[2008] CSOH 154



in the cause







Pursuer: A Smith, Q.C., Munro; Digby Brown

Defender: Shand, Q.C., HBM Sayers

7 November 2008


[1] Mrs Smith is a teacher. She is a teacher who has special gifts. She described herself as a peripatetic support teacher, one who lends support to a class teacher from nursery to sixth form. Her special gift is that she has a sufficient command of no less than eight foreign languages. She was there to help the children of immigrants to learn in our schools; children to whom English is a second language. She described her job as very rewarding. In 2003 she worked over schools mainly on the south side of Glasgow often with Punjabi and Urdu speaking children and she gave the court examples of helping children of other races. She lived in Prestwick and described her life as living beside a beach and driving the short distance to Glasgow to do a job she loved.

[2] Events on 20 January 2003 have blighted her life. She went to work as usual that day. She drove her car northwards on the A77 road and when she was near to Kilmarnock she was involved in a serious accident which was not her fault. A lorry came out of a lay-by and Mrs Smith moved into the offside lane to avoid it. The behaviour of the lorry caused her to brake and as she did so a car coming at speed from her rear ran into her. Her car was lifted up, spun round and hit the central reservation ending up facing to the south. I shall return to look at the details of all of this later, but what has since befallen her is the subject of this action.


[3] Let me begin by looking at what is said on Record. The pleadings are in the abbreviated Coulsfield form. That has not caused any problems in what became a complex case. That was due to the commonsense and mature attitude of experienced counsel. Condescendence 4 narrates the facts of the accident in January 2003, when the pursuer was 54. The facts are admitted. It discloses a collision from the rear which the evidence proved to have been violent and at high speed. Article 5 narrates the loss, injury and damage which falls into discrete areas. There is a claim for her physical injuries and anxiety disorder which were treated in hospital and by her doctor and others. There is a claim for loss of earnings and certain miscellaneous costs. There is then a statement that in November 2004 she was diagnosed with Parkinson's Disease and "... it is likely that the accident brought forward the development and diagnosis by a period of up to seven years ...". The defender's response inter alia states that the accident did not bring forward the development of Parkinson's Disease.

[4] The case began in January 2007 and for a variety of reasons did not conclude until 6 March 2008. It occupied thirteen Court days. The notes of evidence were extended for the hearing. They are not of good quality. There are many gaps and omissions and some obvious errors including spelling. This may not be the fault of anyone since the transcript was prepared in Devon, with the inevitable difficulty in England of Scottish voices. It does, however, make for problems in achieving accuracy and I have had to rely on my notes and the helpful written arguments of counsel.

[5] There is no dispute that really the only issue in the case is the very important and difficult legal and medical questions of whether the accident (I use the word generally) accelerated the development of Parkinson's disease (hereafter referred to as P.D.) in the pursuer who was already suffering from it (the "causation question"). That she was so suffering is not a matter of dispute. I was assisted in this matter by the two eminent doctors viz Dr Grosset for the pursuer and Professor Bone for the defenders. Both gave evidence according to the highest tradition of their profession and completely objectively. In the end of the day, for reasons which will appear, it was not necessary for me to have to prefer one over the other. Both of them were in agreement that P.D. is idiopathic and that the causation question depended upon epidemiological studies and trauma to the head,. To that I will return in due course. It was also not disputed in the evidence that there is a difference between Parkinson's disease which is in issue here and arises from the brain not producing dopamine; and Parkinsonism. The latter evinces many of the symptoms of the former but arises from separate causes. Often boxers suffer from it due to repeated blows to the head and it can be manifested in persons taking psychotropic drugs. However, I should like to observe that in a case of this nature decisions have to be taken by both sides as to how best to present their case through experts as to fact and opinion. The Court often cannot make any assessment other than through the experts. Inevitable problems arise when the expert has to rely on the studies of others. Sometimes those others are witnesses, sometimes, not. In this case no epidemiologists were called on either side. Both doctors however, spoke at length about the studies. Passages in learned journals were read to them at length for comment. All of this can make the task of the judge of first instance acutely difficult. Though nothing now turns on it, it is interesting to note that all the learned papers were lodged by the defenders.

[6] There are a number of other things which were agreed or were not seriously in dispute which I should mention. It was accepted that as the pursuer was already subject to P.D., though unaware of it at the date of the accident, she would inevitably have developed it at some stage. There was no disagreement that she suffered certain physical injuries of a minor nature and that she may have suffered some personality change and loss of confidence. Also there was no challenge to the fact that soon after the accident she experienced a throat tremor with associated dysphagia and a tremor on her left side which would not go away. These symptoms were evident in 2003/4 and were spoken to by her and other witnesses. The medical records confirm them. It was also not disputed that she had none of the warning symptoms before the accident.

[7] Other matters were specifically agreed in two joint minutes of agreement. The first of these agrees a number of medical records, pay information and other accounts. They are not, strictly, agreed as accurate but nothing was made of that. The second agrees timings at and after the accident including hospital treatment to 10.55 on 20 January 2003, her Glasgow Coma Scale, what she said to the doctors, what they recorded and the contents of No 6/4 of Process. In evidence much was made of the Glasgow Coma Scale findings (paras 4 and 12).

[8] It is necessary to say something about how Parkinson's disease happens. This was not a matter seriously in dispute.

[9] Parkinson's disease is a neuro degenerative disorder. The degeneration takes the form of accelerated ageing in areas deep in the brain which control movement. Normal smooth active movements become slowness, stiffness and tremor. In the brain are nerve cells which produce a chemical called dopamine. Dopamine is a chemical messenger producing impulses into the limbs and the voice. It is a link in the chain producing all the movements a person takes for granted. The brain sends a signal and dopamine communicates that to the limbs (See Vol.3, page 124). If dopamine runs low then the communication process slows and so does movement. It is vital for health that the exact amount of dopamine is produced for the relevant brain signal. Too much dopamine (eg. by drugs) can have the wrong side effects. Dopamine is found in the brain, the kidneys and the heart. The condition was first noted by a London general practitioner, Dr Parkinson, in the early 19th century. At present there is no known cure. (Vol 16 p.204)

[10] An important factor in its development is age with older people being more vulnerable. Family history can be a known risk factor. Cases have occurred as young as thirty but the average age of presentation is sixty.

