Was Mr Lowe's condition caused solely and independently of any other cause?
84 In light of the reasons and conclusion expressed above to the effect that Mr Lowe does not suffer from hemiplegia as that term is used in the Policy, it is not necessary to address this question. However, as there is a substantial body of evidence directed to the issue, and the matter has been fully argued, it seems to me desirable that I express my views on the issue. I will deal first with the contemporaneous documentary evidence, and then deal with the expert evidence given at the hearing, before turning to the relevant legal principles and their application.
85 Following the 2016 Injury, the contemporaneous medical reports contained a number of references to "signal change in the cord" (which Dr Coyne said indicated a structural abnormality within the spinal cord: T86.28-30), oedema (i.e. swelling: Dr Coyne at T86.32-33) and myelomalacia (i.e. scarring: Dr Coyne at T86.34) on Mr Lowe's spinal cord noted in MRI scans performed on his cervical spine:
(a) the first MRI report taken two days after the 2016 Injury by Dr Geoffrey Haussman noted "significant deformity of the cord" (CB116);
(b) the MRI report of Dr Alan Boles dated 9 January 2017 noted that "the pre operative study does demonstrate minor cord oedema at the C5/6 level however this appears to have largely resolved" (CB437). In his oral evidence, Dr Coyne recalled after this scan "a little bit of residual signal change within the spinal cord on subsequent MRI scans" (T67.1-2);
(c) the MRI report of Dr Tyson Reeve dated 1 April 2017 initially stated "no cord oedema", but an amendment was added on 3 April 2017 noting that "there is very subtle hyperintense signal in the left lateral aspect of the cord which could reflect mild cord oedema or myelomalacia…given the history of new symptoms, this does raise the possibility of recent injury to the cord" (CB125-6). When asked about this scan in cross-examination, Dr Coyne opined that there was some oedema in that scan, and "any signal change [within the spinal cord] is probably of some significance because it means a spinal cord has had a physical injury" (T70.8-71.7);
(d) the MRI report of Dr Charlotte Slaney dated 4 May 2017 noted it was possible "that there is a subtle area of increased T2 signal within the left lateral aspect of the cord which may indicate mild oedema or myelomalacia." Dr Slaney also noted that "it is possible that there is a small amount of oedema in the left lateral cord at the site of indentation by the focal disc bulge"(CB132-3);
(e) in Dr Guazzo's letter to Dr Ball dated 5 May 2017, Dr Guazzo noted his review of Mr Lowe's MRIs that "[t]he small area of signal change in the cord was evident on the previous MRIs and relates to the initial disc protrusion" (CB131). In cross-examination, Dr Coyne opined that any change was "pretty marginal" and that "there wasn't significant change" (T73.13-16);
(f) the MRI report of Dr Alan Boles dated 8 June 2017 noted that "the disc protrusion effaces the CSF space anterior to the cord with some distortion of the left side of the cervical cord…The increased signal intensity within the left side of the cord at this level extending over the 14mm longitudinal length is similar to previous imaging" (CB135);
(g) the MRI report of Dr Kurundeniya Prematunga dated 31 August 2017 noted that "There is anterior indentation to the thecal sac and the spinal cord. There is oedema of the cord extending from the lower border of C4 to upper border of C6. The oedema is best demonstrated on sagittal images … There appears to be minimal progression of the cord oedema craniocaudally as demonstrated on sagittal images" (CB137);
(h) the MRI report of Dr Dimmick dated 19 July 2020 recorded that "[h]yperintensity within the left hemi cord extending from the level of the mid C5 vertebral body to the middle C6 vertebral body (1.8 cm in length) appears to be a combination of oedema and myelomalacia" (CB140-1). In his oral evidence, Dr Coyne opined that this scan showed "that there has been sort of an extension or progression of the residual disc protrusion that was left behind after the 2016 surgery" (T77.1-9);
(i) Dr Farey's letter dated 2 November 2020 recorded, from a review of MRI scan on Mr Lowe's phone, "the presence of a large central and left sided disc protrusion at the C5/6 level with marked cord compression and myelomalacia" (CB147, 345, 386);
(j) the MRI report of Dr Gaurav Khera dated 3 November 2021 noted "Reduced volume of left hemicord with bright signal area suggesting chronic myelomalacia at C5/6 level. This is likely sequala to old injury" (CB390); and
(k) the letter from Dr Parkinson to Dr McDonald dated 25 November 2021 noted that repeat MRI imaging showed "residual myelomalacia consistent with a previous cord injury for which the surgery was required" (Exhibit D).
