Biomechanics of the lumbar spinal canal

Clinical Biomechanics

1986; 1: 31-43

Printed in Great Britain

31

Biomechanics of the lumbar spinal canal J. D. G. Troup

PhD of Orthopaedic

Department

and Accident Surgery, University of Liverpool, P.O. Box 147, Liverpool L69 3BX. UK

Summary The normal mobility of the vertebral column, particularly in the cervical and lumbar regions, gives rise to major changes in the length and lumen of the spinal canal and of its volume. Its contents must therefore adapt to these changes without disturbance to their several functions. The contents are partly fluid, partly neural tissue, but also connective tissue: all with differing physical characteristics. Thus, all respond differently to changes in the space in which they are contained. When pathological changes supervene, the spinal meninges, the spinal cord and nerve roots may be adversely affected by the increases in the resting tension, by compression or bending stresses. Because the mechanical state of one region of the spine has a more than local effect, all these factors have to be consideredparticularly for the interpretation of the symptoms and clinical signs of lumbosacral root pathology. Key Words:

Biomechanics, Stenosis

Clinical tests, Disc prolapse,

Mobility,

Introduction The spinal cord and nerve roots need space within the vertebral canal to enable them to function freely. Whenever that space is jeopardised. neurological dysfunction may follow. This is most evident after an injury to the vertebral column which leaves it unstable; and it is obvious when, for example. a tumour grows into the canal. At a much commoner level, restriction of the space in the spinal canal and foramina is aetiologically significant in a variety of conditions. The midsagittal diameter of the cervical canal is narrower than and normal in those with cervical spondylosis myelopathy’.‘.3 and recently it has been shown that, in cervical injury, the narrower the canal the greater the likelihood of neurologic involvement.‘. Similarly in the lumbar spinal canal, it is now well established that the mid-sagittal diameter is narrower in those with the commoner lumbar syndromes’.h.7.X. The dimensions of the canal are thus a major factor in both myelopathies and radiculopathies. Compression has been recognized as the typical pathomechanism but the trigger, whether for acute injury or for is generally movement. Cauda chronic symptoms, equina symptoms are provoked when the space available is reduced by lumbar extension and tend to be relieved by flexion when the canal lengthens and widens: hence the ‘bicycle test’ for lumbar stenosis’.”

reprint requests to: Dr J.D.G. Troup PhD. Depar~rnent of Orthopkdic and Accident Surgery, Ukersity of Liverpool, P.O. Box 147, Liverpool L69 3BX. UK. Corremondenceand

Nerve roots, Sciatica, Spinal cord,

and the need in myelography to see the thecal image in both flexed and extended postures. Thus both the dimensions and the posture of the canal are significant. Within this conceptual model of the biomechanics of the vertebral canal, the idea of compression as a major pathological factor has become dominant. Compression results from pincer action between hypertrophic encroachments and the bony barriers which oppose them, or from space-occupying lesions such as a neoplasm, and it is compounded by the presence of oedema. Mechanisms other than compression have received comparatively less attention. Roots. archetypically, became ‘compressed’ and the only rational approach to a root thus compromised was, whatever was actually done at operation, to ‘decompress’ it. It was assumed that the cord and roots were relatively unaffected by vertebra1 motions other than those that caused compressive ischaemia. Brelg ” in 1960 was one of the first to demonstrate beyond reasonable doubt that the pons-cord tract, from the brain-stem to the emergent sacral roots, was in fact highly plastic. Under the influence of the normal ranges of spinal motion the physiological changes in length, diameter, shape and direction that they underwent were considerable. Breig’s studies”.” showed the very great variation in resting tension to which the cord, the roots and the meninges are normally subjected. In addition to compression as a cause of ischaemia, he showed that adverse tension, leading to tensile ischaemia, in these tissues was a major pathological factor. He demonstrated” that, for example, the symptoms of idiopathic trigeminal neuralgia on cervical

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1986; 1: NO 1

flexion or rotation arose from stretching of the trigeminal nerve root; or that the respiratory centre could be adversely affected by tension in the spinal cord in cases induced when axial traction was of kyphoscoliosis, surgically applied, if the neck was unduly flexed. Moreover, symptoms from cervical spondylotic radiculopathy or from cervical myelopathy could readily be provoked on flexion, when the cervical cord and roots are stretched, or relieved when the appropriate treatment led to their relaxation’2,“. A dynamic approach to the understanding of those symptoms and signs which stem from disturbances in or near the spinal canal is therefore inescapable. And one of the first essentials is to appreciate that the effects of spinal motion in one of its regions are not confined to that region; that the adverse mechanical effects of a lesion in the spinal canal can extend far beyond its site, both cephalically and caudally. Cervical motion and root tension

