Spinal_Cord

Spinal Cord Injury

Mr. AA (Photo below) was involved in a head-on collision on 16/12/1999, aged 32, in which his brother died and his wife sustained multiple fractures. He sustained an unstable fracture of L1 – L2 vertebrae, and a spinal cord injury (SCI) - an American Spinal Injury Association Level B injury (ASIA B) (Appendix_1, [High-Resolution] discussed below). Of importance is the fact that he sustained a high velocity injury, which would cause a disruption of the spinal cord anatomically. The unstable vertebrae were stabilised surgically on 29/12/1999. A colleague, Dr BB, was requested by a friend of the patient to treat him homoeopathically. She in turn requested my guidance on treating a patient with a spinal cord injury, since I have previously treated a total of four patients with spinal cord dysfunction. She furthermore informed me that the assistant surgeon who operated on the patient told her that the patient’s spinal cord was badly injured.

I advised her to treat him with Hypericum 1M 1 2 3 three times daily till he was fully functional. She was only able to commence administering the Hypericum three weeks after the injury on 05/01/2000. His hospital records confirm that he had power 0 in his lower limbs, from L2 distally. One week later, on 12/01/2000, a doctor entered a note in his file (Appendix 1): “Toes are now moving bilat!!” He therefore recovered power from L2 to L5 within one week. He walked with a frame by 03/02/2000, and was fully functional by 02/03/2000, 8 weeks after commencing Hypericum, as confirmed in Appendix_2 [High-Resolution] the physiotherapist report. The photo was taken in 2007 which depicts him standing independently. Appendices 1-2 are documents from his hospital file.

Appendix 1:

Kindly note that the date 7/12 should be 17/12, or 17/12/1999. The notes were written by one of the Consultants. I transcribe it as follows:

MVA

δ paraplegic

Sensation intact lower limbs

Power grade 0

Anal ?????? tone ± (Anal sphincter tone ±)

Perianal sensation intact

Incomplete cord injury

At the bottom of the page dated 12/01/00 are the following notes: “Toes are now moving bilat!!”

Mr. AA

The Consortium for Spinal Cord Medicine PDF provides details of the dire outcomes of SCI patients. Hurlbert and Tator discuss the ongoing lack of effective treatments to reverse most injuries. Ditunno presents on slides 47 – 50 one example of a ‘miraculous’ recovery of a young quadriplegic athlete, who recovered the ability to run in 6 months time. Ditunno naturally questions this "miraculous" recovery which defies established outcomes.

Hurlbert says:

"The devastating consequences of traumatic spinal cord injury (SCI) continue to haunt the corridors of medical science now into the 21st century. Few conditions cause such degree of permanent disability in previously high functioning individuals who after injury remain fully cognitive and become faced with the Herculean challenges of reintegration into society. Whether it is by walking, riding, jumping, or flying, it is the individual engaged in enjoying life that most frequently becomes afflicted by this tragic condition in the span of a heartbeat or two."

"The consequences of SCI are as permanent as they are sudden and devastating. Despite a rich tradition of medical successes in the last 100 years spanning the discovery of insulin to gene splicing technology, the progress in the treatment of acute SCI has been painstakingly slow."

Tator says:

"The field of spinal cord injury (SCI) is remarkable for the high number of treatment trials in humans. Unfortunately, none has produced a major improvement in neurological recovery or a meaningful increase in function, although much effort and resources have been expended. The high level of trial activity in this relatively small field, which encompasses only 11,000 new cases annually in North America , is likely related to the large personal and societal costs of these injuries with respect to loss of function and financial costs, and the fact that previous trials have not led to a breakthrough. Scientists are attracted to this field because of the high clinical need and the lack of effective therapy."

Nevertheless, I have approached academic colleagues for evaluation of my results, or to propose a clinical trial. Professor Glasziou et al wrote an article on dramatic clinical effects, as such I submitted 2 patients' cases to him, to which he responded as follows:

Dear Dr Jeggels,

Thanks for these interesting cases. Unfortunately they don't fit the type that we describe in the BMJ article.

In general we need a long period *before* treatment with no change in health state, then a treatment and a rapid change.

In your examples, the pre-treatment period is short and the change after treatment takes some time.

The only other way if could fit is if someone had a hundred or so similar cases to the 2 you describe who could act as a comparison,

Best wishes,
Paul Glasziou

I therefore submitted a research proposal for a phase 3 randomised controlled trial employing Hypericum as per the above patient to Professor Dunn in Cape Town. He refused categorically to be involved in the trial. He stated the following in his first letter to me on the 22nd April 2010, from which I removed non-relevant aspects:

Dear Dr Jeggels

I appreciate your enthusiasm and have had a quick look at the proposal.

