that once a person is thinking in an abnormal way, then their driving potential becomes erratic and unpredictable because they may not be responding to things that are there, or doing it for a purpose which is obvious to an observer. The degree of agitation would be quite pronounced as well, and a person’s ability to think clearly to concentrate appropriately would be significantly impaired. They would also show impairment in relation to the way they would respond to other events on the road, in the sense that they may not respond at all. Professor White said that users at this level may simply fail to notice things that are obvious, or they may respond inappropriately. At this level, he said that an individual’s extreme or obsessive focus could form part of a person’s inability to notice and respond appropriately.

24. Professor White went on to refer to a number of articles that were tendered. In summary, whilst some of the studies have low amounts of subjects, they all support the view that in particular, at higher ranges of methylamphetamine, there are negative effects upon the capacity of an individual to drive a motor vehicle effectively. One of the papers, an article by Elvik[37] concludes that there is an estimated risk of between 5 and 8 fold of the likelihood of an accident whilst an individual is under the influence of methylamphetamine.

    [37]   Exhibit P17.

25. Turning in particular to the circumstances of this case, Professor White said that the level of ketamine that was located in the blood of Mr Wells, was consistent with a therapeutic amount of that drug. That is consistent with the finding that it was administered by the medical staff en route to the Royal Adelaide Hospital, as I have referred earlier. In respect of the amphetamine that was located in the blood sample taken, he said that he would regard that as a bi-product of the methylamphetamine.[38]

    [38]   TT 95.

26. Professor White was asked to assume that the reading obtained two hours after the collision was 0.56mg/L. He said that assuming the concentration of methylamphetamine was decreasing between the time of the collision and the blood sample being taken (i.e. assuming that the accused had not consumed methylamphetamine after the collision) and it is being eliminated at an average rate, then he estimated that the level at the time of driving was 0.66mg/L. At those levels, the effects could include increased risk taking and impairment in thinking and decision making, a failure to properly concentrate on the road due to tunnel vision or tunnel focus on other aspects such as the surroundings, and a potential for more erratic driving than might otherwise occur.

27. He said that in relation to methylamphetamine, there are two phases; the first is the stimulating phase which begins shortly after a person has ingested the methylamphetamine, and thereafter, what is referred to as a rebound phase.[39] It is during this phase that a person can be fatigued and have difficulty concentrating for different reasons. He said that sometimes people will be impaired in their ability to maintain concentration for a period that might be 24 hours or more after the drug effects wear off. Insomnia in particular, may continue for extended periods of time, as may an increase in heart rate. In relation to a reading of 0.56 to 0.66mg/L, he said that it is not possible for a person to be in the rebound phase at those levels because the implication is that their concentration must have been considerably higher at an earlier point in time. When a person is at these levels, they would be at high risk of death from overdose and experiencing extreme effects, including psychotic effects, so they could not be in the rebound phase in the sense of having no direct effects of the drug, and simply fatigued. He described this concentration level as significant. He said there would have been direct effects of methylamphetamine at that time. He also gave evidence that at those levels, a person’s ability to fall asleep “disappears.”[40] He said that at that concentration, it is not realistic to consider that a person would fall asleep. It is one of the primary effects of the drug that it prevents sleep, sometimes for days on end. However, in a binge situation where a person has been taking amphetamines for a period of days, it gets to a point where the person can no longer persist without sleep. This exhaustion can also result in psychotic effects, so a person can start hallucinating spontaneously. If a person has crossed into this situation, you may not see physical manifestations of it, but a person in that situation would not be able to drive properly at all. The effects upon them would be very pronounced.

    [39]   TT 97.

    [40]   TT 98.