Figure 1 shows a diagram of cervical radiographs in flexed and extended postures with the images of C7 superimposed. The normal ranges of cervical motion have been studied numerous bY authors’~.‘~.‘h.~7.‘X.IY.Z(1.2~ using a variety of techniques. Based on radiographic studies, for example, Babin and Capesius2” reported a mean of 97” (sd 13”) for the total sagittal range of motion in a series of 35 subjects. From the extreme of extension to the limit of flexion, there is a consequent change in the length of the cervical canal”. It has been shown that the anterior wall of the canal increased in length by between 6.5% and 13% and the posterior wall by 23% to 30%“‘. The effects of such a change on the cervical cord will depend partly on spinal posture elsewhere, but the stretching effect extends upwards. even to the pans”. On flexion, the cord takes a more anterior route within the canal” so that the epidural space is widened posteriorly. The epidural space is generally increased on cervical flexion for another reason: the lumen of the canal is increased as well as its length”.“‘. This change can be accommodated mainly by a shunt of venous blood and. to some extent, of cerebrospinal fluid.

Figure 1. Diagram based on lateral radiographs of the cervical spine taken in maximal flexion and extension with the images of C7 superimposed: showing the increase in the length of spinal canal on flexion.

Figure 2. Dura, cord and nerve roots in the cervical spine in a cadaver: (A) in extension when the tissues are lax; (BI on full cervical flexion showing the tension in all tissues and the root sleeves pulled into contact with the pedicles. (Figure 2 from Breig’*.)

Neural tissues, even where invested by pia mater, can adapt to the increase in volume and length of the cervical canal by virtue of their plasticity. Yet the cord, cervical roots and meninges are demonstrably stretched on flexing the neck (Figure 2). The dura mater, although it can stretch transversely with relative freedom. is less extensible axially. In the extended cervical spine the dura is folded and only becomes taut towards the limit of flexion or if its resting tension is locally increased by rotation”“‘. yet the effects of cervical flexion are detectable in the lumbar region. Figure 3 shows the separation of cut surfaces in experimental transections of the cord in cervical and lumbar regions when the neck is flexed; and Figure 4a illustrates, in a normal radiculogram, the propagation of tension to the lumbar roots on cervical flexion. The mechanism of exacerbation of pain on neck flexion in cases of prolapsed intervertebral disc is illustrated in Figure 4b, in which the root is seen angulated over the prolapse on cervical flexion. Clinically, it is convenient to test this phenomenon with the patient seated and the chest flexed on to the thighs, but initially with the head up. Then on flexing the neck, symptoms may be induced. Often the pain is in the lower back and it may be inferred that the increased dural tension is resisted locally in the lumbar region by tissues which are irritable, the dura being well innervated2’. In patients with root symptoms, a variant of this test may be pathognomonic. Cyriax2’ described a similar posture for the test but with the knee on the

Troup: Lumbar spinal canal

33

a

Figure 3. Transverse incisions in the cord at cervical (upper, right and left) and lumbar (lower, right and left) levels. On the right side, the cervical spine was extended, the cord relaxed and the cut surfaces are apposed. On the left, the cervical spine was flexed and the cut surfaces of the transection are drawn apart. (Figure 67A from Breig”.) painful

side extended

to the pain-free

result being reproduction

limit:

of the leg pain on cervical

flexion. Thoracic

mobility

Thoracic

motion is substantially

and lumbar the length

less than in the cervical

regions’

and the consequent

and volume

of the thoracic

changes in

canal are not

marked. Nevertheless, flexion results in anterior migration of both cord and dural theta”.“. Clinically, a thoracic origin of adverse tension within the spinal cord arises either

locally,

a space-occupying

b

a positive

lesion within

the canal or a lesion within the cord itself. or from a deformity of the thoracic vertebral column such as a kyphosis.

