Causes Of Segmental Instability

• Primary breakdown of the disc

• Primary breakdown of the facet joints

• Incompetence of the 'bony catch' mechanism of the facet joints

• Weakness and poor coordination of the trunk muscles

Primary breakdown of the disc

In the later stages of breakdown of a stiff spinal segment, the disc degrades to such a degree that it becomes like an inert flattened washer. It dehydrates and loses its buoyant ball of nucleus at the centre which should act as a pivot. The nucleus so lacks internal hydrostatic pressure that it cannot prime the disc and spring-load its vertebra on top to tip as the spine bends. Instead, the vertebra shears forward. The passive non-performance of the disc tugs and stretches the side walls, similar to the way a perishing car tyre veers over onto its wall as it rounds a corner. Thus a flaccid degenerating disc is gradually destroyed by its own vertebra's runaway movement.

Figure 6.4 Lack of internal pressure in the sick disc means the spine skids and slews forward on that level whenever you bend, instead of tipping on a buoyant nucleus.

When the disc has reduced stuffing, the constant weight of the spine bearing down through the weak link is further cause for breakdown. With its much reduced intradiscal pressure, the main brunt of load-bearing is transferred from the nucleus to the walls. They have nowhere to go but billow outwards, like a cardboard box crumpling when a weight is rested on top.

With long periods of sitting, the distension of the walls becomes more marked because a degenerated disc loses its fluid more quickly. As the upper vertebra settles closer to the lower one, the disc bulges circumferentially like an inflatable rubber collar, and the two vertebrae almost touch. The back may be caused to slew sideways on the sick disc by the muscles attempting to lift the pouting wall off the nearby spinal nerve; it may remain kinked into a 'windswept' 'S' bend after rising from sitting, and take a few minutes to

Figure 6.4 Lack of internal pressure in the sick disc means the spine skids and slews forward on that level whenever you bend, instead of tipping on a buoyant nucleus.

stretching back disc wall disappear. A sciatic scoliosis like this is often more long-lasting after attending a seminar for a few days or after a busy period of sitting writing reports.

Figure 6.5 With the disc bulging all around like an inflatable rubber collar both nerve roots are vulnerable.

This process of breakdown can be greatly speeded up by a percussive injury through the length of the spine as if the degenerated nucleus is looking for a way out. The sudden impact can blow a vent through the thin cartilage of the vertebral endplate causing the degraded nuclear material to squirt into the blood-saturated honeycomb bone (spongiosa) of the vertebrae above or below. Endplate fracture when the disc is healthy will not result in the nucleus breaking out, although it will cause rapid deterioration of the disc's health so that eventually it will punch through.

Once the nuclear material has penetrated the bone, the blood cells in the spongiosa attack the toxic disc material as an unwelcome foreign substance, and an auto-immune reaction sets up. This does not limit itself to the dislodged material but continues back through the communicating hole into what is left of the disc. The remnant disc is then devoured by the auto-immune reaction, leaving a flaccid fibrous bag of scar tissue where the disc once was. This process is called primary disc disease.

flaccid c offendei nerves flaccid c offendei nerves

Figure 6.5 With the disc bulging all around like an inflatable rubber collar both nerve roots are vulnerable.

degraded nucleus

Figure 6.6 Disc breakdown can be greatly accelerated when direct vertical impact through the spine extrudes a semi-degraded nucleus into the neighbouring vertebral body.

degraded nucleus

Figure 6.6 Disc breakdown can be greatly accelerated when direct vertical impact through the spine extrudes a semi-degraded nucleus into the neighbouring vertebral body.

Not surprisingly, this is a back problem common to the armed forces. Soldiers who train over assault courses are particularly susceptible through landing on their feet with a heavy pack on their back. Parachutists are also at risk, as are pilots who use ejection seats: they all suffer similar traumatic shocks up through the spine which may be painless at the time. It is also the complaint of the weekend gardener. Forceful tugging at a stubborn root, or unaccustomed heavy lifting, can punch a hole though the cartilaginous endplate which is insufficiently 'seasoned' to tolerate the force.

As the disc becomes incompetent, the segment will only remain stable in the column as long as the other main control mechanism of the facets is up to the task. The strain will eventually be felt on the facets and their highly innervated facet capsules are the first to complain.

Primary breakdown of the facet joints

Segmental instability can also start off when facet joints develop severe arthritic change (see Chapter 3). With poor joint lubrication and the friction of the joint surfaces chafing, the cartilage buffer within the joint can be worn down, leaving room for the two opposing bones to clatter about more as they lie alongside one another. This also causes the joint capsule to pucker and the joint develops excessive play during activity—even though in time it ingeniously moulds its lower bone surface into a cup-shape to hold things stable. Inexorably, the joint slips around with movement and articular destruction picks up apace.

Sometimes, instability can spread from repeated facet locking episodes (see Chapter 4). With each mini-dislocation, the capsule is traumatised and healthy fibres replaced by scar tissue. As the capsule becomes weaker it also loses elastic recoil, thus making it harder to keep its joint snugly together. However, facet locking typically affects one facet only, so instability is less likely to spread across the whole segment from this problem.

Incompetence of the 'bony catch' mechanism of the facet joints

You can also develop segmental instability when the solid bone-to-bone backup of the facet joints becomes incompetent. This can happen in three ways: a congenital malformation (called spina bifida) where the facet joints fail to develop properly in utero; a physical break in the bony neck at the bottom of the catch mechanism, usually caused by trauma (called spondylolisthesis); and when the bony neck of the catch mechanism very gradually elongates, like toffee stretching (called spondylolysis).

