The Leatt-Brace is promoted to protect the motorcyclist’s cervical vertebral column. However, this device may produce “dangers” of its own. Of course, a device cannot be considered “dangerous”: it is motorcycling which is dangerous. However this device could convert relatively innocuous or survivable injuries into injuries with greater morbidity and death.

Although claims are made that injuries to the vertebral column will be reduced if the Leatt-Brace is used, there is no possible way of substantiating this claim. Controlled trials are simply not possible. The tumult of a motorcycle accident and the multiple variables cannot be replicated.  It is certainly not possible to re- visit those injuries and introduce categories as controlled trials.

Motorcycle accidents on the road are difficult to reconstruct.  Race-track injuries are well documented, but these are usually slither-tumble injuries. On the modern race tracks the impact against stationary objects is relatively infrequent. Rarely do these become projection or impact injuries and occasionally “ride-over” injuries.

Motorcycle accidents on the road, however, are more likely to be collisions resulting in impact and projection injuries. Even in a slither event, the rider on the road often hits stationary or moving objects.

Therefore this claim remains a supposition, which is based on rather primitive, linear reasoning which is:

The neck is potentially vulnerable in that it is not protected by a strongl mechanical sheath, the way that the lumbar, thoracic, and intra-cerebral spinal cord is protected. Let us then put a mimicing brace about it, and so “protect” it.

Wish it were that easy.

This linear reasoning appears not to have fully comprehended the functional anatomy of the mechanisms of the cervical vertebral column, which makes it invalid.

If my head is fully protected by a helmet, is it not logical to extend that protection to my neck?

Firstly one must ask what protection the helmet offers.

There can be no debate that the crash-helmet reduces head injury and death in motorcyclists, a worthwhile but not universal protection.

The helmet prevents many penetrating, abrasive and direct contact facial injuries But it offers little protection against rotational injuries (which produced diffuse axonal and brainstem lesions) and may increase these injuries by its inertia if body rotation decreases rapidly.

The helmet reduces deceleration injuries to some extent but concussive and contra-coup injuries will be reduced only by a margin when deceleration is from speeds of excess of 50 km an hour.

Direct blows on the top of the head (axial compression injuries) are a common cause of spinal injuries. These might be increased in some circumstances by the weight of the helmet

The Leatt-Brace will not prevent axial compression injuries and could promote or worsen that injury, because it interferes with evasive actions

There is some evidence that helmets reduce injuries to the cervical vertebral column, but this is poorly documented and the types of spinal injury which are reduced by the use of a protective headgear are not well analysed.

How do we protect ourselves from external forces?

Humans, like most other mammals, have exceedingly good “energy dissipating devices”. What this means is that there are highly sophisticated neuromuscular circuits which are designed to protect the individual from that universal enemy, the force of gravity. It is therefore possible for the human to fall, sometimes heavily, and sustain little or no damage. This is well illustrated in contact sports, notably rugby and professional wrestling.  The sophistication of the martial arts have allowed specific techniques of energy dissipation to be trained into participants early in their martial arts career.

In American and rugby football, energy dissipation or “break fall” is not usually trained: Instead the players rely on intuitive and inherent capacities to protect themselves from injury when their balance is perturbed. Some fondly imaginings this is a “conscious” mechanism: it is not. It is not possible in the time available to rationalise which strategies should be employed. With very few exceptions, there is no time to anticipate the vectors of destructive forces. Humans survive by the blessings of  “hardwired” and intuitive mechanisms [1]

That these mechanisms of energy dissipation exist is easily demonstrated. Most individuals could jump from a table to the floor and suffer no injury. There would be no outward expression of the kinetic forces, such as loud sounds, generation of heat or light or  damage. On the other hand, if a 75 kg facsimile of that individual in granite was pushed from the table the forces of falling would convert to  sound, heat, light and damage. Another example: Robots can do much, even mimic running. But robots do not have the energy dissipating mechanisms of humans. A robot on a rugby field would not survive the first tackle or even, perhaps, the first nudge, without damage.

