Krieger v Bundaberg City Council [2009] QSC 412

[1] The plaintiff, Kenneth Krieger, claims damages for personal injuries suffered when lifting a heavy saw[1] in the course of his employment with the defendant, the Bundaberg City Council. Liability is admitted. It is necessary to assess the quantum of damages.

[2] Mr Krieger was born on 16 June 1959 and injured on the 7 February 2005. So he is presently aged fifty years and was aged forty-five years when he suffered the subject injury.

[3] It is not in contention that as a result of the subject incident Mr Krieger suffered a disc prolapse at the C7-T1 level of his spine. On 7 July 2005 he underwent an anterior cervical discectomy and fusion procedure performed by Dr Richard Williams, a consultant orthopaedic surgeon specialising in spinal disorders.

[2] Nor is it in issue that Mr Krieger has suffered, quite independently of the subject incident, a peripheral sensory neuropathy, the symptoms of which became evident subsequent to the surgery to his spine. The cause of that condition is unknown, not an unusual feature of it.[2] Nor does it seem to be in issue that, again independently of the subject incident, Mr Krieger has a mild carpel tunnel syndrome bilaterally. What is in dispute are the effects of those causally independent conditions.

[3] However the principal issue is whether Mr Krieger has suffered a cervical myelopathy ie damage to his spinal cord at the cervical level, which can be attributed either directly to the trauma of the subject incident, or indirectly eg caused in the subsequent surgery or due to micro trauma resulting from the altered mechanics of the spine due to and following on from the surgery. There is no suggestion that the surgery was not competently performed and hence no suggestion of any novus actus interveniens severing the causal connection as discussed in Mahony v J Kruschich (Demolitions) Pty Ltd.[3]

[4] Whilst there was reference to the principles explained in Fishlock v Plummer[4] in submissions that case was concerned with discrete subsequent events independently causing demonstrable injury. The plaintiff cannot point to any subsequent incident in his life as having demonstrably damaged his spinal cord. Rather, if direct injury not be established, the plaintiff's case is that his spine was put into such a state as a result of the subject incident and subsequent surgery that the everyday incidents of life - which in his case included heavy manual work - resulted in damage to the cord.

[5] I accept as accurate the proposition that if the plaintiff can demonstrate, on the balance of probabilities, that he has suffered injury to his spinal cord and that he would not have suffered such injury but for his physical condition brought about by the defendant's breach of duty then he is entitled to damages for that added injury.[5]

[6] I did not understand the defendant to contest that a legal liability could arise indirectly in this way.

[7] The defendant's case was that the plaintiff did not have a cervical myelopathy and that if he did it could not be shown to be due to the subject incident, directly or indirectly.

[8] As to the first issue the defendant argued that for there to be damage to the spinal cord there needed to be compression of the cord which would have been evident on MRI scan and it was not, that the signs essential for the diagnosis of cord damage were missing, that the symptoms reported were not consistent with cord damage, and that there was an alternative explanation for what symptoms the plaintiff had.

[9] As to the second issue the argument seems to be simply that there was no evidence to support the claimed link there being no contemporaneous onset of symptoms to enable an inference to be drawn in the plaintiff's favour and if there be any encroachment in to the spinal canal (which the defendant disputed) that has occurred in the presence of significant pre-existing degeneration.

[10] In my judgement the plaintiff has failed to make out his case. It will be necessary to examine the evidence closely to demonstrate why I hold that view.

[11] Whilst there is no doubt that Mr and Mrs Krieger were patently honest and sincere, their recounting of the symptoms suffered or observed cannot be accepted at face value. They have lived with these symptoms for years and it is evident that symptoms have changed over time. To expect them to recall with any accuracy when symptoms came on and to what degree is unrealistic. Contemporaneous records are likely to provide a better guide.

[12] As mentioned Mr Krieger injured his neck lifting a heavy saw. He consulted his general practitioner, Dr Tim Adams, on the day following the incident. In a letter of referral Dr Adams notes the complaints then being that Mr Krieger had hurt his neck and had "pain down the (L) arm into the hand".[6]

[13] On the 19 April 2005 Mr Krieger was referred to Dr Bill Ryan orthopaedic spinal surgeon. Dr Ryan recorded restriction of extension of the cervical spine on examination with brachial plexus irritability on the left. He recorded "an absent triceps jerk and decreased power of flexion and extension of the elbow and abduction of the fingers".[7] Dr Ryan expanded on this in another report where he recorded that his clinical findings were of "neck and arm pain radiating into the shoulder and left elbow" and "accompanied by pins and needles in the little and ring fingers and of feeling a weakness and lack of control of the left hand".[8]

[14] Dr Ryan referred Mr Krieger to Dr Richard Williams, a consultant orthopaedic surgeon who specialises in disorders of the spine. He recorded the current symptoms (as at 19 April 2005) as being that Mr Krieger "continues to suffer neck and left arm sensory disturbance although has no left arm pain". He noted that Mr Krieger reported "a loss of fine motor control in the left hand with decreased strength generally in the left arm".[9] On his clinical examination he found a full range of motion in the cervical spine, the ulnar nerve on the left to be non tender with an "absent triceps jerk and super noted jerk on the left" with sensation diminished in the left fifth finger.[10]

[15] I note that Dr Williams' report of no left arm pain is at odds with Dr Ryan's report of the same day. Mrs Krieger gave evidence that Mr Krieger was a poor reporter of his symptoms and it may be there was some breakdown in communication, but all reports to that time indicate that there was a continuing complaint of left arm pain.

