Estate of Hughes v Accident Compensation Corporation (Treatment Injury)

IN THE DISTRICT COURT AT TAURANGA ITE KOTI-A-ROHE KI TAURANGA MOANA [2019] NZACC 70 ACR 180/17 UNDER THE ACCIDENT COMPENSATION ACT 2001 IN THE MATTER OF AN APPEAL UNDER SECTION 149 OF THE ACT BETWEEN ESTATE OF DAVID HUGHES Appellant AND ACCIDENT COMPENSATION CORPORATION Respondent Hearing: 11 April 2019 Appearances: Ms Mckee-Trail for the appellant Ms Miller for the respondent Judgment: 26 June 2019 RESERVED JUDGMENT OF JUDGE DENESE HENARE [Treatment Injury s 32 Accident Compensation Act 2001] [1] This appeal concerns the Corporation's decision to decline the appellant's claim for segmental dystonia involving face, tongue, jaw - variant of orofacial lingual dystonia/edentulous dystonia (segmental or orofacial dystonia) as a treatment injury. The appellant challenges the Corporation's decision dated 6 December 2016 declining cover for a treatment injury. [2] Sadly, David Hughes died in January 2017. The application to appoint Barbara Hughes executor of the estate as the appellant in the appeal is confirmed. I dispense with the formality of sealing and service of the order. [3] The appellant's position is that Mr Hughes' dystonia was caused by stubborn dental extractions causing disruption and injury to the submaxillary nerve ganglion and therefore is a treatment injury. [4] The Corporation's position is Mr Hughes did not suffer a personal injury caused by dental treatment, and therefore the decision to decline cover is correct. [5] A key question for consideration in the appeal is whether Mr Hughes suffered a physical injury that was caused by dental treatment, that is, the dental extractions. Agreed Facts 6] Mr Hughes had a history of periodontal conditions/dental decay and extensive tooth extractions. Between approximately 2005 and 2013 Mr Hughes had all but two teeth removed due to his periodontal condition/dental decay. [7] In February 2014 Mr Hughes' GP referred him to a neurologist. Dr Paul Timmings, with a principal complaint of poor speech, and a tendency for his tongue to protrude through the left corner of his mouth when he was talking. Dr Timmings diagnosed Mr Hughes with an atypical left hemifacial spasm. [8] Mr Hughes was treated with various medications for the hemifacial spasm, without significant effect. MRI assessments revealed no significant abnormality. [9] In April 2015 Mr Hughes was seen by neurologist Dr Barry Snow, who diagnosed him with segmental dystonia, a variant of orofacial dystonia. Dr Snow raised a link between lingual dystonia and tooth removal ("so-called edentulous dystonia") and recommended that an ACC claim be lodged. [10] On 19 May 2015 the appellant's GP made a claim for a treatment injury, described as: Segmental dystonia involving face, tongue, jaw-variant of orofacial lingual dystonia/edentulous dystonia. [11] ACC investigated the claim, including by obtaining Mr Hughes' dental and medical records, and obtaining an expert opinion from neurologist, Dr William Wallis. On 5 November 2015 ACC declined cover on the basis that it had been unable to identify a physical injury which had led to the segmental dystonia. [12] Mr Hughes sought a review of ACC's decision, and on 3 June 2016 the reviewer quashed ACC's decision and directed that it obtain further expert evidence from an oral surgeon and a neurologist, who were required to examine Mr Hughes. [13] ACC obtained further expert evidence from a Maxillofacial Surgeon, Dr Paul Smedley, and a Neurologist, Dr Peter Wright. Both Dr Smedley and Dr Wright examined Mr Hughes as part of forming their opinions. [14] On 6 December 2016 ACC issued a fresh decision to decline cover on the basis that there was insufficient evidence of a physical injury that had led to the symptoms of dystonia. [15] ACC's decision was upheld on review. Medical Evidence [16] In October 2005 Dr Berry, Dentist referred Mr Hughes to Dr Whitley, Oral Surgeon, and noted that: Dave has a sporadic history of dental treatment with a longstanding poorly managed periocondition. Early this year he had a throbbing pain in the lower anterior region and numbness over his chin. 5/05 - I extracted 41, 31, 32. The pain stopped but he still felt numb ... as you can see from the enclosed films the situation had not been good for a long time. [17] The appointment with Dr Whitley did not proceed. Dr Whitley noted: He feels things are okay for now. [18] The dental records of July 2009 of Dr Stutz, Dentist, note Mr Hughes had a