1. Professor White gave evidence that he is not aware of any interplay between methylamphetamine and CPS.

2. Professor White was cross-examined by Mr Jolly. He was cross-examined about the effects on an individual if the drug Endep is taken at the same time as methylamphetamine. He said there is some potential for increasing the effects of methylamphetamine if the drugs are taken concurrently, but it may not be significant unless the person is taking a large amount of methylamphetamine, in which event, it will have an effect upon the brain and a somewhat increased effect of the methylamphetamine may occur. He was cross-examined about some of the studies that he had referred to earlier and also in relation to the effects if a very high concentration of methylamphetamine was found. In relation to the concentration range of 0.5 to 1mg/L, Professor White was referred to the effects of the drug at those levels, and asked whether it was more likely than not that you would see those types of things as referred to in the study occurring on the road. He said that it depends what is happening on the road and the complexity of the driving task. The more complex the driving is, the more obvious the effects may be. He said where there is not a lot of traffic around, not a lot of intersections or signs to respond to, you may not necessarily see any significant worsening of driving performance, but if that same person is in a situation that may be more difficult, or if they may be required to make rapid decisions, then you are more likely to see them make errors and the drug effect becomes more obvious.[41] He agreed that drivers in that situation are still exercising a degree of control and may be aware of what they are doing, and may even be aware they are not making the right decision. In relation to the suggestion that Dr Robertson holds the opinion that at a level of 0.56 to 0.66mg/L, a person may be so fatigued that they fall asleep, Professor White said that could only be possible in the “rebound phase” or when a user is experiencing withdrawal effects. He commented that that would imply that earlier levels were very much higher, so that you would have to be significantly adversely affected by the drugs at an earlier point in time. Secondly, he said that a person can be in the rebound phase and still have persistent effects of the drug such that they would have difficulty sleeping.[42] In all, Professor White’s opinion was that for a person to be at 0.56 to 0.66mg/L, in the withdrawal stage where he could fall asleep, his levels at an earlier stage would have had to have been life threatening.[43]

   [41]   TT 117.

   [42]   TT 121.

   [43]   TT 122.

3. Professor White was cross-examined about the studies particularly with respect to an individual level that was as high as 18mg/L. Professor White said caution needs to be applied in relation to interpreting those studies because they include fatalities such as homicides and suicides where people have intentionally overdosed, and the concentrations can then be many many times more than what would normally be achieved because the intention of that person was to die. He referred to the data from the Forensic Science Centre where the individuals who have come to the attention of the police have an average concentration of 0.19mg/L.

4. In relation to the determination of tolerance of users, Professor White said tolerance can be determined by reference to when they last used and their use patterns over the previous few months prior to the event, rather than many years ago.

5. He was asked whether methylamphetamine can be used as pain relief and said that whilst it is not beneficial in relieving pain, the euphoric effects that it induces could mask the symptoms in the sense that a person’s mood is elevated and they may have difficulty focusing and tend to think a bit less about the pain.

6. Professor White was re-examined about the studies done at the Forensic Science Centre in so called ‘drug driving cases.’ That indicates that 90% of samples had a concentration of less than 0.47mg/L and 95% of samples had a concentration of less than 0.65mg/L, and that being assumed, then a figure of 18mg/L was significantly outside the range of known concentration in living drivers.

7. Dr Michael Robertson was called by the accused to give evidence. He holds a Bachelor of Science Degree with Honours in Pharmacology and Toxicology from Monash University. Having received that qualification, he then went on to work with the Victorian Institute for Forensic Medicine between 1991 and 1996 as a Forensic Scientist, and thereafter, worked in the United States for some years. His qualifications are set out in his curriculum vitae what was tendered.[44] He has now worked for almost 30 years in the fields of pharmacology and toxicology. A list of his publications was tendered.[45] He is a member of number of different organisations including the Australian and New Zealand Forensic Science Society, the International Association of Forensic Toxicologists, Society of Forensic Toxicologists and Forensic and Clinical Toxicologists of Australia. These societies and associations share the results of their research and findings, organise conferences, and communicate about current research. He acknowledged that he does not have expertise in relation to generalised seizures, or, partial seizures. He acknowledged receiving reports prepared by Professor White dated 11 March 2014 and 19 May 2014.

   [44]   Exhibit D21.

   [45]   Exhibit D22.

8. The opinions of Dr Robertson were largely in agreement with Professor White. There were some areas of disagreement and I will deal primarily with those.

