CHIEF CONSTABLE OF STRATHCLYDE POLICE
ON 9 MARCH 2000
I have read in draft the speech prepared by my noble and learned friend Lord Hope of Craighead. For the reasons which he gives I would dismiss the appeal.
LORD NICHOLLS OF BIRKENHEAD
I have had the advantage of reading a draft of the speech of my noble and learned friend Lord Hope of Craighead. For the reasons he gives I too would dismiss this appeal.
I have had the advantage of reading in draft the speech of my noble and learned friend Lord Hope of Craighead. For the reasons he has given I would also dismiss the appeal.
LORD HOPE OF CRAIGHEAD
The appellant is a retired police officer. He was working in the course of his employment as a constable of Strathclyde Police on 11 April 1990 when he was injured in a road accident near the Townhead interchange on the M8 motorway. The driver of a police van in which he was travelling lost control of the vehicle. It swerved violently from side to side, overturned, spun round and landed on its roof. The appellant was thrown about as it did so. He struck his head on a wooden partition inside the vehicle and suffered a whiplash injury to his neck. He emerged from the vehicle dazed and with a sore neck but no serious injuries. He was taken to Stobhill Hospital where it was found that he had an abrasion to his scalp but that his central nervous system was intact and that he had not lost consciousness. He was discharged and returned to the police office before being sent home. Although he had a stiff neck the next day, he worked a normal shift. He was then off duty for three days. He returned to his normal duties at the start of the next week.
The whole event would have been passed off as nothing more than a lucky escape in the course of what turned out to be a minor accident had it not been for the fact that the appellant began to develop the symptoms of multiple sclerosis (“MS”) seventeen days after sustaining his neck injury. On 28 April 1990 he was on duty escorting an Orange Walk. He had been walking for about one and a half hours for a distance of two miles or so when he noticed that he was “dragging” his left leg. He felt as if his leg had gone lame. He was able to complete the march and the problem went away after he had rested. But it recurred about two weeks later when he was walking home. He had walked for about a mile when he again noticed that his left leg was dragging. He eventually had to take a taxi to get home, but once he was there his leg recovered after resting. Various other events then followed, none of which at the time seemed to be particularly significant. In July 1990 he had difficulty in maintaining his balance while strawberry picking. In August 1990 he consulted his general practitioner complaining of a stiff neck. In September 1990 he returned to his general practitioner complaining of blurring of vision while concentrating at work and of continued neck pain. But thereafter his condition began to deteriorate, as he encountered increasing problems with his leg and his balance. By the end of the year he had begun to experience problems of bladder control. In March 1991 when on a nature trail with his family he was unable to complete the walk and had to sit down.
On 2 April 1991 he discussed these problems with his general practitioner who referred him to the Department of Neurology at the Southern General Hospital in Glasgow requesting an opinion regarding a possible diagnosis of MS. He was seen a month later in the hospital by Dr. I.T. Draper, a consultant neurologist. Various tests were done, and on 11 August 1991 Dr. Draper reported to the general practitioner that the results were strongly in favour of a diagnosis of MS. The appellant was informed on 11 September 1991 that his symptoms were probably due to this condition by a registrar in the hospital. By now his impaired mobility had become more noticeable and he had been assigned to light duties in the police force. In April 1993 he was diagnosed as suffering from depression due to ill-health. On 12 August 1993 the Chief Medical Officer of Strathclyde Police wrote to the appellant’s general practitioner to inform him that steps were being taken to retire the appellant from the police force on health grounds. Thereafter his condition continued to deteriorate with tragic consequences for both him and his family. By the end of the following year he was severely disabled by the disease and had become dependant on a wheelchair for mobility. His wife had to give up her part-time work to look after him. Their only source of income was his police pension and his disability allowances.
The possibility that the appellant’s disability might be related in some way to the accident was first raised on his behalf by his solicitors in June 1991. By that time he was undergoing tests in the Southern General Hospital. His solicitors wrote to Dr. Draper on 25 June 1991 requesting a report on his treatment and confirmation that his injuries and condition were directly related to the accident. On 14 October 1991 Dr. Draper provided them with a report in which he said that, while MS was an illness which does occur spontaneously, there had been speculation for many years as to whether it might be provoked or caused to relapse by trauma. He concluded his report by saying that there was clear evidence of damage to the brain and the brain stem of the kind which was associated with MS and that, while proof was not possible to come by, it was reasonable to assume a causal relationship between the occurrence of the MS and the injury which the appellant had sustained on 11 April 1990 when he was in the police van. On 9 February 1993 Dr. William Durward, a consultant neurologist at Glasgow Royal Infirmary, prepared a report for the appellant’s solicitors in which he said that, having examined the appellant and read Dr. Draper’s report, he agreed that the appellant had MS and that he considered on balance of probability that there was a link between trauma sustained on 11 April 1990 and its subsequent development. On 29 March 1993 the appellant commenced these proceedings in which he claimed damages against the Chief Constable.
The proceedings in the Court of Session
By the time when the appellant’s case came to proof before the Lord Ordinary, Lord Dawson, in June 1995 the Chief Constable had admitted liability for the accident. The issue between the parties on the pleadings was focussed by the appellant’s averments on the one hand that MS is a condition which may be provoked by trauma and that the trauma to his head, neck and shoulders in the accident of April 1990 had resulted in the development of his MS, and by the Chief Constable’s averments on the other that MS is not a condition that is caused or influenced by trauma and that any trauma sustained by the appellant in the accident of April 1990 did not cause his MS.
