What Is A Prolapsed Disc

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A 'slipped' disc is a localised bulge in the back wall of a disc. It is caused by the devitalised nucleus losing cohesion and trying to escape through a chink in the cracking disc wall (anulus). The condition needs explaining because for years it has taken the blame as the main perpetrator of back mischief. In the 1930s, 'slipped discs' were nominated as the chief cause of back trouble, and this limited view of what goes wrong has held sway, almost to the present day. It was thought that a disc could pop out of spinal alignment—like a saucer slipping sideways out of a stack—and pinch a nearby spinal nerve. Sometimes a disc wall does buckle (or prolapse) and this painful distension does not disappear when segmental compression is alleviated, but by modern estimates fewer than 5 per cent of back problems are caused in this way.

True prolapse is a localised bulging of the disc wall, caused when a nucleus is 'rendered expressible' by the degenerative process. Inordinate compression (of the type caused by heavy lifting or when the segment remains locked over a period of time by intense muscle focal bulge in disc wall pinched nerve root

Figure 5.1 Disc prolapse is a localised bulge in the disc wall caused when the degenerated nucleus loses osmotic cohesion and tries to escape through a crack in the disc wall.

spasm) can make the nucleus track out of the disc's centre by burrowing through a small chink or radial fissure in the wall. The escaping pocket of nucleus creates pressure against the sensitive outer 'skin' of the disc. The painful stretching of the intact outer layers of the wall creates a particularly unpleasant cramping ache, deep within the back.

The localised mass of a prolapsing disc can also annoy other pain-sensitive structures nearby. A 'posterior bulge' directly out the back of the disc can stretch the highly sensitised posterior longitudinal ligament and also obtrude into the bundle of nerves hanging down inside the spinal canal (the cauda equina). This can cause disturbed bladder control and/or saddle anaesthesia. On the other hand, a postero-lateral prolapse comes out the diagonal back corner of a disc and may squash and stretch (at the same time) the spinal nerve root nearby in its exit canal (foramen). This causes severe leg pain (sciatica) which can be sharp and 'lancinating' in its acute phase or a deep aching cramp when more subdued. The pain is often accompanied by numbness, weakness, positive tension signs in the nerve, and loss of reflexes.

Sometimes the wayward nucleus ruptures right through the few remaining layers of a painfully stretched anulus. This is known as fenestration (or sequestration) and accompanies a kind of crisis with

Positive Nerve Root Tension Sign

focal bulge in disc wall pinched nerve root

Posterior Lateral Spinal Canal
Figure 5.2 A 'posterior bulge' may annoy nerves inside the spinal canal whereas a 'postero-lateral' bulge, in either back corner, may impinge on the nerve root in the exit canal (foramen).

the back, usually as a consequence of a forced lifting movement. At this point, the back pain abruptly disappears, with the release of pent-up pressure behind the wall. However, the leg pain dramatically worsens as the nerve root—though released from the mechanical stretch—is now chemically inflamed by the highly toxic nuclear material. Drastic as it sounds, the extruded nucleus is quite quickly absorbed by the blood stream and surgical removal is not required. Usually, within a couple of weeks, there is very little pain and the problem reverts to a grumbling low-grade discomfort more typical of a stiff spinal segment.

Figure 5.3 With disc fenestration the disc wall bursts and the toxic, semi-degraded nucleus is disgorged, adding further irritation to the already sensitised nerve root.

ruptu disc w escap nuclei mater ruptu disc w escap nuclei mater

Figure 5.3 With disc fenestration the disc wall bursts and the toxic, semi-degraded nucleus is disgorged, adding further irritation to the already sensitised nerve root.

When disc prolapse occurs it is always part of the wider picture of segmental breakdown, when the degenerative process has rendered the nucleus expressible. Neither disc prolapse nor fenestration happens when a spinal segment is healthy. This has been demonstrated in the laboratory when spines of young cadavers were progressively loaded until the bones crumbled rather than the discs rupturing. Even cutting the wall of a healthy disc with a scalpel, and then subjecting it to load, will not cause the nucleus to prolapse or rupture, although this does initiate the disc's slow breakdown in the longer term, as the wall is attacked by enzymatic action.

