Sarah Key is the author of Back in Action and Back Sufferer’s Bible. She is the official physiotherapist to Britain’s Royal Family, for which she was made a Member of the Victorian Order in 2001. Her private practice treats back-pain sufferers and trains medical professionals in back care.

The Body in Action

You Can Keep Your Joints Young

By Sarah Key

Allen & Unwin

Copyright © 2006 Sarah Key
All rights reserved.
ISBN: 978-1-74114-118-4

Contents

Introduction,
1 Your low back,
2 Your thoracic spine,
3 Your neck,
4 Your shoulders,
5 Your elbows,
6 Your wrists,
7 Your hips,
8 Your knees,
9 Your ankles,
10 Your feet,
The 30-minute daily regime,
About the author,

CHAPTER 1

Your low back

WHAT IS YOUR LOW BACK?

Your lumbar spine, or low back, is a short, segmented pillar that sits on the sacrum at the back of your pelvis. It works like a chunky, flexible strut that supports the rest of your spine towering above it. Your lumbar spine passes up through the back of your abdominal cavity, which balloons out in front, and a strong corseting of the abdominal muscles is required to hold your abdominal wall reefed in. Abdominal muscle weakness, common to most of us, allows the abdominal contents to fall forward, and this can have direct consequences for the functioning of your lower spine.

The lumbar spine consists of five lumbar vertebrae. The lowest, L5, is lashed securely to the forward-sloping surface of your sacrum. The sacrum does not participate in spinal mobility. It consists of five fused sacral vertebrae with the vestigial remnant of the tail, the coccyx, extending from the base. Your sacrum makes up the back wall of your pelvis and joins with the two big ear-shaped bones (the ilia) at either side at the sacro-iliac joints, the impression of which you can see as two dimples in your skin. The forward inclination of the sacrum is approximately 50 degrees. Flatter or steeper angulations of your sacrum can have direct consequences for the way your entire spine stacks, and also on the way it absorbs impact.

The vertebral body is the circular brick-like part of each vertebra. It has a narrowed waist to help bear load, though most of its weight-bearing brilliance comes from the honeycomb bone (trabeculae) on the inside of the vertebral body. All weight-bearing bones have trab-eculae, which look like iron filings following lines of force, showing where load is transmitted through the bone. These resemble the structure of a sponge and are an ingenious way of making the bones strong, yet light. If the vertebral bodies were solid bone, the spine would be too heavy to lift and chunks of bone would cleave off under load. The trabeculae form a three-dimensional grid of fine vertical pillars and horizontal struts of bone. The vertical ones sustain load while the horizontal ones provide transverse shoring to prevent the vertical ones buckling. They also prevent the sides of the vertebral body caving in like a cardboard carton.

Your lumbar spine is a bendable pillar of support. Its segments stack around a gentle forward-arching curve known as the lumbar lordosis, which gives your lower back a natural hollow when viewed from the side. The rest of your spine uncoils in an ‘S’ as it rises from your pelvis, like a cobra from its basket. The lumbar spinal curve is maintained by forward angulation of your sacrum, correct muscle balance and the slightly wedged-shape back of both vertebra and disc.

Optimum lordosis is an important factor in sustaining lumbar spinal health. It performs two very important functions: a sinking and springing action on footfall, which provides a very important impact-absorbing mechanism to eliminate juddering during walking, and the more static stacking of the torso on your lower body with minimal effort, most importantly during sitting. It follows that spines with either too much or too little lumbar lordosis suffer mechanical duress. Insufficient lumbar hollowing causes added load to be borne through the front of your spine — thus loading up your discs — whereas too great a lumbar hollow causes the opposite: excessive weight-bearing through the back of your spine at the facet joints.

The intervertebral discs sit between your vertebrae like squashy water-filled pillows to cushion bone-to-bone contact. They are thickest in the lumbar area, where they provide vigorous resilience to compression. In many ways, discs resemble a radial car tyre: the walls consist of twelve to fifteen layers of diagonal meshing, the fibres of each alternate layer running at right angles to the one before. This provides great strength, yet allows the vertebrae to twist and gap open on all sides during movement.

The anulus fibrosis is the circumferential wall of the disc. It is divided into a middle-inner section plus an outer part and — very importantly — their roles are quite different. The middle-inner anulus works like a capsule, with its fibres running in a circular fashion throughout both adjacent vertebral end plates. Its fibres contain the fluid nucleus at the centre of the disc and this part is responsible for bearing load. The walls are prevented from buckling and collapsing under load by the radially ‘outwards squirting’ pressure of the water contained within the nuclear capsule.

The outer disc walls are not involved in weight bearing at all. They are more like a pre-tensioned outer ligamentous skin, which works like a connective stocking-mesh to bind the vertebral segments together. The more radially expanded the disc is by the downward force, squirting the fluid of the nucleus outwards, the more the outer walls are made taut, which gives the segment stability. It works exactly like a fully inflated inner tube of a car tyre making the outer tyre taut.

It is a beautifully ingenious mechanism. The two parts of the disc wall complement each other: the outer wall controls stretch whereas the inner controls compression. The spine then manages to combine flexibility at low load and stability at high load.

