Kenda and Comcare (Compensation) - [2022] AATA 1452

Kenda and Comcare (Compensation) [2022] AATA 1452 (2 June 2022)
Division:GENERAL DIVISION
File Numbers: 2017/6600
2017/6622
2017/7338
2018/2015
2018/4493
2018/5058

Re:Danielle Kenda
APPLICANT

AndComcare
RESPONDENT

DECISION
Tribunal:Dr Stewart Fenwick, Senior Member
Date: 2 June 2022
Place:Melbourne

The Tribunal affirms the decisions made in each of the decisions under review.
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Dr Stewart Fenwick, Senior Member
Catchwords
COMPENSATION – carpal tunnel syndrome right, lateral epicondylitis right, sprain of shoulder and upper arm (subdeltoid bursitis) right – claims of cervical spondylosis with foraminal stenosis and severe headaches, aggravation of temporomandibular joint disorder and complex regional pain syndrome – claims for medical procedures and treatment – claim for permanent impairment right shoulder – decisions under review affirmed
Legislation
Safety Rehabilitation and Compensation Act 1988 (Cth)
Cases
Comcare v Watson (1997) FCR 273
Secondary material
Comcare Guide to the Assessment of the Degree of Permanent Impairment (Ed. 2.1)
REASONS FOR DECISION
Dr Stewart Fenwick, Senior Member
BACKGROUND

This matter involves a series of applications arising from decisions made about a range of physical conditions said to arise from Ms Kenda’s employment as a paralegal at the Australian Government Solicitor (‘AGS’). I will set out here a brief chronology of the decision-making history.
Ms Kenda first made a formal claim for compensation in December 2012 for a number of physical conditions, and for a psychiatric condition. This claim was accepted in April 2013, with a date of injury in October 2012. She subsequently lodged a claim for newly reported physical conditions in May 2017, and this claim was rejected in August 2017 (application number 2017/6622). At the same time, the Respondent determined that it was no longer liable for physiotherapy in respect of the other previously accepted physical conditions (2017/6600). A subsequent request for a sympathetic nerve block to the thoracic spine was declined in late 2017 (2017/7338).
A request for a hydrodilatation procedure for Ms Kenda’s right shoulder was declined in March 2018 (2018/2015). Following this, in July 2018, the Respondent determined that it would no longer accept liability for medical treatment and incapacity payments in respect of the previously accepted physical conditions (2018/4493). Also in July 2018, Ms Kenda applied for consideration of a permanent impairment claim in respct of her ‘right shoulder’ and ‘right upper limb’. A decision was made in August 2018 to deny liability for permanent impairment, as a result of the then recent denial of ongoing liability (2018/5058).
The physical conditions, for which liability was accepted in 2013, are all conditions of Ms Kenda’s right upper limb: aggravation of carpal tunnel syndrome; lateral epicondylitis; and sprain of shoulder and upper arm (subdeltoid bursitis). These were said to have arisen in February 2011. Ms Kenda had undergone carpal tunnel decompression surgery in December 2010, which was privately funded.
The conditions newly reported in 2017 were: cervical spondylosis with foraminal stenosis and severe headaches; aggravation of temporomandibular joint disorder (‘TMJ’); and complex regional pain syndrome (‘CRPS’) right upper limb. The reported dates of onset for these conditions being: October 2012 for the spine condition; April 2013 for the TMJ; and February 2011 for the CRPS.
While I have accepted, for the purposes of this background material, that Comcare rejected the claim for CRPS in August 2017 (and the parties submissions reflect this assumption), I note that the denial of liability dated 14 August 2017 states that the CRPS of right upper limb, arm, right hand and shoulder will be subject to independent assessment and a separate decision. I have been unable to identify this separate decision in the materials, but do not consider that this affects these reasons.
Ms Kenda worked for the AGS in a range of clerical capacities between 1986 and late 2018. At virtually all relevant times, Ms Kenda was employed part time in duties associated with handling legal files, including copying and collating documents, mouse and keyboard work, and telephone attendances. In brief, the substance of Ms Kenda’s claims is that she has been affected by the repetitive and high volume nature of her duties, in a high-pressure work environment.
I set out here a very brief summary of some key events:
(a)Ms Kenda reports lodging an incident report in relation to her right forearm in the mid-1990’s;
(b)Ms Kenda also lodged an incident report in April 2005 for neck and shoulder pain;
(c)Ms Kenda underwent right side carpal tunnel decompression surgery in late 2010, as noted, and returned to work in January 2011;
(d)Ms Kenda lodged an incident report in March 2011 for aggravation of a wrist condition;
(e)the initial claim for compensation was accepted in April 2013, with a date of injury in October 2012;
(f)Ms Kenda underwent right sided radial nerve release surgery in November 2014;
(g)in April 2017 Ms Kenda was deemed unfit for all work;
(h)newly reported conditions were advised, as noted, in May 2017; and
(i)Ms Kenda retired on medical grounds in November 2018.
The Applicant lodged a Statement of Facts, Issues and Contentions (‘SFIC’) and closing submissions (totalling 125 pages, including a Reply to the Respondent’s Closing Submissions). The following material was received in evidence at the hearing:
(a)Statement of the Applicant, dated 2 November 2018 (Exhibit A1);
(b)Timesheet calculations for November, dated 6 December 2005 (Exhibit A2);
(c)Statement of Richard Boughton, dated 19 November 2018 (Exhibit A3);
(d)Statement of Peta Heffernan, dated 20 November 2018 (Exhibit A4);
(e)Paper of Dr Peter Blombery titled, ‘The Role of Occupational Factors in Carpal Tunnel Syndrome’, June 2019 (Exhibit A5);
(f)Clinical diagnostic criteria for complex regional pain syndrome proposed by the International Consensus Conference, Budapest, 2004 (Exhibit A6);
(g)Report of Dr David Wiesenfeld, dated 8 July 2019 (Exhibit A7); and
(h)Report of Associate Professor Jack Gerschman, together with supplementary report, dated 3 January 2019 (Exhibit A8).
The Respondent lodged documents pursuant to s 37 of the Administrative Appeals Tribunal Act 1975 (‘T documents’) in respect of each claim, as well as Supplementary T (‘ST’), and Further Supplementary T (‘FST’) documents.[1] The Respondent also lodged a SFIC and closing submissions. The following additional material was received as exhibits at the hearing:
(a)Report of Dr Gautam Khurana, dated 14 November 2018 (Exhibit R1);
(b)Report of Mr Ronald Haig, dated 11 December 2018 (Exhibit R2);
(c)Radiology report, dated 19 June 2019 (Exhibit R3);
(d)Supplementary report of Dr Tony Kostos, dated 7 July 2020 (Exhibit R4); and
(e)Reports of Dr Andrew Howe, dated 7 August 2019 and 4 December 2019 (Exhibit R5).
[1] In these reasons references to T documents will be in the format: file number/T document number/page number.
The hearing was conducted in two blocks, 12 months apart. This arose from reliance during expert medical evidence on research material which the Respondent’s representative submitted required consideration in advance of cross-examination. An adjournment was granted and further delays arose during the production of written submissions by the parties.
LEGISLATION
Under s 14 of the Safety Rehabilitation and Compensation Act 1988 (Cth) (‘the Act’) compensation is payable in respect of an injury, which is a term specifically defined in s 5A.
An injury may take two forms, either a physical or mental injury arising out of, or in the course of, employment (s 5A(1)(b) of the Act); or it may take the form of a disease. An injury may also arise in the form of an aggravation of an injury, whether or not that injury arose out of, or in the course of, employment (s 5A(1)(c) of the Act).
‘Disease’ is also specifically defined, in s 5B of the Act. It is an ailment or an aggravation thereof that was contributed to to a significant degree by employment. Ailment is defined to mean any physical or mental ailment, disorder, defect or morbid condition (whether of sudden onset or gradual development) (s 4 of the Act). ‘Significant degree’ means a degree substantially more than material (s 5B(3) of the Act).
In determining whether employment contributed to a significant degree to the development of an ailment, the following non-exhaustive list of matters may be taken into account pursuant to s 5B(2) of the Act:
(a)the duration of employment;
(b)the nature of, and partuclar tasks involved in, the employment;
(c)any predisposition of the employee to the ailmaent or aggravation;
(d)any activities of the employee not related to the employment; and
(e)any other matters affecting the employee’s health.
Compensation can be provided for medical expenses (s 16 of the Act) and for incapacity for work (s 19 of the Act). Compensation can also be provided for injuries resulting in permanent impairment (s 24 of the Act) and for non-economic loss (s 27 of the Act).
ISSUES
The issues requiring determination are as follows:
(a) whether the Respondent is liable to pay compensation in the form of the medical expenses arising for the procedures that have been denied Ms Kenda;
(b) whether the Respondent is liable for compensation in respect of the injuries for which liability has been denied; and
(c) whether the Respondent is liable for compensation for a permanent impairment.
In determining these issues, it is necessary to identify Ms Kenda’s conditions, and give consideration to their nature in the terms of the legislation. That is, to determine whether they are ailments or injuries, each of which involves a different test of causation. No compensation of any form is payable if a claimed condition does not meet the overall definition of an injury.
For any injury found, consideration will need to be given to any of the related treatments for which Ms Kenda has sought payment, and to any permanent impairment arising.
EVIDENCE
Witnesses at hearing
Ms Kenda
Ms Kenda confirmed the contents of her written statement (Exhibit A1). In this statement, relevantly, she states:
(a)in December 1996 she worked with a litigation support database involving intensive use of a computer mouse, for which she lodged an incident report, was promoted to another role within approximately six months, and took voluntary redundancy in mid-1998;
(b)that she returned to AGS in mid-2000, and was engaged on a time-based costing model (with a bonus component), in which her billing target was met within ordinary daily work hours;
(c)at this time she was engaged in a range of paralegal duties, including drafting documents, writing file notes, using databases and compiling Tribunal documents of between 300-1800 folios, and inspecting and copying files;
(d)her workload became hectic in late 2004/early 2005, and she lodged an incident report for neck and shoulder pain;
(e)she began to feel tingling and numbness in her right hand and wrist in September 2010 and was diagnosed with CTS, undergoing surgery in December 2010;
(f)at this time she worked in the Bankruptcy and Winding up areas of the practice, which involved keyboard and database use, as well as document preparation and filing, and she returned to this work wearing a splint after her surgery;
(g)she lodged an incident report in March 2011 for aggravation of her wrist condition, and was experiencing quite pronounced symptoms in her hand and elbow;
(h)that she continued to experience pain in her arm and neck and was troubled by her work, which included photocopying thousands of pages each day;
(i)in late 2012 she experienced difficulty sleeping due to numbness and pain and she commenced medication for this, and she would constantly ruminate about the implications of her condition for her employment;
(j)later in 2012 she experienced right shoulder pain, and by early 2013 she was experiencing difficulties managing her physical conditions, and a secondary anxiety condition, and found it challenging to perform cooking and household chores;
(k)that she experienced jaw and neck pain in April 2013, and her General Practicitioner (‘GP’) emphasised that she should stick to her work restrictions, and that later in 2013 she spoke with her GP about her worsening anxiety over performance targets, as well as migraines and teeth grinding;
(l)that in November 2013 she was ‘granted budget fee relief backdated to July 2013’, however work restrictions were ‘never complied with/implemented by my employer’;
(m)in March 2017 a psychiatrist recommended treatment by a psychologist, and in or about April 2017 her rehabilitation file was closed by her employer;
(n)in June 2017 she travelled to Europe on long service leave, and commenced seeing a psychiatrist in February 2018; and
(o)that due to her injuries, she experiences difficulties with dressing and personal care, food preparation, household chores, shopping and gardening.
In oral evidence, Ms Kenda stated that her work with a litigation support database involved a ‘large’ mouse. She stated that her work copying documents could involve up to 1,500 or 3,500 pages.
Ms Kenda stated that, at a point after her return to work in 2000, she was moved from a workstation to a ‘mail alcove’, at which time she experienced neck and shoulder pain. She believed this was from cradling a telephone with the attached supporting device. This was later replaced with a Bluetooth system.
In her evidence about her work practices during her first and second engagements with AGS, Ms Kenda stated that she chose to work through lunchbreaks. In the late 1990s this was in order to complete four days’ work across only three days. Ms Kenda stated that in around August 2010 her casual engagement was changed to permanent, and she worked an eight and a half hour day, again working through lunch.
In respect of her work duties, Ms Kenda stated that at a point in time she was no longer permitted to charge for travel time involved in trips out of the office to copy documents. She considered this time lost time that she had to make up for, and she was also conscious of the bonus payment system in place, which she treated as a form of overtime.
Ms Kenda confirmed that she underwent carpal tunnel decompression surgery as a private patient as she did not want her employer to know her business. She considered there was a stigma attached to being thought of as ‘an Applicant’. She stated that she was not honest with her supervisor about the cause of her CTS until mid-2011, although her employer knew about the surgery. Ms Kenda also stated that she did not conform to her surgeon’s (Mr McCombe) recommendation about reduced tasking following treatment, because she felt guilty about seeing the workload of her colleague increase during her absence.
Ms Kenda stated that Mr McCombe was irate with her about the recurrence of symptoms following her return to work, and her hand was visibly swollen. She was placed on a restricted work arrangement, and a subsequent workplace assessment led to her computer mouse being changed. Upon resuming normal hours, Ms Kenda stated that she would work between eight and a half and ten hours a day, three days a week.
Upon the apparent diagnosis of lateral epicondylitis, Ms Kenda began taking anti-inflammatory medication, which she stated helped ‘alleviate that searing pain’. At this time her duties changed and she worked a lot more slowly than before.
Ms Kenda began to experience waking during the night in September or October 2012, with numbness and the inability to feel her right hand. Her GP, then Dr Zebic, recommended examination of her cervical spine. She was able to sleep better with insomnia medication. At around this time, Ms Kenda also began experiencing panic attacks, for example developing a fear of entering the City Loop when commuting to work on the train.
Ms Kenda stated that it was pain in her teeth and jaw that led to her to see her GP about TMJ in 2013. Ms Kenda stated that the loss of teeth and pain from TMJ affected the manner and quality of her eating. She stated that she also noticed migraines, about every two months, when she experienced problems with grinding her teeth.
Ms Kenda stated in evidence that when receiving physiotherapy from Mr Stephens, they agreed to avoid treatment of the hand and forearm due to pain. Ms Kenda also stated that Mr Stephens had observed her hand ‘going quite a deep – quite deep – a different colour of purple …’.
In late 2013, Ms Kenda was granted ‘budget relief’ in respect of her billing target, and her GP recommended she work only 65-75% of normal duties and no longer compile Tribunal documents. The latter recommendation was not implemented for nearly ten months, by which time she had been able to train a replacement to perform this task. Ms Kenda later agreed that this work stopped in about April 2014.
Ms Kenda explained that she transferred to Dr Navani after Dr Zebic ceased handling compensation work. She was shocked when Dr Navani reviewed her file in early 2017 and informed her that she was not fit to work in her current state.
At different points in her evidence Ms Kenda elaborated upon her difficulties with domestic duties. She confirmed that she has for some time experienced difficulty with many household tasks including, in particular, cooking (kneading, whisking, chopping) and personal care.
When prompted about using her right arm when brushing her teeth or hair, Ms Kenda added: ‘What I notice about my hand is when I have used it repetitively, it will often change colour. It will go a dusky, sometimes like purple. Sometimes when it’s swollen it will go swollen and a dark purple’. She stated that this had happened earlier on that very day of her oral evidence. Ms Kenda also stated that she does not drive for more than about 15 minutes because of the pain caused by gripping the steering wheel.
In cross-examination, Ms Kenda was asked why she had not made a complaint to her GP about employment conditions causing pain, but rather first raised the issue of symptoms arising at home. She responded that she recalled telling her GP that she had been ‘working in the house’, and that she only attributed the symptoms to what she had been doing perhaps the day before.
When asked about her decision not to inform her employer about CTS, Ms Kenda stated that she was aware from a recent case how difficult it was to establish a link to employment. She did not wish to put herself through the process of trying to prove this connection.
Ms Kenda acknowledged that documents in her matter did not disclose a link to employment, but denied that she went to great lengths to conceal her condition. It was suggested that Ms Kenda had determined for herself that employment caused her symptoms. She responded that she was just concerned about how to deal with them.
Ms Kenda agreed that when she was certified fit to return to normal duties in April 2014 her symptoms were occasional or sporadic tingling and numbness.
When asked whether her supervisors directed that she work long hours, Ms Kenda responded that her work was dictated by the ‘amount of work that had to be completed by the end of the day’. She understood her part time work arrangement to involve ensuring that no work was left uncompleted during the other days. Ms Kenda accepted that she made a financial gain by working longer hours due to the fee system in place.

