Scottish Court of Session Decisions

OUTER HOUSE, COURT OF SESSION [2011] CSOH 178
	OPINION OF LORD WOOLMAN in the cause MARTIN WILSON Pursuer; against (FIRST) NORTH LANARKSHIRE COUNCIL AND (SECOND) THE BOARD OF MANAGEMENT OF MOTHERWELL COLLEGE Defenders: ­­­­­­­­­­­­­­­­­________________

Pursuer: Party

Defenders: D I Mackay, Q.C.; Wilson; Simpson & Marwick

25 October 2011

Introduction

[1] In August 1994, Mr Wilson went to his general practitioner complaining of back pain. The position worsened in 1995. He suffered a lumbar disc herniation. Scans of his spine disclosed degenerative changes. Since then, he has suffered from back pain. The condition has had a marked and adverse effect on his life. He is 54 years old and has not worked for the last 15 years.

[2] Mr Wilson attributes his back problems to his former employment. Between 1987 and 1996, he was a music lecturer at Motherwell College. On his account, he was required to lift and carry musical instruments and equipment to and from his classes. The items were awkward and heavy. They had to be carried some distance. During term time, Mr Wilson required to undertake this task daily and sometimes several times a day. He contends that the repeated "micro-trauma" to which his back was subjected led to degenerative changes in his intervertebral discs.

[3] He claims that his employers knew that his activities were causing him to develop back problems, but failed to provide him with assistance. Accordingly, they were at fault at common law. He also alleges that they were in breach of their statutory duties to carry out a risk assessment and to provide instructions in manual handling.

[4] Mr Wilson seeks damages of £2,592,000 "with more to follow", together with interest since 1996. That sum is based on a number of propositions: (a) that he is incapable of working again; (b) that but for his back injury, he would have continued working in the educational sector until retirement with various promotions; and (c) that he would have also developed a parallel career as a conductor of classical music concerts.

[5] In 1993, the second defenders took over responsibility for the management of Motherwell College from the first defenders. In this action they both have the same legal representation and mounted a unified defence. They contest every branch of the claim:

(a) On the facts, they contend that Mr Wilson did not need to carry the items, as he could have asked a janitor to assist him and a trolley was also available. They dispute the weight and size of the materials he had to carry, as well as the frequency of the task and the distance he had to carry them.

(b) With regard to knowledge, they maintain that they did not know that Mr Wilson was carrying the equipment, or that he was developing back problems that he attributed to his work.

(c) On causation, they dispute the "micro-trauma" model. They argue that whether or not a person develops degenerative disc disease is principally a matter of genetics. They found upon a cluster of recent epidemiological studies to that effect.

(d) So far as the question of damages is concerned, the defenders say that the calculations underpinning the sum sought by Mr Wilson are speculative and without foundation. If the claim succeeds, only a modest award should therefore be made.

[6] The proof was heard in four parts between November 2009 and May 2011. Although Mr Wilson originally had the benefit of legal representation, he has conducted the case as a party litigant for a number of years. During the course of the proof, he had the benefit of two "Mackenzie Friends": Mr Craig Dunbar followed by Mr Douglas Nicol.

[7] Mr Wilson is a tall man, about six feet four inches in height. To allow for his back problems, each day's hearing was punctuated with breaks every hour or so. Sometimes with the leave of the court he sat down to ask questions, but for the most part he was standing. One of the consultant orthopaedic surgeons who gave expert evidence, Mr Mackay, was asked for his view of Mr Wilson as he observed him in court. He replied that Mr Wilson seemed to stand as comfortably as many persons of his age.

[8] Mr Wilson's close involvement in the outcome of the action was plain in the course of the proof. For example, he found it very difficult to maintain perspective when cross-examining witnesses whom he believed to be giving evidence hostile to his position.

[9] The defenders chose not to insist upon their plea of time bar. But the passage of time did have a significant effect on the evidence. The events in question took place over the lengthy period of about 8 years nearly two decades ago. Not surprisingly the witnesses, including Mr Wilson himself, sometimes found it difficult to recollect matters in detail.

Mr Wilson's Career

[10] Mr Wilson attended the Royal Scottish Academy of Music and Dance between 1974 and 1978, where he obtained a Diploma in Musical Education. He then proceeded to Glasgow University, from which he graduated with an honours degree in music in 1983. Subsequently, he worked in a number of capacities. He held a temporary post as a production assistant with the BBC Scottish Symphony Orchestra. He also wrote programme notes for concerts, studied conducting, worked as a music critic, and gave occasional lectures.

[11] Mr Wilson's long-term aim has been to pursue a career as a professional conductor. His intention was to save money from his salary for that purpose. The post at Motherwell College was his first full-time job. He was appointed to develop a course in music therapy at the College. He spent the academic year 1987-88 arranging a curriculum and materials for the proposed course. It did not, however, attract sufficient students and it was decided that it was not viable.

[12] Mr Wilson was then allocated other duties. His main tasks were to teach keyboard skills to nursery nurses and to special needs students. In addition, he undertook evening classes and "outreach" classes at local schools. Two members of the College management thought that Mr Wilson was disappointed by the turn of events. One of those individuals was David Wilson, who was his head of department for part of the relevant period. To avoid confusion, I shall refer to him as "David Wilson" and to the pursuer as "Mr Wilson" in the course of this opinion.

[13] During the period of Mr Wilson's employment, there was a reducing demand for music classes at the College. This matter was discussed with him at a meeting held on 25 November 1993. He countered by stating that there was an increased demand for music at evening classes. The trend appears, however, to have continued as the defenders suggested that he retrain as a lecturer in computer studies. Sometime in 1995, Mr Wilson agreed to undertake a Higher National Certificate course in that subject. The course coincided with the period when his back pain was at its most acute and he undertook some of the work at home.

[14] In February 1996, Mr Wilson was invited to attend a disciplinary hearing to discuss his failure to complete the HNC course. He was still on long-term sickness leave and did not attend. The hearing eventually took place in his absence on 17 June 1996. On the same day, a letter was sent to him terminating his employment with immediate effect.

[15] Mr Wilson's subsequent claim for unfair dismissal was upheld. The Employment Tribunal awarded him over £4,000 by way of compensation. An appeal to the Employment Appeal Tribunal was refused.

Mr Wilson's Back Problems

[16] In the course of his evidence in court, Mr Wilson traced his back problems to about 1991. That was when they were "... becoming progressively more troublesome". He also stated that: "I first experienced back pain approximately a year after I began work at Motherwell College ... maybe 18 months." The history he gave to the defenders' expert, Mr Mackay, during the course of an examination in 2006 was that the problems began "shortly after starting work at Motherwell College ... possibly within one year".

[17] If correct, that might be thought to be surprising. During that first year, he was devising a syllabus for the new course, not undertaking any lifting work. One cross-check is to consider when Mr Wilson took time off work with back problems. His self-certified absences in this connection are as follows:

November 1989	3 days
January 1991	3 days
April 1991	2 days
September 1991	2 days
October 1991	2 days
June 1992	1 day
March 1993	1 day
August 1993	5 days

[18] Mr McMaster, another orthopaedic surgeon who gave expert evidence, made the observation that this record might be regarded as abnormal. He explained that the absences from work are relatively level, year on year. In Mr McMaster's experience, most people with back problems have a more chequered absence history.

[19] It might be thought that the general practice records would provide the surest guide to this problem. They are, however, only available from 1994 onwards. An entry on 30 September 1994 refers to back pain that was thought to be a bout of sciatica. There are further entries throughout 1995. They contain nothing to suggest that Mr Wilson linked his back complaints to his working conditions until after his employment terminated. For example, an entry on 15 February 1995 reads "No triggering trauma".

[20] Mr Wilson queries the reliability of these records. He told Professor Mulholland, an orthopaedic surgeon who gave evidence on his behalf, that the GP records did not reflect the degree of back pain he was having whilst he was working, as he generally self-certificated.

[21] With regard to hospital records, Mr Wilson was seen in the orthopaedic clinic of the Western Infirmary, Glasgow on 5 June 1995. At that time, he did not make a connection between the problems and his work. The history notes that he had developed low back pain at about the time he was on holiday in Eastern Europe the previous year. That fact is subsequently recorded by several different doctors in various letters and clinical notes.

[22] The apparent discrepancies between these accounts were explored in cross-examination. Mr Wilson explained that the hospital records were mistaken. According to him, one doctor must have misunderstood his account. The others had repeated the mistake without taking a separate history.

[23] I found that explanation curious. A natural reading of the records suggests that more than one history was taken. In addition, tracing the back problem to the holiday coincides with other evidence given by Mr Wilson. He mentioned having a week of back discomfort before going on the holiday, which was sufficiently severe for him to attend his GP. The reason that he went on holiday appears to have been because it had cost him about £1,500.

[24] Looking at all these materials together, I conclude that Mr Wilson was not experiencing significant back problems prior to his disc herniation in 1995.

[25] When the herniation did manifest, Mr Wilson was treated by physiotherapy, as well as a TENS machine, with minimal relief. He had restricted movement in his lumbar spine and straight leg raising was also restricted. There were no motor weaknesses and the X-rays were normal. A Magnetic Resonance Imaging ('MRI') scan was performed on 13 July 1995. It showed bulging of his L5/S1 disc, but no evidence of nerve root compression. He was reviewed on 24 July 1995 and advised to take bed rest and commence anti-inflammatory medication.

[26] On 30 October 1995, it was noted that Mr Wilson's back and right leg pain had become more severe after physiotherapy and that he had been in bed for the previous six weeks. On examination, there was no significant change. It was thought that he had compression of the S1 nerve root and he was prescribed a lumbo-sacral support.

[27] On 14 November 1995, Mr Wilson was seen at Stobhill Hospital, Glasgow. He reported pain radiating down his right leg and that he had difficulty in sitting. On examination, spinal movements were restricted. Straight leg raising was slightly improved. Mr Wheelwright, consultant orthopaedic surgeon, wrote to inform the GP that there was a disc herniation, but that no surgery was indicated. He added that there was: "... considerable disc degeneration at this level with reactive changes affecting the adjacent end plates of the L5/S1 disc space."

[28] Mr Wilson was seen in the Neurosurgical Department of the Southern General Hospital, Glasgow on 18 January 1996. He was still complaining of pain in his back, but his right leg pain had resolved. On examination he had a good range of movement in his lumbar spine. Straight leg raising was to 30 degrees on the right and normal on the left. A CT scan of his lumbar spine dated 30 November 1995 was reviewed. It showed an L5/S1 disc prolapse causing nerve root compression. Again, no treatment was thought necessary.

[29] Mr Wheelwright again saw Mr Wilson on 1 August 1996. He noted that his condition had generally improved. His leg pain had resolved, but he still had a dull ache in his back. He was able to sit for up to one hour without trouble. A review by Mr Wheelwright on 19 February 1998 noted that there had been no change since he was last seen. However, Mr Wilson was now able to stand and sit for longer periods. By 14 April 1999 his sciatica had resolved, but he still had pain in his back. It caused him to wake at night.

[30] Another MRI scan performed in August 2001 showed that the disc protrusion at the L5/S1 level was less obvious. Dr Annesley Williams, a consultant radiologist who gave expert evidence, explained that the disc bulge now showed some evidence of resolution. It had become less prominent. Speaking broadly, the other parts of the spine were of relatively normal appearance for a middle-aged man. There were established degenerative changes.

[31] On 15 May 2002 Mr Wilson was seen by Professor Kennedy in the Neurology Department of the Southern General Hospital, Glasgow. It was noted that he had developed a new problem in June 1999, with an episode of pain and slight shaking in both hands. On examination there were no neurological abnormalities.

[32] There has been no material change in his condition since that time.

Mr Wilson's Duties

The Witnesses

[33] Mr Wilson was the first witness at the proof. Unsurprisingly, he found it difficult to question himself. He adopted his written pleadings as an accurate summary of the facts. In chief and cross-examination, he then amplified and clarified his position. Various other former employees of the College gave evidence. Some were fellow lecturers. Others were members of the management team.

F Block

[34] Motherwell College comprises a number of buildings situated on a campus. About 200 metres from the main building there is an annexe known as F Block. It contains three classrooms known as FG3, FG4 and FG5. Most of Mr Wilson's classes took place there. He stated that until about 1991, he primarily used FG5. In the later part of his employment, he tended to use FG3 and FG4. The weight of the evidence from the other witnesses placed Mr Wilson mainly in FG3 or FG4.