couple of teeth removed in Australia and "unable to chew and speech issue .. generalised perio issues". Eighteen months later in January 2011, the dental records note: Quite badly swollen face while away placed on antibiotics by GP. [19] In September 2012 the dental notes record: Significant speech issues feels getting worse, feels due to bad fitting denture. [20] Further extractions were recorded in 2013 with denture adjustments in 2014. [21] In February 2014 Dr Timmings, Neurologist, saw Mr Hughes with a major complaint of "poor speech, and a tendency for his tongue to protrude through the left corner of his mouth when he is talking". [22] In a letter dated 20 February 2014 Dr Timmings reported: He has had several sessions of dental work and a number of extractions, an upper denture made, and a partial plate fitted to the lower jaw, but these restorations have made no difference to his speech and face symptoms. Dave also mentioned that sometimes he has spontaneous spasm affecting his left lower face, which is transient, the cause is marked left lower face distortion. ... Conclusion and opinion: The history and findings today are suggestive of atypical left hemifacial spasm. Neuroimaging is appropriate, and further management will ensue. [23] Mr Hughes was prescribed medication, and an MRI brain cerebral carotid MRA was performed on 14 March 2014Dr Timmings reported the MRI showed minor age related change, but "no worrying or concerning abnormalities": [24] On 26 March 2014 Mr Hughes was reviewed by Dr Timmings, who reported to Mr Hughes' GP some slight improvement to the hemifacial spasm. He also noted that: You will be aware that his MRI scan was satisfactory, and although this is reassuring it is also a little bit disappointing that we do not have a specific diagnostic cause. [Emphasis added] [25] Dr Timmings saw Mr Hughes again on 24 July 2014 and reported that "He still clearly had left lower hemifacial spasm which was intermittent and variable - almost dystonic. Cranial nerves were otherwise normal". Mr Hughes' medication was increased, and the need to obtain a surgical opinion was also discussed. [26] On 13 November 2014 Mr Hughes was seen by Mr Hussein, Neurosurgeon, who noted the "MRI brain scan did not reveal any major vascular compression or tumour". Mr Hussein arranged for a special MRI scan "to study the course of the Hypoglossal nerve and to focus on the brain stem & neck". [27] The subsequent MRI was reported by Dr Swarbrick, Radiologist who stated: No abnormality identified in relation to the trigeminal nerves on either side to account for the patient's symptoms ... [28] Mr Hussein reported to Dr Timmings on 5 March 2015 that: There is no obvious neurovascular compression syndrome or lesions to explain his symptoms. 29] On 11 April 2015 Dr Snow, Neurologist, reported his assessment of "orofacial dystonia" and stated: In summary, I agree that David has segmental dystonia involving the face, tongue and jaw. Thus it is a variant of an orofacial lingual dystonia. As you know this disorder is seldom satisfactorily explained. There is a link between lingual dystonia and tooth removal so-called edentulous dystonia. In David's case I believe it is likely that this link occurs, although there is not a good pathophysiological explanation. [Emphasis added] [30] On 14 May 2015 Mr Hughes' GP, Dr Hughes, filed an injury claim form. Dr Hughes diagnosed the injury as: Dystonia, unspecified. Left ... Confirmed is under care of Dr Paul Timmings, neurologist and has seen Dr Barry Snow, neurologist to confirm diagnosis of orofacial lingual dystonia. This is believed to be linked to previous dental surgery [31] Under the heading "Injury and Employment details - Description" Dr Hughes wrote: Has had extensive dental surgery with multiple extractions over a 5 year period. David is now suffering from orofacial dystonia, which is believed to be a result of this dental surgery. [32] In a file review of 1 October 2015 Dr Wallis, Neurologist noted, among other things: ... there is good evidence that he had dental extraction starting at least around 10 years ago, possibly before that time. Subsequent typed notes describe multiple dental procedures after 2005, and mention "significant issues with speech" on 4.9.2012. Of note, this would be roughly congruent with Dr Snow's estimate that the movements began two years before he saw Mr Hughes that is around 2012 or 2013. Using these dates, the dystonia appears at least 6 to 7 years after the first