1. In each proceeding, the claim for compensation under Part 3 of the Transport Accident Act 1986 (Vic) is dismissed.
2. No order as to costs.

Mr Pinkstone of counsel, instructed by the Transport Accident Commission

1. Mr Paproth was injured in a transport accident on 17 September 2014. A truck collided into his utility vehicle on the Princes Freeway near Werribee.
2. He was injured in the accident. It is accepted by both parties that his injury included an end plate fracture of vertebra T7 within his thoracic spine.[1]
3. Mr Paproth had worked full time as a floor leveller immediately prior to the accident.
4. He made two claims for compensation from the Transport Accident Commission ('the TAC') as a result of the transport accident under Part 3 of the Transport Accident Act 1986 (Vic) ('TAA').[2]
5. The TAC considered these claims, including supporting medical reports and other documents provided by Mr Paproth.
6. In both instances, the TAC rejected Mr Paproth's claim on the basis that it was not satisfied that there was a causal connection between the transport accident and the compensation claimed.
7. In summary, it did not accept there was sufficient evidence of autonomic dysfunction or that Mr Paproth sustained a spinal cord injury at the thoracic level, which it regarded as necessary to establish his current symptoms were caused by the transport accident.
8. Mr Paproth sought review of both these decisions at the Tribunal, under s 77 of the TAA.[3]
9. As at the date of the final hearing, Mr Paproth sought compensation in the first proceeding (Z1162/2018) as a result of claimed autonomic dysfunction, including thermoregulation dysfunction.[4] Mr Paproth claimed that this condition was directly related to and caused by the transport accident.
10. He sought compensation towards utility bill payments and for retrofitting his home to make it less susceptible to temperature changes, as well as a contribution towards transport to take his son to childcare when he is/was unable to do so.[5]
11. As at the date of the final hearing, the second claim (Z481/2021) seeks rebates for prescription medication, Minirin spray (Desmopressin), for the regulation of urinary output.[6]
12. I heard submissions for both parties.[7]
13. Mr Paproth gave evidence under oath and answered questions from the Tribunal and counsel for the TAC.
14. The TAC called expert evidence from Dr John Waterston, a neurologist who had prepared a joint medico-legal report on behalf of the parties for the proceeding. Mr Paproth asked questions of Dr Waterston by way of cross examination, mainly targeted to whether his analysis of the radiology results could be interpreted differently.
15. After the hearing, I made orders for the provision of additional reports referred to in oral submissions by Mr Paproth.[8]
16. I provided him with an opportunity to call expert neurological evidence from one of his treating specialists, Dr Victor Gordon. However, Mr Paproth did not elect to take up this opportunity.
17. I also made orders as requested at the hearing for the TAC to make closing or reply submissions in writing after it had received the transcript of the hearing.
18. A copy of the transcript was provided to the Tribunal and Mr Paproth and the TAC provided its final submissions on 27 March 2025.
19. I have considered all relevant evidence and submissions provided by the parties in making this decision in these two compensation proceedings.
20. For the reasons below, I am not satisfied that Mr Paproth is entitled to compensation as claimed in either proceeding.
21. In summary, I am not satisfied that the symptoms he exhibits constitute an injury 'as a result of a transport accident'. This is the precondition for an entitlement to compensation under Victorian legislation.

1. The issues in dispute narrowed as the hearing progressed.
2. The TAC did not dispute the fact that Mr Paproth was in generally good health before the accident, and that he did not exhibit the symptoms he now relies on in his claims for compensation.
3. Mr Paproth explained that he has experienced significant health problems, including extensive 'burning' back pain in the months immediately following the transport accident (lasting approximately 7-9 months).
4. He submitted that he also now suffers from the condition of autonomic dysfunction.
5. The condition of autonomic dysfunction was explained in evidence of Dr Waterston as a dysfunction which affects the sympathetic and parasympathetic nervous system, with the nervous system controlling bodily functions. He advised that it could have a functional cause, a structural cause (such as a neurological basis) or may arise from genetic factors.[9]
6. Mr Paproth described key symptoms, including an inability to regulate his bodily functions during hot/cold conditions, blood pressure and heart abnormalities and digestive and urinary issues.
7. The TAC did not substantially dispute the fact that Mr Paproth suffers from the majority of symptoms he has identified.[10]
8. Given this position, I was not persuaded that it would be appropriate to adjourn the hearing to enable Mr Paproth to have additional medical testing and analysis relating to other potential symptoms, such as a repeat ECG in an attempt to document abnormal heart function.
9. The TAC disputed the fact that he suffers from the neurological condition known as autonomic dysfunction. It considered this had not been demonstrated sufficiently in specialised medical tests.[11]
10. For reasons I outline below, I do not consider it necessary to make any concluded findings as to whether Mr Paproth has this specific condition, as distinct from whether he experiences relevant symptoms.
11. Notably, the TAC submitted that there is no sufficient evidence that Mr Paproth's symptoms were caused by the transport accident.
12. This is the key point of difference between the parties in this case.
13. The TAC distinguished between an injury to Mr Paproth's spine - which was accepted (being the T7 end plate fracture) - as distinct from an injury to his spinal cord - which was denied.