9. He gave evidence that in relation to methylamphetamine, a tolerance can be built up. He explained it as, the more you use the drug the less effect it will have on an individual at the same dose, therefore in order to experience those positive effects, the dose has to increase. In this way, the dose itself is irrelevant, because the individual will take the dose appropriate to obtain their desired positive effects, and the dose will vary based on the drug taking history of the individuals. He said in relation to the stimulation phase of the effects of methylamphetamine, at lower concentrations it can improve driving, so particularly if you are fatigued, it may have little effect, if you are a user of methylamphetamine. If a person is fatigued or going through withdrawal it can normalise them. It is a general way of easing distraction. He went on to say tracking, that is, making sure the car stays in the lane, can be disrupted, risk taking can increase because of the feelings of euphoria and grandiosity, and a person may drive more quickly, speeding for instance, driving through red lights may occur because you are no longer afraid of the consequences.[46] He described the generally accepted therapeutic range is of about 0.05mg/L, with the majority of publications referring to it as being 0.05 to 0.1mg/L. He said in this range there were more likely improvements in performance that have been documented and there are also documented degradation of some performance tasks. It depends on who is taking the drug, how they are taking it, and whether they are regular users.

   [46]   TT 207.

10. He said that when you get in a range of above 0.5 or 0.6mg/L, you are moving into a higher range. Dr Robertson said that 0.8mg/L and above is a high concentration. However the effects depend, again, on the tolerance of the user. He said the simulation phase is generally regarded as two to four hours post dose but that can vary if taken orally. Initially there is dysphoria then as the concentration plateaus it drops and the dysphoria gives way to fatigue. Fatigue can be exacerbated by sleep patterns and a lack of sleep may have an effect on the fatigue of an individual. He said that if a higher dose is taken to achieve stimulation, then during the withdrawal phase the concentration will also be high because it can take 10 to 15 hours for the concentration of methylamphetamine in the blood to halve, yet fatigue can occur six to eight hours after use. In relation to the factors that affect sleep, he said that a naïve or intolerant user, at a level of 0.4mg/L that may have used it two to three hours prior, would probably not be able to sleep but a concentration of 0.4mg/L in someone who had used a higher dose and was at 0.6 or 0.7mg/L some hours before, may reasonably fall asleep particularly if they are fatigued. If they have used the methylamphetamine by binging, which is reasonably common with methylamphetamine users who use it constantly for a period of 24 hours or more, sleep is achievable even though the concentration of methylamphetamine in their blood stream is still relatively high. He said without knowing the drug use patterns and the drug use history of an individual, it is difficult to predict how methylamphetamine may affect them. He described a regular user as a daily user of the drug, that is, someone who has used in regular amounts so that the chemistry of their brain is not reverting back to normal. In these cases, the physiology of the brain changes because of the substances that are in the system. It is in this way that a tolerance is built up to methylamphetamine. He also referred to the need for a regular user to be using daily over months. They may use more than once a day in small amounts but it would take a period of time to build up a tolerance. In terms of their sleeping patterns, he likened it to caffeine use, where certain individuals cannot have a coffee after midday because it keeps them awake, whereas others have a coffee before going to sleep. He said that the physiological effects on the brain are not permanent, they can revert back, but only after a number of months.

11. Dr Robertson said that he has heard the term hyper focus used in relation to methylamphetamine, but he is not specifically clear on what it is meant to relate to. He said he has not read about obsessive traits in the publications in relation to an individual grinding their teeth or fidgeting but as far as focusing on one thing to the exclusion of others he is not familiar with that.

12. Dr Robertson gave evidence that in order to predict the likely effects of methylamphetamine at a particular level, it is important to know whether they are a tolerant user or not. He explained it in these terms: if an individual has a peak concentration of 0.3mg/L but is tolerant to the drug, it may have less impairing effects upon them than someone who is using it for the first time or is a less tolerant user. It may also be that the level of 0.3mg/L is not the peak concentration but rather a residual amount from a drug consumed many hours earlier when that individual may have in fact peaked at 0.6 or 0.7mg/L and it is now dropping. In that case you would not be dealing with stimulation at all but rather dealing with individuals who ware fatigued and in the withdrawal stage. In this sense, the reading that is obtained from the blood analysis is a quantification of the concentration of the drug in the blood at that particular time.