recorded tooth extractions. In other words, the movements, as documented in the supplied records, began well after Mr Hughes started to have progressively more tooth extractions. [Emphasis added] [33] Mr Wallis went on to explain that segmental dystonia or orofacial lingual dystonia involves "sustained involuntary muscle contractions causing twitching or repetitive movements" and that "an underlying cause is often difficult to prove". He noted that literature refers to three forms of such dystonia: [a] Idiopathic dystonia: "as the name suggests, no explanation is found"; [b] Tardive dystonia: "occurs after treatment with neuroleptic agents and occasionally with phenothiazines. It sometimes begins immediately after starting these treatments but other times only later ..."; and [c] Peripheral dystonia: "... a term popularised by ... Dr Joseph Jankovic. It is defined as a type of dystonia triggered by trauma to the peripheral or cranial nerves. One of the forms ... is peripheral edentulous dystonia ... [which] presumably originates after dental trauma or procedures causing chronic oral pain." [34] As to peripheral dystonia, Dr Wallis opined that: Dr Jankovic compares peripheral dystonia to idiopathic dystonia and points out hat with peripheral dystonia (as suggested might be the cause of this patient's conditions) the latency between the trauma and the dystonia is measured in days up to one year. Pain is a prominent feature with peripheral edentulous dystonia but not with idiopathic edentulous dystonia ... [Iff this patient's dystonia were caused by tooth extraction, there are atypical features. The first is that his tooth extractions began many years before the onset of dystonia. The second is that pain is not a prominent feature, at least as outlined in the reports from Drs Timmings and Snow. [Emphasis added] [35] Dr Wallis concluded: In all likelihood this patient has a form of idiopathic orolingual dystonia associated with the edentulous state ... There is no proof as far as I can tell from the supplied records, that dental extractions have caused the condition. Rather, it is likely that the edentulous state, caused by many years of having teeth removed, is the cause of the dystonia rather than the dental procedures themselves. One accepts, however, that it is impossible to be sure about this, but on the balance of probabilities Mr Hughes has an idiopathic form of orolingual dystonia, possibly related to the edentulous state but not caused by dental procedures. [Emphasis added] [36] The evidence was considered by the Corporation's Complex Claims Panel on 22 October 2015 who recommended advice be sought from an internal medical advisor whether dystonia is caused by damage or harm to body tissue, that is, whether there is a physical injury. [37] On 27 October 2015 Dr Chris Moughan, the Corporation's Medical Advisor commented on this question and advised: The difficulty with edentulous dystonia is that there is no good mechanism proposed of directly neurological toxicity or injury not a good pathophysiological explanation. As noted by Dr Snow, the disorder is seldom satisfactorily explained. There is a link between lingual dystonia and tooth removal - so called edentulous dystonia - which Dr Snow believed to have occurred in this case. However he noted there was not a good pathophysiological explanation. ... Although one of the suggested possible mechanisms includes destruction of sensory to motor connections of nerve cells, with the development of edentulous dystonia there is not a good pathophysiological basis of nerve injury (as there is for tardive dystonia - with basis of direct neuronal toxicity). [Emphasis added] [38] In a review decision dated 3 June 2016, the Reviewer quashed the decision and required the Corporation to make the decision again in accordance with directions. The reviewer explained: In my opinion the medical evidence has not explicitly or fully considered whether the dental treatment Mr Hughes received has caused a physical injury (for example nerve damage) and whether this is a possible cause of his dystonia. [39] The reviewer directed that: [a] An independent oral surgeon and neurologist must be provided with copies of all relevant documents, including the review decision; dental records, and reports of Drs Timmings, Snow, Wallis and Moughan; [b] The oral surgeon and neurologist must examine Mr Hughes; [c] The question for the oral surgeon is whether Mr Hughes' dental treatment is likely to have caused