1. In my view, the remaining matter in dispute can be distilled from the TAC's hearing submissions:[12]

Without an injury to the spinal cord there is no causal connection between any autonomic dysfunction or thermoregulation dysfunction symptoms and the transport accident.

The principal issue for determination is whether the transport accident caused an injury to the spinal cord at the thoracic level.

1. The parties agreed at the hearing that I would not make any direct assessment of the monetary value of the claims.
2. If Mr Paproth was to succeed in either claim, the TAC wanted the opportunity to consider the appropriate form of compensation.
3. Ultimately, for the reasons that follow, this will not be necessary.

1. The TAA establishes a regime for compensation for people injured in car accidents in Victoria.
2. Section 35 of the Act provides the relevant entitlement to compensation in the following terms:

35 Persons entitled to compensation

(1) A person who is injured as a result of a transport accident is entitled to compensation in accordance with this Act if -

(a) the accident occurred in Victoria...

[Tribunal emphasis added]

1. 'Injury' is defined broadly in s 3(1) as meaning physical or mental injury.
2. The claims procedure is provided in Part 4 of the TAA. Mr Paproth followed this procedure.
3. I have conducted an independent review of the TAC's decisions in these proceedings to arrive at the correct and preferable decision.

1. As I explained, the key issue in this case is whether I can be satisfied on the particular facts before me that Mr Paproth's symptoms were caused by the transport accident he was involved in.
2. There are a number of relevant case law principles to my analysis, including Rus v Transport Accident Commission[13] which summarises and confirms that:
   • the transport accident only needs to be a cause of the injury or symptoms, not necessarily the only cause;
   • neither party bears the burden of demonstrating this connection; the Tribunal is to make this independent enquiry on review of the material before it; and
   • the assessment is to be made on the basis of the balance of probabilities, in that it must be more likely than not that the accident was a cause of the symptoms.
3. There is no formal standard of proof for determining causation. In Rzanovski v Transport Accident Commission[14] the Tribunal considered:[15]

... the question now to be answered is whether the evidence before the Tribunal is such as to justify an inference of probable connection between the transport accident and the cardiac arrest.

1. In Sahin v Transport Accident Commission[16] the Tribunal observed:

That state of satisfaction may be reached where the evidence before the Tribunal is such as to justify an inference of a probable connection between the transport accident and the condition. Any inference must be based on facts established by admissible evidence. The process of reasoning must constitute a valid inference as distinct from speculation or guesswork. The totality of the evidence may be considered together in order to ascertain the weight of the evidence as a whole.