[16] Dr Williams' comments should be read in the context of his later qualification which appears in the report of 7 June 2005 when under the heading "Current Symptoms" Dr Williams reported: "He continues to suffer neck and left arm sensory disturbance. At the time of initial review he reported little in the way of left arm (sic) although did have inter scapula pain radiation into the left trapezial region....He reported a degree of lost fine motor control in the left hand and of strength in the left arm."[11]

[17] Eventually Dr Williams performed surgery on 7 July 2005.

[18] Mr Krieger appears to have done well following surgery. Whilst his oral evidence was that there was no significant change, that was not how he presented to Dr Williams six weeks following the surgery. Dr Williams reported that Mr Krieger was "very happy with the result". Dr Williams cleared Mr Krieger to return to work suggesting he start with half days and increasing to full active duty over a month. He also noted that Mr Krieger "should have no restriction in his activities from the start".[12]

[19] Mr Krieger returned to work. He had episodes of increased symptoms particularly following two periods of heavier manual labour, the first involving jack hammering in September 2005. He persisted with his work, but principally on lighter duties. On 22 February 2006 Mr Krieger was again put into heavy manual tasks at his work place. He was required to lower heavy sandbags into a two metre deep trench. He again reported an increase in neck and left arm pain.

[20] That accords with the history given when he returned to see Dr Williams in April 2006. Dr Williams found that the left arm pain was in the C8 distribution. The imaging available to Dr Williams at that time suggested that there was no ongoing neural compression. Mr Krieger told Dr Williams then that he took Panadol tablets rarely and an occasional Mersyndol.[13]

[21] On 5 June 2006 Mr Krieger attended on his general practitioner, Dr Adams, who noted: "wants a record of pain upper arms to the elbows, under the arms, axilla (R) and back of neck, tingling both index and middle fingers".[14] This seems to be the first record of pain in both arms. This report may be contrasted with his presentation to Dr Ryan a year before when he complained of pins and needles in the little and ring fingers with a feeling of weakness and lack of control in the left hand.[15]

[22] At some point Mr Krieger commenced to have symptoms of tenderness and pins and needles in the soles of his feet. I discuss the timing of onset below.

[23] On 16 May 2007 the plaintiff's position with the Council was terminated.[16]

[24] By the time of trial Mr Krieger used a cane to ambulate, had weakness and giving way of his ankles, a tremor and weakness in his hands, his hands would go numb and tingle and spasm and cramp, bad headaches, pain across the back of his neck and down his arms, the tops of his thighs would begin to burn if he sat in one place for too long and he suffered from urinary urgency.

[26] The plaintiff's claim that there was radiological evidence to support the presence of cord damage was based principally on an MRI scan of 15 June 2006[17].

[27] The original report of that scan prepared by the consulting radiologists (Dr Joe Savage and Dr John Mitchell) recorded their impression of the C5/C6 level of the spine that there was "some effacement of the anterior CSF space" and that there "appears to be some compression of the cord with high signal and this could be the aftermath of compressive myelopathy". Their report went on that "the cord at C6/C7 also looks hyper intense and flattened although the anterior CSF is only minimally compressed". Their "impression" was recorded as "satisfactory appearances at the level of the anterior fusion of C7/T1 with no canal compromise. Mild disc bulge at C5/6 and C6/7, broad based and central with mild spinal canal stenosis with a slight reduction of anterior dimensions but there is however flapping of the cord and high signals suggesting compressive myelopathy."[18] The report was plainly strongly supportive of the plaintiff's case.

[28] As well Dr Todman, an experienced neurologist, said that the scan was "hard evidence that this man has cervical compressive myelopathy".[19]

[29] Despite those views I am satisfied that the scan does not support the plaintiff's case. I do so essentially for the reasons explained by Dr Mitchell, who resiled from the views that he expressed in his report.

[30] First, the particular image[20] relied on by the plaintiff as showing compromise of the "CSF space" - that is the space around the cord occupied by the cerebrospinal fluid - is at odds with another image taken in the same plane moments later[21] which seems to clearly demonstrate no such compromise at all. So much is evident to a layman's eye. If the structures surrounding the cord intruded into the canal then the images should have been consistent with each other. All witnesses who were asked about the two images agreed with that proposition and the lack of compromise on the second image.

[31] The explanation for the first image probably lies in the inherent problems of obtaining a clear scan. The accuracy of the images produced can depend on a variety of factors including the ability of the patient to stay still through a thirty minute process. The second image was a T1 sequence which was a faster sequence than the first image which was a T2 sequence. Hence the T1 images have a greater prospect of showing a more accurate image if movement of the patient is a problem. Dr Mitchell thought that the appearance of the first image was an artefact, as did Dr Williams.

[32] Second, as Dr Mitchell pointed out, the T2 sequence can exaggerate the appearance of any bony ridge indenting the thecal sac and hence result in geometric distortion in the image. If the distortion did not show on the T1 image then it inclined him to think that the appearance was not real. In a similar vein Dr Williams was of the view that the image, to his eyes, was taken a little off line - at a slight obliquity - which would result in a distorted image.

[33] Third, the images taken in the axial plane, again shortly after the image on which the plaintiff relies, apparently demonstrate the lack of any compromise of the CSF space[22] - I must rely on the expertise of the witnesses for the accuracy of the statement. The opinion was uncontested.

