Plastic Spinal Cord

First published in The Lawyers Weekly October 4, 2002,  Vol. 22, No. 21

[Neuroplasticity means that spinal cord and brain may be...altered...permanently by pain events.]

Plastic (Greek, plastikos, relating to moulding) not as the latest bionic prosthesis, but because the functioning of the spinal cord is capable of being permanently shaped, formed or moulded by acute pain events.

Neuroplasticity, not a dozen years old, is a central concept in chronic pain litigation.

In 1644 René Descartes illustrated the startling proposition that phlogiston (fire) set in motion a spot on the skin of the foot, causing it to pull on a thread that travelled through the leg and spine to ring a bell in the brain.

The "electrical wiring" model of sensation that evolved eventually was not challenged until 1952 when Glen Player proposed the idea that nerves could be "restrained" from transmitting pain messages.

1965 was the year Melzack and Wall published their Gate Theory: a pain train approaching the brain could be stopped by throwing a track switch to favour a train on another converging track.

The Gate Theory explains how stimulating the spinal cord inhibits pain - the basis of Transdermal Electrical Nerve Stimulation (TENS).

However this is not an "all-or-none" switch, and pain can be not only attenuated but also enhanced.

A soldier can escape from the battlefield despite a shattered leg, but a hammered thumb can be overwhelmingly painful to the reluctant Do-It-Yourselfer.

Anatomists and physiologists have now demonstrated specialised nerve pathways from the brain to the dorsal root ganglion of the spinal cord that can not only dampen but also amplify pain signals.

Neurophysiological research during the last 35 years has revealed some of the immensely complex chemistry whereby this modulation of pain is effected in the dorsal horn of the spinal cord.

In 1990 McQuay and Dickenson suggested that the highly sophisticated spinal cord was also plastic.

Neuroplasticity means that spinal cord and brain may be physiologically and anatomically altered long-term or even permanently by pain events.

Although pain is primarily a sensory experience, it also has emotional and cognitive aspects.

That emotions, attitudes and psychological defences impact the experience of pain is self-evident.

The modified Gate Theory explains how activities of the cerebral cortex of the brain modulate acute pain, but there are also prolonged or permanent anatomical and physiological changes in the spinal cord following severe pain.

To understand these changes, we need to distinguish between the experience of pain and the physiological effects of stimulating pain fibres in nervous tissue.

If a tree falls in the forest and there is no-one there to hear it, does it make a sound?

If a patient is unconscious, is the surgeon’s knife painful?

Philosophical and semantic debate aside, the physiological answer to the second question is yes.

Not only do pulse rate and blood pressure rise with the first operative incision, but changes in blood chemistry and muscle activity are well recognised responses to surgery.

This is the basis of muscle relaxant medication during general anesthesia.

What is only just being found for the first time is that postoperative pain can be materially reduced by enhancing unconsciousness during surgery (general anesthesia) with complete pain relief (epidural analgesia).

Such pre-emptive analgesia is a developing clinical application of neuroplasticity.

Neuroplasticity also explains various other phenomena with which Personal Injury counsel must grapple.

Spontaneous pain may develop in the absence of any evidence of tissue damage.

Emotional amplification of pain is part of the fabric of Personal Injury litigation.

Most relevant to Personal Injury lawyers is this "new" model of chronic pain.

In a previous article, I alluded to the concept that 3 months after soft tissue injury the connection between tissue damage and nociception (awareness of tissue injury) has already broken, but the pain-suffering-behaviour persists as chronic benign pain.

The plastic spinal cord model is of central importance in addressing and litigating chronic benign pain after soft tissue Personal Injury.

Because the soft tissue damage is long healed, expert testimony by the traditional "tissue injury" specialist is largely irrelevant.

In their stead, chronic pain specialists (anesthetists and psychiatrists) need to be asked explicitly to explain this current understanding to the Court.

However, this model has a further modification of importance to Personal Injury litigators.

Additional factors are involved in the post-traumatic development of allodynia (experiencing touch as painful) and widespread chronic pain (FibroMyalgia Syndrome, FMS).

The neuroplastic changes that cause these more generalised conditions of allodynia and FMS usually long precede the Personal Injury and may be initiated by traumatic early experiences, particularly various forms of childhood abuse.

Responses to other life events trigger fluctuations in symptoms both before and long after the event being litigated.

Whereas these latter conditions rarely occur de novo after soft tissue Personal Injury and are Causally attributable for only weeks or months, new onset localised chronic benign pain may be disabling long-term.

For decades we have been seeking in vain for tissue changes that explain localised chronic pain following soft tissue injury.

Physicians and lawyers alike have been focussing on the injured part or the psyche, to explain a permanent change after an acute injury that is long healed.

We have been looking in the wrong parts of the body.

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