NGAI PING KWAN v. CHOI YAT HUNG

HCPI 537/2010

IN THE HIGH COURT OF THE

HONG KONG SPECIAL ADMINISTRATIVE REGION

COURT OF FIRST INSTANCE

PERSONAL INJURIES ACTION NO. 537 OF 2010

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D E C I S I O N

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I. INTRODUCTION

1.  On 9 January 2009, the Defendant’s taxi collided with the taxi driven by the Plaintiff (“Accident”).  A few days later, the Plaintiff evolved an ischemic brainstem stroke.  On 14 October 2010, he commenced the present action to claim against the Defendant for damages for personal injuries as a result of the Accident.  The Plaintiff claims his stroke and current disabilities are due to flexion-extension or whiplash neck injury caused by the Accident.  The Defendant admits negligence but denies the Plaintiff’s stroke and/or current disabilities are caused by the Accident.  He further avers that such disabilities are due to the ischemic stroke to which the Plaintiff was constitutionally disposed, and as a fallback he says that the Plaintiff’s claim for damages should be reduced to take into account inter alia his pre-existing medical condition.  Such dispute is significant because the Plaintiff’s claim for damages is substantially premised his stroke.

2.  Before commencing the present action, the Plaintiff has obtained two solo neurology expert reports dated 29 March and 28 July 2010 (“Woo 1^st and 2^nd Reports”) by Dr Edmund Woo (“Dr Woo”).

3.  On 18 March 2011, Dr Woo and the Defendant’s neurology expert Dr Yu Yuk Ling (“Dr Yu”) compiled a joint neurology expert report on causation and quantum (“Jt Report”).  Drs Woo and Yu (collectively, “Experts”) have reviewed the treatment medical reports/notes/records of Tuen Mun Hospital (“TMH”) and Pok Oi Hospital (“POH”) and the radiological images relating to the neuroimaging studies in respect of the Plaintiff for the Jt Report.

4.  At the Checklist Review (“CLR”) on 13 May 2011, the Plaintiff opposed the Defendant’s application for leave to adduce expert evidence from a radiologist with expertise in neuroimaging (“Issue”) as a result of (a) differences in opinion between the Experts over the interpretation of the radiological evidence, and (b) modifications of Dr Woo’s own views over such interpretation.  The Issue came before me for substantive argument on 29 July 2011.  

5.  Background information in relation to the Issue as set out below is elicited from the Plaintiff’s and the Defendant’s witness statements dated 28 May and 14 December 2010 respectively, TMH’s treatment medical reports, Woo 1^st and 2^nd Reports, and the Jt Report.  Mr McLeish, counsel for the Defendant, and Mr Sakhrani, counsel for the Plaintiff, have referred me to only two pages of the treatment medical notes/records in the hearing bundle.

II. LEGAL PRINCIPLES

6.  Expert evidence must be relevant, necessary and of probative value. Chu J (as she then was) in Wong Hoi Fung v American International Assurance Co (Bermuda) Limited & anor HCA 4576/2001 (unreported, 8 October 2002) said at para.12 that expert evidence must be relevant in the sense that it is helpful to the court in arriving at its decision on one or more issues to be resolved.  The learned judge cited Baring plc (in Liquidation) & anor v Coopers and Lybrand & ors Lexis Transcript, 9^th February 2001, paras.44-45 in which Evans-Lombe J said the court can exclude expert evidence if it is of the view that calling such evidence will not be helpful to the court in resolving any issue in the case justly, eg where the issue to be decided is one on which the court can come to an informed decision without such expert evidence.  Whether to grant leave to adduce expert evidence requires an exercise of judicial discretion, and pertinent considerations will include (a) how cogent the proposed expert evidence will be, (b) how helpful it will be in resolving any of the issues in the case, and (c) how much it will cost and the relationship of that cost to the sums at stake.

7.  Recently, Bharwaney J in Fung Chun Man v Hospital Authority & anor HCPI 1113/2006 (unreported, 24 June 2011) has given further guidance on the court’s power to grant leave for a party to adduce expert medical evidence:

“ 9. The enactment of the CJR did not result in a change to O.38, r.36 of the Rules of the High Court …… However, after the enactment of the CJR, it is clear that the court’s discretion, whether or not to grant leave to a party to adduce expert evidence, is to be exercised within the ambit of the court’s management powers. Those powers must be exercised in the light of the underlying objectives of the CJR, including the need to ensure the cost effectiveness of the proceedings; to ensure that the case is dealt with expeditiously; to ensure reasonable proportionality having regard to the amount of money involved, the importance of the case, the complexity of the issues, and the financial position of each party; to ensure procedural economy in the conduct of the proceedings; and to ensure fairness between the parties.

10. The courts recognise that the primary aim of its case management powers is to secure the just resolution of the dispute in accordance with the substantive rights of the parties. However, the substantive rights of the parties to a personal injury action do not include a legal right to call experts of their choice.

11. The expert evidence can only be adduced with leave of the court and, in deciding whether or not to grant leave, the court must ensure that such evidence is admitted only if it is likely to be of real assistance to the determination of the issues, and that it is adduced in the most effective and economic way consistent with the objectives of the CJR.

……

  15.  In summary, the expert evidence must be in a recognised discipline, reasonably required to enable the court to resolve the issues in dispute, and proportionate.”

III. PLAINTIFF’S MEDICAL HISTORY

(a)  Nasopharyngeal carcinoma

8.  The Plaintiff had nasopharyngeal carcinoma in 1993.  He presented with cervical lymphadenopathy, and a course of radiotherapy was delivered to the nasopharynx and neck.  He attended follow up every half year from 1994 to 2002, which was reduced to once a year after 2002 and once every 18 months at the time of the Accident. The doctors told him his nasopharyngeal carcinoma was in remission.

9.  The Plaintiff developed panhypopituitarism (hypofunction of the pituitary gland which lies within the radiation portal) as a complication of the radiotherapy, and was referred to POH’s endocrine clinic for management since August 2008. He has been kept on life-long pan-hormonal replacement including thyroxine, testosterone and as-needed hydrocortisone.

(b) Hearing impairment

10.  The Plaintiff also has bilateral hearing impairment (left worse than right), dysarthria (slurring of speech) with occasional choking, vocal cord palsy and weakness/fasciculation of his tongue due to multiple lower cranial nerve damage as a result of the radiotherapy.  It is documented in the TMH records that the Plaintiff “[claimed] right mouth-angle dropped all along after radiotherapy”.

(c) Hypertension

11.  The Plaintiff was found to have hypertension in March 2008 when his blood pressure was elevated to 174/99 at the visit to POH’s endocrine clinic.  Anti-hypertensive medication (nifedipine) was prescribed.

IV.  ACCIDENT

12.  According to the Plaintiff’s witness statement and the Jt Report, at the time of the Accident he was travelling at a speed of 40-50kph when the Defendant’s taxi suddenly cut into its path, and the right front of his taxi collided with the left rear of the Defendant’s taxi.  He was wearing a seat belt at the time, but his head was thrown forwards and then backwards once against the head rest of the driver seat (ie flexion-extension or whiplash movement).  He told the Experts the degree of head and neck movement was not excessive, and it was similar to that when he braked his taxi abruptly. He had no loss of consciousness.

13.  The Plaintiff’s witness statement states he did not feel any immediate discomfort.  Indeed, he was able to alight and inspect the damage to his taxi.  When he was examined by Dr Woo on 22 March 2010, he said he did not have any headache or neck pain.  But when he was examined by the Experts on 11 January 2011, he said he was uncertain if he had any pain at the back of his neck but even if he had it was mild and momentary.

14.  The Plaintiff claims that both taxis were damaged and the right front of his taxi was damaged quite seriously. But the Defendant says that the impact of the collision was mild, and both vehicles were only slightly damaged at the points of impact (ie the front of Plaintiff’s taxi and the rear of the Defendant’s taxi).

15.  The Plaintiff’s passenger left the scene without leaving any contact details.  The Plaintiff then made a report to the police, and when they arrived and asked whether he was injured, he gave a negative answer because he did not feel any discomfort at that time.  No ambulance was summoned to the scene, and he did not seek immediate medical attention. The medical report of the department of medicine and geriatrics (“DMG”) of TMH dated 18 April 2009 confirms no significant injury was noted at the time.  Thereafter, the Plaintiff parked his taxi and took a bus home.

V. AFTERMATH OF THE ACCIDENT

16.  The Plaintiff went to bed at about 3:00-4:00am on 10 January 2009.  He claims that when he woke up at 2:00pm (ie about 15 hours after the Accident) he noted some weakness in his right hand (eg it could not hold a cup of water properly), but he did not appreciate its significance or pay attention to it.  He went to pick up his taxi, and drove it to a garage for repairs before taking a bus home.

17.  The Plaintiff claims that when he awoke from sleep at about 1:00pm on 11 January 2009 (ie about 38 hours after the Accident) he experienced generalised right-sided weakness which was more apparent.  He had to drag his right leg on walking, his right hand was weaker than the day before, and his speech was slurred.  He could still eat and swallow, but choked when drinking water.  He wanted to see a doctor, but upon recalling it was a Sunday thought he would wait until Monday.

18.  At about 9:00am on 12 January 2009, the Plaintiff went to see a private doctor and was told he might have suffered a stroke.  He was immediately referred to TMH.  He attended the accident and emergency department (“AED”) of TMH at 10:30am.  According to the medical reports by TMH’s AED and DMG dated 8 November and 18 April 2009 respectively, the sudden onset of stroke (presenting with right-sided weakness and slurred speech) was about 3:00pm on 11 January 2009, but such reports note there was no limb numbness, headache or neck pain.

19.  According to the medical report by TMH’s AED dated 8 November 2009, initial examination showed no slurring of speech or facial numbness.  Physical examination showed right-sided weakness with power grade 4/5, right-sided hyperflexia and upgoing plantar response.  Clinical diagnosis was compatible with cerebrovascular accident with right-sided weakness.  The Plaintiff was admitted to TMH’s medical ward for further management.

20.  According to the medical report of TMH’s DMG dated 18 April 2009, the Plaintiff was conscious and alert on admission with a normal Glasgow coma scale of 15/15.  He had dysarthria (slurring of speech) and partial right facial palsy.  There was also bilateral tongue fasisculation and the tongue was deviated to left. Power in the right extremities was diminished at 4+/5, but left side power was full.  There was associated right upper limb clumsiness with pass-pointing (ataxia of the right upper limb).  His blood pressure was 98/66.  Routine blood test (including renal function), ECG (electrocardiogram) and chest x-ray were unremarkable. CT (computed tomography) brain scan done on 12 January 2009 did not show any intracranial haemorrhage, obvious infarct or other abnormality (“TMH CT”).

21.  The Plaintiff informed the attending doctors he had the Accident prior to the onset of his right-sided weakness.  The doctors suspected he might have had some vascular injury to the vessels in his neck.  On 20 January 2009, they arranged MRI (magnetic resonance imaging) and MRA (magnetic resonance angiogram) of the brain (“TMH MRI/MRA”), which revealed recent left pontine infarct with suspicious underlying left vertebral artery dissection.  The clinical diagnosis was acute ischemic stroke resulting from left vertebral artery dissection.