[34] Fourth, MRI scans prior and subsequent to the 15th June 2006 scans do not support the presence of any compromise of the canal to a degree that would involve compression of the cord nor is there any high signal intensity shown which would be indicative of damage to the cord.[23] It is relevant to note that the quality of the images can vary from machine to machine. The evidence suggested that the Bundaberg radiology MRI device had lesser strength than the devices used in Brisbane.

[35] The MRI scans to which I refer are those of 11 May 2005, 31 January 2007 and 22 December 2008. I will set out the relevant sections of the reports.

[36] An MRI scan of 11 May 2005 carried out by Queensland Diagnostic Imaging at the Holy Spirit Northside was reported as showing, so far as is relevant, the following:

"The canal appears satisfactory throughout. Intrinsic cord signal is normal....neural foramen widely patent....At C5-6 there is more marked uncovertebral osteophytosis with osteophytic encroachment into the neural foramen (C) bilaterally although the changes are more marked on the left then (sic) the right....There is a minor diffuse annular bulge with anterior flattening of the thecal sac. AP diameter of the canal is small but appears satisfactory....

[37] Queensland X-ray performed an MRI at the request of Dr Coroneos on 31 January 2007. Dr Medoro reported that at the C5/6 level there was "mild effacement of the cord" caused by a small central disc protrusion with bilateral posterior lateral osteophytic ridging. At the C6/7 level he reported "a small central disc protrusion with mild indentation of the cord. There is no definite neural compression. Mild bilateral foraminal stenosis is evident secondary to osteophytic ridging." He also reported that there was no "intrinsic cord signal abnormality". [24]

[38] Bundaberg Radiology was again asked to perform an MRI of the cervical spine on 22 December 2008 at the request of Dr Todman. Dr Bharati reported that "the signal intensity from the bodies of the cervical vertebrae (C2-C6) appear normal". Relevantly he also reported that there was "mild indentation by the disc osteophyte complex on the anterior CSF space at the C5/6 and C6/7 levels, mildly narrowing the spinal canal. No direct indentation on the spinal cord is noted at these levels. The neural foramina appear narrowed at these levels on both sides due to encroachment by the osteophytes at the uncovertebral joints." His conclusion was that there were "mild degrees of indentation on the anterior CSF column with mild narrowing of the spinal canal at C5/6 and C6/7 levels. No obvious cord compression noted. Bilateral neural foraminal narrowing at these two levels due to encroachment by osteophytes at the uncovertebral joints."[25]

[39] Thus, while expressions such as "mild effacement", "mild indentation" and "encroachment",[26] occur in reference to the cord or CSF space, the reports are consistent in noting no evidence of cord compression or abnormal signal. Dr Cameron pointed out that one could have cord indentation without compression and hence damage. I did not understand that view to be contested.

[40] Fifth, five experts with very substantial experience in the assessment of these radiological pictures, Drs Williams, Hall, Mitchell, Cameron and Nave, were of the view that there was no radiological evidence to support the presence of spinal cord compression or damage. A sixth, Dr Coroneos, who did not give evidence but whose reports were tendered, appeared to conclude, after reviewing Dr Cameron's nerve conduction studies, that the probable diagnosis was idiopathic sensory neuropathy.[27] His views are of limited weight given that he assumed the absence of motor and bladder symptoms.

[41] I am conscious that Mr Morton did not restrict his case to the MRI scans but called in aid the CT scans that had been performed. I note that the MRI was acknowledged by all witnesses to be the more sensitive of the two scanning methods.

[42] Nonetheless I will set out the relevant CT scan reports. One thing that the CT scans do demonstrate is the presence of quite significant degeneration.

[43] A CT scan was performed on 17 February 2005. So far as is relevant the reporting radiologist, again Dr John Mitchell, analysed the scan as showing:

"At C5-6 there is mild discophytic lipping of the vertebral m plates with moderate degenerative changes in the neuro central joints and mild degenerate changes in the facet joints. There is mild to moderate bi lateral foraminal stenosis. There is also mild encroachment on the anterior aspect of the thecal sac with narrowing of the antero-posterior diameter of the vertebral canal to approximately 9mm.

At C6-7 there are degenerative changes in the neuro central joints bilateral with mild to moderate narrowing of the right neural foramen and moderate to mark narrowing on the left. There is very prominent discophytic lipping of the vertebral endplates and there appears to be a left postero-lateral disc protrusion which appears to indent the anterior aspect of the thecal sac. There is narrowing of the antero-posterior diameter of the vertebral canal to approximately 7mm and this could encroach on the cervical cord. Considerable artefact is present in this region and definition of the disc and the thecal sac is sub optimal.

At C7-T1 the appearance of the disc, spinal canal, recesses and posterior intervertabal joints are all within normal limits. No abnormality is seen in the surrounding soft tissues.

The most significant pathology appears to be the C6-7 level where there is prominent discophytic lipping of the vertebral endplates and there appears to be a central to left paracentral disc protrusion indenting the anterior aspect of the thecal sac and extending into the left lateral recess to some degree. This could encroach on the cervical cord and could well impinge on the nerve roots exiting at this level. In view of the clinical symptoms, if intervention is considered further assessment with magnetic resonance imaging is recommended."[28]

[44] A CT scan of the cervical span was performed on 24 April 2006. The report is that the spinal canal at the C5/6 level was "of adequate calibre". At the C6/7 level the report records that the intervertebral foraminae are narrowed bilaterally and that there were "osteophytes arising from the posterior margins of C6 and C7 [which] encroach into the canal. These and the disc margin indent the thecal sac which is mildly compressed." The radiologist concluded that there was a C6/7 posterior disc protrusion evident in association with osteophyte formation and bilateral foraminal stenosis and he or she could not exclude a lateral disc protrusion at C5/6 on the right.[29]

[45] Mr Morton placed particular emphasis on the restricted diameter of the spinal canal at the C6/7 level as reported in the first of those CT scans. Obviously the more narrowed the canal the greater the risk of injury to the cord.[30] While it seems plain that the canal is narrower than might be considered optimal - the evidence was that 9mm or preferably 11mm would be more normal[31] - I am not persuaded that the CT scan report should be accepted as necessarily accurate.