13. Dr Robertson agreed that if the blood test was taken two hours after the collision and revealed a reading of 0.56mg/L and assuming that the individual had not ingested in the hour or two prior to the collection of the sample, shortly before the collision a level of 0.66mg/L was reasonable.[47] At that level he said it was likely to have had an effect on the driving of the accused if 0.66mg/L represents recent use as it is more likely that the individual was stimulated. If 0.66mg/L represents residual drug from a higher concentration 10 to 15 hours earlier then the effects are likely to be different from a person who was stimulated. Dr Robertson was asked to assume that at the time of the collision the range was 0.56 to 0.66mg/L of blood of methylamphetamine, that the substance had been consumed orally, that Mr Wells was a regular and high user of methylamphetamine up to 2009 when he stopped cold turkey and on two occasions relapsed once in 2011 and once either in the middle of 2012 or slightly earlier when he used intravenously. He was then asked to identify what effects if any there may have been manifested by Mr Wells just before the collision. Dr Robertson gave this answer:[48]

    AThe effects of tolerance I do not believe to be relevant if his last exposure was mid-2012, that is, his central nervous system would likely to have reverted to normality, if I can use that term. Therefore the concentration is relatively high in someone that would be an irregular, or I can almost classify him in the non-user in the relevant period. That being said, that number in isolation again just allows the interpretation that either the effect of stimulation would have been greater depending upon when the drug was ingested, that is, I still cannot determine from the information whether the 0.56 to 0.66 is a peek concentration from recent use or a residual concentration that may have been consumed, be that orally, or injected, or smoked 10 to 15 hours earlier, it’s still to difficult to determine what phase someone was in regardless, in this case, of their drug-use pattern.

    QCan I now build on that scenario a bit more by asking you to assume this information; that the motor vehicle that Mr Wells was driving effectively veered or drifted off the road onto the shoulder of the road and struck a stationary vehicle. Can I also get you to add in that there was no evidence that Mr Wells made any attempt to slow down, or to avoid that collision. Can I also ask you to assume that there were no objects, hazards or wildlife in the vicinity of the collision that would have caused Mr Wells to take evasive action and that the road was straight. It was one directional, that is, a completely separate road to the oncoming traffic. The conditions on that day were bright and clear and I ask the question again with that additional information; are you able to give some assistance in the likely effect of that concentration of methylamphetamine, that is, 0.56 to .66 on Mr Wells just prior to the collision.

    AIn my experience, the absence of evasive action or braking and so on and so forth are consistent. When I say ‘my experience’, what is both in review of the literature as well as my own personal research into driving-related crashes, that the absence of braking is consistent with either falling asleep or loss of concentration for a protracted period of time or some other medical event, obviously that may have occurred, the phase of the individual, an individual can be distracted and that may lead to some drifting off perhaps. So I can’t exclude that as a possibility. But the absence of braking or evasive action when otherwise I would have expected an observation of a car to be based there, based on what you have just described to me, appears to be more consistent with fatigue or withdrawal, an individual falling asleep, or another alternate cause.

    QGiven the scenario that’s now been painted for you, are you able to say with any certainty as to whether it was the stimulation phase or the withdrawal phase that Mr Wells was in just prior to the collision.

    ANot with certainty. I can’t exclude either scenario with certainty. I would suggest it’s more likely that it is a fatigue-withdrawal type scenario, loss of concentration due to fatigue or indeed falling asleep that has led to that loss of concentration, if I assume it only to be methylamphetamine-related. That is I’m setting aside potential other causes.

    [47]   TT 224.

    [48]   TT 227-229.

