Pain following Spinal Cord Injury (SCI): Understanding mechanisms to develop treatments

SCI patients often have severe pain that is the main factor preventing return to a fulfilling life. This program is part-funded by a competitive program grant from NSW Health in a special initiative stimulated by a visit of the late Christopher Reeve (‘Superman’).

This basic research program is one of only a few in the world to use two different models of SCI to permit intensive study of mechanisms and new treatments of SCI pain. Basic studies are closely linked to clinical studies in SCI patients, about 60% of whom have SCI pain due to mechanisms linked to nerve tissue damage.

Unfortunately results from other types of nerve injury have not proved to be useful for SCI pain. Therefore currently available drugs are ineffective for SCI pain with one new exception that has partly arisen from our concept of persistent SCI pain as a disease in its own right.

The basic research program is led by Assoc Prof Janet Keast and uses models of SCI of relevance to problems that occur in people such as traumatic SCI (eg horse, car and surf accidents), cancer, MS and other neurological conditions.

Although nerve regrowth to obtain normal function again is desirable, unfortunately after SCI some nerve regrowth is abnormal and leads to nerve-related pain.

Thus it is important to study such regrowth and factors that control it: firstly, to contribute to treatment of SCI pain; secondly to aid SCI regrowth studies to enable patients to regain function without pain.

Many of the methods of Program I will be used in this SCI research but more emphasis is placed on growth factor studies and in particular studies of the glial cell line derived neurotrophic factor (GDNF) family. The glial cells form the support (‘scaffolding’) of the nervous system and release powerful pain-related growth factors and transmitters of relevance to persistent pain.

In the SCI models, studies will be carried out on the spinal nerves, spinal cord and brain. PMRI studies have already revealed abnormal activity of spinal cord neurons above the level of spinal injury, and associated changes in release of neurotransmitters.

The loss of input to the brain in SCI is believed to cause increased sensitivity of brain nerve cells in the pain pathway. PMRI studies are revealing new abnormal nerve cell connections and neurochemistry in SCI patients.

Back