22.  The Plaintiff was treated with antiplatelet (aspirin) medication.  His fasting glucose was normal, but he was found to have mild hypercholesterolemia for which lipid-lowering medication (simvastatin) was prescribed.  His blood pressure while in hospital varied from 120-150/60-90.

23.  The Plaintiff made good recovery from his ischemic stroke and remained neurologically stable.  As his symptoms remained static, he was discharged home on 20 January 2009.  At that time he was ambulatory with the aid of a cane.  After another 2 months, he could walk unaided and could continue his daily activities independently.  Aspirin was continued, and he was offered early follow up appointment at TMH’s medical clinic to assess any change in his clinical condition.

24.  The Plaintiff’s neurological symptoms and signs improved on follow up assessment.  Since 9 February 2009, another antihypertensive medication (lisinopril) at low dose was added for the control of his blood pressure which was elevated to 159/88 that day.  However, his blood pressure subsequently dropped to very low levels, so lisinopril was discontinued after a few months.

25.  Videofluoroscopy swallowing study on 24 April 2009 showed silent aspiration and accumulation of food residue in the valleculae and pyriform sinuses in the pharynx.

26.  The Plaintiff in his witness statement claims he has received physiotherapy and occupational therapy treatments.  According to the Jt Report, he attended follow up at POH’s endocrine clinic where he was dispensed with antiplatelet (aspirin), lipid lowering (simvastatin), antihypertensive (nifedipine) and hormonal (thyroxine and testosterone) medications, and at the radiotherapy clinic of Prince of Wales Hospital for serial evaluations of his nasopharyngeal carcinoma that was in remission.

VI.  AGREEMENT BETWEEN THE EXPERTS

27.  The Experts agree that the Plaintiff has pre-existing deficits in the form of hearing loss, dysarthria and weakness/fasisculation of his tongue as a result of the radiotherapy for his nasopharyngeal carcinoma.  Apart from occasional choking when drinking fluid, he is able to swallow normally.

28.  The Experts further agree the Plaintiff had brainstem stroke in January 2009.  Clinically he had right hemiparesis and worsening of dysphagia and dysarthria, and radiographically a small infarct in the left paramedian pontine region was demonstrated on the TMH MRI/MRA.  The deficits as a result of his brainstem stroke include right hemiparesis, urgency of micturition, and an increase of bulbar dysfunction (with dysphagia and dysarthria).  Now that two years have elapsed since the stroke, further significant improvement in his neurological functions is not expected.

VII.  POSSIBLE CAUSES OF THE STROKE

29.  The medical reports of TMH’s DMG dated 18 April and 10 December 2009 say the Plaintiff’s suspected vertebral artery dissection could have resulted from a minor trauma to the neck at the time of the Accident, but the definite or exact relationship between the Accident and the suspected dissection could not be accurately or properly determined.

30.  Whilst the Experts disagree over the cause(s) of the Plaintiff’s brainstem stroke (see Part VIII below), based on the Plaintiff’s medical history and on the radiological findings as a whole, they agree that three possibilities need to be considered, ie (a) dissection of the extracranial segment of the left vertebral artery, (b) radiotherapy-induced atherosclerosis, and (c) hyperintensive cerebrovascular disease (collectively, “Three Possible Causes”).

(a) Dissection of extracranial left vertebral artery

31.  Cervicocerebral arterial dissection refers to dissection of the cerebral arteries (internal carotid artery and vertebral artery) at the extracranial (cervical) or intracranial segment.  Arterial dissection usually arises from an intimal tear that allows the development of an intramural haematoma (false lumen) or less commonly as a result of rupture of a primary intramural haematoma into the intima.  Woo’s 1^st Report says that pathologically dissection is accompanied by haemorrhage into the subintimal or medial layer of the vascular wall.

32.  Dissection can be iatrogenic (from catheter procedures) or due to severe trauma in which cases the causes are obvious, but most occur spontaneously or are associated with antecedent trivial trauma including sudden head movement.  Arterial injury results from mechanical stretching of the vessel.

33.  For spontaneous dissection of the vertebral artery, extracranial vertebral artery dissection is more common whereas dissection of the intracranial vertebral artery is uncommon.  It may cause ischemia of the brain parenchyma either as cerebral infarct or transient ischemic attack usually on the ipsilateral (same) side of the dissected artery. The mechanism is through haemodynamic disturbance due to narrowing or occlusion of the artery, or by distal embolism from the thrombotic segment, or both.  Unlike atherosclerotic vascular occlusion, luminal compromise from dissection most often resolves with complete recanalisation of the vessel, which may take weeks or months.

34.  MRI/MRA currently offer sophisticated non-invasive imaging of cerebrovascular arterial dissection in the acute phase and for follow up assessment.  Characteristic MRI findings of the dissected artery include the diminution or absence of signal flow void and the crescent sign indicating an intramural haematoma within the arterial wall.  In addition, subtle abnormalities include (a) high signal intensity from the entire vessel, (b) significant compromise of the vessel lumen by adjoining abnormal increase in signal tissue, (c) enlargement of the vessel diameter, and (d) poor or no visualisation of the vessel.  Fat suppression technique needs to be applied in cross-sectional MRI images at the level of dissection to differentiate small intramural haematomas from surrounding soft tissues.  In relation to detection of these abnormalities, a study published in 1994 reported that MRI brain had 60% sensitivity (ie it would miss 40% of cases) while MRA had 20% sensitivity (it would miss 80% of cases) (“1994 Study”).  Their specificities, on the other hand, are 98% and 100% respectively (ie there are rarely false-positive findings).

35.  Invasive catheter-based conventional angiography is warranted if MRI/MRA findings are non-diagnostic in spite of high clinical index of dissection.  It yields excellent delineation of the characteristic abnormalities associated with dissection, including intimal flaps, intraluminal clots, tapering occlusions, double lumen, vessel stenosis with string sign, and post-stenotic aneurismal dilatations.

36.  The outcome of extracranial vertebral dissection is generally good. Complete or excellent recovery occurs for 75%-85% of patients.  Mortality is less than 5%, and significant neurological deficits persist in only 5%-10% of patients.

(b) Hypertensive cerebrovascular disease

37.  In long-standing or poorly-controlled hypertension, the recognised complications include atherosclerosis, stroke (cerebral infarct or haemorrhage), coronary heart disease, hypertensive heart disease and kidney failure.  Such adverse effects take time to evolve so thrombotic complications do not usually occur until hypertension has been present for many years.  Radiologically, hypertensive cerebrovascular disease manifests with multiple areas of signal changes in the white matter in the subcortical and periventricular regions of the cerebral hemispheres (such being attributed to small vessel disease) on MRI, and with irregular areas of narrowing and stenosis in the cerebral blood vessels (such being attributed to large vessel disease) on MRA.  These radiologic changes are irreversible.

(c) Radiotherapy-induced injury

38.  Radiotherapy is the mainstay treatment for nasopharyngeal carcinoma.  The radiation portals generally cover the nasopharynx and adjacent regions and the neck, including the skull base, pituitary gland and anterior parts of the temporal lobes.  The posterior extent of the radiation portals covers the whole clivus and extends about 1cm posterior to the clivus and sometimes more, thus possibly covering the basilar artery.

39.  Woo’s 1^st Report says that radiotherapy treatment delivered to the neck may cause accelerated atherosclerosis of the vertebral arteries so that they are prone to vascular thrombosis.  Woo’s 2^nd Report states that radiation for the Plaintiff’s nasopharyngeal carcinoma may induce atherosclerotic changes in the blood vessels within its radiation portals, ie the main cerebral arteries in the neck and at the base of the brain.  The Jt Report says that radiotherapy-induced injury of these structures may occur as early as 6 months after irradiation, and can occur anytime thereafter. Once established, they are irreversible in the majority of cases.

VIII. DISAGREEMENT BETWEEN THE EXPERTS

40.  The Experts have arrived at different conclusions as to the cause(s) of the Plaintiff’s pontine infarct.

(a) Dr Woo’s conclusions

41.  In Woo’s 1^st Report, Dr Woo notes that although the Plaintiff had no immediate symptoms after the Accident, he evolved an ischemic brainstem stroke with a left pontine infarct over the next 48 to 72 hours.  Dr Woo opines that the flexion-extension (whiplash) movement of the Plaintiff’s head and neck at the time of the Accident probably resulted in a mild dissection of his vertebral artery.  He says this is the immediate precipitating factor of the Plaintiff’s stroke, but the Plaintiff’s pre-existing radiotherapy and hypertension probably also played a contributing role even though the TMH MRA does not reveal any sign of atherosclerosis.

42.  Although there is no accurate guide for assessing the relative contribution of the Three Possible Causes towards the Plaintiff’s brainstem stroke and residual neurological disabilities, upon taking the whole clinical picture and the radiological findings into consideration, Dr Woo estimates the Accident and the dissection account for 60% whilst the combined effects of the pre-existing radiotherapy and hypertension account for 40%.  Dr Woo opines that in such circumstances most probably the Plaintiff would not have suffered his current disabilities but for the Accident.

43.  In Woo’s 2^nd Report, Dr Woo accepts that all Three Possible Causes could have pre-disposed to the Plaintiff’s stroke.  He says there has been no MRA radiological change to support the diagnoses of hypertensive cerebrovascular disease and/or radiotherapy-induced atherosclerosis, but dissection cannot be excluded since radiological changes for dissection are very subtle (especially when the TMH MRA images are not of superior quality) and reversible (so it could have been missed if MRA is not performed within the appropriate time window).

44.  In the absence of any definitive MRA clue, Dr Woo considers the temporal course of events to be far more relevant and significant.  Taking the whole clinical picture into consideration and on the balance of probabilities, there is 60% chance the Plaintiff’s stroke was caused by dissection, 20% chance it was caused by hypertensive cerebrovascular disease, and 20% chance it was caused by radiotherapy-induced atherosclerosis.  Putting it in another way, pre-existing hypertensive cerebrovascular disease and radiotherapy-induced atherosclerosis each resulted in 20% narrowing of the left vertebral artery, but did not cause any haemodynamic compromise (since a blood vessel has to be narrowed by at least 70% before haemodynamic disturbance ensues). They were clinically insufficient to cause a stroke, but a stroke resulted when the dissection occluded the remaining 60% of the vessel.  Dr Woo maintains that but for the Accident most probably the Plaintiff would not have had a stroke or suffered his current disabilities.

45.  In the Jt Report, Dr Woo concludes that the Plaintiff had a sudden flexion-extension neck movement at the time of the Accident which could have resulted in mechanical stretching of the vertebral artery.  Although the Plaintiff had no immediate symptoms, he evolved an ischemic brainstem stroke with a left pontine infarct over the next 24 to 48 hours.  The Plaintiff’s MRI/MRA changes are suspicious of a dissection, but definitive conventional angiography has not been performed despite high clinical index of suspicion.  Dr Woo says that clinically the temporal evolution of events is strongly indicative of dissection as the underlying cause.  