A significant amount of time was taken in cross-examination to scrutinise the nature of Ms Kenda’s duties in her varyious paralegal positions. She was unable to specify an average volume of work related to compiling Tribunal documents. The cross-examination in general appeared to confirm that Ms Kenda’s duties varied not only between roles, but during the course of her different roles within AGS. She also confirmed that when photocopying documents at volume she used her left hand to place sheets on the copier. She also stated that when she was preparing Tribunal documents that she turned pages with her left hand and wrote with a texta using her right hand.
It was put to Ms Kenda that she did not pursue dental treatment when consulting dentists over her TMJ in the period from 2006 to 2009. She disagreed, pointing out that she has had three splints made over a ten year period.
During re-examination, Ms Kenda stated that during her examination by Dr Kostos she pointed out to him that she considered her hand was discoloured, stating that it was mainly her fingers and thumb that were a purple colour. She considered this had been triggered by recent physiotherapy.
Richard Boughton
Mr Boughton provided a statement (Exhibit A3) in which he describes his experience as a senior lawyer with AGS. Mr Boughton states that he knew Ms Kenda since approximately 2005, and confirms the nature of her paralegal duties; adding that she worked very hard and to court-imposed deadlines.
Mr Boughton describes her as busy and diligent. He states that he was on leave when Ms Kenda had her 2010 surgery, and he expressed concern when he saw her continue to work in a splint. He states that she rarely complained, and had a stoic attitude.
In cross-examination, Mr Boughton agreed that it was likely that he was Ms Kenda’s direct supervisor for approximately two years during her employment with AGS.
Peta Heffernan
Ms Heffernan did not give evidence at the hearing. In her statement (Exhibit A4), Ms Heffernan states that she worked closely with Ms Kenda between December 2000 until July 2016.
Ms Heffernan states that Ms Kenda impressed her with her ‘prodigious’ work effort. She states further that Ms Kenda was ‘always extremely capable and efficient’ in her tasks. As Ms Kenda’s direct supervisor from late 2012, Ms Heffernan observed that ‘even though her work performance was impaired due to her physical injury she was still able to perform some of her work duties and did so extremely capably’.
Dr Vijay Navani
Dr Navani confirmed he had been Ms Kenda’s treating GP since February 2017. In his evidence, he was taken to his report of 14 June 2017 (6600 and 6622/T35). In this report he diagnoses: CRPS; cervical spine spondylosis with bilateral foraminal stenosis at C5/C6; aggravation of CTS right; persistent right lateral epicondylitis; and, severe Adjustment disorder with Major depression and Generalised anxiety, described as a ‘significant factor in her TMJ and severe headaches’.
In this report, Dr Navani also records symptoms of pain at all points in Ms Kenda’s right upper limb and into the neck. He confirmed that they ‘worsened with activity’, meaning small hand movements performed during examination.
Dr Navani confirmed in evidence that he observed ‘obvious swelling and discolouration’ quite a few times. He described this is ‘puffiness’, and a bluish colour. Dr Navani observed weakened grip using a grip test on his fingers, and tingling and numbness in the hand and forearm.
He stated that he confirmed his diagnosis of CRPS using the ‘Budapest consensus criteria’ (‘the Budapest criteria’) and that no other diagnosis better explains Ms Kenda’s symptoms. He stated that cervical spondylosis was age-related, but rendered symptomatic by work duties.
Dr Navani stated that physiotherapy every two to three weeks would not cure Ms Kenda, but would help ease her symptoms. He considered a T2 and T3 nerve block a reasonable option, to see if it relieves her symptoms. Hyrdrodilation is also reasonable, given her limited shoulder movement.
In cross-examination, Dr Navani was challenged about the quality of his patient notes (ST31). He stated that because of her chronic injury state, it was not necessary to make an examination each visit. Dr Navani agreed that there was no record made of hyperaesthesia or allodynia, nor temperature difference. He also accepted that he had not used an instrument to conduct the strength test of Ms Kenda’s hand.
Mr Douglas Gardiner
Mr Gardner, orthopaedic surgeon, addressed in evidence the findings of his report dated 13 June 2018 (5058/T8) from an examination of the same date. In his report, Mr Gardiner diagnoses: CRPS Type 1; mild to moderate rotator cuff arthropathy causing subacromial bursitis and impingement; right lateral epicondylitis with partial ligament tear; cervical spondylosis without neurological compromise, with left periscapular back pain of uncertain origin; and, recurrent CTS. Mr Gardiner determined a combined Whole Person Impairment (‘WPI’) of 29% for Ms Kenda’s orthopaedic conditions.
In his oral evidence, Mr Gardner stated that he accepted Ms Kenda’s descriptions of her pain symptoms, and that on examination she demonstrated stiffness and an excessive response to light touch. He found none of the significant swelling, shininess, temperature, or colour change that are usually part of a diagnosis of CRPS.
Mr Gardiner stated that he disagreed that Ms Kenda had a chronic pain syndrome, as diagnosed by Dr Kostos, as this is characterised by generalised pain and symptoms not confirmable by examination. Mr Gardiner supported the CRPS diagnosis made by Mr Blombery, and stated that he was familiar with the latter’s expertise in this field.
Mr Gardiner confirmed that he found significantly weakened grip strength on the right side, noting that, as a voluntary action, this was not highly diagnostic. He described the right shoulder condition as arising from stiffening of ligaments which reduces movement, and stated that hydrodilatation is a reasonable means of addressing this.
With respect to Ms Kenda’s wrist, Mr Gardiner stated that CTS is considered recurrent if a patient experiences ongoing symptoms, but was unable to identify any relevant signs upon physical examination. In his opinion, keyboard and mouse use do not necessarily contribute. He stated that ‘continuous lifting and pressure’ can cause pain and increased swelling at the site of surgery ‘if a person turns to vigorous work too early after the carpal tunnel release’.
Mr Gardiner stated that Ms Kenda’s conditions could be considered ongoing, and that her prognosis was guarded. He described his finding of a WPI for the right upper extremity of 10% as ‘conservative’, but reasonable. It was an overall assessment, and he leaned toward the major and obvious features of her condition.
In cross-examination, Mr Gardiner affirmed his observation that sensory abnormalities in Ms Kenda’s hand and forearm were ‘non-dermatomal’. That is, her subjective sensory loss was not attributable to known nerve pathways.
Mr Gardiner stated that CRPS could not explain Ms Kenda’s cervical spine symptoms. He restated his opinion that there is no relationship between CTS and computer work. He also stated that a person with neck or shoulder pain may experience continuation of pain in those areas from adopting a fixed position.
I asked Mr Gardiner what activity might, in his opinion, account for Ms Kenda’s shoulder condition. He replied that rotator cuff disease usually arises from vigorous activity at or above shoulder level. Mr Gardiner assumed this was accounted for by continuous lifting of heavy files onto shelves. On the assumption there was no evidence of this kind of activity, Mr Gardiner suggested that reaching down to lift from a box, or reaching out with files could irritate the rotator cuff.
Mr David McCombe
Mr McCombe confirmed in evidence his speciality in hand, plastic and reconstructive surgery. He provided numerous reports in the form of letters to Ms Kenda’s pervious GP (ST documents) including a referral for symptoms consistent with recurrent CTS in December 2012 (ST5). At this time, Ms Kenda also exhibited elbow pain and crepitus, and radiology showed a ligament tear.
Following an MRI, Mr McCombe was unable to see any compression on the median nerve, but identifies a ‘reformed retinaculum’ (ST6). He describes scarring following decompression surgery causing some restraint of the tendon, and fresh elbow imaging showing mild lateral epicondylitis.
When referred in evidence to his medico-legal report to Comcare of 23 January 2013 (6600 and 6622/T7), Mr McCombe confirmed that a nerve conduction study after surgery was normal, but subsequent studies were consistent with a recurrence of CTS. He stated that the history provided to him was of a recurrence of symptoms with work duties, and he was not aware of any other activity or systemic medical reason that might explain their recurrence.
Mr McCombe referred Ms Kenda to a sports and exercise physician, who reported paraesthesia, or pins and needles, upon pressure to the top of the forearm and hand on 7 May 2013 (ST9). As most of the pain was related to soft tissue in the shoulder, Ms Kenda was referred for physiotherapy, which Mr McCombe considered a good idea for symptom relief.
In his letter of 6 February 2014 (ST13), Mr McCombe agrees with the view that Ms Kenda’s symptoms were myofascial, or soft tissue related. There were persistent neurological symptoms related to the radial tunnel. Mr McCombe conducted radial nerve decompression of the posterior interosseous in November 2014. He disagreed with the observation made by Dr Kostos in his report of 17 October 2017 (6600 and 6622/T50) that Ms Kenda had never in fact had nerve impingement.
Mr McCombe decided not to perform further carpal tunnel release surgery as Ms Kenda’s ongoing symptoms were ‘diffuse’; meaning he was not convinced she had a recurrence of the condition (ST26). He notes nerve conduction studies are not necessarily an accurate guide to recurrent symptoms, as there may in fact have been successful release during surgery.