Dr. Draper and Dr. Durward both gave evidence in support of the appellant’s case, but they made it clear that they were not qualified to engage in a detailed debate on this subject as their primary concern had always been with the practical problems relating to the diagnosis and treatment of MS. In this situation detailed evidence on the critical issue as to the causal relationship, if any, between the appellant’s accident and his development of the symptoms of MS was left to two rival teams of eminent expert witnesses. The appellant’s experts were Professor Peter Behan, Professor of Neurology at the University of Glasgow, and Dr. Charles M. Poser of the Harvard Medical School and Beth Israel Hospital, Boston. Those for the Chief Constable were Professor D.A.S. Compston, Professor of Neurology at the University of Cambridge, Professor William A. Sibley, Professor of Neurology of the University of Arizona and Dr. Leonard T. Kurland, Senior Consultant at the Mayo Clinic, Rochester, Minnesota.
It was not possible to complete the proof in June 1995 and further evidence was held in December of that year. On 6 November 1996 the Lord Ordinary pronounced an interlocutor in favour of the appellant and awarded him £547,250 as damages. The Chief Constable reclaimed, and on 5 March 1998 the First Division (the Lord President, Lord Prosser and Lord Caplan) allowed the reclaiming motion with the result that the appellant’s award was reduced to £1,500 which was agreed as the solatium due to him for the injuries which he received in the accident: 1998 S.C. 548. The appellant has now appealed to your Lordships’ House against the First Division’s interlocutor.
It is necessary at this point to mention two features of the way in which this case was dealt with in the Court of Session, as they have had a profound bearing on the nature of the material which is before your Lordships in this appeal. The first is that, while the Lord Ordinary’s opinion provides a useful and accurate summary of the factual background and of the evidence given by the expert witnesses, it lacks any analysis of their evidence. Much of it was the subject of detailed criticism by the witnesses on both sides. But it is impossible to tell what the Lord Ordinary made of those criticisms as he has failed to explain the grounds on which he decided to accept some parts of the evidence and to reject other parts, as he must have done in order to find the appellant’s case proved. There is no indication that he based his decision to any extent on the demeanour of the witnesses when they were giving evidence, although he noted – as is indeed obvious from the transcript – that Professor Behan and Professor Compston in particular both held strong views on the points which were at issue and were at pains to express them at considerable length in answers which often bore little relationship to the questions which had been asked. The exercise of his judgment was wholly dependent on an evaluation of the substance of all the expert evidence, but there is no discussion of these matters in his opinion. The First Division held that the Lord Ordinary’s decision as a whole was unsatisfactory and, applying Lord Thankerton’s well-known dicta in Thomas v. Thomas 1947 S.C.(H.L.) 45 at p. 54 and Lord Keith of Kinkel’s observations in Stephen v. Scottish Boatowners Mutual Insurance Association 1989 S.C.(H.L.) 24 at p. 61, they decided that it was open to the Inner House to review the whole matter. The appellant accepts that they were entitled to reach this view.
The second feature of the case is the outstanding quality of the opinions which were delivered by all the judges of the First Division, and especially – if I may say so – that of the Lord President. This has more than redressed the absence of detailed reasoning in the opinion of the Lord Ordinary. Great care has been taken to explain the anatomy and physiology which formed the background to the debate between the expert witnesses and to identify and analyse the grounds on which the propositions on each side of the argument were based. The complex nature of these issues is underlined by the fact that, although the judges were unanimous in their decision to allow the reclaiming motion, they gave different reasons for reaching this view. In the result it has been much easier than it might otherwise have been for your Lordships to identify and explore the points which lie at the heart of this appeal.
The proceedings in this House
Section 40(1) of the Court of Session Act 1988 provides that it shall be competent to appeal from the Inner House to the House of Lords without the leave of the Inner House against a judgment on the whole merits of the cause. The decision of the Inner House in this case is such a judgment. The right of appeal to this House may be directed to issues of fact as well as issues of law. As Lord Reid said in Benmax v. Austin Motor Co. Ltd.  A.C. 370, 375, apart from cases which are expressly limited to questions of law, an appellant is entitled to appeal against any finding, whether it be a finding of law, a finding of fact or a finding involving both law and fact. Appeals from the Court of Session on issues of pure fact are unusual. The House will only review concurrent findings of fact in the Outer and Inner House of the Court of Session which depend on an assessment of credibility by the trial judge if it can be clearly demonstrated that the findings are erroneous: Islip Pedigree Breeding Centre and Others v. Abercromby 1959 S.L.T. 161, 174 per Lord Reid; Brodie v. British Railways Board 1972 S.L.T. (Notes) 37, per Lord Kilbrandon. But that rule of practice cannot be applied in this case, and the appeal has been quite properly taken on what is undoubtedly an issue of pure fact. The matter is further complicated by the absence of any detailed reasoning in the opinion of the Lord Ordinary. In the result the decision of the Inner House – which is based entirely on the printed evidence – must be regarded as open to scrutiny by your Lordships in the same way as if it had been taken at first instance and was at large for consideration by the appeal court.
