Long v GIO General Ltd

CERTIFICATE OF DETERMINATION OF MEMBER
CITATION:	Long v GIO General Ltd [2021] NSWPIC 489
APPLICANT:	Phillip John Long
RESPONDENT:	GIO General Ltd
MEMBER:	Paul Sweeney
DATE OF DECISION:	30 November 2021
CATCHWORDS:	WORKERS COMPENSATION - Claim by worker for compensation pursuant to section 66 for loss of sight of both eyes and for referral of a threshold dispute as a result of injury on 5 April 2001; unanimous evidence of ophthalmic surgeons that worker’s visual system is normal; claim put on the basis that workers spatial difficulties are caused by a traumatic brain injury on 5 April 2001; by a Medical Assessment Certificate dated 18 August 2011 an Approved Medical Specialist had certified that the worker did not suffer a traumatic brain injury; Held – in view of the conflicting evidence, appropriate to refer the matter to a medical assessor for an opinion as to whether the worker’s visual difficulties result from injury.
DETERMINATIONS MADE:	1. Substitute GIO General as the name of the respondent in these proceedings. 2. Remit the matter to the President for referral to a Medical Assessor (neurosurgeon or neurologist with an interest in the brain) to express an opinion on the papers as to whether the applicant’s visual impairment results from the injury on 5 April 2001 bearing in mind the conflicting opinions of Dr Fearnside and Dr Benjamin, on the one hand and Dr Fraser and Dr O’Sullivan on the other, as to whether the applicant suffered a traumatic brain injury. 3. Medical Assessor to have access to the Application to Resolve a Dispute, the Reply, the Applications to Admit Late Documents and the documents attached to each together with a copy of my reasons for this decision. 4. On receipt of the Medical Assessment Certificate list the matter for a further telephone conference at my first available time slot convenient to the parties.

STATEMENT OF REASONS

BACKGROUND

On 5 April 2001, Phillip John Long (the applicant) fell from a ladder and struck his head on a concrete floor in the course of his employment with Colin Green. It is accepted that he suffered an injury to his neck and a fracture of his skull as a result of the fall. GIO General Ltd (the respondent) accepted liability for the injury and the applicant has been paid weekly compensation and permanent impairment compensation in respect of permanent impairment of his neck and permanent loss of use of his left arm at or above the elbow.
Since the injury, the applicant alleges that he has experienced loss of sight of both eyes. On 22 December 2008, he made a claim for permanent impairment compensation in respect of 55% permanent loss of sight of both eyes and for pain and suffering pursuant to s 67. The claim is based upon the report of Dr Peter Duke, an ophthalmic surgeon dated 4 December 2008.
The respondent did not accept that the applicant suffered loss of sight as a result of the injury. It relied on the opinion Dr Frederick Benjamin, a consultant ophthalmologist who had treated the applicant. After referring the applicant to several specialists for investigations, Dr Benjamin, in a report dated 24 February 2009, expressed the opinion that the applicant’s symptoms were due to “non-organic” factor.
On 18 August 2011, Dr Michael Fearnside, a neurosurgeon, was requested to assess the applicant’s whole person impairment as a result of the injury on 5 April 2001 to resolve a medical dispute between the parties. In addition to the injury to the cervical spine and left upper extremity, he assessed the applicant’s nervous system (mental status and cognition). After considering the extensive medical history available to him at the time and examining the applicant, he concluded that the applicant did not “sustain a traumatic brain injury”. The issue of loss of sight or impairment of the applicant’s visual system, however, was not part of the medical dispute referred for assessment.
In 2016, a neuro ophthalmic surgeon, Dr Clare Fraser, expressed the opinion that the applicant did suffer a traumatic brain injury in the incident and that his impairment of sight results from that injury.

PROCEDURE BEFORE THE COMMISSION

By these proceedings the applicant claims compensation for loss of sight of both eyes and for consequential pain and suffering pursuant to s 67. As the claim for compensation was made prior to the enactment of the Workers Compensation Legislation Amendment Act 2012, the applicant is entitled to maintain the claim for pain and suffering. The respondent, of course, disputes that the applicant is entitled to compensation for loss of sight.
When the matter came on for conciliation and arbitration on 28 October 2021, Mr Willoughby of counsel represented the applicant and Mr Hunt of counsel represented the respondent. The conciliation conference and arbitration hearing were conducted over the telephone. I used my best endeavours to bring about a resolution of the dispute, however, I was informed by counsel that they were unable to resolve the threshold question of whether the applicant suffered loss of sight in both eyes as a result of the injury of 5 April 2001. I am satisfied that the parties had ample opportunity to settle the dispute but were unable to formulate a mutually satisfactory resolution of the claim.

EVIDENCE

The documents before the Commission are as follows:
(a)     the Application to Resolve a Dispute and the documents attached;
(b)     the Reply and the documents attached;
(c)     an Application to Admit Late Documents dated 2 November 2021 which was lodged with the Commission on 2 November 2021 in accordance with a direction I made at the arbitration hearing. and
(d)     an Application to Admit Late Documents dated 23 November 2021 containing an MRI report of 14 August 2013.
During the conciliation conference, Mr Hunt objected to reports of Dr Stern and Dr Harrison. He submitted that they breached cl 44 of the Workers Compensation Regulation 2016 which prohibits the use of a multiplicity of forensic medical reports. Mr Willoughby conceded that this was the case and the opinions of those doctors will be excluded from the evidence considered by the Commission.
Mr Hunt also objected to aspects of the primary report of Dr Briers, but I ruled that this report was admissible and should be admitted into evidence. Otherwise, there was no objection to any of the material identified above. There was no application to adduce further written or oral evidence.
After commencing to write the decision, it became apparent that the report of an MRI scan dated 14 August 2013, which formed the basis of the opinion of Dr Fraser, was not in evidence. The MRI report was lodged with the Commission at my request.