A disc never slips to cripple you with one blinding movement. Healthy discs are extraordinarily strong and never dislodge with one ill-considered move. Discs are very superior segmental connectors. They make powerfully bendable fibrous unions between the vertebrae and are one of the main agents keeping the spinal segments together. Believe me, nothing slips freely anywhere.

Perhaps the pure expressiveness of the term 'slipped' has captured the imagination of patients and specialists alike and slowed the pace of change. When a back is devastatingly and persistently brought low, the very word conjures images of something bad; of something slipping off centre and jamming the works, even though spinal mechanics are far too sophisticated for anything so crude to occur. It is ironic that for so long so much has been attributed to such an unlikely cause; that this rare condition could have obtained such wide currency as to be inversely proportional to its true incidence.

Mild disc prolapse is extremely common and usually asymptomatic. This has been borne out with the advent of 'magnetic resonance imaging' (MRI) where large cross-sections of populations not suffering back pain can be scanned, minus the radiation hazard of X-ray myelography. Results have shown an astonishing one in five under the age of 60 and one in three over the age of 60 with disc prolapse—all without symptoms. Nearly 80 per cent of those scanned had bulges.

Healthy discs broaden by half a millimetre or two as they take weight and all healthy discs bulge considerably more by the end of the day when they have lost up to 20 per cent of their fluid. Less healthy discs bulge more readily because they have a lower proteoglycans content and consequently have trouble holding their fluid. Like a car tyre with a slow leak, degenerating discs are drier, so they have a low hydrostatic pressure which causes their walls to bulge.

But there is another factor which comes into play once a spinal segment has started degenerating: muscle spasm. Any pathology of a motion segment causes protective spasm of the spine's extensor muscles. If the protective response is intense and continuous, eventually the compression makes disc distension irrevocable as enzymatic action attacks the walls. Though impossible to say how many Newtons of compression force is exerted by the clenching hold of muscle spasm, the sustained loading causes disc cells to die. In a direct analogy to the rubber of a car tyre perishing, a buckling wall of the disc cannot be 're-inflated' when it has been flat for too long.

This makes it only too clear how urgent spinal decompression and muscle relaxation exercises are when backs are in extremis. When a disc has remained buckled for longer than a few weeks it is no easy job to rehydrate it. This factor alone has implications for the urgency of effective spinal treatment when a back problem is in its acute stage. Even if the original pathology is not discogenic, the disc will eventually be destroyed if it remains compressed by muscle spasm. These are the cases which require surgical excision of the distending disc wall; formerly laminectomy and more latterly, discectomy.

bulging disc inflamed nerve inflamed capsule

Figure 5.4 When a spinal segment is locked by the compression of muscle spasm all its soft-tissue structures inflame and swell. In this instance, the disc is the easiest to section out, though its removal makes the facet bear more load and its capsule pucker.

bulging disc

Figure 5.4 When a spinal segment is locked by the compression of muscle spasm all its soft-tissue structures inflame and swell. In this instance, the disc is the easiest to section out, though its removal makes the facet bear more load and its capsule pucker.

Disc prolapse is really a culmination of events; a secondary or tertiary phenomenon rather than a primary entity. True disc prolapse always has a history of pre-existing breakdown of the segment (see Chapter 2) usually with a grumbling backache over several years, though it may have been fairly 'silent' with few symptoms along the way. Eventually it becomes something different, as the original back pain disappears and a new type of pain develops in the leg.

Diagnostic techniques

In the past, discs were difficult to 'see'. Because disc material is not radio-opaque it is not possible to get a clear picture on X-ray. To find out if a disc was protruding into the spinal cord (in the spinal canal) or the spinal nerve (in the intervertebral exit canal), a radio-opaque dye was injected into the space around the cord and its investments, then the patient tilted this way and that to make it trickle around the discs. Afterwards an X-ray was taken to reveal the discs' outline. The procedure is called a myelogram.