But it is not practicable for the means by which such decision at first instance is normally scrutinised in the Inner House, by the reading of the evidence to the judges from the transcript and then subjecting it to argument, to be adopted by your Lordships in this House. Lord Steyn pointed out in Smith New Court Securities Ltd. v. Citibank N.A.  AC 254, 275 that the prime function of the House of Lords in English appeals is to review questions of law of general public importance. He said that it could not properly discharge that function if it often had to hear appeals on pure fact. Similar considerations require that regard must be paid to the need for economy in the time taken in Scottish appeals to present arguments on questions of pure fact. With that in view, their Lordships took the unusual step of holding a preliminary hearing in this case to discuss the procedure which was to be adopted in the preparation of the appeal.
An essential element in that procedure was the exchange between the parties of their written cases prior to the lodging of the final written cases in the Judicial Office. Both sides were asked to ensure, when preparing their written cases, that they set out not merely the heads of argument but also an outline of the argument to be advanced under each head and that the parts of the judges’ opinions which were under challenge were clearly identified by page number. They were also asked to provide cross-references to the particular passages in the evidence or the medical reports on which they proposed to rely in support of any submission that the judges’ treatment of the facts was materially incomplete, inaccurate or otherwise in need of supplementing by reference to the words used by the witnesses. Counsel on both sides are to be commended for the care and attention which they have given to these details, and for the fact that their cases gave identical paragraph numbers to the competing arguments on each point. Their Lordships were greatly assisted by the quality of the written cases in their preparation for the hearing of the appeal and in their consideration of the case after the conclusion of the oral argument.
The medical background
As the Lord President observed at p. 558, the matters in dispute between the parties are medical. They were debated with the witnesses against the background of a shared knowledge of the relevant anatomy and physiology and of the nature of the medical conditions which were being discussed. The Lord Ordinary was at a disadvantage in dealing with these agreed matters because he was not provided with an elementary text to guide him through these chapters of the evidence. Following a suggestion which was made at the procedural hearing, a description of the anatomy and physiology of the central nervous system, a copy of the relevant chapters in Richard S. Snell’s Clinical Neuroanatomy for Medical Students, 4th edition, and an excerpt from Grant’s Method of Anatomy were included in the Appendix. But the best guide to the medical background is to be found in the Lord President’s opinion at pp. 558-563 where he set out his understanding of these matters with great clarity and commendable attention to detail.
It is not necessary for me to go over all the ground which he has described so fully and so well and is illustrated so helpfully by the material which was included in the Appendix. But I must mention some of the more important points described by the Lord President which were common ground among the witnesses.
MS is a disease of the central nervous system (“CNS”). The brain and the spinal cord which together make up the CNS are connected with each other by nerve fibres. The spinal cord contains nerve cells which control movement. Signals are transmitted from the nerve cells to all parts of the body by nerve fibres. These fibres also transmit signals from other parts of the body to the spinal cord. The nerve fibres are covered in a sheath of myelin, which has an insulating effect on the electrical signals which they transmit. Damage to the spinal cord is liable to interfere with these signals and may cause paralysis. In MS the myelin which covers the nerve fibres within the CNS becomes depleted, although the nerve fibre itself remains intact. This process is known as “demyelination”. When demyelination occurs the nerve fibres are deprived of their sheath, and this impairs their ability to conduct electricity. It results in the formation of plaques within the CNS which become scarred or sclerotic as they develop and get older. Symptoms occur when a plaque develops in an area which affects the operation of a sensory or motor function of a part of the body such as the arms or the legs. It is a characteristic of the disease that it affects different parts of the brain at different times. Symptoms may appear for a short period and then disappear. They may manifest themselves later in a different way because the myelin is being attacked in some other part of the CNS. In a high number of cases the disease becomes progressive and the patient suffers a decline, becoming more and more disabled as time goes on.
There is no proof of what causes MS. But it is common ground that trauma never causes the disease. So, as the Lord President put it at p. 562, the dispute is as to whether trauma can “trigger” it. MS occurs among certain races and not others, and only certain people within these races are liable to develop it. They were referred to by the witnesses as “potential demyelinators”. The consensus view is that a genetic factor is involved, and that those with the necessary genetic characteristics become potential demyelinators due to a microbial or viral infection in their childhood. Not all potential demyelinators develop symptomatic MS. For many the reason why they become symptomatic is a mystery, as its clinical manifestation starts without being preceded by any obvious event which could be said to have caused or “triggered” it. It appears to be accepted by the experts that exposure to a virus is the most common trigger. The area of dispute is whether symptomatic MS can ever be triggered by trauma.
The body is supplied with an immune system which responds to an attack by a foreign body by producing organisms known as lymphocytes. These are of two kinds. B-lymphocytes produce antibodies which react with the foreign body and render it harmless. T-lymphocytes attack the foreign body in various ways which complement the role of the B-lymphocytes. The immune system can however work in an incorrect way. This results in its failure to distinguish between foreign bodies and other bodies from within the body against which it reacts. When the system is in this condition the activated T-lymphocytes may behave in a deranged manner in a way that is associated with the development of MS plaques.