[11] The pursuer in evidence gave the following description of her accident which was not disputed and I accept as correct. She was driving north on the A77 and had gone through the Bellfield interchange to the east of Kilmarnock. She was in the offside lane. An articulated lorry which had been parked in a lay-by near a railway bridge moved out and into her lane. The pursuer braked to avoid the lorry. The defender's car which was travelling at high speed behind her struck the rear of the pursuer's car causing it to lift off the road, spin round and hit the central reservation. The pursuer escaped from her car (which was a "write off"). She felt sick and experienced severe lower back pain. Other drivers stopped to help her. She made contact with her husband. The pursuer had been wearing a seat belt and her car was fitted with head restraints. She was taken by ambulance to hospital. She was by then in a head restraint as she was suffering severe neck pain. She continued to feel sick, nauseous and dizzy. Later the same day she was discharged home. She experienced pain to her neck, back and left leg. She took painkillers, and was confined to bed. She became aware of pain in her left arm when moving it. She was off work for some weeks and latterly attended a gym to get fit. By then she noticed that her left arm was beginning to shake. She tried acupuncture without success. At work she noticed lack of movement with the fingers of her left hand. Her father became aware of a problem with her left arm. When she walked her left arm did not swing.

[12] Associated with the problems affecting her left arm, the accident had an immediate impact on her ability to work. She lost confidence in herself, her appearance and her willingness to drive to the Renfrewshire area. As time went on she did not want to socialise or for anyone to know the extent of her disabilities. She would have wanted to work full time until she was 65. She was 54 at the date of the accident and by the date of the proof she had ceased to work in Renfrewshire and was employed in Ayrshire.

[13] A number of matters can be held as established since there was no dispute about them. The accident was in January 2003. By November 2004 she was found to be suffering from Parkinson's disease. It is accepted that the physical injuries she sustained in the accident were (fortunately) minor and for these alone a relatively small amount of damages must be made. If, however, Parkinson's disease was caused or triggered by the accident a significantly greater award of damages would be justified. There are a number of other facts, medical and otherwise, which are not seriously in dispute and I will deal with these as they arise. One thing I am clear about is this. The proof is not a scientific inquiry into whether this condition can be caused in general by a high impact road traffic accident. I have to decide a different question which is whether the onset of the condition to the pursuer was caused by the accident. That is a much narrower question and can only depend on the evidence put before me. It is not for me to speculate about what other evidence might have been led or evidence I would have liked to hear.


[14] Having set out in summary what was the medical evidence about P.D. I now turn to the areas of dispute and there are a number of these. The first is the issue of head injury. Said in this way it seems a simple concept but it is not. It matured into brain injury, head trauma and both of severity from mild through moderate to severe. The learned papers did not speak with one voice on the subject, were open to interpretation and at times seemed to have some internal inconsistencies. I am quite clear in my opinion that unless there is proof that the pursuer suffered a head injury her major claim cannot be proved.

[15] The second area of dispute is as to the correct meaning to attribute to the studies actually produced but not spoken to by their authors. Allied to that is a question as to what to make of studies not produced but whose conclusions clearly appear in review papers. Subsidiary questions arise as to why negative papers were not produced and in general what to make of the methodology of the epidemiologists. The way they go about their research has changed over the years and, of course, the court does not have to evaluate the documents and questionnaires relied on by them to produce their results and statistics. Since none gave evidence the testing of their conclusions cannot be scientifically accurate and has to be a matter of impression. There is of course a legal test given to me to apply.

[16] Before leaving this subject I should say a little about it in general. Medicine is not a pure science. It is an applied science. That means that when medicine is in issue legal advisors have the difficult task of deciding how high and how far to pitch their case. Do they rely only on doctors? Do they need to lead the background medicine of the epidemiologists? To do both can almost lead the court unwittingly into a kind of satellite litigation on issues away from the pursuer's case. Sometimes that will be necessary, sometimes not. There are at least two recent examples in Scotland where lengthy and expensive litigation over a long period resulted. There is also a separate matter in all of this which cannot be overlooked. A claim such as this is at the frontier edge of causation. The condition is known to be idiopathic, and as a matter of law and medicine the causing is not as obvious as it would be with purely physical injuries and well known and researched diseases. Even these latter e.g. pneumoconiosis were once the subject of speculation and research. Here it is a matter of minute cell anatomy within the mystery that is the human brain allied to bodily beneficial chemicals which allow us all to move with ease. The court has to be careful and circumspect in the interests of all, pursuers, insurers and the development of the law of reparation. Otherwise what is being sought is described as "quite a leap", a "reach" or "a bridge too far" (my own words).


[17] When looking at any conflicting medical opinions in this case I have to consider the epidemiological basis on which it is founded. The proof of the case depends upon studies which may show a link to head injuries causing the disease. That of course is not quite the same question as whether it accelerated an already pre-existing condition. However, leaving that aside for a moment what is the proper test to apply to such studies. It is to be found in the Opinion of the Court in Main v Andrew Wormald Ltd 1988 SLT 141. In the first place it is clear that medical witnesses are entitled to refer to medical literature in their field including papers by epidemiologists even though they themselves are not epidemiologists. Indeed it is part of their duty.