[35] Each student being taught musical skills by Mr Wilson used an electric keyboard. They were placed on the desks and plugged into a power point. From time to time, other equipment was also used, including a "ghetto blaster" and Marshall amplifiers. Because the locks on the classroom doors were broken, the various items were kept in a locked storeroom. It is located beside FG3 and FG4, but some distance away from FG5. It is along a corridor containing two sets of swing doors.

[36] The equipment was kept on the floor at the rear of the storeroom. That was because it contained no shelves. Mr Wilson described what he did as follows:

"[I] lifted, twisted and turned the equipment from the floor and handed it to those students who were there. Similarly if any students had come with me to the store after the class, I took it from them... twisting and turning as I did so, and indeed in every class that I taught I carried at least seven or eight keyboards. And I always carried the heaviest items of equipment, such as the stereo, the ... speakers ... and amps."

[37] For a period of months, perhaps as long as a year, a large photo-processing machine blocked the entrance. That caused Mr Wilson to twist and turn as he entered or left the storeroom and to lift the equipment higher than normal.

[38] Mr Wilson stated that he would take the materials out in the morning and return them to the storeroom at lunchtime. He often remained in classes during the morning and afternoon breaks to prevent theft. Sometimes - he estimated about fifty per cent of the time - he would return the equipment to the storeroom between periods. He stated that he carried between 3 and 5 keyboards at a time.

[39] Each class had a maximum of about 24 students. Mr Wilson maintained that his class numbers remained "healthy". However, in cross-examination he appeared to accept that his classes reduced in size during the course of his employment:

"Well isn't that what happened in 1993 and 1994? The numbers for your classes were dropping off to virtually nil? - That was because the department had targeted my classes ..."

Stewart Hall

[40] Mr Wilson taught special needs students in Stewart Hall, another building on the campus. These students had below average learning skills, but they did not have physical difficulties. He transported the same type of equipment to and from F Block.

[41] The maximum number for these classes appears to have been much lower than for those in F Block. A memo dated 2 October 1991 (from Irvine Kinghorn to David Wilson) headed "Music Option (Keyboarding)" states that:

"On Wednesdays the MLD link groups operate to an average of 8 students. I am prepared to make this the maximum for keyboarding but cannot limit the class to 6 students as requested by Martin Wilson."

[42] These classes took place in the early part of Mr Wilson's employment. David Wilson sent a memo dated 17 January 1992, which reminded Mr Wilson that he had been informed some time ago "that there should be no reason for you to use the Music Room in Stewart Hall."

Outreach Classes

[43] Mr Wilson taught outreach classes at Viewpark Community Education Centre and Burnhead Primary School in Uddingston until March 1995. He used his own car to transport similar items to those he used for his classes at the College. At Burnhead, Mr Wilson said that he required to carry the items a considerable distance and to negotiate stairs and doors. In addition he was often required to maneouvre chairs and desks into a suitable position. He suggested that there might have been between 7 and 10 students in these classes. However, the documents lodged in process indicate that there were only 6 or 8 students in 1991 and only 4 students in March 1994.

Evening Classes

[44] Mr Wilson also taught in the evening:

"... I was teaching up to three evening classes a week at one point, and this meant that when I was coming in to college at half past eight in the morning, I would be leaving at half past ten in the evening. So these were long working days. And they required me to do the setting up and dismantling of equipment for several classes. I was teaching, for example, all day in four different classes and I would be taking the equipment in and out ... four times a day approximately... And then again in the evening."

Timetable

[45] Mr Wilson's position was that for the bulk of his period of employment, he undertook a full teaching timetable. That meant 24 contact hours with students each week. The defenders said that he only required to teach a maximum of 16 hours a week. Mr Wilson characterised that assertion as "plainly false".

[46] To support his account, Mr Wilson relied in large measure on the position of a fellow employee, Mrs Swift. She had been employed part-time for many years to teach music to special needs students. It was College policy not to employ a part-time member of staff, unless another member of staff in the same discipline was already on a full teaching timetable. That led Mr Wilson to state: "if I was only doing 16 hours a week, what on earth was Mrs Betty Swift doing being employed at the same time?"

[47] Mr McCallum gave a different account. According to him, at the time of Mr Wilson's appointment, it was intended that Mrs Smith would continue with her duties. When the music therapy course was cancelled, it was decided out of fairness that she would not be sacked. I found that explanation cogent and convincing.

[48] A number of Mr Wilson's timetables were produced. Although he had lodged them himself, he appeared to dispute them in evidence. One timetable dated 11 June 1991 shows that Mr Wilson had no classes on Monday, Thursday & Friday mornings, or Friday afternoons. Another appeared to show that by 1995, he was only teaching music to evening classes. When asked to clarify the position, he responded: "these timetables do not cover all of the classes that I was teaching ... for the last six months." He refused to "even guess" at the numbers of pupils who attended the evening classes.

[49] The uniform evidence of the management staff (David McCallum, David Wilson and Mary Trayner) was that Mr Wilson never had a full timetable. They stated that his maximum number of contact hours was about 15 hours per week. Shortly before David Wilson transferred to another department in 1994, he informed the College Principal that Mr Wilson was doing less than 12 hours per week.

Keyboards

[50] Mr Wilson said that when he began teaching, only half-size keyboards were available. They were unsuitable. He ordered replacement full-sized keyboards. They covered 5 octaves and were in use from about the beginning of 1989.

[51] The evidence of the other witnesses was inconsistent. Some agreed that he taught using large keyboards. At least two thought that keyboards of different sizes were used. Others, however, recollected mainly small keyboards being used.

[52] Mr Wilson compiled a list of the instruments and equipment he claims he was required to transport. He conceded, however, that it omitted the Casio MT240 keyboard, which was the smallest and lightest model. When questioned further about it and in particular the fact that it was only a 4 octave keyboard, he replied: "Well, again, I don't have any of the evidence before me, so I can't comment."

Other Equipment & Materials

[53] The pursuer stated that he was also required to carry (a) a portable stereo radio, or "ghetto blaster"; (b) a glockenspiel; and (c) two Marshall amplifiers - a 100 watt and a bass amplifier, which he carried a few times a year. He also mentioned carrying percussion instruments, guitars, recording sets, desktop music stands and music folders.

[54] On occasion, Mr Wilson said that he also carried photocopying from the main building to F Block. He spoke of a box of paper containing 400 to 500 pages. He was reticent about how often that occurred. While he accepted that it was rare, on repeated questioning, he stated: "it was a weekly occurrence, at least".

Weight

[55] Mr Wilson estimated the weight of the various items as follows: keyboards (6-61/2kgs); ghetto blaster (6kgs), amplifiers (22.4kgs), and glockenspiel (85kgs). The evidence of the defenders was that, including batteries, the Casio MT240 keyboard weighed 2.6 kgs and the ghetto blaster 4.6 kgs.

[56] Mr Lawson the janitor said that he had carried keyboards from the storeroom without difficulty. He estimated that they weighed about 1kg. During the course of the proof, the macer and two of the expert witnesses, Mr McMaster and Mr Mackay, lifted a Casio keyboard in court without any apparent difficulty. Mr McMaster also lifted the stereo unit and the Marshall amplifier. He thought it unsafe to try and lift three keyboards at a time and could not conceive why anyone should choose to do so. David Wilson made a similar remark. He commented that he thought it a bit stupid for anyone to carry three or four keyboards at once.

Janitorial Assistance

[57] According to Mr Wilson, he undertook virtually all of the lifting and carrying for his classes himself. From about 1991:

"... I would request but not necessarily always received... some assistance from some students from some classes, that is I would lift, twist and turn every piece of equipment that was used in the class, handed it to them, they would carry it across and ... I would always carry the heaviest items of equipment... to the classroom."

[58] Mr Wilson also stated that during the last six months of his tenure, Tom McEwan assisted him with the outreach classes. In support of his claim that no handyman was available prior to that period, Mr Wilson referred to several minutes of college meetings. They included requests for support from a technician. None of them, however, specifically records that Mr Wilson asked for assistance with lifting and carrying keyboards or other equipment.

[59] Mr McEwan was employed between 1989 and 2008 as 'a driver - service support'. His main function was to carry and transport equipment using a van to various sites outside the College, mainly to about 80 outreach centres. From time to time he worked within the College. In practice he mainly worked for the horticulture department. He said that he did assist Mr Wilson at Burnhead and Viewpark. However, he did not assist him in transporting equipment and classroom materials on the College campus itself.

[60] Mr Lawson held the post of janitor between 1986 and 1996.He stated that:

(a) His room was close to classrooms FG3, FG4 and FG5.

(b) He was available to assist if asked: "that's what I was paid for".

(c) He was not aware of lecturers having difficulty in contacting him.

(d) He did on occasion assist Mr Wilson with lifting and carrying.

(e) He did not recall, however, Mr Wilson ever asking him for assistance.

(f) If any such request had been made, Mr Lawson would have classed that as a priority. He would have worked his schedule around it to ensure that it was done.

[61] George Birrell began by stating that he had never seen a janitor lifting or carrying any keyboards and that there was no janitor permanently based in F Block. In cross, his position altered. He accepted that a janitor "may have been permanently allocated there, but he was certainly not permanently present". He added that janitors were very seldom present and hard to find.

[62] Mr Wilson's own testimony also fluctuated between chief and cross-examination. His initial position was that Mr Lawson never assisted him in lifting and carrying items. When pressed in cross, however, Mr Wilson reluctantly conceded that he had never once approached Mr Lawson for assistance. In my view that was a striking admission. Given the back problems he describes, why did he not request assistance?

[63] There was also a technician, but Mr Wilson was not contradicted when he said that Mr Hay never worked in F Block:

"Nobody ever saw him there. He was based in ... the main building, several hundred yards away. So it might have been theoretically available, but it was never practically made available."

I therefore discount any idea that he provided assistance.

Complaints about Lifting

[64] The clearest evidence that complaints were made to the defenders about lifting came from Craig Dunbar. He stated that he did complain on Mr Wilson's behalf. As the trade union representative, he sought a meeting with David Wilson to raise the risk to health and safety being presented to Mr Wilson by his work. As Mr Dunbar put it: "I was complaining about the fact that he was having difficulty carrying these keyboards around the corridors and through the doors, and in conditions which could cause him to perhaps slip and fall ..."

[65] Mr Dunbar thought that the matter was first raised in 1988 or 1989 and that he approached David Wilson: "somewhere between about half a dozen and ten times". According to Mr Dunbar, David Wilson said that he would look into the matter, but nothing happened. He also mentioned that Mary Traynor was present at more than one of the meetings.

[66] When it was suggested to Mr Dunbar that a technician or janitor was available to assist Mr Wilson, he responded:

"... that's absurd, because that's exactly what we were trying to obtain in our discussions, and the furthest we ever got was that we'll look into it. There was no ... if that had been the case, they would have said, oh we have somebody and we can show you who he is, and that never, ever happened."

[67] Neither David Wilson nor Mary Traynor could recollect these complaints being made. Further, they had no memory of Mr Wilson himself complaining to them about lifting or moving equipment. Mr McCallum was to similar effect.

[68] It is a difficult task to adjudicate on this conflicting evidence, because I do not doubt the credibility of Mr Dunbar, David Wilson, Mr McCallum, or Mrs Traynor. I conclude, however, that no complaints were made. In making that finding, I rely on these factors. First, the absence of any supporting documentation. Many minutes of staff meetings and memoranda were produced. One feature is remarkable. Not one includes a complaint about Mr Wilson's back problems.

[69] Secondly, all three management witnesses emphasised that Mr Wilson was prone to complain. David McCallum stated that Mr Wilson left notes of complaint in his office almost every day. The flavour of the correspondence between David Wilson and Mr Wilson is illustrated by a memo dated 11 June 1991. It begins: "May I remind you again, and hopefully for the last time, that Mary Traynor is your Senior Lecturer and anything appertaining to the music section is initially under her jurisdiction. DO NOT RAISE MATTERS WITH ME WHICH SHOULD OBVIOUSLY BE ADDRESSED TO HER."(sic). In cross-examination, David Wilson stated: "Any time I spoke to you, you were unhappy about things."

[70] Thirdly, there was no reason for the defenders not to take steps to address the problem. They could have simply directed Mr Wilson not to pick up the keyboards, and instructed Mr Lawson to carry out the task instead.