How is this done?

The human frame, in its vertical axis is designed as a complex zigzag from the toes to the skull. Each of the angles of these zigzags is controlled by muscle allowing these zigzags to be compressed, concertina-like. During this compression, muscles response near instantly by tensioning, and by using their inherent energy allow the external energy to be slowly and safely dissipated.

Rotational movements are also used to dissipate energy, and allow the limbs to flex, reducing their lever-arm length, or tucking the limbs beside or behind the trunk.

There seem to be priorities in the methods of protecting the body. The head brain and eyes seem to have a priority re. protection. The hands and mouth are next in this triage and the feet follow.

Why a high head and a thin neck?

It is no coincidence that the head is placed high on the body. Better surveillance is an obvious benefit. Perhaps more important, by its height the brain high is maximally protected from injury. Whilst accepting that the phrasing which I use is teleological, the “purpose” of the mobile and relatively thin neck is that it allows the head a great freedom of movement and consequently the maximum capacity to protect the brain from jarring or other forces (including rotation) which could damage the enclosed brain. It is well-recognised how, when people fall, the head is “lifted” away from a potential point of contact with alacrity.

Now that is considering the tumult such as occurs in motorcycle accidents. This freedom to move the head will likely be the critical component to the broader “energy dissipating mechanisms” and its contribution to protecting the head from impact.

Where the body thrown towards an impacting surface, even a few centimeters of intuitive movement of the head away from the potential point of impact (perhaps transferring impact to the shoulder or the upper limbs) could prevent severe injury to the head. If this flexibility is lost and the ability to move the head is prevented (as it would be with the Leatt-Brace) that latitude is lost.  . Even distances of one or 2 cm might be critical in preventing severe brain damage. Immobilisation by a neck brace might therefor result in severe injury

Whilst the Leatt-Brace could protect the neck from flexion injuries, by imposing immobility it is equally likely to make damage to the brain more common and more serious than any neck injury would have been.

Other functions of the head.

Inasmuch as movement of the head plays an important role in protecting the brain, the head also plays a vital role in the overall posture of movement, particularly movement during falling. The head weighs the equivalent of two bricks and functions as a counterbalance. The capacity to move the head rapidly and induce “coupling” dynamics in the physics of equilibrium is immensely important. If the head is restrained, for example by the Leatt- Brace, it becomes impossible to posture the body in space. This use of the head as a counter balance is well illustrated by springboard divers  to control backwards and forward somersaults. Without a free range of neck movement it would be impossible for the diver to obtain a posture safe for entry into water, or the gymnast to land on a surface. Try jumping from a step wearing a Leatt-Brace! Make sure that it is not more than a step, since jumping from a height of even half a meter, wearing the Leatt-Brace, could produce a sever injury including a fracture of the base of the skull.

I am not aware that this concept is discussed in standard textbooks of medicine, and for most medically and biologically trained people this is not considered.

Is the neck especially vulnerable?

The cervical vertebral column could be mistakenly considered a “vulnerable” area region. This might be because spinal cord injuries invoke highly emotive responses because they are potentially so incapacitating and incurable. However, taken overall injuries to the cervical vertebral column are less common than injuries to the brain. There are also specific situations where the vertebral column is at higher risk One is the diving into shallow water which has produced this devastating injury many thousands of times. The reason is that the diver does not expect to strike the head, and none of the “head / neck protection” mechanisms are recruited. Injuries to this vital part of the vertebral column also occur in road traffic accidents generally. These are far less specific and the victims range from pedestrians through to individuals who have survived motor vehicle accidents, and finding themselves inverted and held by seatbelts, then suffer catastrophic injury when a “helpful” individual releases the seatbelt: the victim then falls onto the (inverted) roof of the vehicle, and suffers cervical spinal cord injury.

How can we find out more?