[46] First the report itself sets out the qualifications on the opinion - there is artefact present and the definition is sub-optimal. Second, a neurosurgeon of considerable experience, Dr Hall gave evidence, and he was not contradicted, that four MRI scans did not support the measurement. I note that the report of the MRI of 31 January 2007, consistently with that opinion, described only "mild narrowing" of the spinal canal. Third, while neither Dr Williams nor Dr Cameron spoke in terms of millimetres both seemed clearly to hold the view that the canal was of adequate size. I accept these opinions.

[47] I conclude that the radiological evidence does not support the plaintiff's case. That is not conclusive of the issue but the absence of such support must be seen as significant. Dr Hall said that damage would usually show on MRI, but may not. Dr Williams said that he has not seen a myelopathy, that is, clinical signs of the condition, without cord compression. Dr Cameron agreed. Dr Todman apparently held a contrary view. Whether he felt that was simply theoretically open, or whether that was his experience in practise was not made clear. The evidence supports the conclusion that the presence of a cervical myelopathy without radiological evidence of compression of or damage to the cord, whilst possible, would be unusual to a significant degree.

[48] I turn then to a consideration of the signs and symptoms.

[49] A significant problem for the plaintiff's case is that a number of medical practitioners, with great experience in this field, held the view that the plaintiff's presentation, that is the clinical signs that were present, was not consistent with a cervical compressive myelopathy.

[50] There were several matters of significance. All specialists were agreed that damage to the cord should result in increased tone and brisk reflex responses. Dr Williams described brisk reflexes as the first and most persistent change with the cervical compressive myelopathy and the feature most concordant with such a disease.[32]

[51] All doctors are agreed that Mr Krieger's reflexes, far from being brisk, were in fact slowed. Dr Todman suggested that the absence of brisk reflexes might be explained by the sensory peripheral neuropathy which it is accepted slows the reflexes.

[52] I find that a puzzling statement. If the damage to the cord that the plaintiff postulates is sufficiently severe to cause an alteration to his gait, and the peripheral neuropathy is a mild one not sufficient to explain alteration in gait, then it is puzzling that the neuropathy wins out over the myelopathy in relation to the reflexes.

[53] Dr Cameron observed that Dr Todman's theory was a "strange statement". No evidence was advanced in the form of case studies, experience, or the like to justify the theory. Without such support the mere assertion of the possibility I find unpersuasive.

[54] However the difficulties for the plaintiff's argument go well beyond the absence of brisk reflexes.

[55] There is a gait disorder, described by some of the doctors as a "spastic gait" marked by rigidity and stiffness in the legs, typical of cervical myelopathy. While there can be some variation from one patient to another all of the specialists called thought that Mr Krieger's gait was not of that type. Dr Williams pointed out that to him the gait was quite the opposite of what he expected from a myelopathy.[33] Again it may be said that is not conclusive but the alteration to gait present here is plainly atypical. And once it is accepted that it is atypical then, as Dr Hall observed, his leg symptoms could be due to a number of conditions.[34]

[56] As the specialists called by the defendant pointed out there is an absence of all other signs that they expect to see with a compressive cervical myelopathy. Dr Cameron spoke of the absence of alteration in tone, the absence of clonus, the absence of toe extensor responses all of which he would expect to see if there was a spinal cord problem of sufficient significance to cause upper motor neurone problems and hence being responsible for the alteration in gait.[35]

[57] Dr Hall's evidence was to the same effect[36] - he spoke of the absence of increased tone, the absence of increased rigidity, the absence of a Hoffman sign[37] in the upper limbs and the absence of a Babinski response[38].

[58] The absence of a gait disorder typical of the condition and the absence of the signs typical of the conditions are each again unusual features and significantly against the plaintiff's argument. Again the absence of any one these can be accepted as not conclusive of the issue but the absence of all significantly impacts on the probabilities.

[59] The other symptom that the plaintiff calls in aid of his argument is the onset of urinary urgency. The difficulty in attributing any great significance to the presence of the symptom is that it is explicable by means other than cervical myelopathy.

[60] Whilst Dr Cameron accepted that the symptom can be a reflection of a spinal cord disturbance, and in this he was in accord with Dr Todman, he considered that it was also consistent with the condition of progressive neuropathy diagnosed and as well commonly caused in men of Mr Krieger's age by prostatic hypertrophy with bladder outlet instability, a possibility that is yet to be explored.[39] If all other potential causes were excluded then one might accept myelopathy as the most probable explanation but that is not the position here.

[61] To complicate matters further Dr Hall did not accept that renal urgency was a classic sign of myelopathy - he indicated that urinary retention, not urgency, was the classic sign and in that regard he was supported by Dr Williams who said that he had never seen bladder disturbance from a cervical myelopathy.[40]

[62] The conclusion that I draw from this is that the presence of urinary urgency does not significantly impact on the probabilities of the case.