[18] Such material has to be looked at critically because without the writer it cannot be cross-examined. Also if a witness (as here) adopts a published work or a passage from it the Court has to determine whether the work or the passage is convincing or not. For the science to be an important factor it has to be "intelligible, convincing and tested" (Lord Cooper in Davie v Magistrates of Edinburgh 1953 SLT 54 at 57). The Court also has to be sure that the experts have drawn the correct inferences from the studies. The personal experience of both experts in this medical field is not an issue. Nor do I think that in every case it would be necessary to call as witnesses epidemiologists. If that became widespread it would simply result in much satellite litigation.

[19] I was referred to three main authorities on how to approach the question of proof in a case of this kind.

[20] In Bryce v British Railways Board, Outer House, the issue was whether trauma to the head had accelerated multiple sclerosis from which the pursuer was already suffering. The Lord Ordinary was Lord Prosser and any opinion under his hand must be accorded the greatest respect. A railwayman had been injured while working under rolling stock. He struck his head in a confined space between the tracks on a part of a ballast cleaner. On liability, the Lord Ordinary found fault and for the unpleasant though minor injuries, a moderate sum of damages was due. However, the main issue argued was whether the head injury made a pre-existing multiple sclerosis deteriorate (see p.6 and 7). There was a complication of a head injury ten years previously. The case is, of course, very different to the matter before me, but I am principally interested in the type of evidence led before the Court. It consisted of two clinicians (one of whom gave evidence to me). There was no evidence then (1994) from any epidemiologist but documents were lodged of studies from eminent people whose work was quoted later by them in Dingley viz McAlpine, Poser and Sibley (p.26/28).

[21] It appears that both doctors made reference to the literature in a limited and general way directed to the question of whether there was a causal relationship between exacerbation of multiple sclerosis and trauma. The Lord Ordinary had to consider that, other causes (eg electrocution), anecdotal evidence of a link and coincidence. From what was placed before him, his analysis had to be generalised. From it all he concluded thus (p.32/3)

"... my impression is that trauma ... can and does on occasion cause a significant relapse or deterioration in multiple sclerosis. I do not regard this as certain but I do see it as probable. That being so in any individual case, trauma is at least a possible cause of a discovered deterioration, the actual likelihood depending on a number of different circumstances ..."

The problem for the pursuer was that at his age, what happened to him was not abnormal or beyond the range of what one could expect. That range had to be fairly board and inspecific. Lord Prosser found that his deterioration in the time frame was not so unusual or unexpected as to identify trauma as the probable cause (page 34). The defenders were only responsible for the minor results of the injury and no more.

Dingley came later, by which time the evidence was more, more detailed and more complex. As will be seen, Lord Prosser with better evidence would find again on the same legal tests, that trauma could trigger multiple sclerosis.

[22] Dingley v The Chief Constable, Strathclyde Police 1998 S.C. 548, was a case concerning multiple sclerosis. The Inner House were of the view that the Lord Ordinary had failed properly to analyse the evidence and reach a view on divergent opinions. The Lord President then undertook that task.

[23] Much was said about this case by both sides and the defenders' Counsel read most of it in Court. Out of respect to the work put in on this authority I must say something about it. In the first place it concerned multiple sclerosis not Parkinson's disease. In the second place, the kind of proof led in the Outer House was quite different to what was led before me. In Dingley the pursuer's witnesses were a mix of eminent doctors who had clinical, research and epidemiological experience; the defenders leading three witnesses of similar experience. It was criticised that no statistician was led and no illustrated anatomical texts were provided to help the Court. (Commenting on these pages 557/8 the Lord President said that he hoped this would be done in future. It was not before me). By the time the case reached the House of Lords they were faced with some conflict of opinion in the Inner House. They found it necessary to have a procedural hearing (2000 SC (HL) 77 at 82E), exchange of written cases, out-line arguments and an appendix containing excerpts from two medical text books and other matters to be agreed. It was pointed out that the Lord Ordinary had none of these advantages. I have considerable sympathy with the late Lord Dawson faced with the case he had. It lasted many days and was subject to lengthy adjournments.

[24] Though the medical condition in Dingley was different, the facts raised issues not dissimilar to what I have been asked to decide. There were broadly two questions, one medical and legal viz could the trauma cause or accelerate the disease as a matter of medical science and then did it cause it in the case before the court. To both of those the Court had to apply the standard of the balance of probabilities which is a low test. The Lord Ordinary had evidence of clinicians and epidemiologists on the various papers presented. So far as the latter were concerned, the single judge ought to have been sufficiently instructed by them on their discipline methods and conclusions to enable him to draw his own conclusions about the subject matter and what if anything can be taken from it. I have no doubt that Lord Dawson well understood all the technical matters laid before him. However the Court was of the view that his expressed analysis and preference was not sufficient. In the result the whole evidence was examined in detail again. The Lord President devoted many pages to this and his analysis is a master class in legal exposition of very complex matters. That opinion and those of the other judges received the highest praise from the House of Lords (see Lord Hope at page 81G) (such a detailed exercise was carried even further in McTear as I will take up in due course).

[25] However, there is one matter about Dingley which causes me concern. It is that the judges in the Inner House were not unanimous in their reasoning on all points, though concurring in the result. This may make the ratio of the case less clear insofar as it is binding on me. It can be put in this way.

[26] On the medical question, the Lord President having found that trauma could never trigger MS, did not deal with the legal question. Lord Caplan agreed on the medical question but said that he had found the other way, he would have found for the pursuer on the facts. Lord Prosser found that trauma could trigger MS but it did not do so in the pursuer's case. In the House of Lords, the only issue was whether the Lord President had taken the correct approach to the evidence. They held that he had. What I take from Dingley is this. The Court has to undertake some analysis of the medical and scientific evidence and only with the assistance of the experts. I also think the case shows that epidemiology alone can never prove an individual case. It also shows that care has to be taken where expert opinion is divided, where there are alternative explanations and where coincidence is a factor. Like the pursuer in the present case Dingley probably had his condition before his accident (p.563).