14. Dr Robertson was cross-examined. He described the ways that observations of an individual post-collision can provide useful pieces of information. This may include observations of whether a person is in the stimulating phase or the withdrawal phase at the time of, or immediately after the collision and their respective levels. He agreed with the proposition that a person’s driving can be significantly impaired without the person exhibiting obvious features to an outsider.[49] He agreed that the absence of outward signs of impairment is not a good indicator of a person’s ability to drive safely. Ms Matteo put to Dr Robertson the scenario that had been painted by the accused during the course of his evidence about his methylamphetamine use in the years and months before the collision. Dr Robertson said that he would regard a person with this degree of use as being intolerant and it would put a person in the same position as a first time user in respect of their tolerance. The exception to this would of course be that they would know what to expect if they used the substance in relation to the effects of stimulation at this level in someone who was intolerant. Dr Robertson said he would expect significant stimulation or profound stimulation that may lead perhaps to agitation and irritation at the level of the accused. He did not think it would be high enough to induce psychosis and hallucinations, but he said that it would certainly produce significant stimulation, amplified feelings of grandiosity, feelings of being “bullet-proof,” distraction, rapid thought processes and impaired tracking.[50] He said the impaired tracking can occur in both the stimulation phase and the withdrawal phase. In peak tracking, a person’s  ability to watch, keep the car moving in line, and so on, can be due to the stimulation phase because they have got rapid thought processes, they are distracted by a lot of things and paying less attention to where the car is in the lane and observing things around them. It can also occur in the fatigue stage, which is when they are tired, have poor concentration and so on.[51] He said that tracking is one of the aspects that is studied in the literature, and that following the recent ingestion of methylamphetamine, tracking is often impaired. For a person who was intolerant and exhibited a blood concentration level of 0.56 to 0.66mg/L, the withdrawal stage would also produce greater effects relative to someone who is tolerant.[52] Dr Robertson said that these rebound effects are more to do with concentration, a feeling of emotional flatness, and feelings of being tired and exhausted that may lead to sleep. It may also lead to a condition where someone is slower to react.

    [49]   TT 248.

    [50]   TT 250.

    [51]   TT 250-251.

    [52]   TT 251.

15. Dr Robertson was also cross-examined about the 2004 article that he had written, about a study in which he had been involved that was said to have presented: [53]

    good evidence that drivers killed in motor vehicle crashes and taking psycho active drugs, particularly cannabis and strong stimulants, or two or more drugs in combination were more likely to be responsible for the crash than those taking neither drugs nor alcohol.

    [53]   TT 254.

16. He agreed that that was the conclusion of the study and said that the study did not know whether the participants were in the withdrawal or stimulation stage in respect of stimulants that they had consumed. He said the majority of the cases related to methylamphetamine and agreed that the use of methylamphetamine significantly increased a driver’s risk of a serious road crash.

17. After the final address had been delivered, counsel for the accused sought leave to reopen the defence case to present evidence that the accused had been tested for the presence of methyamphetamine in 2012, and that the results had been negative. This was opposed by the prosecution. I heard argument and permitted the evidence to be admitted. A report in relation to results was tendered.[54]

    [54]   Exhibit D26

18. Both counsel addressed. The addresses were comprehensive and well constructed. I have taken into account the arguments of both Ms Matteo and Mr Jolly.

    Findings of fact

19. Considering all of the evidence, I am satisfied beyond reasonable doubt of the following facts. At approximately 3.00pm on 23 March 2013 a motor vehicle driven by AK stopped on the Sturt Highway on the gravel shoulder of the roadway. It was well off the lane for south eastern bound travel at that time. AK alighted from the driver’s door and walked towards the rear of the utility. As he was doing so, AP alighted from the passenger door and observed a motor vehicle driving towards them. This motor vehicle was a Barina being driven by the accused. He was the sole occupant of that car. The Barina drifted from the left hand lane of the road directly towards the utility. At that time, it was doing a speed of about 110km/h. The accused did not brake, or take any other evasive action, as the Barina came towards the rear of the utility. The Barina collided with the rear of the utility. As a consequence of the collision, AK was struck and sustained serious injuries that amount to serious harm.

    Was the accused driving voluntarily?

1. In order to answer this question, it is necessary to consider what aspects of the evidence I am prepared to rely on. It requires an assessment of all of the evidence including the accused’s evidence and the statements he had made to others. I must then determine whether I am satisfied that the prosecution have proven beyond reasonable doubt that the accused’s driving was voluntary. To put another way, I must be able to exclude even as a reasonable possibility that the accused did not suffer from a CPS that rendered his driving at the time of the collision involuntary.