[63] A further matter against the plaintiff's arguments is the history of the onset of the symptoms in the legs. Mr Krieger's evidence was that around about the time of the jack hammering incident, and shortly prior to it, he had commenced to have symptoms of tenderness and pins and needles in the soles of his feet.[41] Eventually this developed to the extent that Mr Krieger said that he started using a cane because he had become unsteady and found that he would trip when walking.[42] He was using a cane at the time of trial.

[64] Putting to one side the timing of onset, that description accords with the history given to Dr Cameron on 29 November 2006. The history obtained by Dr Cameron at that time was that around June of 2006 Mr Krieger noticed "altered sensation and tingling in the soles of the feet. This now seems to encompass his feet and spreading into his lower legs. His toes feel numb and his feet cramp. His legs feel weak. He has had some bladder frequency but no bowel problems."[43]

[65] Dr Cameron said of this description that it was typical of an upper peripheral neuropathy and quite distinct in its manifestation to what one expects from a cervical myelopathy.[44] Dr Cameron indicated that he had examined Mr Krieger "on several occasions" and found the same "glove and stocking pattern" compatible with sensory neuropathy.[45]

[66] Thus the manner of onset and the description of symptoms are both more consistent with a neuropathy than a cervical myelopathy.

[67] Dr Cameron claimed that nerve conduction studies confirmed his views. The initial study was normal but he said "with time there was evidence of gradual impairment of sensory...motor function in his lower limbs".[46]

[68] Dr Cameron's conclusion was that his clinical examination and findings strongly supported the diagnosis of peripheral sensory motor neuropathy of the arms and legs.[47]

[69] Dr Cameron has the advantage of having seen Mr Krieger on five occasions - 27 November 2006, 31 January 2007, 1 March 2007, 11 April 2008 and 5 June 2009. He has conducted nerve conduction studies on several occasions. He has seen progressive deterioration. His examinations were initially for the purposes of treatment and his opinions formed in that context. He formed the view that his nerve conduction studies not only demonstrated an advancing condition but eventually a "prominent sensory motor neuropathy".[48]

[70] Dr Todman disagreed with Dr Cameron's views concerning the seriousness of the sensory neuropathy condition. Dr Todman performed conduction studies himself on 17 December 2008 and considered that those showed "normal motor conduction velocity and normal F waved latencies" consistent with mild peripheral neuropathy.[49]

[71] Neither side sought to cross examine either specialist on their respective nerve conduction studies, on what might be normal, and where one would draw a line between mild and "prominent". I merely note that in the absence of such a cross examination it is not possible for me to compare one study with another, and that Dr Cameron had the advantage of the latest study, of seeing Mr Krieger over a greater length of time and on more occasions than Dr Todman.

[72] I have determined to reject the views of Dr Todman and prefer those of Dr Cameron. I will explain my reasons. First, Dr Todman clearly based his views on the assumption that the MRI scan of June 2006 demonstrated "conclusively" the presence of cervical compressive myelopathy[50], a view I cannot accept as I have explained above.

[73] Second, the other matters that Dr Todman thought supported his analysis that leg weakness was attributable to cord compression I find unpersuasive. He referred to the appearances of the MRI scan of January 2007 which he said showed disc protrusions in the neck which were touching the cervical cord, symptoms of bladder urgency, and what were described as "L'Hermitte's" symptom, a symptom typical of such compression.[51]

[74] Dr Todman's point concerning the MRI of January 2007 can at best be considered neutral. I have referred above to Dr Cameron's views.[52] The absence of any abnormality in the intrinsic cord signal is indicative of, but not conclusive of, an absence of damage to the cord.

[75] As I have indicated the debate concerning bladder urgency does not assist in resolving the issue - there are other potential causes not excluded and, given the absence of the many signs that the doctors would expect from a cervical myelopathy, causes more probable than myelopathy.

[76] The claimed presence of L'Hermitte's symptom (an electric shock type sensation on tilting the head forward) depends entirely on the report of Mr Krieger that the symptom exists. Neither Dr Cameron nor Dr Todman could reproduce the symptom in their clinical examination. The description of a symptom by an admittedly poor reporter that cannot be reproduced is not of great weight.

[77] In summary the signs that the doctors expect from cervical myelopathy are not present, the symptoms that are demonstrably present are explicable by another diagnosis namely that of a degenerating peripheral sensory motor neuropathy which the plaintiff undoubtedly has, there are potentially other explanations for some symptoms that have not been excluded, the manner of onset of the leg symptoms is more consistent with the developing neuropathy, the gait disturbance again is not typical of a cervical myelopathy but more consistent with the neuropathy, and the matters that Dr Todman calls in aid of his views are no better than neutral and not particularly persuasive.

[78] I conclude that I am not persuaded on the balance of probabilities that Mr Krieger can demonstrate the presence of a cervical myelopathy.

[79] There is a further problem for the plaintiff's case. If a cervical myelopathy was assumed to exist then it is essential for the plaintiff to demonstrate on the balance of probabilities that the damage to the cord was connected in some way to the subject incident.

[80] Three mechanisms were suggested - injury to the cord in the incident itself, injury through surgery, or injury through minor trauma from everyday life, but particularly noting the two incidents at work of aggravated symptoms, brought about by the altered mechanics of the spine following from the surgery.

[81] Given my conclusion as to the absence of any damage I will not analyse the evidence extensively. The highest the case reached was that there were disc protrusions in the neck which might well be touching the cervical cord (and so in theory responsible for any damage). That is how Dr Todman put it in his last report.[53] But there was no evidence to show that those disc protrusions were causally connected to the subject incident.