The organs of the CNS require to be supplied with various nutrients which are delivered by means of the blood stream. But the brain could be damaged if harmful substances were to be allowed to pass into the brain. A structure exists between the blood and the brain whose function it is to prevent this. It is known as the blood brain barrier (“BBB”). It consists of a layer of cells, each of which is opposed to the other by a tight junction. As the Lord President explains at p. 561, it is incorrect to think of the BBB as a wall or some other similar kind of barrier. It operates in a selective fashion by admitting some and excluding other substances. When it is operating normally it allows beneficial nutrients to pass into the brain but it excludes harmful substances. Among the substances which pass in and out of the brain in a healthy subject is a modest, or low-level, supply of lymphocytes. When the body is responding to an attack such as an infection the BBB alters so as to allow an increased supply of lymphocytes to pass into and out of the brain to fight the infection. A key question in the case is whether, and if so in what circumstances, trauma may also alter or open up the BBB so as to allow activated and deranged T-lymphocytes to enter the brain.
The main chapters of evidence to which the expert witnesses turned in order to justify the conclusions which they reached on the critical issues in the case against this general background consisted of the following. For the appellant Dr. Draper, Dr. Durward, Professor Behan and Dr. Poser relied on their own clinical experience and reports of cases in the medical literature, including a summary of the reports linking trauma with the onset of MS provided by D. McAlpine and N. Compston in their epidemiological study, “Some aspects of the natural history of disseminated sclerosis”, Quarterly Journal of Medicine, New Series, vol. 21 (1952), 135-167. Professor Behan and Dr. Poser relied in addition on a series of experiments on animals. Dr. Poser also drew support for his position from an article by R. Gonsette and others published in Acta Neurologica Belgica, vol. 66 (1966), 247-262 and a paper by D.R. Oppenheimer, “The cervical cord in multiple sclerosis”, published in Neuropathology and Applied Neurobiology, vol. 4 (1978) 151-162. For the respondent Professor Compston, Dr. Sibley and Dr. Kurland also relied on their clinical experience. Professor Compston drew support for his conclusions from two other epidemiological studies. One, which was referred to as “the Arizona Study”, was carried out by Professor Sibley and his colleagues in the Department of Neurology at the University of Arizona and was the subject of two papers: C.R. Bamford and others, “Trauma as an etiologic and aggravating factor in multiple sclerosis”, Neurology, vol. 31 (1981), 1229-1234; W.A. Sibley and others, “A prospective study of physical trauma and multiple scelorosis”, Journal of Neurology, Neorosurgery and Psychiatry, vol. 54 (1991), 584-589. The other, which was referred to as “the Mayo Clinic Study”, was based on records from Olmstead County, Minnesota and was the subject of a paper by A. Siva and others including Dr. Kurland, “Trauma and multiple sclerosis”, Neurology, vol. 43 (1993), 1878-1882.
The issues in this appeal
The Lord President said at p. 564B that the question whether the appellant’s injury caused the onset of his symptomatic MS could be broken down into two questions. The parties to this appeal adopted that approach when they were presenting their arguments. The first, or “general”, question is whether trauma can ever cause, or “trigger”, the onset of symptomatic MS in a susceptible individual. The second, or “particular”, question is whether, if trauma can trigger symptomatic MS, it did so in the appellant’s case. The word “trigger” is used to describe the mechanism that turns asymptomatic MS into symptomatic MS.
There is however a close relationship between these two questions which requires that they be defined more precisely. The first symptom which the appellant noticed after the accident was the dragging in his left leg. There was ample evidence to show that this was a symptom of his MS, and that the disease had become symptomatic because he had developed a plaque or plaques on his spinal cord. This is because the spinal cord is an area in which the development of plaques of demyelination will produce that kind of symptom. The Lord President said at p. 565C that he was prepared to proceed on the basis that shortly after the accident the appellant had a plaque or plaques of demyelination on his spinal cord. He also said that he was satisfied that the spinal cord could have been damaged by a whiplash injury. The respondent has not challenged either of these findings, and I accept them as justified by the evidence.
There was no direct evidence that the whiplash injury which the appellant sustained in the accident did in fact damage the spinal cord, as there is nothing in the records of the hospital where he was treated after the accident to indicate that he sustained this particular injury. For damage of this kind to occur the whiplash injury must disrupt the spinal canal within which the spinal cord is located in such a way that the cord is bruised or damaged. No X-rays were taken or other findings recorded to indicate that the appellant suffered any kind of damage to those structures in his neck. But it is possible to establish that this was so by inference, and the appellant’s witnesses sought in this way to link the development of a plaque or plaques on his cervical cord to the type of injury which he sustained in the accident. The critical questions therefore are (1) whether a whiplash injury which damages the nerve pathways in the spinal cord can ever trigger symptomatic MS and, if so, (2) whether it can be inferred from the fact that the appellant developed a plaque or plaques on his spinal cord shortly after the accident that his whiplash injury was of the kind which causes damage to the nerve pathways in that area.
The reasons given by the judges in the Inner House
I mentioned earlier that the judges of the First Division gave different reasons for allowing the reclaiming motion. In the Statement of Facts and Issues the following summary of the conclusions which they reached is given:
- “(a) the Lord President
- (i) that trauma could never trigger MS in a potential demyelinator
- (ii) that he therefore did not require to address the issue of whether trauma had brought about the pursuer’s MS
- (b) Lord Caplan
- (i) that trauma could not trigger MS in a potential demyelinator
- (ii) were it to have been shown to have been probable that MS can be triggered by neck trauma, he would have been inclined to hold that the appellant was one of those with a neck injury which has caused MS
- (c) Lord Prosser
- (i) that trauma could trigger MS in a potential demyelinator
- (ii) but that it did not do so in the pursuer’s case.”