1. I have applied these broadly accepted principles to the facts before me in these proceedings.

1. Mr Paproth did not call any person to give expert evidence on his behalf at the hearing.
2. Instead, he relied on the numerous medical assessments that had been undertaken and recorded in reports in the Tribunal Book.[17]
3. Being a self-represented litigant, in his hearing presentation, there is some blurring between submissions and evidence.
4. In any event, Mr Paproth was sworn in at the hearing and to the extent he was giving evidence, it was tested through cross-examination and by questions from the Tribunal.
5. Mr Paproth described a series of symptoms starting with a burning pain in his upper thoracic spine, a blocked nose, then a runny nose, then sweating, vomiting (or reflux more recently), irregular blood pressure, then diarrhoea.
6. Mr Paproth gave evidence that he has experienced the following symptoms since the summer of 2015, which he attributes to the transport accident:
   • heart and blood pressure irregularities, including claimed atrial fibrillation in the heat;
   • an inability to regulate his body temperature in the heat or cold, including extensive sweating above the nipple line when dysregulated (especially in hot weather);
   • noxious stimulation and vomiting, diarrhoea, constipation and severe liver pain on occasion;
   • excessive urination;
   • orthostatic intolerance; and
   • restless leg.
7. He suggested that he has become more sensitive to his symptoms as time progressed.
8. He explained that these symptoms are significantly reducing his quality of life by requiring him to limit his time outside the home which consequently limits his access to fresh food and has generated marital and family pressure.
9. He claimed that his symptoms, including pain and restricted movement, have resulted in an inability to work and he now suffers from anxiety.
10. Mr Paproth explained that after the accident, he purchased a smaller home and paid approximately $70,000 for additional insulation to make it more liveable.
11. As to proof that the injury/symptoms resulted from the traffic accident, Mr Paproth referred me to the reports of Dr Victor Gordon, one of a number of consulting neurologists.
12. Mr Paproth considered that he had undertaken an MRI that showed traumatic oedema to his spinal cord.
13. However, he confirmed he was unable to locate an MRI earlier than 26 November 2014,[18] and subsequently confirmed through his GP that there had not been earlier MRI imaging undertaken.
14. Nevertheless, Mr Paproth was of the view there had been swelling or compression/distortion of his spinal cord (possibly not visible on imaging because of swelling) that had led to his claimed condition.
15. In general, he expressed the view that there may have been poor radiology reports (as he claimed to have experienced with diagnosis of his knee injury pre surgery) which did not reflect the 'severity of the car accident'.
16. He said he was told by his treating doctors that some nerves 'get better', but he would not experience a total recovery. He believed this was not unexpected because he claimed that one of his treating neurologists had told him the impact on his body was comparable to hitting a wall at 240km.
17. In response to cross examination, he explained that he had hit his head on the top right hand side and was told later that this was from impact with the side window of his utility vehicle.
18. Mr Paproth last saw Dr Gordon in 2022. He believed that Dr Gordon had changed his earlier advice and concluded that there was evidence of autonomic abnormality after reviewing ECG reports.
19. He provided an outline of the general chronology of his various treating specialists, particularly the neurologists. He considered that three specialists had said that he suffered from 'autonomic dyreflexia', (a condition characterised by a high blood pressure in individuals with spinal cord injuries above a certain level).
20. However, I note that in a letter from his consulting neurologist, Dr Victor Gordon, dated 23 May 2018, this very severe condition was expressly discounted. Instead, Dr Gordon considered he had 'more long term dysregulation of autonomic function'.[19]
21. I summarise key findings of Dr Gordon below when I outline the medical testing and reports contained within the Tribunal Book as relevant to the issues in dispute below.
22. Mr Paproth claimed to have undertaken additional testing including a thermography scan, and I directed him to provide copies of these reports to the Tribunal and TAC.
23. However, after further checking, Mr Paproth confirmed by email to the Tribunal and TAC that all recorded material in his possession has been provided to the Tribunal.

1. The TAC confirmed its position that it does not accept that Mr Paproth's symptoms amount to the neurological condition diagnosed as autonomic dysfunction.
2. But, even if they did amount to autonomic dysfunction, it does not accept that his symptoms i.e. the injury was related to the transport accident.
3. In its view, this would have required damage (i.e. an abnormality or injury) to Mr Paproth's spinal cord that the TAC claims has not been demonstrated by way of evidence.
4. On the latter, the TAC submitted that there was no radiological evidence or clinical findings sufficient to deduce any spinal cord injury.