[82] In the absence of contemporaneous onset of symptoms consistent with damage to the cord it is difficult to see why an inference should be drawn that there was such damage caused in the incident itself. No symptom claimed to be consistent with the condition - assuming the plaintiff's view of the leg symptoms - is clearly shown until over 16 months later.

[83] The spine was plainly degenerate - in July 2006 Dr Coroneos described it as "long standing degeneration". It is not apparent that the incident caused any change to the natural progress of the degenerate disease. As Dr Hall pointed out the MRI scans from 2005 through to 2008 demonstrated that the disc disease at C6/7 was unchanged over the period.[54] Whilst the absence of change in appearance on such scans is not conclusive there is simply a complete absence of evidence of any change and the theoretical basis urged for assuming such change is unconvincing.

[84] One theory is that the presence of the fusion at C7-T1 throws onto the higher disc at C6/7 greater stress so that it will degenerate at a greater rate.

[85] One difficulty in applying that theory to Mr Krieger is the short period of time that is in question - the surgery was performed in mid 2005 and the symptoms I assume to have come on in the soles of the feet sometime after July 2006. What is known is that over the three and a half year period between the MRI scan of May 2005 and the last scan of December 2008 there was no change in appearance. Thus it is not shown that there is any ongoing change, let alone significant change over and above that which might have otherwise have occurred in what is plainly a degenerate spine.

[86] A second difficulty with the theory is that the C7-T1 disc is not, to use the words of Dr Hall, "a mobile disc". There is little movement at that level. Thus a fusion at that level does not make any great difference.[55]

[87] So the theory must be that at a level where one would not expect any significant effect from the fusion there ought to be an assumption of degeneration sufficient to impact on the spinal cord, over a timeframe that seems remarkably short, and not only with an absence of any evidence of that occurring in the radiological pictures, but those pictures suggesting no impact on the cord. The theory is not probable. I note Dr William's emphatic rejection of the hypothesis.[56]

[88] It seems plain that the surgery itself did not cause harm. As mentioned Mr Krieger came to surgery on 7 July 2005. Dr Williams' report to the general practitioner of the operative procedure contains no suggestion of any untoward event in the course of the operation.[57] The evidence, as one might expect, was that the operating surgeon had a responsibility to report untoward events such as any interference with the spinal cord.[58]

[89] Thus there was no suggestion of any cord damage being evident to an experienced spinal surgeon six weeks after that surgery. The uncontested evidence from Dr Hall was that if surgery was the cause of any damage to the cord then one would expect the patient not to recover well and not get back to work.[59]

[90] The alternative theory advanced was that the spinal cord had been subjected to repeated minor trauma brought about by the everyday incidents of life but which included two significant periods of hard manual labour at which time Mr Krieger experienced an increase in his neck and arm symptoms.

[91] The first difficulty with the theory is that it was highly theoretical and not in accord with the experience of the bulk of the specialists called.

[92] Secondly, it depended on the premise that the spinal canal itself was sufficiently narrowed to permit such minor trauma to the cord to occur. That was not demonstrated.

[93] Thirdly, any attempt to attribute the damage to the episodes of significant manual effort as the trigger suffers from the fact that the symptoms in the legs came on well after those work incidents.

[94] The timing of the onset of these symptoms isn't entirely clear. In September 2006 Dr Olsen had a history of onset at the time of the sandbagging work ie in February 2006.[60] As noted above in the November 2006 visit to Dr Cameron Mr Krieger had the symptoms commencing the previous June. That is at odds with the history recorded by Dr Coroneos. Despite Mr Krieger's claim that he was referred to Dr Coroneos because of leg symptoms[61] there is no reference to any such symptoms in the referring letter of Dr Adams[62] or in Dr Coroneos report of 11 July 2006.[63] That would be a remarkable omission if Dr Coroneos was told of the symptoms. Equally it would be remarkable that Mr Krieger, no matter how poor an historian, would forget to tell him if the symptoms were present and the cause of the visit.

[95] No leg symptoms were recorded by Dr Williams in April 2006, Dr Adams's in June 2006[64] or Dr Coroneos in July 2006. The probabilities are that the symptoms came on after the visit to Dr Coroneos.

[96] Thus the timing of onset of the leg symptoms is not contemporaneous to any particular event in Mr Krieger's life and particularly not to the jack hammering or the work involving the sandbags. The onset was months later. Those two events were the most strenuous of the activities that Mr Krieger could identify and the ones that Mr Morton attempted to advance as those most likely to cause damage to the cord.

[97] When symptoms come on contemporaneously with an event then it is often logical to draw the conclusion that there is a causal link. An argument of that type is not open here. And while some of the opinions expressed accepted that there could be a delay between the damage and the onset of symptoms that does not establish the causal link.

[98] A final difficulty is that while it might be said that all things are possible no expert thought that the jack hammering work or the work involved in the lowering of the sandbags provided a probable mechanism for damaging the spinal cord.

[99] In my view the only conclusion open is that whatever be the cause of the symptoms complained of by Mr Krieger it is not shown on the balance of probabilities that they are attributable to the subject incident directly or indirectly.

[100] The onus lies on the defendant, once a causal link between the breach of duty and a condition or symptom is established, to separate the effects of the claimed supervening cause from those that are compensable with some reasonable precision: Watts v Rake[65]; Purkess v Crittenden[66]; cf. Malec v JC Hutton Pty Ltd[67]; Smith v Topp[68]; Hopkins v WorkCover Queensland[69].