Fortunately this very clumsy and unpleasant procedure (which often left the patient with headaches for days but much more seriously, sometimes caused 'arachnoiditis'—a longstanding inflammation of the tissue coverings of the spinal cord) has been completely superseded, first by CT scans and then by MRI (magnetic resonance imaging). Although MRI in particular is expensive, it shows increasingly clear (almost 3D) images of soft tissues and bone alike, making it much easier to interpret the state of play of all spinal structures, not just the discs.

It is impossible for people like me to feel the discs with our hands because they are around the front of the spine and far out of reach of our probings. It is only possible to feel the state of the neurocentral core by palpating it through the vertebra's backward tail (the spinous process). Although there may be a typically 'gummy' feel of the surrounding tissues when there is a tense disc bulge, this may be difficult to pick up. Sometimes however, the slight palpatory pressures disturb a bulge and provoke pain further afield, probably by the swollen wall rubbing against the nerve root.

If minimal pressure brings on a cramping leg pain, it spells out a high irritability of the nerve—although it is important to exclude facet involvement, rather than disc. This is done by palpating 1-2 cm laterally from the centre, over the facets.

Because it is impossible to feel the disc we must rely on objective signs to show if the spinal nerve root is under duress. They are all called 'neurological signs' and they indicate the degree of irritability of the nerve and the extent to which it has stopped working. The straight leg raise test (SLR) involves raising the leg to a right angle and not allowing the knee to bend. By increasing the tension on the nerve roots you can tell if one is inflamed. If there is a marked nerve inflammation the leg barely gets off the bed before it exacerbates the leg pain. Other signs of nerve involvement are dulled or absent reflexes (behind the ankle and below the knee), numbness of the skin on the leg and loss of muscle power. It is confusing that severe inflammation of a facet joint gives almost the same signs (see Chapter 3). I believe you can only conclude that symptoms are caused by disc prolapse if there are disturbances of bowel and bladder function (which a facet cannot cause).

Friction Bulge
Figure 5.5 Thumbs can feel through to a swollen facet but not the disc. Indirect pressure delivered via the spinous process can provoke leg pain by causing friction of the disc bulge against the nerve.

True disc prolapse is one of the most difficult spinal conditions to fix conservatively but, given time, it will eventually regenerate. Even with stark evidence of disc prolapse on MRI it can be nothing short of miraculous how well cases like this can do. Admittedly, once the nucleus is out of the centre of the disc it is difficult to get back (it is often described as getting toothpaste back into a tube) but mobilising the segment releases it from compression which improves disc nutrition. The manual loosening also relaxes the muscle hold which lessens the pressure on the bulge and allows the disc to imbibe fluid. It also frees the disc to suck and blow to promote cellular activity and repair. And finally, the introduced movement also restores a better circulation of blood through the whole area (not the disc which is avascular) to reduce inflammation caused by the many other swollen structures of the segment, all pressing and chafing against one another, the disc being but one.

Coaxing a crimped spinal segment to move can dispel even the most menacing leg pain, even though a nerve root, once inflamed, retains a lowered threshold for some time. For many months it may be susceptible to flare-ups, especially after periods of slumped sitting, which stretches the covering (dura) of both the spinal cord and the nerve roots. With even the vaguest return of muscle spasm, or if the disc's circulation becomes sluggish for other reasons, shades of the familiar leg cramp can start up.

Disc surgery

The fact that the whole 'metabolic climate' inside an inflamed segment contributes to the irritation of a nerve root may explain why removing a disc with surgery is so often unsuccessful. Some figures estimate that 50 per cent of operations for a slipped disc leave the patient worse or at least no better. Removing the disc may not be removing the problem; it may be worsening it. If indeed the facet is the main source of pain, wholesale disc removal obliterates the disc space and brings more pressure to bear on the facets. After the operation the leg pain is much worse—which is very disappointing after all you have been through. No sooner are you upright than all your symptoms return, as bad as they ever were.