Disc hydration is the key to maintaining spinal health. A disc lacking fluid develops a lower hydrostatic pressure. It also means the walls will not be fully radially expanded, like a car tyre lacking air, and the outer walls will sag or bulge. All discs bulge more by the end of the day as they naturally lose fluid and less healthy discs bulge more readily because they have trouble holding their fluid. But moderate bulges alone are no bad thing. This is not quite the case with major disc wall prolapse over a sustained period.

In major disc prolapse, the outer disc wall can be painfully stretched, which can be a source of low back pain. It is important to note that only the outer ligamentous skin of the disc wall is innervated, meaning it behaves exactly like any other ligament of the body — it elicits pain if it is over-stretched and develops scar tissue after injury. With sustained wall prolapse (especially when a spinal segment is locked by extreme spasm of the spinal muscles) there can also be enzymatic breakdown of the wall, which means the disc will not expand again, even when the muscle spasm releases.

The watery nucleus of each disc behaves exactly like a liquid ball bearing. The compression of each spinal segment stacked vertically on its disc provides the pre-tension for each intervertebral link, thus allowing the whippy, elongated movement of the spine as a whole.

Proteoglycans is the magical x-factor of discs. It constitutes 65 per cent dry weight of the nucleii and exerts a powerful electrostatic attraction to water. Thus proteoglycans is the active osmotic agent that drags fluid into the discs, keeping them buoyantly plumped up despite the weighing down effects of gravity. Even so, fluid is gradually squeezed from the discs by day so that we all go to bed approximately 2 centimetres shorter at night. Lumbar discs lose more than those higher up because they are the cushions at the bottom of the stack. Fluid loss throughout the day is regained at night — imbibed during sleep when your body is stretched out horizontal and relaxed. The tidal exchange of discal fluids squeezed out by day and sucked back in by osmosis overnight is one of the main mechanisms of feeding your discs. If you are tense during sleep and do not relax your muscles the discs will not get back their full complement of fluid, and disc nutrition suffers. The stateliness of this diurnal fluid exchange is only tolerable because the metabolic rate of the discs is so slow. It also means that discs are only just viable, even in their normal healthy state; they are slow to break down, and also slow to repair.

A vital adjunct to the daily exchange of discal fluids is the ‘pump imbibition’ mechanism provided by pressure changes created by movement. This mechanism mainly works during daylight hours, when physical stretching and bending exerts a squirt–suck effect on your spinal segments, creating an ancillary circulation of discal fluids. So a full range of activities during the day keeps the discs additionally nourished. In later life, or when the discs degenerate, this secondary pump mechanism becomes more important, both to offset reduced proteoglycans content of older discs and the calcification of small holes in the endplates, through which fluids pass to and from the vertebral bodies. At the very outset, this explains why movement is such an important factor in spinal rehabilitation — more so as you get older.

Each vertebra joins its neighbour through the vertebra–disc union, but it also makes bone-to-bone contact at the back of the bony ring. As one vertebra sits on another, they make two bony notches behind the intervertebral disc, flanking the central neural tube that houses the valuable spinal cord. These bone-to-bone notches are called the apophyseal or facet joints.

The facet joints are synovial joints like many others in the body, such as the finger joints or the knee. The facets’ role is to notch the segments together in a loosely articulated column that then protects the central core from excessive movement, which could cause the disc walls to fray. The congruent interfaces of the facet joints are held together by their own joint capsule and their opposing cartilaginous surfaces are washed and lubricated by the supremely lightweight and slippery synovial fluid. The facet surfaces are the first to suffer rub if the washer-like disc of the same level loses water and deflates. This is another important source of lower back pain.

Like other synovial joints, the facets are strained easily and prompt pain follows. Unlike the intervertebral disc, they have a highly sophisticated nerve supply. At each intervertebral level two spinal nerves branch off the cord inside the spinal canal and issue from the column through the intervertebral foraminae. These short bony canals are situated between the segments, equidistant between the intervertebral disc at the front and the facet joint behind. Thus, the spinal nerves exit the spine right through the spinal hinges, running the gauntlet between two potential aggressors and, not surprisingly, it is fairly easy for the nerve roots to be irritated by a bulging unhealthy disc wall or an inflamed facet joint. Either condition can cause leg pain or sciatica.

HOW DOES YOUR LOW BACK WORK?

As you’ve just discovered, your lumbar vertebrae provide the stacking support, whereas the intervertebral discs perform the dual roles of shock absorption and gluing the cotton-reel vertebral bodies together. The facet joints steady the flamboyant column of segments by providing bone-to-bone notching, which ultimately stops them toppling off one another.

Your low back positions the thinking–acting, upper part of your body and you could say the main role of your lumbar spine is to support your upper body while letting it bend with safety through the middle.

Your spine acts as the central strut to the internal scaffolding of your body. It is tall and narrow with a handsome repertoire of movement. Bending forward is its most grandiose — and most risky — action though the combination of your spine’s hard anatomy and soft tissues makes it possible.