46.  Dr Woo says that although the Plaintiff’s pre-existing hypertension and radiotherapy were pre-disposing factors for atherosclerosis (and in this respect of the possible presence of atherosclerosis in the extracranial vessels in the neck and not in the intracranial basilar artery), there is no radiological change to indicate that such atherosclerosis was present (ie the TMH MRI shows no deep white matter lesion, and the TMH MRA shows all vessels to be pristine with no evidence of severe vascular disease in the form of irregularities, narrowing and/or stenosis in multiple cerebral arteries), so the Plaintiff was not at risk of blockage of any of these vessels and/or imminent stroke at any time.

(b) Dr Yu’s conclusions

47.  On the other hand, Dr Yu points out that the Plaintiff has two pre-existing medical conditions (ie he was diagnosed to have hypertension in March 2008, and he sustained radiotherapy-induced injuries of the pituitary gland, the 9^th, 10^th and 12^th cranial nerves bilaterally, the right facial nerve, and the cerebral arteries as a result of the radiotherapy for his nasopharyngeal carcinoma in 1993).  At the time of the Accident, the Plaintiff had one cycle of flexion-extension neck movement (which was of mild intensity) but no external injury, but within 38 hours of the Accident he developed features of a brainstem infarct.  Ten days after the stroke, the TMH MRI showed an acute infarct in the left paramedian region of the pons, and the TMH MRA showed a vestigial left vertebral artery with no evidence of dissection and no atherosclerotic narrowing of the major cerebral arteries.

48.  Carotid Doppler ultrasound study of the extracranial arteries (neck segment of the cerebral arteries) for ruling out stenosis performed on 24 February 2009 (ie more than a month after the Plaintiff’s stroke) (“TMH DS”), whereby the calibre of the blood vessels and their flow were evaluated using ultrasound, shows diffuse atherosclerosis and multiple non-calcified plaques in the common carotid and internal carotid arteries bilaterally.

49.  Based on currently available evidence, Dr Yu opines that the pontine infarct can be better explained by atherosclerosis of the basilar artery and/or its pontine branches due to irradiation and hypertension.  He cast doubt on the suggestion in Woo’s 2^nd Report that the temporal evolution of events (ie flexion-extension injury followed by pontine infarct in 24 to 72 hours) is strongly indicative of dissection as the underlying cause, a major reason being the lack of radiologic evidence of dissection. He also refers to the following considerations:

(a) the one cycle flexion-extension neck movement was mild with minimal or no neck pain, and was unlikely to bring about dissection of the vertebral artery;

(b) following the Accident there was absence of the common initial symptoms of dissection, eg there was no headache, and neck pain was either absent or minimal;

(c) the deep pontine infarct is more typical of an infarct due to atherosclerosis of the basilar artery and/or its paramedian branches than dissection;

(d) there is radiological evidence of atherosclerosis with multiple non-calcified plaques in the carotid arteries bilaterally;

(e) the left vertebral artery was vestigial;

(f)  the aspirin treatment the Plaintiff received catered more for cerebral infarct due to atherosclerosis than extracranial vertebral artery dissection;

(g) given the extensive radiotherapy-induced injuries the Plaintiff already had before the Accident, radiotherapy-induced vascular injury (atherosclerosis) of the basilar artery and/or its paramedian branches supplying the pons was a distinct possibility;

(h) hypertension may also have a role in the atherosclerosis in this case;

(i)  cerebral infarct due to atherosclerosis can occur any time, and the temporal proximity of the Accident and onset of the stroke could have been coincidental.

IX.  RADIOLOGIC INVESTIGATIONS

50.  The Issue focuses on whether neuroradiology expert evidence will be helpful to the court in elucidating the cause(s) of the Plaintiff’s stroke, especially in light of the Experts’ conflicting views on whether or not there is radiological evidence of dissection of the extracranial segment of the left vertebral artery and/or of atherosclerotic changes due to irradiation and hypertension.  It is therefore appropriate to first turn to the available radiological evidence.  Apart from the TMH CT, the TMH MRI/MRA and the TMH DS referred to above, MRA brain was repeated on 1 June 2010 at Axon Scanning Centre Limited (“Repeat MRA”).

(a) TMH CT

51.  The TMH CT shows the brain parenchyma to be unremarkable.

(b) TMH MRI/MRA

52.  The radiology report of the TMH MRI/MRA by TMH’s radiologist Dr Vincent Lai (“Dr Lai”) states inter alia as follows:

“CLINICAL HISTORY:

Known [history] of [nasopharyngeal carcinoma] with [radiotherapy] done. Admitted this time for stroke [presenting with] right hemiparesis, preceded by some neck pain and neck movement / manipulation. Suspected dissection of the neck arteries.

……

FINDINGS:

Focal T1W [T1-weighted] hypointense T2W [T2-weighted] hyperintense lesion is seen at left pons showing restricted diffusion, in keeping with recent infarction. Rest of the brain parenchyma shows no signal intensity.

……

Marked reduced calibre of left vertebral artery is evident with diminished signal and irregularity. Axial T1W FS [T1-weighted fat suppression] sequence shows suspicious hyperintense signal at the lower end of left vertebral artery with absence of flow void. Findings are suspicious of underlying vertebral artery dissection. Right vertebral artery and basilar artery are patent.

Rest of the major vessels is also patent.

OPINION:

Recent left pontine infarct with suspicious underlying left vertebral artery dissection.

……”

53.  The Experts have reviewed the TMH MRI/MRA images for the Jt Report, and agree they show a small infarct about 1cm in diameter in the left paramedian pontine region.  They also agree the left vertebral artery is small and attenuated in its cervical segment indicating a vestigial artery.  However, they differ on other findings, but more of that below.

(c) TMH DS

54.  The radiology report of the TMH DS by TMH’s radiologist Dr Cho Hing Yan (“Dr Cho”) states inter alia as follows:

“FINDINGS:

There is diffuse atherosclerotic changes along the common and internal carotid arteries bilaterally.

Multiple non-calcified atheromatous plaques are evident at the distal common carotid arteries and carotid bulbs bilaterally.

The right vertebral artery showed antegrade flow.

The left vertebral artery was not identified on the colour doppler study.

……

OPINIONS:

Bilateral carotid atherosclerosis with no haemodynamically significant stenosis.”

55.  The TMH DS did not examine the intracranial cerebral arteries including the basilar artery since this is not part of the standard investigation.

(d) Repeat MRA

56.  In the Jt Report, the Experts agree that (a) the Repeat MRA is of better imaging quality than the TMH MRA, (b) the other cerebral arteries appear normal with no evidence of atherosclerotic narrowing, and (c) the left vertebral artery remains small and attenuated as shown in the TMH MRI/MRA, thereby confirming its vestigial nature.

X. PRELIMINARY POINTS

57.  It is convenient to set out my initial observations on several points raised by Mr Sahkrani for they form an underlying thread in his submissions to which I shall return from time to time in my discussion below.

58.  First, Mr Sakhrani suggests that in raising the Issue the Defendant is seeking to go behind the views expressed by Drs Lai and Cho in their respective radiology reports for the TMH MRI/MRA and the TMH DS. He says that such reports are professional reports, and hence the Defendant’s present application premised on Dr Yu’s suggestion to obtain neuroradiology expert evidence is an impermissible attempt for a “second bite of the cherry”.

59.  In my view, the above proposition fails to recognise the distinction between clinical and forensic evaluations.  Wu Leung Kui Jacky v Leung Ming Yun & ors DCPI 1154/2008, H H Judge Mimmie Chan (unreported, 7 March 2011) at para.62 underlines such distinction as follows:

“Professor Mak has fairly pointed out the difference in the role played by a treating psychiatrist and a forensic expert. She highlights the fact that in clinical situations, there is an underlying trust between the patient and the treating psychiatrist, who share a common goal in that the patient wants to get well and the psychiatrists helps the patient to get well. When the psychiatrist acts as a forensic expert assisting the Court, the psychiatric expert has an obligation to critically evaluate all the sources of information in order to assess the reliability of the plaintiff and his assertions. ……”

In my decision in Pun Kwong Cheung v Tang Shiu Wo trading as Luen Yick Decoration & Design Co & anor HCPI 587/2008 (unreported, 23 February 2010) paras.54-57, I have also noted the different roles of medical professionals/doctors in clinical and forensic settings:

“In the usual clinical setting involving doctor-patient relationship, the patient suffering from psychiatric disorder or symptoms comes to seek medical help for those problems, and it will be unusual for the clinician to critically question whether or not the patient is actually experiencing those problems or whether he is exaggerating or even malingering. It is also not normally expected for the psychiatrist clinician to seek corroboration of a patient’s information or complaint to the same extent as will a forensic examiner. ……”

60.  The above observations are applicable also in the context of radiological medicine.  Forensic radiology operates at the interface of law and radiology where scientific/clinical radiological expertise is applied in the legal context.  A forensic radiologist is not the evaluee’s “doctor”.  He provides evaluative “expert” medical opinion on diagnostic issues whilst the radiology therapist gives professional “fact” evidence on the diagnosis made for treatment purpose.

61.  In such context, therapeutic and forensic decision-making in radiology medicine may differ.  As explained by Professor Mak in Wu Leung Kui Jacky, the primary goals of therapeutic activity in the best interest of the patient must be cure and palliation.  In the treatment context, it is to be expected that therapists will rather maximise the detection of pathology than risk the serious consequence of failing to detect a potentially threatening symptom or condition.  To put it in another way, the risk of false positives is regarded as a lesser evil than false negatives (ie undiagnosed diseases).  But selectivity is more important in a forensic setting.  After all, it falls on the claimant to prove (and the defendant to challenge) causation between the accident and the injury and between the injury and the current disabilities.

62.  Since the therapist is primarily interested in promoting the patient’s well-being, his expertise is focused on diagnosis and treatment.  But the forensic expert is expected to critically evaluate the claimant’s specific complaints and the historical accuracy of his medical narrative on the basis of scientific knowledge and forensic techniques in order to assist the court in its adjudication of the legal dispute, including any dispute on the issue of causation of medical conditions and residual disabilities.

63.  It is therefore not unusual for forensic experts to disagree with therapists, eg expert psychiatrists may find claimants to be malingerers with no diagnosable psychiatric illness even though they may have received extensive psychiatric or psychological treatments, or expert orthopaedists may find claimants to have grossly exaggerated their physical limitations even though they may have received extensive physiotherapy and/or occupational therapy treatments with little objective signs of musculoskeletal injury.  

64.  Even in the area of radiology, it is not surprising for experts to disagree with therapists as to, say, whether a hairline fracture is shown on X-ray or whether an annular tear is evident on CT discography.  Indeed, in Woo’s 1^st and 2^nd Reports, Dr Woo says his review of the TMH MRI/MRA and the TMH DS images fails to confirm dissection of the left vertebral artery and/or atherosclerotic changes along the common and internal carotid arteries as reported by Drs Lai and Cho. Does it mean that the Plaintiff (by his neurology expert Dr Woo) is also making an impermissible attempt to go behind the views of Drs Lai and Cho for a “second bite of the cherry”?