Because it is so difficult to get sufficient information from road traffic accidents a possible model could be rodeo injuries, which are well documented. A number of rodeo injuries are caused by falls from height, such as would happen to a projected motorcyclist after hitting a stationary object.

In order to illustrate the effects on the neck of these types of falls, illustrations of Gauchos can be used to analyse the mechanics of the injury. Even more important is the analysis of the fail safe mechanisms which are spontaneously recruited by the rider. It is improbable that any rodeo rider would allow himself to be restricted by a Leatt-Brace – and it would be highly unethical to even suggest this.

Is there a way to protect this vulnerability of the cervical vertebral column, and perhaps the brain as well? This seems possible and the author has researched this in much detail. That research has included a detailed investigation into the (complex) locus of movement and angular velocities of the

Gaucho falls5

1. “Bunionectomy”.
This is a brutal procedure which simply chisels off the metatarsal condyle – damaging perfectly normal bone and ultimately destroying  (almost always) perfectly normal joints.
Conceptually it is flawed, as it ignores the underlying causes.
Technically this is the crudest of surgery, often damaging or destroying the digital nerve, with the risk of a neuroma and permanent pain
It is irrational in that the very structures which keep the great toe from deviating towards the lesser toes are destroyed. The metatarso-phalangeal join is, in the long term, doomed by this procedure (see page Is “conventional” forefoot surgery proven as beneficial?)
Not surprisingly the long term outlook is poor and recurrence of problems inevitable.

2. “Metatarsal Osteotomy”. Many grandiose names are given to the variants such as Chevron, Akin, Scarf and many more, the titles implicating that these are scientifically established as valid treatment. What success there is, in the short term, is primarily by producing a cosmetic approval, plus the illusion the “what looks normal will function normally”. Again it ignores the underlying cause.

What studies which have been done have measured  the short term results (see “Noxious Placebos”), and this  academic poverty is conceded by the Cochrane reviews.
Again the long term outlook is poor, also resulting in destruction of the joint at the base of the great toe.
This causes pain, often incapacitating, in the last decade of life – the very period n when the patient is so dependent upon their feet for independence, and when maximum painless balance and stability are necessary to prevent falls.

The illustration below shows a typical long-term outcome. This woman had metatarsal osteotomies, “bunionettes” removed and arthrodesis of the toes. Each of these procedures produced progressive destructive changes in different parts of the foot. Far from protecting the joints, these joints became the victims of these procedures (see The Hallux Paradox)

It might be thought that she had in parallel a destructive arthropathy which produced these changes, independent of the osteotomy. This is not the case. None has ever been identified during careful monitoring, including that by her general practitioner husband. The result is that normal joints have been relentlessly destroyed as an effect of metatarsal osteotomies.

See this popular site:
Patient.co.uk http://www.patient.co.uk/doctor/Hallux-Valgus.htm from which is extracted the text below. Much of the text should be regarded with skepticism, some is diametrically wrong. Some is merely loose speculation, such as:
“Displacement of the joint gives the tendons mechanical advantage and this displaces the joint further. As this occurs, tension is created on the medial aspect of the joint (with compression laterally). Medial tension causes ligaments to pull and cause the bone to proliferate on the dorsomedial aspect of the first metatarsal head. Lateral tension causes the sesamoid apparatus to stick in a dislocated position laterally.”
“Prognosis (for bunion surgery). The outlook is highly variable, as is that of the patients who are treated. Hence there is a shortage of adequate trials to compare the outcomes of the various forms of treatment. A Cochrane review found very little good evidence on which to assess either conservative or operative treatments.9”
Cochrane Database Syst Rev. 2004;(1):CD000964.

He is registered in many countries, and has worked in all five continents. He is a professor of Orthopaedic Surgery, and has worked as a teaching hospital consultant with experience of the National Health Services of the United Kingdom, Canada, New Zealand and others. He has extensive experience in many underdeveloped countries, and has worked in military, public and private practice.