nerve damage or other physical injuries (which might explain his orofacial lingual dystonia). [d] The question for the neurologist (in light of the report from the oral surgeon) is whether any nerve damage or other physical injury identified by the oral surgeon as likely having been caused by the dental treatment - was "probably a material cause of Mr Hughes' orofacial lingual dystonia". (40] In a report dated 15 August 2016 Dr Smedley, Oral Surgeon, advised he spent "some considerable time reviewing all the documentation that had been provided" and he had physically examined Mr Hughes on 28 July 2016. Dr Smedley reported having undertaken a comparative review of x-rays: A new "OPG" was taken to compare radiographically the mandible and maxillary bone and alveolar bony bases from the OPG taken in June 2005, with dentition and the current edentulous mouth. That 2005 OPG and the accompanying periapical radiographs show considerable alveolar bone loss associated with chronic periodontal disease is relevant because with this amount of disease there is little and in some areas no bony support for the teeth, and as such there would be little in any trauma in removing these teeth (sic). It is also worth noting that the patient, when asked, said that all of the teeth were removed using simple dental forceps and NO surgical procedures were required. The new OPG radiograph when compared to the similar radiograph shown in he notes (2015) now demonstrates absence of all teeth, healing alveolar bone in the recent extraction and normal bone elsewhere, an intact inferior alveolar nerve canal on the right side with no evidence of any trauma to the canal (this does not totally exclude trauma to the inferior alveolar nerve) but makes it extremely unlikely as one has to look at the bone surrounding the nerve rather than the nerve itself. [41] Dr Smedley concluded: From this examination x-rays and patient discussion, it is my conclusion that no abnormal dental procedures were undertaken and the dentition was removed relatively atraumatically on a sequential basis and partial dentures were provided until the current new full dentures. As such I support the statement that on the balance of probabilities Mr Hughes dental treatment is unlikely to have caused nerve damage or other physical injuries which might explain his lingual dystonia. While being sympathetic to this patient and his disability I cannot link the dental treatment to this disorder. In making this decision I have considered all my eminent neurological colleagues reports and accompanying papers ... [Emphasis added] [42] The Corporation then arranged for Mr Hughes to be seen by Dr Wright, Neurologist whose report in September 2016 indicated he reviewed the medical records and reports, medical literature and completed a clinical assessment, including questioning Mr Hughes about discrepancies in the reports. In response to specific questions, Dr Wright advised: 2. Are you able to identify an injury (damage or harm to body tissue) which has resulted in the orofacial dystonia in this case? If so, please describe this injury. Reply: the minor sensory nerve injury that occurred in 2005 is not causally linked to the dystonia. A probable pathological disruption in the basal ganglia circuits controlling orofacial movements has been triggered by pain and altered sensory inputs from the mouth. The proprioceptive sensory pathway disruption at the basal ganglia level of the brain in theory underlies this presentation. 3. On the balance of probability, what is the probable cause of this injury? Reply: the painful dental extraction of 12.03.2008 4. Have the dental extractions made a material contribution to the injury described? If so, please describe the mechanism by which this has occurred. Reply: the painful dental extraction and the subsequent edentulous state with adequate dental prosthesis is compatible with an evolving secondary "peripheral edentulous dystonia". I note the expected evolution over time is not unusual. I note the lack of clear causal actiological link in the published literature, but the consensus that there is a clear association between the injury and the syndrome, through probable pathological disruption in the basal ganglia circuits controlling orofacial movements triggered by pain and altered sensory inputs from the mouth. [Emphasis added] [43] The Corporation then arranged for Dr Brown, Medical Advisor to review and comment on whether Dr Wright's description of a "pathological