65.  In my view, on the above analysis of the different functions of forensic and clinical evaluations, neither the Plaintiff nor the Defendant is making any such impermissible attempt.  Indeed, as Mr McLeish submits, the court is not necessarily bound by the treatment medical evidence.  Ultimately, the question is whether the proposed neuroradiology expert evidence is relevant, necessary and of probative value in assisting the court in its evaluative and adjudicating function.

66.  Secondly, Mr Sakhrani submits that radiological studies are but one type of diagnostic tools (and for this the radiology reports of Drs Lai and Cho are already available), and the Jt Report demonstrates they cannot replace neurological expert opinion in assessing the significance of the radiological findings against the whole clinical picture and other factors that are relevant to the issue of causation (see paragraph below).  Mr Sakhrani also argues that since the radiological studies will not obviate the need for interpretation by the neurologist Experts, there is no basis for Mr McLeish’s submission that the reason for neuroradiology expert evidence is to avoid interpretation by the neurology Experts.

67.  It is true that in the Jt Report both Experts have expressed different views over a number of clinical features and other factors in their deliberations as to the cause(s) of the Plaintiff’s stroke, for example:

(a) the significance or otherwise of the temporal proximity of the Accident and the onset of the Plaintiff’s stroke;

(b) the likelihood or otherwise of the one cycle flexion-extension (whiplash) neck movement at the time of the Accident being the suspected underlying cause of extracranial vertebral artery dissection;

(c)  whether or not a diagnosis of extracranial vertebral artery dissection is supported by clinical features, such as headache or neck pain, or by the site of the infarct;

(d) whether the medications prescribed for treatment of the Plaintiff’s stroke is consistent with stroke due to atherosclerosis or stroke due to arterial dissection.

68.  But it is equally true that the Experts also rely on the available radiological evidence, and they have premised their differing views as to the cause(s) of the Plaintiff’s stroke on their respective interpretation of such radiological evidence from a neurological perspective and on medical postulations and/or conclusions drawn from such interpretations.

69.  I believe Mr Sakhrani’s submissions reflect a misunderstanding of the Defendant’s stance, which in my view does not seek to doubt the value of neurological expert opinion.  As I understand it, Mr McLeish’s point is that given the fundamental and material differences between the Experts in their interpretation of the TMH MRI/MRA, the TMH DS and the Repeat MRA, and further given Dr Woo’s modifications of his own views over such interpretation, which differences and modifications have led to their conflicting conclusions on the medical causation of the Plaintiff’s stroke, expert neuroradiological interpretation of the radiological evidence being an admittedly relevant diagnostic tool will be helpful to the court by providing specialist scientific criteria for evaluating and assessing the differing opinion of the Experts.

70.  Dr Yu accepts that neurologists are well-versed in interpreting magnetic resonance findings in the majority of cases, but in cases where the radiological findings are crucial for decisions on diagnosis and management the neurologists will consult radiology colleagues. Although Mr Sakhrani says that “[with] respect, this does not follow”, I disagree.  Radiologists are experts in image capture technology, and are specialists in radiographic image interpretation and reporting in a clinical setting.  Plainly, there must be a clinical interface between the referring clinician and the imaging specialist.  I do not see anything illogical in Dr Yu’s views that neurologists will consult radiology colleagues where the radiological findings are crucial for clinical decisions.  Even Dr Woo accepts that the opinion of a radiology colleague would often be sought in doubtful cases.  

71.  Likewise, I expect that where imaging diagnosis is crucial and/or complicated, the radiologist will correlate image findings with clinical insight from the primary care clinicians as to the pathology, physiology and therapies of the underlying disorder.  Indeed, I see every advantage in combining the patient insight, clinical experience and disease-focused interpretation skills of the clinical specialist with the technologic, consultative and broad-perspective imaging interpretation skills unbiased by clinical specialisation of the radiology specialist, so that their inter-disciplinary collaboration will result in co-ordinated image interpretation within the clinical context of medical symptoms and disease aetiology for the benefit of the patient.

72.  In light of the above, I see little reason why optimal neuroimaging forensic evaluation should not require both neurological and radiological input in appropriate cases where skilled radiographic interpretation is necessary and desirable.

73.  Chum Oi Wa & anor v Kong Sai Wah Kelvin & anor HCPI 766/2001, Suffiad J (unreported, 6 May 2004) is a medico-legal case arising out of abruptio placentae complications in relation to the pregnancy and labour of the 1^st plaintiff and the birth of the 2^nd plaintiff by her.  The parties adduced neuroradiology expert evidence on the MRI readings in addition to obstetric and neonatal paediatric expert evidence.  The neuroradiology experts were instructed to “study the neuroimaging in order to diagnose the pathology underlying the (2^nd plaintiff’s) neurological disabilities and by correlation with the history to comment on the causation and timing of the brain damage”.  The plaintiffs’ neuroradiology expert gave opinion on the cause of the brain damage to the 2^nd plaintiff, but disagreed with the defendants’ neuroradiology expert over the timing of such brain damage.  Whilst I am not concerned with the substance of their disagreement, it is pertinent to note that neuroradiology expert evidence was considered relevant and admissible in that case even though both experts agreed that the timing of the onset of the brain damage “must be correlated with the birth history by obstretic and neonatal expertise”.

74.  In Carter v Basildon & Thurrock University Hospitals NHS Foundation Trust [2007] EWHC 1882 (QB) (30 July 2007), the deceased mother died from the effects of cerebral venous sinus thrombosis (CVST), a comparatively rare form of stroke that sometimes present itself during perperium shortly after childbirth.  The defendant claimed that the hospital’s negligent treatment made no difference for nothing could be done to prevent her death. So the court had to ascertain whether the evolution of the deceased’s presentation and symptoms should have alerted the medical staff to her serious and developing problem such that earlier proper treatment would have prevented her death.  On such issue, basing at least in part on what was eventually shown on the CT scan done in the evening, the parties neuroradiology experts opined that (a) a CT scan done in the morning would have shown evidence of thrombosis but it would not have been possible to identify the location of the CVST at that stage, and (b) a competent radiologist would have described the changes on the CT scan and included some description of the existence of thrombosis in the cerebral veins.

75.  Such neuroradiology expert evidence that analysed the radiological studies as to how the deceased’s CVST developed and that postulated the likely radiological presentation of neuronal damage on an earlier notional CT scan was considered relevant and admissible notwithstanding neurology expert opinion was available to assist the court in resolving the essential issues of the timing of any significant occlusion and/or whether or not earlier differential diagnosis would have resulted in earlier administration of anticoagulant for the deceased.  

76.  These authorities show that the availability of expert opinion by clinician experts (be they neurologists, obstetricians or neonatal paedistricians) and/or of radiological images/reports obtained during the treatment process do not necessarily result in exclusion of neuroradiology expert evidence.  In my view, the true question in the context of the present action is, as suggested by Mr McLeish, whether neuroradiology expert opinion will be helpful in assisting the court in its adjudication.  Dr Yu says that given the conflicting views between the Experts as to whether or not there is radiological evidence of dissection of the extracranial segment of the left vertebral artery, radiological interpretation is crucial for elucidation of the diagnosis, and hence neuroradiology expert evidence is necessarily helpful.  On the other hand, Dr Woo fails to see how such expert opinion can have any impact on the final diagnosis, bearing in mind that normal MRI/MRA does not exclude dissection and definitive conventional angiography has not been performed.  This will be discussed in greater detail below.

77.  Thirdly, Mr Sakhrani argues that since the existing radiology reports of Drs Lai and Cho have not prevented disagreement between the Experts, further neuroradiology expert opinion is unlikely to resolve such disagreement or narrow/reduce the area of such disagreement, and may even lead to more disputes.  Putting it in another way, Mr Sakhrani says there is nothing to demonstrate that further neuroradiology expert evidence will be “determinative of the issue in relation to dissection and atherosclerosis and do away with the need of [the opinion of the Experts]”, and there is no reason to conclude that such expert evidence is likely to reveal anything not already known, particularly from the TMH MRI/MRA and TMH DS before us.

78.  But it is not the Defendant’s case that neuroradiology expert evidence will be determinative of the issue of causation of the Plaintiff’s stroke.  Rather, Mr McLeish suggests that such expert evidence will be of real assistance to the court by offering skilled analysis based on scientific criteria of the important diagnostic tools that the Experts have relied on for their deeply divided views.

79.  As explained above, the fundamental purpose of expert medical evidence is to assist the court in its adjudication of the disputed issues.  If expert medical evidence is relevant, necessary and of probative value in the context of a particular case, it should not be excluded for the reason that (a) the parties’ respective experts are likely to have divided views, (b) their views may differ from the therapist’s diagnosis and management, or (c) it may raise more medical considerations than canvassed by the therapist. I do not agree that such expert medical evidence will necessarily “confuse the issue” as suggested by Mr Sakhrani.  If genuine medical issues that have impact on the interpretation of the factual evidence and/or the determination of the disputed issues before the court are reasonably raised in the litigation, it is the duty of the court to adjudicate on such medical issues no matter how many and how complex, and this is where medical experts who have special skill and experience not possessed by ordinary laymen come in. Medical certainty is not a criterion for adducing expert medical evidence. After all, the expert’s role is to furnish the judge with the necessary scientific criteria for forming his own independent judgment by the application of these criteria to the facts proved in evidence (see Davie v Edinburgh Magistrates [1953] SC 34, 40).

XI. NEURORADIOLOGY EXPERT OPINION

80.  Before I consider counsel’s submissions as to whether or not there is a need for neuroradiology expert opinion, it is necessary to consider what issues are proposed to be canvassed by such expert opinion.

81.  Mr McLeish submits the specific questions for the neuroradiology expert are whether (and if so, in what way) the available radiological investigations (ie the TMH CT, the TMH MRI/MRA, the TMH DS and the Repeat MRA) show (a) dissection of the lower cervical segment of his left vertebral artery and/or (b) atherosclerosis, which questions go directly to the causation issue that will determine whether or not the Plaintiff is entitled to recover damages from the Defendant as he claims.

82.  Mr McLeish submits that if such expert agrees with Dr Woo’s interpretation as to whether there is radiological evidence of dissection, the Plaintiff’s case that his stroke was caused by flexion-extension (whiplash) movement of his neck at the time of the Accident would be strengthened.  On the other hand, if such an expert sides with Dr Yu on the issue of whether there is radiological evidence of atherosclerosis, the case for concluding the cause of the Plaintiff’s stroke was his pre-existing hypertension and radiotherapy would be strengthened.  Even if such expert is of the opinion that there is radiological evidence of both dissection and atherosclerosis or alternatively there is no (or minimal) radiological evidence of either dissection or atherosclerosis, it will still be of assistance to the court because in the former case the focus can move on to the issue of the relative contribution of each of the Three Possible Causes, and in the latter case it will place more weight on other evidence in determining the causation issue.

83.  Mr Sakhrani disagrees and in his submissions raises the spectre of widening the dispute between the parties if the neuroradiology expert evidence opens the door to a host of as yet unknown medical issues.  For example, will there be fresh MRI/MRA investigation or further Doppler study?  Will there be further radiological or neuroimaging study of the Plaintiff’s basilar artery?