Complaints about Back Problems

[71] I found it difficult to understand Mr Wilson's evidence in court on this point. Accordingly, I asked him to clarify when he notified the defenders of his back complaints. He replied:

"Suffice to say we had all been promised these facilities, they never appeared. And there were ... that was the beginning ... letters or memos seeking assistance and verbal requests for assistance were made by myself and other members of staff regularly at section meetings, staff meetings, by memo, and they simply weren't met with any competent result. And we were left to get on with it as best we could ...And that state of affairs continued ... until the last six months of my tenure when ... I did receive some assistance ... in lifting and carrying materials in and out of Burnhead Primary School."

I found that to be a vague and oblique answer to a simple question.

[72] At another point in his evidence, Mr Wilson stated that he spoke to Mrs Barr after returning from sickness absence:

"[she] enquired if I felt there was anything at work which was contributing to my back injury. And I said well I don't know, but the lifting and carrying certainly isn't helping. To that [she] said 'Well the janitor is available to assist' ... and I pointed out that theoretically the janitor may be able to assist... but in practice he was never available ..."

[73] David Wilson, David McCallum and Mary Traynor were unaware that Mr Wilson was off work with back injuries. His absences from work were neither frequent, nor lengthy. As they were self-certified, in my view there was no reason for the defenders to be aware that he was complaining of back problems associated with his work.

Trolley

[74] There is then the question of the trolley. There was conflicting evidence as to whether one was provided or not. Mr McEwan thought that a trolley was kept near the boiler house at F Block. Latterly he was supplied with a barrow, or something similar, for his own use. Mr Lawson stated that he used an ASDA supermarket trolley, which was kept in the storeroom for two or three years when Mr Wilson was employed. Mary Trayner recollected seeing a trolley, but she did not know where it was kept and never saw Mr Wilson using it. I find that no trolley was provided.

Credibility and Reliability

[75] The witnesses from Motherwell College all struck me as trying to tell the truth. Apart from the issue of Mr Dunbar's complaints, there was no matter of material importance where a conflict in testimony arose.

[76] Mr Wilson is in a different category. His evidence requires to be considered separately. He accepted several times that he was unable to recollect all the details after such a length of time. In other words, he was unreliable in relation to certain matters. Senior counsel for the defenders went much further. He submitted that Mr Wilson was wholly unreliable - someone prepared to say anything that advanced his case.

[77] I begin by observing that Mr Wilson had a poor relationship with the College management. That can perhaps be inferred from some of the evidence mentioned above. Mr McCallum in particular had a negative view of him. He described Mr Wilson as "lazy" and "a very difficult member of staff to supervise". He spoke of Mr Wilson arriving at work late and leaving early; of supervising the students with his feet upon the desk while reading the Herald newspaper; of absenting himself in the staffroom or playing snooker. In Mr McCallum's view, Mr Wilson would not lift anything as he did not see it as part of his job.

[78] I have considered the whole evidence to determine Mr Wilson's credibility and reliability. As I have already explained, his evidence is critical. If I cannot accept his account, then a large part of the foundation of his claim disappears.

[79] Mr Wilson has been preoccupied with this case for over sixteen years. During that period, he has not undertaken any other form of employment. Instead he has concentrated on the litigation. He finds it very difficult to be dispassionate. He is inclined to ignore or dispute any version of the facts that does not square with his account. His instinct is to exaggerate. Various illustrations of these tendencies can be given.

[80] Mr Wilson was keen to supply details when he spoke of matters that supported his position. But when hard questions were put to him, he was inclined to prevaricate and to take refuge in a lapse of memory.

[81] When asked why the teaching timetables appeared to show less than a full complement of student contact hours, he stated that he didn't wish to comment in the absence of the facts. Documents that appeared to show that he was no longer teaching outreach classes in the summer of 1995 were: "...wholly unreliable and tainted by the fact that they got all of these things wrong."

[82] Mr Wilson stated that when he was retraining in computer skills, the defenders did not meet his request to be supplied with a laptop to work at home. Two documents were then put in front of him in cross-examination: (i) a letter by him dated 7 December 1995 acknowledging receipt of a laptop; and (ii) a minute dated 15 February 1996 stating that he was using it. Confronted by this evidence, Mr Wilson stated that he would have to check the documents and that his memory is problematic because of his heavy medication and the length of time which has elapsed.

[83] Mr Wilson lodged a DVD containing video footage of the various locations at which he worked. It was shown to various witnesses. During the cross-examination of Mr Mackay, there was a technical problem and the court copy would not play. With the agreement of the defenders, Mr Wilson's own copy was put into the DVD machine. Once it began playing, it appeared to contain extra footage. I queried this with Mr Wilson. He equivocated and then said that the footage had been seen before. This assertion turned out to be wrong. But he did not offer any explanation or apology.

[84] Mr Wilson refused to accept that he told medical staff that his low back pain began on holiday in Eastern Europe in 1994. He suggested that the Registrar "got it wrong" and all the other doctors repeated his mistake. But Dr Pickering confirmed that the history set out in the hospital records was consistent with the GP records.

[85] It is plain that Mr Wilson holds a deep sense of grievance towards the defenders. He described himself as having sustained a "catastrophic" injury. Two of the experts regarded that term as an inappropriate one to use for his injury. During the course of the proof, Mr Wilson attempted to introduce irrelevant matters with the design of blackening the reputation of Motherwell College. He made a number of tendentious comments about his former employers. He did so despite the repeated warnings that I issued.

[86] There was also the issue of Mr Wilson amending a GP's letter without permission. He accepted that he had done so:

"... [I] altered a single letter of support from my GP to Scottish Office Pensions Agency having sought my GP's consent beforehand. She was unavailable to give that consent and I redacted or I withdrew eight paragraphs which gave a misleading account to Scottish Office Pensions Agency based upon the information which I had given to my GP at the time she wrote the letter."

I did not find that explanation convincing.

[87] In short, I found Mr Wilson to be an unsatisfactory witness. I was only able to accept his version of events when it was supported by other reliable evidence. While I accept that he did lift instruments and equipment in the course of his employment, I do not accept his account in relation to (a) the number of keyboards lifted at any one time; (b) the weight of that equipment; (c) the frequency with which they were lifted and (d) the distances over which they were carried.

[88] The defenders made the following submission: "It is inconceivable that the pursuer, who complained about the slightest thing, would not have complained repeatedly about having to lift and carry the items he says he was required to lift and carry, particularly if he had had the slightest difficulty with any such activities." I agree.

[89] Mr Wilson's account gives rise to several questions that remain unanswered. Why did he carry the keyboards back to the storeroom at breaks? Why did he not ask for the locks on the classroom doors to be fixed? Why did he carry several keyboards at a time, particularly after he alleges the back problems developed? Why did he not ask for assistance?

[90] Because no one else could give a clear account of the actual amount of lifting undertaken, it is impossible to pin down what tasks Mr Wilson was doing throughout the eight year period of his employment. That would be guesswork. Accordingly, he has failed to discharge the burden of proof in establishing the activities which he founds upon in his claim.

[91] I also hold that the defenders did not know (a) that Mr Wilson was lifting and carrying instruments and equipment to and from the storeroom; (b) that he was doing so in a manner that would give rise to a risk of injury; and (c) that he was suffering from back pain which he attributed to his work. Accordingly, the common law case fails.

Risk Assessment & Instruction in Manual Handling

[92] The Manual Handling Operations Regulations 1992 came into force on 1 January 1993. On the evidence, the defenders did not discharge their duties in terms of regulation 4. They did not carry out risk assessments, or offer manual handling training to their employees.

[93] If a risk assessment had been made, it would have disclosed to the defenders that Mr Wilson was carrying and lifting the equipment. If they had provided instruction in manual handling techniques, then he would have known how best to fulfill his duties.

[94] In my view, Mr Wilson has therefore established a breach of statutory duty.

Causation

[95] The issue of causation occupied the greater part of the proof. It unpacks into two questions. Firstly, can repetitive trauma cause disc herniation? Secondly, did the lifting carried out by Mr Wilson at Motherwell College cause his injury?

[96] I received assistance on these questions from a number of distinguished experts. Those called on behalf of Mr Wilson were: Professor Adams, biomechanical engineer; Professor Mulholland, orthopaedic surgeon; Dr Goldman, neurologist; and Dr Annesley Williams, radiologist. The defenders called three orthopaedic surgeons: Mr McMaster, Mr Mackay and Professor Dickson, together with Dr Rankine, radiologist.

[97] I should add that Dr Clive Andrews, an ergonomist, was also called by Mr Wilson. In my view, however, he was not qualified to give evidence on causation.

[98] The clinicians have a wealth of experience, having collectively performed or observed thousands of operations. There is also a significant body of literature on the subject. A large number of papers from scientific and medical journals were cited in the course of the proof.

[99] In evaluating the detailed and complex evidence, I applied the following principles, which I derive from Dingley v Chief Constable of Strathclyde Police 2000 SC (HL) 77; Davie v Magistrates of Edinburgh 1953 SLT 54; Main v Andrew Wormald Ltd 1988 SLT 141; McTear v Imperial Tobacco Ltd 2005 2 SC 1; and Sarah Smith v Lorna McNair [2008] CSOH 154:

(a) The Court must analyse the medical and scientific evidence with the assistance of the experts, but they cannot usurp the function of the judge.

(b) The science must be "intelligible, convincing and tested".

(c) The experts can assist with the epidemiological evidence, even though they themselves do not work in that field.

(d) The Court must assess the whole evidence to determine whether the pursuer has discharged the burden of proof.

The Significance of Back Problems

[100] Disorders associated with disc degeneration are very common:

"Back pain is a major public health problem in Western industrialised societies. It causes suffering and distress to patients and their families, and affects a large number of people; ... with around 10% of sufferers becoming chronically disabled. It also places an enormous economic burden on society; its total cost, including direct medical costs, insurance, lost production and disability benefits, is estimated at £12 billion per annum in the UK and 1.7% of the gross national product in The Netherlands."

Urban and Roberts, Arthritis Research & Therapy (2003) 5:120-130

[101] Several years ago, the European Union funded a project called EURODISC, which published a report in 2004, with a follow up paper in 2006. Seven laboratories throughout Europe combined to investigate the interaction between ageing, genetics and life-style in the development of intervertebral disc degeneration. The study estimated that disc degeneration "... is significant in around 10% of teenagers and more than 70% of people over 50 years."

[102] The position in the United States of America is similar:

"The lifetime prevalence of low back pain is approximately 80 percent; 31 million Americans have low back pain at any given time. In the United States, low back pain is second only to the common cold as the reason patients cite for seeking medical care. The estimated cost of medical care for patients with low back pain exceeds $8 billion annually. Although there has been no increase in the incidence of this problem, over the past 30 years the rate of disability claims related to low back pain has increased by 14 times the rate of population growth."

Jensen et al; N Engl J Med 1994; 331, Magnetic Resonance Imaging of the Lumbar Spine in People without Back Pain

Discs and Disc Degeneration

[103] The intervertebral discs are:

"... the joints of the spinal column. They have a primarily mechanical role in transmitting loads through the spine and providing flexibility to the spinal column (allowing bending, flexion and torsion). The disc has a complex structure." Eurodisc

[104] A healthy disc has a high water content, but:

"... with increasing age the nucleus generally becomes more fibrotic and less gel-like ... With increasing age and degeneration the disc changes in morphology, becoming more and more disorganized...There is frequently cleft formation with fissures forming within the disc, particularly in the nucleus. Nerves and blood vessels are increasingly found with degeneration"

Urban and Roberts (supra)

[105] The precise physiological process involved in degeneration is not yet known. Professor Dickson suggested that a Nobel prize awaits the scientist who discovers the answer. What is known is that as the disc loses water, the vertebrae come closer together and the disc height narrows.

[106] Because of the technical nature of some of the expert evidence, it is also necessary to give a more technical description of the process:

"The internal mechanical functioning of the intervertebral disc is such that a young healthy disc has a water-rich nucleus and the annulus fibrosus enables it to act like a fluid. ... Compressive loading of the spine forces some water away from the nucleus pulposus ... thereby resisting further compression. On removal of the load, the normal disc height and equilibrium conditions are restored. However, as the person ages, the disc water content decreases, especially in the nucleus. Now it is the annulus that acts as a fibrous solid to resist compression directly. Thus, any parameter that decreases proteoglycan concentration or weakens the collagen network will compromise disc function.