It seems to me however that the process of reasoning by which they reached these conclusions as disclosed by their opinions was closer together than this summary might suggest. The question to which they had to direct their attention was whether the appellant had proved his case on a balance of probabilities. The matter was complicated by the fact that the critical issues in the case had to be decided by analysing the evidence of expert witnesses who, applying their minds to these issues as scientists, profoundly disagreed with each other about the conclusions which could be drawn from known facts. The standard of proof which they were applying was not that which is applied in civil proceedings by a court. A judge is entitled to find a fact proved if it is established to his satisfaction on a balance of probabilities. This is not a very exacting standard, and the margin on either side of the balance may such that the decision can quite reasonably go either way. It would not be surprising to find that there were differences of view among the judges as to where the balance lay on the first issue which relates to the general question whether trauma can ever cause MS. In these circumstances the process of reasoning, rather than the individual conclusions reached on each chapter, is more important when your Lordships are considering whether the decision as a whole stands up to examination or should be set aside.
My understanding of the reasons which each of the three judges gave for the conclusions which they reached on the first question is as follows.
The Lord President noted that there was an obvious conflict between the appellant’s witnesses, who referred to a number of cases in their experience where patients previously in good health had developed symptoms of MS after trauma, and the respondent’s witnesses, who said that they had not had that experience. He said that the fact that someone like Professor Behan had been able to assemble 16 such cases was something which anyone trying to understand the possible cause of the disease must take into account, as was indicated by the fact that Dr. Poser had been led by similar reports and experiences to put forward the hypothesis that they pointed to a causal relationship between certain traumas and the development of MS plaques and to shape a theory as to why there might be such a causal relationship. But in his view such a hypothesis had to be tested. He proceeded to examine first the epidemiological studies, one of the purposes of which was to test that hypothesis, and then the validity of any theory put forward to explain any assumed relationship between trauma and the development of MS. His conclusion on the epidemiological studies was that they did not support the view that there was a causal relationship between trauma in general and the onset of symptomatic MS, and that this was important because it focused attention on the question whether there was such a relationship between trauma to the spinal cord and the onset of such symptoms. Having examined the theories which were advanced based on the animal experiments, on Gonsette’s paper (1966) and on Oppenheimer (1978) he said at p. 601G-H that he did not find it proved, on a balance of probabilities, that trauma in general or whiplash injury in particular could ever trigger the onset of symptoms of MS. He then said that, in view of this conclusion, he did not need to go on to answer the second question. But he observed that he had difficulty in seeing how, even supposing “that it were possible” for trauma to trigger the onset of MS, the evidence established that trauma “was” a trigger in this case rather than coincidental to its onset.
Lord Prosser said at p. 612 that the account of what happened to the appellant in the accident and of his neck symptoms shortly thereafter seemed to him to show an actual trauma which was at least “quite likely” to show an appropriate injury with damage to the blood brain barrier, and that he would be content to infer that there was indeed such an injury if the general question could be answered in the appellant’s favour (my emphasis). This forced him back to the general question, as to which he said that if all one could say in answer to that question was that these cases cannot all be mere coincidence one would lack any positive pointer, in any particular case, as to whether that case was one where the traumatic breach was used by the lymphocytes to penetrate the barrier. Reviewing the evidence on the general question and having noted the discrepancy between the witnesses as to their clinical experience, he said that he accepted that the experience of Professor Behan and Dr. Poser was as they described it and that Oppenheimer’s theory sufficed to give an understandable mechanical explanation for the clinical experience. But he found no basis to justify the conclusion that traumatic breach rather than chemical breach was probably the explanation for the symptoms in any particular percentage of cases or more probably than not. That being so, he said at p. 618H that he did not feel able to hold that the appellant “probably” sustained an appropriate injury or, even assuming such an injury, that in this case the traumatic breach rather than chemical breach led to the symptomatic MS. At p. 620 he said that the evidence had in his view established that trauma “can” trigger MS, but that that general conclusion was not enough for the appellant. He could find no basis for treating coincidence as rarer, or as less likely, than traumatic cause in this case.
Lord Caplan indicated at p. 628 that he was unable to accept the evidence of the appellant’s witnesses based on their clinical experience unless it was tested by other evidence. He did not find it possible to find firm support for their evidence from the experiments with animals or in the papers by Gonsette or Oppenheimer. He observed that the precise mechanism for the activation of dormant MS remained unclear. In his view the epidemiological studies had failed to throw up any positive connection between the onset of MS and trauma. As for the nature of the injury which the appellant sustained in the accident, he said at p. 634F that he found the question whether the cervical cord was damaged hard to answer in the abstract as deductions about the nature of that injury were to a degree dependent on the force of any evidence which could establish a recognised link between MS and neck trauma. If it were clearly shown that neck trauma was a recognised facilitator of MS he would be inclined to hold that in the appellant’s case the combination of circumstances was not a coincidence, and that the probability was that his neck injury caused MS. But that all depended on it being “probable” that MS could be triggered by neck trauma, which he was unable to find proved.