86 The 2016 Surgery involved, among other aspects, the removal of free disc fragments arising from the 2016 Injury (CB120, 122). For the 2020 Surgery, Dr Parkinson's Operative Findings noted a "[f]loating bone fragment due to previous foraminotomy also causing some foraminal compression" (CB144). This is direct evidence of fragments from the 2016 Injury contributing to the compression of Mr Lowe's spinal cord in the 2020 Injury. Dr Coyne said that Mr Lowe was at a higher risk following the 2016 Surgery because of the "floating" fragments of disc that could not be recovered in the 2016 Surgery, although that increased risk could not be quantified (T67.41-68.6). After the 2016 Injury and after the 2016 Surgery, MRI scans revealed that Mr Lowe continued to suffer a persistent, albeit reduced size, left posterior paracentral disc protrusion (CB437, 125-6, 132-3). Dr Guazzo emphasised in correspondence in 2017 that Mr Lowe's risk of further injury had increased following the 2016 Injury, stating on 6 April 2017 that "[t]here must be some increased risk in view of the disc protrusion" (CB127) and on 5 October 2017 that Mr Lowe "must be at slightly increased risk of cord injury if he sustains a serious injury to his neck" (CB136).
87 The contemporaneous documents also show that Mr Lowe was asymptomatic after the 2016 Surgery, in particular Dr Guazzo's letters to Dr Ball of 3 November 2016 (CB123), 12 January 2017 (CB124), 6 April 2017 (CB127), 12 June 2017 (CB134) and 4 December 2017 (CB139). Those findings are consistent with the background that Mr Lowe had continued to play rugby league in the NRL competition during the 2017, 2018 and 2019 seasons, and up to Round 10 in the 2020 competition, and had also suffered the 2017 Injury. Mr Lowe himself said in his affidavit that he had no ongoing symptoms during that period associated with the 2016 Injury (paras 37, 42, 43 and 45-47).
88 In his expert report, Dr Coyne addressed the question: "Insofar as the Claimant suffered a medical or physical condition following the 2016 incident, was it aggravated by the 2020 injury, or combined with the 2020 injury so as to result in the Claimant's current medical condition?", and provided the following evidence (p. 8):
It is likely that both the 2016 and 2020 incidents have contributed to Mr Lowe's current condition. The 2016 incident likely left the C5/6 disc with a predisposition to further injury, including disc protrusion, in the event of a further significant force to the cervical spine, noting that imaging following Mr Lowe's 2016 cervical spine surgery demonstrated some degree of residual central/left disc protrusion. The subtle signal change within the cervical spinal cord following the 2016 incident indicates that Mr Lowe's spinal cord possibly had less reserve to deal with a second insult.
It is likely that the first incident resulted in a predisposition to a further injury in the event of significant force to the cervical spine. As such both incidents have likely together resulted in Mr Lowe's current condition. However is it possible that even in the absence of the first incident sufficient force to the cervical spine as in the second incident may have resulted in a de novo C5/6 disc protrusion with the same outcome.
As I have indicated above, in the context of Dr Coyne's evidence as a whole, I read the word "likely" in that passage as meaning "more likely than not", in contradistinction to the use of the words "possibly" and "possible" in the last sentence of each paragraph in that passage.
89 In his cross-examination, Dr Coyne readily conceded on numerous occasions that Mr Lowe was asymptomatic after the 2016 Surgery. Dr Coyne was taken to Dr Guazzo's letter of 4 December 2017 referring to Mr Lowe being "completely asymptomatic" following the 2016 Injury involving an orbital fracture and significant extension of his neck, and accepted that that was an important matter in indicating that Mr Lowe's neck was capable of sustaining some significant force without any further injury (T74.41-43). However, Dr Coyne did not accept that that demonstrated that Mr Lowe's spine was capable of withstanding the kind of force that can fracture the orbital socket, as distinct from showing that Mr Lowe "got lucky that time" and he did not get lucky a few years later (T74.45-75.9). Dr Coyne accepted that the increased risk resulting from the 2016 Injury of a further disc injury and further neurological symptoms in the future could not be measured and expressed as a figure (T75.35-44; and see T74.26-33). Dr Coyne also accepted that the 2020 Injury was a new injury with new neurological symptoms, but said that the MRI scans showed that it was an extension or progression of the residual disc protrusion that was left behind after the 2016 Surgery, and the 2016 Injury provided the platform on which the 2020 Injury occurred: T76.13-77.18. Dr Coyne was asked specifically about the opinion in his report that the subtle signal change within the cervical spinal cord following the 2016 Injury indicates that Mr Lowe's spinal cord possibly had "less reserve" to deal with a second insult, and agreed that what he was saying is that there was a susceptibility to a greater degree of injury rather than any root cause of injury (T78.42-44).