Lumbar disc disease progresses as a series of pathophysiologic events, beginning with asymptomatic fissuring and fragmentation within the disc. The decrease in water content and disc height leads to degeneration of the annulus fibrosus resulting in radial tears through which the posteriorly migrated nucleus pulposus herniates, followed by herniation of the disc into the spinal canal or the neural foramen.

Disc herniation in the typical posterolateral region may cause nerve root impingement. Though the nucleus pulposus has relatively little in the way of nerve supply, the annulus fibrosus is well innervated. Thus, annular rupture, with prolapse of the herniating nucleus pulposus, usually manifests as mild to severe back pain, often with the pain radiating to the pelvis and legs. This back pain typically involves multiple exacerbations and remissions."

Cheung et al (2008); Current Understanding of low back pain and intervertebral disc degeneration: epidemiological perspectives and phenotypes for genetic studies; Current Orthopaedics (2008) 22, 237 -244

[107] The key feature of degeneration is dehydration. As degeneration occurs, cracks appear within the disc like those in an oak beam as it loses turgor with age. In consequence, the disc then tends to bulge, rather like a flat tyre coming into contact with the ground.

[108] Surprisingly, there is no clear agreement on terminology in this field. The leading authors in this field state:

"... then there is the deceptively simple issue of defining disc degeneration. The term ... is commonly used for an overall subjective impression of imaging findings, including signal loss, bulging, herniation, endplate irregularities, osteophytes, and narrowing of the disc space, but no universally accepted standard definition exists."

Battié & Videman The Twin Spine Study: Contributions to a Changing view of Disc Degeneration The Spine Journal 9 (2009) 47 - 59

[109] These terms require further clarification.

signal loss A normal disc appears white on an MRI scan. As the disc degenerates, it loses water and begins to turn grey and then black.

fissures, clefts and tears These terms are synonyms. The defenders' experts prefer to use the term "clefts", as they occur without any form of trauma.

"disc prolapse" and "disc herniation" These terms are also used interchangeably. They cover a variety of disc problems: bulges, protrusions, and extrusions.

disc bulge This involves a contour abnormality of the disc. The bulge is circumferential and symmetrical. Such bulges are very common and part of the degenerative process.

disc protrusion A protrusion is a segmental or localised bulge. In other words it involves one portion of the disc, so the contour abnormality is asymmetric. A protrusion is a more focal bulging of an already bulging disc.

disc extrusion An extrusion is a large protrusion. The neck adjacent to the disc is narrower than the material that protrudes into the spinal canal.

disc sequestration A sequestration occurs when the extruded disc material is no longer connected to the disc from which it came.

endplates These are-as the name suggests-at the end of the discs. They are currently being investigated by a number of researchers to see if they play a role in degeneration.

Matters of Agreement

[110] The experts appeared to agree on a number of matters:

(a) disc degeneration normally begins when persons are in their 20s

(b) some children, however, show signs of disc degeneration and in rare instances, may have a protrusion

(c) degeneration continues throughout life until death

(d) disc protrusions mainly occur between the ages of about 20 and 40

(e) they are typically located in the lower lumbar spine (L4/L5 or L5/S1)

(f) disc degeneration and disc protrusions are usually associated

(g) protrusions don't often occur after the age of about 60

(h) that is because after a certain stage, the discs are too desiccated to protrude

(i) many people with disc degeneration are asymptomatic

(j) it is not known why someone who is asymptomatic becomes symptomatic

(k) Mr Wilson had a disc protrusion at L5

(l) his discs showed no evidence of endplate damage

(m) it is normal not to operate in such circumstances; conservative treatment being thought to be the best option

[111] In theory, ageing and degeneration are discrete processes. However, differentiating between them is very difficult:

"It is well known that the lumbar intervertebral disc undergoes progressive morphological and cellular changes with age and degeneration. Although many clinicians and scientists make a distinction between 'pathological' and the inevitable 'age-related changes', there is no clear definition between the two." Cheung (supra).

[112] The experts all emphasised that disc degeneration is extremely common. Looking around the court when giving his evidence, Professor Mulholland remarked that while not everyone in the room had disc degeneration, possibly all those aged over 50 did so. He thought that up to half the population was affected and that many people are walking round with protrusions and extrusions that are entirely asymptomatic. Professor Adams stated that: "It's unusual for an old man to escape without degenerative changes, we all get them in the end."

[113] In Mr McMaster's clinical experience, an MRI scan of someone over the age of 50 would disclose a disc protrusion. Dr Rankine estimated that about 60% of the middle-aged population have disc protrusions. He stated that it is simply not known why some people are symptomatic and others are asymptomatic. Urban and Roberts found that more than 70% of asymptomatic people have disc prolapses that pressurise the nerve roots.

The Developing Scientific Thought

[114] A number of causes have been suspected of causing disc degeneration. They include heavy manual labour, smoking and vibration (in the case of HGV drivers). An influential series of papers published by Kelsey et al in the 1970s and 1980s concluded that heavy manual labour was the main cause. The authors' position is summarised in: 1990 Low Back Pain/Prolapsed Lumbar Intervertebral Disc Epidemiology of Rheumatic Disease vol. 16 p.699.

[115] All the orthopaedic surgeons testified that it became the received view that disc degeneration had a mechanical cause. Mr McMaster said that when he was appointed to a consultant post in 1975, it was widely accepted that heavy work activity was the predisposing factor in people developing degenerative change to their backs. Professor Dickson stated that 30 or 40 years ago, it was generally felt that trauma might have a significant part to play. Professor Mulholland agreed that the mechanical model gained ascendancy in the 1970s and 1980s.

[116] Dr Rankine is perhaps the most interesting witness in this connection. He submitted his doctoral thesis on degenerative disc disease in 1998. After reviewing the existing state of knowledge, he accepted the theory that trauma was the main causal agent for the condition. However, he now regards that part of his thesis as a historical document. That is because of a seminal paper published in 1995. Dr Rankine explained that it took some time to recognise the paper's significance.

The Battié & Videman Papers

The 1995 Paper

[117] The paper in question is entitled Determinants of Lumbar Disc Degeneration Battié & Videman et al Spine 20 (24): 2601-2612. It reported on an epidemiological study involving 115 pairs of identical twins aged between 35 and 69 years. They were drawn from the "Finnish Twin Cohort", which included virtually all twins born in Finland before 1958 and alive in 1975. They were selected based on one of five sets of discordance in each pair: occupational materials handling, sedentary work, exercise participation, vehicular vibration and cigarette smoking. Questionnaires were sent to each participant, followed by a structured interview that included the taking of a detailed occupational history.

[118] The aim of the paper was to identify the cause or causes of disc degeneration. The monozygotic twins were chosen precisely because of their identical genetic make-up. They were divided into two groups: those who had performed (a) very light activities; and (b) heavy activities. The study made a clear and startling finding. The major contributing factor to people developing degenerative changes in their back was genetic. Heavy physical activity had only a very modest effect: "In the lower lumbar levels, leisure time physical loading entered the multivariate model explaining 2% of the variability."

[119] The authors concluded that:

"The study findings suggest that disc degeneration may be explained primarily by genetic and early environmental influences and unidentified factors, which may include a complex interaction between environmental factors and individual spinal anthropometrics that lead to largely unpredictable effects."

[120] All the experts acknowledged that this paper was the most important work in decades. Although speaking as clinicians, rather than as epidemiologists, Professor Mulholland, Mr McMaster and Dr Rankine thought that the methodology was impeccable. The results were "incredible" and "remarkable". Mr McMaster described it as the paper that changed everything. It shed a completely different light on matters.

[121] While none of the experts disputed the findings of the paper, its interpretation did open up divisions between them. The defenders' experts took the view that, following its publication, the mechanical trauma model could no longer be supported.

[122] The pursuer's lead expert, Professor Adams, described Battié & Videman as the most highly regarded authors in the field. He was of the opinion, however, that although the 1995 paper is "startling" (a) it is relevant to disc degeneration, not to disc herniation; and (b) that the unidentified factors mentioned by the authors include micro-trauma.

[123] On the first point, he was of the view that the 55 per cent unexplained element is mainly mechanical in nature. Dr Rankine, Mr McMaster and Professor Dickson took the opposite position. They inferred that the 'unexplained' part must exclude physical loading. On their interpretation, the study had set out specifically to consider the effect of "heavy leisure time physical loading" and concluded that it only explained 2 per cent of the variability in degeneration scores. It was therefore unjustifiable to try and add physical loading back into the "unexplained" section. They pointed out that the paper specifically considered the type of herniation found on Mr Wilson's MRI scan.

[124] To underline his interpretation, Mr McMaster referred to a histogram in the 1995 paper (page 2608). It shows three causes: unexplained, familial aggregation and physical loading. As physical loading is included, that must exclude it in either of the other two categories. Dr Rankine also stated that there is no evidence that the "unexplained" section is mechanical.

[125] On the second point, another fault line opened up between the experts. Professor Adams' position was that twisting and carrying contributes to both disc herniation and disc degeneration. However, he said that it is more linked to disc herniation than disc degeneration. He stated that the old view that an individual had to have disc degeneration before herniation disappeared about 15 years ago.

[126] The defenders' experts rejected that view. Based on their extensive clinical experience, they said that a prolapse only occurs in a lumbar disc that exhibits soft tissue degenerative change. It does not take place in an otherwise normal disc. According to them, that view is held be everyone who works in the field.

[127] I should add that at a late stage of the proof, during his cross-examination of Dr Rankine, Mr Wilson appeared to question the validity of the 1995 paper. In response to a specific question from me, he agreed that was the case. I found that baffling. Without any basis in the evidence, he disputed a paper that his own experts relied upon.

Later Papers

[128] Battié & Videman and their fellow authors have continued to publish papers in this field. What follows is an attempt to summarise those of their later findings which were discussed by the experts and are pertinent to this case.

[129] In 2004, they published a review paper: Lumbar Disc Degeneration Spine 29 (23): 2679 - 2690. Its aim was "to synthesize the scientific literature on the prevalence of lumbar disc degeneration and factors associated with its occurrence, including genetic influences." The paper makes two key points. First, herniation is a common degenerative finding. That suggests that the authors were addressing herniation as well as degeneration. Secondly, it reiterates that the effects of loading at work are minor:

"Physical loading associated with upright postures and normal everyday life appears to affect disc degeneration, as suggested by substantially greater findings at the lower lumbar discs when compared with the upper lumbar region, but specific occupational and sport exposures appear to have minor additional affects."

[130] The authors continue to accept that the position is unclear:

"... yet the additional effects of specific loading exposures studied to date, whether work, sports, or leisure related, beyond those of the normal range of activities of daily living, are unclear or appear to be relatively minor. ... It is certain, however, that both environmental and constitutional factors have some role in disc degeneration phenotypes and that their magnitude can vary. In other words, the genetically determined 'natural progression of disc degeneration' is modified to some degree by behavioural and environmental factors."

[131] The next paper was published in 2008: Genetic and Environmental Effects on Disc Degeneration by Phenotype and Spinal Level Spine 33 (25): 2801. It contains the following statements:

(a) "Disc degeneration is likely the result of the contributions and interplay of many genes and environmental influences."

(b) "Our results confirm a substantial genetic influence on disc degeneration, with heritability estimates ranging from 29% to 54%, depending on the particular phenotype and lumbar level."

(c) "... although some genetic influences are shared, the majority of genetic and environmental effects on disc degeneration seem to be unique to either the upper or lower lumbar levels. This finding ... strongly suggests that the upper and lower lumbar regions should be considered separately."

[132] Professor Adams called this the "best paper" and noted that it lowered the percentage attributable to genetic factors from those set out in the 1995 paper. He said that

"... [it] showed that if you just concentrate on disc degeneration at L4/5 and L5/S1, then genetic inheritance accounts for 35 per cent of the variance."

[133] He was also keen to stress that, like the original paper, it concerned disc degeneration:

"We do know that disc prolapse is more heavily dependant on environment than disc degeneration, but we can't come up with a similar figure because there's not enough identical twins who've got disc prolapse. So you are stuck knowing that the inheritability of intervertebral disc prolapse/herniation is somewhat less than the 35 per cent, but we don't know how much less, because the information is not even obtainable."

[134] The defenders' experts also regarded the 2008 paper as important. But they placed a different construction upon it. In their view, it reinforced the thesis that genetic factors are the main known cause of disc degeneration in the lower lumbar spine. While the 2008 paper shows a slight reduction in the genetic component, it does not reduce the physical loading component. In other words, the causal effect of heavy manual lifting is still minimal.