In cross-examination, Mr McCombe confirmed that testing recurrent CTS was always more difficult. Asked about the finding in September 2015 that there was no neuropathy in Ms Kenda’s right arm (ST23), Mr McCombe agreed it was reasonable to assume there should have been objective evidence of a worsening of her condition. He agreed that where there had been previous severe median nerve compression, it is reasonable to expect detectable changes in nerve conduction studies.
Mr McCombe was asked whether myofascial pain syndrome might provide a better explanation for Ms Kenda’s condition. He responded that it was difficult to achieve a unifying theory for Ms Kenda, and her upper arm symptoms were all common problems.
In response to questions from me, Mr McCombe confirmed that he had particular expertise in treatment of CTS. He said that there is a documented relationship between certain occupations such as abattoir workers, but the link with administrative work was more difficult due to the varied nature of the tasks. In summary, he described CTS as a ‘very common condition and a broad range of people get it’. Surgery is usually a durable solution, and he considered the risk of recurrence to be around five percent.
Dr Peter Blombery
Dr Blombery confirmed in oral evidence that he is a specialist in vascular medicine and pain medicine, with particular experience over 30 years in CRPS. Dr Blombery provided a report dated 24 April 2018, and a supplementary report dated 8 June 2018 (5058/T5 and T6). In his main report after examination of Ms Kenda in April 2018, Dr Blombery diagnoses CRPS based on the Budapest criteria, a ‘good history’ of changes in temperature and colour, and observed differences on examination. He further assessed Ms Kenda with 15% WPI, based on carpal tunnel compression of the median nerve, and reduced range of shoulder movement.
In this report, Dr Blombery also states that Ms Kenda’s employment contributed to her cervical spondylosis. He states that there is a well-documented association between ‘heavy and repetitive use of the arm and wrist’ and carpal tunnel compression of the median nerve. Her lateral epicondylitis is also said to be consistent with the heavy and repetitive work she performed, as is her shoulder condition.
In his supplementary report, Dr Blombery states his opinion that Dr Kostos ignored evidence of autonomic dysfunction in reaching his diagnosis of chronic, or non-specific, pain syndrome.
In his oral evidence, Dr Blombery described a chronic pain condition as arising, in many patients, due to pain pathway sensitisation. It had previously been considered to be psychological in origin. He stated that CRPS is a disorder characterised by changes to the autonomic nervous system following an injury that leads to changes in colour, temperature, or swelling and altered hair or nail growth. Dr Blombery stated that the most common cause of CRPS is carpal tunnel release surgery. He had treated about 700 patients with CRPS, but did not see many patients for carpal tunnel issues.
Dr Blombery confirmed that he had produced a study into occupational factors in CTS (Exhibit A5). He stated that ‘the evidence is now overwhelming that rapid and heavy movements of the wrist are likely to cause an increased risk incident of carpal tunnel compression of the median nerve’. When asked what ‘heavy’ was in this context, Dr Blombery stated that even keyboard work of an hour’s duration has been shown in ultrasound studies to swell the median nerve. A combination of repetition and load further increased the risk. However, Dr Blombery noted development of the condition is multifactorial.
He stated that handling and marking large volumes of documents at a fast pace would qualify as repetitive movement, as discussed in his paper. He confirmed that there was less dramatic association between CTS and occupational keyboard use than in other industries, but this link had been validated in more recent studies.
Dr Blombery considered that Ms Kenda’s recurrence of symptoms after returning to work following surgery was supported by nerve conduction studies in October 2012. He stated that the apparent absence of median nerve neuropathy in 2015 was ‘very curious’, and recommended the testing be repeated.
With respect to treatment, Dr Blombery stated that a sympathetic nerve block was unlikely now to be effective, hydrodilatation was appropriate, and that Ms Kenda may well benefit from physiotherapy. He added that Ms Kenda did not give a particularly strong history of working with a heavy load, which is usually associated with the kind of tendon tear found in her shoulder.
Dr Blombery stated that the Budapest criteria had been changed to require observation of physical signs, rather than relying only on patient history. He himself had noted that Ms Kenda’s hand appeared darker in colour, her right forearm was 1.5 degrees cooler than the left, and there was tenderness in the hand and elbow.
Dr Blombery stated that reduced sensation to light touch could not be attributed to Ms Kenda’s documented wrist or elbow conditions. He was not sure what that symptom might represent, as it was associated with the C5 nerve distribution.
In cross-examination, Dr Blombery stated that some studies of CTS do not find a positive link with clerical duties. He reiterated that there was a link in the median nerve studies previously referred to, and that Ms Kenda was not only engaged in keyboard work but also handling paper.
It was put to Dr Blombery this was not ‘heavy’ work, and he stated that studies indicate that repetitive use of hand and wrist is associated with increased risk of CTS. He disagreed that the ‘jury was out’, stating that with every passing year the link to clerical occupations is clearer. Dr Blombery acknowledged that most studies relate to other kinds of movement to that arising in keyboard work.
He confirmed that he observed the back of Ms Kenda’s right hand to be ‘duskier’, and that he used an infrared thermometer to identify the forearm temperature variation. He stated that colour change would need to be observed on more than one occasion.
I asked Dr Blombery during cross-examination to confirm what made CRPS a ‘regional’ pain syndrome. He responded that it is usually a limb on one side only. He provided the example of symptoms predominantly involving the hand but that ‘often just extend proximally up to the shoulder’.
Andrew Stephens
Mr Stephens confirmed that he was Ms Kenda’s sports physiotherapist between 2013 and 2018. She consulted him on approximately 55 occasions in relation to myofascial pain, meaning muscular pain. He considered physiotherapy would form part of Ms Kenda’s ongoing management, but rather than ‘manual therapy’ he would now offer her proactive strategies to improve fitness, perhaps once every two to four weeks.
Mr Stephens observed that Ms Kenda’s symptoms had, in the past, been exacerbated by manual treatment, with an increase in pain, paraesthesia, numbness and tingling. However, when treating Ms Kenda he did not observe any of the signs associated with CRPS. He also stated that he tried to reinforce with Ms Kenda that her pain was out of proportion to levels of damage reported in scans. Ms Stephens accepted that this is a feature of CRPS.
Mr Stephens considered that Ms Kenda’s symptoms improved after her nerve release surgery and when on holiday. He considered her pain ‘seemed to be certainly stirred up’ by stress, and that ‘work pressures increased her experience of pain’.
In cross-examination, Mr Stephens stated that Ms Kenda did not give a history of lifting objects above shoulder level. He added that ‘frozen shoulder’ is known as idiopathic adhesive capsulitis and ‘we don’t know why people get it’, and accepted that it can develop in the absence of specific trauma.
Mr Stephens explained that the reference in his clinical notes to ‘pain behaviour’ exhibited by Ms Kenda was to the alteration of movement to avoid all pain, perhaps where pain is out of proportion to the level of damage.
Dr David Wiesenfeld
Dr Wiesenfeld provided a report dated 8 July 2019 (Exhibit A7) for the Respondent, and was called as a witness on Ms Kenda’s behalf. Dr Wiesenfeld is qualified in dental science, with a specialisation in oral maxillofacial surgery. He reviewed Ms Kenda in May 2019 and reports that the main factors contributing to her TMJ are clenching and grinding, which may be stress related. He notes the loss of seven teeth including several molars, describing a complex dental history with multiple cracked and repaired teeth.
Dr Wiesenfeld stated in evidence that there are patients who continue to experience bruxism after the withdrawal of a stressor, due to muscle and stress patterns becoming ingrained. Ms Kenda’s TMJ may become more severe if she is unable to overcome it, and Dr Wiesenfeld considered that her reports to other treaters of headaches was typical of the condition.
In cross-examination, Dr Wiesenfeld acknowledged that materials he had been provided (ST35 and 36) indicated Ms Kenda was diagnosed with TMJ in 2006, and tooth cracking was also noted at that time. Dr Wiesenfeld also agreed that stress arising from surgery or physical conditions could contribute to TMJ. He added that the process of anaesthetising patients during surgery can also exacerbate the condition.
Dr Wisenfeld agreed that stressors can take different forms, and that he was not apprised of a history of personal stress in 2006 (6600 and 6622/T46.3). When asked about Ms Kenda’s history of medication between 2006 and 2009, Dr Wiesenfeld stated that he considered her problem is not the result of any single event.
Associate Professor Jack Gerschman
Dr Gerschman provided two reports, both dated 3 January 2019 (Exhibit A8). He confirmed his extensive qualifications in dental science, oral medicine and psychology (among others). His primary report provides an extensive summary of Ms Kenda’s treatment history for TMJ, including summaries of the reports of other specialists. Dr Gerschman found mild to moderate muscle pain on palpitation. He concludes that chronic work injury and associated anxiety have aggravated Ms Kenda’s bruxism. Dr Gerschman states that Ms Kenda’s TMJ is likely to lead to degenerative changes. The supplementary report of the same date makes parallel findings, but includes references to psychological consultations.