84.  In paragraphs 77-79 above, I have already dealt with the Plaintiff’s concerns over the possibility of neuroradiology expert evidence widening the scope of dispute over medical matters. As regards the possibility of further radiographic investigation, if neuroradiology expert evidence is necessary and desirable, it will be for the neuroradiology expert(s) to explain and justify what further radiographic investigations (if any at all) that will aid interpretation of the available radiological evidence and/or elucidation of any radiological basis in respect of the cause(s) of the Plaintiff’s stroke, especially when the Experts agree that radiological changes for hypertensive cerebrovascular disease are irreversible (see paragraph 37 above) and those of radiotherapy-induced injuries are irreversible in the majority of cases (see paragraph 39 above).  This will be no different from an orthopaedic or neurology expert recommending a CT scan, discography, ECG, nerve conduction test or other medical examination to aid forensic evaluation of the relevant diagnosis and management.  If it is the neuroradiologist’s considered view that fresh radiological investigation will not be of assistance, then he will apply his expertise and experience in the interpretation of the available radiological evidence.

85.  I agree with Mr McLeish that a neuroradiologist would possess the necessary recognised expertise to assist the court in the interpretation of radiological evidence.  I further agree with Mr McLeish that Chum Oi Wa & anor (see paragraph 73 above) and Carter (see paragraphs 74-75 above) are clear illustrations of such proposition.  Here, neurology opinion by the Experts suggests that it is technically possible for radiography (through diagnostic imaging) to provide direct and/or indirect evidence of arterial injury or dissection (see paragraph 34 above), and to detect the existence, extent and severity of atherosclerotic changes or disease (see paragraphs 37-38 above).  So even though conventional catheter-based angiography (which according to Dr Woo is the standard of reference in the evaluation of arterial injury) has not been performed, the question is still whether it is relevant, necessary and of probative value to obtain neuroradiology expert evidence in the context of the present case.  Both Mr Sakhrani and Mr McLeish submit that the answer can be found upon a study of the opinion expressed by the Experts to which I now turn.

XII. DISCUSSION

86.  The Experts disagree as to whether the available radiological images show evidence of dissection or atherosclerosis.

(a)  Dissection

87.  Apart from considering the clinical features and other factors, the Experts turn to the available radiological evidence in forming their conclusions on whether there has been any dissection of the lower cervical segment of the Plaintiff’s left vertebral artery.

(1)  Dr Woo’s opinion

88.  The TMH MRI/MRA was reported by Dr Lai as showing a suspicious dissection of the left vertebral artery.  But when Dr Woo first reviewed the TMH MRI/MRA images for Woo’s 1^st Report, he finds that the images fail to show classical radiological features of dissection, and the appearance of the left vertebral artery attenuated in its cervical segment to be suggestive of a vestigial artery instead of dissection.  However, the presence of a dissection within the first few days of the Accident cannot be excluded as the TMH MRI/MRA was performed some 10 days after the ictus (during which time the Plaintiff had been treated with antiplatelet medication and his clinical status had improved to the extent that he was ready to be discharged home on the day he had the TMH MRA).  Dr Woo says it is plausible that the dissection, especially if it were mild, to have resolved spontaneously.  He therefore opines in Woo’s 1^st Report that probably a mild dissection of the Plaintiff’s left vertebral artery has resulted from the flexion-extension movement of his head and neck at the time of the Accident, and this was the immediate precipitating factor for his brainstem stroke.  The Plaintiff most probably would not have suffered from his current disabilities but for the Accident.

89.  In Woo’s 2^nd Report, Dr Woo reiterates that after reviewing the TMH MRA images for Woo’s 1^st Report, he took a different view from Dr Lai, ie the radiological changes of a small attenuated left vertebral artery point to a vestigial vessel with congenital and not acquired changes.

90.  The Repeat MRA was not available at the time of Woo’s 1^st Report. In Woo’s 2^nd Report, Dr Woo says that careful review and comparison of the TMH and Repeat MRAs show a very faint signal change in the mid-segment of the left vertebral artery in the TMH MRA, but this signal change cannot be detected in the Repeat MRA.  The difference can be interpreted as indicating a small intramural clot in the vessel in the TMH MRA which has since resolved.  Such sequence of events suggests there may have been a small dissection in the vestigial left vertebral artery.

91.  Dr Woo goes on to say that dissection cannot be excluded as its radiological changes are very subtle (especially when the TMH MRA images are not of superior quality and the interpretation is difficult), so one can only suspect but cannot be certain of the presence of a dissection.  Further, failure to convincingly demonstrate dissection on the TMH MRA can be explained by the fact that it was not performed until 11 days after the Accident.  As radiological changes of dissection resolve with time and the Plaintiff improved during the intervening days and was clinically stable at the time of TMH MRA, so any radiological changes of dissection could have been missed if the MRA were not performed within the appropriate time window.  Dr Woo postulates that had the MRA been performed on, say, 13 or 14 January 2009, the changes could have been visualised.

92.  In the Jt Report, Dr Woo also says that when he first reviewed the radiological images for Woo’s 1^st Report he did not feel the changes represented dissection although the intramural clot signal at the lower segment of the left vertebral artery associated with slow flow signals at more distal levels can be considered as compatible.  Upon review of the TMH MRI/MRA for the Jt Report, Dr Woo says the T1W FS sequence shows a signal change at the lower segment of the left vertebral artery suggesting a small intramural clot in the vessel compatible with arterial dissection.  There are signal changes at more distal levels in the left vertebral artery, but they took on a different configuration and are compatible with slow blood flow. Dr Woo opines that the MRI/MRA changes are suspicious of a dissection.  The Repeat MRA (which is to evaluate if the left vertebral artery is indeed vestigial and not to look for any further evidence of dissection which evidence should not be present after almost 18 months) is of better imaging quality.  The left vertebral artery remains small and attenuated as in the TMH MRI/MRA, thereby confirming its vestigial nature.  The signal change previously observed at the lower segment of the left vertebral artery is still present though to a lesser extent, and there also remains the other signal changes at the more distal segments of the left vertebral artery.

93.  Further, Dr Woo says that the TMH MRI/MRA show that blood flow was undoubtedly present, though diminished, in the vestigial left vertebral artery, so when dissection occurred, even if it was a small one, there was further flow disturbance in a low-flow artery and ischemic deficits would evolve in the downstream region.  As the left vertebral artery is not the major blood supplier to the brainstem (as compared to the right vertebral artery), clinical deficits resulting from its dissection are likely to be milder. Dr Woo says dissection of the whole left vertebral artery is unlikely as it would probably have resulted in more significant deficits, but the radiological signs are clearly not florid enough to support that view.

94.  Dr Woo says that since the radiological changes on the TMH MRI/MRA are not florid (being limited by the fact that the left vertebral artery was small and attenuated in its cervical segment thereby indicating a vestigial artery, and that the MRI/MRA were not performed until 10 days after the onset of the Plaintiff’s illness when his deficits were stabilised and improving), the dissection might or might not have resolved at that point in time, but it was more unlikely to be active (ie it was not causing further reduction in flow).  The dissection improves on its own, and aspirin does not cure the dissection but merely acts to minimise the amount of thrombosis at the site of the dissection.

95.  In the Jt Report, Dr Woo therefore concludes that an intramural clot was likely present in the lower segment of the left vertebral artery in January 2009 but it resolved with some remaining scar tissues in June 2010.  He reminds that MRI/MRA are not sensitive and refers to the 1994 Study which suggests that MRI misses 40% of cases and MRA misses 80% of cases.  The fact such study was still cited in medical literature in 2004 suggests that the low sensitivities of MRI/MRA have not improved in those 10 years, and even allowing for improved techniques in more recent years there remains appreciable false-negatives.  But unfortunately definitive conventional angiography, which is warranted when MRI/MRA changes are non-diagnostic, was not performed by TMH in this case despite a high clinical index of suspicion.

(2)  Dr Yu’s opinion

96.  Dr Yu opines that in the axial slices (at the level of the C5 vertebra) of the T1 fat suppression sequence for the TMH MRI/MRA, there is a tiny area of hyperintense signal in the lower segment of the left vertebral artery.  Similar tiny areas were also present in axial slices at the same and other vertebral levels.  As for the tiny area of hyperintense signal at issue, there are two possibilities, the first of which is more likely: (a) this may be due to a slow flow artefact or adjacent vertebral veins as are similar tiny areas in the other slices; or (b) it may represent a small intramural clot (a sign of dissection) but its appearance is atypical of an intramural clot and there are no other recognised magnetic resonance signs of dissection.

97.  Dr Yu says that since conventional angiography has not been performed, the analysis should be based on the available radiological evidence.  He opines that on the TMH MRA the tiny dot visualised on the fat suppression sequence of MR T1 axial slices at the lower segment (at C5 vertebral level) of the left vertebral artery probably does not represent an intramural clot:

(a) this tiny dot is more likely to be a flow artifact or a vertebral venous flow signal;

(b) the common site of extracranial vertebral artery dissection is at the C1-C2 vertebral level, which site is involved in half to two-thirds of all vertebral artery dissections, and in 80% to 90% of rotation-related dissections, but while most cases of rotation- related dissection are at such site it does not mean that such site is uncommon for cases of non-rotation dissection;

(c) the lower segment of the vertebral artery remains an uncommon site for both rotation-related and non-rotation dissection;

(d) if there had been dissection, the intramural clot would not have been so limited in its extent;

(e) there are no other recognised MRA features for arterial dissection.

Dr Yu therefore opines there is no radiological evidence for dissection at the lower cervical segment of the left vertebral artery.

98.  Dr Yu further opines that when a vertebral artery is vestigial, there is substantially reduced blood flow, and the contralateral vertebral artery takes over much of its role in supplying blood to its designated territory and to the basilar artery.  Here, the TMH MRA shows greatly reduced flow and the TMH DS shows no flow in the left vertebral artery.  Even if there had been dissection of this vestigial vertebral artery, it is unlikely there would have been further and critical reduction of blood flow.  Moreover, given the very narrow calibre of this vestigial artery, a dissection would most likely have caused complete obstruction of the artery; but this is not the case on the TMH and Repeat MRAs.

99.  Dr Yu further opines that it is unusual for magnetic resonance features of dissection to have resolved by the time of the TMH MRA (ie within 10 days), which images do not show classical features of dissection.  He points out that aspirin takes time to act, and it only prevents platelet aggregation and further thrombosis but does not dissolve blood clots.  Clinical improvement represents the functioning peri-infarct brain tissues taking over the function of the infarcted tissues, and does not equate to resolution of dissection of the artery.  Further, since there has been substantial improvement in magnetic resonance technology in the 15 years after the 1994 Study, the sensitivity of magnetic resonance procedures in detecting dissection was much higher in 2009, and MRI/MRA have become the mainstay for diagnosis of dissection in clinical practice.  Dr Yu says the likely explanation for the 1994 Study to be quoted in medical literature even in 2004 is that such study has not been repeated on newer generations of magnetic resonance machines rather than because the data was still applicable.