disruption of the basal ganglia" provided a description for a physical injury. Dr Brown reviewed the medical reports and medical literature and noted the National Institute of Neurological Disorders (NINDS) divided dystonias into groups of idiopathic, genetic and acquired or secondary. He noted form the studies that the pathophysiology of dystonia is complex, and cerebellar dysfunctions may also be involved. The conclusion of a study by Kovojic' is that dystonia represents one of many possible states. Dr Brown advised: The physical injury proposed by Dr Wright, 'a probable pathological disruption in the basal ganglia circuits controlling orofacial movements' appears to be so broad that it must be considered in context with the underlying diagnosis. It is apparent in the case of Mr Hughes, despite having the consideration of four or more neurologists, a neurosurgeon and a maxillofacial surgeon, that there is no expert consensus as to whether he has primary, idiopathic, genetic, or an acquired secondary form of dystonia. Dr Wright himself uses three different terms to describe the outcome in Mr Hughes' case: peripheral edentulous orofacial lingual dystonia, peripheral edentulous dystonia, and oromandibular dystonia. . . . ... it is more likely that Mr Hughes' condition is the result of subtle changes in neuronal function and microstructural brain alterations, particularly in sensorimotor circuits that are associated with motor learning and memory, that have created a susceptible substratum for dystonia to occur. In this way, through maladaptive sensorimotor plasticity, disruption or dysfunction or normal coordination leads to a disabling motor disorder, such as unfortunately experienced by Mr Hughes. Maladaptive sensorimotor plasticity, a disturbance of the normal physiological state does not nevertheless amount to a physical injury. In my opinion, having considered all the circumstances of treatment in the case of Mr Hughes, the description of "pathological disruption of the basal ganglia" does not provide evidence of a physical injury. [Emphasis added] The Requirements of a Treatment Injury [44] In order to establish cover for a treatment injury the requirements of s 32(1) of the Accident Compensation Act 2001 ("the Act") must be satisfied. Section 32(1) relevantly provides: Kovojic M, Parees I. Secondary and primary dystonia: pathophysiological differences. Brain 32 Treatment injury (1) Treatment injury means personal injury that is- (a) suffered by a person- . . . ii) receiving treatment from, or at the direction of, 1 or more registered health professionals; or . . . b) caused by treatment; and (c) not a necessary part, or ordinary consequence, of the treatment, taking into account all the circumstances of the treatment, including- i) the person's underlying health condition at the time of the treatment; and (ii) the clinical knowledge at the time of the treatment. [45] In this case the primary question is whether the treatment, that is the multiple extractions caused a personal injury, that is, segmental dystonia. The submissions of the parties [46] Ms Mckee-Trail submitted the extractions that Mr Hughes endured caused the injury resulting in the oral mandibular dystonia and that injury is a treatment injury. [47] Ms Mckee-Trail submitted: [i] Dr Snow's views are based on his physical assessment of Mr Hughes, his experience and his research. [ii] Dr Timmings noted there is a recognised link between lingual dystonia and tooth removal and in Mr Hughes' case it appears likely the two are connected. [ifi] Dr Wright identified the physical injury when noting on 12 March 2008 there was a difficult tooth extraction that was perceived as very painful. Dr Wright opined a probable pathological disruption in the basal ganglia circuits controlling orofacial movements has been triggered by pain and altered sensory inputs from the mouth. 