[27] In McTear v Imperial Tobacco Ltd 2005 2 SC 1 the issue was whether smoking cigarettes had caused lung cancer in the pursuer's late husband.

[28] The facts and problem (smoking and lung cancer) were quite different to the present case but the principles in law were the same. A number of experts including epidemiologists gave evidence. The judge had to deal with what evidence the parties chose to put before him and it is obvious that the case had international importance. Most of the evidence was complex, detailed and highly technical. A great deal of it concerned epidemiological studies. Most of the opinion was devoted to the most careful and exhaustive and necessary analysis of that. Indeed the whole case itself occupies one volume of Session Cases.

[29] The tests which were applied were those enunciated in Dingley and which I have to follow. I observe again that the kind of evidence before the Court seems to me to be becoming satellite litigation. Although the correct (and lower) civil standard of proof was correctly applied by a very experienced judge it must have been a problem to disentangle this from the scientific standard adopted by some of the experts.

[30] It is quite clear that Lord Nimmo Smith preferred the clear evidence of the witnesses Idle and Cohen (para.6.152/3) to that of Doll, Hastings and Friend. I detect a note of disappointment with the way their evidence was given disclosing, as it apparently did, a degree of ad hominem rivalry.


[31] Mr Smith in opening the hearing invited me to find in favour of the pursuer on all issues. Liability was admitted and the real issue was what he called "the link". The symptoms were accelerated by the accident not caused by it. The Court had heard about two distinct conditions viz Parkinson's disease and Parkinsonism. This case concerned the disease which was a neurological degenerative disorder affecting nerves in the "substantia nigra" area of the brain and causing a dopamine deficiency.

[32] The Court should not be concerned to seek a medical truth overall about Parkinson's disease, but only about this case. The papers produced are all about causation not manifestation. As to causation there was some support for mild trauma causing it, the experts had filtered the papers, and produced only the ones they thought important. The context of the study was limited to causation not acceleration which was a different question.

[33] The mechanism had to be known. If mild trauma could cause it could greater trauma accelerate an existing condition.

[34] Counsel continued by saying that there has to be acceptable evidence that the pursuer had sustained head trauma. It was also important to take note of when depleted levels of dopamine would become symptomatic. Some would exhibit signs of a level of 70 and everyone at 40 although the reasons were not fully understood. He again emphasised that the case was about accelerating the condition in someone predisposed and not about causing the condition. It was all a matter of opinion from the literature together with a mechanism and backed by the experience of the witness. Grosset saw many more patients than the Professor now did. His expertise was not in doubt. Under reference to various passages in Volume 5 of the evidence it was all a mater of post hoc ergo propter hoc.

[35] Mr Smith then moved to look at the recent literature produced saying that it was not for the Court to review the literature to see whether it justified the point in issue. All the articles were responsible and respected. They had never been criticised. All conclude that there may be a link as to progression and even cause. Counsel at this point summarised his view of Professor Bone by saying that the witness, without seeing the pursuer accepted that the literature showed causation could occur but not in this case. Grosset on the other hand was sure. This was not like the multiple sclerosis debate where there were two opposing camps.

[36] As to the papers the Court should have no regard to papers not produced. Grosset had referred to the papers by Semchuk and Stern. What was important was brain injury (not head injury) and the symptoms. The pursuer exhibited three symptoms viz dizzy sickness, personality change and weakness in her arm soon after the crash. One of these was enough according to Stern.

[37] Counsel referred to the evidence concluding that the pursuer's brain must have moved when her head hit the restraint. The degree of violence did not need to figure on the Glasgow Coma Scale. As to the papers they were as recent as 2002 and in respected journals. The ones in the pursuer's favour had never been criticised. As to the mechanism of causation Mr Smith said that damage anywhere along the dopamine route could have occurred. Such required a brain stem injury. The nausea and dizziness were symptoms of this. A question then arose as to how quickly all of this had accelerated the disease. Given that she already had the condition the range of acceleration at her age of 54 was between one and a seven years. The mid point was appropriate i.e. 3.5 years. She wanted to work until 65 and might not have been symptom free to 61 but would probably have ceased work at age 611/2. There was thus a wages loss for 31/2 years.

[38] Counsel then looked at the authorities in some detail beginning with Dingley. He accepted that the facts and the conditions were different. There were two distinct camps of medical thought. Various passages in the case were read especially on the need to address the scientific evidence. This was a civil proof not a medical one and the barrier should not be set too high (Lord Prosser at 602/3) Bryce was referred to, to a lesser extent.

[39] Counsel then looked at damages with reference to his written submission. He invited me to put the case out By Order with the opinion for a discussion on interest.

[40] Miss Shand in opening for the defender submitted a written argument which I refer to for its terms. In addition she made the following points.

[41] The main issue was whether the accident caused the onset of Parkinson's disease or not. If it did not then solatium would be in a modest sum plus agreed outlays. There was, however, no evidence that the accident had accelerated the disease. There was no causal connection and no studies, scientific, animal or other, vouched it. The learned papers do not establish acceleration nor do statistics prove causation. Dr Grosset was not an expert in head injuries or in epidemiology and the pursuer should have led an epidemiologist. There had to be evidence about the papers being tested otherwise Dr Grosset was merely an advocate. Counsel referred me to McTear at various passages, particularly pages 135 and 140. In Dingley evidence was led to allow the Court to form an opinion. There was a body of medical evidence but that was not enough. There was no such detail in the present case. Counsel examined Dingley at many places and read much of the case to me. The onset in that case of multiple sclerosis was more sudden. Counsel drew my attention to the different approach taken by Lord Prosser in Dingley to that of the majority. She also read from the subsequent appeal to the House of Lords.

[42] Counsel noted that all the studies which had been referred to and relied on by the pursuer were produced by the defender. They dealt with a different question and not the issue of acceleration of the disease. Dr Grosset could not say that the pursuer would not have got the disease if there had been no accident. The studies produced did not show causal connection beyond statistics and coincidence.

