EXP v Barker

The Claimant, (“EXP”) was born on 18 June 1965. She is married with two teenage daughters.

On 5 September 2005 the Claimant was appointed to the role of full-time District Judge, having previously worked as a barrister for about eighteen years. By 2011 the Claimant was sitting as a District Judge.

The Claimant had been involved in a road traffic accident in 1991 leading to discomfort in her neck and back. The Claimant had been referred to a consultant orthopaedic surgeon, Mr Osborne, in November 1991.

The Claimant made a relatively good recovery from her neck and back whiplash injuries within 18 months of her accident in 1991. In 1997 the Claimant suffered a recurrence of the problems in her neck after a toddler jumped on her and pulled her neck awkwardly.

In about March 1999, whilst working as a barrister in court, the Claimant experienced an episode of visual disturbance that lasted approximately 90 minutes. The Claimant was taken to A & E at the Queen Alexandra Hospital in Portsmouth, where her vision returned to normal and she was advised to see her GP for further investigation.

The Claimant attended at her GP on 4 March 1999 and was privately referred to Mr Harley, consultant orthopaedic surgeon, with symptoms of longstanding neck pain extending into the back. The Claimant was seen by Mr Harley on 24 March 1999 at the Wessex Nuffield Hospital in Chandlers Ford. Mr Harley made a provisional diagnosis of spinal spondylosis and organised an MRI scan on the spine. In his letter to the Claimant’s GP of the same date, Mr Harley went on to comment that: “I am not happy that this explains her double vision and her incoordination could be primarily a neurological problem, rather than a mechanical compression. I think there must be some concern that demyelination is a possible diagnosis. I have therefore arranged for her to have an MRI scan of her brain, visual evoke potentials and have checked her routine bloods. I will see her again once we have the results”

The Claimant subsequently underwent an MRI scan of the lumbar spine and MRI scan of the brain on a private basis. The Claimant retained the original packaging for these scans, which indicated by way of annotation that the MRI of the lumbar spine was reviewed by Dr Vince Batty and the MRI of the brain by the Defendant, Dr. Charles Simon Barker.

Dr. Batty and Dr. Barker were both consultant radiologists working in Southampton at that time. Dr Barker had specific expertise in the reporting of brain scans.

On about 12 April 1999 the Claimant saw Mr Harley again to discuss the results of the MRI scans. At this consultation, the Claimant was told that she had the hb57 gene for ankylosing spondylitis and that the MRI scan of the lumbar spine had revealed multi-level degenerative changes. As a result Mr Harley recommended referral to a consultant rheumatologist.

Mr Harley told the Claimant that her brain scan was entirely normal. In his letter to the Claimant’s GP dated 12 April 1999 Mr Harley confirmed: “I am pleased to say that her brain scan is entirely normal and so I think this rules out any demyelinating problem”.

On 8 September 2011, some 11 years later, the Claimant had returned to her home after a judicial training course in London and then proceeded to go downstairs with her daughter to do an exercise DVD together. The last thing that the Claimant can remember is complaining of a headache, following which she collapsed and lost consciousness.

The Claimant was taken by ambulance to Accident and Emergency at the Queen Alexandra Hospital in Portsmouth where the Glasgow Coma Scale was noted to be 4 on arrival (having been 3-4 upon attendance of the ambulance crew).

A CT brain scan was performed which revealed a 5 x 4.5cm acute parenchymal haemorrhage centred on right temporal lobe with a 2½cm shift from the midline. The appearances of the scan were reported as most likely representing a right sided middle cerebral artery (MCA) aneurysm that had ruptured.

The Claimant was then transferred to the Wessex Neuro Centre during the early hours of 9 September 2011. A CT angiogram taken at 01.29 hours on 9 September 2011 revealed a partially thrombosed aneurysm originating from the right middle cerebral artery.

Emergency surgery was carried out by Mr. Duffill (consultant neurosurgeon) who identified a large clot in association with a bi-lobed aneurysm which was partly calcified. Mr Duffill proceeded to clip the MCA aneurysm and evacuate the haematoma.

Further CT scanning post surgery revealed a right sided haematoma and associated MCA aneurysm. The appearance of the aneurysm was noted to be complex with features of local arterial dissection.

The Claimant was discharged home on 30 September 2011 into the care of the Community Stroke Rehab Team. The Claimant now suffers from a range of disabilities, including a left homonymous hemianopia (left field visual field loss causing 50% blindness); left sided hemiparesis; paralysis/weakness in the left leg; chronic pain and spasticity; weakness and imbalance; cognitive impairments; impaired speech, hearing, swallow, smell and taste; fatigue; headaches; periodic bowel and bladder incontinence; disinhibited behaviour; depression and panic attacks.

The Claimant was seen by Mr Duffill at an outpatient appointment on 14 December 2011. The Claimant took the 1999 images with her to that appointment and on viewing those images Mr Duffill believed that he could identify on them the aneurysm that had subsequently ruptured. Mr Duffill subsequently wrote to the Claimant’s GP on 28 December 2011, noting the Claimant had brought copies of the MRI brain imaging taken in 1999 to the appointment and that “I think in retrospect one can see that the middle cerebral artery bifurcation on the right is abnormal and that this represents a small aneurysm which was present twelve years ago.”