2013 Jul: 136 (P+7): 2038-49. [48] Ms Mckee-Trail submitted Dr Smedley's report is flawed due to a number of factual errors namely: if He refers to a tardive form of dystonia in his reports and this is not the type of dystonia that Mr Hughes had contracted. [ii] He is under the impression Mr Hughes' teeth were extracted easily and without any force applied which is incorrect. Both Dr Berry and Dr Stutz stated in their clinical notes Mr Hughes' teeth were stubborn and required considerable effort to extract them. [ifi] His opinion is outlier and the assessments of Dis Snow, Simpson, Timmings and Wright are to be preferred. [49] Relying on the evidence of Dr Wallis, Dr Smedley and Dr Brown, Ms Miller submitted the weight of the evidence is that the dystonia was not caused by dental treatment. [50] Ms Miller submitted Dr Brown had particularly conducted careful review of the literature and concluded a probable disruption of the basal ganglia did not amount to a physical injury. [51] Ms Miller submitted Dr Wright's evidence establishes risk of causation. His opinion amounts to an alternative theoretical explanation. Discussion [52] There is no doubt the history in this case is extensive as noted in the background section to this judgment. There is also no doubt the complexity of the case is marked by the involvement of no less than four neurologists, a neurosurgeon and a maxillofacial surgeon. [53] Causation is the issue. The key question agreed by the parties is whether Mr Hughes suffered a physical injury caused by his dental extractions. [54] The Court of Appeal has established principles to guide understanding of causation. In Ambros', the Court stated the evidence must be robust, and that risk of causation does not suffice. [55] In Thompson, 3 Collins J discussed the legal test of causation in treatment injury cases. He said: [39] A court faced with a treatment injury claim that requires a causation analysis would be expected to carefully assess: (1) Whether the applicant had discharged the legal and evidential burden of establishing his or her personal injury was caused by treatment. While the legal burden remains with the claimant, the evidential burden may shift to ACC where a claimant adduces some evidence of causation. Whether the evidential burden shifts at any point during a case involves a careful evaluation by the decision-maker. (2) Whether causation has been established by all relevant evidence, including valid inferences and evidence relating to proximity. Causation is not necessarily determined on the basis of expert evidence except where the expert evidence establishes there is no connection between the treatment in question and the claimant's personal injury. This point was explained in the following way by the Court of Appeal in Accident Compensation Corporation v Ambros: "... [A] court's assessment of causation can differ from the expert opinion and courts can infer causation in circumstances where the experts cannot. This has allowed the court to draw robust inferences of causation in some cases of uncertainty ... Judges should ground their assessment of causation on their view of what constitutes the normal course of events, which should be based on the whole of the lay, medical, and statistical evidence, and not be limited to expert witness evidence ..." [56] It is settled law that pain of itself is not a personal injury. A physical injury must be identified with some precision. It must be established on the balance of probabilities that the segmental or orofacial dystonia is, in terms of s 32(1)(a) and (b), a personal injury caused by treatment. Accident Compensation Corporation v Ambros [2008] 1 NZLR 340 (CA). Thompson v Accident Compensation Corporation [2015] NZHC 1640. Studman v Accident Compensation Corporation [2013] NZHC 2598. [57] I agree with the Reviewer the evidence provided at the first review did not address the question of personal injury. I find the reports of the neurologists provided at the first review are largely grappling with diagnosis and treatment. However, the neurologists noted a research base acknowledging a causal connection between dystonia and dental extraction. [58] Dr Hussain ruled out a neurovascular compression syndrome which he did not explain. Dr Timmings, Dr Snow and Dr Simpson confirmed diagnosis of orofacial lingual dystonia involving the face, tongue and jaw, linked to previous dental surgery. This disorder was noted in May 2015 by Dr Hughes GP to have "significantly affected his ability to work as a school principal" from 27 April 2015. [59] Ms Miller urged me to review the opinion of Dr Wallis carefully. It is the case, as Dr Wright acknowledged, that Dr Wallis is a senior and experienced general neurologist. In this case Dr Wright is the acknowledged independent expert. I find the reports of Dr Wallis and Dr Wright taken together provide a synthesis of opinion and conclusion so that I find the 2008 dental extraction was causative of a personal injury in this case. [60] The distinguishing feature between the reports of Dr Wallis and Dr Wright is that the opinion of Dr