He has had a particular interest in surgery of the foot and extensive experience in the management of vertebral pain and the entrapment neuropathies.

It causes difficulty in making the finger “flat” with the hand, and the passively flexed distal phalanx catches whilst tucking sheets or reaching into a pocket. Catching a ball difficult and it is regarded as an important aesthetic loss in a woman. Because adaptive strategies are difficult it may merit surgical correction.

Conventional management is not always simple or effective.
In addition the “scientific” documentation of this injury is often poor,  illustrating an incomplete understanding of the surgical biology.

Below are extracts from the most frequently consulted web sites.

WIKIPEDIA: http://en.wikipedia.org/wiki/Mallet_finger
It results from hyper-flexion of the extensor digitorum tendon (1), and usually occurs when a ball (such as a softball, basketball, or volleyball), while being caught, hits an outstretched finger and jams it – creating a ruptured or stretched (2) extensor digitorum tendon.
The splint allows the tendon to return to normal length (3), if the finger is bent during these weeks the healing process must start all over again. Surgery is used to reattach the tendon and is usually performed within a week of the injury
It should be determined via radiograph if the Extensor Digitorum tendon has avulsed from the phalange, which will require surgical intervention to reattach the tendon and should be done within 10 days of the injury. Surgical treatment is used when the mallet finger presents as an open injury or if the bony mallet involves more than 30% of the articular surface of the joint. If passive extension cannot be achieved, surgery will put the finger in a neutral position and drill a wire through the DIP to the PIP, forcing immobilization and eliminating patient compliance for re-injury(4).
There are errors here:
1. Not so. It is hyper-flexion of the distal inter-phalangeal joint. The extensor tendon cannot hyper-flex.
2. Incorrect. Breakage (rupture) occurs. The tendon cannot “stretch”.
3. Fanciful. The tendon is unlikely to return to “normal length”, because the natural tendency of muscle is to retract the tendon. No splint provides the forces essential to pull the tendon back distally and so draw the tendon ends anatomically together.
4. It is assumed that the author means ”non-compliance which will perpetuate the injury or increase the deformity”

AMERICAN ACADEMY OF ORTHOPEDIC SURGEONS:

http://orthoinfo.aaos.org/topic.cfm?topic=A00018

AMERICAN SOCIETY FOR SURGERY OF THE HAND  has good illustrations and valid comments: http://www.eatonhand.com/hw/hw015.htm
How Successful is the Treatment?

Although this may seem like a trivial or simple injury, a cosmetically perfect correction is not likely with any form of treatment. However, with proper therapy and effort on the part of the patient, this problem can usually be improved to a tolerable level most – that is, the end joint of the finger may not fully straighten, but it will work well enough to be used for normal activities.
• Unless the injury is due to a cut on the back of the finger or there is some other associated problem, many hand surgeons believe that the final outcome and complication rate are at least as good with splinting alone compared to surgical repair. This may change as new techniques are developed to improve the results of surgery.
• Surgery is a reasonable consideration if the finger remains unacceptably bent after a full trial of splinting or if splinting is not possible – for example, if a skin reaction develops beneath the splint. Surgery is only considered if the outcome of surgery is expected to be better than the outcome of treatment without surgery.
What Happens if you have no treatment?

• Without any treatment, the appearance and ability to straighten the end joint of the finger will not improve. Additionally, if the injury is less than a month old, the problem may be worsened by using the finger without a protective splint of some sort.
• If the injury is more than three months old and has not been treated, it is unlikely that it will get better or worse on its own. Injuries more than three months old are not likely to be improved with anything short of surgery.

My Summary.
Conventional, non-intrusive management of mallet finger by splinting will not correct deformities (but might prevent worsening).