In his oral evidence, Dr Gerschman was taken to Ms Kenda’s statement in which she refers to work stress in late 2004/early 2005, including an incident report referring to neck and shoulder pain. Dr Gershman observed that individuals suffering stress can experience pain in different muscle groups. He stated further that most clinicians dealing with Ms Kenda have considered that her TMJ was due to stress at work.
Dr Gerschman was reluctant to be drawn on the implications of Ms Kenda’s use of various medications related to her mental health. He added that in his supplementary report he makes a clear finding that employment contributed to her condition, based ‘on what the psychologist found’.
Dr Gerschman stated that his observation of Ms Kenda’s jaw opening of 46mm was normal. He stated that Dr Wisenfeld’s observation of ‘very restricted movement’, given the lateral movement noted, ‘doesn’t make sense’. He stated that the jaw opening of 20mm observed by Dr Howe may have been due to the effect of her medications, and not the jaw condition itself.
Dr Gerschman was asked to explain the main conclusion in his report. He stated:
So I’m agreeing with the psychologist who said the same, that it’s an opinion that – well, if she’s got anxiety and depression related to her work injury, this was either the psychologist or psychiatrist, that would aggravate and maintain nightly tooth grinding.
Dr Gerschman opined that given that radiology indicated minor degenerative change in Ms Kenda’s jaw, wearing a splint was required ‘forever or as long as it takes’, and considered she should have Botox.
In cross-examination, Dr Gerschman acknowledged that bruxism is a multifactorial problem, and that Ms Kenda was diagnosed with bruxism and TMJ, probably in 2005. Dr Gerschman stated he did not know Ms Kenda’s full history, and confirmed he had relied on information about psychological factors supplied by others.
Dr Gautam Khurana
Dr Khurana provided a report for the Respondent dated 14 November 2018 (Exhibit R1), and in his oral evidence confirmed his specialisation as a brain and spine neurosurgeon. In his report, Dr Khurana states that in physical examination Ms Kenda exhibited ‘symptoms in excess of objective signs and in the presence of a Waddell/non-organic overlay’. Radiology and nerve studies did not, in his opinion, disclose a cause for her presentation. Dr Khurana notes that the weight of opinion is that repetitive mechanical duties at work contributed to Ms Kenda’s CTS; Ms Kenda’s cervical spondylosis is constitutional and not properly related to work; her chronic pain is non-organic; and, she may benefit from ongoing psychological treatment.
In his oral evidence, Dr Khurana stated that he obtained a history from Ms Kenda of having a ‘Shrek hand’, but did not recall any other reference to physical change in appearance. He was unable to undertake a proper physical examination of her limb due to her perceived pain behaviour. Ms Kenda could feel light touch, but also reported areas of numbness.
Dr Khurana accepted that he did not address radiology for Ms Kenda’s limb. However, immediately prior to attending the hearing he reviewed the most recent neck radiology (Exhibit R3). This confirmed the presence of a multilevel constitutional process, affecting five discs and he stated: ‘there was no pathology on the right hand side of the cervical spine that could account for any neurogenic symptoms’.
Asked about his conclusion regarding CTS, Dr Khurana stated that the information provided at the time of his report indicated that symptom onset was ‘temporally associated with work duties at the time’; his opinion was not intended to address causation. He stated that CTS is well recognised to be genetic, or constitutional, in origin.
Dr Khurana accepted the proposition that Ms Kenda presented with a chronic pain syndrome, but it was ‘one hundred percent’ non-organic, and he described her presentation as ‘very bizarre’.
In cross-examination, Dr Khurana agreed that he was not able to comment in detail on CRPS, but did make a practice of looking for non-physiological features in patient presentation. He accepted that he had found tenderness in the scapula with the onset of hand numbness and pain, which he described as ‘paradoxical’.
Mr Ronald Haig
Mr Haig prepared a report for the Respondent dated 11 December 2018 (Exhibit R2). In his oral evidence he confirmed his expertise as an orthopaedic surgeon. In his report, Dr Haig states that on examination Ms Kenda exhibited ‘quite abnormal pain behaviour’. He states that Ms Kenda had a ‘bizarre constellation of symptoms in the right upper extremity which do not fit any pattern for a clinical diagnosis’. Specifically, Mr Haig concludes:
(a)Ms Kenda does not have CRPS, but rather a chronic pain syndrome;
(b)her CTS is constitutional in origin;
(c)she ‘may’ have lateral epicondylitis;
(d)any shoulder restriction is not secondary to another condition, and minor changes are not unexpected for her age;
(e)there is some cervical spondylosis unrelated to employment;
(f)Ms Kenda is not in need of any treatement including physiotherapy; and
(g)Ms Kenda has no permanent impairment from an orthopaedic point of view.
In his oral evidence, Mr Haig stated that he recorded Ms Kenda’s daily living activities as being able to drive, cooking but no longer baking, difficulty cleaning toilets, and carrying shopping in her left hand. He stated that upon examination, Ms Kenda had difficulty opposing her thumb and little finger, but had no anatomic deformity to prevent her doing so.
Mr Haig explained that he administered a test to induce altered sensation in the distribution of the median nerve. In response, Ms Kenda reported tingling in the finger tips including the little finger, which is not part of the associated nerve distribution.
Mr Haig described observing tenderness where it was not expected, and facial grimacing during movement tests. Tenderness was observed in the shoulder and neck on minimal palpitation, which he considered unexpected. All Ms Kenda’s range of movement was ‘much reduced’, but Mr Haig questioned her compliance.
Mr Haig confirmed that he did not observe hand discolouration and found none of the other signs required for a diagnosis of CRPS.
With respect to CTS, Mr Haig cited the American Medical Association (‘AMA’) Guide to Evaluation of Disease and Injury Causation, a meta-analysis which indicates that demographic and disease related variables are more likely to cause CTS than occupational factors.
Mr Haig did not disagree that heavy and repetitive work with the hands may be associated with development of CTS, but did not consider keyboard and mouse work to meet this description.
Asked about lateral epicondylitis, Mr Haig stated that too much emphasis had been placed on an ultrasound finding of a small tear. This did not account for the symptoms that Ms Kenda had complained of at that time, being paraesthesia down the back of the forearm and hand. Mr Haig considered Ms Kenda did not meet the vast majority of the criteria required for diagnosis by the AMA text quoted above.
Mr Haig agreed minor changes in the shoulder were not unexpected, but radiological findings do not mean they are the cause of any symptoms. Mr Haig also confirmed that he had allocated a rating of four for permanent impairment relating to chronic pain.
In cross-examination, Mr Haig stated that he was aware of the nature of Ms Kenda’s work duties. He stated that a return to work after carpal tunnel decompression could be in the order of a week or ten days for someone in a sedentary occupation.
Mr Haig stated that he had some reason to doubt the outcome of a second nerve conduction study undertaken in 2012 which indicated recurrence of CTS, and that symptoms reported by Ms Kenda were not typical of the condition.
Dr Tony Kostos
Dr Kostas provided the following reports: 13 November 2017 (6600 and 6622/T50); 30 April 2018 (4493/T4); 16 July 2018 (5058/T10); and 7 July 2020 (Exhibit R4). Dr Kostos stated his expertise to be rheumatology, with a particular expertise in musculoskeletal medicine. Dr Kostos examined Ms Kenda once in October 2017, and later reports were supplementary.
In his November 2017 report, Dr Kostos states that Ms Kenda exhibited: restricted neck movement; some tenderness about the cervical spine; some restricted right shoulder movement (elevation) and diffuse tenderness; pain free movement of the right elbow except for extension; no lateral epicondyle tenderness; full wrist movement and no observable changes, but markedly reduced right grip strength; and, reduced pinprick sensation throughout the entire arm. Dr Kostos diagnoses chronic regional pain syndrome, and finds no CTS, and no lateral epicondylitis. Dr Kostos considers Ms Kenda’s shoulder symptoms not consistent with any underlying condition. He also considers cervical spondylosis not relevant to Ms Kenda’s current symptoms, and concludes that no treatment will assist her.
In his July 2018 report, Dr Kostos comments on additional clinical information not previously provided. On the basis of this material, dating to 2005, Dr Kostos states his view that the information strongly suggests Ms Kenda had pre-existing problems in her neck and right upper limb. Dr Kostos goes on to:
(a)state that Dr Blombery’s diagnosis of CRPS is not properly substantiated by clinical findings;
(b)identify research papers countering the view that keyboard work is associated with development of CTS;
(c)state that Dr Gardiner’s findings in respect of Ms Kenda’s conditions reflect findings that can also be made for asymptomatic patients; and
(d)respond to findings in a report of Dr Nitin Shukla, psychiatrist, dated 13 February 2018 (2068 and 2015/T12), stating that this report details the non-physical factors responsible for Ms Kenda’s chronic pain syndrome, a diagnosis that is supported by that psychiatrist.
In his July 2020 report, Dr Kostos responds to the evidence provided in the hearing by Dr Blombery. Dr Kostos reiterates his view concerning the CRPS diagnosis, and observes that Dr Blombery is not an expert in musculoskeletal conditions.