Figure 4. a Lumbar radiculogram showing relaxation of the lumbosacral roots (A) with the cervical spine extended; and the tension in the roots induced in (6) when the cervical spine is flexed. (Figure 123 from Breig’*.) b Lumbar radiculogram showing a disc prolapse at L4/5: (A) the lumbosacral roots relaxed by cervical extension, and (B) on cervical flexion, showing the nerve root pressed against and stretched round the prolapse. (Figure 138 from Breig”.) Lumbar Lumbar

mobility sagittal and frontal

mobility

25 ‘7.2X.ZL).30.31.~2.~3.i4

studied - ‘-

have been widely

The ranges vary with age and race: sagittally from 25” in elderly Europeans to 105” in young Bantus and frontally from 10” to 70”. .

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1986; 1:

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Figure 5 shows a ‘normal’ range of lumbar sagittal motion with the fully flexed and fully extended postures. In the former, the lumbar spine is comparatively straight. The lumbar discs being thicker than thoracic or cervical discs, the combined disc height contributes substantially to the length of the anterior wall of the lumbar canal, particularly on flexion because of the increase in posterior disc height. The length of the lumbar spinal canal increases when flexed; though, as in the cervical spine, the greatest increase in length is posteriorly. As its length increases, so does its lumen. On extension, the dura is lax and folded as in the cervical region’“.‘6. The posterior longitudinal ligament bulges more on the anterior wall and the ligamentum flavum, on the posterior. Any tendency to disc protrusion will therefore be increased on extension. The effects of lateral flexion are illustrated in Figure 6. On the concave side, the side to which the spine is laterally flexed, the lumbar meninges and roots are lax but on the convex side the resting tension is fully taken up and the tissues are straightened to the shortest possible routes. On ipsilateral flexion the intervertebral foramen is narrowed, while on the contralateral side it is opened up. Lumbosacral

root mobility

Unlike the cervical roots which are normally tethered in the intervertebral foramina. thus protecting the cord from root avulsion when traction is applied traumatically from the periphery37.“s. the lumbar. roots are relatively free. On movement of the lower limbs, on straight leg raising for instance. the first sacral and

Figure 6. Cadaveric specimen of the lumbar spinal canal showing the dura, cauda equina and nerve roots on lateral flexion relaxed on the concave or ipsilateral side and under tension on the convex or contralateral side. (Figure 140 from Breig”.)

lower

lumbar

roots

therefore

move

infero-antero-

laterally through the foramina by as much as 1 cm at S1 hut decrcasingty from L5 upwards~~.““.3”.J0.J’.37_.43. It

Figure 5. Diagram from radiographs of the lumbar spine flexed and extended with the images of the sacrum superimposed: showing the increase in length when the spine is flexed.

has also been shown that tension in the sacral plexus can be further increased, and thence transmitted to the root by concomitant medial rotation of the hip44. Sugiura (11~1.‘~ inserted pressure transducers between the nerve roots and the discs in cadaveric specimens. They found that the resulting angulatory stresses imposed on the root by straight leg raising were also detectable on adduction and abduction of the hip. The mobility of the root in the foramen may be constrained by the occasional ligamentous bands of the transforaminal fascia, the commonest being the superior corporotransverse, which runs from the accessory process of the transverse process obliquely down to the posterolateral margin of the vertehrat body4”. They are randomly arranged and the variants which occurred at

Troup: Lumbar spinal canal

35

Figure 7. Dissections of the lumbar spine of a 17 y.o. male to show thickenings in the transforaminal fascia at the level of L3. On the right side (A, B and C) two thickenings bridge the emergent root, leaving it free. On the left side (D and El the single thickening is inserted into the perineurium of the L3 root. if the root becomes tethered L3 in a I7-year-old

male are shown in Figure 7: on one

side with two ligamentous

hands bridging the emergent

nerve root and. on the other.

attached

perineurium

of the root. so limiting

Pathological

increases in root tension

In a posture of extreme

directly, to the

its mobility.

taken

clearly

not so much

be stretched.

as to cause ischaemia,

thanks in part to the tortuosity of radicular vessels when the root is lax. But any abnormality which increases the resting tension of the root may lead. under extreme conditions. to ischaemia and diminished conductivity.

Theoretically,,

below the site of adhesions. Resion

reproduces

this may arise either

when a

root cannot. transmitted the root the site When in root

when neck

in sciatica’”

the root.

no further.

the

to the

and frequently

On straight

leg raising,

tension induced in the sacral plexus and because of adhesions in the foramen,

be

above it. Thus the consequent stretching of

Cervical

flexion.