The Claimant alleges that the Defendant negligently failed to identify and to report the presence of a right middle cerebral aneurysm in his analysis and reporting of the MRI brain scan carried out on 6 April 1999. That is now the only issue in the trial before me. Mr McCullough QC, who appeared at trial for the Defendant having been instructed shortly before trial, no longer pursues the pleaded defence on causation. For completeness, however, I shall briefly mention the Claimant’s case on causation.

The Claimant maintained that, if the aneurysm had been correctly identified in April 1999, the Claimant would have been referred for a neurosurgical/neurovascular opinion. If she had been referred, the aneurysm would have been characterised by means of either CT angiogram or a digital subtraction angiogram and on the balance of probabilities, a bi-lobed aneurysm measuring around 5-6mms would have been identified.

It was then very likely that active treatment would have been offered due to the Claimant’s young age. In 1999 this may have taken the form of either a coiling or clipping procedure. It was most likely that a clipping procedure would have been offered.

The Claimant would have accepted the diagnosis and the recommendation for active treatment. The Claimant would have proceeded to open operation and a craniotomy to clip the aneurysm.

Given that this was an incidental aneurysm that had not ruptured, the clipping procedure would have had a 95-98% certainty of curing the aneurysm and have a largely unremarkable post-operative course and outcome. The Claimant would have returned to her full activities within 6-12 weeks.

The long-term prognosis would have been excellent, albeit her blood pressure and hypercholesterolaemia would have been scrutinised more carefully. Even if the Claimant would not have decided to have the aneurysm secured, the Claimant would have been subject to ongoing surveillance and annual MRI imaging. Given that the aneurysm upon rupture in September 2011 was significantly larger than at the time of the MRI brain scan in April 1999, the ongoing surveillance would have identified this progression and led towards active treatment for the same. On either scenario the catastrophic events of 8 September 2011 would not have occurred.

The issue is now a relatively narrow one, namely, whether the MRI scan in 1999 did indicate the presence of an aneurysm which a reasonably competent neuroradiologist would have identified and reported. The issue, though narrow, has sharply divided the two neuroradiology experts who gave evidence before me.

The Claimant relied on Dr Paul Butler MRCP FRCR. Dr Butler is a consultant neuroradiologist in the department of neuroradiology at the Barts and The London NHS Trust. He also consults privately at the King Edward VII Hospital, Beaumont Street, W1G 6AA. Dr Butler has been a consultant since 1986, holding appointments at a number of hospitals and clinics. He was an examiner for the FRCR examinations at the Royal College of Radiologists, as well as lecturing in neurology. He has made many presentations in his specialist area and has been involved in various publications.

In his report of August 2014 Dr Butler stated:

“As a neuroradiologist one is first and foremost influenced by the clinical details on a request form and initial attention is directed to the regions on the scan relevant to these. There follows a general survey as Dr Barker describes. The reasonably skilled neuroradiologist should include a perusal of the basal cerebral arteries in this survey.

Even taking a sceptical view there is, at the very least, a high index of suspicion of an aneurysm on the 1999 scan, notably study 2, image 33 on that study. I would have expected that a responsible neuroradiologist would have raised this possibility in the report and requested further imaging, notably a magnetic resonance angiogram.

The site of the subsequent haemorrhage was centred this region and, on the balance of probabilities, the aneurysm identified in 1999 was responsible for it.

DISCUSSION OF THE 2011 CT ANGIOGRAM

Because the suspected aneurysm was not characterised fully in 1999 it is not possible to make a direct comparison between the ‘routine’ cranial MR scan at that time and the September 2011 CTA.

Equally it is not possible to comment on the precise shape of the aneurysm on the 1999 MR scan.

By far the more likely scenario is that the aneurysm, which I firmly believe to have been present in 1999, ruptured in 2011 and correspondingly it is extremely unlikely that an aneurysm arising ‘de novo’ in exactly the same location was responsible for the haemorrhage.”

Earlier in his report Dr Butler had depicted image 33, study 2, taken from the relevant MR study, which related to the right sylvian fissure, transmitting the right middle cerebral artery. Dr Butler drew an arrowhead pointing to what he considered was “an aneurysm on that artery and not tortuosity of that artery”. In discussing the cranial CT scan from The Portsmouth Hospitals NHS Trust of 18 September 2011, he said:

“There is a right temporal haematoma intimately related to the right sylvian fissure. There is widespread subarachnoid haemorrhage. There is evidence of raised intracranial pressure with shift of midline structures to the left and effacement of the basal cisterns”.

In referring to the CT angiography from Wessex Neurosurgical Centre of 9 September 2011 Dr Butler observed that it showed a right middle cerebral artery aneurysm in close relation to the temporal haematoma. As to the MR scan, Dr Butler said:

“On such a routine investigation the aneurysm cannot be characterised fully, nor can its size be accurately measured. It is however of the order of 5mm.”