I have serious doubts about the causal relationship between St Johns wart and neurological improvement.

We also accept that ASIA B has the ability to recover with time.

I doubt any ethics committee would approve such a study.

Regards

RD

Prof Dunn also insisted that I must resort to basic animal studies before anything else. I was very surprised and disturbed at his belief (not evidence) that ASIA B has "the ability to recover" when compared to other authors (see the Guidelines below). The manner in which he states his conviction suggests that the ability of ASIA B patients "to recover" is the norm - all such patients recover to an identical degree. However, within less than two weeks the "evidence" for his generalisation was revealed. Prof Dunn et al had an article published on rugby related spinal cord injuries at the end of April 2010 in the South African Medical Journal. In this article they record that 2 out of 3 ASIA B patients recovered to E. These findings thus form the basis for Prof Dunn's conviction that "ASIA B has the ability to recover with time". The following is from this article:

"The ASIA admission neurological status is depicted on the vertical axis of the table and the outcomes distributed over the horizontal axis (Table IV). Complete motor and sensory loss is A, residual sensation is B, power less than 3/5 in at least 50% of distal muscle groups is C, power greater than 3/5 in at least 50% of distal muscle groups is D, and E is normal. Accordingly, 8 patients presented as complete; none of these improved, and this group included the 2 who died. Strikingly, two of the Bs (i.e. sensory preservation) improved to normal. All the C and D patients improved by one grade."

"Accordingly, 14 catastrophic injuries (ASIA A - C) occurred; of these patients 2 died, and 2 improved to normal and 3 to near-normal status. At follow-up there were 7 surviving players with residual catastrophic neurological deficit. The more severe neurological injuries did not correlate with injury type or age; they had relatively rapid access to definitive care with an average delay of 7.8 (3 - 12±2.7) hours."

Prof Dunn does not provide exact details of the severity of the each patient's injuries in order to make scientific analyses and conclusions on the relationship between the severity of the injuries and the spontaneous recovery thereof, even if he may claim that his cohort was not part of a formal study. Nevertheless, the "Guidelines for the conduct of clinical trials for spinal cord injury (SCI) as developed by the ICCP Panel: Clinical trial inclusion/exclusion criteria and ethics" clearly state the following:

Abstract: Page 222

This is the third of four papers. It examines inclusion and exclusion criteria that can influence the design and analysis of clinical trials in SCI, together with confounding variables and ethical considerations. Inclusion and exclusion criteria for clinical trials should consider several factors. Among these are (1) the enrolment of subjects at appropriate stages after SCI, where there is supporting data from animal models or previous human studies; (2) the severity, level, type, or size of the cord injury, which can influence spontaneous recovery rate and likelihood that an experimental treatment will clinically benefit the subject; etc.

Lesion anatomy considerations: Page 225
Modern imaging techniques provide the opportunity to characterize lesions at the time of treatment to support subsequent outcome analysis in the trial. Thin-plane sagittal and axial MRI imaging through a lesion site can provide data regarding lesion location, size, associated oedema, parenchymal sparing, and the extent of hemorrhage. A possibility exists to stratify analysis by the nature of the lesion on MRI. Such analyses could enhance matching of enrolled subjects into treatment and control groups, supporting exploratory effect analyses in Phase 1 and 2 trials.

In the light of the above:

Prof Dunn unfortunately does not provide categorical evidence as specified by the "Guidelines", which negates scientific analyses and comparisons especially between the ASIA B patients. Since 2 of his ASIA B patients returned to E, while one remained a C, there must have existed different degrees of severity of the injuries between the three patients, which played a very crucial role in their spontaneous recovery. He is correct to state that "This potential recovery from complete injury is thought to be even more likely in low-velocity rugby injuries, where the cord is compressed rather than disrupted anatomically." Thus, his ASIA B patients did not suffer from severe trauma. But, he also says that "The more severe neurological injuries did not correlate with injury type or age; they had relatively rapid access to definitive care with an average delay of 7.8 (3 - 12±2.7) hours." He terms ASIA A, B and C "catastrophic" injuries, but is unable to correlate injury type to them. Thus his conclusions on the basis of his data is irretrievably unsatisfactory and unscientific, especially since he rejects the outcomes of my patient who suffered from a high velocity injury. In concluding this part, the question to be answered is what the spontaneous recovery of an ASIA B patient truly is.