2. The accused had a level of methyamphetamine in his blood of about 0.66mg/L at the time of the collision. This level is so significant that no matter when he had consumed the drug, in the opinion of both experts, it would have significantly impaired his capacity to drive a motor vehicle effectively. However, this fact alone does not inform me about whether he also suffered a CPS at a time proximate to the collision, and by reason of a brief period of unawareness or unconsciousness, was so impaired by that event that it caused him to drive in the manner that I have described above.

3. It is clear on the evidence from Professor White, Dr Robertson and Dr Marantos that there is no reason to think that the ingestion of the methyamphetamine would have brought on, or caused, the CPS. If I accept the evidence of the accused in relation to these episodes then they had probably been occurring for some time prior to the collision but he was unaware of them. If I accept the evidence of the accused, such an episode may have accounted for the collision that occurred in February and the events that his son observed.

4. I accept that Matthew Wells made observations about his father in the way he described in his evidence.  Matthew Wells was a considered witness who expressed genuine concern for his father.

5. However I do not accept the evidence of the accused on a number of crucial issues.

6. I do not accept that he had not relapsed in relation to consuming methyamphetamine at a time prior to the collisions in February and March. I accept his evidence that he had been a very heavy user of the drug prior to 2009 and then stopped using, and that he had relapsed after that, including in 2012. I accept that the urine tests[55] confirm that he did not have methyamphetamine in his body at the time he was tested. However, the last test was in August 2012.[56] In evidence he said in relation to the relapse in 2012:[57]               

   [55]   D26.

   [56]   I note that these tests were conducted by DCS and draw no adverse inference against the accused in this regard.

   [57]   TT 159.

   QHow long before that car crash or that collision had you last taken methamphetamine, as far as you’re aware.

   A2012, somewhere around there, I think.

   QWhen in 2012; beginning, middle or end.

   AIn the middle somewhere round there. Might’ve been a bit before that.

   QDid you take any methamphetamine in the second part of 2012.

   ANo.

   QDid you take any around Christmas 2012.

   ANo.

7. When the accused gave his history to Dr Marantos in May 2013, he referred to methylamphetamine in an historical sense, without going into detail about his usage at the first consultation or later when he had become aware of the hospital blood test results. One explanation for him not having mentioned his drug use to Dr Marantos may be that he did not consider it relevant.  Another may be that his son was present at the first consultation and the very reason that the accused had stopped taking drugs was because of an ultimatum from his son in 2009. When his son gave evidence in this case, he said he was unaware that the accused had relapsed at all nor was he aware that the accused had methylamphetamine in his blood at the time of the subject collision. He said he had taken the accused at his word that he had stopped using the drug.[58] It is therefore possible that the accused was not willing to admit to Dr Marantos that he had recommenced using methylamphetamine while his son was present and at later consultations it was not an issue that was raised.

   [58]   TT 279.

8. When Matthew Wells was giving the history to Dr Marantos, he said he had first made his observations at about Christmas 2012. However in evidence, he was less certain about the times and thought it could have been 9 months to a year prior to the collision in March 2013, but noticed his father being dazed around Christmas time.[59] The description given by Matthew Wells in evidence, of his observations of his father “falling asleep,” was very different from the history recounted by Dr Marantos. In court, he demonstrated the accused falling asleep with his head nodding forward and losing tone. This is, according to Dr Marantos, inconsistent with a CPS. During a CPS a person may look forward, stare or eyes roll back. The clear description by Matthew Wells in evidence was seeing a person who fell asleep.

   [59]   TT 267, 273.

9. The regularity with which Matthew Wells appears to have observed these events, being every time he saw his father during this period of time,[60] also makes it unlikely, in my view, that the explanation for what he was describing was always a CPS, rather than perhaps a number of events occurring, including the withdrawal stage of methylamphetamine use.

   [60]   TT 264, 273.