On 6 October 2014, in answer to a question on behalf of the Defendant, Dr Butler sought to clarify his opinion by stating:

“Rapidly flowing bloods in arteries (and blood flowing in patent arterial aneurysm) is displayed as a ‘signal void’ on MRI and is black on T2 and T2 FLAIR sequences.

The middle cerebral arteries travel in the sylvian fissure on each side. In EXP’s case the signal void in the right sylvian fissure is too prominent to be explained on the basis of the normal middle cerebral artery and its branches alone. There is no evidence of undue arterial tortuosity or arterial ectasia on the subsequent CT angiogram and the two sides on the MR scan are different, the left being normal.

A CT angiogram is a special investigation utilising thin axial sections of 1mm to display arterial anatomy in some detail, incorporating 3D.

The MR examination of 1999 was a routine scan with a slice thickness of the order of 5mm. Accordingly the abnormal signal void in the right sylvian fissure is a composite mainly of the aneurysm sac and immediately adjacent arteries. ”

In the Joint Report dated 17 November 2014 Dr Butler maintained his opinion. As to the location, direction and measurements, he said that in the 1999 scan the aneurysm was in relation to the distal M1 segment of the right MCA. It was not possible to determine the detailed anatomy of the aneurysm. However, the aneurysm was likely to be in the order of 5-6mm. The direction was “difficult to determine because of the limitations of the scan”. Dr Butler agreed that on the CT angiogram of September 2011 the (ruptured) aneurysm was “laterally directed from the posterior aspect of the vessel.”

Dr Andrew Molyneux MA MB B.Chir. D.Obst RCOG FRCR, honorary consultant neuroradiologist, University Hospital of North Staffordshire NHS Trust, gave evidence for the Defendant. He was consultant neuroradiologist at the Radcliffe Infirmary, Oxford, from 1999-2004. Among other positions he was an examiner for the MSc degree in radiology, and honorary senior clinical lecturer at Oxford University. His main interest has been in the development of science, practice and techniques of interventional neuroradiology, primarily the treatment of cerebral aneurysms and brain AV malformations by endovascular techniques. The Radcliffe Infirmary was the leading UK centre and had one of the largest experiences in the world in the treatment of cerebral aneurysms by interventional techniques. His curriculum vitae provided an impressive list of articles in peer reviewed journals since 1998, a large number of which covered his special area of aneurysms.

In his report dated 6 August 2014, Dr Molyneux stated:

“MRI scan of Brain performed at Alliance Wessex Nuffield on 06 April 1999. This scan is provided as hard copy images. This scan consists of Axial Dual echo (Proton density and T2 images), Saggital T1 and Coronal FLAIR images.. I have reviewed the findings on this scan and in my opinion there is no abnormality seen in the brain. I am not able to identify any clear evidence of a cerebral aneurysm on this scan. The right sylvian fissure is prominent, with a prominent CSF space. The proximal middle cerebral arteries (MCA) are quite prominent on both sides, and all the vessel flow voids seen in the circle of Willis are quite prominent. I am not able to definitely identify an aneurysm on this scan. The findings on this MRI scan are within the range of normal in an adult patient and I would have reported this scan as such.”

Later in the report, he stated:

“I have received the MRI scan done in 1999 again. There is no visible abnormality on the 1999 MRI scan at the right MCA bifurcation. The aneurysm that 12 years later ruptured and caused the subarachnoid haemorrhage and intra-cerebral clot in 2011 was pointing laterally from the posterior aspect of the trifurcation of the right MCA.

In addition, Dr Molyneux stated:

Incidental intracranial aneurysms occur in the adult population with a frequency of about 3%. The time course of formation and rupture of intracranial aneurysms is unknown. The most widely held opinion amongst experts in this field is that the majority of small aneurysms that present with rupture causing a SAH do so relatively soon after their formation. This is the only realistic explanation for the discrepancy in the observed natural history of small unruptured cerebral aneurysms found incidentally which, based on the best literature evidence, have a very low likelihood of rupture and the observed fact that in the most patients who present with a haemorrhage after an aneurysm rupture, the size of the aneurysm is small and usually less than 7mm.”

In an attachment to his report, showing image 14, study 2 and headed “EXP MR1 April 1999”, Dr Molyneux drew a blue arrow with the legend “Axial Proton density image showing tortuous MCA trifurcation anteriorly of the artery”. In respect of image 33, study 2, Dr Molyneaux drew a blue arrow with the legend “Axial T2 Image same slice level showing slightly tortuous MCA trifurcation anteriorly”.

In the Joint Report Dr Molyneux said:

“… the findings on the MRI scan of 1999 are shown in retrospect to represent what [I regard] as complex bifurcation pattern of the right MCA and that the findings are within normal limits”.

In respect of image 33, study 2 of the MRI scan, Dr Molyneux stated that the flow voids “relate to the complex branching pattern of the MCA shown on the later CT angiograms”.

As to the location of the aneurysm found on the CT angiogram in September 2011, Dr Molyneux repeated that the aneurysm was “arising from the posterior aspect of the proximal MCA at the first branch of the artery just proximal to the second branch origin which is arteriorly directed”, and that the aneurysm on the CT angiogram was not the same aneurysm postulated by Dr Butler on the MRI in April 1999.