However, many back operations are extremely successful. In the past, a more radical procedure called a laminectomy was performed which removed the entire disc (like tearing away three-dimensional pieces of fingernail with pliers) and then part of the bony foramen

inflamed facet inflames the nerve

Figure 5.6 If both disc and facet capsule are swollen, changeable leg symptoms are more likely to come from the facet. The facet's rich blood supply makes its behaviour mercurial.

an inflamed facet inflames the nerve

Figure 5.6 If both disc and facet capsule are swollen, changeable leg symptoms are more likely to come from the facet. The facet's rich blood supply makes its behaviour mercurial.

above and below the nerve root was removed with bone cutters. Sometimes a spinal fusion would then be performed during the same operation to deal with the instability created by destroying the fibrous union. A fusion would be performed either by packing out the empty disc space with bone chips (usually taken from the hip bone) or inserting two large screws through the facet joints. More latterly, metal cages have been used which though unable to absorb shock, at least preserve the disc space and prevent facet loading.

Disc removal has also been refined to make it less upsetting to the streamlined spinal mechanics. A microdiscectomy is a much more discreet surgical procedure and smacks less of removing the tyre and letting the wheel run along on the rim. This operation is carried out through a tiny cut in the skin and takes as little disc as possible (virtually the bulge only). With a smaller wound and less cutting, the scar formation is also kept to a minimum.

Apart from the essentials of skill, the most successful surgeons repair the surgical division made in the thoraco-lumbar fascia before they close up. This means the spine retains its ability to clench the vertebral segments vertically a few micro-seconds in advance of spinal action, which helps avoid instability problems developing later on. It also pays to keep the blood and oozing fluids to a minimum during the operation, and mop up as much as possible before closing the wound. Many surgeons demand the resumption of normal activity as soon as possible after a disc is removed. (The most successful surgeon I ever worked with, would not discharge his patients until they could touch their toes—usually ten days after surgery.) Early activity gets the working parts of the spine moving again, dispersing old bleeding and the collection of lymph in the tissues. In turn, this means that scar tissue is kept to a minimum with fewer 'adhesions' to clag the spine's delicate machinery.

withered nerve root

Figure 5.7 Scar tissue is like living undergrowth that invades the working machinery of a spinal segment and chokes the nerve.

withered nerve root

Figure 5.7 Scar tissue is like living undergrowth that invades the working machinery of a spinal segment and chokes the nerve.

The more selective surgeons have strict guidelines, and operate only if there is evidence of the nerves in the saddle area and legs not working properly. Pain alone is no reason for opening a back and removing a disc. Pain is subjective and too emotive to be any sort of guide. And besides, there are many other spinal disorders which can produce similar pain.


Pre-existing breakdown alters the properties of the nucleus and weakens the disc wall

Bending and lifting stress breaks down the back wall of the disc

Pre-existing breakdown alters the properties of the nucleus and weakens the disc wall

Discs are shock absorbers and are meant to bulge. In their healthy state, the girth of each one swells imperceptibly as we transfer support from leg to leg during routine weight-bearing activity. As compression passes downwards through the spine, forces are transmitted outwards in all directions via the fluid of the disc's nucleus. Through the mechanics of an hydraulic sack, compression is converted to a springing-apart buoyancy which gives the spinal links their tensile strength and prevents the column juddering as we make contact with the ground.

As the spine sinks and springs with movement there is a synchronised to-and-fro exchange of energy. This passes between the briefly distorting nucleus and a moment later, the stretching mesh of the disc wall as it accommodates the force. When the wall nears its limits of stretch, its elastic recoil bounces the energy back to the nucleus causing it to puff up and thrust the spine aloft. This sublime dynamic uses the tension of the disc walls to off-load the weight of the spine bearing down from above and gives us a bouncing spring to our step.

The transfer of energy works well while the nucleus and the disc wall are in peak condition. As long as the nucleus retains its proper viscosity and the wall its tensile strength, a disc can dissipate on-off compression almost indefinitely. But early breakdown of facets or the disc—or overzealous muscle spasm protecting either—can change everything. Simple stiffness of the front or back compartment can eventually lead to disc prolapse, simply by localised muscle clench hampering disc nutrition.

As the disc dries out and the nucleus becomes more viscid, it is more easily deformed under pressure. Instead of being a tightly contained ball of fluid at the centre of the disc, the nucleus loses cohesion and spreads out laterally inside the disc when compressed. As it squirts this way and that with different activities of the spine, the nucleus bumps up against the internal layers of the disc wall. Over time, the battering against the interior walls amounts to trauma and eventually they start to perish from the inside out.

unhealthy depressurised disc with flattened walls

Figure 5.8 As a disc degenerates it flattens and the nucleus deforms laterally under pressure.