90 As I have indicated above, Dr Mobbs was not asked specifically to address this question, but expressed the following opinions in her report which are relevant to it:
(a) although symptomatically returned to normal after the 2016 Surgery, Mr Lowe may have had ongoing spinal microscopic compromise from the 2016 Injury that meant a vulnerability to more severe injury (p. 3, para 2); and
(b) the 2020 Injury was almost certainly made worse by the neural vulnerability created by the 2016 Injury (p. 3, para 5).
As I have indicated above, Dr Coyne expressly agreed in his oral evidence with the latter proposition.
91 In her cross-examination, Dr Mobbs accepted that the signal changes at the C5/6 level which existed prior to the 2020 Injury indicated spinal cord damage, insult or compromise, although she described that as "mild" (T54.45-55.9). Dr Mobbs accepted that ongoing traces of oedema and myelomalacia indicated a process of damage to the spinal cord but said that it would not necessarily indicate an ongoing active process and said that if it was a pathological process then it was "minor" (T55.17-23).
92 As I have indicated above, I accept the evidence of Dr Coyne, and in cases of inconsistency I prefer his evidence to that of Dr Mobbs.
93 Turning to the question of legal principle as to the meaning of the expression "solely and independently of any other cause" used in the definition of "Bodily Injury" in the Policy, the relevant authorities on similar wording were considered by the New South Wales Court of Appeal in Preston v AIA Australia Ltd [2014] NSWCA 165. In that case, the policy wording referred to a physical injury "which results solely and directly and independently of a pre-existing condition or any other cause in total disablement". That language is arguably more difficult for the insured to satisfy than the wording in the Policy, because of the reference to "pre-existing condition" in addition to "any other cause". However, the authorities reviewed by the Court of Appeal involved substantially the same wording as is used in the Policy in the present case, in referring to the injury being caused solely and independently of all other causes.
94 In Preston, Sackville AJA (with whom Meagher and Gleeson JJA agreed), drew a distinction between two situations (at [80]):
The first is where a dormant or inactive condition creates a propensity in the insured to suffer disabling consequences from what otherwise might be a relatively minor injury. The second is where a significant medical or physical condition is aggravated by the injury or combines with the injury so as to result in disability.
Counsel for both parties in the present case accepted that the approach taken in Preston at [80] is applicable to the Policy here.
95 In the first situation, the accidental injury will ordinarily be regarded as the sole, direct and independent cause of the disability. That is illustrated by three cases. In Fidelity and Casualty Company of New York v Mitchell [1917] AC 592, the insured severely sprained his wrist and in the ordinary course the sprain would have healed in about six months. However, about ten years before the accident, the insured had experienced a tubercular infection in one lung resulting in a lesion which had completely healed and would have remained harmless but for the accident. The presence of tuberculosis in some form within the insured's system prevented the sprain from healing and resulted in total disablement. In Silverstein v Metropolitan Life Ins Co (1930) 171 NE 914, the insured suffered abdominal injuries while lifting a milk can and during surgery on the insured's abdomen, the surgeon found a perforation through which the contents of the insured's stomach escaped, leading to peritonitis and death. A duodenal ulcer about the size of a pea was located at the point of the perforation. But for the accident, the ulcer would have had no effect since it was dormant and not progressive. Even so, the ulcer weakened the wall so that the impact of the blow on the abdomen was followed by perforation at the point of least resistance. In Lipertis v Australian Casualty Company Pty Ltd [1983] 2 VR 280, the insured suffered a soft tissue injury to his thoracic spine at work, and subsequently developed a "decompensation reaction" which produced a disabling psychiatric condition. The psychiatric condition was causally related to the trauma of the accident. In the reasoning of Kaye J (at 286), although the insured had a particular type of personality which was susceptible to a decompensation reaction, it was the accident alone which caused the insured to react to his physical injuries in a manner which disabled him from pursuing his normal lifestyle and means of livelihood.