The Defendant gave evidence. He had no recollection of reviewing the MRI in April 1999, but explained the normal procedures he would have followed in any event. That evidence was not challenged as such. The inescapable inference was that, if he had reviewed the relevant images, he had found them to be normal and to reveal no indication of any aneurysm, in particular, no evidence of any aneurysm at the location of the ruptured aneurysm later shown by the CT angiogram in 2011. The Defendant expressed no view either way as to what he now thought, having had the opportunity in the context of this litigation to review all the relevant images from the MRI scan of April 1999, in the light of the angiogram of September 2011. He left the interpretation of those images to the rival experts.

The Claimant also relied on an expert report of Peter Kirkpatrick BSc MB Ch.B MSc FRCS (SN) F Med Sci, consultant neurosurgeon at the University of Cambridge Hospital Trust since 1995. In his report dated 11 August 2014, after reviewing the available neuroradiological material, including the MRI scan of April 1999, he stated:

“On the T2 – weighted horizontal images a flow-void in the region of the right middle cerebral artery is identified. The globular flow declares very clear aneurysm in the region of the middle cerebral artery bifurcation. It looks multi-locular It measures about 5-6mm in its maximum dimension. The lesion is also identified on the TI – weighted images but is slightly less obvious.”

Later in his report, under the heading “Comments on the Defence Pleadings”, he stated:

“The key issue here relates to whether or not the images of 06.04.99 were abnormal. I have reviewed these myself, and from a neurosurgical perspective who sees hundreds of MRI scans on an annual basis, the images are clearly abnormal and, unequivocally in my view, demonstrate the presence of a sizeable right middle cerebral artery aneurysm measuring between 5-6mm in its maximum dimension. This is not a small aneurysm, and the suggestion that the images show no vascular abnormality, or at best a small aneurysm, in my view is wrong. It would of course be for the expert neuroradiological and general radiological commentary to identify standards of reporting in this matter, but from a neurosurgical and neurovascular perspective I have no doubt in my mind what the MRI scans show. Indeed, I note the commentary from Dr Paul Butler in his expert report that he also considers that the aneurysm was visible on the cranial MRI scan performed in April 1999. He considers that the site of the subsequent haemorrhage was centred in this region and on balance of probabilities the aneurysm identified in 1999 was responsible. From the neurovascular point of view I would totally agree with his views.”

There was a written report, and two purported “supplementary reports” in November 2014, on behalf of the Defendant, from Mr Paul Bryne FRCS (SN), consultant neurosurgeon at the Nottingham University Hospital NHS Trust. Mr Byrne was not called to give evidence, and the Defendant did not seek to rely on his report. However, I should note the following two paragraphs in Mr Byrne’s main report of August 2014:

“In 1999 I was part of the neurovascular team in my neuroscience centre and was involved in the management of incidentally found unruptured cerebral aneurysms.

In 1999 I would have referred to the enclosed article (New England Journal of Medicine Volume 339 No.24 10 December 1998 pages 1725-1733 “Unruptured Intracranial Aneurysms – Risk of Rupture and Risks of Surgical Intervention. The international study of unruptured intracranial aneurysms investigators” (ISUIA) That paper, which was widely held as the definitive scientific evidence on the risk of rupture of unruptured aneurysms, looked at a group of patients from 53 participating centres in the United States, Canada and Europe. In patients who had no history of subarachnoid haemorrhage the conclusion of the paper was “The likelihood of rupture of unruptured intracranial aneurysms that were less than 10mm in diameter was exceedingly low”. The risk was noted to be about 0.05% per year. The paper notes “The management of unruptured aneurysms depends on the natural history of these lesions and on morbidity and mortality rates associated with repair. On the basis of the rupture rates and treatment risks in our study, it appears unlikely that surgery will reduce the rates of disability and death in patients with unruptured intracranial aneurysms smaller than 10mm in diameter and no history of subarachnoid haemorrhage”.”

In the event the important witnesses at trial, who were extensively cross-examined, were Dr Butler and Dr Molyneux (consultant radiologists) and Mr Kirkpatrick (neurosurgeon). All these witnesses expressed views on the core issue, and in essence their views remained the same as those expressed in their reports.

The Defendant attached a curriculum vitae to his witness statement of 10 July 2014. It showed that he had received his medical education at the teaching hospitals in Bristol and Birmingham, before he became a registrar in radiology at “Oxford RHA” in August 1984. He remained a registrar until March 1989, when he became senior registrar in neuroradiology at the Radcliffe Infirmary, Oxford. He remained in that position until October 1991. He stated that he had spent four and a half years in “general radiology”, saying that:

“The Oxford course provided a wide general radiological experience as well as the specialised techniques of a teaching Hospital, the latter allowing concentrated experience of body computed tomography, ultrasound, neuroradiology, angiography and interventional radiology….”

As to his “neuroradiology training”, Dr Barker stated:

“The Department of Neuroradiology, Radcliffe Infirmary, provided comprehensive service for the Oxford Region. I spent a total of nine months on rotation through the Department prior to my appointment as Senior Registrar in Neuroradiology and then two and a half years in this specialist post. I received training in myelography, angiography, computed tomography, magnetic resonance imaging and interventional neuroradiology.”