Muscle spasm at this point can convert a fleeting problem to a permanent one if the protective hold locks in and cannot be persuaded to disperse. The muscle clamp keeps the segment compressed in a vertical vice which hinders the dynamics of on-off squash and suck through the disc. As the compression persists, the disc wall starts to bulge at points on its circumference where pockets of escaping nucleus start pressurising the walls from within.

Activities that create sustained pressure inside the disc accelerate its breakdown. With generalised slumped sitting for example, when the pressure within the discs is raised, more force is directed towards the back wall of the disc. But with bending and lifting, which always involves some twist, the force is directed to the left—or right-hand back corner of the disc.

Bending and lifting stress breaks down the back wall of the disc

When the nucleus is on the run, ever-present bending of the spine has dire consequences. The intradiscal pressure is great when the spine bends forward. If there is a degree of twist as well, the pressure is even greater, because intense muscle effort increases the clamping-down pressure on the disc. If the twisting action is always in the same direction the nucleus damages the same part of the inner wall and breaks it up, strand by strand, like elastic fibres in a corset perishing at the points of greatest wear.

Hot And Cold Water

unhealthy depressurised disc with flattened walls

Figure 5.8 As a disc degenerates it flattens and the nucleus deforms laterally under pressure.

Strenuous lifting can be the last straw. It places enormous stresses upon the spine, particularly the lowermost discs. It raises the intra-discal pressures to unparalleled heights and as more fibres break in the same spot, a radial split opens up in the wall from the inside out. With more lifting and more pressure, the squirting nucleus burrows its way into the opening and prises it apart as it makes tracks towards the periphery. Eventually the whole wall may split open, disgorging its nucleus into the spinal canal. This is known as fenestration.

Figure 5.9 With torsional lifting strains, multiple fibre breakage at one point in the disc wall creates a small 'V'-shaped nick which the runaway nucleus burrows into.

Intensifying the breakdown

Rupture of the disc happens faster if the weight being lifted is held out from the body or if the lifting is heavy work—both of which increase the internal pressure of the disc. It also happens faster if you bend over using a large twisting element to lift. The disengaging of the facets as the segment goes forward makes the disc even more vulnerable to torsional strain and the alternating layers in the wall tend to separate, making circumferential tears in the outer zones. This appears to happen more readily in kidney-shaped discs, where the wall buckles around the sharper corners of the disc. With marked internal derangement of a disc, a radial split can meet up with a circumferential one and the nucleus can squeeze through many parts of the wall.

Pars Interarticularis

these tears are caused by the layers of wall separating as the segment twists

Figure 5.10 Circumferential tears tend to be more common in the acute-angled back corners of the walls of kidney-shaped discs.

these tears are caused by the layers of wall separating as the segment twists

Figure 5.10 Circumferential tears tend to be more common in the acute-angled back corners of the walls of kidney-shaped discs.

The combination of the internal squirting pressure of the degraded nucleus and the rotatory strains on the wall means discs are most likely to disintegrate at the points on the clock face corresponding to 11 and 1. This explains the preponderance of postero-lateral disc bulges. In a good example of Murphy's Law, these two points of breakdown are exactly where the sciatic nerve roots make their way out of the spine, having branched off the spinal cord higher up. The nerves travel down inside the canal as multiple strands and then exit via the left and right intervertebral foramen at their designated level.

With a posterior protrusion the nerve is blighted inside the roomy central spinal canal, but a postero-lateral bulge irritates the nerve inside the much narrower exit foramen. The lack of room in the foramen means the nerve can get doubly assaulted; squashed up against the other wall while at the same time being stretched over the back of the bulge, like squeezing past the fat lady in the bus.