It seems to me that Lord Prosser and Lord Caplan were in broad agreement in their approach to the second question. Adopting Lord Prosser’s words at p. 612, they would both have been content to infer that the appellant sustained an appropriate neck injury in the accident if they had felt able to hold that symptomatic MS could “probably” be triggered by an injury of that kind. This, as Lord Prosser said, forced them both back to the first or general question, which was the only question that the Lord President found it necessary to answer. As to their conclusions on that question, there was a clear difference of view between the Lord President and Lord Prosser. The Lord President was unable to find it proved on a balance of probabilities that whiplash injury could ever trigger the onset of symptoms of MS, whereas Lord Prosser was satisfied that trauma “can” trigger symptomatic MS. But the significance of this difference is much reduced once one appreciates that the critical question for Lord Prosser was whether it had been proved that traumatic breach was “more probably than not” an explanation for these symptoms. Only if the evidence had persuaded him that this was so would he have been able to hold that in the appellant’s case the relationship was more than a coincidence. Agreeing on this point with Lord Caplan, his conclusion was that it had not been proved that trauma was a more probable explanation.
The significance of the difference of view between the Lord President and Lord Prosser is further reduced by an examination of the views which they expressed about the study which was carried out by Oppenheimer. In what the witnesses on both sides acknowledged to be a paper of high quality, Oppenheimer set out his conclusions after examining the spinal cords in 18 cases of MS. He found that lesions in the cervical cord were more common than at lower levels. In view of their shape and their frequency he expressed the view that mechanical stresses play a part in determining the site of these lesions, and that such stresses are commonly transmitted to the cord during flexion of the spine through the denticulate ligaments. These ligaments run down each of the two lateral aspects of the spinal cord and hold the cord in position within the spine. His conclusion was that in patients with MS neck flexion was dangerous and that patients with the disease should be protected against the effects of full flexion of the head and neck.
Lord Prosser said at p. 618C that he was persuaded that Oppenheimer’s theory sufficed to give an understandable mechanical explanation for the appellant’s witnesses’ clinical experience. But, as the Lord President pointed out in his detailed analysis of this paper at pp. 594-599 and as Lord Caplan also observed at p. 630, that theory was subject to important limitations. Among these were the fact that he was considering the effects of chronic stress, not sudden trauma such as a whiplash injury, and the absence of any compelling explanation as to why lesions similar to those which he observed in the spinal cord and attributed to movement occur in other areas which are not subjected to movement of that kind. I think, with respect, that much of the force of what Lord Prosser took from this paper is removed by the fact that in his treatment of it he did not subject the paper to the same detailed analysis as the Lord President.
I have concluded therefore that the outcome of this appeal depends upon what your Lordships are to make of the opinion of the Lord President. The differences between his reasons and those of Lord Prosser on the first question are so marginal in the whole context that the fact that these differences exist does not of itself not serve in any way to undermine the Lord President’s opinion on this question, and on all essential matters Lord Caplan agreed with the Lord President. So the appellant must show that the Lord President misdirected himself by approaching the evidence in the wrong way or by failing to understand the nature and significance of that evidence. Only if that hurdle can be overcome would it be open to your Lordships to look at the whole matter afresh and re-examine the question where the balance of probabilities lies on the difficult issues raised by the first question.
The Lord President’s opinion
It has to be said at the outset that the attention to detail and the depth and quality of the analysis which the Lord President brought to bear on the evidence is of such high quality that the task which the appellant has set for himself is a formidable one. Nevertheless it is right to bear in mind that there is an important difference between the exacting standards of thought and analysis which the academic will expect of medical scientists and the task of a judge when he is considering whether the essential elements in a pursuer’s case have been established on a balance of probabilities.
This is not to say that the judge need not examine the detail of the evidence. Of course he must, as his task is to identify the real issues in the case and then determine where the balance lies between the competing positions revealed by the evidence on each side. In a case such as this, an important part of his task is to assimilate and understand the oral and written evidence and to penetrate the arguments which have been developed by the expert witnesses. But when it comes to the point of exercising his judgment on these issues, he must be careful to avoid applying the standard of proof which the expert would apply to them. As Lord President Cooper said in Davie v. Magistrates of Edinburgh, 1953 S.C. 34, 40:
- “Expert witnesses, however skilled or eminent, can give no more than evidence. They cannot usurp the functions of the jury or judge sitting as a jury, any more than a technical assessor can substitute his advice for the judgment of the court.”
The function of the judge in a civil case is to decide where the truth lies, or whether the case has been made out, on a balance of probabilities. One cannot entirely discount the risk that, by immersing himself in every detail and by looking deeply into the minds of the experts, a judge may be seduced into a position where he applies to the expert evidence the standards which the expert himself will apply to the question whether a particular thesis has been proved or disproved – instead of assessing, as a judge must do, where the balance of probabilities lies on a review of the whole of the evidence.
This was a point which clearly troubled Lord Prosser, who introduced his opinion at pp. 602-605 with some general observations on the questions of probability and proof. As he put it at p. 603G-I, he thought it right to labour these issues as he had found it important, and sometimes difficult, to keep bringing them to mind when looking at the evidence of particular witnesses. At the end of this passage, at pp. 604I-605A, he observed that, while a conclusion may seem to be insufficient until one can find an identifiable possible mechanism as a basis for finding that a causal link is proved or established in ordinary or scientific terms, that feeling of insufficiency is much less appropriate if one stops short of such claims and contents oneself with saying that the causal relationship is marginally probable as civil litigation requires. At first sight there is perhaps an indication here that the explanation for the difference of view between the Lord President and Lord Prosser on the first question – although Lord Prosser stopped short of answering that question in a way which would have led him to answer the second question in the affirmative – may have been due to the bringing of different standards of proof to bear on the evidence.