In these passages Dr Barker did not mention Dr Molyneux at all. Dr Molyneux produced a curriculum vitae, as already noted, in which he stated that he had been a consultant neuroradiologist at the Radcliffe Infirmary, Oxford.

Someone comparing these respective CVs would reasonably infer that Dr Barker would have had contact, possibly significant contact, with Dr Molyneux from about August 1984, and in particular from about March 1989, when he became senior registrar, until October 1991 when he became a consultant neuroradiologist in Southampton. However, someone looking at the respective CVs would not know the exact nature and extent of any connection between Dr Barker and Dr Molyneux, because neither of them in their written statements condescended into setting out particulars of any such connection. On the contrary, neither referred explicitly to any such connection.

Mr Angus McCullough QC, on behalf of the Defendant, suggested that the respective CV’s should have put the Claimant, or at least her legal representatives and proposed experts, on notice that there was likely to have been some sort of connection, and that they ought then to have pursued the matter with the Defendant.

I do not accept that suggestion. In my view, the burden was fairly and squarely on the Defendant, in particular on Dr Molyneux who was to be the Defendant’s key (in the event, sole) expert witness at the trial, to state frankly, with adequate particulars, the nature and extent of any connection between Dr Barker and Dr Molyneux.

The Defendant knew the details; it is both fair and economical that the Defendant should disclose them. The Claimant should not be expected to engage in the time consuming detective work, the output of which might be incomplete or inaccurate, in order to ascertain the full picture bearing on Dr Molyneux’s independence as an expert witness. Furthermore, if the Claimant had been given full particulars, the issue of Dr Molyneux’s independence could have been explored, as it should have been explored, before the trial began.

It emerged only in cross-examination at the trial that the connection between Dr Barker and Dr Molyneux had been lengthy and extensive. Dr Molyneux had trained Dr Barker during his seven years of specialist radiology training, and in particular had trained him for two and a half years as a registrar and senior registrar in neuroradiology, including the particular area of interventional radiology in which Dr Molyneux specialised and in which Dr Barker had a special interest. It is clear that they had worked together closely over a substantial period. They had written together a paper for the 14^th International Symposium on radiology, a paper not shown on Dr Molyneux’s list of publications, and Dr Molyneux told the Court that they might have co-operated on other papers which he could no longer specifically recall. Dr Molyneux helped Dr Barker to obtain foreign placements: Dr Barker had been a Visiting Fellow at the Department of Neuroradiology, University of California at San Francisco in February and March 1990; and William Cook International Fellow, Department of Neuroradiology, Sahlgren Hospital, Gottenberg, with Dr Barker taking care, in this instance, to note in his CV that this enabled him to gain further practical experience “under the supervision of Dr P Svendsen”. Dr Barker accepted that Dr Molyneux had guided and inspired his practice, and Dr Molyneux had helped Dr Barker become a consultant in Southampton. They had also been officers together on the committee of the British Society of Radiologists, Dr Barker having been Treasurer at the time when Dr Molyneux, being a committee member, was nominated President.

It also emerged that Dr Barker had suggested that Dr Molyneux should be a defence expert. He had first been asked in cross examination whether he had chosen Dr Molyneux as an expert, which he denied, and he had had to be prodded with a further question to elicit the full picture.

Mr McCullough QC suggested that most, if not all, of the above cast no real doubt on Dr Molyneux’s independence, because it was now in effect ancient history. I also reject that suggestion. Where a medical practitioner such as Dr Molyneux has played a relatively prominent part as mentor of another practitioner’s career, the bond may well have a very lasting effect, and it is imperative that the connection, even if well in the past, should be disclosed if the mentor is to be put forward as an independent expert witness whose evidence would benefit the person who had been under his or her tutelage. In any event, Mr McCullough’s suggestion was wholly undercut by Dr Molyneux, perhaps in an unguarded moment, referring to Dr Barker in his oral evidence by his first name, “Simon”. I was somewhat taken aback by this use of nomenclature, because it both tended to show that traces of the relevant bond could still be found, and also that Dr Molyneux was not presenting himself as an expert having the necessary emotional distance from, and professional objectivity about, the practitioner whose competence had been called into question.

In my judgment, there was in this case a very substantial failure indeed, both on the part of the defence more generally but also specifically on the part of Dr Molyneux himself, to disclose, with adequate particularity, the nature and extent of Dr Molyneux’s connection with Dr Barker, so that the Court would have a complete understanding of all matters that could realistically affect Dr Molyneux’s independence as an expert witness. That failure occurred nothwithstanding paragraph 17 of the order of Master Cook on 2 June 2014 in which he specifically directed that:

“Experts will, at the time of producing their reports, incorporate details of any employment or activity which raises a possible conflict of interest.”

In these circumstances Mr Grahame Aldous QC, on behalf of the Claimant, submitted that I should entirely exclude the evidence of Dr Molyneux. I was taken to a number of authorities in support of, and in opposition to, that submission. However, those authorities have been analysed with considerable scholarship in Phipson on Evidence at paragraph 33-29, and it seems to be that at paragraph 33-30 the learned editors summarise the principles that emerge from the authorities with admirable lucidity, as follows:

“The current state of the law may be summarised by the following principles.