(3)  Analysis

100.  Mr McLeish submits that neuroradiology expert opinion will be of assistance in considering the difference in opinion between the Experts as to whether there is radiological evidence demonstrating signal changes that reflect the occurrence of dissection.  Even if the neuroradiologist says there are no such signal changes, “the focus can [then] move to the significance of this ……”.  He fails to understand the Plaintiff’s reluctance to have neuroradiology expert opinion since there is always the possibility that the neuroradiologist may side with Dr Woo’s opinion in which case the Plaintiff’s case on dissection as the precipitating cause of the stroke will obviously be strengthened.

101.  Mr Sakhrani argues that neuroradiology expert evidence will not bring the matter further because (a) Dr Yu agrees that MRI/MRA is the mainstay for diagnosis of dissection in clinical practice, and (b) Dr Lai’s report in respect of the TMH MRI/MRA has categorically concluded that the findings are suspicious of underlying vertebral artery dissection.  He says there is no basis for assuming that further neuroradiology expert opinion will come to a different conclusion, but if it does, it will only add confusion and may lead to further applications, costs and delay.  Mr Sakhrani also criticises Dr Yu for attempting to contradict Dr Lai’s report by saying there is no radiological evidence for dissection at the lower cervical segment of the left vertebral artery.

102.  As explained in paragraphs 58-65 above, forensic medical experts are not necessarily bound by the radiological interpretation and consequent findings by the treatment radiologists, especially when the radiographic images are available for review by the neurology and/or (where necessary and desirable) the neuroradiology forensic experts.  Again, as explained in paragraphs 66-79 above, the fact that forensic experts do not agree with the therapists as to diagnosis and/or management is not necessarily an evidential evil that needs to be avoided.  If different forensic opinion is necessary, relevant and of probative value in the sense that it is helpful to the court in elucidating the medical dispute, then such evidence is admissible for just determination of the disputed issues before the court.

103.  In fact, Dr Woo also does not just take the word of Drs Lai and Cho. He himself has reviewed the TMH MRI/MRA in coming to his own interpretations of the radiological evidence (see paragraphs 88-95 above), and indeed in Woo’s 1^st Report, Dr Woo has even disagreed with Dr Lai’s interpretation of the TMH MRI/MRA (see paragraphs 88-89 and 92 above).

104.  It is interesting to follow Dr Woo’s modifications of his interpretation of the radiological evidence presented by the TMH MRI/MRA.  In Woo’s 1^st Report, he notes the absence of classical radiological features of dissection, opines the radiological appearance of the left vertebral artery is suggestive of a vestigial artery instead of dissection, and merely says dissection cannot be excluded because it is plausible that dissection, especially if mild, would have resolved spontaneously by the time of the TMH MRI/MRA.  Woo’s 2^nd Report confirms that Dr Woo’s view expressed in Woo’s 1^st Report that the radiological changes pointing to a vestigial left vertebral artery are congenital and not acquired.

105.  But in Woo’s 2^nd Report, by comparing the TMH and Repeat MRAs, Dr Woo opines that (a) the very faint signal in the “mid-segment” of the left vertebral artery in the TMH MRA can be interpreted as a small intramural clot signal that has “since resolved”, (b) such signal is suggestive of a small dissection, and (c) such signal change “could not be detected in the recent scan” (ie the Repeat MRA).  But in the Jt Report, Dr Woo says that (i) in the TMH MRA the signal change at the “lower segment” of the left vertebral artery is suggestive of a small intramural clot compatible with arterial dissection, (ii) such intramural clot “has resolved with some remaining scar tissues in June 2010”, and (iii) such signal change is “still present though to a lesser extent” in the Repeat MRA.

106.  I note there has been no mention of any signal change indicative of an intramural clot in Woo’s 1^st Report notwithstanding his forensic review of the TMH MRA.  Even when Dr Woo modifies his interpretation of the TMH MRI/MRA (see the above paragraph), there are still differences in his description of the radiological presentation on the TMH and Repeat MRAs as highlighted in (a)-(c) and (i)-(iii) in the above paragraph.  In my view, these matters at the very least reflect difficulty in the interpretation of the TMH MRI/MRA which (as Dr Woo admits) is not of superior quality and does not show any florid radiological changes.  In my view, this provides solid reason for forensic input by a neuroradiologist with particular skill and experience in diagnostic interpretation of radiological evidence.

107.  This view is strengthened when one considers Dr Woo’s opinion against Dr Yu’s. Contrary to what Dr Woo suggests, Dr Yu opines that the hyperintense signal in the lower segment of the left vertebral artery is more likely to be a slow flow artefact or a vertebral venous flow signal rather than a small intramural clot.  Even ignoring for present purpose the clinical features considered by Dr Yu, he points out that the appearance of the hyperintense signal is atypical of an intramural clot, and there are no other recognised radiological signs of dissection (see paragraph 34 above).  I bear in mind there are signal changes at the distal level in the left vertebral artery. There is little analysis by the Experts on this in the Jt Report, but Dr Yu says the hyperintense signal like the other “similar tiny areas in the other [axial] slices” may be due to slow flow artefact or a vertebral venous flow signal, and Dr Woo also says such signal changes are “compatible with slow blood flow”. This requires a critical radiological study of not just the hyperintense signal in question but also the signal changes at the distal level for a comprehensive radiographic picture.

108.  Dr Yu adds that dissection is unlikely because (a) a dissection of the vestigial left vertebral artery (with substantially reduced or nil blood flow demonstrated by the TMH MRA and TMH DS) would most likely have caused complete obstruction of the artery, but this is not the case on the TMH and Repeat MRAs, and (b) contrary to what Dr Woo says, it is unusual for radiological features of dissection to have resolved by the time of the TMH MRA.  On the other hand, Dr Woo says even a mild dissection would have caused further flow disturbance in the low-flow artery, which is not the major supplier to the brainstem, thus causing milder clinical deficits.

109.  There is further disagreement between the Experts as to the sensitivity of magnetic resonance technology in 2009 (ie at the time of the TMH MRI/MRA) in detecting dissection.  Dr Yu says the sensitivity is much higher than suggested by the 1994 Study so that MRI/MRA have become the mainstay for diagnosis of dissection in clinical practice (and yet there are no classical features of dissection in the TMH MRA).  Dr Woo says the 1994 Study cited in medical literature in 2004 indicates there are still appreciable false negatives in MRA detection of dissection.  In my view, the technologic aspect of MRI/MRA is plainly a matter within the particular expertise of neuroradiologist.

110.  I agree with Mr McLeish that this case cries out for neuroradiology expert evidence.  The fact that Dr Woo has modified his own interpretation of the TMH MRA and that he differs from Dr Yu over interpretation of the radiological evidence demonstrates that particular technologic and diagnostic interpretation skills of the neuroradiologit are relevant, necessary and of probative value in the present case.

111.  Dr Woo suggests that neuroradiology expert evidence is of no assistance because no definitive conventional angiography has been performed.  I agree with Mr McLeish that such suggestion misses the point, because in determining whether or not particular expert medical evidence is required, the court does not look for medical certainty but considers whether such expert evidence will be helpful to the court in deciding on the balance of probabilities the cause(s) of the Plaintiff’s stroke.  Leave to adduce expert medical evidence should not turn on the fortuity or otherwise of diagnostic investigations having been performed during medical treatment.

(b) Atherosclerosis

112.  The Experts also rely on imaging evidence to support their respective views on whether or not the Plaintiff’s stroke was caused by pathological lesion in the basilar artery as a result of radiotherapy-induced or hypertensive atherosclerosis.  

(1)  Dr Yu’s opinion

113.  The Plaintiff underwent radiotherapy for nasopharyngeal carcinoma in 1993.  Dr Yu opines he has sustained radiation-induced injury:

(a) The Plaintiff has panhypopituitarism as a result of damage to the 9^th, 10^th and 12^th cranial nerves bilaterally, which nerves are affected because they traverse two high dose irradiation zones, ie the region where they exit the skull base and the upper neck.

(b) The Plaintiff probably also has a mild right facial palsy as documented in the medical notes: “[claimed] right mouth-angle dropped all along after radiotherapy”.  The radiation injury may affect the facial nerve at any site, but since the facial canal and stylomastoid foramen region are in the low dose irradiation zones the facial nerve is more likely to be affected at its intracranial sites.

(c) Since the posterior extent of the radiation portal covers the whole clivus and extends about 1cm (and sometimes more) posterior to the clivus, thus possibly covering the basilar artery which is situated at the ventral aspect of the pons between the posterior aspect of the clivus and the pons, it is likely that radiotherapy-induced vascular injury (atherosclerosis) of the basilar artery and/or its paramedian branches supplying the pons was present causing the pontine infarct.

114.  As regards the Plaintiff’s pre-existing hypertension, Dr Yu considers such hypertension diagnosed in March 2008 to be of a relatively short duration.  His review of the ECG reading taken on admission to TMH shows left ventricular hypertrophy which according to the voltage criterion (S_V2 + R_V5 = 43mm; normal ≤ 35mm) is a sign of early hypertensive heart disease indicating that hypertension has caused tissue changes in the heart muscles.  He disagrees with Dr Woo’s interpretation that the ECG was normal. After all, the Plaintiff is of average built and probably does not have a thin chest to justify spurious voltage abnormality.  Dr Yu also does not agree that an early sign can be dismissed because it is not accompanied by other signs which indicate more advanced disease.

115.  Dr Yu notes that in the report for the TMH DS Dr Cho has clearly stated his findings of diffuse atherosclerosis and multiple non-calcified atheromatous plaques in the common carotid artery and cervical segment of the internal carotid artery bilaterally, but there is no atherosclerotic narrowing on the serial TMH and Repeat MRAs.  These findings on one hand confirm the absence of atherosclerotic stenosis of those arteries and on the other hand demonstrate diffuse atherosclerotic changes with non-calcified plaques on the arterial wall that can be due to hypertension or radiotherapy-induced vascular injury, or both.  Dr Yu opines that such discrepancy is more apparent than real because MRA provides direct visualisation of changes in the artery lumen and enables indirect inference of status of the artery wall, ie it can pick up gross changes such as stenosis, occlusion or deep ulcerated plaques, but it cannot detect changes within the vessel wall, mild atherosclerosis or shallow plaques.  In other words, MRA does not possess the capability of the Doppler ultrasound in this respect. But without ultrasound evidence, the absence of gross atherosclerotic narrowing or changes of the basilar artery on the TMH MRA is not equivalent to the absence of atherosclerosis. 

116.  Stroke may be caused via one of the two mechanisms: (a) reduced blood supply when the feeding artery is significantly narrowed (>70% stenosis) or (b) artery-to-artery emboli dislodged from the atheromatous plaques (see paragraph 33 above).  Even though the TMH DS has not examined the intracranial arteries including the basilar artery, the diffuse atherosclerosis and multiple non-calcified atheromatous plagues demonstrated in the TMH DS show it is likely that “atherosclerosis similar to that in the right and left common carotid arteries and internal carotid arteries has been present” (my emphasis, p.26 of the Jt Report) or “the same changes were present in the basilar artery and its branches” (my emphasis, p.28 of the Jt Report).  Dr Yu adds that these plaques pose a greater risk than calcified plaques in terms of artery-to-artery embolisation.