[135] Battié & Videman et al published a further paper in 2009 in which they restated their opinion about the causes of disc degeneration:

"The once commonly held view that disc degeneration is primarily a result of aging and 'wear and tear' from mechanical insults and injuries was not supported by this series of studies. Instead, disc degeneration appears to be determined in great part by genetic influences. Although environmental factors also play a role, it is not primarily through routine physical loading exposures (eg, heavy vs. light physical demands) as once suspected."

The Twin Spine Study: Contributions to a Changing view of Disc Degeneration; The Spine Journal 9 (2009) 47 - 59

[136] In this paper, the authors also make an interesting observation:

"Our findings provide evidence that more cumulative or repetitive physical loading in the form of greater body mass is not harmful to the disc and, instead, appears to delay L1-L4 disc desiccation slightly. The study results suggest that a gradual increase in routine physical loading is not bad for our discs."

[137] Professor Mulholland observed something similar when he first went to work in Nottingham. He conducted research into back problems in coal miners and was confident of finding many such problems, including disc protrusions. However, that turned out not to be the case. He speculated that the miners typically went down the mines at the age of 16 and developed a thick disc annulus.

[138] Dr Rankine said that patients with disc degeneration were recommended to keep active. They would not be made worse off by doing cyclical loading. Moreover, ninety five per cent of disc herniations resolve without intervention.

[139] Professor Adams did not consider the 2009 paper to be a major contribution, because it is a literature review. He also suggested that the authors do not understand body bio-mechanics very well. His approach rests on the view that once loading goes above a certain threshold, harm begins. According to him, most informed people regard excessive mechanical loading as a key feature of disc herniation.

[140] Two further papers in this sequence were published in 2010. Both came too late to be considered by Professor Adams in his evidence. In the first, the conclusion can be gleaned from the title: Videman et al Challenging the cumulative injury model: positive effects of greater body mass on disc degeneration The Spine Journal 10 (2010) 26-31. The second paper is Hancock, Battié & Videman The Role of Back Injury or Trauma in Lumbar Disc Degeneration Spine 35(21):1925-1929. It concludes that "back injury based on patient report is not an important predictor of future disk degeneration". All the defenders' experts agreed with that conclusion. They regarded the thrust of all the papers as refuting the bio-mechanical model.

The "Micro-Trauma" or "Cumulative Fatigue" Model

[141] As the lead expert for Mr Wilson, it is worth scrutinising Professor Adams' evidence in more detail. His first degree was in physics, followed by a doctorate in bio-mechanics. He currently holds the chair of Spine Biomechanics at the University of Bristol and has published many articles in peer-reviewed journals. He has received several prizes and eleven of his papers have been cited over 100 times.

[142] For the past 30 years he has conducted research into two areas. First, carrying out measurements on living persons to assess the forces acting on the human spine. Secondly, applying these forces to cadaveric spines to find out what injuries they can create. He does not treat patients and explicitly stated that he "should have no clinical opinion."

[143] Professor Adams said his speciality is "meccano biology". He prefers the term "cumulative fatigue damage" to describe this model. That is because the key to injury is the fatigue resulting from the repetitive nature of the activity.When a disc is subject to repeated loading, it can suffer micro damage. "Trauma" is less appropriate as it suggests a high level of loading.

[144] In his report on Mr Wilson dated 15 May 2008, Professor Adams states:

"Laboratory experiments on human cadaveric spines have shown that a high proportion of lower lumbar discs from middle-aged people will herniate if loaded severely in bending and compression. Early experiments removed the neural arch in order to visualise the herniation but later experiments did not. The forces required varied greatly between specimens, suggesting that some discs are substantially weaker or stronger than others, but generally either the compression or the bending exceeded normal physiological limits. In other experiments, neither the bending nor compression was exceptionally high, but several thousand loading cycles were applied in order to cause disc herniation as a gradual injury. Failure in response to repetitive loading is called 'fatigue failure' and is caused by the gradual accumulation of microscopic damage over time. Fatigue mechanisms of disc herniation appear to be facilitated by adding lateral bending and torsion to the complex loading to simulate a person twisting while lifting. These cadaveric experiments are supported by the results of experiments on animal spines, and by mathematical models."

[145] That passage might be said to encapsulate his position. Professor Adams goes on to state that there have been a number of such experiments and that "The applicability of these experiments to living people is no longer challenged in the scientific literature, or in leading scientific societies."

[146] Before discussing his views in more detail, it is worth quoting a passage that expressly queries that model:

"A cumulative injury model of disc degeneration has traditionally been predominant in spine care. This view of spinal degeneration suggests that disc structures are damaged through the cumulative effects of occasional excessive forces and repeated loading, often resulting from occupational exposures or leisure-time physical activities. An injury model of disc degeneration might predict that a patient-identified inciting event was the final injury in a cascade of events culminating in annular rupture and displacement of disc material. Although some epidemiologic studies have found associations between occupational exposures and LDH or sciatica, other studies have failed to find such an association. Similarly, there is conflicting evidence for the possible association of leisure-time physical activities with LDH or sciatica."

Suri et al (Boston) 2010 Herniation; Intervertebral disc displacement; Etiology; Trigger; Event; Activities of daily living; Exercise The Spine Journal (2010) 388-395

[147] In court, Professor Adams confirmed his views on cadaveric experiments:

"... these experiments have shown... that if you apply the right kind of mechanical loading that's sufficiently severe then you can get the discs to herniate ... not every time, but most of them can be made to herniate if the load is sufficiently severe on them. And you don't need to have a particular state of degeneration or a particular age for that to herniation to occur. The discs which herniate most easily, about 70 per cent of discs that herniate, will herniate if you load them severely if they are on the lumbar spine and if they are from somebody aged about 35 to 50. That is the age where it is easiest to get them to herniate."

[148] Professor Adams rejected the allegation that his approach was outmoded. Despite the Battié and Videman papers, Professor Adams stated that in the last ten years, the view of the scientific community is that the importance of mechanical forces to the degeneration of discs has increased in the last ten years. He founded on the fact that in the last three years, the most prestigious spine research society - the ISSLS -has awarded about half of its prizes to papers discussing either the mechanical initiation of disc degeneration, or the mechanical causes of disc prolapse. He mentioned that two of his own papers have been heavily cited by nearly everybody working in the field: 'Mechanical Initiation of Disc Degeneration' and a review paper 'What is Intervertebral Disc Degeneration and What Causes It?'(Adams and Roughley, 2006).

[149] He stated that there has been a move towards integrating the mechanical with the biological and that his views were widely accepted: "most scientists would agree or wouldn't quarrel with that evidence, they would be convinced."

[150] Curiously, Professor Adams was not asked to speak to any papers to explain the basis of the "micro-trauma" model. Nor were such papers put to the defenders' experts. In my view, this was a material omission. In order to complete the picture, it is necessary to add that Professor Adams acknowledges that it is impossible:

(a) to say precisely how strong an individual's back is; it depends upon age, gender, genetic inheritance, and previous "wear and tear";

(b) to measure the peak forces acting on the spine during some particular incident; other men would have managed Mr Wilson's lifting tasks without injury; and

(c) to observe micro-trauma in any living person.

[151] Professor Adams appeared to be clear about one matter: "The widely held opinion ... that a disc must always be 'degenerated' before it will herniate appears to be based on tradition ..." He then, however, stated:

"... disc degeneration shouldn't be confused with disc herniation. Very many people have disc degeneration. Disc herniation or disc prolapse is a particular feature of a degenerated disc, but most degenerated discs are not herniated. Most people at a certain age will develop age related changes, which then can merge imperceptibly into degenerative changes. So these are very widespread. And these degenerative changes are mostly biochemical. We lose water from the tissue because the tissue, which becomes yellowy, it becomes more vulnerable to injury. That is different from disc herniation. And disc herniation doesn't increase with age. The epidemiological surveys link disc herniation much more closely to environmental factors, such as mechanical loading ..."

[152] That passage appears to link the two conditions very closely. Professor Adams also stated that "... but then you mustn't confuse disc degeneration with the pathology that Mr Wilson has suffered which is disc herniation. This is a very particular feature of disc degeneration." He did not quarrel with the statement in Cheung (supra) that "Prolapse intervertebral disc which constitutes a form of disc degeneration".

[153] To my mind, taking his evidence as a whole, the supposedly clear line between herniation and degeneration was blurred.

[154] Professor Adams' approach to those who disagreed with him tended to be brusque. He suggested that those people who reject his approach either have not read the relevant papers, or do not understand them. He commented: "personal dislike, or ignorance, of new evidence should not be confused with scientific debate." He speculated that certain "elderly clinicians" did not accept his views, because they were not prepared to accept new evidence. He was particularly dismissive of Professor Dickson's report, on which he wrote a critique.

[155] The defenders' experts thought these comments were condescending and insulting. Mr McMaster said that they were not worth commenting on. Professor Dickson described them as "intemperate" and "pejorative". I found it surprising that Professor Adams thought it necessary to make such ad hominen comments. They struck me as being contrary to the scientific approach that he strongly advocated.

[156] Professor Adams was the lead expert for Mr Wilson. Dr Goldman, Dr Annesley Williams and Professor Mulholland all agreed with his opinion on causation. I shall therefore review their respective evidence in less detail.

[157] Dr Goldman is a neurologist and is the medical chairman of the State of Utah Labour Commission. He explained that he is frequently called upon to provide a second opinion on whether an individual requires surgical intervention to the spine. He also acts as the Medical Director of Research for a private company of which he co-founded and serves as an expert witness.

[158] The defenders' experts queried whether Dr Goldman could give expert assistance in this area. They suggested that a neurologist is not the appropriate expert to provide an opinion on the cause of degenerative disc disease.

[159] I am not inclined to take a narrow view of matters. It appeared to me that Dr Goldman did have an appropriate degree of expertise, although others had either more clinical or research experience. On causation, Dr Goldman stated:

"... you need to have something environmental or some external force, perhaps superimposed upon a genetic predisposition, but it could be a single event or it could be a repetitive event"

[160] He accepted, for example, that a disc herniation can occur as a result of a sneeze in bed. It is therefore "not necessary that these people have had experience of heavy lifting, heavy exertion and the like for this condition, that is the prolapse, ... to occur." So "people can have degenerative disc problems ... without being involved in any physical activity at all".

[161] While Dr Goldman considered that Mr Wilson's protrusion was related to his work activities, he accepted that "there's always been controversy as to the cause of such disc protrusions."

[162] Dr Annesley Williams was led primarily to give evidence about the radiological position. On causation, she was (quite properly) reluctant to express an expert opinion. She expressed her understanding that disc degeneration is a multi-factorial process, involving chronic micro-trauma, genetics and other factors as well. But given her candid recognition that this is not in the area of her expertise, it is unnecessary to consider her evidence in this regard further.

[163] Professor Mulholland has had a notable career in the area of spine research and back pain. Although broadly adopting the views of Professor Adams, it was clear that Professor Mulholland took a less rigid position. He accepted that (a) protrusions only occur in degenerate discs; (b) soft tissue degenerative changes in the lumbar spine are relatively common in the normal population; and (c) a minority of people with degenerative disc disease will then develop a disc protrusion of varying degrees.

[164] More importantly, Professor Mulholland accepted that there has always been controversy as to the cause of disc protrusions. In this connection, he made two important statements:

"The cause or causes of degenerative disc disease are simply not known in the large majority of people, and it's possible to have such degenerative disc disease for prolonged periods before symptoms develop."

"It doesn't seem to me that they are specifically related to trauma, either acutely or following repeated activities. The common presentation of a disc protrusion would be with sciatic symptoms appearing without any history of trauma."

[165] Although Professor Mulholland disagrees with the defenders' experts, he accepts that their opinion is a legitimate one to hold and is not based on some outdated or discredited scientific approach.

Review of the Cumulative Fatigue Model

[166] The defenders' experts all agree with the conclusions of the Battié & Videman papers without qualification. In their view, the papers demonstrate two things. First, that genetic inheritance is a significant causal factor in disc degeneration. Secondly, that heavy physical loading has a very limited effect. They were keen to stress that their views, rather than those of Professor Adams, accurately reflected the prevailing thinking among the medical and scientific community.

[167] In rejecting what they refer to as "the micro-trauma model", the defenders' experts also relied on the following propositions: (a) that cadaveric and animal experiments are inappropriate models; (b) that drawing on their clinical experience, degenerative disc changes are always present prior to herniation; (c) that it is common to find localized disc degeneration; and (d) that herniations are common events. I shall consider these matters in turn.

