The Disc Breaks Down

As your back gets progressively less mobile the changes to the lower discs become more difficult to reverse. The diminished water content allows the vertebrae to settle closer together and the fibrous walls of the disc bunch down and become less stretchable. When this happens the buoyant nucleus become imprisoned by the hardened mesh walls, rather like the four wing-nuts in each corner of a flower press screwing down the plate. The once-robust bouncing-back nucleus is kept penned inside where it gradually loses life. Instead of being watery and translucent it becomes a yellowy-brown colour and more viscid (sludgy). It also becomes harder to visually differentiate nucleus from anulus.

Figure 2.15 A buoyant healthy nucleus imparts a quivering up-thrust to the spine when it receives compression whereas a degenerated disc receives load with a thud through the bunched-down disc wall (anulus).

As the disc degenerates, load bearing transfers from the wizened nucleus to the disc wall. Since the outer wall is tensile rather than compressive it collapses like a buckling wicker basket as it bears weight. The bulging disc becomes an inert spacer which manages to keep its vertebrae apart simply by its bulk. The pulverising forces of load also create friction between the fibrous layers of the disc wall (lamellae) creating circular separation and radial splits from the inside anulus out. Eventually, the wall destruction can lead to 'disc prolapse' (see Chapter 5) as the degraded nucleus, which has lost the osmotic cohesion and spreads under compression, starts to burrow through chinks in the wall to the periphery. However, this turn of events is uncommon and accounts for fewer than 5 per cent of back problems.

As the disc progressively hardens it ceases to be a stretchable connector and a band of stiffness develops across the spine's length. As the spinal segments pull away from one another in movement, like a beautiful streamlined concertina, the problem link cannot let go. Fibres of the disc wall ping as stretch is demanded of a link that cannot provide it and pain signals are elicited from both the chemical and mechanical receptors. The low back emits a low-grade constant ache, with sharp jabs of pain whenever you stretch.

It is also difficult for a flatter disc to cope with spinal bending because there is no buoyant nucleus on which its superincumbent vertebra can pivot. When it cannot see-saw, the upper segment shears instead and the walls are stretched. Atrophy of the small intrinsic muscles (multifidus) controlling segmental movement also traumatises the brittle link. The weakness comes about partly through reflex inhibition (the less they contract, the less the painful segment is compressed) and also because they have so little to do because the segment is too stiff to move.

Restoring mobility makes a stiffer segment less vulnerable to physical assault, although strengthening weakened intrinsic muscles must be the final step in the rehabilitation process. (Note: strengthening the abdominal muscles is the first step.) Remember, whenever spinal strengthening starts it makes your back sore (see Chapter 7) but being aware of this at the outset should dissuade you from taking fright and repairing to your bed. Getting it right with treatment is all about getting the rate right.

If a disc continues to stiffen and degenerate with chronic muscle spasm locking it away, it eventually becomes a mass of scar tissue. As it loses its functioning nucleus it cannot rock and pivot to ride out shock waves passing through and it becomes an easily 'knockable' link; a sitting target waiting to get hurt. Instead of a tightly contained ball of fluid, the disc resembles a wedge of compressed carpet which is repeatedly flattened by compression. It develops multiple large-vent ruptures of both endplates, making deep fissures through the disc that are invaded by blood. The pain network can augment with increasing numbers of nerve endings growing into the heart of the sick disc; in effect 'seeking out the pain'. Rare cases such as these are ideal for disc removal and surgical fusion of the segment.

Long before this point, however, the aim of spinal therapy is to rehydrate a drier stiff disc to make the spinal link more mobile. Improved mobility allows the disc to suck fluids through to nourish itself, generating the pressure changes to gear up the metabolic factory within. This healing process is not instantaneous because discs have such a slow metabolic rate but remember, discs do regenerate. 'Therapy' is simply about helping discs repair through enhancing nutrition. It is not rocket science; it just takes knowledge . . . and perseverance.

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