[101] While it is plain that the leg symptoms are not attributable to the subject incident things are not so clear in relation to the arm symptoms. Generally I prefer the views of Dr Cameron for the reasons explained above.[70] It seems to me that he has had the most to do with the plaintiff over an extended period of time and is in the best position to offer an informed view of what is an obviously complex picture. Dr Cameron concluded in the last of his reports that the progressive sensory motor neuropathy that he had diagnosed accounted "predominantly for his hand and lower limb symptoms, poor balance, gait instability and bladder and erectile dysfunction."[71] As well account must be taken of the mild carpal tunnel condition.

[102] "Predominantly" does not mean exclusively. Pins and needles and loss of control and weakness in the left hand were recorded by Dr Ryan and Dr Williams in April 2005 and long before there is any suggestion on nerve conduction studies of any sensory neuropathy[72] or carpal tunnel condition. No specialist suggested that the damage to the C7/T1 disc could not be responsible for the symptoms and all assumed at the time that it was. I note that Dr Cameron said that intention tremor was associated with the peripheral neuropathy.[73]

[103] I will proceed on the basis that whilst the complaints that Mr Krieger makes about his hands spasming and cramping and his inability to hold a mouse, a telephone or reach out to a keyboard are largely unrelated to the subject incident there seems to be a component of them that can be accepted as related to the neck injury and which therefore makes worse what would otherwise have been the case.

[104] The symptoms that seem to me to be attributable to the injury sustained on 7 February 2005 include neck pain, pain across the back of the neck and shoulders, and pain into the arms. Symptoms which seem to me not to be attributable to that incident include altered sensory feeling in the soles of the feet, spasming in the legs, altered gait, and the bladder frequency. Some component of the loss of fine motor skill in the hands and loss of strength in the hands and arms is due to the unrelated conditions.

[106] It is plain that Mr Krieger has a very serious disability attributable to the subject injury. Drs Nave and Williams assessed the degree of permanent impairment at 25% whole person.[74] Whilst part of that impairment relates to pre-existing degeneration,[75] there is no reason to think that the condition would have necessarily become symptomatic but for the subject incident.

[107] Mr Krieger is in constant pain. He has debilitating headaches. The pain radiates to his arms and into his fingers. At times he requires strong medication.

[108] The onset of the unrelated conditions has worsened the effects of the compensable neck injury. He is now called on to rely on his arms to support himself when using a cane and that will aggravate his pain.

[109] Mr Krieger has a life expectancy of 35 years.

[110] Mr O'Driscoll contended for an award of $50,000. That seems to me to understate the full effects of the condition. I propose to allow $75,000 under this head.

[111] Mr Krieger's employment history includes working as a shop assistant after leaving school at age fifteen, work as a van salesman selling potato chips and then working in the building industry firstly as a labourer and then as a plasterer. He then worked in structural landscaping and eventually took up employment with the Bundaberg City Council in 1997 and 1998. He was working as a plasterer in his own business immediately before starting with the council and plainly was extremely hard working. He spoke of working seven days a week. His wife confirmed that account. Mr Krieger started as labourer with the council and was promoted to ganger, leading hand. He occasionally relieved in the overseers' position when they were on leave. His work as a ganger plainly involved manual labouring work. Mr Krieger indicated that it included "everything associated with the construction of the jobs that I was doing". Those jobs included major building works, drainage, curb and channel, road works and building construction.

[112] It seems to me that Mr Krieger's capacity to carry out the sort of manual work that he was accustomed to do prior to the subject incident was seriously and adversely affected by the injuries suffered in the subject incident. Dr Williams' evidence was to the contrary but he seemed to assume that Mr Krieger made a full recovery following surgery and before the onset of the unrelated conditions. I don't accept that is the true picture. It seems clear that Mr Krieger sought and obtained lighter duties and when called on to do normal, but heavier, duties he had a significant exacerbation of his pain.

[113] The difficulty in the assessment is that the problems attributable to unrelated conditions plainly would substantially interfere with his capacity to carry out such work and indeed much sedentary or semi-sedentary work.

[114] Mr Krieger was asked about his own views as to his capacity to hold down a supervisory position or a relevantly sedentary position. He thought that he would be unable to do that. The reasons he nominated included that with any requirement for mobility he would get a burning in his thighs; if he spent time where he had to reach and use his arms extended for any long period he would get "really bad headaches" and the muscles in his arms would begin to ache; that his hands would tingle and commence to spasm such that he wouldn't have the ability to use a mouse or hold a telephone; that he couldn't reach out to a keyboard as he has similar problems. Driving occupations also he would rule out for much the same reasons. Reaching out to the steering wheel apparently causes his hands to go numb and tingle about an hour into the driving.[76]

[115] Mr Krieger said that if he didn't have his arm and neck problems he could hold down a "sitting down job" explaining that he would have the ability to get up and move around and so alleviate his symptoms of leg discomfort when the symptoms arose.[77] The difficulty with accepting that self assessment, apart from its hypothetical nature given that Mr Krieger has never experienced what it is like to have the one set of symptoms and not the other, is that it assumes that all the upper limb symptoms are to be ignored.

[116] Nonetheless Mr Krieger is plainly very stoical and determined. Some idea of his character and of the comparative effects of the various conditions can be gained from Mr Krieger's determination to mow his own lawn. The weakness in the legs would, one might expect, totally preclude even the attempt, given the presence of neck and upper limb pain. Nonetheless Mr Krieger persists and completes the task despite the activity causing him considerable distress. It might be expected that without the debilitating headaches and pain emanating from his neck Mr Krieger would have had the stoicism and drive to obtain, and persist in, some form of employment.