(a)  Cadaveric and Animal experiments

[168] Professor Adams stated that the results obtained from cadaveric experiments since the 1970s are widely accepted within the scientific community: "...most scientists would agree or wouldn't quarrel with the evidence. They would be convinced".

[169] The general view of the defenders' experts is that it is highly artificial to rely on cadaveric experiments. That is firstly, because they involve hyper-flexion, that is, flexion beyond the normal physiological range. As the forces then applied to the discs were greater than one would expect in normal day-to-day living, Mr McMaster said it's not surprising that you have various abnormal findings reported. What would be surprising is the opposite result.

[170] Secondly, in cadaveric experiments the disc is separated from its normal environment. By removing muscles, ligaments and in some cases the laminae, the structural support tissue is no longer present. Mr McMaster described the abdominal pressure on the muscles as acting as a splint to the spine. Thirdly, such experiments take no account of ability of living tissues to repair. As Professor Mulholland put it in his report: "The difficulty with any bioengineering study which involves repetitive stress, is that these are carried out on cadavers which have not got the ability to heal."

[171] There is a study that shows that normal forces can affect the spine: Gordon et al Mechanism of Disc Rupture: A Preliminary Report Spine Volume 16 Number 4, 1991 (2613-2625). It concludes:

"We contend that prolapse of the intervertebral disc is primarily the result of peripheral injury, namely annular disruption. We conclude that when the appropriate combination of flexion, rotation, and compression operate over an adequate length of time, annular separation and subsequent prolapse will occur."(page 456)

Although this study does support the mechanical model, it predates the Battié and Videman papers and is therefore less influential.

[172] Professor Adams also relied on animal models:

"... there is a whole wealth of scientific literature here to show how mechanical damage will lead to degenerative changes in intervertebral discs. For obvious reasons these experiments are done on animal discs, they are called animal models of disc degeneration, and the easiest way to get that disc degeneration is to create trauma in the disc, you cut into it, you stab it, you overload it ..."

[173] For a long time, it was thought that animal models might assist in the quest for causal factors. That is reflected, for example, in the following passage from Urban and Roberts (supra):

"For many decades it was suggested that a major cause of back problems is injury, often work-related, which causes structural damage. It is believed that such an injury initiates a pathway that leads to disc degeneration and finally to clinical symptoms and back pain. Animal models have supported this finding."

[174] But ultimately the same authors question the validity of such studies:

"... there is a lack of a good animal model. There are significant anatomical differences between humans and the laboratory animals that are traditionally used as models of other disorders. In particular, the nucleus differs... In addition, although the cartilage end-plate in humans acts as a growth plate for the vertebral body, in most animals the vertebrae have two growth plates within the vertebral body itself, and the cartilage end-plate is a much thinner layer than that found in humans. Thus, although the study of animals that develop degeneration spontaneously and of injury models of degeneration have provided some insight into the degenerative processes, most information on aetiology of disc degeneration to date has come from human studies."

[175] Two recent papers confirm that no animal model has yet been devised, where the findings can be accurately translated to humans. The first study concludes:

"Many techniques have been applied to develop a successful, experimental animal model of human disc degeneration. However, no particular model currently parallels the complex nature of human disc degeneration. Naturally occurring animal models have the drawback that the basis for the high rate of disc degeneration is not known. The availability of animals is based on the rate of occurrence, and so a predictable experiment is difficult. Although the interventions in artificial animal models are known, the true relationships of these to the actual events leading to disc degeneration in humans are not. The careful comparison of data obtained from an animal model with those from human pathologic specimens will shed light on the detailed mechanisms of disc degeneration. With recent progress in biomechanics, cell biology and molecular biology, an easily reproducible and valid animal model may help unlock the complex cascade of events surrounding human disc degeneration. Only then might it be possible to offer insight into the prevalent and disabling condition of back pain." (emphasis added)

Singh et al Animal models for human disc degeneration The Spine Journal 5 (2005) 2675-27957/45

[176] In cross-examination, Professor Adams accepted the underlined statement as being correct. Indeed he went further. He conceded that care was required in translating the results of cadaveric and animal experiments to living human beings. That echoes what is stated in the second paper:

"Although animal models are invaluable to increase our understanding of disc biology, because of the differences between species, care must be taken when used to study human disc degeneration and much more effort is needed to facilitate research on human disc material."

Alini et al Are animal models useful for studying human disc disorders/ degeneration? 2008 Eur Spine J (2008) 17:2-19

(b) Clinical Experience

[177] One consistent theme in the evidence of each of the defenders' experts was their own clinical experience. Mr Mackay explained it in this way. He said that his views have strengthened since the identical twin studies were published, but that the "larger reinforcement is my experience."

[178] The defenders' experts were at one in stating that pristine discs do not protrude or extrude. That only occurs in severely degenerated discs. They also thought that herniation is part and parcel of the degenerative process. Radial clefts form, which weaken the integrity of the disc. In Mr McMaster's view, disc protrusions are so common that they can be regarded as normal. When one takes place, it causes nerve root irritation or compression. That results in pain radiating into the leg, often accompanied by a feeling of tingling or numbness.

[179] Mr McMaster described the intervertebral discs as the most inviolate, protected part of the spine. In his experience, patients with spine fractures never have disc prolapses. In order to damage a normal disc, one would almost have to dislocate the spine through that disc. That only occurs in severe road traffic accidents. It does not occur through normal stresses and strains. He therefore does not accept that ligamentous injury generally affects discs. Mr McMaster had operated on many teenagers with disc herniations. For every 100 adults between the ages of 30 and 50, he had operated on someone under the age of 20. Those children had clearly not been engaged in heavy physical occupations. That therefore reinforced his view that the herniation had occurred spontaneously.

[180] Dr Rankine was to similar effect. He has had extensive experience in imaging prolapsed discs. He had not come across partial tears of ligaments where there was a prolapse. He had never seen areas of pathology, except in major spinal trauma, for example high velocity road traffic accidents.

[181] Mr Mackay stated that none of us can avoid disc degeneration. While some individuals are more susceptible than others, most individuals will have a degree of degeneration in their lower back, often at the level L5/S1. It is a common clinical experience to find that such persons are asymptomatic. It is also a common pattern for people to have acute episodes and then for their symptoms to go into hibernation. As Mr Mackay put it, the natural history of disc degeneration is one of resolution. But he was also clear that lifting does not cause disc degeneration.

[182] In Dr Rankine's view, the research has established that the most important cause of disc degeneration is genetic. He accepts that the causes are multi-factorial, but at present science does not know what the other causes are. In his view, the theory that activity causes degeneration has not been proved in patients in vivo. He sees teenagers with disc degeneration disease, even some with disc prolapse. He does not think that is the result of their doing something traumatic to spine. It's just that they have inherited a particular set of genes.

[183] Professor Dickson prefers the expression degenerative disc disease, because that accurately reflects the process involved. But at a certain point, the disc becomes too dry to herniate.

(c) Localized Disc Degeneration

[184] I have discussed above Professor Adams' view that there is no need for pre-existing degeneration prior to a herniation. Another feature of his thinking is that it is odd to find localized degeneration when a herniation occurs. He argues that if it is genetic, one would expect the degeneration to be present throughout the spine.

[185] This is contradicted by the defenders' clinicians. In their experience this finding is common. Dr Rankine stated that degenerative disc disease is frequently seen only at one level. Commonly, it is observed at L5/S1. The anatomical reason is that the greatest loading is at that level as one goes about everyday life. It is often seen when individuals are in their mid to late thirties and will usually progress with age.

(d) Prevalence of Herniation

[186] Professor Adams rested part of his theory on the rarity of herniation:

"... the definitive study on this is by Jensen, and that was published in the New England Journal of Medicine in about 1994 ... a very highly regarded journal, it gets cited more even than Nature. And this paper looked at MRI scans of 100 people without any back pain, and sure enough, they showed that many people have slight age related degenerative changes, but only 1 of the 100 had a disc herniation. So it's not true to say that many people are wandering round with great big disc herniations."

[187] The paper to which he was referring is Jensen et al Magnetic Resonance Imaging of the Lumbar Spine in People without Back Pain; N Engl J Med 1994; 331 69 - 73. In this study, MRI examinations of the lumbo-sacral spine were carried out on 98 asymptomatic people. The results were then classified into four categories: normal, bulge, protrusion, and extrusion. The authors found a high prevalence of abnormalities. About half of those examined had at least one disc bulge. About a quarter had at least one protrusion. Only 36 per cent had normal intervertebral discs at all levels.

[188] The conclusion drawn was that "Given the high prevalence of back pain in the population, the discovery of a bulge or protrusion on an MRI scan in a patient with low back pain may frequently be coincidental." Accordingly, it is unclear why Professor Adams relies on this paper. It shows that the commonest cause of back pain is non-specific, but that a majority of people had herniations of one sort or another.

[189] Two other studies support the finding that herniations are common, whether symptomatic or asymptomatic. The first paper is Boos et al 1995 Spine Volume 20 Number 24, (2613-2625) The Diagnostic Accuracy of Magnetic Resonance Imaging, Work Perception, and Psychosocial Factors in identifying Symptomatic Disc Herniations.

[190] In this study, MRI scans were carried out on two groups of patients. One group contained people who had no back symptoms. The other group comprised people who had symptoms. The study found that the MRI findings were very similar. A disc herniation (protrusion, extrusion, or sequestration) was present at least in one level in 76% of the asymptomatic volunteers. That compared with a similar percentage in those who actually had symptoms.

[191] Professor Dickson, Mr McMaster and Professor Mulholland all regarded the Boos paper as important. They agreed that clinicians should focus on history, examination and (most importantly) experience. MRI scans should be looked upon as supporting evidence.

[192] Professor Adams took a different view. He discounts this paper. In evidence he said that he had spoken to Boos at conferences and thinks Boos would now alter his position from the one set out in the paper.

(e) Current Views of the Scientific Community

[193] There are four highly regarded papers that attempt to set out the current state of scientific thinking. The first is Urban & Roberts; Degeneration of the intervertebral disc Arthritis Res. Ther. 2003, 5:120-130. The authors begin by looking at the role of mechanical forces:

"Although herniation is often thought to be the result of a mechanically induced rupture, it can only be induced in vitro in healthy discs by mechanical forces larger than those that are ever normally encountered; in most experimental tests, the vertebral body fails rather than the disc. Some degenerative changes seem necessary before the disc can herniate ..."

[194] They then review the influence of mechanical load and injury

"Over the past decade, as magnetic resonance imaging has refined classifications of disc degeneration, it has become evident that, although factors such as occupation, psychosocial factors, benefit payments and environment are linked to disabling back pain, contrary to previous assumptions these factors have little influence on the pattern of disc degeneration itself. This illustrates the tenuous relationship between degeneration and clinical symptoms."

[195] With regard to genetic factors in disc degeneration, Urban & Roberts state:

"More recent work suggested that the factors that lead to disc degeneration may have important genetic components. Several studies have reported a strong familial predisposition for disc degeneration and herniation. Findings from two different twin studies conducted during the past decade showed heritability exceeding 60%. Magnetic resonance images in identical twins, who were discordant for major risk factors such as smoking or heavy work, were very similar with respect to the spinal columns and the patterns of disc degeneration."

[196] It is worth recording Professor Adams' view of this paper and its lead author. He knew Dr Urban and thought that there were areas of agreement and disagreement in their respective views. However, he thought her work very good and often cited it. He indicated his surprise that she had not chosen to look at experiments where repetitive mechanical loading has been applied without such severe loading. He thought it would have been appropriate for her to look at studies where more moderate mechanical loading had been applied cyclically to create radial fissures, followed by disc herniation.

[197] I asked Professor Adams whether it was at best curious that an eminent person in the field was apparently unaware of these experiments. His reply is worth recording in full:

"Yes. I think she wasn't aware of it because I spoke with her at length about it just over a month ago and I was talking about just this kind of experiment and she didn't seem to recognise what I was saying. Now, I couldn't say for certain that she just didn't agree with me and was too polite. I don't really know but she's a specialist in the cell biology side and she knows quite a bit about biomechanics, but there is just so much literature these days that she may not have been aware of these papers or chose not to give them the prominence of mentioning them. In a review paper you normally build up a theme and she's developing a theme which is presumably the future of research in this area. The kind of research that she does ... it's what scientists do tend to do. It's not bad behaviour. Putting a slant on it, you're not refusing to accept information you know about but you're accentuating certain information."