SUBMISSIONS

The submissions of the parties are recorded and I do not propose to reiterate each argument of counsel in detail. However, given the nature of the matter, it is probably appropriate to set out the general thrust of counsel’s argument at the outset.
Mr Hunt relied primarily on the opinions of Dr Benjamin and Dr Fearnside. He submitted that those doctors who expressed the opinion that there was a causal nexus between the applicant’s head injury and his loss of vision did so on the basis of an inadequate history. Either they did not have an accurate history of the applicant’s level of consciousness following his fall, or they did not have access to the results of the extensive investigations carried out by the applicant’s treating doctors in the several years following the injury, particularly MRI scans of the applicant’s brain which was taken in 2002 and 2010.
Mr Hunt submitted that the opinion of Dr Claire Fraser, a neuro-ophthalmic surgeon, who supported a causal nexus between injury and loss of vision, must be discounted as she did not have access to the earlier scans of the applicant’s brain and because she gave no adequate explanation of her opinion.
Mr Hunt also suggested that the applicant’s account of his visual ability was unreliable. He relied on an observation of Dr Benjamin in February 2009 that despite his reported impairment of peripheral vision, the applicant was able to move between various rooms in his surgery without assistance.
Mr Willoughby argued that the contemporaneous medical evidence on which Dr Fearnside relied was “tenuous at best”. The applicant was in no position at the time to give a coherent account of his level of consciousness. Further, he was not seen by the ambulance officers for several hours after the incident and was not admitted to hospital until the evening of the incident. Rather, the Commission should rely on the opinions of the neuropsychologists who had seen him on referral from his treating medical practitioners. Dr Georgius had recorded that the applicant had no recollection of the incident for several days and expressed the opinion that post-traumatic amnesia of this duration was typically the result of a moderate or severe head injury.
Mr Willoughby argued that the applicant’s medical case was quite straightforward. The applicant clearly suffered a significant head injury at the time of the fall as evidenced by the fracture to his skull. Dr Fraser, the only neuro-ophthalmologist, who had seen the applicant had explained his right hemifield neglect and his difficulties with spatial perception and visual processing on the basis of the left sided gliosis seen on his MRI scan. She specifically stated that the gliosis was not an “expected age-related change”. The respondent’s qualified ophthalmic surgeon, Dr Weschler, did not take issue with this analysis. While he stated that he had no qualifications to deal with this issue, he expressed the opinion that Dr Fraser’s opinion provided the most probable explanation of the applicant’s visual problems.
Mr Willoughby submitted that the medical practitioners and neuropsychiatrist’s who had seen the applicant after his first consultation in 2013 unanimously accepted that the applicant’s visual problems were caused by brain damage.
It will be necessary to return to the submissions of counsel when resolving the issues in dispute. It is first necessary, however, to record the evidence of the applicant and the long history of his medical treatment relevant to his alleged loss of vision. What follows is not intended to be a comprehensive survey of the evidence. Rather, I set out the salient aspects of the evidence so that the manner in which the Commission has resolved the dispute can be understood.

THE APPLICANT

The applicant’s primary evidence is contained in an initial written statement dated 17 July 2001 and supplementary statements dated 27 November 2018 and 29 January 2020. By his initial statement the applicant recounts the circumstances of his injury. He says that on the afternoon of 5 April 2001 he was standing on the fourth rung of a ladder undoing bolts with a shifting spanner which he was using with his right hand. He was also carrying a pinch bar in his left hand. He continues:
“After undoing a number of bolts I then placed the shifting spanner in my back pocket while still carrying the pinch bar in my left hand. I then slid the timber rafters/battens down on to the ground and commenced to climb down the ladder to take the timber to the truck where it was to be loaded.
As I commenced to climb down the ladder my right foot buckled through the fourth rung of the ladder and I lost balance. My right leg went through the ladder whilst my body fell backwards. I could not grab onto the ladder with my left hand because I was carrying the pinch bar and although I tried to grab the ladder with my right hand, I know that I had fallen too far backwards to reach the ladder.
The back of my head then struck the concrete forcing my chin on to my chest. I cannot remember anything further until Colin Green came around and into the garage and picked me up. Apparently when he came to the garage I was on my hands and knees holding my head and had blood coming out of my right ear.”
The applicant to recounts that Mr Green came to his assistance. He drove him to his home. As the applicant was able to “get up” an ambulance was contacted. The statement continues:
“The ambulance officers placed a neck brace on me and then transported me to Maitland Hospital where I was x-rayed. The results of the x-ray showed that I had suffered a fractured skull as well as a fractured C2 in my neck. I remained in Maitland Hospital for 7 days where I was treated by Dr Lynette Reece, an orthopaedic surgeon before being discharged.”
The applicant says that he has been unfit for all work duties from the date of the accident. He says that he is unable to drive a motor vehicle and that he suffers from dizzy spells, blurred vision, headaches and fatigue.
By his first supplementary statement, the applicant says that he has not been able to return to work since the injury. He reiterates that he had no difficulties with his eyes or vision prior to the incident. He states, however, that:
“Ever since I fell I have had blurred vision. Ever since the accident I have not been able to read newspapers or documents.
I am now in receipt of a blind pension.”
By a second supplementary statement dated 29 January 2020, the applicant states that subsequent to the injury he has suffered dizzy spells, blurred or blotchy vision and nausea. He says that when he was in hospital following the injury he could not read a newspaper “because of blurred vision”.
The applicant recounts that his general practitioner, Dr Wong referred him to Dr Benjamin who prescribed glasses but “they did not make any difference”. The applicant says that prior to the injury he was able to ride a motor-cycle. Subsequent to the injury he was unable to drive a car for three years “until I felt confident enough to drive”.

MEDICAL EVIDENCE

Following the injury, the applicant was treated at Maitland Hospital for a C2 fracture and an undisplaced fracture of the left occipital bone. He then came under the care of Dr Wong, a general practitioner of Kurri Kurri, who referred him to Dr Benjamin, the ophthalmic surgeon. By a report dated 3 July 2001, Dr Benjamin recorded that the applicant initially had difficulty with his vision for both distance and close work. He recorded that:
“Now his distant vision is clear but he has had increasing discomfort with close work.”
Dr Benjamin concluded that the applicant had a “disturbance of accommodation following the head injury” and a need to change spectacles from time to time. He expressed the opinion that a visual field analysis should be performed before changing the prescription for the glasses. He referred the applicant to a neurologist.
Dr Milder, a consultant neurologist, saw the applicant at the request of Dr Benjamin on 26 July 2021. In his report of that date, he recorded the following:
“The perimeters of the visual fields, as determined by confrontation, were entirely normal. The remaining neurological examination was normal.”
Dr Milder expressed the opinion that the applicant’s visual disturbances may be migranous in origin as he appeared to suffer daily migranous headaches. He prescribed Prothiaden. If there was no improvement in three weeks, consideration would need to be given to electroretinography and visual evoked responses.
On 14 August 2001, the applicant saw Dr Colin Reed, an otolaryngologist, on referral from Dr Reece. He took a history that the applicant had positional vertigo when rolling in bed to the right and when bending over, and headaches and visual disturbances. After performing a series of tests, he expressed the opinion that the likely diagnosis was one of benign paroxysmal positional vertigo affecting the right posterior semi-circular canal. He instructed the applicant in the “modified Epley or particle repositioning manoeuvre” which he stated was successful in helping 80% of patients with this problem.
On 18 September 2001, Dr Wong referred the applicant back to Dr Benjamin as vision disturbance had not improved with the glasses prescribed at the last consultation and the applicant was still visually restricted in a number of areas. On 18 September 2001, Dr Benjamin wrote to Dr Wong stating that the applicant was unhappy with Dr Milder’s diagnosis of post-traumatic migraine and “was not happy at all to take medications that had been recommended”. After referring to the examination that he performed he continued:
“I have explained to him that I could not find any ocular cause for the blurred vision and it would be desirable to go through the electroretinogram and visual evoked responses.”
He stated that in view of the personality clash between the applicant and Dr Milder this might best be done by Dr Burton at Newcastle.
On 29 November 2001, Dr Burton, a consultant neurologist saw the applicant and recorded complaints of recurrent dizziness as well as episodes of “blotchiness” of his vision. He noted that the applicant had been referred to Sydney Eye Hospital where he had been seen by a neuro-ophthalmologist. He thought that further neurological investigations were necessary in view of the nature of the applicant’s complaints. He also referred the applicant for an MRI scan of the brain and neck.
Insofar as it is relevant, the MRI scan of 29 January 2002 reported that there were “white matter changes adjacent to the posterior horn of the left lateral ventricle which are non-specific” and possible early stenosis of the left internal carotid artery. It was suggested that it may be prudent to further assess the carotid arteries with a doppler ultrasound.
On 6 March 2002, Dr Burton wrote to Dr Benjamin regarding his EEG examination. His interpretation of the examination was that:
“This is a normal recording in which there were no focal asymmetries of the cerebral background activities present.”
On 25 March 2002, Dr Burton wrote to Dr Benjamin enclosing the results of the Trans Cranial Colour-Coded Duplex Examination of the applicant. He recorded that the intracranial arterial circulation was examined by Trans Cranial Colour-Coded Duplex and by Trans Cranial Pulse-Wave Doppler. He concluded that these tests “did not demonstrate any definite evidence of intracranial stenotic disease”. He did note the presence of asymmetric distal middle cerebral artery flow profiles and he thought the relevance of this observation “remains uncertain in the context of his presenting complaints”.
In April 2002, Dr Burton carried out visual evoked potentials and oculomotor and caloric testing. He concluded that the former test did not demonstrate any evidence of “a delay in conduction involving the anterior visual pathways”. The latter test did not provide any evidence for the presence of “a persistent, unilateral vestibular lesion”.
On 19 April 2002, Dr Burton reported that he had carried out a Brainstem Auditory Evoked Responses (BAER) test and a Vestibular Evoked Myogenic Potentials (VEMP). He concluded that the combined BAER and VEMP studies did not demonstrate any delay in conduction in the vestibular cochlear pathways.
On 26 April 2002, Dr Burton reported that the applicant’s investigations revealed “some subtle changes yet those findings do not appear to be of immediate clinical relevance”. He raised the possibility of the applicant undergoing multifocal ERG studies at Sydney Eye Hospital should his visual impairment remain unexplained.
On 28 August 2002, Dr Petsoglou, the senior registrar to Dr Billson, reported that the latter doctor had seen the applicant at the Save Sight Institute on 13 August 2002. He recorded:
“Mr Long underwent extensive electro-physiological examinations. I have included copies of these reports for your reference. All the results show that the electrical signals from both eyes were within normal limits. There was no significant loss of vision reflecting his poor performance on prior field tests.
In general, it can be concluded that the eye and visual pathways to the brain are intact and normal. They have not suffered any injury from his fall. It is uncertain whether his visual symptoms are due to some type of higher order problem.”

On 28 September 2002, in a report to the applicant’s then solicitors, Dr Benjamin reviewed the investigations that had been carried out by Dr Milder, Dr Burton and Dr Billson. He reported:
“It was concluded that the eye and the visual pathway to the brain were intact and normal and had not been injured in any way from his fall. The absence of any injury to the eye and the absence of any abnormality to the electro-physiological tests strongly suggest a non-organic explanation for his continued symptoms.”
Dr Benjamin stated that he was unable to offer a diagnosis explaining the applicant’s visual symptoms. He continued:
“His symptoms of blotchy vision is applicable to both eyes, but there has been no evidence of injury to the eyes or visual pathways. The only positive detail is tunnel vision in both eyes, the only condition which produced this was lesion of the visual pathway bilaterally, but this has not been demonstrated by any of the electro-physiological tests which have been done.”
He also stated:
“His visual acuities, clinical examination of the eyes and electro-physiological tests do not show any permanent damage or impairment of sight. However, the visual fields show about 50% loss of visual function.”
Dr Benjamin postulated that the latter responses were not entirely accurate as “responses could be suppressed by non-organic factors affecting his brain”. Therefore, he paid more attention to the results of the electro-physiological tests “which cannot be suppressed by higher centres of the brain or non-organic factors”.
On 23 January 2008, Dr John Harrison, an ear, nose and throat surgeon in Brisbane, forwarded a report to CGU in respect of his examination of the applicant. His opinion is not in evidence.
On 4 December 2008, the applicant saw Dr Peter Duke, an ophthalmic surgeon at the request of his solicitors. The doctor had available to him a copy of the results of the Visually Evoked Potentials carried out by Dr Burton on 1 April 2001. He noted that those studies did not “demonstrate any evidence of delayed conduction involving the anterior visual pathways (i.e. optic nerve)”. He made no further comment on this. He concluded that the applicant had total visual incapacity of 55% and whole person impairment of 52%.
On 24 February 2009, the applicant saw Dr Benjamin after a lapse of 6½ years. His “visual field test” demonstrated peripheral constriction amounting to tunnel vision. He stated:
“I felt there was marginal increase in the concentric peripheral scotoma leaving only a very small area in the centre through which he could see. My estimate of the disability was around 55-60 percent.
However I observed that in spite of the extensive peripheral visual defect he walked through the surgery quite comfortably. He walked from the waiting room to the consulting room then to the fields room and back to the consultation room without bumping into any objects. Both eyes were straight and had full range of movements. The pupils were normal in size and reaction. The ocular media were clear, the fundi did not show any abnormalities, the optic disc did not show any pallor indicating damage to the visual system. There was no cupping of the discs nor papilloedema. The intraocular tensions were normal. He had no bruit over the carotid regions.”
Dr Benjamin repeated his assertion that the applicant had visual field constriction due to non-organic cause. He stated that the restriction had been consistent and was estimated to be between 55 to 60%. As it was non-organic, he thought that it was likely to remain permanent.
On 23 August 2009, Dr Duke reported that he had read the reports of Dr Benjamin and Dr Petsoglou. He stated:
“The concussive head injury may have led to bilateral occipital cortical injury but the electro-physiological tests do not support this and a higher frontal cortical function impairment may be responsible.
The electro-physiological tests could be repeated but I doubt that they would document any change in the former findings.
The opinion of a psychiatrist or psychologist with an expertise in visual physiology may be helpful.
I do not consider that Mr Phillip Long is feigning his apparent visual impairment.”
He suggested that a further consultation may assist in conjunction with updated electro-physiological laboratory techniques.
On 7 January 2010, Dr Wayne Reid, a clinical neuropsychologist, saw the applicant at the request of Dr Buchan of Cooran. After carrying out a battery of tests, Mr Reid stated that:
“On current neuropsychological assessment he was found to show specific deficits in his serial auditory verbal learning, reduction in his planning and organisational abilities, ability to form concepts and adapt and regulate his behaviour given feedback and speed and flexibility of thinking. From my assessment I could find no evidence that he was deliberately exaggerating his cognitive problems. In the context of his history and looking at the mechanisms of brain injury from his fall it seems on the balance of probability he sustained a contra-coup injury to his frontal lobes mainly affecting the orbital basal surface causing a most notable change in his personality and behaviour where he has become more apathetic, anxious, has difficulties with serial auditory verbal learning, thinking quickly and flexibly, adapting and changing his behaviour based on feedback. In addition Mr Long shows evidence of depression and anxiety.”