In his oral evidence, Dr Kostos stated that on examining Ms Kenda, all the Budapest criteria were absent, noting that the concept of a disproportionate level of pain was the most subjective part of the criteria. There was no radicular component to Ms Kenda’s right sided arm pain, and a diagnosis of CRPS means ‘persistent pain in the absence of any objective physical abnormality’.
He stated that Dr Navani had not provided evidence for each of his diagnoses in respect of Ms Kenda. When referred to Dr Navani’s clinical note of ‘blueing discolouration and some swelling in the right hand’, Dr Kostos stated this may have indicated autonomic dysfunction, but that signs and symptoms for CRPS ‘don’t come and go’.
He stated that the condition was previously named ‘reflex sympathetic dystrophy’ on account of the trophic changes; being wasting of muscle, and thinning of hair and nails. Dr Kostos explained this was a result of overactivity of the sympathetic nervous system.
Dr Kostos stated there is confusion about Ms Kenda’s right elbow condition. He considered the ultrasound and later MRI to have indicated different problems; and there was no evidence of an acute lesion.
Dr Kostos restated his view that any further intervention would fail with Ms Kenda. This was because treatment would be directed at individual radiological abnormalities without looking at the whole patient, who in this case had a chronic pain syndrome.
He confirmed the finding in his report regarding inability to diagnosis a shoulder condition. Dr Kostos stated that it is not his practice to order radiology for shoulder and elbow conditions, but he has experience treating shoulders. Dr Kostos further stated that most changes observed in radiology are genetically determined, and the notion that you can ‘wear out’ joints through work was not correct.
In cross-examination, Dr Kostos stated that physiotherapy should provide relief within two to three sessions. If only occasional temporary relief was experienced, then massage would be as useful. He did not agree that reduced pinprick sensation met one of the Budapest criteria, and stated that a person with chronic regional pain have tenderness ‘everywhere’.
Dr Kostos stressed in his oral evidence that, in his opinion, CRPS signs and symptoms would be evident in Ms Kenda’s hand, whereas Dr Blombery noted a temperature change in the forearm. Dr Kostos stated that the hand would be affected, as this is predominantly where the changes resulting from reflex sympathetic dystrophy occurs.
I put to Dr Kostos that a previous witness had given evidence as to CRPS being by definition a ‘regional’ condition. He responded:
Well I’ve never seen it involve anything else other than the hand to begin with. Some patients, if they’re not responding to treatment, they can develop allodynia further up the arm … clinical experience tells us that the vast majority of cases of CRPS type one involve a distal area, usually hand or foot.
When asked in evidence about a range of contrary findings by other specialists, Dr Kostos stated that Ms Kenda had been serially treated for a wide range of different conditions, but her symptoms remained the same. This was a ‘long tortuous’ path he had frequently seen.
Dr Andrew Howe
Dr Howe provided reports dated 7 August 2019 and 4 December 2019 (Exhibit R5). He confirmed his expertise in dental surgery. Dr Howe was unable to examine Ms Kenda for the purposes of the report and notes seven missing teeth and only one molar. He notes that her bruxism predates the accepted dates for her claim, and heavy restoration was also prior to that date. In one instance, Ms Kenda lost a tooth after failing to pursue treatment. Dr Howe was unable to determine whether employment contributed to her further experience of the condition.
Dr Howe examined Ms Kenda in November 2019 for his second report. Ms Kenda showed him a soft nightguard which had split, with signs of considerable wear. He recommends a hard splint combined with physiotherapy, psychological counselling and palliative measures including medication, and states that Botox may also be effective. Dr Howe confirms that Ms Kenda was diagnosed with TMJ in 2006, and had a splint made prior to this time. Hence, her employment did not contribute to the onset of this condition.
Dr Howe stated that Ms Kenda was unable to open her jaw more then 20mm without pain, and that more than 40mm is a normal range. He confirmed that Ms Kenda could not produce lateral movement, but that because of the evidence of grinding she did indeed have the capacity for lateral movement.
Dr Howe acknowledged Ms Kenda’s report of both temporal headaches and migraine, but the latter is not normally associated with TMJ. He agreed that deterioration of Ms Kenda’s teeth could have been arrested had she used an appropriate guard, or had other dental treatment.
In cross-examination, Dr Howe agreed that information contained in Ms Kenda’s statement addressing her workload issues in late 2004/early 2005 would have been important to consider. He opined that stress is generally accepted as being associated with bruxism and TMJ, and surgery could also be a stressor.
Other medical evidence
Ms Kenda was referred to Mr Stephens for physiotherapy by Dr Paul Blackman in May 2013 (ST9). Dr Blackman is a sports and exercise physician who also corresponded with Mr McCombe. In reporting to Mr McCombe (ST9), Dr Blackman states that he suspects the majority of Ms Kenda’s pain arises from myofascial sources, particularly in the forearm and shoulder.
Dr Blackman reported to Ms Kenda’s previous GP, Dr Steven Zebic, in November 2013 (ST12) that Ms Kenda provided ‘telling’ information to Dr Blackman that she felt better after a much easier week at work physically. Dr Blackman reports that he: ‘had a protracted discussion with Danielle today explaining that from a medical point of view I remain to be convinced she can do much more to treat her current pain scenario’.
Dr Zebic wrote to Mr McCombe with a similar perspective in October 2013, when referring Ms Kenda for further review (ST11). Dr Zebic stated that Ms Kenda is: ‘still suffering from considerable symptomatology because she is not/her employer really keeping to the restrictions as outlined in her certificates’.
In considering his treatment response to Ms Kenda’s radial nerve issue, Mr McCombe reported to Dr Zebic in February 2014 (ST13) that he agreed with Dr Blackman: ‘the majority of her symptoms appear to be myofascial in origin and hence unlikely to respond to surgery’.
Mr McCombe subsequently reported to Dr Zebic later in February 2014 (ST14) about his exploration of radial tunnel syndrome. He states:
It is possible that this has something to do with Danielle’s symptoms however as I explained to her today the procedure of decompression of the posterior interosseous branch of the nerve which is potentially compressed here is not guaranteed to resolve her pain and she does have some atypical features with a fairly diffuse pain symptoms and also sensory symptoms …
I would be happy to explore the nerve here for her but only on the understanding that this may not resolve her symptoms. At this stage I am not sure that Danielle has reached this point.
Some years later, Mr McCombe referred Ms Kenda to Mr Paul Smith, neurosurgeon, who examined her and reported in February 2017 (ST28). Mr Smith did not consider Ms Kenda’s cervical spine to contribute to her symptomatology. He examined her right hand and arm conducting pinprick and light touch assessment. Mr Smith states: ‘she reported quite diffuse sensory disturbance and asymmetry between the two hands, but I found it hard to identify a clear cut pattern that was definable’.
At the same time, in February 2017, Dr Neels Du Toit, sports medicine physician, reported to Dr Navani (ST29):
The most likely diagnosis that I can make is that she has symptoms and signs of complex regional pain syndrome. Her symptoms are slightly atypical, given that she has minimal trophic signs of the hand and nails and today there were no clear colour changes to the hands and forearms …
At some point we will have to make a decision that we are not going to find the specific structural cause for her symptoms. I started the discussion with her in regard to pain and symptomatic management.
Dr Du Toit wrote in March 2017 (6600 and 6622/T27) in support of a request for the sympathetic nerve block (2017/7338). He states there that Ms Kenda’s symptoms ‘closely relate to complex regional pain syndrome of the right forearm and hand’.
Also in March 2017, Ms Kenda attended Dr Mary Wyatt, an occupational physician, who then reported to Comcare about her examination (6600 and 6622/T26). Dr Wyatt notes:
At the conclusion of the examination, Ms Kenda pointed out that her right hand had become purple. This was confirmed on examination. The right hand became dusky-purple in colour, particularly over the volar aspect, with slight swelling. Ms Kenda said this would likely take five or ten minutes to settle or at times could take longer …
From her description of her problems at this stage, I think it is best to describe her right arm problem as a chronic pain disorder …
Ms Kenda’s current symptoms are consistent with the multifactorial nature of her problem …
Ms Kenda’s symptoms are of quite variable severity.
Dr Wyatt provided a supplementary report in June 2017 (6600 and 6622/T36) concerning the observations of Dr Du Toit and the issue of a sympathetic nerve block. Dr Wyatt concurs with Dr Du Toit’s indication that Ms Kenda’s symptoms are ‘closely related to complex regional pain syndrome’. Dr Wyatt accepts that in her previous report she addressed autonomic dysfunction, but adds the colour change noted during examination: ‘was suggestive of a milder degree of problems in line with complex regional pain syndrome, but not meeting the diagnostic criteria’. Dr Wyatt states further that the chance of success of a nerve block procedure is relatively low, with a small evidence base.

The clinical notes of Dr Navani (ST31) throughout 2017 and into early 2018 make numerous references to discolouration. The notes appear to repeat the same format each time with the relevant entries largely as follows:
REASON FOR CONTACT:
Right hand dorsum swollen /pain / bluish discolouration ++
sore Right arm / Neck
PROGRESS SINCE LAST VISIT:
…
not able to cope ++struggling
has swollen / bluish discolouration of Right upper arm…
In correspondence to Comcare in February 2018 (2068 and 2015/T11), Dr Du Toit refers to the rejection of his proposal for sympathetic nerve block and hydrodilatation. He states that these procedures are in response to Ms Kenda’s physical response to CRPS, which has been lack of use of her shoulder. He describes CRPS as the primary diagnosis, and of longstanding, which has therefore lead in his opinion to her adhesive capsulitis.
Finally, I note the findings of Dr Shukla (2068 and 2015/T12), who prepared a report upon referral from Ms Kenda’s GP, Dr Navani. In addition to an anxiety and depressive condition, Dr Shukla diagnoses ‘chronic pain syndromes’. He records under the heading ‘Impression’:
Loss of role appears to have a very destabilizing affect on her. Her description of her problem as ‘Still pining and grieving for my job’ sums it up quite well. Her beliefs and Anxious traits in personality are contributing to maintenance of the problem. Ambivalent and conflicted as what she wants is return to work and to not rest, but that’s what the treatment needs, at least on a short term [sic]
CONSIDERATION
It follows from the nature of the legislation that compensation is only payable for an injury that causes incapacity or impairment. This must be an injury as defined in the Act. There are different tests of causation (the link to an individual’s employment) depending upon whether a finding is made as to the existence of an ‘injury’ or an ‘injury in the form of a disease’.
Further, key authorities in the compensation jurisdiction lead to two important riders, which are: that decision making is progressive, that is, it takes account of the evolving medical opinion; and, that for liability to pertain, there must be a finding as to a continuing causal connection to employment.
I will not attempt a summary of the very extensive submissions made in these matters. However, I note that I have considered them, and draw on them in shaping these considerations, as well as relying on the brief summary of evidence above, and other relevant material.
Reviewable decisions have been made in respect of six different conditions, and in respect of three treatment types said to relate to those conditions, in addition to the permanent impairment decision. Given the significant overlap between medical conditions and symptoms, and the divergent diagnoses, I will deal with the conditions in groups. I will make determinations in terms of the legislation with respect to these groups of conditions.
Preliminary considerations
Prior to addressing the claims as outlined above, it is appropriate to take into consideration Ms Kenda’s employment history and duties. This is not only pertinent to the exploration of the necessary causal connection, but because of the considerable focus placed in the presentation of Ms Kenda’s case upon this issue.
The Applicant’s submissions, for example, refer to the following elements of Ms Kenda’s evidence:
(a)her database entry work in the late 1990’s using a large mouse intensively and repetitively;
(b)the demanding responsibilities of her paralegal work, including supporting a team of lawyers and working in a time-based fee structure;
(c)file inspection duties, including copying and collating, and preparation of Tribunal documents;
(d)her extremely heavy and hectic workload in the early to mid 2000’s; and
(e)the lodging of incident reports at various times.
I note that Ms Kenda introduced evidence from members of the professional staff at AGS. However, I do not consider this material to have provided specific insights into Ms Kenda’s actual workload or work practices. Nonetheless, it is relevant to note that the Respondent’s submissions include the explicit acknowledgment that Ms Kenda found her duties demanding, and that this was supported by the evidence of Ms Heffernan.
I am satisfied that, on the basis of the evidence overall, Ms Kenda was engaged in part time employment at the relevant times. Her pattern of work was, in the main, a three day week comprised of non-consecutive days at the office. I accept Ms Kenda’s evidence that she worked long hours on those days.
I am also satisfied that Ms Kenda’s duties were diverse. It is apparent from the evidence that there were some periods during her employment where certain duties, be it database work, telephone work, or handling files, may have predominated. However, I consider that, overall, the better view is that her duties included a range of clerical tasks.
Right upper limb conditions
Lateral epicondyltitis
This condition forms part of Ms Kenda’s first set of accepted claims. The first medical reference appears to be to a ‘sore elbow’ in a consultation with Dr Zebic on September 2011 (6600 and 6622/T6.1).
There is radiology material from late 2012 indicating mild or low grade pathology in Ms Kenda’s right elbow (6600 and 6622/T4P, T5.3). The first is an ultrasound report that states there is a suggestion of a tear in the lateral collateral ligament. The second is an MRI that states there may be either a sprain or partial tear in the medial collateral ligament. It also notes a signal associated with the common extensor origin compatible with low grade tendinopathy. I note this structure is on the lateral aspect, or outside, of the elbow.
I note that Dr Gardiner in his report observes that radiology from 2011 indicated no abnormality in the elbow. He would, however, appear to have been satisfied that the radiology explained Ms Kenda’s reported symptoms.
Mr McCombe also appears to have been so satisfied, and to consider employment duties capable of explaining the condition. Equally, he accepted in cross-examination that all of Ms Kenda’s conditions are quite common. There is correspondence from Mr McCombe to Comcare, dated 22 August 2014 (6600 and 6622/T14), in which he expresses the view that Ms Kenda’s lateral forearm symptoms at that time were the result of the identified issue with her radial nerve compression. He subsequently performed surgery for this on 21 November 2014 (6600 and 6622/T15).
In contrast, Mr Haig was not satisfied that the radiology accounted for Ms Kenda’s symptoms. Dr Kostos stated that there has been confusion about this condition due to the contradictory findings of the radiology, which he also describes in his report as unreliable.
Dr Blombery accepted that he is not an expert in musculoskeletal conditions. On this basis, his opinion as to the underlying pathology in the elbow is somewhat less relevant. However, in his written and oral evidence he appears to have had difficulty integrating Ms Kenda’s elbow symptoms into his overall diagnosis. Indeed, as with Mr McCombe, he considered there may be a cervical issue behind them.
Ms Kenda has been examined by two neurosurgeons, Mr Khurana and Mr Smith, neither of whom consider there is an identifiable neurological element to Ms Kenda’s presentation, including her elbow. That is, her lateral epicondylitis was not explained, in their opinion, by any spinal condition.
Sprain of shoulder and upper arm (subdeltoid bursitis)
The issues relating to Ms Kenda’s shoulder are apparently both longstanding and diverse. There is a rather non-specific note from a medical consultation in April 2005 (6600 and 6622/T46.1A) referring to neck and shoulder pain and peripheral tingling. There are otherwise numerous references throughout the medical history to various upper arm issues. Ms Kenda’s claim form of December 2013 (6600 and 6622/T3) refers somewhat generally to ‘shoulder restriction’.
There is some consistency across radiology reports, specifically in December 2012 (6600 and 6622/T5.2) and March 2018 (6600 and 6622/T21). The first report of an ultrasound identifies mildly thickened subdeltoid bursa, but no rotator cuff issue or tendinosis. The latter report, also of an ultrasound, similarly states that the imaging is ‘suggestive’ of bursitis. It also notes background degenerative change.
In contrast, a report of radiology in the form of an x-ray and ultrasound in May 2015 (6600 and 6622/T17), describes the result as ‘largely normal’. It also identifies background osteoarthritic change. It suggests the possibility of adhesive capsulitis (or ‘frozen shoulder’) and identifies no rotator cuff involvement.
Mr Gardiner, seemingly in spite of the quite specific radiology findings to the contrary, considered Ms Kenda had mild to moderate rotator cuff arthropathy. Moreover, his evidence at the hearing revealed that he considered certain movements above shoulder height to be the cause of Ms Kenda’s shoulder pathology. He proffered lifting from boxes in the alternative. The former is not supported by any direct evidence. The latter may find some, but weak, support in the evidence.
Mr McCombe has consistently identified Ms Kenda as exhibiting soft tissue pathology, including for her shoulder. Dr Blombery saw no aspect of Ms Kenda’s history as adequately accounting for her shoulder symptoms. Mr Stephens, consistent with Mr Gardiner’s first theory, also saw no relevant activity history to account for Ms Kenda’s shoulder presentation.
Mr Haig was of the view that the state of Ms Kenda’s shoulder is explained by her age. In the context of her guarded behaviour, he did not consider her symptoms to be clearly explicable by pathology. Dr Kostos was also relatively emphatic in his rejection of a formal diagnosis consistent with the conditions claimed.
Aggravation of CTS
Ms Kenda has a documented history of diagnosis for, and surgical treatment of, right CTS. This was not the subject of a claim for compensation.
Ms Kenda had approximately six weeks off work after surgery in December 2010. She was approved to return to work in late January 2011 on modified duties, including minimal keyboard work (6600 and 6622/T4B/T4C/T6.5). She had further time off with a medical certificate in February 2011, and was offered hand therapy, with a graduated return to work to be signed off by the surgeon (6600 and 6622/T4D).
On 7 March 2011 Ms Kenda submitted an incident report concerning aggravation of her CTS, said to be caused by ‘overuse of keyboard and mouse’ (6600 and 6622/T4G). She confirmed her need to work on modified duties in an email dated 17 February 2011 (6600 and 6622/T4H).
In August 2011 nerve conduction studies conducted by the same neurologist who had diagnosed CTS previously (Dr David Frielich) found no evidence of CTS (6600 and 6622/T4J). A subsequent study in October 2011 found evidence of CTS (6600 and 6622/T4N). An MRI of the right wrist conducted on13 December 2012 found ‘no evidence of compression of the median nerve’ (6600 and 6622/T5.3).
Ms Kenda’s claim of 15 December 2012 for this condition was accepted (6600 and 6622/T10). The decision to accept liability was based upon nerve conduction studies and Mr McCombe’s assessment of recurrent CTS, for which he considered her repetitive work to be responsible in part (6600 and 6622/T7).
Some time later, in September 2015, Dr Martin Short performed a nerve conduction study (ST23) and found no evidence of median, radial or ulnar nerve neuropathy.
Mr Gardiner’s evidence is somewhat ambiguous. He appears to have not found any clear evidence of CTS, but was prepared to accept that Ms Kenda’s work circumstances contributed to aggravation. The evidence here does not appear to have taken into account the passage of time between her return to work after surgery, and his examination of her conducted in 2018. Further, he was not of the view that keyboard work contributes to CTS.
Mr McCombe was not convinced in 2017 of the recurrence of CTS. He also accepted that nerve conduction studies were not a definitive tool in diagnosis and expressed clear reservation about a link between CTS and administrative tasks.
The question of a possible occupational link was one of the major issues of dispute in the evidence of Dr Blombery and Dr Kostos. I do not consider it necessary to address the literature relied on by these witnesses as their opinions were thoroughly aired in evidence. I note that Dr Blombery referred more than once to a link between CTS and ‘heavy’ work. He maintained that Ms Kenda’s duties qualified, albeit also acknowledging that most occupational studies relate to other hand movements. Dr Blombery also accepted that he did not see many patients with CTS.
Dr Kostos expressed significant doubts about the diagnosis of CTS, to the extent that he questioned whether it may have ever been an appropriate diagnosis. This opinion was, appropriately, qualified with his observation that he did not examine Ms Kenda in 2010. I accept from his evidence that he holds experience in nerve conduction studies, and expressed reservations about their value.
Dr Khurana found no direct association between Ms Kenda’s condition and her employment. Mr Haig agreed that her CTS was constitutional in origin, albeit he acknowledged not being well informed about her particular duties.
Summary findings
The Applicant appears to contend that she experienced aggravation of her CTS and that this is an injury pursuant to s 5A of the Act. In the alternative, it is contended that this condition was contributed to by her employment to a significant degree. It is contended that her right shoulder and upper arm conditions were also significantly contributed to by her employment. I take these to be references to a claim under s 5B of the Act.
The Respondent’s written submission on these conditions appears to stress the opinions of its medical expert witnesses, and states that their views should prevail. There does not appear to be a submission expressed in terms of the legislation.
There is little robust evidence before me on which to conclude that Ms Kenda suffers from some clearly definable elbow pathology. I consider the better view of the medical evidence is that there is only dated, and quite equivocal, radiological material. Moreover, any condition that may have been clearly diagnosable at some point appears at best to have been a mild problem.
Moreover, the evidence in general points only to a possible, broad correlation between Ms Kenda’s work duties and the experience of elbow pain as a symptom. There is no evidence before me suggesting a specific incident that was responsible for the suspected tear.
The evidence about Ms Kenda’s shoulder is also quite equivocal. My reading of the material and evidence suggests that the balance of opinion is that Ms Kenda may have some form of shoulder condition, but that the link to her employment is speculative. As with the elbow, there is an absence of any specific evidence demonstrating some form of traumatic injury.
I consider that the evidence demonstrates more than a temporaral connection between Ms Kenda’s employment following carpal tunnel decompression surgery and a flare up in symptoms. However, whether the symptoms experienced in the years following her return to work support a diagnosis of aggravation of CTS is less than clear. I consider the lengthy exploration at the hearing of an occupational link with CTS to raise significant doubts about whether this is a reasonable clinical diagnosis.
Regardless of this concern, more importantly, there does not appear to be any contemporary evidence of relevant pathology supporting a diagnosis of aggravated CTS at present. I note that Ms Kenda separated from her employment some time ago.
In summary, I am not satisfied that any of these claimed conditions meet the statutory definition of injuries in accordance with the Act. They are they not marked by the kind of identifiable change required to be an injury, particularly in the absence of adequate evidence of a precipitating incident. They also do not satisfy the statutory test of ailment in order to qualify as disease, as required under the Act. This is because, regardless of associated symptoms at different times, I consider there to be insufficient persuasive evidence categorically linking them to Ms Kenda’s employment beyond merely a material degree.
To the extent that there may be any relevant symptomatology in Ms Kenda’s right upper limb, I consider this further in respect of the other conditions in issue.
Cervical spondylosis with foraminal stenosis and headaches; aggravation of TMJ
There are indications in the material that Ms Kenda reported neck, shoulder and upper back symptoms during 2005. A radiology report of 31 August 2005 (ST1) of the cervical spine found no abnormalities.
In August 2007 Ms Kenda appears to have experienced cervical pain and headaches originating in the neck after gardening (6600 and 6622/T6.1).
Ms Kenda was referred to Dr Jonathan Tversky, oral medicine specialist, who reported in December 2008 on ‘assessment and management of her tooth clenching’ ((6600 and 6622/T46.3). He took a history of tooth grinding for two years, conciding with anxiety, panic and the use of Aropax (an antidepressant). Dr Tversky refers to the ‘multifactorial nature of bruxism’, which in recent times has been considered to be ‘a movement disorder with a central cause and aggravated by peripheral and exogenous factors’, which includes stress and tension. He expressed the suspicion that her psychotropic medication plays a role.
In September and October 2011, Ms Kenda appears to have complained of arm pain associated with either the C4/5 or C6/7 distribution (6600 and 6622/T6.1). Some degeneration appears to have been found in one site in radiology of 23 September 2011 (6600 and 6622/T4K), with no findings of nerve involvement.
A radiology report of 22 October 2012 (6600 and 6622/T4L) identified ‘mild multilevel chronic degenerative disease’, with mild right side foraminal stenosis at C5/6.
It appears that in December 2015, Mr McCombe suggested exploration of Ms Kenda’s cervical spine due to her ongoing hand symptoms (ST24). He summarised her situation at that time based on radiology as follows (ST26): some loss of disc height at C4/5 and C5/6 ‘without obvious foraminal stenosis’, with some lateral disc protrusion mainly related to the left side. He did not consider these changes ‘significant enough to warrant further intervention’.
I have noted above briefly the findings of Mr Smith in 2017, who did not consider Ms Kenda’s cervical spine to be contributing to her symptoms.
It is from this point in the record that there is greater focus on TMJ, headaches, and the cervical spine; and Ms Kenda lodged her notification of these as newly reported conditions in May 2017.
Ms Kenda was referred again to Dr Tversky, who reported on 12 June 2018 (5058/T7). Dr Tversky considers that Ms Kenda had a TMJ disorder, and also identified myalgia (pain) secondary to her neck and shoulder complaints.
Mr Gardiner diagnosed cervical spondylosis without neuroglogical compromise, and I consider his evidence to indicate that he was unable to understand this in the context of her upper limb symptoms. I do not consider Mr McCombe to have offered helpful insight into Ms Kenda’s cervical spine.
Dr Blombery accepted that he is not an expert in musculoskeletal conditions. I also do not consider him to have offered evidence that contributes to an understanding of Ms Kenda’s cervical spine.
I note the opinions of Dr Khurana and Mr Haig, that Ms Kenda’s cervical spine condition is constitutional and unrelated to employment. I note that Mr Smith was of a similar view about Ms Kenda’s cervical spine.
According to the evidence provided by the dental specialists, and Ms Kenda herself, she has a significant history of dental treatment, including for TMJ and bruxism, dating back to the mid 2000’s.

Dr Wiesenfeld considered bruxism could become ingrained following withdrawal of a stressor. He appeared not to have a comprehensive understanding of Ms Kenda’s history of stress, and when pressed on causation, identified multiple factors of which work practice may have been one.
Dr Gerschman, particularly in his written material, placed considerable emphasis on Ms Kenda’s chronic work injury and anxiety conditions. While he stated that most treaters had associated Ms Kenda’s TMJ with work, he also accepted the proposition that there was no consistent agreement in her case. Dr Gerschman also appears to have been quite ambivalent about the nature and origins of Ms Kenda’s reported headaches.
Dr Howe was of the view that reported migraines were unrelated to TMJ, but accepted Ms Kenda’s reports of headaches. He accepted that at the time of reporting he would have benefitted from a more detailed work history. Dr Howe experienced difficulty in his physical examination of Ms Kenda, and was unable to determine if her employment contributed to the aggravation of her TMJ.
Summary finding
The Applicant contends in written closing submissions that her cervical spine condition was aggravated by ‘constant, repetitive, fast paced upper limb activites with twisting, turning of the neck and upper spine’ (which activities are said to be supported by the evidence). It is also contended that the opinions of Dr Gardiner and Dr Blombery support this finding.
It is also contended that Ms Kenda’s severe headaches are caused by her TMJ, and that the evidence supports a finding that her TMJ is a result of work-related stress ‘across her employment with the AGS’. This is submitted to be in keeping with the evidence of Dr Gerschman, Dr Wisenfeld and also Dr Howe.
The Respondent contends that the preponderance of relevant expert evidence is that Ms Kenda’s cervical spondylosis with foraminal stenosis and severe headaches is not causally connected with her employment. The Respondent also contends, citing Mr Smith, that no right sided radiculopathy has been identified.
The Respondent’s submissions about aggravation of TMJ are more complex. It is contended that:
(a)Dr Tversky considers Ms Kenda’s TMJ as secondary to her neck and shoulder complaints, which are not injuries for the purposes of the Act;
(b)it is open to the Tribunal to find that there were weaknesses in Dr Wiesenfeld’s evidence, including a failure to consider the breadth of relevant causative factors, and his opinion as to causation should be dismissed as unsatisfactory;
(c)Dr Gershcman’s evidence is of no assistance to the Tribunal;
(d)Dr Howe considered Ms Kenda had suffered from TMJ since the mid-2000’s, that it has been attributed to anxiety by Dr Tversky, Ms Kenda did not appear to be using the correct splint, and she had a history of failing to have teeth restored, and had a poor prognosis overall; and
(e)Dr Howe’s evidence should be preferred over the evidence of other witnesses.
With respect to Ms Kenda’s cervical spine, I consider the opinions of Dr Khurana and Mr Haig to be relevant and persuasive, and to be supported by the findings of Mr Smith.
On the basis of these opinions, I am satisfied that Ms Kenda has an ailment in the form of mild degeneration of the cervical spine. On the basis of the evidence overall, however, I am not satisfied that this has any relevant association to her work duties, and certainly not to the standard of causation required.
Headache symptoms have been linked, through the nature of the claim made, to Ms Kenda’s cervical spine condition. However, overall, the evidence appears to suggest that medical consideration of headaches has fallen largely to the dental specialists.
There is virtually unanimous agreement among the medical opinions that bruxism and TMJ can be stress-related, and that they are multifactorial. The evidence about what Ms Kenda may have experienced in both personal and work spheres, and at what particular time in her lengthy history of dental concerns, is quite mixed. There is no disagreement in the opinions, nor on the evidence, that certain stressors or the pain and discomfort, associated with Ms Kenda’s physical conditions, including their treatment, might amount to a relevant stressor.
I am satisfied that Ms Kenda has experienced TMJ for some considerable time. It would appear that this was aggravated at an indeterminate point in time, most likely at a point before her referral to Dr Tversky. I am satisfied that this should be considered an ailment.
Nonetheless, on the basis of the weight of the medical evidence, I am not satisfied that the relevant causal connection to employment can be made out. That is because of a consideration of matters that arise under s 5B(2) of the Act, specifically: the condition of TMJ is multifactorial; Ms Kenda has a lengthy and complex history of dental treatment, including apparently failure to pursue treatment; there is a mixed factual history about life stressors; and, the evident role of Ms Kenda’s psychological condition and its treatment.
I note that I am aware from the materials, and indeed from the content of submissions, that Ms Kenda appears to have an accepted claim for anxiety. However, this was not a subject of direct evidence at the hearing, nor of any substantive submission as to the manner in which it may, or may not, impact upon considerations arising in respect of the matters addressed in these reasons.
Complex regional pain syndrome
The first clear reference in the materials to CRPS appears to be that of Dr Du Toit in February 2017, which I have noted above. He notes atypical features, in the context of a further recommendation that there may be no structural cause for her symptoms. His subsequent correspondence regarding the sympathetic nerve block contains a more equivocal reference to CRPS. I also note the February 2018 correspondence, in which Dr Du Toit states that Ms Kenda’s CRPS was a longstanding condition.
I have noted also the opinions of Dr Wyatt. Her fingings were not conclusive, but her principal opinoin was that Ms Kenda had a chronic pain condition. Indeed, I read Dr Wyatt’s second report as ruling out a diagnosis of CRPS, given her view that Ms Kenda’s physical signs were variable, and also of a lesser kind than would be expected in CRPS.
Dr Navani stated in evidence that he did indeed observe signs relvent to a diagnosis of CRPS during his examinations of Ms Kenda.
I note also that Ms Kenda saw Dr Scott Chambers, psychiatrist, in March 2017 (6600 and 6622/T25). His diagnosis focussed on aspects of anxiety and depression, described as being in the context of Ms Kenda’s history of chronic pain and physical limitations.
Ms Kenda formally notified her claim of CRPS in May 2017 (among other conditions).
Ms Kenda was assessed by Dr Philip Haynes, occupational physician, in August 2017 (6600 and 6622/T45), apparently with respect to her fitness for duty. It is not clear from his report what material he was briefed with, but it would appear that his physical examination included identifying signs related to CRPS. He notes slight swelling of the right hand, but ‘no marked discolouration’ or temperature change. Dr Haynes diagnoses a ‘regional pain syndrome affecting the right arm’.
Dr Gardiner gave evidence in respect of CRPS, but I consider it falls somewhat short of a robust diagnosis. He stated that confirmation of diagnosis of CRPS in his report was based on the finding of other reporters. He stated further that he did not observe signs necessary for a diagnosis.
Mr Haig was of the opinion that Ms Kenda has a chronic pain syndrome, and that her upper limb symptoms were bizarre, and not refererable to a clinical diagnosis.
As previously noted, Dr Kostos diagnosed a chronic regional pain syndrome, first in November 2017, and Dr Blombery has maintained contrary diagnoses. In summary:
(a)there is a distinct disagreement between them as to whether Ms Kenda exhibits, or has exhibited, signs requisite for a diagnosis under the Budapest criteria;
(b)Dr Kostos was of the opinoin that any signs of autonomic dysfunction should be evident each time a patient presents for examination;
(c)Dr Kostos did not consider Ms Kenda’s pain presentation to satisfy the diagnostic criteria of pain disproportionate to an inciting event;
(d)significantly, Dr Kostos was of the view that Ms Kenda should clearly exhibit symptoms in the hand;
(e)Dr Blombery considered that Dr Kostos had ignored signs of autonomic dysfunction;
(f)in Dr Blombery’s opinion, CRPS is characterised by pain sensitisation following injury, including commonly by carpal tunnel release surgery; and
(g)both specialists have differing views about Ms Kenda’s other conditions.
Summary finding
It is submitted on the Applicant’s behalf that CRPS has been properly diagnosed by Dr Navani and Dr Blombery. It is contended that this condition can be considered as being singificantly contributed to by Ms Kenda’s employment, which I take to be a submission that it should be understood as a disease.
I will only briefly summarise the contentions raised on behalf of the Applicant with respect to the key witnesses relating to CRPS:
(a)Dr Blombery possess relevant expertise given his experience in a field of specialised knowledge (vascular and pain medicine);
(b)Dr Blombery considered that signs may change from time to time, and their observation on a single examination was sufficient;
(c)Dr Kostos appears to have ignored information and observations about Ms Kenda’s reported signs and symptoms; and
(d)Dr Kostos took a restrictive and narrow interpretation of the Budapest criteria given the way he interpreted various signs and symptoms, and accordingly his evidence should be considered unreliable.
The Respondent contends that the diagnosis of CRPS rests largely on the opinion of Dr Blombery, who does not possess a relevant specialist expertise, and on Dr Du Toit. Its submissions appear largely to contrast the opinion of Dr Du Toit, who was pursuing treatment options for Ms Kenda, with that of Dr Wyatt.
With respect to Dr Blombery, the Respondent further contends that he is not qualified to dismiss the competing diagnosis of chronic pain syndrome, nor to render opinions about Ms Kenda’s other conditions. The submissions also question the adequacy of Dr Blombery’s observations on his single examination of Ms Kenda.
The Respondent also raised further contentions about the diagnostic criteria and status of CRPS more broadly, which relates primarily to the separate question of a WPI assessment.
The central contentious issue is that across the body of material overall there is a divergence of opinion as to the diagnosis of CRPS. The focus of this question is the consistency and range of observable signs arising from the diagnostic criteria (Exhibit A6) over time and across examiners.
No witness questioned the existence of CRPS as a condition. However, there is some disagreement, or at least lack of clarity, about the extremity of a limb as the primary site affected in cases of CRPS, and also the extent of the ‘region’ intended by that word in the condition’s title.
Taking all of the evidence into account, I consider that Dr Blombery is in the minority in his categorical diagnosis of CRPS. I do not, however, discount his evidence on the basis of expertise, as contended by the Respondent. This issue was not ventilated thoroughly at the hearing, and his medical opinion in any event has played a role throughout the various stages of Ms Kenda’s claims management.
I place limited weight on Dr Navani’s evidence due to the issues raised about the quality of his clinical notes, and his lack of specialist expertise. I place little or no weight on the final report of Dr Du Toit, as it stands in contrast to his two prior reports which were ambivalent at best.
Dr Blombery appears to place some stress on his findings with respect to Ms Kenda’s other upper limb conditions. I do not consider this to be helpful in the context of diagnostic criteria that require an exclusion of other plausible explanations for symptoms. I also accept the Respondent’s contention that Mr Blombery is not a musculoskeletal specialist. That is, despite the potential contradiction in diagnostic approach I have noted, he is not in a strong position to draw together a holistic impression of Ms Kenda’s other conditions.
I consider the most important feature of the evidence overall to be that, over a relatively extended period of time, the majority of examiners have not in fact made a clear diagnosis of CRPS.
The question arising is therefore what condition, if any, explains Ms Kenda’s presentation. Two neurologists have also not been able to identify a physiological explanation for Ms Kenda’s symptoms, and Dr Khurana identified a non-organic overlay. Mr McCombe leaned towards a mysofascial pain syndrome, but defered to pain specialists, as he had difficulty arriving at a unifying theory. I do not consider Mr Gardiner to have offered a cogent perspective.
It appears that Dr Kostos has relied upon Dr Shukla’s assessment in February 2018 that Ms Kenda’s mental state is contributing to the maintenance of her problem. Dr Shukla’s report itself, however, does not appear to contain a comprehensive assessment of physical and non-physical conditions, nor does it appear to contain a definitiave assessment of the contributors to her diagnosed psychological conditions.
Nonetheless, I consider the better view of the evidence overall is that Ms Kenda has a form of chronic pain condition, and that this condition is considered to be non-physical in origin.
I do not consider it reasonable, or necessary, to take this consideration any further, given that I have not been provided with submissions directed at Ms Kenda’s state of mental health nor any diagnosed conditions she may have. For this reason, I have sought to restrict references to materials addressing this question to those elucidating evidence by witnesses.
Treatment claims
Sympathetic nerve block and hyrdrodilation
Ms Kenda’s claim for a sympathetic nerve block has its origins in Dr Du Toit’s recommendation contained in his report of March 2017. He repeated this recommendation, together with a proposal for right shoulder hydrodilatation, in his report dated 31 October 2017 (6600 and 6622/T49.5).
I note that in the March 2017 report, Dr Du Toit observes that Ms Kenda has been examined for underlying structural abnormalities, and ties the nerve block procedure to his suspicion of CRPS. Dr Wyatt, as noted, expressed reservations about the likely impact of the procedure.
While there are references in reports from both Mr McCombe and Dr Du Toit to the thoracic region, I have been unable to identify any radiology concerning her thoracic spine. I have already noted the opinion of two neurologists as to the absence of identifiable spinal neropatholagy.
The Applicant submits that the procedure constitutes reasonable medical treatment for Ms Kenda’s right hand numbness, a consequence of her aggravation of CTS, and for CRPS. The submissions highlight the evidence of Dr Du Toit and Dr Navani.
With respect to hydrodilatation, the Applicant’s submissions contend that the procedure was supported by Dr Navani, Mr Gardiner, and Dr Blombery, and was recommended by Dr Du Toit.
The Respondent’s submissions highlight the opinion of Dr Wyatt. As the submissions also tie the procedure to Dr Du Toit’s recommendation, including the link apparently made to CRPS, I will not repeat the contentions raised in respect of that condition.
Given the state of the evidence, I am unable to conclude that Ms Kenda has a specific pathology that supports the need for a sympathetic nerve block at T2 and T3. Furthermore, given my findings above in respect of the primary conditions, there is no injury, in the terms of the Act, to which such a procedure might reasonably relate.
The findings above in respect of primary conditions, particulary with respect to Ms Kenda’s right shoulder, also mean that there is no injury to which the hydrodilatation procedure might reasonably relate.
Physiotherapy
The question as to final medical treatment, being physiotherapy, must be placed in the context of the timeline of decision-making. The decision to cease payment for Ms Kenda’s physiotherapy was made in August 2017, and affirmed in October 2017. Comcare’s decision that liability no longer pertained to the previously approved conditions for which physiotherapy had been provided was made later, in July 2018. I note that in his report, Dr Haig observes that Ms Kenda continued to privately fund physiotherapy after the decision.
Accordingly, despite my findings above in respect of the related primary conditions, it remains a possibility that any physiotherapy undertaken prior to this later decision may be considered medical treatment obtained in relation to an injury (s 16(1) of the Act).
Comcare’s decision to no longer accept liability for physiotherapy (6600 and 6622/T38) refers to the March 2017 report of Dr Wyatt. In addition to the observations cited above in respect of CRPS, in this report (6600 and 6622/T26) Dr Wyatt also states:
Ms Kenda is currently attending physiotherapy every three weeks and feels this is of some beneft, though the benefit is only termporary. In these circumstances, with the current troublesome limitations, this seems reasonable to continue, though it is not likely to result in any long term change in the condition.
In its decision of August 2017 (6600 and 6622/T38), Comcare refers to the principles in its Clinical Framework for Health Services, statintg that 50 treatment sessions had not demonstrated a therapeutic benefit. Accordingly, it determined that ‘it is reasonable to conclude that the provision of further physiotherapy treatment would not be in line with the Clinical Framework…’.
To summarise the medical evidence in relation to this treatment:
(a)Dr McCombe considered the treatment, when first proposed, appropriate for symptom relief;
(b)Dr Navani considered phsyiotherapy would ease Ms Kenda’s symptoms and Dr Blombery considered she may benefit from it;
(c)Dr Stephens stated that a form of treatment beyond ‘manual therapy’ would form part of a future treatment plan;
(d)Dr Haig did not see any indication for any form of treatement, including physiotherapy;
(e)Dr Kostos considered in his November 2017 report that no treatment would assist Ms Kenda; and
(f)Dr Kostos expanded upon this in his July 2018 report, stating that physiotherapy was not reasonable given the lack of efficacy demonstrated to date, and he added in evidence that phyiostherapy should have an impact within a short number of sessions.
The Applicant submits that the definition of medical treatment includes ‘therapeutic treatment obtained at the direction of a legally qualified medical practitioner’ and includes physiotherapy (s 4 of the Act). It is further contended that pain relief can properly be regarded as medical treatment (citing Comcare v Watson (1997) FCR 273).
I add to the Applicant’s submission about the definition of treatment by noting that therapeutic treatment, contained within the definition of medical treatment, is also defined in the Act as including treatment given for the purpose of alleviating an injury (s 4 of the Act).
The Respondent’s submissions consist of a summary of the medical evidence.
Mr McCombe referred Ms Kenda for physiotherapy in 2013 on the basis that he considered her condition to be soft-tissue related. This, combined with the technical aspect of Dr Kostos’ evidence regarding the anticipated time required for physiotherapy to show impact, supports a finding that as at the date of the decision in question, physiotherapy was not medically required. This opinion is also held by a number of other witnesses and I consider that, taken together, these opinions outweigh the countervailing view that symptom relief continued to be a sufficient justification for prolonged treatment.