Lumbar

ffexion.

Flexion

upon

pain

increased tension have to be borne in mind:

Lumbar

impinges

For example,

limb

may be locally increased tither above or below of the adhesions. interpreting the signs of pathological increase tension (Figure 9). all the possible sources of

de-

lesion

though

the increased

forms it or distrains it from its normal path (Figure 8); or

space-occupying

lower

root at the site at which it is irritable.

fingers on toes and their necks not only is the rcstin, (7 tension in the system

though

only when tension is induced in the root either above or

adherent.

flcxion. as when agile people sit

up but the roots will undoubtedly

In the latter increased but

tension induced by cervical flcxion is transmitted

with legs outstretched. flexed;

by adhesions.

cast. the resting tension is not invariably

lateral flexion. of the lower limb as in straight leg raising.

36

C/in. Biomech.

1986; 1: No 1

s

A

C

D

Figure 8. Diagram showing the effect of a prolapsed disc on tension on the dura and root: (A) and (D) represent the normal condition with the cervical spine flexed and extended respectively; (B) and (Cl represent the prolapse with the resulting increase in the resting tension of the dura and root with cervical flexion and extension respectively. (Figure 137 from Breig12.)

roots,

Root compression When canal or foramina encroachment there

depending

squeezed are narrowed

by hypertrophic

or by any other space-occupying

is an increased

Figure 10. Representation of the stress in a nerve root that is stretched and simultaneously angulated over an unyielding structure (white arrows), as visualised in a photoelastic model using an Araldite block (A) bending stress from downward forces (black arrows) and (B) with combined axial tension. (Figure 136 from Breig”.)

risk of compression

action on the cauda equina

lesion.

by pincer

itself or on one or more

on the

between

two

effect is produced canal or foramen flexion,

particularly

The

neural

tissue

surfaces.

is

The

when the space in the

is decreased.

respectively.

rounding

site.

non-compliant

by extension and lateral

It is exacerbated

when the sur-

soft tissues,

or the roots themselves, are Compression may also be evident when

oedematous.

an encroaching lesion impinges on the root when under tension: as when a root is stretched tight across an osteophyte.

Such a condition

a photoelastic

is illustrated

model in Figure

by means of

10.

Mechanisms of root pathology The root may be subjected

to compressive,

tensile and

bending stresses in the course of the commoner nical derangements

may become adherent it is subjected

to mechanical

or chemical

experiments

in which venous stasis was in-

tion or after compression ability of neural damage the

ischaemia

circulation

irritation.

Rydevik et al.”

duced in the tibia1 nerve of rabbits after

which

it

at any point of contact at which

In a review of the pathomechanisms. described

mecha-

of the lumbar spine. In addition,

The prob-

depends on the duration

is maintained.

was rapidly

15% elonga-

by 60~80mmHg.

restored

After

and normal

for

2 hours. function

regained. But much depends. experimentally, on the initial rate of application of force as well as its magnitude”.j”.~“. Percussion, for example, can readily cause permanent

loss of conductivityJH.

Nevertheless,

after feline sciatic nerves had been stretched their

initial

weakness Figure8. Diagram of the lumbar canal with lumbosacral roots and sacral plexus under the influence of (1) increased tension in the sciatic nerve and (2) increased tension induced by cervical flexion. The borders of the intervertebral foramina are shown darkly shaded. Asterisks indicate the potential sites of transforaminal thickening or adhesion. The lightly shaded area shows the roots and plexus relaxed. In the ‘inset’ a prolapse is seen to ‘borrow’ relaxed tissue from inferiorly, drawing the dural root sleeve, the root and the spinal ganglion up towards the spinal canal. (Figure 134from Breig’ .)

length,

resulted

but motor function

well

beyond

their

to twice

elastic

limit,

and was still present 24 hours later had recovered

within

14 days”‘.

Capacity for recovery of conductivity after periods of experimental ischaemia depend on their duration. Lundborgs’

used a sphygmomanometer

hind limbs of rabbits and concluded

cuff on the

that if endoneurial

oedema developed, then recovery was jeopardized. If compression in the human spinal nerve root is maintained for long enough or repeated often enough with-

out

adequate

time

for recovery,

so that

endoneurial

Troup: Lumbar spinal canal

oedema ensues, the oedema itself would have a compressive effect, particularly in a stenotic canal or foramen. There appears to be a combination of factors in lumbosacral radiculopathy. Compression alone on healthy nerve fibres leads merely to loss of conductivity, not to pain. Repeated mechanical insult, whether compression, tension or angulation, induces a state of chronic tissue irritation predisposing the nerve root to endoneurial oedema. to epidural root fibrosis and to arachnoiditis in the root pouch. With ischaemic compression and oedema, axonal damage and Wallerian degeneration will follow if both compression and oedema remain unrelieved. Then. clinical signs of motor, sensory or reflex dysfunction are likely, but they are not necessarily accompanied by the other signs that are typically associated with root involvement. Positive neurological signs, though related to tension signs, can occur independently. Blower’” conducted a prospective study of 100 patients undergoing their first episodes of sciatic pain and found no relation between positive neurological signs and the severity of limitation of straight leg raising. Clinically it is common to find patients with symptoms and signs of cauda equina compression but unrestricted straight leg raising. The mechanism of root compression is thus reasonably clear but it is often quite distinct from the mechanism of adverse root tension. Tension signs are usually dominant in patients with acute attacks of sciatic pain but the neurological signs are generally negative: not invariably, by any means. Combinations of angulation, tension and local compression are not uncommon. Epidural root fibrosis, restricting root mobility, will lead to signs of increased tension in the presence of root compression. Posture and sciatic pain

With acute sciatic pain, posture and walking patterns are disturbed and there is a variety of contributory factors. Weight-bearing on the affected leg is painful because the muscles, in particular, are hyperalgesic. In earlier descriptions of sciatica. the sciatic nerve itself was the site of interstitial neuritis”” and this, though now a comparatively rare finding, gives rise to exacerbation of pain whenever the sciatic nerve is touched or stretched. But stretching of the sciatic nerve from whatever cause will be transmitted to the sacral plexus and roots and this leads the patient to avoid any movement or posture in which the resting tension between the roots and the periphery is increased: they walk on their toes with the knee flexed to avoid stretching the popliteal nerve and their stride length is reduced to limit sciatic tension. When sciatic pain arises from acute disc prolapse there is the added problem of minimizing the bulge of the prolapse. The bulge is greatest on extension or on ipsilateral flexion. The logical solution is to flex or contralaterally flex the spine; but this increases dural and root tension. The conflict can be resolved, more or

37

less, in a variety of postures. The sciatic list with a flattened lumbar spine is seen relatively commonly. The lumbar flattening or flexion reduces the bulge of the prolapse and the list towards the painful leg reduces the tension that side. But there are no hard and fast rules. Given all the potential causes and contributory factors in radiculopathy, from disc prolapse and epidural fibrosis to hypertrophic osteoarthrosis. in any of the anatomic sites in which such changes may arise, the range of postural adaptations to pain is considerable. Edgar” studied the relationship of the side of sciatic list to the site of the prolapse and the position of the affected nerve root seen at operation. The pattern was not wholly consistent and the sciatic list from a central prolapse could vary from one side to the other. Observation of the patient’s posture and movements aloire is not enough because, however typical the pattern may appear, it is unlikely to be pathognomonic.

Clinical signs of root pathology

The names of Lasegue.sh Fajerstajr?’ and a host of others, many of them reviewed by Dyck,” appear throughout the literature. But eponymous signs can be singularly unhelpful as the name gives no guidance on how to conduct the test. Indeed. few of those who routinely report whether ‘Lasiguc’ is negative or positive perform the test as originally described. And there is the added point that the first author to described the test can easily remain unread. Deutsch. for example, noted that medial rotation of the hip tightened the sacral plexu?” some 60 years before the fact was rediscovered4’. The aim of the clinical tests of root pathlogy is to identify first, the individual root in trouble but secondly. the precise anatomical site at which the damage or irritation is arising. The first category presents a mainly neurological problem and it is the tests of motor dysfunction that appear to be of most value’“. The site of root pathology is more difticult to determine. Generally speaking. the more evidence there is. the greater the likelihood of focusing on the precise spot. But, unless surgery is contemplated. the number of justifiable investigations may be limited. Here. it will be enough to consider those tests which relate to root compression or root tension and the radiographic evidence available on plain films.

The tension tests Cervical flexion tests

With the patient seated, the trunk is flexed on the hips as far as symptoms permit. The neck is gently flexed, so increasing dural tension. Sometimes this just causes neck pain. When back pain is elicited. it may be inferred that the lumbar dura is in an irritable state; or that the dura may be adherent to the wall of the spinal canal, particularly at the site of disc protrusion or

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Clin. Biomech. 1966; 1: No 1

Figure 11. Cervical flexion with the trunk flexed and the knee extended on the side of sciatic pain as a test of increased r&t tension24. hypertrophic osteoarthrosis. The sign was found to be positive in 22% of all cases of back and sciatic pain seen in an industrial survey and in 35% of those of them who were referred to hospitalH’. When there is unilateral pain in a lower limb. the test can be modified”: after flexing the trunk, the knee on the painful side is extended to the limit of pain and then the neck is gently flexed (Figure 11). If thjs elicits the leg pain, it can be assumed that the increased dural tension is transmitted to a dural root sleeve that is either in an irritable state or both irritable and adherent. tension being increased above the level of adhesion.

Straight leg raising (SL R) Passive elevation of the limb with the knee straight lengthens the hamstring and hip extensor muscles but also, as the pelvis begins to rotate and the lumbar spine to flex, the erector spinae. Thus a number of tissues, any one of which may be the site to which primary back pain has spread and which are therefore hyperalgesic, are stretched. Often one or more of them may be the site of the pain on SLR but this is not evidence of increased root tension. Qualifying tests are needed. For this, a passive movement is made which does not further lengthen the extensor muscles but which does stretch the neural pathway between +e spinal canal and the periphery. The SLR test has therefore to be conducted under well controlled conditions if it is to be more than a pain-tolerance test of the range of hip flexion with knee extended. The patient must be lying without later51 flexion on a firm surface with only a low pillow, except for those patients with pronounced thoracic kyphosis who may

need to be propped up. The legs must be together and when one is raised, there must be no hip rotation. The endpoint of the SLR is pain or discomfort. The range of movement to the painfree limit must therefore be measured with a suitable goniometer (Figure 12). At the same time. the site of pain is noted. There are no clear guidelines as to what constitutes a normal range of SLR. In healthy, symptom-free subjects with no lumbar spinal disorder, the normal range is between 50” and 120”. Much depends on their regular physical activities. The clinical emphasis is on differences between the two sides. In an epidemiological survey. the criteria used by Troup et al. ” were a difference between the two sides of 15” or more. or a limitation of SLR to 4S”, irrespective of unilateral difference. Blower” used a difference between the two sides of 30” as his criterion for a prospective clinical study. But it is probably unwise to adopt too hard and

Figure 12. Measurement

of the pain-free range of SLR.

Troup: Lumbar spinal canal

39

fast a rule diagnostically, except for the convenience of categorization, because the range of SLR motion is not the only indicator. The difference on the two sides may be confined to symptoms: hence the importance of recording precisely where pain or discomfort is felt on SLR.

The ‘well leg ’raising test When, in patients with unilateral sciatic pain, symptoms are provoked by SLR on the pain-free side, the ‘well leg’ raising or ‘crossed sciatica’ test is positive”‘. The test was deemed to be pathognomonic of prolapsed disc, being positive in 97% of cases”. The mechanism is that SLR of the pain-free leg stretches the sacral plexus and roots on that side quite normally, but the tension is transmitted medially across the dura and dural root sleeves on the painful side, so increasing the angulation”.

SLR qualifying test5 After recording the pain-free range of SLR and noting the site of symptoms elicited, SLR is reduced by 2” or 3 and one or other of the qualifying tests performed: Passive dorsiflexion of the ankle (PDA) stretches the popliteal and sciatic nerves and thence the roots: Medial rotation of the hip (MHR) stretches the sacral plexus (Figure 13)“; Cervical flexion (CF) stretches the dura”. A variant is the ‘bowstring test”” for which the knee is flexed a few degrees at the painfree limit of SLR and the popliteal nerve stretched by direct pressure (Figure 14). Undoubtedly other qualifying tests for root and dural tension have been deviscd’s. What they should have in common is that the meningeal or neural pathway is stretched without further stimulus to the muscles or joints of the lumbar spine and hips. For any one of these qualifying

tests to be positive.

the pain induced

on SLR

must be reproduced-whether it be in the back, hip or legs-and this emphasizes the need for precision in noting the site of pain on SLR.