(1)

It is always desirable that an expert should have no actual or apparent interest in the outcome of the proceedings.

(2)

The existence of such an interest, whether as an employee of one of the parties or otherwise, does not automatically render the evidence of the proposed expert inadmissible. It is the nature and extent of the interest or connection which matters, not the mere fact of the interest or connection.

(3)

Where the expert has an interest of one kind or another in the outcome of the case, the question of whether he should be permitted to give evidence should be determined as soon as possible in the course of case management.

(4)

The decision as to whether an expert should be permitted to give evidence in such circumstances is a matter of fact and degree. The test of apparent bias is not relevant to the question of whether an expert witness should be permitted to give evidence.

(5)

The questions which have to be determined are whether:

(a)

the person has relevant expertise; and

(b)

he is aware of his primary duty to the Court if they give expert evidence, and are willing and able, despite the interest or connection with the litigation or a party thereto, to carry out that duty. ”

(6)

The judge will have to weigh the alternative choices open if the expert’s evidence is excluded, having regard to the overriding objective of the Civil Procedure Rules.

(7)

If the expert has an interest which is not sufficient to preclude him from giving evidence the interest may nevertheless affect the weight of his evidence.

Even where the court decides to permit an expert to be called where his independence has been put in issue, the expert may still be cross-examined as to his independence and objectivity.”

The authorities emphasise the importance of disclosure, indeed early disclosure, of any conflict. The Guidance of the General Medical Council published on 25 March 2013, with effect on 22 April 2013, entitled “Acting as a witness in legal proceedings” also rightly emphasises the importance of early disclosure, as follows :

Conflict of Interest

If there is a possible conflict of interest – for example, you have been professionally or personally involved with one of the people involved in the case in the past, or you have a personal interest in the case – you must follow our guidance on conflicts of interest. “You must also make sure the people instructing you, the other party and the judge are made aware of this without delay. You may continue to act as an expert witness only if the court decides the conflict of interest will not affect the case.” (my emphasis)

Failure to make early disclosure may lead to the kind of chaotic situation that has arisen in this case, where the nature and extent of the conflict became clear only in the course of the trial and led to a submission, after all the evidence had been heard, that the evidence of the Defendant’s expert, upon which the defence in the event exclusively depended, should be ruled inadmissible by the Court. Failure to make early disclosure, particularly of an obvious conflict, also tends to raise a natural suspicion that the default was not inadvertent, and to reinforce the Court’s concern that the witness has, most exceptionally, become so compromised that the evidence must be altogether excluded.

Dr Molyneux apologised for his failure, but I must look at the issue objectively. Dr Molyneux also said that the conflict had not in any way affected his impartiality, independence and objectivity as an expert witness. He referred to other cases where he had not hesitated to state an expert opinion that was adverse to the interests of a practitioner who was known to him. I am not in a position to evaluate the strength of such a point. However, a further matter did arise which again raised doubts in my mind about Dr Molyneux’s independence in this case.

I have already referred to an extract of Mr Byrne’s expert report. Anyone reading the relevant passage (see paragraph 43 above) would reasonably have believed that the paper referred to was a model of scientific excellence in its day and was uncontroversial. However, “Surgical Neurology” in 1999 asked several well known vascular neurosurgeons to comment on the article published in the New England Journal of Medicine. The published response was highly critical, the dominant themes being that the study suffered from systemic bias in the selection of patients, was contrary to current orthodoxy and at odds with accepted medical practice. In January 2002 the Journal of Neurosurgery published a number of articles and editorials about the study, and the conclusions drawn contradicted those of the report, with the editorial echoing the original criticisms in 1999. The editor of Surgical Neurology in 2002 went as far as saying that the credibility of those involved in the challenged study had been “severely compromised” and that the interpretation of the retrospective arm, at least of the study, was scientifically flawed.

In these circumstances it was wholly unclear why Mr Byrne had referred to the study in the terms that he did and why he had made no reference at all to the criticisms mentioned above. He did not give evidence, so the mystery remained. The significance of this in the present context is that Dr Molyneux had been an executive committee member of the ISUIA and could have been expected to know of the criticisms of the study and to realise that Mr Byrne’s evidence was seriously deficient and misleading. Dr Molyneux accepted in cross examination that he had seen a copy of Mr Byrne’s proposed report that contained the relevant passage and he also agreed that the study could not accurately be described in the terms used by Mr Byrne, given the criticisms and controversy already mentioned.

He knew that Mr Bryne’s report was being relied upon in respect of what, until very shortly before the trial, was an important contested issue, yet Dr Molyneux did nothing at that stage to draw the attention of Mr Bryne, or anyone else, to what he knew to be the case. The justification for this appeared to be that Mr Byrne was the expert on neurosurgery, and it was not within Dr Molyneux’s remit to comment on any aspect of the neurosurgical evidence.