[43] I should briefly summarise what counsel said about the various studies. She began by noticing that "head injury" varied widely, and where the categories were broad it was less easy to see where the facts fitted in. Here it could not be suggested that the pursuer had suffered any serious head injury. The Stern paper depended on a long time lapse. Factor and Weiner looked at a smaller number of controls. Semchuk was vitiated by observer bias. Lai was a review paper not a primary study. Bower studied small numbers but again depended on a long time log.

[44] Counsel then looked again at Dingley and said that where medical opinion depended on a theory, that theory had to be capable of testing. Where the theory or area of expertise was not in dispute then normally it would be a simple question of preferring one expert over another. Here, however, that could not be done since the very science was in dispute. That was also compounded by a failure to prove any brain injury.

[45] In the reply to the defenders Miss Munro tendered a written submission which I refer to for its terms. In her argument to the Court she urged the following points upon me. There was nothing in the decided cases to compel a finding that the pursuer here had not discharged the onus resting on her. There are two proper questions. Could Parkinson's disease ever be caused or symptoms accelerated by head trauma? Did that occur here? Dr Grosset was entitled to base his opinion on the epidemiologists and the statistics and Main was Inner House authority for that (see also McTear 5.12 and 5.15). There was very little written material on the point and it was proper to refer to it. There were other studies mentioned but no evidence was led about them. The studies founded on were not criticised and that was all the Court had to go on. The witness was entitled to form a view on the studies and where the precise cause of the disease was not known as a scientific certainty the Court had to work to the lower threshold of probability, and marginal probability was enough. Counsel referred me to Bryce at page 15.

[46] Here the trauma unmasked the Parkinson's disease. Grosset did not deviate from his view and what he said was not just an oracular pronouncement. Medicine was an applied not an exact sentence. This pursuer was in a better position than the pursuer in Dingley where the anecdotal evidence in clinics was contradicted by the learned papers. McTear only had epidemiology with no experts on cause and effects. The Lord Ordinary rejected the pursuer's experts as not being objective. Anecdotal evidence is not worthless and here there is also epidemiology. The defender's expert concentrated too much on the general question of "can it cause" and did not address the other of "did it" in this case. Dr Grosset, on the other hand, had properly "mapped" the pursuer and taken account of the "coincidence" theory.


[47] In one sense in this case the answer to it all is simple or it is not. Can it be said on the evidence that the pursuer has proved that she sustained any kind of head injury or not. I am quite clear that there is no direct evidence by word or document that she did. If she did it has to be a matter of inference from facts and circumstances. How then does the evidence lie. I begin with the pursuer. She described her pain which was in her neck and lower body. She felt sick and was dizzy. That is not a description of a blow to the head. However, she was wearing a seat-belt and her seat had a head rest. Given the speed of the impact it is likely that the back of her head struck the head rest. I am prepared as a matter of commonsense to infer that that probably happened. It is also possible of course that only her neck would suffer injury and that is consistent with what she said, her pain and the evidence of the surgeon, Mr Tait. The Hospital Records at A & E Crosshouse do not show head injury. The admitted Glasgow Coma Scale of 15 is inconsistent with head injury (both experts agree on that, see e.g. Grosset - vol 4, 129, Bone vol 5, 118/125) and the pursuer made no claim of any head injury when she saw Professor Bone (volume 5, p.117). It seems clear then that there was no objective evidence of head injury at the accident or at Crosshouse Hospital and no complaint by the pursuer then or subsequently. It may now be an analysis of the obvious but on this evidence it is impossible to conclude that the pursuer did sustain any head injury.

[48] If, however, I am wrong on this point a head injury would have to be inferred and the inference would have to be a reasonable one based on the facts and circumstances of the collision. Let me assume this in her favour, though to do so poses many new questions. As the learned papers interpreted in the evidence show there is no consensus as to what kind of head injury would be relevant for the purposes of causation. It would have to be one sufficient to result in damage to the dopamine producing cells in the substantia nigra in the brain and make them unable to produce dopamine in sufficient quantities. My impression from the evidence about the papers produced is that such a head injury would have to be categorised as a brain injury and probably of at least moderate range if not severe.

[49] The evidence which is purely medical in this case is not in dispute. It was given, on the main issue, by Dr Grosset for the pursuer and Professor Bone for the defenders. Both are eminent clinicians in this area of medicine. It is possible that Dr Grosset has more recent and extensive experience of Parkinsons Disease since the Professor has retired. However the experience is really the same. Both gave evidence in a moderate, restrained and thoroughly professional manner. Between them there was no ad hominem element which surfaced in some of the experts in the cases cited to me. It is difficult to prefer one over the other. That problem may be solved, however, in relation to the epidemiology which was central to each of their opinions.

[50] I hold it established that the pursuer had symptom free Parkinsons Disease before the accident. (See Grosset Vol.4 p.14/15). After the accident she showed symptoms which I have already described and in November 2004 Dr O'Leary diagnosed the condition which a brain scan confirmed early in 2005. The relevant records from the hospital are only agreed to be what they are but there is no reason to think they are not accurate. The doctor's letters of 15 November 2004 and 10 January 2005 confirms the worst fears with dopamine loss and classic body dysfunction and tremor as described by him. Dr O'Leary was not a witness and it might have been useful to have had his view. However, Dr Grosset's report makes it clear that the issue is causation. He concludes, as he would have to, that the pursuer must have had a sufficiently severe head injury which caused the manifestation of the pre-existing condition. He reaches that conclusion from the later symptoms. In other words he makes the reverse reasoning spoken of by Lord Prosser in Dingley at page 609 ("consequences back to cause"). Secondly, he is prepared to conclude from four of the studies (Lai, Factor, Semchuk and Stern) that there is a link between head trauma and Parkinson's disease. Whether that relates to pure causation or to unmasking of pre-existing Parkinson's disease is not clear in his report. The whole matter was expanded upon in his evidence to which I now turn in summary. At the risk of repetition I also give his view on the studies elsewhere.