10. I do not accept as a reasonable possibility, the assertion of the accused that he was not regularly using methylamphetamine at the time of the collision. His reading was in a range that renders it impossible for him to have been unaware of it given the high level of methylamphetamine recorded in his blood. I do not accept that his food or drink was spiked at a BBQ at his friend’s house on the evening before the collision, and that the methylamphetamine in his blood at the time of the collision was the residual amount. To accept this evidence would have necessitated the following findings:

    ·that shortly after the oral consumption, at about 7.00pm on 22 March 2013 his level of methylamphetamine was around 0.88 – 1mg/L. This amount could be sufficient to cause an over dose in a naïve user;

    ·that he was unaware of the presence of the drug. On his evidence he drove to his mother’s home, had a good nights sleep, got up and went to work the next day, all the time seemingly unaware that he had this drug in his system; and

    ·that he was unaware of the presence of the drug in light of the evidence of both experts, that at the level of 0.66 mg/L there would be significant, or profound stimulation that may lead perhaps to agitation and irritation. It may not be high enough to induce psychosis and hallucinations but it would certainly produce significant stimulation, amplified feelings of grandiosity, feelings of being bullet proof, distraction and rapid thought processes and impaired tracking.[61] This of course, needs to considered in the context that if the evidence of the accused was accurate, his level was significantly higher the previous evening and he was an intolerant user therefore the effects would likely be more pronounced.

    [61]   TT 250.

11. I find that the accused was untruthful about his abstinence from methylamphetamine at the time of the alleged offence.

12. I do not accept the evidence of the accused that his last memory on the day in question is working on the tipper and that he has no recollection about the day before or after that. In this regard, I refer to his history to Dr Marantos on 1 May 2013, including a memory of getting his shopping, and getting into his car and driving off.[62] There is no medical explanation for him having this memory on 1 May 2013 and no longer remembering this event when giving evidence. Indeed, this assertion on 1 May 2013, is inconsistent with his assertion to the Police Officer on 9 May 2013, when asked if he can recall even the incident leading up to the collision, and in response, the accused shakes his head.[63]

    [62]   TT 290.

    [63]   Exhibit P19.

13. I found the accused to be an unsatisfactory witness. He prevaricated, was untruthful and unconvincing, even allowing for his personal shortcomings and inability to articulate clearly. For the reasons that I have expressed, I am satisfied beyond reasonable doubt that he was a regular and significant user of methylamphetamine by the time of the collision on 23 March 2013.

14. I find that he was dishonest when he gave his history to Dr Marantos. Dr Marantos has relied upon the history of both accused and his son to diagnose CPS, as he must. However, his diagnosis is only as good as the history given. In this case I find that there were significant deficiencies, the most notable of which was in relation to the untruths or “gaps” regarding the accused’s consumption of methylamphetamine. There are no medical tests that support the diagnosis of CPS.  Dr Marantos has a very limited understanding of the effects of methylamphetamine and the different stages associated with its use, and frankly admitted so when he gave evidence.

15. The opinion of Dr Marantos was based on the assumptions[64] that he was asked to make in relation to the condition of the accused, at a time proximate to the collision. These assumptions included that the accused was not a regular user of methylamphetamine.[65] It is not possible that the accused was a naïve user at the time. It would be impossible to have achieved these levels and be functioning without an awareness of his own intoxication. Dr Marantos does not have a good understanding of the effects of the proven level of methylamphetamine. Indeed it seems to have played no real part in relation to his opinion or diagnosis.

    [64] See above at [48].

    [65]  Ramsay v Watson (1961) 108 CLR 642 at 645.

16. The question of the conversation between the accused and Ms Robertson was not raised with Dr Marantos in evidence in chief. In cross examination he said that it was possible for the accused to have seen a man at the back of the car to then suffer a CPS and veer off the road but if he veers off while seeing the man then that is not consistent with a CPS.[66]

    [66]   TT 317-318.

17. I have reservations as to whether the accused has even suffered from CPS. However it is not necessary for me to decide this issue. Even if the diagnosis of CPS is correct, I reject beyond reasonable doubt that the accused suffered from a CPS event proximate to the collision.

18. I am satisfied that a statement was made by the accused to Ms Robertson shortly after the collision, to the effect that he had seen a man “behind the car and, as he was coming up he seen him coming around the side.”[67] In cross-examination it was put to Ms Robertson that in statement she gave to the police on 17 October 2013 she said “during part of our conversation, the male said he had seen someone at the back of the ute and that he had been walking towards the driver’s door when he hit him.”[68] Ms Robertson agreed she had said that to the police.