I find that explanation difficult to accept. Dr Molyneux was put forward as, and indeed is, an eminent neuroradiological expert with exceptional and extensive expertise in respect of aneurysms. He held an important position in ISUIA, and he well knew, as he admitted, that the 1998 ISUIA paper was not generally accepted in the neurosurgical community as scientifically unbiased and reliable. The issue of causation between the parties remained important. I would have expected Dr Molyneux in these circumstances to have done something to alert someone to what he knew to be the case. That failure, in my view, reinforced the concern that in this case Dr Molyneux might not have been as disengaged from the party in the litigation as he said that he had been in other cases.

Where does all this leave the Court? I must say that, in the light of the accumulation of facts and matters that I have set out at some length above, I came very close indeed to ruling that Dr Molyneux’s evidence was not admissible, on the ground that I could not properly have the confidence which the Court demands it should have in the impartiality and objectivity of an expert witness. However, I did hear the evidence, and the consequence of non admission would be potentially fatal for the Defendant. There is no doubt about Dr Molyneux’s expertise and competence to assist the Court on the remaining central issue.

I believe that I can fairly admit the evidence, but I must bear powerfully in mind, when I assess the weight that I should give to the evidence, the reservations that I retain about Dr Molyneux’s independence and objectivity in this case.

It is first important to appreciate that the Defendant was engaged with a patient where the concern related to double vision, not to the possible presence of an aneurysm. The specific MRI scan in 1999 was not intended to detect aneurysm, and all the experts agreed furthermore that such a scan was in general not an effective instrument for reliably determining the possible presence of an aneurysm. The alleged abnormality appears on only a few images from about 80 images in all. The minimum size of detectable aneurysm was about 4-5mm, and, if there was an aneurysm in 1999, it would have been at about the minimum that could with any degree of confidence have been detected. If the neuroradiologist believed, incorrectly and without sufficient reason, that there might be an aneurysm shown on the scan, and further investigation was pursued (as would be likely), the patient would be likely to undergo an angiogram, a procedure that carries its own risks and that would on this hypothesis be unjustified. On the other hand, if there is an aneurysm, and it remains undetected and untreated, the potential consequences are devastating. Even allowing for the context in which the relevant scan was carried out in this case, and the significant limitations of the scan for detecting aneurysms, the consideration of the scan for the possible presence of an aneurysm, given those potential consequences, called for close scrutiny.

Three practitioners believed that the 1999 imaging showed the presence of an aneurysm in the location of the actual aneurysm that ruptured in 2011. The operating surgeon, Mr Duffill, expressed that opinion when he viewed the relevant imaging in 2011. However, Mr Duffill did not give evidence, and I do not believe that I should attach significant weight to his opinion, particularly as it might have been informed by an understandable confirmation bias, a matter that could not in the event be explored in cross-examination.

Mr Kirkpatrick, a neurosurgeon, believed that the 1999 imaging showed a “very clear aneurysm”, “a sizeable right middle cerebral artery aneurysm… not a small aneurysm”, “a very obvious aneurysm”. This language was much stronger than that used by the Claimant’s expert neuroradiologist.

Mr Kirkpatrick is not a neuroradiologist, but, as a neurosurgeon, he has substantial experience in reviewing and interpreting MRI scans for the purpose of, among other things, considering whether there is evidence of the possible presence of an aneurysm. The Defendant criticised Mr Kirkpatrick’s evidence in a number of respects. For example, he had initially stated that “the size of the aneurysm described by Mr Duffill and reported on the radiological material at the time of the ictus in 2011 was substantially larger than on balance the aneurysm would have shown some degree of progression over the years and this would have promoted a re-visit towards active treatment”. However, on proper analysis of the evidence, there was no reliable support for the conclusion that the putative aneurysm had enlarged, or that the actual aneurysm was a “giant” aneurysm measuring 3.5cms in dimension.

Notwithstanding these criticisms, I am entitled to give some weight to Mr Kirkpatrick’s opinion, as a neurosurgeon, that the 1999 imaging revealed an abnormality. At the end of the day, however, the critical neuroradiological evidence for the Claimant was that of Dr Butler, which is set out at length in paragraphs 26-31 above. I have no doubt that Dr Butler is a distinguished neuroradiologist and that he was honestly and carefully stating his opinion on the core issue in the case. What objectively divided Dr Butler and Dr Molyneux was whether the 1999 imaging, notwithstanding its acknowledged limitations, displayed such features of “abnormality” as to require further investigation for the possible presence of an aneurysm. Dr Molyneux considered that the imaging did no more than reveal “tortuosity”, and did not display any “abnormality” that required further investigation. The use of the word “tortuosity” was perhaps unfortunate, if not misleading, because it suggested, and was taken to suggest, unusual branching of the brain vessels that would not ordinarily be expected in someone of the Claimant’s age. However, it became clear when he gave oral evidence that Dr Molyneux was not referring to any such unusual characteristics. With the aid of a textbook of brain anatomy (Brain Atlas) he explained that the relevant region under consideration was where the MCA divides into different branches, that those branches may twist in ways that differ from person to person, and that for an individual the branching pattern may differ from right side to left side. Dr Molyneux believed that the branching would better explain what otherwise might have been considered to be an "abnormality" in the 1999 imaging: the apparent broadening of the signal flow void in that region was explicable by reference to normal, not unusual or worrying, anatomy.