[198] Standing the object of the paper and its coincidence with the views expressed in a number of other papers, I found that a surprising position to adopt. I was also struck by the similarity of Professor Adams' approach to Boos and Urban respectively.

[199] Dr Rankine described Jill Urban as the biggest name in the United Kingdom in her field. He confirmed that clefts were part and parcel of the natural degenerative process. He did not accept Professor Adams' opinion that clefts are traumatically formed. He pointed again to the incidence of degeneration in children.

[200] The second paper is the one published by Eurodisc in 2004. As stated above, this was a collaborative project set up to examine why intervertebral discs degenerate. Geneticists, epidemiologists, spinal surgeons, and research scientists from across Europe were asked to examine the question. Their summary is very similar to that of Urban and Roberts:

"The reasons for the dramatic degenerative changes in the disc are poorly understood, but ageing is the biggest determinant. There have been many epidemiological studies over the past 30 years. They have revealed heavy physical work, truck-driving and smoking as risk factors for back problems, based on an 'injury' paradigm. This model implies that overloading results in structural damage, which leads to disc degeneration causing symptomatic conditions. This model does not, however, examine the biological capacity of the musculoskeletal system to adapt to external exposures. In addition, improvements in the workplace and ergonomic interventions have not resolved the problem of disc degeneration-associated pain and disability, rather the incidence is increasing arithmetically. This may be explained by population studies over the last decade, which have shown a genetic predisposition to back pain problems. Although disc degeneration is strongly genetic, degenerative changes are an outcome of interactions between genetics, age and cumulative exposure to environmental factors."

[201] The Eurodisc paper stresses another important point:

"The disc is always exposed to mechanical loads - not only due to body weight and daily exercise but also during sleeping as even muscular activity of breathing causes measurable changes in intra-discal pressure as shown by in vivo measurements."

[202] Dr Rankine said that he supported entirely the Eurodisc findings. In particular: (a) it is not possible to overload a human disc to the extent that damage can be caused to it by trauma; (b) cracks in an unloaded disc are part and parcel of degeneration; (c) the correlation between damage in the disc and external mechanical load is poor.

[203] The third paper is Cheung et al; Current Understanding of low back pain and intervertebral disc degeneration: epidemiological perspectives and phenotypes for genetic studies Current Orthopaedics (2008) 22, 237 -244. It confirms that:

"The conventional belief that heavy physical loading can result in early degenerative disc disease has not been supported by studies. ... Interestingly, studies in occupational medicine suggest that repeated physical activity is beneficial. ... there is no clear dose-response relationship between the amount of physical loading and degenerative disc disease."

[204] Cheung also acknowledges the key role played by genes, while allowing for other factors:

"... a number of studies show that genetic influence plays a significant role in intervertebral disc degeneration. Although genetic inheritance, being the highest risk factor, accounts for approximately 50- 70% of the variability in disc degeneration between identical twins, there is potent intra-subject dependence of disc degeneration at the spinal level, which reflects environmental influences."

[205] The paper concludes that:

"The emerging importance of genetics in the aetiology of degenerative disc disease behoves us to reinterpret the existing literature and review all the methodologies that are available for the study of genetics and degenerative disc disease. Further exploration of the role of genes that have been found to be associated with degenerative disc disease is warranted."

[206] Both Professor Adams and Professor Mulholland broadly agreed with the content of this paper. But their approach mirrored the one they took to the Battié and Videman studies: that a distinction must be drawn between disc herniation and disc degeneration and that mechanical rather than genetic influences are more important for the former.

[207] The fourth paper is Suri et al Inciting events associated with lumbar disc herniation The Spine Journal 10 (2010) 388-395. It arrives at a similar conclusion to the earlier papers:

"There was no significant association between the occurrence of a lifting-related event and the severity of the clinical presentation. Although these findings do not refute either the cumulative injury model or genetic model of disc degeneration, neither do they suggest that physical activity is associated with the occurrence or severity of disc herniation.."

Conclusion on Micro-trauma Model

[208] In my view, the causal link between micro-trauma and disc degeneration has not been proved. I accept the evidence of the defenders' experts. I conclude that the views expressed in the Battié and Videman sequence of papers and the four just mentioned express current scientific and medical thinking. It appeared to me that it was difficult to use a mechanical model to explain disc degeneration in children, or herniations in those adults who had never engaged in heavy manual labour.

[209] I found it difficult to know precisely which papers Professor Adams relied upon in support of the cumulative injury model. He repeatedly mentioned papers of his own and others, which were not lodged in process. Some of these papers were then produced by the defenders and he was questioned about them in cross-examination. At that stage, I found his answers less convincing than they had appeared in chief.

[210] Mr McMaster stated that he did not particularly want to criticise Professor Adams, because he has done much good work, but his approach is unique: "It is not accepted by anyone else in the clinical field."

[211] I reject the supposed distinction drawn by him between scientific and medical literature. I was persuaded that clinicians do not work in isolation. Dr Rankine in particular kept himself abreast with scientific developments, especially in the field of biomechanics. I accepted his opinion that compressing cadaveric spines is the historic approach, in which the scientific community is no longer interested. I concluded that it was Professor Adams, rather than the defenders' experts, who supported an outdated model of causation.

[212] I therefore hold that whether a person has degenerative changes to their spine is, by and large, genetically predetermined. The influence of heavy physical work is very modest. It follows that Mr Wilson fails on the question of general causation.

End Plates and Schmorl's Nodes

[213] For the sake of completeness, I shall discuss two matters that figured in the evidence, but which I found were not relevant to the present case. First, a number of papers were cited relating to disc end plates. It seemed to be suggested that end plates had a role to play in disc degeneration. Some of the papers indicated that chronic micro-trauma to the end plates led to disc degeneration in a genetically susceptible individual. The theory rested on the notion that a sclerotic end plate prevents nutrients coming into the disc, which will degenerate and die.

[214] However, end plate damage can be set to one side in this case. That is because Dr Annesley Williams did not find any evidence of end plate damage in Mr Wilson's back. Further, Dr Rankine confirmed that it is not possible to associate physical loading with end plate change. He is currently conducting research into the nutrition of end plates. The current view is that they play an integral part in the degenerative process. However, it is not known whether end plate damage occurs secondary to a degenerative disc, or if it is a primary problem at the level of the end plate that then affects the disc. In other words, there is uncertainty as to whether it is cause or effect.

[215] The second matter related to Schmorl's nodes. DrAnnesley Williams did find evidence of these on the scans of Mr Wilson's back taken on 30 September 1994. However, according to Dr Rankine, one in five persons has Schmorl's nodes and it is not a finding of clinical significance. The disc spaces narrow in response to an end plate defect. They develop during adolescence when the spine is soft and there is a higher incidence of them in elite athletes. Importantly, Schmorl's Nodes do not play a role in disc degeneration. Accordingly, their existence is of no relevance to Mr Wilson's degenerative disc disease and prolapse.

Individual Causation

[216] If my analysis of the question of general causation is wrong, then I must consider the question of individual causation. I begin by making an observation. According to the clinicians who gave evidence, patients often link their back problems to playing sports, lifting, coughing, sneezing or even tying their shoelaces. Mr Wilson might therefore be thought not to be unusual in attributing his lumbar disc herniation to a specific activity.

[217] A recent study has examined the incidence of such patient reports: Suri et al Herniation; Intervertebral disc displacement; Etiology; Trigger; Event; Activities of daily living; Exercise The Spine Journal (2010) 388-395. Contrary to the clinicians' experience, the authors found that only 6 per cent of patients referred herniation to trauma or heavy lifting. About "62 per cent of lumbar disc hernias did not have a specific patient-identified event associated with the onset of symptoms."

[218] If disc degeneration has a genetic basis, then as the authors point out there would be "little relevance between patient identified inciting events and the occurrence of [lumbar disc herniation]." But even if the micro-trauma hypothesis is correct, Mr Wilson must establish that his work activities caused his back problems. He must prove that the actual lifting, twisting and carrying he undertook at work were the true causal agents.

[219] The expert witnesses led on Mr Wilson's behalf all based their respective opinions on his account of his duties at Motherwell College. Professor Adams referred to his "exceptional work activities" at Motherwell College:

"... the key factors that suggest Mr Wilson's work damaged his disc are: the considerable weight and awkward bulk of the objects lifted; the fact they were lifted from the floor; the frequency of lifting; the need to carry the objects for considerable distances; the stressful working atmosphere which would encourage haste; and Mr Wilson's age and height."

[220] He continued:

"Having to carry the lifted objects along corridors and through doors, and having to repeat the tasks many times, would have lead to fatigue in Mr Wilson's back and trunk muscles. Muscle 'fatigue' is a metabolic condition which reduces a muscle's ability to contract rapidly and forcefully when required, and laboratory experiments have shown that fatigued back muscles allow the spine to bend forwards more than usual, and so allow the spine to be subjected to greater bending stresses."

[221] In his report, Dr Goldman stated:

"It is my opinion... on a reasonable balance of probabilities, that Mr Martin Wilson ... has, in fact, sustained a cumulative trauma injury in his lumbosacral spine, with a resulting radiculopathy, from the repetitive and continual lifting, carrying and manipulating of musical instruments and associated equipment ..."

[222] In response to a question from Mr Wilson in his evidence in chief, Dr Goldman confirmed his view:

"My impression is that you sustained what I refer to as a musculoskeletal injury, tendons, ligaments, muscles, there's no way to really know which one of those, with some nerve root injury, as a result of the physical activities that you were involved with. ... I feel in the balance of probabilities ... that your injury has come from the repetitive stress and straining activity, physically, that you underwent during your employment with Motherwell College."

[223] Dr Goldman could think of no other cause of the disc problems. He stated several times that the disc herniation developed as a result of "repetitive strain" and "a repetitive trauma injury". However, he also indicated that it could be an acute injury and that Mr Wilson "may have just had to hurt himself once or start a cascade of dominoes with a one time event."

[224] Dr Annesley Williams stated that the disc prolapse was predominantly caused by acute trauma linked to lifting and twisting. Professor Mulholland's view was essentially that Mr Wilson had a genetic predisposition to disc degeneration. His injury was largely caused by ten years of carrying awkward equipment. There was no reason to suppose he would have otherwise have developed a herniation, but for the twisting and stretching involved in his work.

[225] What was the information provided by Mr Wilson to his experts? He stated:

"... I don't recall actually specifying how many people I taught. I simply recall telling my experts that I was required to lift and carry classroom equipment, musical equipment and transport materials up to eight times a day and often under the pressure of time. I did not say that I had to lift and carry classroom materials and musical equipment eight times every day."

[226] The experts' respective opinions were based on the assumption that he had given them an accurate report. Professor Mulholland stated that if there had been "a significant exaggeration", he would depart from his conclusion. Professor Adams said that he would require to reconsider his opinion if the facts were not as outlined to him.

[227] As I am unable to accept Mr Wilson's evidence, I conclude that even if the question of general causation had been established, he has failed to prove that his work activities led to his disc herniation.

[228] In any event, I found the evidence of the defenders' experts in this regard to be cogent and persuasive. In arriving at his opinion, Mr McMaster accepted Mr Wilson's account in respect of the lifting and carrying he undertook at Motherwell College as being accurate. Mr McMaster concluded, however, that Mr Wilson would in any event have developed disc degeneration, followed by a disc prolapse. His back problems were "predetermined".

[229] In Mr McMaster's opinion, a bulging or protruding disc for someone in their late thirties is so frequent that you could call it normal. The fact that the onset of symptoms was spontaneous is typical of most persons with degenerative disc disease. In his experience, the vast majority of patients did not have a precipitating event.

[230] Mr Mackay expressed his views with restraint and objectivity. He did not believe that the activities described by Mr Wilson would have led to degenerative disc disease or the disc protrusion. Mr Mackay stated that:

"The common presentation of a disc protrusion being with sciatic symptoms appearing without any history of trauma."

He was not aware of anything in the published material that contradicts his view.

[231] During his evidence, he lifted the keyboards and the stereo unit. He thought that he could manage to carry three or four keyboards going through doors, although he would prefer to lift them separately. In his view there was nothing related to the weight or shape of the equipment, or the distances it was carried, or the twisting to get through doors that would influence his view on causation.

