The colloquial term 'slipped disc' is one almost all of us are familiar with, associating the condition with excruciating low back pain.

But what actually happens when a disc slips is far more complex than the term implies.

This article aims to answer why something that sounds so benign can be so painful.

Lying between the vertebrae in your spine are intervertebral discs. Discs act as shock absorbers preventing wear and tear injuries on the joints of your spine.

They also make the spine mobile, squashing like suspension in car to allow you to bend.

The anatomy of an intervertebral disc comprises of two components: The gel-like nucleus pulposus in the centre, and the tough, fibrous capsule called the annular fibrosis.

Their design is very clever.

Because the annular fibrosis is phenomenally strong in tension, having a moveable fluid centre means that whatever position you move in they are always under tensile stress.

This system helps minimise injuries by keeping the annular fibrosis under strain in a manner in which they are most resistant.

The annular fibres are so strong that in experiments where the spines of cadavers have been loaded to failure, it has been the vertebrae that fail first (White and Panjabi, 1990).

Because of this strength, it is exceptionally rare for a disc to slip, or herniate, suddenly (Dickson and Butt, 1992).

Onset is a gradual process with increasing damage to the annular fibres. This process is known as disc derangement.

However, symptoms of disc herniations are often sudden in onset. This doesn't match what is known about the pathological process of disc derangement, so the question is why do patients experience this sudden deterioration in symptoms?

As a disc protrudes, it begins to displace the adjacent nerve.

This is usually tolerated rather well, because intervertebral foramen (the space through which your nerves pass) is relatively large to allow the nerve to move and stretch without damaging as you move your limbs.

Symptoms may begin when the annular fibres finally fully rupture. Because the nucleus pulposus has been encapsulated since birth your body reacts to it as a foreign substance, producing an acute inflammatory response (McCarron et al, 1987). This can cause severe back pain and a temporary nerve irritation with associated sciatica.

This is a temporary response, but is the most common cause of severe pain associated with disc derangements.

Sciatica lasting for more than several days may be caused by direct pressure on a nerve by herniated nucleus pulposus material.

Despite the logic in extruded matter pressing on adjacent nerves, due to the small amount of nucleus pulposus this is a rare cause of pain.

This is not a cause of back pain, but only referred pain. This tends to aggravated by position.

Advances in imaging (MRI and CT) have shown that up to 25% of the asymptomatic adult population have nucleus pulposus material impinging on nerve tissue (Wiesel et al, 1984), and follow up images of patients show little or no change in nucleus pulposus position despite remission of symptoms (Willberger and Pang, 1983).

This demonstrates further that direct nerve impingement is not necessarily responsible for symptoms.

Damage to annular fibres does not occur through normal loading and, as such, poor posture and muscular imbalance have a very important role to play in disc injuries.

The altered biomechanics that cause disc injuries induce pain from joint irritation and muscle spasm. This is the most clinically significant origin of pain in patients with lumbar disc injuries, and can be both local and radiating (Webster, 2007).

The structures with the most nociceptive (pain receiving) nerves in the spine are the facet joints (Ashton et al, 1992), and it is no coincidence that these joints are put under more strain in patients with back pain and disc injuries.