Not surprisingly, disc prolapse and fenestration is often brought on by strong physical work. Heavy lifting with a twisting action is the worst: moving bags of cement or digging with a long-handled shovel. Nurses are particularly prone to back trouble, though not always discogenic. Bad lifting techniques can 'hurt' the outer ligamentous wall but the disc will not prolapse until its nucleus has been rendered expressible by the pathological processes typical of a stiff spinal spinal nerve root spinal nerve root

Figure 5.11 Repetitive bending-twisting actions weaken the two back corners of the disc, right where the nerve root passes.

segment. Most commonly, nurses get a bad back when they save a patient from falling. This may create a virgin injury or, more probably, it strains a dormant link in the spine which was too stiff to accommodate the wrench passing through.

The acute phase

Sciatic pain usually creeps up over several days after hurting your back. You can often recall exactly what you did, though your back did not 'go'. You probably felt a slight strain, with a momentary deep pain inside which quickly passed off.

You often hurt the back by awkward lifting, where the object is unwieldy rather than unliftable. You may be hauling up one end of a sofa for example, and attempting to push it across the floor, when a corner snags. The difficult wrestling which follows is often the last straw, causing a sharp feeling of strain in your back. It becomes more sore and tight over the next few days, and then the pain down the leg starts.

The overwhelming feature is a painful tension deep in your buttock and down the leg which develops into a nasty cramp-like


pain. In the beginning it feels like a pulled muscle or a tightly pulled string in the leg. It often originates in your buttock and moves down into the thigh, missing out on the knee and reappearing in the calf. You can usually locate a trigger point deep in your buttock by digging in through the layers of muscle with your fingertips, and for some reason, pressure here relieves the pain in the leg.

The nerve may be so inflamed and sensitive to stretch you cannot even get your heel to the floor when standing. Your back often acquires a lateral 'windswept' bend (sciatic scoliosis) to relieve the tension of the nerve root and the whole back takes on a painful crippled appearance. Sometimes the sciatic scoliosis can be so pronounced, with the hips out one side and the shoulders the other, you look as if you won't fit through a doorway. From the rear view the spine looks completely hunched over and weak. As well as its

Figure 5.12 True disc prolapse is a pathetic sight. It is impossible to take weight on the leg or get the heel to the ground and walking is reduced to a hobble because you cannot stretch the nerve to take the leg forward.

lateral 'S' bends it will have a lumbar hump instead of a hollow lordosis. The buttock of the bad side can be flat and wasted, making a continuous line with the rounded low back. Both spinal deformities are protective mechanisms to minimise the tension on the inflamed nerve root.

If you have to stand, you rest your weight on your toe and keep the knee bent to avoid stretching the nerve, and the leg often shakes uncontrollably. Walking is reduced to a pathetic hobble. Every time you take a step forward there is a dreadful, mind-numbing pain down the leg like a jagged, red-hot spear through the tissues (in the textbooks this is described as 'lancinating' leg pain). Bending forward is just as impossible. As you attempt to go over, there is a crippling pain down your leg and the spine slews off more into its 'windswept' deformity to avoid the stretch.

Sitting is often unbearable because the bunching down of the spine increases the pressure on the disc and hence the tension on the nerve. After a few seconds the pain can be so bad you have to get up and lean on something to hang your leg to take the weight off. The pain can be just as unbearable after a few minutes of standing, when the pressure on the disc increases to a crescendo of cramping pain. (You hear of people on their way to being admitted to hospital having to lie down on the floor of the elevator to find relief.) Often, the most comfortable position is lying on your side in the foetal position with a pillow between the knees.

What causes the acute pain?

The back pain of acute disc prolapse is caused by the stretching of the disc walls and the pain genesis here is not dissimilar to that of stretching a stiff disc (see Chapter 2). The pressure of the localised bulge stimulates globular mechanical receptors between the fibres which manifests as a very uncomfortable pain deep inside your back, not relieved by the pressure of hands.

Only the outer layers of the disc wall have a nerve supply which explains why lesser bulges, which are so common, are invariably painless. These can be thought of as full-thickness bulges where the intact inner layers of the wall absorb most of the pressure of the nucleus discharging laterally. They take up the slack and save the more sensitive outer layers from the head of pressure caused by a runaway nucleus.