[51] The doctor had to address the precise mechanism of the worsening of the pursuer's condition. I have looked carefully at my notes and the printed evidence but I cannot find anywhere a medical diagnosis of why there was found dopamine deficiency in this pursuer. The best that is said is that the blow to the head (assuming there was one) does something to the brain. (See his evidence for example Vol.4, page 15 onwards). That is not an understandable clinical diagnosis. It may be, that with the state of medical knowledge no precise statement of causation can be made. (See also his evidence in chief Vol.3, page 26 onwards).

[52] Dr Grosset admitted that for causation he had to rely on published epidemiology papers, especially four of them produced to the Court (Vol.3, page 30 onwards. Vol.4 page 16 onwards. (I am satisfied that in cross Miss Shand fairly, and at length, put the defenders' contrary argument to the Doctor in general and in particular). He accepted that his choice of papers was selective in favour of his theory (see Vol.4, page 118). As I have said in more detail elsewhere I cannot accept that I have been furnished with enough material about those studies to make an informed decision about their validity on the general question of head injury and link to Parkinson's disease and that is fatal to the facts of this case. Dr Grosset was driven to agree that the link was not "clear" (Vol.4, page 107) and was "controversial" (page 123). As to the coincidence factor he admitted (page 23) that he could not say that the pursuer would not have developed the signs of the disease when she did even with no accident.

[53] I am conscious that parties may think I am being selective in the Doctor's evidence, but nowhere can I find that he was or could be dogmatic about the link. In that situation the case for this pursuer on the main issue is simply not proved.

[54] What then was Professor Bone's position since he also saw the pursuer and furnished a report (No.7/1). The report is short and is mainly concerned with the question of whether there was any head injury and whether, if so, that could accelerate Parkinson's disease. His finding is that there is no evidence of head injury, only injuries to the soft tissues of the neck and back. In relation to causation he was of the opinion that a serious head injury could increase the risk but there are other factors more significant. He concludes that there was no relationship between the accident and earlier presentation of Parkinson's disease.

[55] In his evidence he confirmed that position. In chief he emphasised two points of importance. In the first place (Vol.5, page 166/7) he said that there were no studies about acceleration due to head injury. That matter was never disputed. At the same passage he said that the papers look for a head injury early in life with manifestation later in life. That is what the papers call the time lag. Here the time lag is very short with symptoms appearing within months.

[56] Much of the remainder of his evidence dealt with the papers as I relate. He made the interesting point that with Parkinson's disease the literature on head injury is not nearly as extensive as it is for Multiple Sclerosis where there is an "enormous literature". He stressed that it was important to be able to classify head injuries carefully before any conclusions could be drawn. Where I found his evidence most impressive was where he dealt with mechanism at Volume 6, page 215. He said, and I accept this, that unless a mechanism is known there can be no link of causation from head injury. He did, however, concede earlier that if there was proof of direct brain damage or breach of the blood brain barrier then acceleration of Parkinson's disease was possible (Vol.6, page 100). Dr Grosset was less inclined to look for or speculate about mechanism and on this issue I prefer the Professor. I do not see how causation can arise with this pursuer unless a mechanism is known. As I have said already, that may be beyond the current medical knowledge.


[57] Let me now move on to deal with the evidence of the epidemiological studies. There were eight of these produced and spoken about. They were all defenders productions and were properly put as a package and in detail to the pursuer's expert Dr Grosset. Often very lengthy passages were read, and comment invited from the witness. None of the authors of the papers was called as a witness. I should add some observations established in the evidence. It was not a matter of dispute that these articles appeared in learned medical and scientific journals. Both experts commented on these individually but I heard more (unchallenged) detail from Professor Bone (see Volume 5 pages 108/9). The articles are "peer reviewed" before publication. The more prestigious the journal of publication, the greater the impact of the research. Both experts attached importance to the methodology of the research which was mostly not known in any detail. That is where evidence from the writers would have helped. Plainly any conclusions depend on the quality, depth and extent of the research and the minimisation of any bias inevitably occurring.

[58] I now look at them individually in their order. All were located by computer research by both experts.

[59] The first is No 7/3 of process by Lai and three others dated 2001. It is Canadian Review article.

[60] Next is an article dated 1999 in the American Journal of Medical Genetics by Taylor and six others. It is No 7/4 of process. (Not used)

No 7/5 is an article in Neurology, May 2003 by Bower and five others.

No 7/6 is by Lui and others in Environmental Health Perspectives 2003.

No 7/7 in a French Journal by Lus (1997). (Not used)

No 7/8 is a study by Semchuk, Love and Lee in the journal Neurology (1993).

No 7/9 is an article in Movement Disorders 1999 by Factor and Weiner.

Finally No 7/10 is by Stern and others (1991) in Arch Neural.

[61] I begin with the Report of Lai and others published 2001 by Elswier in Canada. It has eight pages of actual text. It provides an overview of occupational and environmental factors which may be linked to Parkinson's Disease (P.D.). A number of factors are looked at including "head injury".

[62] Head injury is written up in paragraph 2.5. Any link is said to be "controversial". It suggests that any head injury in some of the studies would have to be "severe" and even amounting to "brainstem haemorrhage". It then goes on to distinguish the different syndrome experienced by boxers and categorised as Parkinsonism (often called the punch drunk syndrome).

[63] As to head trauma it concludes that the link is unclear and reports in a number of cases have to be interpreted with caution due inter alia to the different definitions of head trauma. It is a tentative and inconsistent link requiring more study and agreed methodology. There seem to be clearer links to family history, rural living, farming well water drinking and exposure to pesticides. Smoking is an inverse risk factor.