No doubt with this in view Mr. Mitchell Q.C. for the appellant began his criticism of the Lord President by contending that he had misdirected himself by applying a higher standard of proof, that of scientific proof, to evidence which required to be addressed in terms of a balance of probability. If there were force in this criticism it would go a long way to opening up the whole issue. This would be a misdirection in law which must be taken to have affected the whole of the Lord President’s analysis. It is a difficult issue which I have thought it right to examine very carefully.
The Lord President said that he had had the advantage of reading a draft of Lord Prosser’s opinion after he had completed his initial draft, and that Lord Prosser had articulated some of the problems which he himself had experienced. That he was fully alive to the problem is plain from these observations at p. 600:
- “…in their evidence the experts refer at times to a standard of scientific proof which is different from the standard of proof which the court applies when deciding matters of fact. For a court a fact is proved if the court holds that it is more probable than not, even if it is only marginally more probable. By contrast scientific experts will obviously require a much higher standard before they hold that something has been established. I have tried to keep this difference of approach in mind when reaching my conclusion”
This still leaves the question whether he was successful in that endeavour as he made his way through each chapter of the expert evidence and reached his conclusion at the end of it. But, having read his opinion again and again and having examined for myself much of the evidence, I am unable to detect anything in his opinion which would justify the criticism that he has applied the wrong standard of proof to that evidence. He has undoubtedly subjected all aspects of the appellant’s case to a rigorous analysis, especially in those passages where he has insisted that propositions advanced in one part of the evidence must be tested against the evidence which is to be found in other parts. The methods which he has used are well-tried in the field of scientific analysis. The nature of the evidence led on both sides invited that approach to its assessment. But the fact that he has used these methods in order to test the evidence does not persuade me that, at the end of the day, he applied the wrong standard when he came to the point of deciding what had been proved. In my view his opinion is not open to this criticism.
I turn now to the detailed criticisms of the opinion which Mr. Mitchell developed in the course of his argument. He said that the reasons for the decision on the first question were unsound, that they showed that the Lord President misunderstood the evidence and that the Lord President ought not to have expressed the view which he does at the end of his opinion on the second question without giving reasons for that view.
The main thrust of Mr. Mitchell’s attack on the decision on the first question was that the Lord President did not give proper weight to the clinical and historical evidence in his summing up on this chapter at p. 569E-G. This led him to reject that evidence when testing it against the epidemiological evidence. He ought not to have done this, as the conclusions which he drew from the epidemiological evidence were unsound and unsatisfactory. At p. 585D the Lord President said that the epidemiological studies might not be perfect but that they were the best source of scientific information on the point which was available. But the fact that they were the best source of information that was available was not a sound reason for attaching weight to them in comparison with the clinical and historical evidence. He was right to discount the study by McAlpine and Compston (1952) for the reason given at p. 585F that the figures in that study were built up of many different types of trauma including peripheral trauma. But he should have applied the same reasoning to the Arizona and Mayo Clinic studies, as neither of them had been designed to investigate the specific types of trauma which were said to produce MS plaques. All these studies were subject to the same criticism that they examined a wide range of different types of trauma and were not designed to address the particular point put in issue by the clinical and historical evidence. This had been recognised by Lord Prosser, who said at p. 619B-C that he could not find anything in these studies which threw any useful light on the narrower question as to the specific category of physical injuries which might damage the blood brain barrier. The Lord President accepted at p. 579H-I that weaknesses in Professor Sibley’s grasp of the detail of the articles had been revealed in cross-examination. But he then said that the statistical calculations and conclusions should be accepted unless they were actually shown to be wrong. This was an error, as the articles could not speak for themselves and the onus was on the respondent to lead the necessary evidence. The need for evidence of that kind was demonstrated by the Lord President’s observation at pp. 580I-581A that the Mayo Clinic study was difficult to follow as its format was not well constructed.
I think that the answer to these and a number of other detailed criticisms which are set out in the appellant’s printed case about the Lord President’s treatment of the epidemiological evidence is that the observations to which they were directed must be seen and understood in the context of the Lord President’s opinion as a whole. It has not been demonstrated that his narrative of the evidence was inaccurate, and I am not persuaded that he misunderstood the evidence. The question is whether he was entitled to use the evidence as he did, bearing in mind its limitations and the absence of evidence either to support or to undermine the statistical exercises. As regards the statistics, the Lord President was right to point out that the question whether the worked figures were incorrect or overlooked in the analysis was not explored in the evidence. The parties did not join issue on this point. As can be seen from Professor Sibley’s cross-examination at pp. 1440C -1445A for example, it was the use to be made of the published material which was in dispute. In these circumstances the Lord President was entitled to proceed upon the basis that the calculations and conclusions should be accepted for what they were worth unless they were shown to be unsatisfactory by contrary evidence, and to concentrate on the use which ought to be made of them. This is in accordance with the usual practice in the treatment of published material which is relied upon by expert witnesses. As regards the use to be made of it, the opinion shows that the Lord President was fully aware of the various criticisms which had been advanced by the appellant’s witnesses for disregarding or at least for attaching no significant weight to this material. There was a difference of view between him and Lord Prosser as to the conclusion which was to be drawn from it when it was compared with the clinical and historical evidence. But this of itself does not mean that the Lord President’s conclusion at pp. 585C-586D must be rejected as unsound.