117.  Dr Yu further opines that stroke from flow-compromised thrombosis and from artery-to-artery embolisation can present in an abrupt or gradual manner.  In the former case, the blockage is complete at the start, the thrombus or embolus being large.  In the latter case, the blockage is incomplete at the start, but blood flow reduction is progressively reduced within hours or days so that artery-to-artery embolisation occurs in repeated bouts also within hours or days.  Dr Yu considers the mode of evolution of the Plaintiff’s stroke as compatible with either flow disturbance or artery-to-artery embolism of the basilar artery and/or its pontine branches.

(2)  Dr Woo’s opinion

118.  In the Jt Report, Dr Woo accepts that (a) the radiotherapy to the Plaintiff’s nasopharynx and neck for his nasopharyngeal carcinoma in 1993 may induce atherosclerotic changes in the blood vessels within its portals (ie the main cerebral arteries at the base of the brain anatomically adjacent to the nasophraynx and the pituitary gland) and also in the large arteries of the neck, and (b) the Plaintiff’s pre-existing hypertension and radiotherapy are pre-disposing factors for atherosclerosis (and in this respect of the possible presence of atherosclerosis, ie changes in the extracranial vessels in the neck but not the intracranial basilar artery).  The MRI/MRA appearance for atherosclerotic changes as a result of radiotherapy-induced injury or hypertensive cerebrovascular disease are similar taking the form of accelerated atherosclerosis with irregular narrowing, stenosis and/or moya-moya pattern (which changes are irreversible once established).

119.  In Woo’s 1^st Report, Dr Woo states that other than changes in the left vertebral artery the TMH MRA does not reveal any sign of atherosclerosis and the other cerebral vessels appear normal with no evidence of any atherosclerotic change.

120.  Woo’s 2^nd Report again says that other than changes in the left vertebral artery, the TMH and Repeat MRAs show that the cerebral vasculature was normal in calibre/appearance without any atherosclerotic change, and there is absence of MRA radiological change to support the diagnosis of hypertensive cerebrovascular disease and/or radiotherapy- induced atherosclerosis.  The TMH DS done more than a month after the Plaintiff’s stroke has been reported as showing diffuse atherosclerotic changes along the common and internal carotid arteries bilaterally with no haemodynamically significant stenosis.  Yet Dr Woo’s “review of the Doppler pictures failed to confirm such atherosclerosis.  In addition, the more definitive [MRA] (which provides a direct and more accurate image of the blood vessels) did not show atherosclerotic narrowing or stenosis of the cerebral vasculature”.  “In the absence of any definitive clue from the [MRA]”, Dr Woo concludes in Woo’s 2^nd Report that “there was no radiological change in the [MRA] to support the diagnosis of hypertensive cerebrovascular disease and radiotherapy-induced atherosclerosis”.

121.  However, on further review of the TMH DS for the Jt Report, Dr Woo says that one can accept a very mild degree of non-ulcerated atheromatous change along the extracranial common and internal carotid arteries bilaterally in the neck with no haemodynamic disturbance. Dr Woo opines that they are not prone to strokes.  After all, they are found only in the carotid vessels (which anatomically supply the cerebral hemispheres) and cannot possibly be the cause of the brainstem stroke, and the TMH DS has not examined the intracranial vessels including the basilar artery.  The above changes must be interpreted together with the absence of any radiographic evidence of atheroma, atherosclerotic narrowing, stenosis or occlusion of those vessels in the TMH MRI/MRA, and with the normal appearance of the cerebral arteries in the Repeat MRA (which is of better imaging quality than the TMH MRA) with no evidence of atherosclerotic narrowing.  Hence, the two serial MRI/MRA studies show the vascular tree or cerebral vasculature to be completely pristine and normal in calibre and appearance with no evidence of atherosclerotic change or disease in any of the blood vessels.   Dr Woo considers MRA to be “more reliable in assessing the vascular trees as it provides a direct image of the blood vessels and it is the usual investigation procured in evaluating the status of the cerebral vessels in everyday clinical practice”.  In the circumstances, the atheromatous changes in the common and internal carotid arteries in the neck cannot possibly be extrapolated to the basilar artery or its branches.  

122.  Dr Woo says this is further supported by the fact that the extracranial carotid arteries in the neck are at the centre of the radiation portals so that mild radiotherapy-induced atherosclerotic changes in these vessels can be accepted, but the basilar artery is at most in the peripheral rim of the radiation portals so that radiotherapy-induced atherosclerotic changes are most unlikely.  The most common anatomical site of cranial nerve damage due to radiotherapy for nasopharyngeal carcinoma is not intracranially in or immediately adjacent to the brainstem at the peripheral rim of the radiation portals but at the skull base at the centre of the radiation portals where the cranial nerve(s) exit the intracranial cavity to reach their destination in the head and neck.  This applies to the facial nerve and all lower cranial nerves that arise from the medulla (causing vocal cord palsy, dysphagia, dysarthria and weakness/fasciculation of the tongue in the Plaintiff’s case).  As such, a cranial nerve is much more likely to be injured in its course within the skull base (eg the facial nerve within the facial canal and not at the stylomastoid foramen) than in its intracranial segment in the posterior fossa (close to the brainstem).  Dr Woo therefore opines that radiotherapy-induced damage to the facial nerve in its intracranial segment in the form of pre-existing droopiness of the right angle of the mouth cannot be taken as a surrogate marker of basilar artery damage.  All these strongly militate against a pathological lesion in the basilar artery as the cause of the stroke and/or a diagnosis of radiotherapy-induced atherosclerosis.

123.  In respect of Dr Yu’s suggestion that stroke can be caused by artery-to-artery emboli, Dr Woo says that such an event occurs suddenly in that blood to the affected area is abruptly cut off by the embolus. Clinical deficits appear acutely and are maximal at onset. On the other hand, a flow compromised thrombotic stroke evolves gradually, and as blood flow is progressively impaired, the affected area becomes progressively ischemic with gradual enlargement of the infarct zone.  Clinical deficits commence insidiously and build up over the next few days.  The Plaintiff’s stroke evolved over an interval of 24 to 48 hours (ie it commenced with some hand clumsiness on 10 January 2009 and it spread to bulbar dysfunction and leg weakness on 11 January 2009).  Such a clinical evolution strongly militates against an embolic phenomenon and argues in favour of a flow disturbance which is consistent with luminal compromise in dissection.

124.  Woo’s 2^nd Report also says there is little corroborative evidence to support hypertensive cerebrovascular disease as the cause of the Plaintiff’s stroke.  He was diagnosed as having hypertension in March 2008 when his blood pressure was elevated at 174/99, and antihypertensive medications were commenced from that time, so his hypertension has not been long-standing (at most a year).  His blood pressure on admission to TMH on 12 January 2009 was 98/66, and it stayed at 120-150/60-90 during the remainder of his hospitalisation from 12 to 20 January 2009.  These values indicate his blood pressure is not poorly controlled.  There is also no evidence of target organ damage to the heart (his chest X-ray was normal) or kidneys (his renal function was normal).

125.  Dr Woo’s interpretation of the ECG is that it is normal, ie (a) spurious voltage abnormality suggestive of left ventricular hypertrophy may be seen in thin-chested individuals, (b) the more reliable and more stringent voltage criterion of eitherS_V1 + R_V5 or S_V1 + R_V6 being ≥ 35mm has not been met, and (c) there is no electrocardiographic change of left ventricular strain.  

126.  Of even greater significance is the absence of any abnormality in the TMH MRI/MRA to indicate hypertensive cerebrovascular disease, ie no parenchymal white matter change in the brain to indicate small vessel disease, and all cerebral vessels (except the left vertebral artery) are pristine.  If MRI/MRA show severe vascular disease in the form of irregularities, narrowing and/or stenosis in multiple cerebral arteries, then one can accept the Plaintiff’s circulatory status was precarious as a result of his hypertension and his radiotherapy so that any of these vessels could have been blocked and a stroke would have been imminent at any time.  But that has not been the case, ie the vessels are pristine so the Plaintiff was not at any risk.

(3) Analysis

127.  Dr Yu opines that the stroke was caused by atherosclerosis of the basilar artery and/or its paramedian branches due to hypertensive cerebrovascular disease and radiotherapy-induced vascular injury via one of two mechanisms: (a) reduced blood supply when the feeding artery is significantly narrowed (>70% stenosis) or (b) artery-to-artery emboli dislodged from the atheromatous plaques, which pose a greater risk that calcified plaques.

128.  Both Experts rely on the clinical features and other factors in coming to their respective views. Dr Yu relies on the Plaintiff’s panhypopituitarism, mild facial palsy (caused by facial nerve damage), and the scope/extent of the radiation portals to support the likelihood of radiotherapy-induced vascular injury (atherosclerosis) of the basilar artery and/or its paramedian branches.  Dr Woo suggests the basilar artery is unlikely to have been affected by the radiotherapy treatment because it is at the peripheral rim of the radiation portals, so that damage to the facial nerve in its intracranial segment cannot be a surrogate marker of basilar artery damage. Likewise in respect of the pre-existing hypertension, Dr Yu says that although the diagnosis of hypertension is of relatively short duration the ECG reading on the Plaintiff’s admission shows signs of early hypertensive heart disease.  Dr Woo, on the other hand, considers such reading to be normal.

129.  Apart from considering the clinical features, Dr Yu has reviewed and interpreted the available MRA and Doppler ultrasound studies as presenting signs of hypertensive cerebrovascular disease and radiotherapy-induced vascular injury, and he makes medical postulations on such foundation.  On the other hand, Dr Woo disagrees there is any radiological evidence of hypertensive cerebrovascular disease and radiotherapy-induced vascular injury.  Although Dr Woo has discussed the clinical features supporting his stance, he also analyses the radiological evidence in coming to his conclusion that it is impossible to support Dr Yu’s postulations as to any haemodynamic and/or embolic phenomena from the available MRA and Doppler ultrasound studies.

130.  It should be noted that notwithstanding his aforesaid views, Dr Woo does not dispute that the Plaintiff’s pre-existing hypertension and radiotherapy contributed to his stroke.  Indeed, in Woo’s 1^st and 2^nd Reports and the Jt Report, Dr Woo opines that the combined effect of these two factors account for 40% contribution towards the Plaintiff’s infarct and his residual neurological disabilities (see paragraphs 42, 44 and 46 above).  In Woo’s 2^nd Report, he says that this means these two factors resulted in 40% narrowing of the vessel (which is less than the 70% narrowing for haemodynamic disturbance or stenosis to ensue), but a stroke resulted when the dissection occluded the remaining 60% of the vessel (see paragraphs 44 above).