[64] On table 4 (page 303) are listed thirteen case-control studies. Three were produced to me as will appear. Some nine of these show no significant difference between patients and controls. None of these were produced so I cannot examine them. What then did the experts have to say. Dr Grosset accepted that this was a review paper in a journal of reasonable quality. He had to accept that in this review paper there was mention of a number of studies which showed no association with Parkinson's disease (Vol.4, 105 onwards).

[65] The Professor (Vol.6, page 4) was of the view that this paper showed that it remained unclear that head trauma might be a factor in the development of Parkinson's. While discussing this he was drawn to the Bower paper to which he attached greater importance.

[66] Liu's study is No.7/6. Again it is American in the Environmental Health Perspective Issue of June 2003. It does not deal with head injuries and the report was not pursued after an objection in the re-examination of Dr Grosset.

[67] The paper by Factor and Weiner (No.7/9) 1990 (Movement Disorders) deals only with head trauma. In the article many of the other papers are discussed.

[68] This raises a number of problems and the authors fairly concede (page 228 both columns) that the methodology contains flaws and further studies are needed. It seems to me to be of importance that there is a report of head trauma damaging the substantia nigra (See footnote 9 which refers to Jellingar's letter). None of that material has been produced. The role of head trauma has to be regarded as tenuous.

[69] Dr Grosset looked at this paper (Vol.5, page 3) though at the end of his cross examination it was not wholly clear what he made of it. He did say there was no analysis of a short time lag from trauma and that the causative effect was not shown on a balance of probabilities. At best he said if there was brain injury there was an inference of association but in the present case there was no evidence of brain injury.

[70] Professor Bone (Vol.5, 186) was critical of the paper since he did not know the questions asked in the survey. At the end of his cross examination on the paper he stressed that it was essential to know a mechanism and be able to "map" that on to any acceleration. He was unable to see how medicine could achieve that.

[71] No.7/8 is an excerpt from Neurology 1993. The article is by Semchuk and others. It is not entirely clear in the article what the writers mean by head injury. At one place "serious head trauma" is used and in other places merely "head trauma". The conclusion is that head trauma significantly increases the risk of Parkinson's disease. The writers do not offer any theory which identifies the specific causative gene or agent involved in the development of Parkinson's disease. More research is needed. Two more negative studies are specifically mentioned at page 1178 (Tanner and William). Their methodology was, however, criticised.

[72] This article and all the others acknowledge that many other factors can be associated with the disease.

[73] What I think is important about Dr Grosset's evidence about this is that the text does not make clear what is meant by head injury (Vol.4, p.223 onwards).

[74] Professor Bone did state that the journal neurology was of top quality but was critical of the article as it did not define head injury (Vol.5, at 168). Again he thought it important to note that the causes are thought to be multi-functional (p.175).

[75] The Report by Stern and others (No.7/10 of process) 1991 Arch Neurol is an American publication. It looked at what environmental agents might act as neurotoxins to destroy neurons in the substantia nigra. Head trauma was considered inter alia and categories of that with fairly serious consequences are discussed at page 904. These include dizziness and personality change (of importance in the present case). The problem with this study, even on an uninformed reading, is that the statistics and calculations cannot be within judicial knowledge to understand. The conclusion at 906, column 3 is that head trauma may be one of many risk factors to induce the complex and unknown chemical events that cause nigral cell death and Parkinson's disease. Before that there is mention of other studies suggesting that trauma of different kinds can worsen Parkinson's disease.

[76] Dr Grosset broadly agreed with this report but was unable to explain the symptoms as related to head injury. The passage at Vol.5, page 25 onwards show the risks of generalising on the effect of one symptom, eg dizziness. He also said that none of the papers have definitive evidence on mechanism (page 29). Professor Bone (Vol.6, page 217) was critical of the study where it did not break down the categories of head injury by symptoms and relate them to the disease.

[77] In the Neurology journal (May 2003) is an article by Bower (No.7/5 of process). It addressed only head trauma. The authors recognise that only a small number of subjects were studied and the study relates to causation not acceleration. They recognise (page 3) that there are three types of head injury and (page 4) the association was restricted to the more severe cases (by which they meant the symptoms described on page 3 none of which were found in the pursuer). The writers found a long time lag between trauma and onset (median 29 years). The authors offer a theory of causation viz possible lowering of nigral neurons, disruption of the blood brain barrier with delayed nigral degeneration and thirdly overexpression of proteins causing cell death.

[78] The conclusion is that the results suggest an association between head trauma and the later development of Parkinson's disease.

[79] Dr Grosset did not deal with this document in his report but it was put to him (Vol.5, page 87) briefly without significant comment and then departed from. The Professor on the other hand thought it was the best of the papers, up to date and from a clinic with an international reputation. He attached importance to the suggested mechanisms, adding that there may be ones of yet unknown (See Vol.6, 44 and following especially 51, 164 to 173 in cross). The Professor seems to accept the possible link to causation if the trauma is severe enough but not otherwise. The difficulty he sees in the individual case is mechanism. The background of the Bower paper discusses mechanisms (three possible) and the Professor's final word (215/6) is that, without that being shown causation cannot be shown.

[80] What then is to be made of this chapter of the evidence which is crucial to the general medical question and, of course, overlaps into the pursuer's circumstances. In the first place I have some sympathy with both Dr Grosset and Professor Bone who were outwith their chosen discipline and abroad in the field of epidemiology which depends on its own experts, methodology, statistics and conclusions. Built into all that are problems described in evidence as observer bias, recall bias and other technical terms. The way questions were put to them may not have assisted. At times long passages were read out to them upon which it was plainly difficult to give a meaningful answer. I feel that many of the problems might have been helped if the authors of the reports could have been called and there had been some statistical evidence. Without that the judge is at once disabled from being able properly to evaluate the worth of the study or to draw the proper conclusions.