1. The Tribunal Book contains extensive medical records following assessments of Mr Paproth since the accident.
2. I note that he self-presented to a medical clinic but was not admitted to hospital after the accident.
3. The first assessment was an X-ray of his chest and thoracic spine on 18 September 2014, with a CT scan of his thoracic spine on 18 September 2014.
4. These examinations observed 'spinal cord has a normal appearance as far as it could be seen' and confirmed a 'wedge compression fracture involving T7'. At that stage, the radiologists' reports also confirmed no paraspinal hematoma was seen, and there was 'no evidence of...neural compression'.[20]
5. The first MRI was undertaken on 26 November 2014 and confirmed the superior end plate fracture of T7. It explained that 'the more diffuse signal abnormality in the T7 vertebral body is likely to relate to post traumatic marrow odema. A focal underlying legion is not identified'.[21]
6. Mr Paproth was then referred to a spinal specialist, Mr Greg Etherington, to investigate his claimed exacerbation of back pain.
7. In summary, the evidence indicates that Mr Etherington noted that Mr Paproth complained of symptoms including constipation and sweating on the upper part of his body.
8. Mr Etherington concluded in a referral response dated 11 June 2015 that 'unfortunately I cannot explain either of these symptoms on the basis of imaging'.[22]
9. Mr Etherington also arranged a further MRI of Mr Paproth's thoracic spine on 17 June 2015 and concluded after further review with the patient that the MRI 'showed no significant cord compression and no cord signal changes'.[23] A subsequent review by Dr Etherington in November 2016 confirmed there was 'no significant canal intrusion'.[24]
10. Dr Etherington suggested Mr Paproth see a neurologist because 'interestingly, these symptoms [sweating etc] are similar to the sympathetic nervous system dysfunction commonly seen in quadriplegics'.[25]
11. Mr Paproth first stated seeing Dr Victor Chong, a neurologist in July 2015 who recorded Mr Paproth's observations including dizziness and sweating on his upper torso.
12. Dr Chong reported to Mr Paproth's solicitors in December 2015 that:[26]

I conveyed to Mr Paproth that there is no convincing clinical or laboratory evidence of autonomic dysfunction. The cause of Mr Paproth's dizziness and associated symptoms remain unclear.

1. Mr Paproth also attended the Melbourne Cardiovascular and Autonomic Clinic in October 2015. Its report concluded:[27]

His ABPM and autonomic function testing, which was also reviewed by Prof O'Callaghan, revealed some mildly reduced heart rate variability but otherwise no postural blood pressure drops, and autonomic function testing did not demonstrate any autonomic failure.

1. A subsequent report from that clinic reported 'no overt autonomic failure demonstrated on ABPM or autonomic function testing'.[28]
2. Associate Professor Chris O'Callaghan also consulted with Mr Paproth on a number of occasions and concluded that:[29]

He has numerous and unexplained symptoms, and they certainly have an autonomic flavour to them, but autonomic testing has not demonstrated a clear abnormality. That is not to say that he does not have a problem with the autonomic nervous system...

1. Mr Paproth sought medical advice from numerous specialists, and was seen by Dr Victor Gordon, a specialist autonomic neurologist from August 2016. His examination records included:[30]

On examination the autonomic reflex screen shows that he had oscillations on his blood pressure on standing but did not actually have a formal tachycardia or hypotension. General neurologic examination is non-contributory.

I think he probably does have some autonomic dysfunction on the basis of his partial spinal cord injury at the T4-T7 level. It is not a formal autonomic dysreflexia but rather an instability of autonomic function caudal to this level.

1. Dr Gordon summarised what I regard as the nub of the concern for Mr Paproth in a letter to his GP at the time, as follows:[32]

We are left with a difficult problem. In essence the summary of his symptoms is of a disorder of autonomic instability with a varied temperature both body temperature and environmental temperature sensitivity of his bowel function. In essence what he has is a thermal instability mostly manifest with gastrointestinal dysfunction.

1. Yet, a further MRI report in 2017 documented that 'cord signal remains normal throughout'.[33] Consequently, Dr Gordon advised that:[34]

In essence, I agree with the report that there is no convincing evidence of spinal cord injury. There is some disruption to the structure of the spine as noted in the T5-T8 levels. There is an area of cord contact at the T5-T6, although there is no signal change ... at that level.

In the end, I think the diagnostic formulation is that he does have spinal cord dysfunction at the level of the spine injury at T5-T8.

1. The most recent MRI was conducted on 29 January 2021.[35] The associated report recorded that the thoracic cord had a 'normal signal' and that:

At T5/T6, there is a small central disc protrusion, which causes mild cord compression.

At T6/T7, there is a small right paracentral disc protrusion, which abuts the cord.

At T7/T8, there is central to paracentral disc bulging, slightly more prominent to the right. This abuts the cord.

At T8/T9, there is a similar appearance.

At T11/T12, there is a disc bulge, with no neural compression.

