Research Review by Dr. Shawn Thistle©


Oct. 2006

Study Title:

A hypothesis of chronic back pain: ligament subfailure injuries lead to muscle control dysfunction


Panjabi MM

Public Information:

European Spine Journal 2006; 15: 668-676.


This paper outlines a hypothesis regarding the etiology of chronic back pain (including low back and neck) from one of the most respected spine researchers of our time - Dr. Monohar Panjabi. Famous for his development of the subsystem theory of spine stability (active, passive, and neural…ring a bell?), Dr. Panjabi puts forth his hypothesis of ligament subfailure as a mechanism for the development of chronic spinal pain, which I will summarize below.

While reading this review, please remember that "back pain" here does not refer to back pain resulting from infection, systemic disease, fracture etc.

It is well known that back pain is a very complex problem. One of the most frustrating aspects for clinicians is the fact that in most cases, an exact cause of spinal pain cannot be identified.

There are many theories about how chronic spinal pain develops including: abnormal mechanics, inflammation, biochemical and nutritional changes, immunologic factors, disc pathology, nerve dysfunction, psychosocial factors…the list could go on.

It is commonly thought that most back pain results from one event, an overt trauma, or an accumulation of repetitive microtrauma that eventually exceeds tissue tolerance. It has also been suggested, with moderate supporting evidence, that back pain patients display delayed muscle reaction times when asked to perform a task, to external perturbations, and when the spine is loaded suddenly.

Furthermore, they display poor spinal control and balance, and impaired positioning ability (mainly in whiplash patients).

Panjabi suggests that the spinal column has two major roles:
  1. Structural - to provide stiffness to the spine
  2. Transducer - to provide information characterizing spinal posture, vertebral motion, spinal loads etc. to the neural control system through mechanoreceptors in the ligaments, muscles, disc annulus, and facet capsules
The proposed hypothesis is prefaced by stating that abnormalities in the structure of the spine (ex. injury or degeneration) cause increased muscular activity to compensate the loss and maintain spinal stability. This model incorporates structural compromise and is much written about. But, what if the transducer function of the ligaments of the spine is compromised? This is the focus of this hypothesis.

There is preliminary evidence from animal studies demonstrating that stimulation of spinal ligaments (disc, facet capsules, spinal ligaments) causes spinal muscle firing. This relationship is known to be influenced at least in part by spinal posture, ligament fatigue, and cumulative microtrauma.

The observations from these studies, with the possibility of transducer malfunction in chronic pain patients, form the basis of the following hypothesis.

Sequential Steps in Ligament Subfailure Model
  1. A single event or cumulative microtrauma results in a subfailure injury of the spinal ligaments (and hence the mechanoreceptors embedded in the ligaments).
  2. Tranducer signals during subsequent movements or responses to load are corrupted (i.e. not normal).
  3. The neuromuscular control unit (in essence, the nervous system) has difficulty interpreting these signals.
  4. The muscle response generated by the nervous system is corrupted, which affects the temporal and spatial coordination and activation of each spinal muscle.
  5. The corrupted muscle response leads to corrupted feedback from muscle spindles and tendon organs, which further corrupts the muscle response.
  6. This corrupted muscle response results in higher than normal stresses and strains in spinal structures leading to further subfailure of various structures and overloading of passive tissues (discs, facets etc.).
  7. The abnormal forces produce inflammation of spinal tissues, which input abundant nociceptive signals to the nervous system.
  8. Over time, chronic back pain may develop.
I feel Dr. Panjabi presents an interesting hypothesis - simple and logical. However, I think the last point could have been strengthened by some mention of recent thoughts on neuroplasticity and increased peripheral nerve sensitivity as a further mechanism in the development of chronic pain.

Conclusions & Practical Application:

One key point emerges from this hypothesis - the injured spine behaves differently than a healthy spine. This is something we all know, and evaluate and treat everyday. The problem remains in determining how to interrupt "corrupted" input or information and normalize spinal stability and function.

Dr. Panjabi explains that current evidence supports the general idea that injured spines demonstrate greater variability in almost all parameters. Further, all patients respond differently to pain. This new hypothesis can explain this observation, as subfailure injuries to ligaments can occur along a spectrum of severity ranging from tearing of a few fibres to partial/complete disruption of the entire ligament.

While noting some limitations of this hypothesis, Dr. Panjabi reiterates that pain is a subjective experience that cannot be explained by a single hypothesis. In addition to corrupted transducer input, ligament injury could also directly influence muscle atrophy and disuse. Muscle atrophy and disuse can then alter spinal function - you see how this gets very complicated. He states that there are likely many studies in support of this theory, and many that would refute or alter it.

Further, the treatment and recovery implications for this hypothesis are uncertain. The hope in publishing this paper is to stimulate thought and future research to elucidate some of the important issues that remain in spinal pain research.