[232] Speaking as a musculo-skeletal radiologist, Dr Rankine was of the opinion that the degenerative changes shown on the radiological images of Mr Wilson's spine between 1995 and 2001 are normal. Professor Dickson adhered to his view that the idea that discs can in some way be damaged or made to degenerate by trauma is unsustainable.

[233] In their opinion, Mr Wilson would have developed degenerative changes in the discs of his lower lumbar spine, irrespective of his work at Motherwell College.

Quantification of Damages

[234] There is no dispute that Mr Wilson suffered injury when the herniation occurred. His general practitioner, Dr Pickering, found him on his back at his home unable to move. At issue is the extent and consequences of his injury.

[235] As I mentioned earlier in this Opinion, Mr Wilson thought that he had sustained a "catastrophic" injury. He believed that it had incapacitated him for any form of work. But that was at odds with the fact that he was able to conduct the lengthy proof, as well as numerous procedural hearings. Tellingly, he described the litigation as "a full time job". He has been in receipt of state benefits for many years.

[236] Mr Wilson called two experts to give evidence regarding his mental health. They gave an insight into his current symptoms. Dr Tom Brown, consultant liaison psychiatrist, stated in his report dated 7 March 2006:

"I think that Mr Wilson's unfair dismissal and the events preceding and following it have significantly contributed to the production of his psychological symptoms, including his sleep pattern, nightmares and indeed his low back pain. Although his low back pain has an underlying physical cause there is no doubt that psycho-social stress is one of the major determinants of chronicity in low back pain ..."

[237] Given that it was five years since his examination, Dr Brown was rightly reluctant to state what stressors are now affecting Mr Wilson. He was, however, prepared to give a provisional view on the basis that Mr Wilson is complaining of the same symptoms and in particular if he is still having nightmares. On that hypothesis, Dr Brown thought that this prolonged litigation, together with his sense of grievance over what he believed had happened to him at Motherwell College, are likely to be affecting him. Professor Espie, consultant psychologist, agreed that this case "has become totally preoccupying" for Mr Wilson.

[238] Perhaps the best person to assess Mr Wilson is his general practitioner, Dr Pickering. She gave her evidence in a level and straightforward manner. She prefaced her remarks by saying that it was extremely difficult to answer questions about his capacity because of his severe disc problem. In her view, anything he does is limited by his condition. Over the last ten years of litigation, she has seen his general ability decrease. She mentioned his poor sleep pattern and said he had become a "shadow of his former self". However, she thinks that his condition has been stable in the last year.

[239] Dr Pickering confirmed her view that Mr Wilson would have been fit to resume the computer re-training course in June 1996, on the basis that it involved private study at home. She suspected that he would have been fit for some sort of part-time employment in November 1996. It remains her view that he should try to obtain some form of work.

[240] When Dr Pickering's view was put to Mr Wilson in evidence, he stated: "My GP is not a medical expert. She is an expert in medicine on a general level of practice." I found that a glib and arrogant response.

[241] Her views corresponded with those of Mr Mackay, who examined Mr Wilson in 2006 and found:

"... normal power and dexterity in both upper limbs, no obvious consistent tremor, no obvious sense of disturbance and no muscle wasting, forearm and wrist joint movements appeared normal."

[242] In his view, intermittent back symptoms tend to be the norm following a disc protrusion. They may include back pain, stiffness and referred symptoms into the lower limbs. He pointed out that these flare-ups occur because of the degeneration of the disc, rather than the acute episode of protrusion. He mentioned that back problems are largely treated by conservative measures such as analgesics, anti-inflammatory drugs and physiotherapy. Some patients visit osteopaths and chiropractors. He noted that Mr Wilson had taken lessons in the Alexander Technique. Mr Mackay did not think that surgery was warranted either in 1995 or now.

[243] Mr Mackay considered that following an acute disc protrusion, an absence from work for perhaps a few months, possibly up to 6 months, would not be unreasonable. However, many people will return to lighter work at an earlier stage. He continued:

"It is hard to consider that at this stage, some 12 years later, his absence of work can be entirely related to degenerative disc disease bearing in mind that he is 49 years of age, is of relatively slim build, is able to walk in a straightforward manner and has no convincing weakness in the lower limbs. Most people in this situation, whether there is a degree of chronic pain, will report symptoms are controlled to some degree by many of the therapies mentioned earlier and it would not be unusual, at least in my experience, to meet people in a worse situation with a long history of low back pain functioning reasonably satisfactorily in relatively sedentary or indeed light physical work. To that extent it seems to me that his perceived level of disability at present is quite markedly out of proportion to what one would normally expect following the onset of degenerative disc disease and a disc protrusion."

[244] Mr Wilson invited me to reject these views prefer the evidence of Dr Goldman, who examined him in November 2009. Dr Goldman offered the opinion that Mr Wilson was not able to work 9 to 5 in a salaried position, but might be able to work at home at his own pace:

"I think you are suffering from the effects of a prior ruptured disc, with a radiculopathy. You do have a chronic pain syndrome. ... If it just affected your work abilities it would be a disability, but ... I think that it is a significant impairment as to your everyday activities."

[245] But he also offered the view that: "I don't think that job exists, so from a practical standpoint... I do not feel that you can do a competitive open labour market job." It was, however, the case that Mr Wilson was able to pursue a career in music. That was confirmed by Mr Martin Dalby, the former head of BBC Music Scotland. He thought that there were several possible careers notwithstanding a bad back - for example, as a music lecturer, music critic, music arranger and potentially composing.

[246] Against that background, if Mr Wilson had been successful on the merits, I would have made an award of £10,000 in respect of solatium. In my view, his problem could be classified as a moderate back injury in terms of the Judicial Studies Board Guidelines (10^th Edition):

"Many frequently encountered injuries to the back such as disturbance of ligaments and muscles giving rise to backache, soft tissue injuries resulting in exacerbation of an existing back condition or prolapsed discs necessitating laminectomy or resulting in repeated relapses. The precise figure depends on the severity of the original injury and/or whether there is some permanent or chronic disability.

£8,250 to £18,250

Minor strains, sprains, disc prolapses and soft tissue injuries from which a full recovery or recovery to "nuisance' level has been made without surgery:

within about five years £5,150 to £8,250

within about two years Up to £5,150"

[247] In making that award, I would have taken into account (a) the chronic nature of the condition; (b) the fact that no surgery was required; and (c) there had been no repeated prolapses. I would have allowed interest at half the judicial rate for a period of two years from 30 September 1994. That is when Mr Wilson attended his GP in connection with his back. Subsequently I would have awarded interest at the full judicial rate of 8% to date.

[248] With regard to wage loss, I would have been minded to award Mr Wilson the sum of £20,000 by way of loss of employability. On the evidence before me, I could not have justified anything other than a broad brush approach.

[249] I therefore regard as fanciful Mr Wilson's claim that he is entitled to compensation of £2,592,000 "with more to follow". It is based upon reports on quantification prepared by Mr Rosenthal, a chartered certified accountant. He qualified in 1960 and is no longer in practice, having sold his accountancy business some 12 years ago.

[250] The report proceeds on the basis of three main pillars. First, that Mr Wilson is incapable of working again. Secondly, that but for the injury, he would have been promoted to a higher grade within the College. Thirdly, that he would have become a successful conductor earning on average £5,000 per concert. In my view, all three assumptions are untenable. Let me consider them in turn.

[251] As I have explained above, on the basis of the evidence Mr Wilson has the ability to work. There was no evidence that Mr Wilson would have progressed in his academic career. He had previously been refused promotion and there is no indication that a successful career lay before him.

[252] As to the suggestion that Mr Wilson would have become a successful conductor, there is one inescapable fact. When he ceased work aged 38 in 1996, he had not conducted a single concert in public. I regard his own evaluation of his prospects as being without foundation. It appeared that the sanguine view that he himself had and which is contained in his CV and another document written by him entitled 'Prospects of Successful Musical Career' was based upon flimsy evidence.

[253] That evidence consisted of the following: (a) an unsolicited testimonial which he received after lecturing to an extra mural class for Glasgow University in 1987; (b) the fact that his father asked him to write a programme note in 1988 and to arrange a particular concert; (c) that Jerzy Maksymiuk, the conductor laureate with the BBC Symphony Orchestra, had agreed to offer him free conducting lessons; and (d) the evidence of two friends of his late father, Thomas Wilson CBE, a well-known musician and composer.

[254] Let me say a word more about the evidence of these two individuals. The first was Mr Dalby (mentioned above). He was of the opinion that Mr Wilson had potential: "what you have shown me here about what you did is ideal groundwork for somebody going on to creative things, as it were, conductor or composer ..." Mr Edward McGuire, a composer, gave evidence to similar effect. He conceded, however, that whether or not Mr Wilson had the potential to pursue a successful musical career was "probably an informed guess".

[255] The flavour of Mr Rosenthal's evidence is illustrated by the following passage:

"... in general terms fees earned by professional musicians can vary and of course in a career as a professional musician they can reach what most of us would call astronomical levels such as, I think, there is an example of one leading conductor earning over US $2 million a year and there is no way, certainly not for me, of knowing whether or not Mr Wilson would have achieved such heights. I have taken what I have considered to be a reasonable approach, partly based on Mr Wilson's previous achievements during the course of his work while he was a lecturer and undertaking various types of part-time work in ... related to music work and I have therefore made an assumption that his additional earning could well have been equivalent to his total salaries during the course if he continued to work as a lecturer/senior lecturer/head of department until the date of his retirement... To some extent, of course, that is speculative and has to be speculative because of the unknown factors. I understand that Mr Wilson considers that that is a very modest level of additional income. However, my Lord, I put it to you that on the balance of probabilities based on my knowledge of Mr Wilson's previous achievements this would be a reasonable figure for damages in this instance."

[256] Standing the absence of evidence in relation to "previous achievements", I regarded this assessment of the claim as unfounded. There were a number of other features of Mr Rosenthal's evidence, which led me to conclude that I could place no reliance upon it. I shall summarise them as follows:

(a) He includes within his calculation several heads of loss that are plainly irrecoverable: (i) expenses and outlays; (ii) compound interest; (iii) full payment of salary to the end of his working life; and (iv) punitive damages.

(b) He accepted the information provided by Mr Wilson, but did not "take any steps to ascertain the totals of previous income". He had not examined any taxation or other records: "because they weren't into any dated, or sequential, order".

(c) He had not checked on current salary increases.

(d) He assumed that Mr Wilson would not only remain in post but be promoted without checking the position or taking into account the fact that he had been refused promotion in 1994 and his post had been made redundant.

(e) He did not check the employment position for music lecturers at other educational establishments.

(f) In calculating the future loss of earnings, he failed to follow any of the proposed methodologies set out in the explanatory notes to the Ogden tables.

(g) He accepted that he used guesswork in respect of other musicians' earnings.

(h) He based concert earnings on the basis of the pursuer working 8 weeks a year and earning £5,000 per concert, while still working full time at Motherwell College. He had not considered the terms of the employment contract, which required Mr Wilson to account for outside earnings to the College.

(i) He included calculations for heads of claim, which are not sought in the pleadings: (i) ongoing healthcare costs; (ii) accommodation costs (£1.3M); and (iii) financial advisers' fees.

[257] Mr Rosenthal stated that it was his impression that the teaching profession did not work as hard as the accounting profession and would therefore have spare time to engage in extra-curricular activities. That was an inappropriate and unfounded observation. It is not one that I would expect to be made by an independent expert witness.

[258] Because of the flaws in his assessment of income, there is no appropriate evidence before the court to enable loss of pension to be quantified.

Two Final Points

[259] Let me make two final points. First, in cross examination on 12 November 2009, Mr Wilson disclosed the existence of two offers of settlement made by the defenders. Senior counsel did not seek to elicit this information by his questioning. It was unnecessarily volunteered by Mr Wilson when asked to comment on certain correspondence, in which the reference to such an offer had been redacted. Neither side asked me to recuse myself and I decided not to do so. I put the offers out of my mind when reaching my decision.

[260] The defenders advanced an argument that Mr Wilson had fallen into "a black hole". This related to their respective responsibilities as employers before and after 1993, when the second defenders took over responsibility for the management of Motherwell College. I did not find this argument very attractive, it was not pressed with any degree of conviction by senior counsel and it is unnecessary for me to come to any final view upon it, standing the opinion I have reached.

Conclusion

[261] In light of the discussion above, Mr Wilson has failed in his claim and I shall pronounce decree in favour of the defenders.