131.  Given that the respective views of the Experts rest substantially on a radiological foundation, I am of the view that interpretation of the radiological evidence will play an important role in determining which medical stance (if any) is sound.  At this interlocutory stage when it is inappropriate to form any definitive view, the relevant consideration is whether specialist neuroradiological interpretation of the available radiological evidence will be helpful.  There is a further dimension, ie whether specialist technologic image interpretation skills and broad-based experience in radiological presentation of symptoms in the context of disease aetiology will be of assistance in assessing the viability of any postulations that can be made from the available radiological evidence.

132.  Whilst Dr Woo accepts hypertensive cerebrovascular disease and radiotherapy-induced vascular injury may induce atherosclerotic changes with irreversible radiological appearance (see paragraph 118 above), he says there is no evidence of such in the present case. Initially in Woo’s 1^st Report he says that the TMH MRA does not reveal any sign of atherosclerosis or any evidence of atherosclerotic change (see paragraph 119 above), and in Woo’s 2^nd Report he reiterates there is no MRA radiological change to support the diagnosis of hypertensive cerebrovascular disease and radiotherapy-induced atherosclerosis (see paragraph 120 above).  Even though Dr Cho has reported that the TMH DS shows diffuse atherosclerotic changes along the common and internal carotid arteries bilaterally but without haemodynamically significant stenosis, Dr Woo in Woo’s 2^nd Report disagrees with Dr Cho and says his review of the TMH DS fails to confirm such atherosclerosis (see paragraph 120 above).  But subsequently upon further review of the TMH DS, Dr Woo in the Jt Report accepts there is mild non-ulcerated atheromatous change along the extracrancial common and internal carotid arteries bilaterally in the neck with no haemodynamic disturbance (see paragraph 121 above).

133.  In my view, the above reflects difficulty and/or doubt in the interpretation of the available radiological evidence which calls for specialist input.  It is plainly helpful to have specialist neuroradiology expert opinion on the particular interpretation of the underlying radiological investigations for enabling the Experts to refine their clinical opinion and for assisting the court in its adjudication.

134.  Mr McLeish goes further by saying that in Jt Report Dr Woo merely acknowledges the presence of atheromatous plaques, which acknowledgment does not amount to a clear acceptance of atherosclerotic changes along the common and internal carotid arteries bilaterally, and as such it reflects a sharp difference between the Experts as to whether the TMH DS shows atherosclerotic changes or not, which difference goes to the very question whether clinical and/or radiological postulations can be made on such foundation as regards the basilar artery and/or its branches.  This, of course, adds weight to the application for adducing neuroradiology expert evidence.

135.  But Mr Sakhrani argues that neuroradiology expert evidence serves no purpose because it is not possible for the atheromatous changes in the common and internal carotid arteries to be extrapolated to the basilar artery or its branches.  In making such submission, Mr Sakhrani relies on the following matters: (a) the TMH and Repeat MRAs demonstrate that the cerebral vessels (except for the left vertebral artery) are pristine with no atherosclerotic change or disease, (b) Dr Lai has already reported that the right vertebral artery and the basilar artery are patent in the TMH MRI/MRA, (c) Dr Woo says MRA is more reliable in assessing the cerebral vascular tree, and (d) the TMH DS has not examined the basilar artery.  Mr Sakhrani says there is no evidence of atherosclerosis in the basilar artery, and no corroborative evidence of hypertensive cerebrovascular disease or radiotherapy-induced vascular injury to support Dr Yu’s proposition.

136.  Even though there is no Doppler ultrasound investigation of the basilar artery and/or its branches at the time of treatment, Dr Yu opines that the absence of gross atherosclerotic narrowing or changes of the basilar artery on the TMH MRA does not equate to absence of atherosclerosis, and (contrary to Dr Woo’s emphasis on the reliability of the MRA) says that MRA does not possess the capability of the Doppler ultrasound to detect changes within the vessel wall, mild atherosclerosis or shallow plaques.  Dr Yu says this is borne out by the apparent discrepancy between the diffuse atherosclerotic changes in the cerebral arteries with non-clacified plaques on the arterial wall (which can be due to hypertensive cerebrovascular disease or radiotherapy-induced vascular injury or both) evident in the TMH DS and the absence of atherosclerotic stenosis of those arteries in the TMH and Repeat MRAs.  In Dr Yu’s opinion, the aforesaid discrepant findings (which discrepancy is more apparent than real) merely reflect the different capabilities of MRA and Doppler ultrasound, and leaves open the probability of atherosclerosis in the basilar artery and/or its branches.

137.  Dr Yu has provided a reasoned basis for his views, and it is premature at this interlocutory stage to say (as Mr Sakhrani suggests) his opinion does not hold water.  It will be a matter for trial to see (a) whether or not the TMH DS reflect atherosclerotic changes along the common and internal carotid arteries bilaterally, (b) if so, whether or not such atherosclerotic changes are caused by hypertensive cerebrovascular disease or radiotherapy-induced vascular injury or both, (c) if so, given the radiological evidence, clinical features and disease aetiology, whether or not it is medically possible to postulate the clinical condition and/or radiological presentation of the basilar artery and/or its branches, and (d) if so, whether or not the Plaintiff probably had atherosclerosis in the basilar artery and/or its branches thereby causing his stroke.

138.  In such circumstances, I am persuaded that neuroradiology expert evidence will be helpful in assessing Dr Yu’s postulation (and Dr Woo’s rejection) of basilar arterial damage for this issue plainly cries out for specialist technologic and diagnostic imaging skill and experience.  The need for neuroradiology expert opinion should not turn on the fortuity of having performed Doppler ultrasound of the basilar artery at the time of treatment or otherwise, especially when the Experts disagree over the reliability and/or sensitivity of MRA and Doppler ultrasound in reflecting atherosclerotic changes. In my view, such matter must fall squarely within the particular radiological expertise of the neuroradiologist.

139.  Mr Sakhrani submits that neuroradiology expert evidence is unnecessary because even on the Defendant’s case Dr Yu himself says it is likely the same atherosclerotic changes were present in the basilar artery.  He argues that since the diffuse artheroscleroruc changes and multiple non-calcified atheromatous plaques in the common and internal carotid arteries shown in the TMH DS are insufficient to cause haemodynamically significant stenosis, the Defendant has failed to demonstrate that the first mechanism for stroke (ie reduced blood supply when the feeding artery is significantly narrowed (>70% stenosis)) is possible.

140.  In my view, this reading of Dr Yu’s opinion in the Jt Report is too narrow. In the Jt Report, notwithstanding the absence of Doppler ultrasound investigation of the basilar artery and/or its branches, Dr Yu in fact postulates the existence of similar or same radiological presentation in the basilar artery premised on radiological findings in the TMH DS of atherosclerotic changes along the common and internal carotid arteries bilaterally and multiple non-calcified atheromatous plaques at the distal common carotid arteries and carotid bulbs bilaterally (see paragraph 116 above).  In using the words “similar” and “same” interchangeably in the Jt Report, Dr Yu must have been extrapolating the same nature of atherosclerotic changes and athermoatous plaques to the basilar artery or its branches rather the exact presentation in the common and internal carotid arteries bilaterally shown in the TMH DS.  In my view, this is precisely where the particular skills of the neuroradiologist will be of assistance in helping the court to decide whether Dr Yu’s extrapolation from the radiological evidence on the TMH DS to the basilar artery and/or its branches is viable from a neuroradiological perspective.

141.  For the other mechanism of stroke, ie artery-to-artery emboli dislodged from the atheromatous plaques, Mr Sakhrani argues it has not been demonstrated that it is likely or even possible.  He reminds that (a) Dr Woo says the atheromatous changes in the TMH DS are mild and the plaques not ulcerated, so they are not prone to stroke, and (b) an embolus event occurs suddenly and clinical deficits appear acutely and are maximal at the outset. But one cannot at this interlocutory stage ignore Dr Yu’s disagreement with Dr Woo’s propositions.  Dr Yu says that (i) non-ulcerated plaques pose a greater risk than calcified plaques in terms of artery-to-artery embolisation and (ii) stroke from such mechanism can present in an abrupt or gradual manner.  In my view, it is inappropriate at this interlocutory stage to come to any definitive view on the Experts’ opinion and/or to refuse neuroradiology expert evidence by relying on the opinion of one neurology expert and rejecting that of the other.

142.  Although Mr Sakhrani suggests that the differing views of the Experts as regards the onset of symptoms “is not a matter for the radiologist but the neurologists” in the clinical context, I believe that neuroradiology expert opinion will be helpful in deciding whether atherosclerotic changes and atheromatous plaques evident in the TMH DS is likely to be present in the basilar artery and/or its branches.

(c) Other considerations

143.  For the above reasons, I allow neuroradiology expert evidence to be adduced. Mr Sakhrani warns against the proliferation of expert reports, but I am not persuaded that in allowing such expert evidence in the present context there is any such proliferation.  I find such expert evidence to be relevant and of probative value.  It is not disproportionate and is in fact necessary for the just determination of the disputes in this action.

XIII. CONCLUSION

144.  In the circumstances, I grant leave for expert evidence from radiologist(s) with expertise in neuroimaging to be adduced at trial on the issues of causation and quantum. I therefore grant the following directions:

(a) Within 21 days from today, the parties do jointly write to the PI Master on the following:

(i) state whether the parties will engage single joint or respective neuroradiology expert(s);

(ii) state the name(s) of the parties’ single joint or respective neuroradiology expert(s);

(iii) confirm whether the parties have agreed on the issues to be addressed by the parties’ single joint or respective neuroradiology expert(s);

(iv) state the date when the parties’ single joint or respective neuroradiology expert(s) will complete his/their single joint or joint report;

(v) propose directions for obtaining single joint or joint neuroradiology expert report;

(vi) propose case management directions for extension of time to comply with paragraphs 11-12 and 14-15 of my order dated 24 March 2011;

(vii) propose time period or date for restoring the case for CLR before the PI Master;

(viii) propose all other necessary and appropriate case management directions.

(b) PI Master shall be notified at once and in any event within 3 days if any of the above dates or directions are not met with detailed reasons.

(c) Solicitors for the Plaintiff shall send a sealed copy of this order to the legal aid counsel in charge of this case to ensure there is no delay in compliance with these directions due to late assignment of counsel or due to late issuance of an appropriate certificate.

(d) Liberty to apply.

145.  There is no reason why costs should not follow event.  I grant a costs order nisi that the Plaintiff do pay the Defendant costs of the Issue (including all costs reserved if any) with certificate for counsel, and there be legal aid taxation in respect of the Plaintiff’s own costs.  I further direct that there be summary assessment of such costs, and:

(a) the Defendant  shall within 21 days from today lodge and serve his statement of costs pursuant to Practice Direction 14.3 and the Plaintiff shall within 7 days thereafter lodge and serve his written objection thereto in bullet point format;

(b) each of the aforesaid statement of costs and objection thereto shall be limited to two pages;

(c) if application is made to vary the costs order nisi, such application shall be heard at the same time as the hearing for the summary assessment of costs;

(d) the Defendant do within 21 days from today fix a date with the Listing Clerk for the hearing of the summary assessment of costs to be heard before me in chambers (open to the public) on a date not before 35 days from today with half hour reserved.

146.  It remains for me to thank both counsel for their able assistance.

Representation: