SUMMARY

DECISION NO. 230/97I2

Psoriatic arthritis. The worker suffered a low back injury in February 1981, for which he was granted a 25% pension. The worker attempted to work as a cook in January and February 1982 but stopped working due to pain. The worker appealed denial of entitlement for psoriatic arthritis and various benefits in 1982. The Panel accepted the opinion of a Tribunal medical assessor that the worker was suffering from seronegative spondyloarthropathy and that psoriatic arthritis was one of the conditions associated with that underlying diagnosis. The 1981 accident accelerated and permanently advanced the course of the condition. The worker was entitled to benefits for the condition. The appeal was allowed. The Panel remained seized to deal with any areas of dispute that may arise regarding VR services. [14 pages]

DECIDED BY: Newman; Anderson; Robb DATE: 26/05/98 ACT: WCA CROSS-REFERENCE: Decision No. 230/97I

WORKPLACE SAFETY AND INSURANCE APPEALS TRIBUNAL DECISION NO. 230/97I2 [1]

This appeal was conducted in Toronto on March 6, 1997, by a Tribunal Panel consisting of: E. Newman : Vice-Chair, C.J. Robb : Member representative of employers, J. Anderson: Member representative of workers. The interim decision Decision No. 230/97I was released on April 7, 1997, in which an assessment from Dr. Duncan A. Gordon, Professor of Medicine, University of Toronto was requested. Dr. Gordon’s report, dated December 20, 1997, was received by this Panel, as was the worker’s final and detailed submission, dated February 28, 1998. THE APPEAL PROCEEDINGS The worker brings this appeal from two decisions:

[2]

[3]

1.

the decision of Hearings Officer St. Pierre, dated April 6, 1995, and

2.

the decision of Appeals Officer Coscarella, dated November 20, 1996. The worker attended, unrepresented. The employer did not attend and was not represented.

THE EVIDENCE [4]

The Panel heard submissions from the worker and considered the following documents: Exhibit A:

Case Description two Volumes;

Exhibit #1:

Addendum #1;

Exhibit #2:

Addendum #2;

Exhibit #3:

a package of materials under cover of letter dated February 13, 1997;

Exhibit #4:

a package of documents under cover of letter dated February 16, 1997;

Exhibit #5:

post-hearing Addendum #1;

Exhibit #6:

the worker’s submission.

THE NATURE OF THE CASE [5]

The worker seeks entitlement to workers’ compensation benefits for a condition diagnosed as psoriatic arthritis, for supplementary benefits, for vocational rehabilitation services, for full temporary

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total disability benefits between April 22, 1982, and June 12, 1982, as well as travelling expenses between September 23, 1992, and April 7, 1993. [6]

A description of the factual history involved in this appeal will fail to do justice to the complexity and difficulties which the worker has faced since his compensable injury of February 4, 1981. However, suffice it for the purposes of this decision to explain that on February 4, 1981, the worker suffered from a compensable accident, and injured his low back. The worker is in receipt of a 25% permanent impairment award for the low back disability.

[7]

Immediately after the accident, the worker received temporary total disability benefits at 100%. In January 1982, he made an effort to return to the workforce, accepting a job as a cook in January 1982. The worker describes this job as extremely strenuous, in which he worked long hard hours under difficult and cold conditions, a difficult and ambitious experience for an individual with so severe a back disability. The worker was employed at this job for 52 days, and then, overcome with pain from the back disability, stopped working.

[8]

The Workers’ Compensation Board reinstated temporary benefits as of February 26, 1982. However, the worker suffered a car accident on April 21, 1982, and from then until June 3, 1982, temporary total disability benefits were reduced to 50%, on the understanding that the worker was totally disabled as a result of a non-compensable neck injury suffered in that car accident. The worker has maintained throughout that he was hospitalized for a very brief period of approximately one week for injuries sustained in that car accident.

[9]

Entitlement to vocational rehabilitation services was denied on the basis that the worker was felt not to be making himself available to participate in a vocational rehabilitation program. Supplementary benefits were reduced for the same reason.

[10]

Symptoms of psoriatic arthritis became apparent, according to the worker, during the time when he was employed as a cook in January and February 1982. This condition was not diagnosed immediately, and in fact, the condition was erroneously diagnosed as Reiter’s syndrome. On the understanding that was a non-compensable condition, and not in any way related to the worker’s compensable injuries, entitlement to the worker continued only on the basis that the organic disability to the low back was compensable, and attracted a permanent impairment rating of 25%.

[11]

In its interim decision, the Panel stated the following: First, at hearing, the Panel raised with the worker its concern about the possibility that the car accident of April 21, 1982, may have been a compensable car accident. We shared our concern with the worker, explaining that if the car accident was one which the worker suffered in the course of attending therapy for a compensable condition, it may be an event which attracts compensation. The Panel involved Tribunal counsel, instructed her to assist the worker to determine whether documentation exists which would evidence the worker’s attendance either at physiotherapy, or at a physician’s appointment on April 21, 1982. Decision-making in respect of this aspect of the case must be deferred until that evidence, if any, is made available to the Panel. Second, and of greater significance, is the question of how the Panel might resolve the very difficult and complex issue of whether the worker’s psoriatic arthritis is a condition which was caused by, or

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contributed to in a significant way, by either his compensable accident or the arduous work he performed as a cook for 52 days… In respect of this issue, the worker drew the Panel’s attention to the opinion of a very well respected physician in this area of medicine, Dr. Daphna Gladman. Dr. Gladman is the Deputy Director of the Toronto Hospital Centre for Prognosis Studies in Rheumatic Disease. She saw this worker on November 3, 1994, at the request of Dr. Bell, who had been the rheumatologist in charge of the worker’s case previously. By report dated October 9, 1996, Dr. Gladman wrote to the worker’s then lawyer, Mr. Mark Bailey of the Injured Workers Consultants. Dr. Gladman said that when she saw the worker, there was “no question in [her] mind that the diagnosis was that of psoriatic arthritis.” Dr. Gladman confirmed that the original diagnosis of Reiter’s syndrome was erroneous. Dr. Gladman went on in her report to say: You asked me to comment on whether trauma injury or emotional stress can act as triggers in the onset of psoriasis. That certainly has been reported. There is a chapter in a book on psoriatic arthritis which was published in 1985 where the author, Dr. Frank Vesey, who is current a rheumatologist in Tampa, Florida actually discusses the role of environmental factors including trauma in the development of both psoriasis and psoriatic arthritis. ... We have published a paper on a patient who presented with both psoriasis and psoriatic arthritis following a fall on an outstretched hand. Thus, it is likely that at least in some people, trauma does play a role in both the development and the exacerbation of a condition. With regards to emotional stress, this may be another mechanism. Since we know that stress both emotional and physical alters the immune response such that it is impaired. Immune abnormalities do occur in patients with psoriatic arthritis and the impairment that is precipitated by stress is the same kind of impairment that we see in the patients with the disease. Therefore anything that would impair the immune response may certainly trigger and aggravate the condition. With specific reference to this worker, Dr. Gladman continues to provide a very detailed opinion supporting a causal connection between this worker’s compensable injury and the development of his psoriatic arthritis. She said: My assessment of the situation is that the back pain is due to the injury, that the psoriasis and psoriatic arthritis may in fact have been precipitated by the injury and therefore contribute to his disability. It is based primarily on Dr. Gladman’s opinion that the worker seeks entitlement to compensation for his psorioatic arthritis. The question of the compensability of psoriatic arthritis after trauma is not an easy question. It is one which has only been presented to the Appeals Tribunal on three prior occasions. In Appeals Tribunal Decision No. 199/90, the Panel concluded that there was no medical evidence linking the worker’s compensable accident with the subsequent diagnosed condition of psoriatic arthritis. In Decision No. 540/94, the Panel felt that there was too much uncertainty regarding the dates of the accidents, and too long a latency period between the dates of the accidents and the development of psoriatic arthritis for it to conclude that there was probably a connection. Most recently, in Decision No. 128/96, a panel of the Appeals Tribunal rejected a claim for entitlement to benefits for psoriatic arthritis following trauma. That was a case in which the Panel sought the input of an assessor, Dr. Duncan A. Gordon. Dr. Gordon provided a report to the Appeals Tribunal which confirms the theoretical view of Dr. Gladman, to the effect that trauma may indeed trigger or exacerbate a previously asymptomatic condition of psoriatic arthritis. However, on the facts reflected in Decision No. 128/96, Dr. Gordon reported that based on his observations, he did not feel that the accident did, in fact, have any impact upon the development of

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the worker’s condition. Indeed, Dr. Gordon provided the opinion that with or without the accident, it was likely the worker in question would have been significantly disabled as a result of the condition by age 40. In the instant case, the Panel has the benefit of Dr. Gladman’s opinion that this worker’s compensable accident likely did play a role in the exacerbation or development or aggravation of the psoriatic arthritis. However, because the issue is a difficult and complex one, the Panel feels that it would benefit significantly from the additional input of Dr. Gordon in the instant matter. Tribunal counsel is hereby instructed to arrange for Dr. Duncan Gordon to assess this injured worker. The Panel seeks confirmation of the diagnosis of psoriatic arthritis, and respectfully requests that Dr. Gordon conduct whatever tests he considers necessary to determine the accuracy of that diagnosis. Having had an opportunity to examine the worker and explore the history with him, Dr. Gordon is asked to express an opinion on the likelihood, in this case, that the compensable accident of February 4, 1981, or the arduous work which the worker performed as a cook for 52 days in 1982, played a contributing role in the development of that condition. Dr. Gordon is asked to explain his findings, and reasons for his conclusions. In the event that Dr. Gordon’s findings conflict with the opinion of Dr. Gladman, he is respectfully requested to explain on what basis his opinion differs from hers. Once Dr. Gordon’s opinion is made available to the worker, he will be invited to make additional submissions to this Panel in writing. Once we have received those submissions, the Panel will continue the process of determining the result of this appeal. [12]

The report of Dr. Gordon is critical to the Panel’s findings, and for that reason it is here included in its entirety: I saw this 49 year old man for medical evaluation December 3, 1997 with respect to the worker’s claim “that this psoriatic arthritis was triggered, caused by, or permanently aggravated by his compensable accident of February 4, 1991”. I also note the interim decision based on the Hearing Panel meeting of April 7, 1997 relating to their concerns about the medical issues of this appeal. History of present illness Based on my interview of [the worker], and review of his files, the following information was obtained. He was well and active, engaging in a variety of sporting activities until the period 1967-69 while working in England, walking on hard floors he developed a problem with painful feet. In the period 1970-72, a history of urethritis, balanitis and musculoskeletal symptoms referrable to his feet, wrists, fingers and low back led to his admission to Sunnybrook Hospital in June of 1973 because of the arthritis. At the time he had evidence of ocular inflammation as well as dactylitis, and skin lesions over his feet in keeping with a keratodermia. [The worker] was unable to recall the details of this admission for me except he admits to having a foot rash, painful enough that in July of 1993 Dr. Ted English did metatarsal surgical resections to control foot pain. After that until the spring of 1982, working mostly as a gas pipeline inspector, he was well except for periodic pain of his feet and an occasional penile rash. On February 4, 1981 he injured his back after falling out of a van onto roadside cement while lifting a 50 lbs. bag. X-rays taken at North York Hospital apparently showed “a fractured disc”. He had treatment at Downsview Rehab Centre for a 2 week period that he says aggravated his back, and Dr. Paisley recommended time off work. Attempts to return to modified duties were unsuccessful because of continuing low back pain until January of 1982 when he returned to work as a cook at a drilling camp in the bush near Heart. This involved outdoor living in tents with continuing exposure to cold, with 12 hour work days from 5:30 a.m. He continued 52 days at this “arduous job” and was forced to give it up because of low back pain as well as symptoms referrable to his neck and

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shoulders. [The worker] informed me that about a month after starting this work he developed a rash affecting his hands, elbows and knees along with general aches and pains that led him in March of 1982 to his family physician at the time, Dr. Coutts, in Parry Sound. Subsequently, on April 21, 1982 he was involved in a motor vehicle accident at which time he was the driver of a car that skidded into a guard-rail backwards. He sustained neck and head injuries, and was hospitalized for about a week. On May 13, 1992 he was seen again at Sunnybrook by Dr. Fam, at which time he says he had a rash affecting his fingers, elbows, knees and buttocks. At that time he was complaining of severe neck pain with lumbar stiffness and sacroiliac tenderness, and a macular rash over his trunk with other skin lesions affecting his fingers. His HLA B-27 test was subsequently found to be positive. This positivity was in keeping with the diagnosis at that time of chronic Reiter’s syndrome, or reactive arthritis with synovitis of the right shoulder, right 5th MTP and left foot with recent soft tissue neck injury and mechanical low back pain related to his back injury of February 4, 1981. In retrospect then, we have evidence of a limited rash going back to the 1970’s with the onset of more extensive rash coming on at least by May of 1982, if not earlier. As I understand it, [the worker] had been receiving 50% benefits after the accident of February 4, 1981 that were later reduced to 25% because he believes that Dr. Fam reported his back pain was more related to his chronic Reiter’s syndrome that the accident. A misunderstanding between [the worker] and Dr. Fam seems to be complicated by [the worker’s] inability to accept the idea that he ever had reactive arthritis/Reiter’s syndrome, and further, [the worker] does not seem to understand the wellknown relationship of reactive arthritis to psoriatic arthritis, and the relationship of both these conditions to his hereditary susceptibility to these conditions because of his genetic HLA-B27 positivity. In March of 1983 Dr. Murray Mitchell in North Bay made efforts on behalf of [the worker] for him to obtain more treatment and vocational rehabilitation, but apparently his eligibility for these recommendations was not accepted by WCB. [The worker] was reassessed at Sunnybrook in February of 1984 because of incapacitating low back pain as well as more extensive rash diagnosed as psoriasis by dermatologist Dr. C. Leneck. During this period he received topical therapy for his psoriasis and took Indomethacin for relief of his back pain. From 1987 through to 1992 he was regularly seen by Dr. Leneck for treatment of his psoriasis, and by Dr. Fam for treatment of his polyarthritis. During this period he was considered to have low back pain with features in keeping with mechanical as well as inflammatory disease. His x-rays then showed typical changes in keeping with spondyloarthropathy with fusion of his sacroiliac joints and asymmetric syndesmophytes affecting the thoracic and lumbar spines, typical of the spondylitis of either Reiter’s syndrome or psoriatic arthritis. There was also disc narrowing and facet osteoarthritis in keeping with mechanical back pain. X-rays in 1991 showed features of spondylodiscitis of the cervical spine and because of his ongoing active psoriatic arthritis he was given the antimalarial Chloroquine by Dr. Hugh Little that he took for 8 months. He says it was stopped because it was ineffective. Early in 1993 his care was switched to Dr. Mary Bell at Sunnybrook and in January of 1993 he was started on oral pulse Methotrexate with good improvement over a 6 month period. On November 3, 1994 he was seen by Dr. Dafna Gladman at the Wellesley Hospital, and on two subsequent occasions at the Toronto Western Division of The Toronto Hospital. He was last seen by her September 12, 1995 when he reported overall improvement of his peripheral arthritis and skin except for chronic low back pain that Dr. Gladman attributed to a mechanical problem rather than his well documented inflammatory spondyloarthropathy. Back and neck movements were limited. Active psoriasis of the extremities was noted. His medications since then have been oral pulse Methotrexate 25 mgs. weekly, folic acid 5 mgs. the day he takes the Methotrexate, Cytotec 200 mcs. b.i.d., Talwin 50 mgs. b.i.d., extra-strength

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Tylenol, and Amitriptyline 10 mgs. at night. Indocid SR he took until a year ago, and his topical skin treatments include Betamethasone. He says he is free to go back to either Dr. Bell or Dr. Gladman, but at present has no desire to see them again, even though he has had no follow-up blood test monitoring for Methotrexate for the past 6 months. History of past health and functional enquiry At present he says his weight had been steady. He described eye symptoms after taking the Chloroquine for 8 months, and possible aggravation of his skin. He was unable to recall any details suggesting ocular inflammation. He smokes 1 pack of cigarettes per day and has exertional dyspnea. No history of high blood pressure. He stopped drinking alcohol when he started taking Methotrexate. He was unable to recall any history suggesting either urethritis or balanitis, and was unable to recall any family history of psoriasis although it is recorded his grandfather had it. He did have ultraviolet treatments of his skin at Sunnybrook. He has nocturia once or twice, infering with sleep. No family history of arthritis except his mother has arthritic symptoms. Current complaints The patient describes a non-restorative sleep pattern with morning stiffness affecting this shoulders and back, controlled with Talwin 50 mgs. q.i.d.; neck stiffness with limited rotation; no temporormandibular involvement; both shoulders painful and restricted, worse with internal rotations more than abduction. This pain and limitation has been longstanding. Elbow ranges good; wrists clear; he is able to make a fist; right 3rd DPI and left 3rd and 4th DIP joints are swollen with some MCP and PIP stiffness, but no Raynaud’s phenomenon; some dorsal interscapular aching that is constant, but no rib cage symptoms; lumbosacral pain worse with repetitive bending. He is unable to extend his back without pain. In the past 2 years he has lost his ability to extend the spine and lateral mobility. No radiation of this lumbosacral pain into his legs is evident, but some periodic tingling in his thighs, more in the right; hips and knees clear; ankles and feet not a problem with old foot surgery. He back pain is worse after immobilization, sitting for ½hour; standing and walking are better; he is able to walk about an hour. Before he took Methotrexate he had pain referrable to his costochondral regions, wrists, fingers, knees and ankles, and now says his musculoskeletal symptoms are 80% better. Also, before he took Methotrexate he had active skin involvement of his nails, elbows, trunk, knees, and now he says his skin lesions are 90% better, affecting only the calves of his legs. With respect to this functional abilities he says he is unable to do any shopping or laundry, or meal clean-up although he sometimes prepare meals. He is able to walk several blocks and visit friends. He is able to do some yard work and drive an automobile. In the previous week he had never felt good. He rates his back pain as 7 or 1/10 in severity; fatigue the same rating; his stiffness in the morning he rates as 8 or 9/10; he describes his nervousness or tenseness as 8 or 9/10, and psychological depression he rates as 4 or 5/10. Physical examination On examination he was a healthy-looking, moderately obese man with forward protrusion of his head and neck, and limited chest expansion from 107-109 cms., but good air entry and no clubbing. B.P. 140/100. No cardiac murmurs; good peripheral pulses. Abdomen was obese, soft and nontender. Skin showed small patches of dermatitis over his elbows and knees, both shins. No nail trophic changes were seen. On musculoskeletal examination his wall-to-occiput cervical flexion deformity measure was 20 cms; lateral flexion 10°; rotation 20° bilaterally. With hands behind his head he could only reach his occiput, and with hands behind his back he could only reach the lumbodorsal region. Elbow and wrist range showed no limitation or tenderness; some MCP and finger DIP selling was evident as described under Current Symptoms. Grip strength bilaterally exceeded 300/20.

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On lumbar examination, lumbar lordosis of 10° with forward flexion 60°; he could only reach his knees. There was no extension, and with forward flexion his lumbar spine moved “en bloc”. Hip range was good. There was no sacroiliac tenderness on testing. Hip range was good without limitation of straight leg raising. Knees with some crepitus, but no effusions. Ankles were clear, but metatarsal heads showed previous resection incisional scars with hallux valgus deformity. No signs of joint hypermobility or fibrositic tender points were detected. Radiologic reports X-rays taken November 3, 1994 at Wellesley Hospital were reviewed with my rheumatologic and radiology colleagues. Cervical spine x-rays showed ossification of the anterior longitudinal ligament at C2-3 with anterior fusion at the C4 level with apophyseal sclerosis in keeping with a diagnosis of ankylosing spondylitis. X-rays of the lumbar spine showed bulky paravertebral ossification with non-marginal syndesmophytes in keeping with a diagnosis of Reiter’s syndrome or psoriatic spondyloarthropathy. The sacroiliac joints were fused in keeping with a diagnosis of ankylosing spondylitis and/or B27 spondyloarthropathy. There was anterior ostephyte formation at L4/5 and L5-S1 with grade 1 spondylolisthesis of L5 on the sacrum with lumbar facet sclerosis. X-rays of hands and feet showed evidence of minor erosions involving the 3rd MCP heads, and x-rays of his feet showed erosions of 1st MTP joint with resection of all the proximal phalanges. In summary, radiographs show features in keeping with mechanical degenerative changes at the L5S1 level, and evidence of longstanding inflammatory changes in keeping with seronegative HLA-B27 spondyloarthropathy. Panel questions Based on the foregoing information and literature review, my responses to the questions posed by the panel’s concerns are as follows: 1) What is this worker’s diagnosis? Seronegative spondyloarthropathy. The basis for this diagnosis is outlined in Chapter 11 of the 1997 11th Edition of the Primer on Rheumatic Diseases. Recognized entities within this diagnostic category include ankylosing spondylitis, reactive arthritis/Reiter’s syndrome, the spondylitis, and peripheral arthritis associated with psoriasis or inflammatory bowel disease, and juvenile onset spondyloarthropathy. As in [the worker’s] case, all of these conditions show a striking association with the inherited histocompatibility gene HLA-B27. In [the worker’s] case he shows clinical features in keeping with a diagnosis of reactive arthritis/Reiter’s syndrome, psoriatic arthritis, some features of ankylosing spondylitis, but no suggestion of inflammatory bowel disease or juvenile spondyloarthropathy. The enclosed table outlines the characteristics of patients who fit into the category of seronegative spondyloarthropathy. In [the worker’s] case he has shown either at present or in the past, features in keeping with ankylosing spondylitis, reactive arthritis/Reiter’s syndrome, and psoriatic arthropathy. At present the most dominant features he exhibits are those of the spondyloarthropathy associated with psoriasis. 2) Please provide a brief description of the nature and normal course of this worker’s diagnosis. The clinical description of psoriatic arthritis is outlined in Chapter 10 of the Primer on the Rheumatic Diseases. Patients with psoriasis may be classified into 3 groups 1) asymmetric polyarthritis 2) polyarthritis resembling rheumatoid arthritis, and 3) predominently spinal involvement with or without peripheral joint disease. Psoriasis is a common skin condition affecting about 1% of the general population, and within that population, psoriatic arthritis is at least 5-10 times more common than arthritis in the general population. About 50% of cases fall into the first category of asymmetric polyarthritis. 25% of cases resemble mild rheumatoid arthritis, and the third category, as in [the worker’s] case, affects less than 10% of cases. The skin involvement of psoriasis usually precedes the onset of arthritis, but in [the worker’s] case this relationship in not clear-cut. He had spinal symptoms after the

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accident, coming on before his psoriasis that could have been related to his seronegative spondyloarthropathy. Certainly he had spinal and peripheral arthritis features at the time his psoriasis became well recognized. Most patients, as in [the worker’s] case, show a peripheral arthritis resembling mild rheumatoid arthritis. In a small percentage of cases, unlike [the worker], a more progressive, destructive peripheral arthritis occurs. This is usually seen in patients with widespread, extensive skin involvement. Patients with advanced spinal deformity, as in [the worker’s] case, show worse functional outcome, sometimes without much pain. In [the worker’s] case his low back pain, however, is probably more related to his previous work injury and mechanical factors than his psoriatic seronegative spondyloarthropathy. 3) Are there any know causes for this condition? The causes of the seronegative spondylarthropathies that include psoriasis, psoriatic arthritic and reactive arthritis/Reiter’s syndrome are unknown, but genetic, environmental and immunologic factors appear important. Moreover, any concept of causation must explain the striking association that these disorders share with the inherited, generic histocompatibility antigen, HLA-B27, the same hereditary make-up that [the worker] possesses. Review of these factors may be helpful in better understanding the cause of [the worker’s] seronegative spondyloarthropathy. With respect to psoriatic spondylitis and reactive arthritis/Reiter’s syndrome, the majority of affected individuals have inherited the human leukocyte antigen HLA-B27. Table 11B-1 outlines the clinical features seen in patients with this syndrome, some of which were described in [the worker’s] case before his motor vehicle accident. It is noteworthy that reactive arthritis/Reiter’s syndrome is now recognized to occur frequently in the absence of urethritis or conjunctivitis, and classified as a seronegative spondyloarthropathy. The development of psoriatic arthritis itself appears to be related to a complex interaction of hereditary and environmental influence. For example, the brother or sister of an identical twin with psoriasis has about a 60% chance of eventually developing psoriasis. Similar genetic influences also appear to determine the onset of psioratic arthritis. Environmental factors have also been implicated in triggering psoriatic arthritis, most importantly, infectious agents and physical trauma. Trauma has been implicated in the causation of seronegative spondyloarthropathy including ankylosing spondylitis, reactive arthritis/Reiter’s syndrome, and psoriatic arthritis in anecdotal reports by several authors (see enclosures). In more than a dozen cases, an inciting general or local traumatic event caused peripheral inflammatory arthritis in keeping with the concept that trauma causes release of self-antigens from the injured joints. In other cases of reactive arthritis/Reiter’s syndrome and psoriatic arthritis “trauma appears to induce either an exacerbation of existing disease or new disease in pre-existing normal joints”. In support of these anecdotal reports, Scarpa in 1992 reported a case control study comparing patients with psoriatic arthritis to patients with rheumatoid arthritis, and found 12 of 138 patients with psoriatic arthritis had an acute disorder immediately preceding the onset of their peripheral arthritis, whereas only 2 of 138 patients with rheumatoid arthritis showed a similar preceding event. The traumatic events in these 12 patients with psoriatic arthritis included a surgical operation in 4, articular trauma in 3, abortion in 2, myocardial infarction, thrombophlebitis and phosphoric ester poisoning in one each. Peripheral joint involvement occurred in all twelve, two of whom, like [the worker], also had spondylitis and were HLA B-27 positive. Finally, patients who undergo physical trauma also experience emotional stress that may lead to disturbances in immune function that could induce or aggravate arthritis in susceptible individuals. Thus, it appears that in person such as [the worker] who possess HLA-B27 and heredity for psoriasis, trauma could play a role in either the development, aggravation or advancement of seronegative spondyloarthropathy of the psoriatic type. 4) Based on your medical knowledge, are there any risk factors known to the associated with the development of this condition?