If the deformity is minimal, or otherwise acceptable, non interference is the way to go. However, if leaving the finger “as is” is not acceptable, then surgical treatment is frequently attempted:

Surgical treatment, as currently practiced,  falls into two types,
1. Attempts at repair. This has been attempted by suturing with wire and other materials where there is no fragment of bone attached to the tendon. If there is a fragment of bone then attempts to fix the fragment (by screws or wire) are usual. However the tiny fragment of bone often splits and surgical failure is common. Whilst this repair is healing the position of the finger must be retained (immobilized) by :
• Splinting for several weeks, or
• Pushing a steel pin through the fingertip, then down the marrow cavity of the finger bones. This causes an awkward projection of the pin which has to be kept dry and requires repeated bandaging for several weeks. This penetration of the fingertip can cause small portions of the skin to become “implanted” more deeply with a painful pseudo-tumor resulting. Infection is not rare
2. “Fusion” of the joint leaving it permanently stiff. This prevents some fine movements (such as playing some musical instruments), and leaving the hand as a whole marginally weaker. Fusion also requires immobilization, as above, for several weeks.

Surely there has to be a more certain, safer and quicker solution? A description of my long established technique for managing mallet finger is available in the Store.

The benefits of this technique are that predictable and accurate results can be obtained, and the procedure can be performed electively long after the injury.

Mallet Finger Surgical Technique

Correction of mallet finger, with consistent reliability and low complication rate.

Price: $25

My mother is 66 yrs old and she had a slip and fall and year ago. The bone between her elbow and shoulder was broken and she was operated twice. The first doctor put the rod and plates with screws but that tend to reduce the nerve movement in her wrist and had to be operated the 2nd time. The 2nd doctor removed the plates and screws and did a bone grafting (taking out bone from the waist). Everything went fine but out of 4 support bones (sorry don’t know much about this), one did not join fine and she cannot function fully due to that. We took advice from multiple doctors and there are 2 suggestions: Either go fo another bone grafting or fit a plate. We are confused and we do not want multiple surgeries. Any piece of suggestion or advice is appreciated. I can send her x-rays and other medical repots on email if that would help in any way.

You do not say whether the bone graft was at the upper or lower end of the bone (there are two residual breaks apparent)

A problem currently is that the bone ends are being held apart by the intermedullary rod, and the screws above and below. The lower screw is surrounded by a “lucency” which could be an indicator of infection.

My approach would be to take out both sets of screws (top and bottom). The bone will shorten slightly, which at this stage is irrelevant. The rod should be left in to provide the necessary splinting.

It might be that as the ends of the bones get close to one another, the bone will unite spontaneously. On the other hand, even without uniting, your mother might be, and function, fine with the intermedullary nail as a splint.

The problem with bone grafting now is that there is potential infection. Also, the radial nerve is close to the fracture site, and there is likely to be significant scar obscuring the anatomy and making the procedure more hazardous.

Please ensure that your mother is not deficient of vitamin D, and has adequate other micro-nutrients

1. X-rays are very limited in what they show, and very “observer dependent”, which means some are better than others in interpreting what is shown. Even complex visualization, such as MRI will not necessarily give answers. Diagnosis depends upon a number of skills, such as the history, clinical examination, and other factors such as experience and intuition. All these qualities need to be combined and correlated if high diagnostic accuracy is sought. Matters often go very wrong when the patient takes the attitude of believing (sometimes insisting) that “all will be shown” by an x-ray and similar. Indeed x-rays can show apparent abnormalities, “red herrings”, and mislead completely. In spinal surgery one of the most dangerous instruments is the MRI. It shows so much that apparent abnormalities can mislead the treatment in a hazardous way.  Therefore it is not possible to say “no fault is found”. All that can be said is that that observer found no abnormality.
2. Swelling in the lower limbs is often treated by diuretics, which dehydrate the individual.  That means giving almost every cell in the body a dose of an abnormal chemical. There are other hazards of dehydration, which I will not labour here. Far better is to treat the parts which need treatment. A good start would be to try elasticised stockings. If the problem is a hydrodynamic one the stockings will work.
3. Another benefit of elasticised stockings is that an undiagnosed or preventable deep vein thrombosis can be treated with (properly designed and fitted) elasticised stockings.
4. If lower limb swelling is also present in the uninjured limb, then an entirely different group of diagnoses must be considered.
5. But it must be remembered that infection and problems with the blood vessels also produce swelling in the lower limbs. An entirely normal limb can be made to swell by inactivating it by walking with crutches.
6. If your swelling is localize to only some of the hardware, then local infection must be considered.
7. At this stage a few days wait is unlikely to make any difference. Rather use the time to ensure an accurate diagnosis and reduce the swelling with stockings. In any event you should use the stockings from immediately after the surgery (see earlier posts).
8. No surgery is entirely exempt from complications. However if the tissues are handled gently the chance of infection are considerably reduced. See earlier page on “Painless surgery”. There is a direct correlation between painful surgery (and for that men injurious surgery) and complications.
9. Discuss the method of removal with your surgeon. It is possible to do “subcutaneous” removal of plates and screws through small puncture wounds.