1. Dr Gordon noted in his report dated 5 February 2021 that this MRI was done 'in the context of a fall with some increased back pain'.
2. He observed that he had not seen the [MRI scan] study himself but believed it showed some mild cord compression and paracental disc protrusion in the thoracic spine.
3. Separately from the doctors' reports, I raised an issue with the TAC at the hearing, seeking clarification of its current position in the proceedings in light of earlier (internal) reports of the TAC in 2016, 2017 and 2018[36] that recommend approval of at least parts of the claim, on the basis that the condition was directly related to the transport accident.
4. The first internal TAC review dated 27 October 2016 noted the applicant's symptoms, results of a somatosensory test suggestive of autonomic dysfunction and a mildly abnormal tilt test indicative of orthostatic intolerance. It concluded 'one can argue that he is more likely than not' to have sustained an autonomic dysfunction as a result of the accident.
5. At that stage, the internal review documents that the case manager was seeking additional medical opinion about the condition and how it was related to the accident.
6. The second internal TAC review dated 16 February 2017 reached a similar conclusion and recommendation to approve the use of Desmopressin, and noted 'consultant neurologist opinion is the increased urinary output relates to cord damage at T4-T7 level from the crush T7 fracture'.[37]
7. The third internal TAC review principally related to the reasonableness of funding other medication for Mr Paproth's ailments.
8. Mr Pinkstone responded that it is not the current position of the TAC that the symptoms were caused by the transport accident, having reviewed all the evidence and documentation.
9. He pointed out that the analysis had been undertaken internally within the TAC by consultants within the discipline of occupational medicine, not a neurological specialist.
10. Instead, the TAC relied on the independent evidence of Dr Waterston in forming its current position, who was advanced as a medico-legal expert and had directly consulted the applicant and conducted a detailed review of radiological testing.

1. Dr Waterston is an experienced neurologist with a 'strong general interest' in autonomic disorders.
2. He first saw Mr Paproth in 2016 to undertake an impairment assessment. He prepared a report dated 24 March 2016.[38]
3. He noted that his reflexes were normal, which weighed against a spinal cord injury.
4. At the hearing, he explained that crush fractures do not commonly cause neurological complications unless they involve the nerve roots as they come out of the spine.
5. He observed some apparent sensory loss from a vertebral level of T5 but formed the view this was a disturbance of function in the nervous system which did not follow anatomical pathways, which would be expected if the patient had a structural abnormality.
6. Dr Waterston recorded his review of two MRI scans (in November 2014 and January 2015) and concluded there was no evidence of any cord compression or cord signal abnormality (including a spinal cord lesion).
7. At the hearing, he confirmed that 'for [spinal] cord injuries causing autonomic dysfunction, the autonomic pathways are deep inside the cord and you'd expect to see MRI abnormalities in the acute stage and ... if there's a significant cord injury'.[39]
8. While Mr Paproth experienced tenderness over thoracic vertebrae T5-T7, Dr Waterston explained that this was not reflective of a neurological deficit; rather, in his view, this constituted spinal vertebral dysfunctional damage.
9. Dr Waterston was unable to document any evidence of autonomic instability resulting in postural dizziness from his consultations. He explained he would defer to cardiovascular opinion regarding the cause of any cardiovascular autonomic instability, and that the diagnosis may be clearer after autonomic function and tilt table testing.
10. Dr Waterston subsequently conducted an independent medical assessment and prepared an expert report dated 25 February 2021, with the benefit of additional test results and reports recorded therein.[40]
11. On review of the MRI scan from January 2021, he concluded:

I reviewed the latest MRI scan of the thoracic spine performed on 29 January 2021. Chronic mid thoracic vertebral body compression fractures were present with the most maximal wedging being at T7. There was a small disc protrusion at T5/6 which was causing some minor indentation in the cord but there was plenty of space around the cord posteriorly. There was no abnormal cord signal abnormality. There were a number of other minor disc protrusions.

1. He explained that in his view, there was no indication that the disc protrusion at T5/6 was causing any neurological dysfunction.
2. He opined that:[41]

While some of his symptoms have been suggestive of spinal cord involvement, he only has sensory symptoms and signs and the examination findings are incongruous with a definite spinal cord lesion. Because of the way the thoracic spinal never roots travel along the course of each rib, the sensory level that occurs in a thoracic cord lesion is higher posteriorly than it is anteriorly which is not the case here. There are no other motor signs to support any significant spinal cord damage and I do not think the imaging findings are severe enough to be responsible for spinal cord symptoms.

...

In my experience, patients with autonomic instability following spinal cord lesions usually have clear-cut signs of severe spinal cord damage which is not the case here. There has never been any definite objective evidence of spinal cord damage.