In all cases, the 'bony catch' of the facet's locking mechanism fails to prevent the upper vertebra slipping forward on the lower one. Without the lock of bone against bone—like a row of fingers of one hand hooked up against the same of the other—both the disc and facet capsules slowly stretch, letting the upper vertebra gradually slip over the abyss.

As dramatic as a spondylolisthesis can look on X-ray, with an overhang of sometimes as much as half the upper vertebra, it can be quite stable. The flattening of the disc as the vertebra pulls forward causes the disc wall to harden as it bunches down. Barring some fluke additional mishap knocking it loose (like a hard fall on the bottom or a scrum collapsing in a rugby game) the segment may remain symptom-free for years.

Figure 6.7 With spondylolisthesis, a break in the neck of bone below the lower facet surface can render the bony lock incompetent. With spondylolysis, the bone stretches over time rather than breaks. Both conditions can make a segment unstable.

I see this in clinical practice all the time: people with a low-grade backache unwittingly harbouring a fairly advanced slip, to have it flare up only when they suffer some minor new mishap. The recent trauma may cause an additional slip of a millimetre or two but even so, the upper vertebra usually settles down securely on the lower one quite quickly. The lesser symptoms of a 'stiff spinal segment' then return.

It is not unusual to break the neck of a facet with impact through an over-arched lower back, and we see this often enough with fast bowlers landing heavily on their leading leg at cricket. You can also break the catch mechanism with a fall on your bottom, and an astonishing number of the Inuit population has spondylolisthesis from falls on ice. Some of these cases remain chronically unstable, with fractures on both sides of the bony ring failing to unite. The back then permanently harbours a low-grade ache and a tendency to give way when caught off-guard or with an awkward movement. Even so, broken bones and all, it is often surprising how little pain there is.

Weakness and poor coordination of the trunk muscles

When an intervertebral disc dries and flattens due to the degenerative process, the intrinsic muscles which work the upper vertebra have a harder job. The angle of pull of their muscle fibres is flattened, which means their already poor mechanical advantage is reduced further. Thus it is harder for muscular control of the segment to compensate for weakness of the other two stabilisers, and the vertebra is more vulnerable to slip.

Full-blown instability can also develop from fleeting 'weakness' of a segment because the back is suffering pain; a temporary alteration in muscle balance can cause the segment to loosen more quickly. This happens for two reasons: volitional (conscious) and automatic. The volitional element is because of the way you use your back when it hurts—avoiding bending and making your knees do all the work.

People usually try to bend with their back straight and knees bent because they think this is the right way. Over the years this has been reinforced by old-fashioned back-care programs, in the belief that it puts less pressure on the discs. We now know this to be wrong and, furthermore, that using the back this way only makes matters worse. It emphasises the use of the stronger, clumsier muscles of the spine while under-utilising the smaller, fine-acting ones which control the individual segments. Thus the spine operates en masse in a bulky, non-bending fashion, and loses subtle undulating motion throughout its length. This makes it feel precarious in complex postures and safe only when it does simple, almost robotic actions. As it gets stiffer and weaker, it becomes increasingly vulnerable to shearing strains.

Even preliminary efforts to get the spine bending properly at this stage improves things—and despite your wariness, you often find it happens quite easily. After bending two or three times (preferably using your hands to walk down your thighs with the knees bent like a gorilla) your back immediately feels freer and more supple. You might easily get a sense of how bending might help you!

The automatic element of muscle dysfunction is a little more complicated and is more likely to happen if there is inflammation in the back. If there is an irritable disc or facet joint, the finer acting deep muscles can be 'paralysed' by the dominant activity of the over-protective long back muscles, even though their main purpose is guarding. But the finer group can also inhibit as a pre-emptive measure, to spare the inflamed segment excessive compression of the muscle working normally.

Some speculation

It is possible, though not documented, that transversus abdominus, the deepest acting tummy muscle, reduces activity if there is primary inflammation of a stiff spinal segment—because its action clenches the 'cotton reels' together vertically. Lighter neurocentral compression may lessen the pain, even though it ultimately hastens instability.

On the other hand, multifidus may automatically dampen its activity if there is a primary problem of the facet joints. Although this spares the irritable facet from compression, it too inevitably results in poorer control of the vertebra's tail and makes it more vulnerable to shear and rotational instability.

Whether, first up, there is over-activity of the dominant group or automatic inhibition of the deeper ones, there is no doubt that one fuels the other. The stronger group gets stronger and the weaker one gets weaker.

This is the way it works: whenever there is pain in the back, the long erector spinae back muscles develop 'protective reflex spasm' which splints everything semi-rigid and limits movement. They lock up the length of the spine, like guy-ropes holding a flagpole steady in a gale, jamming its base into the ground. As the low back compresses more, the intrinsic muscles relinquish their hold. This leaves all the spinal segments—but particularly a problem one at the base—more likely to shear when the spine bends.

The mechanism also works in reverse. Once the unstable segment reveals a tendency to shear, a self-fuelling cycle sets in. As if sensing the weak link, the erector spinae clench the spine even more. This makes the whole back board-like, but further disables the control of the segments and a cycle gears up. The spine develops a brittle veneer of stiffness which makes it awkward to move, and the weak link inside ever more prone to shear.

Patients often half recognise this themselves, with their back becoming increasingly sore and stiffness extending right up (people often complain that their neck is starting to click). It also keeps giving way at the base if they don't protect it. They lose confidence with anything involving bending, fearing they might end up in a heap on the floor, and they become hidebound by a multitude of constraints. They creep about, taking the path of least resistance and planning every move, even down to picking up a teacup.

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