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The risk factors know to be associated with the development of seronegative spondyloarthropathy are those cited in my answer to Question 3. These factors refer to hereditary susceptibility in individuals who possess the HLA-B27 gene. Psoriatic spondyloarthropathy predominantly affects males. The usual onset of seronegative spondyloarthropathy is well before the age of 40, but the age of onset of psoriatic arthritis spans a wider range, up to 55 years of age. A variety of environmental factors have been incriminated, and these may include in the case of reactive arthritis/Reiter’s syndrome, venereal or gastrointestinal infection as well as physical or emotional trauma. In [the worker’s] case the spinal and peripheral arthritic symptoms of his seronegative spondylarthropathy associated with psoriasis only appeared after his compensable accident of February 4, 1981 so that any infectious factors related to his reactive arthritis/Reiter’s syndrome would not be applicable. It should also be noted that his reactive arthritis is considered an inflammatory response to an infection remote from the site of inflammation in the joints, although trauma has been implicated in some cases. Despite the evidence for bacterial triggering of the reactive arthritis/Reiter’s syndrome trials of longterm antibiotic therapy for these patients have shown no benefit. 5) Are there any factors which are known or suspected to affect the course of this condition’s process? If so, please explain any such effects. The course of seronegative spondyloarthropathy may be favorably affected by treatment calculated to control the inflammatory aspect of the condition, and physical therapy measures to maintain good mechanical and postural function of the spine and peripheral joints. In the case of spinal inflammation, as in ankylosing spondylitis, a patient with this condition is known to deteriorate with increased pain and stiffness when put to rest. For example, following a work injury or traffic accident associated with enforced bed rest, the onset of spondylitis may become apparent with increasing pain and stiffness. While the trauma itself did not cause the disease, the patient may then develop progressive symptoms related to this underlying condition when active physiotherapy could have prevented this worsening. Moreover, there is some suggestion that injury does not cause spondyloarthropathy, but rather brings it to the patient’s attention, probably through hospital immobilizaiton. 6) Is there a usual period of latency involved in this condition? If so, what would be the normal range of time after injury in which the signs and symptoms of this disease would be expected to develop? The concept of latency would apply to a situation where underlying sero-negative spondyloarthropathy was completely asymptomatic at the time of the physical or emotional trauma. The trauma might then unmask or aggravate this underlying pathologic process, drawing it to the attention of all concerned. On balance, it seems unlikely that trauma in itself could trigger or induce the seronegative spondyloarthropathy, but it might promote the induction of one aspect of that spondyloarthropathy such as psoriasis or psoriatic arthritis. I am not aware of any epidemiological studies or evidence examining the relationship of physical trauma to the onset or course of seronegative spondyloarthropathy or psoriatic arthritis. But, if this were the case I would expect the onset of symptoms after trauma to come on within a matter of weeks or months after it. This notion would apply whether the trauma was associated with the triggering, induction, aggravation, acceleration, or advancement of the seronegative spondyloarthropathy of psoriatic arthritis. In [the worker’s] case, the time lines for causation of psoriasis are more closely related to his 1982 job than his injury of February 4, 1981. 7) Does the latency period differ according to the severity of the injury? I am not aware of any date that addresses the foregoing issues directly. I am, however, aware of the importance of trauma factors associated with more severe injury in whiplash hyperextension/flexion injuries of the neck that commonly occur with rear-end motor vehicle accidents. In these cases, more severe injury is associated with high speed impact, the amount of damage to the vehicle,

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rapidity of onset of neck pain and restriction of movement along with neurologic features, all worse in individuals with underlying pre-existing degenerative disease of the neck. In [the worker’s] case, however, I do not believe that any of these factors can be seriously implicated. 8) There is reference in the file to this worker having a pre-existing condition prior to his accident of February 4, 1981 (C.D. Page 324; C.D. Page 333) refer to a pre-existing condition since 1972. What effect, if any, would this pre-existing condition have on his current condition? Please explain your answer. In C.D. Page 324 memo dated December 9, 1983, Dr. Boyes comments on [the worker’s] pre-existing condition of Reiter’s disease with “spondylitis and/or sacroiliitis which may have a significant effect on the ability of this patient’s back to recover”. Dr. Boyes goes on to comment “the main question is how much of the present back disability is a direct result of the Reiter’s disease”. I believe that this man’s Reiter’s disease is part and parcel of his seronegative spondyloarthropathy that either pre-existed and was aggravated by the motor vehicle accident of February 4, 1981 or was triggered by it. I favor the view that the motor vehicle accident of February 4, 1981 aggravated, accelerated and advanced his pre-existing seronegative spondyloarthropathy of which the reactive arthritis/Reiter’s syndrome was one aspect. With respect to C.D. Page 333, examination at Head Office by Dr. D. Logan June 19, 1984 noted pre-existing degenerative changes of this man’s lower lumbar spine at the time of the accident with neck pain aggravation related to a motor vehicle accident in April of 1982. Recent x-rays in 1984 showed evidence of inflammatory sacroiliitis. Statement is made that “he has also developed psoriasis to which presumably there is no entitlement”. Examination showed tenderness of the right sacroiliac joint with limited painful lumbar flexion. Dr. Logan estimated the organic disability of his low back at 25%, and noted “there is a moderate pre-existing condition”. Again we have based on x-ray evidence, pre-existing lumbar degenerative disease noted at the time of the accident, but the detection of the spinal and sacroiliac inflammatory condition was documented only after the compensable motor vehicle accident of February 4, 1981. Nonetheless, we know that he has the hereditary predisposition to seronegative spondyloarthropathy with pre-existing features of Reiter’s syndrome compatible with that diagnosis. 9) In your medical opinion, did the worker’s compensable accident of February 4, 1981, or the arduous work which the worker performed as a cook for 52 days in 1982, play a contributing role in the development of his condition? Please explain your findings and reasons for your conclusions. The accident of February 4, 1981 and his work as a cook in 1982 appear to have played a contributing role in the detection of his seronegative spondyloarthropathy and the onset of his psoriasis and psoriatic arthritis associated with that underlying diagnosis. The chronology of medical events and their sequence following these accidents supports this view. However, if a link between trauma and his psoriatic arthritis exists, it seems more likely that it may have advanced the course of the disease by a decade or two rather than being fundamentally responsible for it. One might ask the question had these accidents and events never occurred, would [the worker] have developed psoriasis and psoriatic arthritis anyway? This is a possibility, but I believe that on balance, the events of February 4, 1981 and 1982 appear to have played a contributing role in the aggravation and advancement of his condition, notwithstanding the likelihood that his pre-existing spondyloarthopathy may have started with his reactive arthritis/Reiter’s syndrome documented more than a decade earlier. 10) If your findings are in conflict with the opinion of Dr. Gladman (addendum #2, Pg. 710, please explain on what basis your opinion differs from her.