While I also could not exclude the possibility of underlying autonomic dysfunction and indeed I would not deny that many of his symptoms could be related to involvement of the autonomic nervous system, I cannot definitely attribute this to the injury that he sustained as a result of the motor vehicle accident in question. He remains significantly disabled by his ongoing symptoms.

1. At the hearing, Dr Waterston reiterated that he could not exclude the possibility that there 'may be a problem', but that 'it is not in the nervous system'.
2. He also explained that if the condition was attributable to structural damage (i.e. of the spinal cord), he would expect the symptoms to arise irrespective of weather or other conditions, which is clearly not the case as explained in evidence by Mr Paproth.
3. As to whether Mr Paproth's diabetes insipidus may have been caused by the transport accident (albeit of limited relevance to this claim, because a direct claim was made that was out of time and therefore, refused), Dr Waterston concluded:[42]

Post-traumatic diabetes insipidus is usually associated with severe traumatic brain injuries. Since there is no evidence to indicate that he had sustained any significant head injury, certainly any head injury that would be severe enough to cause pituitary damage, I would consider that the diagnosis of diabetes insipidus is also unrelated to the accident in question.

1. Dr Waterston reviewed additional documentation provided by the TAC and confirmed by letter dated 10 July 2023 that his previous opinion was unchanged.
2. Overall, Dr Waterston concluded there was no evidence on any investigations that would support a diagnosis of spinal cord injury. In his experience, he had only ever seen autonomic dysfunction in the setting of a spinal cord injury after severe spinal cord injuries, such as paraplegia or quadriplegia.

1. I accept the sworn evidence of Mr Paproth and recorded medical histories that he has and continues to experience various symptoms that are indicative of dysregulation of autonomic function.
2. Clinically, these symptoms may fall short of the condition diagnosed as 'autonomic dysfunction'.
3. I accept that there is no conclusive medical report confirming that Mr Paproth has been diagnosed with this condition following relevant testing, as highlighted by the TAC.
4. However, I find it is not necessary for Mr Paproth to satisfy the Tribunal that he suffers from the medical condition diagnosed as autonomic dysfunction in order to claim compensation.
5. The definition of 'injury' under the relevant legislation is broad. A collection of symptoms (or even one symptom) could potentially suffice, provided that there is a sufficient demonstrated connection to the transport accident.
6. In my opinion, the potential relevance of the condition diagnosed as 'autonomic dysfunction' in this case is that there appears to be medical agreement that, in the context of a transport accident, such a condition and its associated symptoms are potentially derived from a spinal cord injury.

1. I accept the evidence that Mr Paproth was in good health prior to the accident and had not experienced these symptoms prior.
2. It is clear that these symptoms affect Mr Paproth's day-to-day life and can be debilitating at times.
3. It also appears that Mr Paproth has no longer been able to return to his original trade following the transport accident for a number of reasons.
4. However, I am being asked to consider only two relatively confined claims for compensation in these proceedings.
5. In order to succeed in either claim under the relevant legislation, I must be satisfied that the health issues reported by the applicant were more likely than not related to the transport accident he was involved in.
6. I note that some panels convened by the TAC to formulate its internal position on the applications before it have (at least in part) accepted some causal connection between Mr Paproth's symptoms and the transport accident in synthesising medical tests and reports provided to it.
7. While these are important internal assessments formulated to influence the position taken by the authority at any point in time, in my view, they should be given less weight than the direct evidence of medical tests and reports of the applicant.
8. It also appears that the authors of the TAC internal reports did not consult with the patient and practise within specialties that are more general to transport injuries, rather than neurology which is pivotal to the evidence in this case.
9. I accept that the key issue in dispute relates to whether the transport accident resulted in damage to Mr Paproth's spinal cord, with the answer to this question being most directly related to the neurological speciality.
10. To this extent, I have given preference in these proceedings to the full content of neurological reports and their assessment of radiology, rather than the internal views of the TAC in 2016 and 2017.
11. The best available medical evidence in support of Mr Paproth's case are reports from Dr Gordon, his consulting neurologist.
12. Dr Gordon explained that:[43]

My impression was that he does have autonomic dysfunction on the basis of his partial spinal cord injury at the T4-T7 level. The nature of the autonomic dysfunction tends to be that of instability of autonomic function rather than a fixed deficit.