[81] My conclusion is that the experts were unable to explain the studies which seem to me to raise more questions than answers. On the narrow issue of "head trauma" there is, on paper, no clear consistency of what that means and any link with causation is at best controversial. There is no study to provide any conclusion on "early manifestation" of a pre-existing condition at all. In that situation even on the low standard of proof on the balance of probabilities, I have to hold that it is not established that there is any link between head trauma and any onset of the condition. It may be that in the future more and better studies will make that link and also concentrate on the mechanisms hinted at in the Bower report. In particular an insult to the blood brain barrier may be important since I understand that can be clinically detected. There is of course no such evidence in this case. Another matter of concern is what the reports speak of as, "a long time lag". That is absent in the present case.

[82] There are some other matters which confirm me in the foregoing conclusion. It is clear from at least one of the overview studies (Lai) that a number of studies exist which assert no link to head injury. I am surprised and slightly critical that I was not instructed in these. I cannot draw any conclusion from them save to note that they exist. They are only important in the context of what was produced not even being sufficient in law. It is also important to take account of the fact that there are many other factors which can be relevant to the onset of the disease. All these things matter in a condition which is idiopathic.

[83] Let me say one final word about head injury. Dr Grosset was, I think, attracted to reason that there must have been a head injury because of the supervening Parkinson's symptoms found soon after. That reasoning from symptom back to cause has the powerful sanction of Lord Prosser in Dingley as being valid in logic. I could not agree more but it will not do in this case because of the complete absence of evidence or complaint at the time and the evident presence of the neck and back injuries. It would also be a bridge too far to infer from the symptoms "severe" head trauma.


[84] There remains one final issue which is the matter of damages. Parties were agreed that if the pursuer was not to succeed on the main question of Parkinson's disease she was only entitled to a modest sum of damages for the minor injuries suffered in the accident. Those I have already described in relation to the evidence of Mr Tait. To that may be added the findings of Dr Susan McLaren about Adjustment Disorder and a Phobic Anxiety relating to driving. I accept Dr McLaren's evidence about these unpleasant conditions but, of course, her supervening Parkinson's condition is now bound to contribute to them. In the event I was asked to make an award of £4,500 for the minor injuries and I will do so. I was told this was a sum inclusive of interest to 30 November 2006. No claim is made for past wages loss for the eight weeks she was off work. There is also a small claim for minor items in the pursuer's schedule amounting to £317 inclusive of interest. It was not seriously disputed that this should be awarded.

[85] For reasons I have already given the pursuer has not succeeded on the main medico legal question. However, if I am incorrect about this it is necessary that I indicate what would have been my award. There was no agreement about what this should be. I was asked to look at awards made in cases of multiple sclerosis but I am not at all sure they provide any reliable guide where the illness is of a different kind. There are a number of other unknown factors. It is not clear on the evidence to what extent the pursuer has made progress with any drug treatment for her condition. She may have gone to Majorca before she was 65. As to her employment, there was no evidence from her employers that she would be allowed to reduce her working hours to the level spoken to in Dr Pollock's evidence and which are part of her quantifications. On the other hand there was no contradictor to the actuarial figures for future wages loss and loss of pension, as matters of arithmetical calculation in the actuarial reports. The properly discounted multipliers are within the correct range. The actual net wage is not disputed. The actuary has allowed for death but not for any other supervening illnesses.

[86] All of these matters, however, have to take account of the question of how quickly her condition might have been accelerated by the accident. Can it be said that she has the symptoms three years earlier than she would have had, given that she already had the disease though latent. It could have manifested itself at any time. On the evidence the whole matter must be one of clinical impression based on experience. Dr Grosset in his report and evidence said he would have expected a manifestation between one to seven years. He has then taken the mean figure of one half. See Vol.3 at 106 onwards passim. Professor Bone did not deal with any such detailed figures but my impression of what he did say was that if you already had the latent condition it was near impossible to predict how soon it would become manifest.

[87] The whole loss of earnings and pension thus depends on the proposition that her future working life has been gradually curtailed then stopped at age 611/2, due to earlier manifestation of the disease. The whole matter is of course academic but it was nonetheless strongly resisted by the defender's counsel. There are a number of difficulties, which I have outlined above, in the way of making any award. However, I do not think the Court should abandon the task because it is difficult and make no award at all. If there had been a head injury which could have accelerated her condition, then she is entitled to damages. The future financial losses are in my view correct estimates. She was a good and valued teacher and I cannot think her employers would refuse to allow her to scale down her work. The middle or average figure selected by Dr Grosset is based on experience and statistics and seems reasonable to me. I would thus accept (rounded figures) the calculations in the pursuer's schedule at £112,000.00 for future wages loss and loss of pension.

[88] As to solatium there are no reliable decided cases to guide. The disease may become very serious and has already had a dramatic effect on her life both personal and professional all as she described in her evidence supported by Dr Grosset and Susan McLaren. Though drugs may control it in the future is not encouraging for a lady who loved her work and had an active social life. In all these circumstances I do not think an award of £25,000 would have been excessive (apportioned as per the pursuer's quantification). For completeness, I should add that I have made no interest calculations on any of these hypothetical awards to any date.

[89] Now to return to actual damages, the pursuer is entitled to solatium of £4,500 and the small sum of £317. Since time has moved on since the date of avizandum, I will, in accordance with my usual practice, put the case out By Order with this Opinion in draft for parties to agree any further interest on these awards, advise me of it and await then a final decerniture. Meantime all questions of expenses are reserved.

[90] I cannot leave the case without a final word. I am deeply sorry for the pursuer who presented herself with restraint and moderation. She made light of her condition. Many would not have behaved so. I do not doubt that for ever in her own mind, she will believe that the car crash has brought on her misfortune. Some day medicine and science may prove her correct but that is for future generations.