It did not seem to me that Dr Butler disagreed with Dr Molyneux’s basic propositions concerning brain anatomy. Initially Dr Butler suggested that the absence of “tortuosity” (in the relevant usage) on the left side of the MCA in the 1999 imaging was inconsistent with Dr Molyneux’s interpretation of the right side of the MCA. However, Dr Butler accepted in his evidence that a branching pattern may differ from side to side, and in any event the left side did not appear to have a dissimilar branching pattern in the light of the 2011 CT scan. Ultimately, it appears that Dr Butler was relying upon his considerable experience in concluding that there was sufficient evidence of an aneurysm on the 1999 imaging to require further investigation. That has to be set against the opinion of Dr Molyneux, that it was reasonable for a competent radiologist to interpret the 1999 imaging as showing no relevant abnormality. I have to decide, of course, whether a competent neuroradiologist in the position of the Defendant could reasonably have concluded that there was not sufficient evidence of “abnormality” to require further investigation for the presence of a possible aneurysm.

I have not found it easy to resolve this conflict between two leading experts. I do see force in Dr Molyneaux’s opinion that the features of the 1999 imaging were consistent with the normal anatomy of the brain in that region, and did not evidence abnormality that required further investigation. However, it does appear to me that that opinion in this particular case rests ultimately upon a judgement informed by accumulated experience and expertise in the relevant area. Dr Butler, based on his experience and expertise, believed that the putative abnormality could not be safely and adequately explained by normal anatomy of the brain and that it required further investigation. That was his judgement. It did not seem to me that Dr Molyneux thought that that was an unreasonable judgement, although he did not agree with it.

Where the core issue in a case turns, as it does here, on the court’s ability to evaluate the competing and finely balanced medical judgements of rival experts, the court’s confidence in the independence and impartiality of the respective experts must play an important role. I have to say, with considerable regret, that by reason of the matters set out earlier in this judgment my confidence in Dr Molyneux’s independence and objectivity has been very substantially undermined. On the other hand I have complete confidence in the independence and objectivity of Dr Butler, and I much prefer to accept his judgement, formed on the basis of his great experience and skill, that (i) a competent neuroradiologist would have been considerably troubled by the relevant images from the 1999 MRI scan; and (ii) would not have concluded that those images could be prudently and adequately explained by “normal brain anatomy”, contrary to Dr Monlyneux’s view; and (iii) would have concluded that the images did show the presence of an aneurysm.

I am fortified in accepting Dr Butler’s evidence by the fact that it was supported by Mr Kirkpatrick, and, for the reasons given, I am entitled to give weight to the evidence of Mr Kirkpatrick as an experienced neurosurgeon. On the other hand, the Defendant offered no assistance to the Court in relation to the interpretation of the images of the 1999 MRI scan, even if any such assistance could have been offered only in retrospect.

That leaves only the final question whether there was an aneurysm present in 1999 that ruptured in 2011. As is already clear from the recital of the evidence, the experts divided sharply on this issue. Dr Butler firmly believed that the actual aneurysm that ruptured in 2011 was in the same location as the putative aneurysm visible from the images of 1999 MRI scan. Mr Kirkpatrick held the same opinion. Dr Molyneux considered that the putative “abnormality” in the 1999 images of the MRI scan was not in the same location as the actual aneurysm that ruptured in 2011. A central difficulty on this question was that the 1999 MRI scan was a relatively crude instrument for ascertaining the precise location and exact features of an aneurysm, if an aneurysm were indeed present. Dr Butler stressed the difficulty in seeking to interpret the precise characteristics of the putative aneurysm.

Dr Butler did accept, within the significant limitations of the 1999 MRI scan that the orientation of the feature which he identified as an aneurysm in 1999 appeared to be anterior. It was agreed that the actual aneurysm on the detailed imaging in 2011 emanated from the posterior wall, laterally directed. That apparent discrepancy has to be set against the improbability that the aneurysm that ruptured in 2011, albeit on any view in at least very close proximity to the abnormality that appeared in the 1999 images, was a different and more recent aneurysm. Furthermore, Mr Kirkpatrick in his oral evidence stated that the vessel may have rotated as a result of the haematoma. It is correct that Dr Butler had not mentioned such a possibility but I do nonetheless attach weight in this context to Mr Kirkpatrick’s explanation, given as it was on a matter within his acknowledged medical expertise.

Having considered the evidence on this question, I conclude, following the evidence of Dr Butler and Mr Kirkpatrick, that on a balance of probability the aneurysm that ruptured in 2011 was an aneurysm that was present in 1999, as shown by the abnormality visible in the 1999 images of the MRI scan which revealed the presence of an aneurysm in the same location.

For the reasons stated, I find that a competent practitioner would have concluded that the images in the 1999 MRI scan showed the presence of an aneurysm, and that the aneurysm that ruptured in 2011 was the same aneurysm as that evidenced by the abnormality in the 1999 images of the MRI scan. No questions of causation call for decision and I therefore conclude the issue of liability in favour of the Claimant.