1. I have two concerns accepting this position.
2. First, it is relevant that this 'impression' that Mr Paproth has autonomic dysfunction was not offered as a concluded, objective view.
3. This aspect of his advice is incomplete since he does not provide any explanation for how he has arrived at his 'impression' of autonomic dysfunction on the basis of test results, which did not conclusively demonstrate this condition.
4. Ultimately, however, this aspect is not determinative because as I indicated, the fact that Mr Paproth experiences symptoms is not disputed.
5. I could still find that the accident was a cause of his symptoms i.e. injury if there was a sufficient connection demonstrated by evidence.
6. More significantly, however, I consider that there is no clear or cogent basis expressed in any of Dr Gordon's reports for his finding that Mr Paproth has 'a partial spinal cord injury at the T4 - T7 level' or how this had caused his symptoms.
7. In particular, there appears to be a lack of integration or reconciliation between the relevant results of imaging and Dr Gordon's recorded views.
8. It is not clear how Dr Gordon's finding derives from or aligns with what I accept as consistent imaging results throughout Mr Paproth's assessments (especially before his most recent fall) namely, evidence of a compression fracture in the spine but no clear evidence of spinal cord injury.
9. In late 2017 Dr Gordon himself '[agreed] with the [MRI] report that there is no convincing evidence of spinal cord injury'.
10. In a later report, Dr Gordon referred to 'imaging findings suggestive of trauma to the T6 to T8 level' but it is also unclear how he attributes any symptoms of autonomic dysfunction to this potential injury.
11. It is unclear whether Dr Gordon analysed the MRI scan itself, or just the MRI reports. For example, he notes in respect of the 2021 MRI scan that he reviewed the report only.
12. Even his observations of the most recent MRI report lack clarity and a clear path of reasoning.
13. On the one hand, Dr Gordon observed disruption to the structure of the spine and notes there is an area of cord contact but that there was no change in signal to the spinal cord. He then opined that Mr Paproth has spinal cord 'dysfunction' without explaining how this arises or could be sufficient to cause 'autonomic dysfunction' or relevant symptoms.
14. My caution in respect of Dr Gordon's unresolved opinions aligns with concerns expressed in evidence by Dr Waterston, that Dr Gordon did not appear to have cited any report of examination for evidence of spinal cord injury, therefore it was unclear on what basis he concluded there was an impression autonomic dysfunction on the basis of a spinal cord injury at the T4-T7 level.
15. For these reasons, I am unable to prefer Dr Gordon's opinion over the formed views of Dr Waterston which were tested at the hearing.
16. I provided an express opportunity to Mr Paproth to call expert evidence from Dr Gordon in an attempt to reconcile these deficiencies. However, Mr Paproth did not elect to call Dr Gordon to give evidence when given the opportunity.
17. I am left with real ambiguity about the connection between his tentative findings and the recorded observations of the patient.
18. There is no more persuasive evidence for Mr Paproth submitted in this proceeding.
19. Ultimately, even if I was to accept Mr Paproth's evidence and submissions at their highest, I am unable to find that there was any likely causal connection between the transport accident and his symptoms.
20. A causal connection cannot just be assumed in this case by a potential crossover in timing between the accident and the emergence of symptoms shortly thereafter.
21. A temporal connection of itself is not enough. Even an inference would need to be supported by relevant evidence.
22. Mr Paproth is not medically qualified to provide this opinion or analysis.
23. It is clear from the evidence of Dr Waterston that there may be functional or structural causes of autonomic dysfunction (and related symptoms). He explained that such symptoms are very commonly related to a disorder of function, as opposed to being related to structural pathology in the overall system.
24. In his opinion, the latter would be needed to demonstrate a causal connection between the transport accident and his symptoms, being dependent on spinal cord injury in this instance.
25. There are also other plausible causes of the symptoms that Mr Paproth experiences.
26. This leaves the Tribunal in the position where the most comprehensive and tested evidence is that of Dr Waterston.
27. Dr Waterston had the benefit of extensive medical imaging over a broad range of time, dating from 6 October 2014 to late 2022.
28. Having reviewed this imaging (not only the reports post-imaging), Dr Waterston did not detect any spinal cord abnormality, including contortion or any disturbance in the spinal cord signal.
29. I accept the evidence of Dr Waterston that he does not dispute that Mr Paproth has autonomic symptoms however, he could not find any evidence of spinal cord injury to explain those symptoms, and there are other causes of autonomic dysfunction apart from spinal cord injury.[44]
30. This is entirely consistent with the balance of evidence including the various clinical tests or analysis of radiological imaging that does not support any finding of spinal cord injury.
31. This was also consistent with Dr Waterston's observations during physical assessments.
32. Therefore, I am not satisfied on the basis of the evidence and submissions that it is more likely than not Mr Paproth suffered any injury to his spinal cord as a result of the transport accident.
33. Likewise, I accept submissions for the TAC that there is no other valid basis for me to infer a probable connection between the injury complained of and the transport accident.
34. I asked Dr Waterston whether there could be other ways that autonomic dysfunction may have been 'caused by' the transport accident.
35. He responded in general terms, post-traumatic stress or chronic pain may be factors leading to autonomic symptoms, so it is possible that there is a connection to the accident on the basis of these mechanisms, but not on the basis of a spinal cord injury.
36. It is noteworthy that there is a complete lack of evidence in this case relating to either of these potentially causative factors.
37. No examining specialist has expressed the view that these are likely to be a cause of Mr Paproth's symptoms.
38. There is no evidence that Mr Paproth suffered from a post-traumatic stress disorder (as medically diagnosed), nor that there is any evidence of a connection between the chronic pain he experienced (such as in the months immediately after the accident) and his symptoms of autonomic dysfunction.
39. Any inference of probable connection must be based on proven facts, not mere speculation.[45]
40. There is no basis on which I could reasonably infer Mr Paproth's symptoms are caused by the transport accident other than damage to his spinal cord.