Dr Reid recommended a referral to a psychiatrist and an MRI of the brain.
On 11 March 2010, Dr Rebecca Briers, a consultant in rehabilitation medicine, examined the applicant. She expressed the following opinion:
“The neck, headaches, visual disturbance, balance disturbance related to the incident at hand. He did have pre-existing industrial deafness. His shoulder complaint was only mentioned some months after the accident and it is difficult to determine if these were directly related to the accident or not.”
Dr Briers also expressed the opinion that there had been “an element of mild to moderate traumatic brain injury”. In this respect, she stated it was difficult to assess his degree of brain injury on the “usual factors” such as Glasgow Coma Scores and post-traumatic amnesia scoring “as these have not been undertaken”.
On 18 August 2011, Associate Dr Michael Fearnside assessed the applicant in respect of his orthopaedic injuries and injuries to his nervous system (mental status and cognition). He noted that the ambulance record recorded that the applicant fell 2 metres, that there was no loss of consciousness, and that the applicant experienced immediate neck pain. He summarised the clinical notes from the Maitland Hospital where the applicant was admitted at 17.26 hours, as follows:
“In Maitland Hospital, he was initially seen in the emergency department where he was assessed as being alert and oriented. He was haemodynamically stable and without any abnormal neurological signs in his arms and legs. He was admitted to the hospital. A soft collar was fitted.
When he was admitted to the ward at about 2100 hours, he was complaining of headache and given Panadol … During his in-patient stay, there were no recorded concerns expressed about his neurological state or his level of consciousness. He underwent neurological observations on 6 April 2001 and 7 April 2001 and all of these were normal. His Glasgow Coma Score was 15, a normal level of consciousness.”
Dr Fearnside expressed the opinion that the applicant did not satisfy the criteria for traumatic brain injury under the WorkCover Guides which governed the assessment of permanent impairment at that time. He stated:
“Mr Long had no medically verified abnormality in his GCS. When the ambulance officers came to him, he had normal consciousness and his level of consciousness was not abnormal in Maitland Hospital. Nor was there any record of concern expressed about his neurological state. There was no post-traumatic amnesia recorded. Although he had an occipital fracture this is not indicative of ‘significant intracranial pathology on CT scan or MRI’.
The abnormalities on the MRI are more likely the result of a small vessel disease. He has a history of hypertension for which he is taking Tritace and the periventricular alteration minimal though it is, is not a pattern seen following traumatic brain injury.”
Dr Fearnside specifically considered the opinions of Dr Wayne Reid and Dr Rebecca Briers. He said that a psychological disorder was more likely to be the cause of the applicant’s presentation rather than a frontal lobe injury. He stated that the severity of the applicant’s injury was not likely to cause long-term cognitive impairment and two MRI scans of the brain have not revealed any evidence of diffuse injury. Dr Fearnside criticised the basis of Dr Brier’s assessment of brain damage as he believed it ignored the contemporaneous medical evidence. He thought that the applicant’s presentation recorded by Dr Briers was quite different to his presentation at the medical assessment. He stated:
“It is most unlikely that a head injury with no impairment of consciousness, a normal CT scan and most likely no post-traumatic amnesia would result in such a mental status impairment as 15% WPI. Mr Long reports a multiplicity of symptoms which are more indicative of a post-concussional syndrome and these should be considered under a psychiatric/psychological rubric.”
Dr Fearnside concluded his assessment in respect of mental status by stating:
“It is my opinion that although Mr Long sustained a blow to the head with an occipital skull fracture, he did not sustain a traumatic brain injury, cognitive impairment or a WPI rating under a mental status or cognitive function category.”
On 25 October 2012, the applicant saw Dr Stern, an ENT surgeon, at the request of his solicitors. He examined the applicant and reviewed the long history of investigations undertaken by various doctors relevant to the applicant’s alleged loss of vision. He stated he would prefer to answer the question of whether there was a causal nexus between the injury and the applicant’s visual impairment after he had been reviewed by a neurologist. He recommended a further battery of electro-physiological tests which might be performed at Sydney Eye Hospital or a similar institution in Queensland. His opinion is not in evidence.

57.On 26 November 2014, Dr Ioanne Anderson, an ophthalmic surgeon reported to Dr Buchan that the ocular examination was essentially normal. She continued:
“His symptoms and the lesion on the MRI scan are possibly connected to a disorder of higher cortical function. I note that he was recommended to undergo formal visual neuropsychology which I think is appropriate. I will attempt to arrange this for Phillip expeditiously.”

Dr Jeanne Georgius, a clinical neuropsychologist, provided a neuropsychological assessment report dated 24 September 2014. She assessed significant impairment of the applicant’s higher order executive functioning as a result of the injury. She estimated permanent impairment to be 29% WPI. She stated:
“It is unlikely that Mr Long’s current neuropsychological profile of higher order abstract verbal reasoning deficits, auditory verbal memory weakness associated with information overload and executive dysfunction, is consistent with early Alzheimer’s dementia, vascular dementia or ischemic changes as the severity and pattern of the results are more consistent with a traumatic brain injury. The pattern of Mr Long’s memory difficulties excludes the possibility of an Alzheimer’s or vascular dementia diagnosis to explain his cognitive deficits, as he exhibited intact memory in coding/learning and there was no significant memory degradation over time.”
Dr Georgius did not have access to much of the contemporaneous material as she was “unable to find GCS or PTA scores”. She assumed that the applicant experienced “a significant post-traumatic amnesia after the accident”. She referred to the CT scan of the brain dated 7 April 2001 and MRIs of the brain dated 30 March 2010 and 14 August 2013. The latter was said to reveal gliosis in the left occipital lobe.
On 31 March 2016, Dr Stephen Faux, a specialist in pain management, saw the applicant at the request of Dr Buchan. He took a history from the applicant and reviewed the neuro-psychometric testing and the radiological reports. In respect of the latter, he stated:
“I was able to review the MRI report and the reports of the CT scan and whilst there has been some mention of occipital lesions in the neuropsychiatric reports, there was no evidence of it in the x-ray reports that I have read.”
Under the heading “Impression”, Dr Faux thought there was a possible post-traumatic brain injury and depression associated with poor motivation and possible cognitive impairment “although this is out of keeping with his ability to drive without accident”.
On 20 November 2017, the applicant saw Dr Dudley O’Sullivan, a neurologist at the request of his solicitor. Dr O’Sullivan had access to the historical material including the ambulance report. He recorded that the applicant had been seen by a neurologist Dr Noel Saines in July 2013 who could find no significant neurological abnormality and who commented that:
“The MRI of the brain in 2010 showed only a small posterior subcortical parieto-occipital hypodensity of uncertain origin. The MRI of the orbits was otherwise normal.”
Dr O’Sullivan also had a report from Dr Joanne Alison, a clinical neuropsychologist dated 5 December 2016 who stated that the applicant sustained a mild to moderate brain injury as a result of the accident. Dr O’Sullivan thought that the applicant suffered a traumatic brain injury. He continued:
“His main disabilities in my view relate to his mild cognitive impairment and the visual impairment, the precise aetiology of which remains unclear as he has got normal visual function on clinical testing.”
Dr Clare Fraser, a neuro-ophthalmic specialist at the Save Site Institute first saw the applicant in 2013 at the request of Dr Buchanan. She carried out a series of tests many of which had been previously performed by other medical practitioners. She expressed the opinion that the applicant’s visual pathways from his cornea to the V1 visual cortex were structurally and functionally normal. She added:
“however on basic screening testing he did appear to have problems with right-sided visual neglect and visual processing difficulties.”
She expressed the opinion that this may explain why he continues to bump into objects on the right-hand side, had inconsistent visual field tests and an otherwise normal ophthalmic examination. She suggested referral for in-depth “visual neuropsychology tests”. If the abnormality in visual-spatial perception was confirmed by this testing then the applicant “may be a candidate for rehabilitation”.
On 27 May 2020, Dr Fraser wrote to Dr Theilhaber, and noted that his visual tests were normal. She continued:
“In 2013 his visual acuity was 6/6, N5 and the slight reduction to 6/7.6 is consequent on his cataract. His main visual issues, however, are his right hemifield neglect and his difficulties with object and spatial perception which are visual processing issues. This fits with the left-sided gliosis seen on his MRI as a consequence of his injury. This is not an expected age-related change.
Humphrey visual fields today did confirm the difficulties with right visual field. OCT shows a healthy optic disc with normal macular architecture. This field change is therefore not a consequence of glaucoma or any structural ophthalmic abnormality.”
By a further report dated 22 June 2021, Dr Fraser stated that “on the balance of probabilities the applicant’s head injury caused the left-sided cerebral gliosis and as a consequence of this, he has hemifield neglect and difficulties with objects and spatial perception.”
Dr Ian Wechsler, an ophthalmologist, saw the applicant at the request of the respondent on 17 September 2019. He also recorded a history that the applicant had persistent blotchiness of vision in both eyes, persistent floaters, decreased near vision and a tendency to bump into things particularly on the right. Dr Wechsler noted that the applicant had seen a number of ophthalmologists, all of whom had recorded a similar history and similar recordings for near and distance vision. However, Dr Wechsler observed that the results of the computer visual field test at his examination “was a vast improvement compared to the visual fields documented from previous ophthalmologists.” He continued:
“The visual field changes on my examination are not the pattern of occipital lobe trauma. There is no respecting of the vertical line and the scotoma is extremely peripheral and crosses the vertical line. With occipital lobe trauma the scotoma is homonymous with similar shaped defect on both sides. This is not apparent in Mr Long’s visual field test. It is for this reason that I do not feel that the visual field changes are related to Mr Long’s occipital trauma from the accident on 5^th April 2001.
In addition, Mr Long on a number of times has had normal electro-physiological studies. A/Prof Clare Fraser in her neuro-ophthalmological opinion noted that Mr Long had problems with right-sided visual neglect and visual processing difficulties but structurally and functionally Mr Long’s visual pathways from the cornea to the visual cortex was normal.”

Dr Wechsler noted Associate Dr Fraser’s view that right-sided visual neglect may explain the applicant’s problems. He said, however, that neuro-ophthalmologist problems such as visual neglect and higher order problems with visual association areas near the visual cortex were beyond areas of his expertise. Nonetheless, he stated that Associate Dr Fraser’s diagnosis was the most likely cause for the applicant’s symptoms. He concluded thus:
“My final diagnosis would be a normal ophthalmic examination and no specific ophthalmic problems but a disorder of the higher and visual association areas. Further assessment should be performed by a neurologist particularly interested in neuro-ophthalmology problems as this area is out of my level of competence.”
In answer to a question as to whether the applicant’s employment was a substantial contributing factor to ophthalmic pathology he stated:
“Although there is no direct ophthalmic pathology there are ophthalmic symptoms, i.e. tending to bump into objects and fuzzy vision which Mr Long consistently complains of since the accident where he had a significant brain injury particularly affecting the occipital area. This means that the head injury from his employment must have caused some neurological damage to the visual association areas to cause his symptoms. Any further discussion would have to be from a neurologist with a particular interest in neuro-ophthalmology.”
Finally, he concluded that as there were no ophthalmic signs there was no “permanent loss of vision”.

DISCUSSION AND FINDINGS

71.It is readily apparent from the brief review of the medical evidence above that it is the unanimous opinion of the ophthalmic surgeons who have treated the applicant, or reviewed him for medicolegal purposes, that he has no structural ophthalmic or visual abnormality. As Dr Wechsler recorded his “visual pathways from the cornea to the visual cortex was normal.”

The applicant, therefore, puts his case for compensation for loss of sight on the basis of a traumatic brain injury occurring at the time of his fall on 5 April 2001, which has caused a disorder of the higher and visual association areas of the brain resulting in blurred and distorted vision. As Mr Willoughby argued, that case is supported by Dr Clare Fraser, the only neuro-ophthalmic specialist, whose opinion has been tendered in this case and is not refuted by Dr Wechsler, the ophthalmologist retained by the respondent to provide an opinion on the relationship between the applicants fall on 5 April 2001 and his alleged impairment of vision.
The applicant made a claim for permanent impairment compensation in respect of a traumatic brain injury in 2011,which was assessed Dr Fearnside, an Approved Medical Specialist appointed by the Registrar of the then Workers Compensation Commission to assess a medical dispute. Dr Fearnside determined that the applicant did not suffer a traumatic brain injury for the purpose of the Guidelines for the evaluation of permanent impairment which were in force at the time. It was not suggested, however, that the applicant was precluded from arguing his case by reason of that determination. Neither did the parties address the obvious problem of how a Medical Assessor, with a specialty in ophthalmology, might assess impairment for the purpose of a threshold dispute when it is accepted that there is no abnormality of the visual system.

Mr Hunt made a rather perfunctory attack on the applicant’s reliability by reference to Dr Benjamin’s comments that despite his restricted vision the applicant was able to walk between rooms in his surgery without apparent difficulty. This may have influenced Dr Benjamin’s conclusion that the applicant’s visual difficulties were “non-organic”. There are also a number of references to the applicant continuing to drive a vehicle, probably only in his local area, although no medical practitioner concludes that this activity is grossly inconsistent with his alleged loss of vision. Only Dr Faux , the Rehabilitation Physician suggested inconsistency but that was in respect of the applicant’s “possible” cognitive impairment.
Subject to one matter which I address below, I doubt that the case can be resolved on the basis of the applicant’s reliability. The evidence of Dr Benjamin, standing alone, is insufficient to permit a finding that the applicant’s evidence as to loss of sight is unreliable. More so because there was no application to cross-examine the applicant on this or other inconsistencies in his case during the course of the proceedings.
While it was not referred to in argument, it is evident that the applicant’s account of the circumstances of his injury on 5 April 2001 has changed in a dramatic fashion over the years. By his primary statement, the applicant recounted that following his fall he could not “remember anything further until Colin Green” picked him up from the floor. Thirteen years later, Dr Georgius, the neuropsychologist, took a history that his first memory was “waking in hospital several days after the accident”.
Contrary to Mr Willoughby’s submission, it is probable that the latter account is unreliable. Recollection of events many years previously is fraught with difficulty: see the discussion by Davies JA in The Nominal Defendantv Cordin [2017] NSWCA 6 (3 February 2017) commencing at [165] relating to credibility issues and the fallibility of human memory. For this reason, where it is relevant, I prefer to rely on the contemporaneous evidence rather than evidence, including medical histories, given many years after the injury.
In many respects the outcome of the matter turns on the resolution of the conflicting opinions of Dr Fearnside side and Dr Fraser. Critical to the opinion of each of these medical witnesses is the interpretation of the MRI scans of the applicant’s brain taken since his injury. Undoubtedly, the opinions of the other medical practitioners, who have treated the applicant or were retained to offer an opinion, are relevant. However, their evidence does not address the central issue of whether the applicant’s loss of vision relates to a traumatic brain injury.
As I indicated above, the last of the reports of MRI scans performed on the applicant’s brain on 15 August 2013 was not tendered in evidence at the arbitration hearing. It has been lodged subsequently at my request. Unfortunately, the report is incomplete. However, the findings of the scan and the radiologist’s interpretation seem to be intact. Importantly, the radiologist states that the findings were unchanged when compared with the MRI dated 30 March 2010. The following finding is recorded:
“there is focal gliosis of the left occipital lobe again noted, unchanged when compared with previous. The appearance suggests old trauma or old infarction. This could easily affect the optical radiations although it is not directly involving the visual cortex.”
The radiologist offered the following conclusion:
“no structural abnormality of the optic nerves or chiasm detected. Gliosis in the left occipital lobe is again noted, and is unchanged. This possibly affects the left optic radiations”
Dr Smith, who performed the first MRI scan on 29 January 2002 relevantly recorded that:
“There is no evidence of midline shift.
The ventricles, cisterns and sulci are within normal limits.
There is minimal periventricular changes, particularly in relation to the posterior horn of the left lateral ventricle. No other focal intracranial lesion.”
Dr Smith commented that there were “white matter changes adjacent to the posterior horn of the left lateral ventricle which are non-specific”.
On 30 March 2010,Dr Salanitri reported on the second MRI scan as follows:
“No significant optic nerve abnormality is identified. Increased T2 hyperintense signal within sub cortical white matter of left parietal-occipital lobe. This has a non-specific appearance and maybe post-traumatic in nature with differentials being that of old ischaemic change.”
The 2002 and 2010 MRI scan were made available to Dr Fearnside when he saw the applicant on the 18 August 2011. Dr Fearnside is one of the rare specialists in the case who also had access to the ambulance record, and the notes of the Maitland Hospital where the applicant was treated immediately following his fall. I have set out above his summary of that evidence. He concluded that the applicant had a normal Glasgow coma score, that he had not suffered from a lengthy period of loss of post traumatic amnesia, and that he was neurologically intact when examined after admission to Maitland Hospital. These conclusions are borne out by the contemporaneous documents.
Dr Fearnside states that the Glasgow scale coma score recorded by the ambulance officers is an objective measure of a person’s level of consciousness. A score of 15 means that “the person is responding normally to commands and moving limbs and opening eyes spontaneously.” It is consistent with the ambulance officers record that there was no loss of consciousness. I should note that Dr Wolfenden also records that the Glasgow coma score recorded in the ambulance record was 15.
Dr Fearnside’s task was to determine whether the applicant suffered traumatic brain injury as Defined by the WorkCover Guides. These required objective evidence of injury by way of a verified abnormality in the patient’s Glasgow Coma Scale Score, post-traumatic amnesia of a significant duration, or a CT or MRI scan which revealed “significant intracranial pathology”. It may therefore be argued that his opinion is of limited impact. However, aspects of the doctor’s opinion are relevant to the outcome of this case. He concluded that the abnormalities on the MRI scan were more likely the result of a small vessel disease possibly attributable to the applicant’s hypertension and the “periventricular signal alteration, minimal though it is, is not a pattern seen following traumatic brain injury.”
Subsequently, when dealing with the opinion of Dr Reid, the neuropsychologist, who thought the applicant suffered a frontal lobe injury, Dr Fearnside said this:
“While these impairments were identified by Dr Reid, I consider that an adjustment disorder is more likely because the severity of Mr Long’s blow to the head is not likely to cause long-term cognitive impairment. Two MRI scans of the brain have not revealed any evidence of diffuse injury.”
Dr Fearnside stated that the opinion of Dr Markou, a psychiatrist, supported his conclusion that the impairments diagnosed by Dr Reid were psychologically and not physically determined. This conclusion is similar to the conclusion arrived at by Dr Benjamin, the applicant’s treating ophthalmic surgeon.
Dr Fearnside also discounted the opinion of Dr Briers, an occupational physician, that the applicant suffered a traumatic brain injury on the basis that it was inconsistent with the contemporaneous medical record. However, there is support for his opinion in respect of the MRI scan in Dr Briers supplementary report dated 5 April 2001. When asked to consider the MRI report of 2010, she stated:
“this does not cause me to amend any of my report. The changes described can be as a result of hypertension, which he has a background history for.”
Dr Faux also appears to have concluded that the radiological evidence was, at least, ambivalent although it is not clear from a short report what scans were made available to him.
Much of the subsequent medical or neuro psychological opinion, which suggests that the applicant had a traumatic brain injury at the time of his fall, is based upon an inaccurate history of the circumstances following the accident. Dr Georgius, for example, has recorded an inaccurate history of the applicant’s post injury amnesia and did not have access to, or could not interpret, the ambulance record or the notes from the Maitland Hospital.
Dr Dudley O’Sullivan, however, had access to these documents. He also interpreted the 2010 MRI in the same way as Dr Fearnside. He accepts, however, that the applicant has suffered a traumatic brain injury giving rise to cognitive impairment and “visual impairment as documented”. Dr O’Sullivan’s opinion may partly be based on his consideration of a further neuropsychological report from Dr Joanne Allanson dated 5 December 2016 which is not in evidence. But he is clearly of the opinion that the applicant suffered some brain damage as evidenced by cognitive and visual problems despite the absence of evidence of abnormalities in the Glasgow Coma Scale score, a proven period of post-traumatic amnesia, or significant to intracranial pathology on the CT or MRI scans.
Dr Claire Fraser, the applicant’s treating neuro ophthalmic surgeon, also supports a connection between the applicant’s visual problems and the injury. She states that the applicant’s right hemifield neglect and his difficulty with the spatial perception “fits with the left-sided gliosis seen on his MRI as a consequence of his injury”. She states that the gliosis is not “an expected age related change.”
Mr Hunt suggested that the Dr Fraser did not have access to the 2002 MRI scan and this may be the case. However, I doubt that detracts from her opinion. My understanding of this evidence is that each of the MRI scans record the same left-sided abnormalities.
Given her specialty, there is no doubt that the opinion of Dr Fraser is entitled to considerable weight. The deference displayed by Dr Wechsler, the respondent’s qualified ophthalmologist to Dr Fraser’s opinion is indicative of this. By reason of her specialty, Dr Fraser may be best placed to comment on the relationship between the left sided gliosis found on the MRI scan and the applicant’s visual problems. An acceptance of her opinion would elegantly resolve the difficulties in the case. It would explain the reason why the applicant has complained of restricted vision since the time of his injury. One could conclude that the applicant suffered a subtle brain injury despite the absence of the usual criteria for brain injury.
It is not clear, however, whether Dr Fraser had access to Dr Fearnside’s opinion or, more importantly, the contemporaneous material which he considers negates a traumatic brain injury, or to the conclusions of Dr Benjamin and the numerous investigations, including those carried out by neurologists, on which his opinion was based. It is difficult to resolve an extremely complex medical issue when the competing medical cases have passed by each other like ships in the night. In particular, there are diametrically opposed views as to whether the findings found on the MRI scan are more probably than not post-traumatic or caused by small vessel disease relating to the applicant’s hypertension. Dr Fraser’s evidence on this point is extremely brief.
At the arbitration hearing, I indicated to the parties that that If Dr Fearnside remained a Medical Assessor, I would have referred the papers in the matter to him to express an opinion based on the entirety of the evidence including the recent opinions of Dr O’Sullivan and Dr Fraser. Having spent several days considering the evidence, I have reached the conclusion that it is best if the issue is resolved with the assistance of a report from a specialist neurologist/neurosurgeon which takes into consideration both the competing medical cases.
I, therefore, propose to refer the matter to the President for referral to a Medical Assessor for a general medical dispute. I propose to ask the Medical Assessor to express an opinion on the papers whether the applicant’s right hemifield neglect and spatial perception difficulties results from his head injury on 5 April 2001 taking into account the opinions of the Dr Benjamin and Dr Fearnside, on the one hand and Dr Wolfenden and Dr Fraser on the other.

[2021] NSWPIC 489

30 November 2021