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With respect to Dr. Gladman’s report, I agree with her diagnosis of her diagnosis of psoriatic arthritis, and I believe she clearly accepts Dr. Fam’s diagnosis of reactive arthritis/Reiter’s syndrome, and she draws attention to the point that [the worker] does not seem to understand that “there is a relationship between Reiter’s disease and psoriatic arthritis in the sense that both belong to the same family of arthitides, namely the B27-associated seronegative spondyloarthropathies”. I also agree with her that no matter what the diagnosis, “the treatment would have been the same, and therefore would have made no specific difference to the patient himself”. In my answer to your question 3, I have cited the publications on the relationship of environmental factors including trauma to the development of psoriasis and psoriatic arthritis. With respect to the back injury triggering the development of psoriasis and psoriatic arthritis it is not clear to me whether early treatment can make a significant difference with respect to the development of progressive disability from that condition. I have also cited evidence that a lack of active treatment in the case of ankylosing spondylitis is detrimental, and [the worker] shows features such s his neck involvement in keeping with that diagnosis that may have been worse because of a lack of active treatment. I also agree with Dr. Gladman that [the worker] clearly has evidence of sacroiliitis which is a feature of both Reiter’s disease and psoriatic spondyloarthropathy. The complaints that he has with regards to his back are not those that we see in patients with inflammatory spondyloarthropathy”. I also agree that “his current back pain is mechanical in nature .. clearly related to the injury”. It is noteworthy that since Dr. Gladman last saw [the worker] in September of 1995 his peripheral joint involvement from psoriatic arthritis appears to be much improved with his Methotrexate treatment, and his major clinical problems at present relate to his spine. Moreover, I also agree with her view that his back pain is due to the injury, and although the psoriasis and psoriatic arthritis may have been aggravated or enhanced by the injury, his back pain rather than his spinal deformity is more related to that mechanical injury than the effects of his psoriatic, seronegative spondyloarthropathy. 11) Is there any additional information which you feel would be helpful to the panel and parties in understanding this worker’s condition and its etiology? In order to better clarify and summarize my answers for the panel, I pose the following questions? 1) Were the work-related traumatic events of 1981 and 1982 responsible for [the worker’s] developing seronegative spondyloarthropathy? This is unlikely, because he had evidence of pre-existing reactive arthritis/Reiter’s syndrome with its know relationship to seronegative spondyloarthropathy, well before the accident. 2) Where the work-related traumas of 1981 and 1982 responsible for triggering the onset of the psoriatic arthritis aspect of his seronegative spondyloarthropathy? In a genetically susceptible person such as [the worker], these traumas were possible triggers, but even more likely for reasons outlined above, I believe they permanently advanced the course of his psoriatic arthritis, and the course of his seronegative spondyloarthropathy. 3) Had [the worker] never been involved in these traumatic events, would be have developed and psoriatic arthritis anyway? In my view he likely had seronegative spondyloarthropathy before these accidents that was temporarily aggravated and then advanced by them. However, it is less certain that he would have developed psoriasis and psoriatic arthritis features anyway, is spite of his hereditary susceptibility to these conditions. If [the worker] was destined to develop psoriatic arthritis anyway, that onset might not have been expected until he reached the age of 55 years. If your have any further questions about the information and views expressed in this report, or if I can be of any further assistance to your and the panel, please let me know.

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[13]

The report of Dr. Gordon, taken together with the other medical evidence and in particular that of Dr. Gladman caused the Panel to conclude that the worker’s seronegative spondyloarthropathy is a condition compensable, in the sense that the injury of February 4, 1981, did, more probably than not, accelerate and permanently advance its course. For that reason, the worker is entitled to a permanent assessment and assessment of permanent impairment arising therefrom.

[14]

Part of the worker’s claim was for entitlement to travel expenses, as discussed in the decision of Hearings Officer St. Pierre. These, obviously, are compensable as well. THE DECISION

[15]

The worker’s appeal is allowed. The Workplace Safety and Insurance Board will re-assess the worker’s entitlement to benefits, and to vocational rehabilitation services, in light of this finding. Should specific areas of dispute arise regarding the worker’s entitlement to vocational rehabilitation services, this Panel will remain seized of those matters. DATED: May 26, 1998 SIGNED: E. Newman, C.J. Robb, J. Anderson