These medical meetings correctly emphasise the importance of sensation loss and insufficiency of blood perfusion. However there is another necessary factor in the cause of foot ulcers, which is seldom discussed in these meetings, the abnormalities of alignment of the skeletal structures of the foot.  Examples are clawing, veering and rotation of the toes and dislocations of the toe joints. These cause dangerous high foot-pressure areas which are a necessary prerequisite for foot ulcers.

Such deformities worsen progressively[i], and once deformation has started ulceration in the insensate foot becomes inevitable with time. Therefore these abnormalities require correction immediately they appear, immediately the toes begin to claw, immediately the calluses show on the soles, and immediately any abrasions or corns appear on their feet.

Most non-diabetics with these foot deformities readily seek treatment because they are prompted by pain.

However, those who cannot feel do not complain, and so often progress to ulcers, with eventual loss of the foot by amputation

Naturally vascular supply surgery might also be necessary but, once the ulcers have appeared, other treatments like full contact casts, debridement of ulcers and bone, and various forms of direct application are all too little, too late, and often fail.

This is a tragedy because correction of the anatomical alignment of the forefoot (claw toes, hammer toes, “bunions”, corns calluses, metatarsal high pressure, and similar) can usually be easily, safely and permanently corrected by soft tissue releases. This reduces the incidence of ulceration dramatically and lessens the amputation rate.

Soft tissue realignment procedures are performed regularly on non-diabetics. Why then are they not performed in the far more urgent circumstances of diabetic sensation loss?

One reason is that podiatric and orthopaedic management commonly involves dividing and realigning perfectly normal bones, and often destroying perfectly normal joints. These procedures are dangerous (particularly in diabetics) because divided bones might not unite. Bones infected subsequent to surgical damage are exceedingly difficult to treat. Plates, screws, pins, spacers and Silastic hinges implanted in “conventional” surgery all increase the risks of infection. Further, bone surgery necessitates long periods of immobilisation which is detrimental to the physiology of the lower limb, producing yet another set of dangerous complications[ii]: Those without feeling run a high risk of abrasion by casts or other “immobilising” devices.

Clearly “conventional” surgery to bone is precluded in those without sensation or with complicated diabetes.

The belief that it is necessary to operate on bone has come about, and become entrenched dogma, because of irrationality. Bones cannot produce deformities and it is irrational to assault them. Deformities can only be caused by soft tissues pulling the bones into misalignment. The target for correction should therefore be the deforming soft tissues.

Because diabetologists have also been lead into this misapprehension they shy away from referring their patients for appropriate surgery, to the detriment of those who rely on their advice.

Soft tissue surgery is often performed successfully and safely on diabetics and those with sensory loss.

Leaving foot skeletal abnormalities in diabetics and sensory loss feet in the hope that complications will not occur is a misguided invitation to catastrophe.

[ii] These include oedema, deep vein thrombosis, fungal dermatitis and sensitivities to the contact material.