Wallis is based on a file review. In consequence, he opined an idiopathic dystonia the most likely condition. However, he acknowledged trauma as causative of peripheral dystonia. On the other hand, Dr Wright had extensive consultation with Mr and Mrs Hughes and was able to reconcile and correct discrepancies and fill gaps in the records, particularly as to symptomology and latency. Mrs Hughes is a dental nurse. [61] There is some difference in the use of terminology to describe dystonia. It is acknowledged as complex terminology. That arises from the research on which each specialist referred. I observe all the neurologists, depending on their particular specialty within neurology, used terminology interchangeably. [62] Both Dr Wallis and Dr Wright agree the nature of oromandibular dystonia. They discussed the research by Jankovic. He defined peripheral dystonia as a type of oromandibular dystonia triggered by trauma to the peripheral or cranial nerves. Criteria for peripherally induced oromandibular dystonia include the onset of dystonia measured in days and months up to a year, the trauma is recorded, and it is anatomically related to the site of injury both facial and oral. Pain is often a prominent feature. The research by Jankovic also showed the relationship between trauma and the subsequent development of a movement disorder, and involves the mouth, jaw and tongue movements. [63] I turn to consider the evidence. [64] There were two dental procedures recording extractions in May 2005 and March 2008. Dr Wallis noted the dental records were brief and difficult to read. Dr Hughes GP noted in the Treatment Injury claim form that details and dates were not available in the GP notes. [65] Dr Berry's letter of October 2005 to Mr Whitley noted the pain stopped but Mr Hughes continued to feel numb on the left side of his chin. Mr Whitley later reported Mr Hughes' statement that "he feels things are okay." Ms Miller submitted this statement showed no real problem arising from the 2005 extractions. In my opinion, this statement is to be viewed with the evidence of Mr and Mrs Hughes as recorded by Dr Wright, that the onset of numbness followed the May 2005 extraction procedure. [66] The onset of the dystonia was opined by Dr Wright as having come on approximately one month after what Mr Hughes described as a difficult extraction and severe pain leading to a day off work in 2008. Dr Berry's notes record Mrs Hughes ringing her and advising that Mr Hughes 'not feeling great' and 'going home'. Mrs Hughes said her husband rarely took any time off from his work as school principal. Luca, C Singer, C and Jankovic, J peripheral dystonia Medlink Neurology, 4 October 2014. Sankhta, C Laia, E and Jankovic, J peripherally induced oromandibular dystonia. J neurol eurosurg psychiatry 1998: 65: 722-728. [67] Dr Wright noted Mr Hughes explanation that it was due to the severe pain with the 2008 extraction and his concerns regarding the facial movements that led him to change dentist to Dr Stutz. Dr Wright discerned that the problem of movements disorder began following the extractions in March 2008 and evolved over time. Mrs Hughes explained the spasms on the left side of the face. These symptoms became worse and a speech issue was first mentioned in Dr Stutz's notes in July 2009. Whilst not mentioned again until 2012, Mr and Mrs Hughes confirmed the speech was persistent and worsening over time. [68] In her referral to Mr Whitley in September 2012, Dr Cowan described the onset of the speech disturbance as recent. The reason for this is noted by Dr Wright in his taking of the clinical history that the dystonia was becoming a lot more obvious, the speech was disabling Mr Hughes' ability to communicate with staff. It was around this time Mr Hughes decided to seek further help because he had been using deputy principals to mask the severity of his symptoms. Dr Wright noted there was a discrepancy regarding pain on speaking in the records. Mr Hughes described that it had been hard to enunciate for some time and this became more and more difficult with concentration and muscular control required to speak more intense, from around 2012 onwards. It was this level of effort that appeared to lead to pain when speaking. [69] Ms Miller is correct in her submission that pain is not evidence of a physical injury. I observe Dr Wright noted in the literature that the pain itself is not a crucial component in the dystonia disorder. [70] In my opinion, Dr Wright has