The intervertebral discs provide the dramatic cohesion between your spinal segments. They are tenaciously embedded in the flat upper and lower surfaces of their neighbouring vertebrae, and when your spine bends, their stretching outer walls steady the movement, while the thrusting, hydrostatic pressure of the nucleus helps by pre-tensioning the walls. As the vertebrae pull apart, the outer walls pull up, rather like tugging up garden lattice; the further it goes, the greater the holding tension of the mesh. When bending forwards, the strong reinforcing ligaments of the facet joints capsules — known simply as the capsular ligaments — help control the movement.

The disc walls and the capsular ligaments almost evenly share the job of holding the segments together when your spine bends, but the solid backstop to all this is the bone-to-bone notching of the facet joints. Strong as the disc walls and the capsular ligaments are, they would eventually fray and weaken were it not for the bony inter-lock of the spinal facets.

Your facet joints are the ultimate block to your spine coming undone. Their upper and lower joint surfaces notch together to prevent shear. It’s a bit like locking the hands by cupping the fingertips over each other. You can see the effectiveness of this facet chain in the dry bones of a cadaver (minus the discs). They stack upright fairly securely, the mutual bony surfaces butting against each other, and don’t fall apart until the spine is well advanced in a forward lean. In the living, the soft tissues of the spine — mainly the discs and the facet capsules — prevent the segments coming apart in this way.

Quite apart from being useful, bending has an important role to play in keeping intervertebral discs healthy. Discs do not have a blood supply; they are the largest avascular structure in the body. They require movement of fluids to take in raw materials — particularly the larger molecules — and expel waste products. High fluid content and a robust fluid exchange is the mainstay of disc nutrition and a healthy back. Disc health is all about disc hydration.

Proteoglycans exerts an osmotic pull on water and is a vital essence in disc hydration. A higher concentration of proteoglycans keeps discs better hydrated and degenerated discs have a lower percentage of proteoglycans. Sick discs have trouble holding their water. The synthesis of proteoglycans is stimulated by pressure changes within the discs — and the optimum range is between 0.3 and 2.5 mega-pascals (MPa). This just happens to be within physiological range — 2.5 megapascals is the maximum pressure recorded when lifting a 20-kilogram weight.

Pressure changes are vitally important to the health of discs and for this reason it is essential for spines to move — indeed to lift — to remain healthy. On the other hand, synthesis of proteoglycans declines when discs endure sustained pressures, either high or low. This explains why bed rest is not good for recuperating spines, nor is sustained sitting. Both extremes are not good for disc vitality.

Degeneration of a spinal segment usually happens via the two main mechanisms that hold the segment together — the disc or the facet capsule. Disc drying and thinning is usually the primary process.

As a disc desiccates from spinal compression, its segment becomes stiff and painful in the column. I call this the stiff spinal segment (Stage 1) and believe it is the most likely cause of simple lower back pain. As the disc degenerates and loses hydrostatic pressure, its walls bunch down and the segment loses mobility. Eventually this implicates the facets at the same level, which also lose mobility as the facet capsules become tighter. This puts them next in line in suffering strain and the ensuing inflammations is known as facet joint arthropathy (Stage 2). As the disc becomes distinctly thinner, the facets start to bear load and their bone-to-bone interfaces become eroded and bruised, resulting in frank arthritic degeneration of the facet joints. As a degenerated disc struggles to hold its water its walls distend, like a half-deflated car tyre; more so at the end of the day. Disc walls bulge even further if the segment is locked up by protective muscle spasm. This may be seen with CT and MRI scanning but may be misinterpreted as disc prolapse.

Acute facet locking (Stage 3) happens when a small unguarded movement causes a facet to slightly slip askew as a consequence of early disc thinning and reduced intra-discal pressure. Instantaneously, your spine will lock up in an agonising gust of protective spasm, which can take weeks to dissipate. This fluke mishap is often memorable many years later and can mark your spine’s downfall; the point beyond which it was never the same again.

Alternatively, the segment may go the other more insidious route where low-grade muscle spasm keeps a spinal link pinched in the column. If a disc wall has been buckled and flat for too long, it will be attacked by enzymatic action, like a car tyre perishing as it runs along almost on the rim. After several weeks like this, the disc cannot be rehydrated and the disc bulge becomes permanent, even when the muscle spasm comes off. This is true intervertebral disc prolapse (Stage 4), although it is often diagnosed in error. Disc prolapse is not a common cause of back (or leg) pain.

Once discs degenerate beyond a certain point, they can no longer hold their segments together firmly in the column and they tend to ooze forward under sustained spinal compression. Over time, this recurrent trespass weakens the other main stabilising structures of the segment: the capsular ligaments or the capsules of the facet joints. Eventually, there is a noticeable forward slippage of this segment every time the spine goes to bend. This condition is known as ‘segmental instability’ and it manifests as a weak back with a painful catch when the spine goes forward. It can also manifest as the spine giving way, or simply as a painful arc on bending (Stage 5).

(Continues…)Excerpted from The Body in Action by Sarah Key. Copyright © 2006 Sarah Key. Excerpted by permission of Allen & Unwin.
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