These medical meetings correctly emphasise the importance of sensation loss and insufficiency of blood perfusion. However there is another necessary factor in the cause of foot ulcers, which is seldom discussed in these meetings, the abnormalities of alignment of the skeletal structures of the foot.  Examples are clawing, veering and rotation of the toes and dislocations of the toe joints. These cause dangerous high foot-pressure areas which are a necessary prerequisite for foot ulcers.

Such deformities worsen progressively[i], and once deformation has started ulceration in the insensate foot becomes inevitable with time. Therefore these abnormalities require correction immediately they appear, immediately the toes begin to claw, immediately the calluses show on the soles, and immediately any abrasions or corns appear on their feet.

Most non-diabetics with these foot deformities readily seek treatment because they are prompted by pain.

However, those who cannot feel do not complain, and so often progress to ulcers, with eventual loss of the foot by amputation

Naturally vascular supply surgery might also be necessary but, once the ulcers have appeared, other treatments like full contact casts, debridement of ulcers and bone, and various forms of direct application are all too little, too late, and often fail.

This is a tragedy because correction of the anatomical alignment of the forefoot (claw toes, hammer toes, “bunions”, corns calluses, metatarsal high pressure, and similar) can usually be easily, safely and permanently corrected by soft tissue releases. This reduces the incidence of ulceration dramatically and lessens the amputation rate.

Soft tissue realignment procedures are performed regularly on non-diabetics. Why then are they not performed in the far more urgent circumstances of diabetic sensation loss?

One reason is that podiatric and orthopaedic management commonly involves dividing and realigning perfectly normal bones, and often destroying perfectly normal joints. These procedures are dangerous (particularly in diabetics) because divided bones might not unite. Bones infected subsequent to surgical damage are exceedingly difficult to treat. Plates, screws, pins, spacers and Silastic hinges implanted in “conventional” surgery all increase the risks of infection. Further, bone surgery necessitates long periods of immobilisation which is detrimental to the physiology of the lower limb, producing yet another set of dangerous complications[ii]: Those without feeling run a high risk of abrasion by casts or other “immobilising” devices.

Clearly “conventional” surgery to bone is precluded in those without sensation or with complicated diabetes.

The belief that it is necessary to operate on bone has come about, and become entrenched dogma, because of irrationality. Bones cannot produce deformities and it is irrational to assault them. Deformities can only be caused by soft tissues pulling the bones into misalignment. The target for correction should therefore be the deforming soft tissues.

Because diabetologists have also been lead into this misapprehension they shy away from referring their patients for appropriate surgery, to the detriment of those who rely on their advice.

Soft tissue surgery is often performed successfully and safely on diabetics and those with sensory loss.

Leaving foot skeletal abnormalities in diabetics and sensory loss feet in the hope that complications will not occur is a misguided invitation to catastrophe.

[ii] These include oedema, deep vein thrombosis, fungal dermatitis and sensitivities to the contact material.

Professor Driver Jowitt, I have found your info by accident and what I have read has confirmed some suspicions I have had about my own care for some time.

About 30 years ago I had a Takata type disc extrusion which led to laminectomy discectomy including a dural tear and weeks on my back in hospital. It was not enjoyable.

I have just had a fusion to help with awful foot and leg pain due to instability and bilateral foraminal stenosis.

I still have pain in both legs and feet and my low back feels no more stable than before. I have suspected for a long time that I have not been fully informed on my true condition-based simply on how bad I often feel- and I know that my GP is taking his lead from the latest ‘expert’ and my outpourings are largely dismissed.

After all I have been ‘fixed’ now… so what is the problem???

My insurer is taking an increasingly hard line lately on folks like me. I am about to be sent for assessment by an independent contractor to determine if I can return to my trade as a carpenter. I fully expect this to be found to be true and my exit (from benefits) put into motion. I have not worked full time since 2002 – in great pain and discomfort – and lost my latest (light)job when I agreed to the fusion. I feel let down by my health services.