On the basis of the above information, his theory that "ASIA B recovers with time", is unconfirmed and unscientific due to the following. Recall from the philosophy of science that a theory which states that "all swans are white" will be valid until one black swan is seen, which invalidates the theory. Thus, from among 3 ASIA B patients of Prof Dunn, 2 returned to E, while one remained a C. His theory is therefore proven wrong scientifically.
It is important to note that the “ability to recover”, which Prof Dunn refers to within the context of SCI, points to the spontaneous non-therapeutic and natural ability of a patient to recover - namely, vis medicatrix naturae.
However, what is the spontaneous innate healing ability of an ASIA B motor-complete patient to recover, and to what extent? The Guidelines state that “Almost all people with SCI show some recovery of motor function below the initial ASIA injury level.” But, “spontaneous recovery of motor function in people with motor-complete SCI is fairly limited and predictable” and that some studies show “…recovery in some zero-rated muscles, but only if they were one segment below the zone of partial preservation (ZPP). Recovery two segments below the most caudal segment of the ZPP rarely occurs.” According to the authors of the "Guidelines", Mr. AA’s results are much, much better than that documented for spontaneous recovery of patients with an ASIA B, motor-complete patients. Mr. AA recovered 4 dermatome levels within one week, and was fully functional within 8 weeks. The "Guidelines", as well as Hurlbert and Tator thus refute Prof Dunn's wrong belief that what happened to Mr. AA happens to all such patients - such patients rarely ever have the spontaneous ability to recover to the extent to which Mr. AA recovered!

Prof Dunn and his colleagues world-wide rely on vis medicatrix naturae. Besides the laudable emergency care, surgical interventions and nursing care, etc, they have no effective therapy to reverse the injuries. They therefore wait on nature, or a miracle, to heal where possible the patients' injuries.

When analysed by the philosophy of science, their science and methodology have no "positive heuristics" - they do not solve the medical therapeutic technology problem of SCI.
When analysed by the philosophy of medicine, there is not a right and good healing of a unique individual.
Their practice in the light of the above is immature, "inauthentic, and a lie."

Prof Dunn blunders scientifically by concluding that “I have serious doubts about the causal relationship between St Johns wart and neurological improvement.”

Firstly, he carelessly misspells St Johns Wort as “St Johns wart”.

Secondly, he confuses St Johns Wort with Hypericum. Hypericum is the therapy made from the plant called St Johns Wort through a specific pharmaceutical process. Hypericum is not the herbal therapy St Johns Wort which has been used widely for entirely different indications.

Thirdly, he expresses “serious doubts” about two therapies concerning which he has no knowledge, therapeutic experience or documented worthy outcomes (human competence – see Thomas Gilbert in the Poster's Article). He furthermore does not refute my findings via a demonstration, or at least offer scientific counter-arguments! His statement is mere rhetoric.

Prof Dunn's uncritical adherence to his system places him amongst those concerning whom Imre Lakatos says the following:

"Indeed, the hallmark of scientific behaviour is a certain scepticism even towards one's most cherished theories. Blind commitment to a theory is not an intellectual virtue: it is an intellectual crime."

Prof Dunn’s last sentence is: "I doubt any ethics committee would approve such a study"

Though he may judge scientific matters within his jurisdiction, his judgment has been analysed as flawed and unscientific. This last statement of his implies however that ethics committees would also reject my proposal on its scientific validity. This brings us to the question which Horrobin and Bruce Charlton has raised, namely whether ethics committees were sanctioned to judge the validity of science or to prevent danger and harm from befalling trial patients?

Ethics committees came into being after the Thalidomide disaster. Considering their activities spanning many years, Charlton recalls Horrobin's conclusion that ethics committees as well as peer review stifle innovation and progress in medicine. Charlton therefore wrote that:

"In other words, ethical committees are acting as another layer of peer review of the scientific validity of research, as well as the ethical legitimacy of the project. There are two problems with this. Firstly, that an ethical committee has no right to referee the scientific value of a research project – they were set up to prevent egregious abuse, not to control science. And secondly that these ethical committees are incompetent to referee scientific projects – even if they did have a mandate to do so – since they have neither the time nor the expertise to do a good job. Anecdotal evidence suggests, unsurprisingly, that ethical committees do a very bad job indeed as scientific referees – and they should not be doing the job at all."

Finally, I have approached Prof Tuszynski from the University of California San Diego, however, after many months waiting on an indication what he may or may not do, I decided to throw in the towel.

Conclusions:

I conclude that the patient, Mr. AA, have recovered dramatically from a severe high velocity injury to the spinal cord when analysed with reference to the "Guidelines".