Once a degraded nucleus is on the move, it acts like a wedge which penetrates a small nick in the innermost walls and spreads it wider as it migrates to the periphery. As it gets closer, with fewer remaining layers left to contain it, the tension on the sensitive outer wall becomes immense, further fuelled by the compressive clamp of the muscle spasm. (This may explain the often-observed loud pop when a surgeon cuts through the wall of a sick disc during an operation, expelling nuclear material many metres across the room.)

As the condition worsens the old familiar back pain disappears as the leg pain comes on. This is usually caused by the disc wall breaking which relieves one set of problems but creates another. By this stage, the nucleus is a brownish colour (indicating it is degraded and toxic) and it is a potent chemical irritant on the nerve—especially if the nerve has already been sensitised by pre-existing stretch.

Stretching a nerve root is greatly more irritating than mere pressure. After all, we know from leaning on our funny bone at the elbow that pressure alone does not cause pain. It may temporarily lose conduction as the arm goes to sleep, and it is unpleasant and pins-and-needley while it wakes up again, but never raging pain. Pulling a nerve taut, thus subjecting it to friction as well as tension (as it twangs and rubs past other structures) is a much more potent irritant. Thus a lesser bulge which does not stretch the nerve will not be painful, explaining why such a high percentage of the population has disc bulges with no accompanying pain.

The first effect of pressure (and tension) on the nerve root is to restrict circulation. Fresh blood is prevented from squeezing through to the affected part, and stale blood damming up cannot flush the products of metabolism away. Both circumstances irritate free nerve endings in the local tissues which register another tier of discomfort from the problem area.

Remember, the inflammatory reaction does not apply to the disc itself because it is virtually bloodless. Rather, it applies to all the other red and swollen tissues clustering around the swollen disc and adding to the engorgement. This racks up the muscle spasm to another level, increasing the compression of the disc as everything becomes more inflamed and squashed together in a confined space.

When the nerve is under pressure and also stretched, friction develops between the tightly stretched nerve and its own protective sheath. The physical chafing between the two blood-congested (hyperaemic) surfaces causes much more pain as the inflammation of the nerve intensifies. Clear fluid weeps from the angry, raw surfaces such as you see from a burn of the skin, and the pain becomes unspeakably bad. If you could look inside you would see the nerve grotesquely red and swollen and the surrounding tissues swimming in fluid. This is the metabolic climate which causes agonising pain in the leg and which is very difficult to settle conservatively.

The disc, as the least bloody structure of the segment, is not a bad choice for surgical excision if the problem gets that bad. When everything is locked by irreversibly bloated congestion, this highly pressurised but inert component is the easiest to define and section out. It is a quick and effective way of decompressing a segment when all conservative methods have failed, despite the ill-effects this may have upon the future function of the spine.

The chronic phase

Rather than pressure, the chronic phase of disc prolapse is more about the internal machinery of the segment struggling with the after-effects of inflammation. As a legacy of the previous pitch of inflammation, the weeping exudate from the nerve gradually solidifies into thickened strands of scar tissue (see Figure 5.7 on page 141). This forms a matted mess, gluing the nerve to its sheath and other structures nearby, including the wall of the exit canal. Dry, whitish adhesions permeate everything, creating a choking collar which gradually strangles the nerve. This is called 'root sleeve fibrosis' and is very common after disc prolapse.

The tethering stops the nerve pulling and retracting freely through the bony tube (foramen) as the moving leg exerts traction on it. A dense undergrowth of adhesions dominates, often binding the nerve down to the back of the disc. The nerve is often much thinner than it should be because it has been trapped and choked for so long.

What Tethered Scar Tissue
Figure 5.13 Dural tethering occurs when strands of scar tissue bind the spinal cord to the inside of the spinal canal, just like pegging Gulliver's hair to the ground.

Your leg can feel like a rigid extension of your back. It cannot bend freely at the hip to sit, nor make a step forward to walk, without taking your back along with it. This causes a typical waddling gait, where the low back rotates in a bottom-twisting fashion instead of your leg angling cleanly back and forth at the hip socket. Your back is stiff, with different pains according to what you do, and the pain down your leg comes and goes, depending on how much tension you put on the nerve.