taken a comprehensive and thorough clinical history from Mr and Mrs Hughes as well as file review. He has distinguished two disorders. The first disorder being a minor nerve injury arising from the dental extractions in 2005 is unrelated to the second movement disorder, the onset of which commenced a month following the 2008 extraction and noted by Dr Stutz a year later. This movement disorder progressively affected Mr Hughes' speech and pain when speaking, and tongue protrusion by 2012. [71] I find Dr Wright provides the pathophysiological explanation with which other neurologists were grappling. Whilst pain was a symptom it was not itself a crucial component in the orofacial lingual dystonia. Dr Wallis was unable to identify any particular procedure, and particular symptomology. [72] I find Dr Wright has thoroughly considered the published literature, the medical consensus of causal link between the injury and the disorder and explained the pathological disruption through the altered sensory inputs from the mouth caused by the 2008 dental extraction. [73] Dr Wright took into account Dr Smedley's report. 74] Ms Mckee-Trail submitted there were various flaws in Dr Smedley's report particularly regarding symptomology following the dental extractions. Whilst I accept there is a dispute of fact as to whether trauma was involved in removing the teeth, I take into account Dr Smedley is the sole maxillofacial surgeon in this case. His evidence focussed on whether the dental extraction procedure was abnormal. He noted a degree of relative trauma on a sequential basis. Dr Smedley acknowledged that this does not totally exclude trauma to the nerve "as one is looking at the bone surrounding the nerve rather than the nerve itself". Dr Wright noted Dr Smedley's view the pathology lay within the basal ganglia. [75] On balance, I find Dr Wright's conclusions have carefully applied the criteria, also discussed by Dr Wallis, in concluding the 2008 extraction caused a physical injury. [76] Ms Miller submitted Dr Wright had produced a theory which amounted to risk of causation. I take into account the thoroughness in which Dr Wright took the clinical history both from the records and reports before him and in consultation with Mr and Mrs Hughes. I find his report comprehensive and compelling. 77] Whilst Dr Brown provided a careful review of the literature, not mentioned by the neurologists, Dr Brown placed focus on the 2005 minor nerve injury which Dr Wright viewed as unrelated to the movement disorder. Further, Dr Brown opined Mr Hughes was susceptible for dystonia to occur. No neurologist has reached this conclusion. I take into account that Dr Brown is not a neurologist. Accordingly, I do not give as much weight to his opinion as I accord to the neurologists' evidence in the case. Result [78] I conclude that the March 2008 dental extraction was causative of the orofacial lingual dystonia by altering or disrupting the proprioceptive sensory pathway at the basal ganglia level of the brain. I conclude there is evidence of a physical injury in this case. There is no evidence that any of the exclusions apply. Whilst Mr Hughes had a periodontal condition, the evidence is this condition was causative in part of the need for the dental extractions, but there is no suggestion of their contribution to cause of the physical injury. [79] At hearing, I indicated to Ms Mckee-Trail that a finding of a physical injury is insufficient to meet the tests under s 32 of the Act. There is need to consider $32(1)(c) of the Act whether a physical injury was a necessary part or ordinary consequence of treatment. Ms Miller's written submissions touch on the test. Ms Miller submitted a physical injury that is necessary in order to carry out treatment will not attract cover. However, there is no medical evidence before me in support of the submission. This is understandable when the evidence is focused on the issue of whether a physical injury had occurred. [80] I consider the best approach at this stage is to quash the review decision on the basis of my finding of a physical injury. This means that the Corporation is directed to obtain evidence and consider the application of's 32(1)(c) of the Act in this case. [81] Since the appeal is successful in part, the appellant is entitled to reasonable costs as may be agreed between the parties. Jenese Idlerone Judge Denese Henare District Court Judge Solicitors: Claro Law, Wellington for the respondent ACR 180-17-Estate of Hughes