    [67]   TT 45.

    [68]   TT 47.

19. I am satisfied that the statement of AP accurately describes his observations. When AK was nearing the rear of the vehicle the accused was already veering off the road. To have seen AK in this position at that time the accused had to be conscious. There is no doubt that the veering manoeuvre had already commenced when AP first saw the vehicle.

20. I am satisfied beyond reasonable doubt that the accused was at all stages conscious and aware, but impaired by the effects of a voluntarily consumed quantity of methylamphetamine.

21. I therefore find that the driving of the accused was voluntary at the time of the serious harm was caused to AK.

    Driving in a manner dangerous

22. The Prosecution must prove that the manner of driving of the accused was such a grave departure from the standard of care expected of a driver, that it imposed a risk which any person in the position of the driver would recognise as a real danger to the public. It was explained by Barwick CJ in McBride v The Queen:[69]

    The section speaks of a speed or manner which is dangerous to the public. This imports a quality in the speed or manner of driving which either intrinsically in all circumstances, or because of the particular circumstances surrounding the driving, is in a real sense potentially dangerous to a human being or human beings who as a member or as members of the public may be upon or in the vicinity of the roadway on which the driving it taking place. It may be, of course, that potential danger to property on or in the vicinity of that roadway would suffice to make the speed or manner of driving dangerous to the public, but the need for death or injury to a person to result from impact with a vehicle so driven may make that question unlikely to arise, though the possibility of its doing so must be acknowledged.

    [69]   McBride v The Queen (1966) 115 CLR 44 at 49-50 per Barwick CJ.

23. The manner of driving encompasses all matters connected with the management and control of the vehicle, it also includes the state of the driver. When intoxication is relevant the principle to be applied were considered by Cox J in Greenham:[70]

    The relevant element of the offence created by s19a is the dangerous driving, not the cause of it. The jury will be called upon to make a qualitative judgement about a defendant’s manner of driving in the light of all the circumstantial evidence. Typically there will be one or more acts of overtly bad or at least questionable driving – high speed, veering across the road, poor look out and so on – and sometimes evidence of a causative or explanatory kind as well. For instance, the defendant may have told someone before he got into his car that he was having trouble keeping awake, or his driving error may have coincided with his using a mobile telephone, or there may be evidence of an alcohol intake which, according to an expert, could have effected the defendant’s driving faculties. The jury may take the alcohol evidence into account if, after considering all the evidence including the act or acts of driving, they are satisfied that the alcohol had an influence on the defendant’s manner of driving.

    [70]   R v Greenham (1997) 25 MVR 495 at 500 per Cox J.

24. The accused drove his motor vehicle whilst he had a significant level of methylamphetamine. I have rejected his assertion that he was a naïve user, nevertheless this level of methylamphetamine would, according to the experts, have had an adverse impact on his driving. This is so regardless of whether he was in the stimulation or withdrawal phase. The ability of the accused to properly focus on his driving to the extent that is required when driving at a speed limit of 110km/h was severely compromised. His gross lack of attention resulted in his car leaving the lane in which he was travelling, and without changing speed, to collide with the stationary ute that was parked well off the road. This occurred at a time when the conditions were dry and clear and there was no impediment to the accused’s vision. In all likelihood, the collision was caused by a complete failure to concentrate on his driving, or as a result of his impaired ability to track, as described by both Professor White and Dr Robertson, that led to the accused hyper focusing on the ute, actually causing him to drive towards it. 

25. I am satisfied beyond reasonable doubt that this gross lack of attention, to the point where he actually drove off the carriageway, over the bitumen shoulder and onto the gravel shoulder and hit the ute without taking any evasive action, amounts to driving in a manner dangerous, as opposed to driving without due care.

26. I am satisfied beyond reasonable doubt that this manner of driving was a substantial cause of the serious harm caused to AK.

27. I am therefore satisfied beyond reasonable doubt of each of the elements of the offence of causing serious harm by dangerous driving.

28. Further I am satisfied beyond reasonable doubt that the circumstance of aggravation has been proved.

    Conclusion

29. I find the accused guilty of the offence of Aggravated Causing (Serious) Harm by Dangerous Driving.