96 In the second situation, the court is likely to conclude that the accidental injury is one of two concurrent causes and is therefore not the sole, direct and independent cause of the disability. That is illustrated by two cases. In Jason v Batten (1930) Limited [1969] 1 Lloyd's Rep 281, the insured suffered minor injuries in a motor vehicle accident, and six days later suffered a coronary thrombosis. It was held that there were two concurrent causes of the disablement, one being the insured's pre-existing arterial disease, which would have produced a coronary thrombosis within three years even without the accident. The second cause was the formation of a blood clot as a result of the accident. The arterial disease and the clotting were regarded as simultaneously present together, with each being a necessary condition of the thrombosis. In Preston itself, the insured sustained severe injuries to both ankles requiring surgery, and although he was able to resume full time work those injuries to both ankles had continuing and observable physical consequences. When he injured his left ankle in 2009 his pre-existing condition materially contributed to his disability, in that the 2009 injury aggravated the physical consequences of that accident in both the left and right ankles. While the pre-existing condition from 1996 was unlikely to have resulted in permanent disablement if the 2009 injury had not occurred, there was no evidence that the 2009 injury, independently of the aggravation of the pre-existing condition, would have rendered the insured totally disabled. Accordingly, there were two concurrent causes of the insured's disability, namely the aggravation of his pre-existing condition and the new injuries sustained in 2009.
97 At [97], Sackville AJA said the following:
If it is necessary to distinguish cases such as Mitchell and Lipertis, the distinction lies in the fact that the Insured in the present case had a pre-existing physical condition that was susceptible to aggravation, and the aggravation contributed to his total disablement. This is not a case of an inherent propensity, whether by reason of personality or a benign and symptomless minor condition, to the adverse consequences of an accident unrelated to the aggravation of a pre-existing physical condition.
98 The 2020 Injury was undoubtedly made worse by the 2016 Injury. Both the 2016 Injury and the 2020 Injury were to the same part of Mr Lowe's spine, located at the C5/6 level. The effect of Dr Coyne's evidence is that it is more likely than not that both the 2016 and 2020 Injuries contributed to Mr Lowe's current condition. The point is starkly expressed by Dr Mobbs in her report, to the effect that the 2020 Injury was almost certainly made worse by the neural vulnerability created by the 2016 Injury, a proposition with which Dr Coyne agreed.
99 Nonetheless, the authorities establish that the language used in the Policy does not preclude a claim by the insured simply because he had a pre-existing condition that can be said to have contributed in some way to his injury. As Cardozo CJ observed in Silverstein, the infinite interplay of causes makes it impossible to segregate any single cause as operative to the exclusion of all others. On the approach in Preston, the real question is whether the 2016 Injury left Mr Lowe with a "dormant or inactive condition" or a "significant medical or physical condition".
100 The better view is that the 2016 Injury left Mr Lowe with a dormant or inactive condition, rather than a significant medical or physical condition. The evidence establishes not only that Mr Lowe was asymptomatic between the 2016 Injury and the 2020 Injury, but also that he played rugby league at the highest level throughout that period. Accordingly, Mr Lowe's condition was analogous to the tuberculosis in Mitchell and the duodenal ulcer in Silverstein. The circumstances in Jason and Preston, by contrast, are distinguishable. Irrespective of the accidents said to give rise to liability, each insured was already suffering significant physical consequences (in the case of Preston) or would have imminently suffered such consequences (in the case of Jason). But for the 2020 Injury, the 2016 Injury would have had no physical effect on Mr Lowe.
101 I acknowledge that there is one respect in which the present case is closer to Preston than Mitchell or Silverstein. In Preston and the present case, the insured's predisposition to injury and the injury itself arose from two similar incidents - during the insured's work, force was applied to the injured part of the body. In Mitchell and Silverstein, by contrast, the cause of the insured's predisposition was entirely unrelated to the ultimate injury. The injury was caused by the application of force to the injured part of the body, but the predisposition arose from an infection (in the case of Mitchell) or stomach ulcer (in the case of Silverstein).
102 However, in my view, the physical correspondence between the causes of the predisposition and injury in the present case does not distinguish Mitchell and Silverstein. In the present case, the ultimate question is whether the 2020 Injury was caused by an Accident "solely and independently of any other cause". The 2016 Injury is thus relevant only for its effect on Mr Lowe. As has been explained, the effect on Mr Lowe was analogous to the effect of the infection in Mitchell and the stomach ulcer in Silverstein.
103 In sum, under the dichotomy in Preston, this is a case in which a dormant or inactive condition created a propensity in the insured to suffer disabling consequences. Mr Lowe's injury was made worse by that propensity, but it was still caused by an Accident "solely and independently of any other cause".