1. I have applied the provisions of the TAA in this decision, which require careful assessment of whether it has been suitably demonstrated a person was injured as a result of a transport accident as a precondition for compensation.
2. For the reasons above, principally a lack of any demonstrated sufficient spinal cord injury, I am unable to find that the transport accident was a cause of Mr Paproth's symptoms of autonomic dysfunction or dysregulation.
3. The same finding extends to his need for medication to regulate urinary output.
4. Consequently, I am obliged to refuse both claims.

[1] Confirmed on medical imaging and not disputed by the TAC in this proceeding.

[2] He also advised that the TAC had separately agreed to pay for pain medication, anti-constipation medication and transport to some of his treating medical team.

[3] I understand that Mr Paproth also submitted a separate claim for compensation to the TAC in connection with his diabetes insipidus (potentially in connection with a claimed head injury as a result of the accident), but that this claim was rejected as out of time.

[4] The application as originally lodged referred to a purported denial by the TAC of 'sci injury' being 'related to the car accident'. This pertains to a review of TAC claim No. 14/05506 in which the TAC revoked its decision of 20 February 2017 to pay for a medication, Desmopressin. The TAC's reasons are dated 10 January 2018.

[5] Relating to TAC claim No. 14/05506, with reasons dated 18 June 2021.

[6] It appears that, for a period of time, the TAC accepted this claim but ceased payments for this medication on 20 February 2017.

[7] References to the Tribunal Book in these reasons is to the Joint Consolidated Tribunal Book as at 18 January 2025 of 1005 pages in the PDF version, referred to as 'TB' with the corresponding page number. Given a lack of certainty about whether this included all relevant documents previously filed with the Tribunal, the TAC lodged a Supplementary Tribunal Book following the hearing on 6 March 2025, referred to as 'STB' with the corresponding page number.

[8] By order dated 21 February 2025 with reasons.

[9] Transcript of hearing, page 90 at [9-21].

[10] Although it is unclear whether it accepted that there is any evidence of any relevant heart condition. The TAC also accepted he suffers from diabetes insipidus but explained that an earlier claim for relevant treatment from the TAC for this condition was refused.

[11] Including those conducted on or around 9 October 2015, 9 June 2016 and 8 August 2016.

[13] [2021] VCAT 70.

[14] [2005] VCAT 652.

[16] [2018] VCAT 1418, at [25].

[17] I requested clarification from the TAC as to how the various joint Tribunal Books filed with the Tribunal in these proceedings over the years were to be reconciled. This was provided and I am satisfied that I now have all relevant documentation before me at the time of making my decision.

[29] In his letter 9 March 2018 at TB 516.

[37] It appears this was a reference to a report from Dr Gordon dated 29 August 2016.

[39] Transcript of hearing p86 at [22-26].

[44] Transcript of hearing, page 88 at [19-25].

[45] Sahin v Transport Accident Commission [2018] VCAT 1418 at [25].