I do not specifically rely here upon Dr Kostos’ view that a small number of treatments should demonstrate impact. However, I accept that in principle, ongoing treatment was not medically indicated. I note that Dr Kostos reached that view relatively close in time to the decision under review.
I also note the opinion of Dr Wyatt that it appeared that treatment was only providing temporary benefit. I consider that this further reinforces the finding that there was an absence of a defensible medical justification for the treatment and, notwithstanding the function of pain relief, the absence of a viable medical reason for the treatment is a prevailing consideration.
Permanent impairment
Ms Kenda’s claim for permanent impairment was submitted by way of two separate claim forms dated 7 July 2018 (4493/T7 and T8). The permanent injury or impairment is described as ‘right shoulder’ and ‘right upper limb’. The impairment resulting from the former is dscribed as ‘restricted right shoulder movement’ and from the latter, ‘quite significantly limited right upper limb function’ and ‘chronic neck pain – significant mental distress with poor mood ?extreme anxiety’.
Briefly, the Applicant has received two WPI ratings, from Mr Gardiner and Dr Blombery. Mr Gardiner assessed three sites, being right upper extremity, right shoulder and cervical spine, arriving at a combined 29% WPI. He stated in evidence that this was under Table 9.14 (of the Comcare Guide to the Assessment of the Degree of Permanent Impairment (Ed. 2.1) (‘the Guide’)), which he considered the ‘best fit’. Mr Gardiner considered loss of movement in the upper limb due to CRPS.
Dr Blombery arrived at a WPI of 15%, which he ascribed to Ms Kenda’s CTS and to her right shoulder. In his evidence, he was of the opinion that there is usually some permanent impairment following carpal tunnel release surgery. He also took into account diminished sensation to light touch.
Mr Haig was of the opinion that Ms Kenda experienced no permanent impairment as a result of her orthopaedic conditions, but allocated four points for chronic pain.
The Applicant contends that Mr Gardiner’s assessment with respect to the cervical spine should be disregarded as it is below the threshold 10%. The Applicant submitted that the Tribunal should find, according to Mr Gardiner’s allocations, 10% impairment for the upper extremity under Table 9.14, and 14% under Table 9.11 of the Guide in respect of her right shoulder.
The Respondent raises a substantive challenge to the assessment of Ms Kenda’s permanent impairment. It contends that both the assessments of Mr Gardiner and Dr Blombery are not in accordance with the proper use of the Guide. The Applicant, in her Reply, endorses the Respondent’s interpretation.
Accordingly, I accept the Respondent’s summary contention that there is no assessment that meets the threshold 10%. I note that, on the basis of my findings above with respect to the primary conditions, and in particular Ms Kenda’s shoulder symptoms, there is no injury in the terms of the Act to which the claim for permanent impairment might reasonably relate.
DECISION
For the reasons given above the Tribunal affirms the decision made in each of the decisions under review.

I certify that the preceding 270 (two hundred and seventy) paragraphs are a true copy of the reasons for the decisions herein of Dr Stewart Fenwick

...........................[sdg]..........................................
Associate
Date: 2 June 2022

Dates of hearing:
12, 13, 14 and 15 August 2019
10, 11 and 12 August 2020

Counsel for the Applicant:
Cassie Serpell

Counsel for the Respondent: John Wallace

Dates of hearing:	12, 13, 14 and 15 August 2019 10, 11 and 12 August 2020
Counsel for the Applicant:	Cassie Serpell
Counsel for the Respondent:	John Wallace