I consider that the views which the Lord President expressed in this passage are fully supported by his careful analysis of the evidence and that he was entitled to reach the conclusions which he did based on that analysis. He was right to point out at p. 586D that the epidemiological studies at least showed that one should look carefully at the evidence which was said to support the existence of a causal relationship between trauma to the spinal cord and the onset of symptomatic MS.
Mr. Mitchell then turned to the Lord President’s treatment of the evidence about experiments on animals, of Gonsette and of Oppenheimer. He said that his reasons for finding that the evidence of the animal experiments did not provide material support for the view that trauma can cause the onset of symptomatic MS were unsound, as this conclusion overlooked the purpose of these experiments. He criticised the Lord President’s treatment of the Gonsette paper on the ground that the conclusions which he drew from it at pp. 594B-C and 600F-G were in conflict with evidence given by Professor Behan and Dr. Poser which he had accepted previously. The observation at pp. 598I-599A that Oppenheimer’s hypothesis, which involved the effects of movement, did not provide a compelling explanation of why lesions leading to demyelination occurred in areas of the brain which are not subjected to movement of that kind ignored the fact that there was clear evidence that the preponderance of plaques were explicable by movement and the effects of movement. Due to this and other errors in his reasoning the Lord President did not give the weight to Oppenheimer’s paper which he should have done.
Here again I think that the observations which were criticised must be read in the context of the opinion as a whole. Reading them in this way, I am wholly unpersuaded that the Lord President’s treatment of these chapters of the evidence was erroneous or than he was not entitled to reach the conclusions which he drew from them. There was an acute conflict between the experts as to the bearing which the experiments on animals had on the question whether trauma can cause the onset of MS in humans. Animals do not develop MS and the condition from which they suffer known as experimental allergic encephalitis is not the same as MS. The weight to be attached to these experiments is a question on which views may differ among experts, but in a civil proof this is a matter for decision by the judge on a balance of probabilities. So also is the question as to the weight to be attached to Gonsette’s study of the development of fresh plaques in the vicinity of areas of the brain affected by the procedure known as thalamotomy – the insertion of a trocar, or needle, through the upper layers of the brain through which an electric current is then passed to destroy a part of the brain tissue. At pp. 592-594 the Lord President sets out the evidence from both sides about this study and narrates what the experts on each side had to say about it. He acknowledges the importance of the questions raised by the experiments, and then takes account of the points made in reply by the respondent’s witnesses. The conclusion which he reaches at p. 594G that it did not provide a basis for the conclusion that trauma of the kind that the appellant suffered can cause MS seems to me to be fully justified by the careful reasoning which preceded it.
Similarly, in his treatment of Oppenheimer the Lord President takes full account of the points which have to be borne in mind in doing justice to this study, acknowledges at p. 598G that the paper does indeed suggest that the lateral columns of the spinal cord are a site of preference for the development of MS plaques and accepts that his observations point to a phenomenon that requires to be investigated. At p. 600G he says that, like everyone else involved in the case, he was impressed by this paper and that he accepted that Oppenheimer’s hypothesis that breaches of the BBB may be caused by flexion could support the theory that other types of trauma, such as a whiplash injury, could also cause a breach of the BBB leading to demyelination. But in the end, after weighing up all the factors pointing one way and the other, he says at p. 601G that he does not find this theory proved. As regards this part of the case also I am quite unable to find any defect in the Lord President’s reasoning to justify the view that he was not entitled to reach this conclusion in the light of his examination of the evidence.
In the end the process of reasoning which led the Lord President to this conclusion seems to me to be quite straightforward, and in my opinion it is unassailable. There is a body of clinical evidence that shows that there are many cases of symptomatic MS which cannot be related to trauma. In a small number of cases the onset of symptoms is preceded by trauma. That happened in this case, but coincidences can occur. So the theory that trauma triggers the onset of symptoms of MS has to be tested. Experiments on animals and the study by Gonsette show that violence can open up the BBB in such a way as to permit the brain to be attacked by activated and deranged T-lymphocytes. But there was no question of such violence in this case. In any event this evidence still leaves the majority of cases of symptomatic MS unexplained. The epidemiological studies do not support the appellant’s case. If anything they tend to support the arguments to the contrary. But for present purposes the important point is that they show that the appellant’s case depends upon there being an acceptable theory to explain what it is that overcomes the BBB and permits the development of symptomatic MS. A satisfactory explanation would go a long way to supporting the appellant’s case. But the evidence, which reaches its highest point with the study by Oppenheimer, does not go far enough to provide that explanation. So the appellant’s case fails on a balance of probabilities.
As for the view which the Lord President expressed on the second question, it seems to me that he was simply making the point which I think he was entitled to make in the light of his review of the evidence on the first question that it was not enough for the appellant to establish that trauma in general could trigger the onset of MS. Sufficient support had to be found in the evidence on the first question as to whether the onset of symptomatic MS can be caused by a whiplash injury which damages the nerve pathways in the spinal cord to enable the inference to be drawn that the whiplash injury which he sustained in the accident was that kind of injury. The view which he formed as to where the balance lay after assessing the weight of the evidence on the first question led inevitably to the conclusion that the appellant had failed to prove that there was a connection between the injury and the onset of his MS.
I am in no doubt that the decision which the judges in the First Division reached was one which they were entitled to reach on the evidence. I would dismiss the appeal.
I have had the advantage of reading in draft the speech of my noble and learned friend Lord Hope of Craighead. For the reasons he has given I would also dismiss the appeal.