Dear Patient, I have the greatest sympathy for you. Medical investigatory techniques (including the most recently developed “scans”) are relatively crude. Therefore a meticulously accurate diagnosis is often lacking. At times the view is taken that “nothing shows, therefore nothing is wrong”. This is an inferior conclusion, which I often have to counter in Court. My argument is that “absence of evidence is not evidence of absence”.

By the same token, such an absence of an anatomical diagnosis defeats accurate treatment design.

However empirically and over a lifetime of involvement in vertebral management [both surgical and (mostly) non-surgical] the least dangerous and most effective form of management is in water, as described in my website.

I imagine you are seeking responses to those who might deem you “fit to work” and so cut your grants. If I can help further, please let me know.

Dear Doctor Driver-Jowitt, I have read some of your articles on spine surgery and tried, elsewhere, to contact you.

I am doing some research on my own situation post discectomy/laminectomy for Takata type extrusion (20mm) in 1989 and L5/S1 fusion recently. I have significant ongoing issues. I am a 52 year old ex tradesman.

Can you tell me how I can establish the current status of my ligamentum flavum? After reading what you have written I think I may have instability and weakness due to its removal in 1989. But how on earth would I know??

Dear Patient, As a beginning, it is not likely to be productive to return to the past in terms of unpicking previous events. What counts is to get going on a process of improving what you have at present.

However, having said that, it might also be important to provide your source of social benefits with some reasons why you may never have been truly “cured” following the original disc prolapse.

At the date of your original surgery it was widespread practice to excise the ligamentum flavum, and to strip away the inter-spinous/supra-spinous ligaments, as well as to elevate (and so inadvertently de-nervate) the mutifidus muscles. The last mentioned is an often unrecognised cause of “instability” as well as “transfer pathology” to segments above and below the segment of primary pathology.

Therefore those who might take the stance “you have been correctly treated, nothing can be found by experts now, and therefore you are fit to work as a carpenter” might well be wrong. Add the impairments at the disc level to other (unrelated and often subliminal) changes of age, and you could well have good reasons not to be able to return to work as a carpenter. Indeed if you are expected to build and mount trusses, or work on scaffolds and ladders, you should be prevented from those activities.

Have your hips been checked? An arthritis, at times not appreciated, can often exacerbate vertebral problems.

http://www.nejm.org/doi/full/10.1056/NEJMoa0907797?query=TOC

It is almost impossible to do a random controlled trial (rct) on anterior cruciate ligament (acl) injuries.

The initial difficulty is that the ultimate measure must be an outcome assessment when the subjects (who are usually in early adulthood when injured) are older than 40, then older than 70 to see if they are more prone to osteoarthritis than average.

A second variable is how much proprioception was lost as a result of the original injury. There is strong evidence that the greater the loss of proprioception, so the worse the long-term outcome, whatever the surgical treatment. But there are no standardised comparative tests of proprioception with the required reproducibility and high sensitivity.

Thirdly the acl injuries are usually related to one or more of a number of other injuries to the radjacent  anatomy, the knee co-laterals, meniscii, posterior cruciate ligament or the patella-femoral joint complex. Unless the rct is standardised for these it will be invalid.

Finally outcomes will depend on a number of life-style variables such as return to sport (and which sports), BMI at various stages of life, other injuries to same and other limb, concomitant illnesses, use of alcohol, smoking and chronic septic foci.

Therefore the variables are huge.

But one additional and not insignificant factor which alters the practice of surgery, and often biases rct selection, is patient demand for the “treatment of their choice” as gleaned from the popular press. This demand is often not resistible by the clinician, and becomes disturbing where the clinical objectivity has been perverted by headline-seeking pronouncements in the popular press.

Anterior cruciate ligament injuries (and their treatment) are frequently exposed in the lay press because of the high cult status of many injured sportspersons.