Sometimes the spinal cord is tethered to the inside of the spinal canal. When sitting, the back is not free to slump and there is a dull pulling sensation which spreads high into your back and down into your buttock and thigh. This is called 'dural tethering'. The sitting stretches the spinal cord and tugs it where it adheres to the wall, causing a deep spreading pain which can extend right up to the shoulder blades. Sometimes you can almost feel the tightness inside the spine bowing you forward.

If the tethering is restricted to the nerve root in the exit canal, most of the symptoms are in the leg. With sitting, the buttock wants to come forward to lessen the acute angle at the hip, and the knee bends automatically when you attempt to straighten your leg. After a time, sitting may bring on other symptoms, like numbness of the heel, or a pain under the foot. But the tight dull pain in your thigh will always be worst because the slumped posture causes traction on the nerve root where it is glued to the foramen. Long after all other symptoms have gone away, a lengthy car trip or aeroplane flight can bring on a pain which you have not had for years.

Figure 5.14 A tethered nerve root cannot pull free of the exit canal as the stretching leg puts tension on the nerve. It is like a strand of cooked spaghetti adhering to the pot.

Apart from the cobbled-up leg and the difficulty sitting, there may be other subtle signs of the nerve not working properly. There can be a low-grade wasting of the muscles of the bad side. The buttock can look flat and withered, as can the calf, where the muscle has less tone and is floppy. There can also be less obvious signs, like the arch of the foot slowly dropping which causes the forefoot to splay out, sometimes making you feel your foot is too big for your shoe. You may notice that certain actions are weaker: you cannot stand on your toe or push off with that foot. When you walk, your leg feels heavier and more difficult to control and you have to haul it up when you take a step.

What causes the chronic pain?

Aggressive tension strains on the nerve, such as you might get kicking a football, can cause a localised inflammatory reaction right at the point where the nerve is bound down. Instead of the nerve pulling loose out of its exit canal, like a strand of cooked spaghetti, it is barely free to budge. The wrench may break a few adhesions and cause a small bleed in the otherwise whitish tissues, which then goes on to create more scarring and increases the cobbling effect. In the meantime there is more of the familiar pain in your leg, as the nerve is sensitised by the local inflammatory reaction.

Beyond a certain point, the invasive proliferation of adhesions may cause symptoms of 'vertebral stenosis'—internal narrowing of the spinal canal—because the nerve's own blood supply is hampered by the living junk crowding out the foramen. With this condition you feel pain in the legs whenever they have work to do. You often have to stop and sit down after walking a short distance, even sooner going up hills or steps.

Normally, when your leg muscles have to pump vigorously to move your body, the nerve sucks in blood to keep it relaying messages back and forth to your brain. If conditions are too cramped the nerve cannot puff up to get the blood through. As it suffers anoxia (lack of oxygen) your legs get more and more leaden, until a dreadful cramping pain locks them up completely and you have to stop. You have to rest by bending over or squatting, which broadens the inside diameter of the spinal canal and gives relief by letting more blood through. You can also get vertebral stenosis with facet arthropathy (see Chapter 3) where the arthritic bulk of the facet joint creates a similar effect on the nerve.

After a few moments, the pain eases and you feel more comfortable. When you resume walking, however, the pain starts up sooner and you have to rest more quickly. Each time you start, you travel shorter and shorter distances before your legs become painfully burdensome again and slow you to a halt. By the end of your journey, you feel you have barely started before you must stop. (This feature of shorter and shorter distances covered between respites distinguishes spinal stenosis pain from the cramping leg pains caused by circulatory problems.)

Although there is a tangible organic reason for the legs locking up in this way, it is fascinating how much this can change from day to day. Some days you can walk an entire block and the next you can barely get down the path to the street. The variable in the equation is the degree of muscle spasm in your back. When present to any degree it compresses the segment and further inhibits the blood getting through. In this regard, anxiety and tension also have a role to play because they influence the degree of tone in the muscles. If you are particularly tired or 'uptight', your legs will be harder to move and you will have the familiar wading-through-treacle feeling over the smallest distances. Other days, for what seems no good reason, you could almost be walking on air.

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