[117] Whilst I acknowledge there is no certainty in this assessment it seems to me the probabilities favour a finding that had the subject incident not occurred the developing symptoms due to unrelated causes would have brought Mr Krieger's position with the council to an end at about the time that it did in May 2007. It seems clear from the occupational therapist's report that by April 2007 the condition that limited him the most was the "deterioration in his legs".[78] Thereafter the developing sensory neuropathy would have made it difficult for him to maintain employment. The symptoms of disturbed gait and impairment of hand function unrelated to the subject accident would have rendered most forms of employment for which Mr Krieger was otherwise suited quite difficult.

[118] Taking his condition overall I accept that Mr Krieger is unemployable. I note that was the view of Dr Olsen.[79]

[119] Mr O'Driscoll submitted that the supervening independently caused symptoms alone would have rendered Mr Krieger unemployable.

[120] Mr Morton submitted that if I was against him on the cervical myelopathy arguments nonetheless Mr Krieger would have retained a substantial earning capacity if one assumed he did not have the accident caused symptoms and could for example have worked as an overseer with the council, that apparently being a sedentary type of employment. Despite Mr Krieger's evident ambition to become an overseer there is no evidence that any position of overseer was ever likely to be offered to him.

[121] It seems to me that from May 2007 onwards all that can be assessed by way of damages for impaired earning capacity is a fairly modest global amount to reflect the chance that but for the subject accident and its consequences Mr Krieger may have been able to find some form of suitable employment to enable him to work around the developing symptoms from the sensory neuropathy and carpal tunnel condition.

[122] The period in question is approximately 22 years, from May 2007 to a possible retirement age of 70 years.

[123] Doing the best I can I assess the loss at $75,000.

[124] It is plain that the plaintiff had a need for pain relieving medication prior to the onset of unrelated problems in the latter part of 2006. However, the extent to which that need was exacerbated by the causally independent symptoms is probably impossible to determine. I have allowed approximately one half of the amount detailed in the plaintiff's schedules. Included in that amount is a small component for past travel. The bulk of the travel costs appear to relate to the attendances on Drs Cameron and Coroneos and are unrelated to the subject incident. The Lyrica and Tofranil medications seem to be for conditions unrelated to the cervical disc problem.[80]

[125] The amounts claimed for paid services, future care, future house modifications and future expenses as set out in the schedule entitled "Medicare"[81] all relate, principally, to treatment or needs unconnected with any injury sustained in the subject accident, as best I can determine. No effort was made to distinguish between needs created by the subject incident and needs and expenses resultant from the independent unrelated causes.

[126] In summary I assess the damages as follows:

Past economic loss to 16 September 2005 (including Fox v Wood)

Loss of employer contribution to past superannuation

Impairment of earning capacity past and future assessed globally

[127] I am required to assess damages on the assumption that I am found to be wrong in my findings concerning the cervical myelopathy arguments.

[128] On the assumption that the plaintiff succeeded on those arguments I would have assessed damages in accordance with the schedule tendered by Mr Morton[83] but with adjustments to future economic loss to $385,000,[84] future superannuation accordingly to $34,650, and future house modifications to $15,000 (the evidence in that regard being not particularly clear). The assessment would have totalled $878,251.65 on this basis. Essentially Mr Krieger is now a spinal cripple, with no significant earning capacity, and in need of a modified home and assistance with certain domestic tasks.

[129] There will be judgment for the plaintiff in the sum of $165,080.00.

[1] Perhaps weighing in the order of 74kgs

[3] [1985] HCA 37; (1985) 156 CLR 522

[4] [1950] SAStRp 18; [1950] SASR 176.

[5] See the first of the rules suggested by Malcolm CJ in State Government Insurance Commission v Oakley (1990) Aust Torts Rep 81-003 at 67,577 (WA Full Court)

[12] See p31 of exhibit 3 - a report of 16 August 2005.

[16] See Letter of Termination dated 9 March 2007 at 2.22 of Ex 5.

[20] I will adopt the numbering shown in the top right corner of the image - 102 IMA 7/6 taken at 4.28.27

[22] E.g. Dr Mitchell at T2-51/10-20; 2-52/20-30

[23] As Dr Williams explained the signal reflects water content which in turn reflects the extent to which fibrous tissue has replaced normal tissue due to compression or scarring of the cord: T1-54/20

[26] Assessment is not made any easier by the varying use of terms to describe appearances - see Dr Mitchell at T2-49.

[30] See Dr Williams' evidence at T1-57/45.

[34] T2-5/40 incorrectly numbered T1-5.

[37] Which I understand to be the reflex contraction of the thumb and index finger upon flicking of the middle finger, the presence of the sign indicating the potential for spinal cord compression.

[38] A neurological reflex of the big toe when the sole of the foot is stroked indicating, when present, a problem with the central nervous system.

[39] See p 110 of exhibit 3 and see the evidence to the same effect from Dr Hall - T2-12/55.

[48] For example see p113 of exhibit 3.

[64] Entry of 5 June 2006 - see p164 of exhibit 3 and [23] above.

[65] [1960] HCA 58; (1960) 108 CLR 158.

[66] [1965] HCA 34; (1965) 114 CLR 164.

[67] [1990] HCA 20; (1990) 169 CLR 638.

[68] [2003] QCA 397 at [38].

[69] [2004] QCA 155.

[72] See nerve conduction study of 29 November 2006 at p 88 of Ex 3.

[78] See Report of Dr Olsen 26/4/07 at p 78 of Ex 3.