Figure 14. The ‘bowstring’ test: popliteal pressure as a qualifying test of increased root tension during the SLR tesP.

The qualifying tests for increased root or dural tension are often independently positive”’ but as the results are often equivocal, more than one test may have to be used. If, for instance, a patient has pain down to the calf on SLR but the calf muscles are painful, reproduction of the pain on PDA clearly does not indicate a positive result as the test itself stretches the painful muscle. It would be the same for the ‘bowstring’ test if the popliteal muscles were sore, or if the piriformis muscle were hyperalgesic when performing MHR. Should one of the tests be positive this, diagnostically, may be enough but if it is negative or equivocal then another must be tried. In an industrial survey of back and sciatic pain the SLR qualifying tests were positive in 92 of 442 (21%). In 22 of the 92 ‘positives’ there was no limitation of SLR, only a unilateral difference in the symptoms caused by SLR. Later, on follow-up. two of the qualifying tests were found to have predictive valueh’,64. PDA and MHR were found to be of equal predictive, and diagnostic. value but CF was not’“. There are practical difficulties in passively flexing the neck during SLR when the shorter clinician is examining taller patients. It is more fruitful to do the cervical flexion tests seated, as described above. The ‘bowstring’ and other qualifying tests appear not to have been studied epidemiologically for their predictive value, but this is not to deny their potential diagnostic value.

The femorul stretch test (FST)

Figure 13. Medial rotation of the hip as a qualifying test of increased root tension during the SLR testa.

The femoral stretch test is routinely performed, usually with the patient prone but in one study, laterally recumbent”, and most often the femoral nerves are separately stretched. An alternative, with the patient prone, is to flex both knees, swinging the heels to the buttocks together. This has the advantage of standardizing the range and velocity of motion, making the comparison easier for the patient. Whatever method is used, any pain in the anterior thigh so caused must be differentiated from other diseases of the hip or iliopsoas muscle before the FST is deemed positive.

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C/in. Biomech. 1986; 1: No 1 Radiographic signs

Figure 15. Knee flexion, prone, for the Femoral Stretch Test, showing the resulting passive lumbar extension.

Tests of root compression Passive lumbar extension

Other clinical data emerge from conducting the FST by flexing the knees together. The movement passively extends the lumbar spine (Figure 15) and was described as a test of lumhosacral pathology by Nachlashh. Back pain is commonly elicited in this way-in 25% of all cases of back and sciatic pain seen in an industrial survey -and this has significant predictive value”. The pain appears to be caused by the passive lumbar extension, arising from the post-vertebral tissues: Not uncommonly, the movement provokes pain in the buttock or back of the thigh. though rarely below the knee: apparently due to the reduction of the lumen of the intervertebral foramen on extension. Herron and Phdasanth7 described another test with the same posture and movement. But the knees are held flexed with the heels to the buttocks for 35-60 seconds and the ankle jerk reflexes are then retested. When the reflex response is reduced by this manoeuvre. it is indicative of root compression. The authors described the diminution of other neurological signs elicited in this way.

The ‘bicycle’ test’

Pain and weakness on walking. as a symptom of cauda equina compression. is considered to be due to ischaemia of the nerve roots while the spine is extended but it has to be differentiated from circulatory disturbances of the lower limb itself. A simple test can be performed quickly using an exercise bicycle on which the patient cycles in an erect position with the spine extended until pain makes him stop. The duration is noted and the test, after time for recovery, is repeated. This time when the symptoms begin, the patient is instructed to continue cycling, but with the trunk flexed like a racing cyclist. If the test is positive. the patient can indeed continue without being halted-by pain because the flexed posture relieves the compression in the canal and foramina.

Interest in the size and shape of the lumbar spinal canal and foramina appears to have begun with the recognition of the relation between lumbar stenosis and the cauda equina syndrome. For a period thereafter it tias assumed that narrowing of the canal, whether of congenital origin or developing from hypertrophic osteoarthrosis with the resulting change in the lumen of the canal to a trefoil shape, arose from a consistent reduction of all its dimensions, including the interpedicular distance’*. That this is not so became clearer when the size of the canal was measured in a broader range of patients. Baddeley’ presented data from plain radiographs from patients with cauda equina syndrome due to lumbar stenosis, patients with sciatic pain and subjects without lumbar symptoms. He found first that the interpedicular distance was not significantly different in the three groups but that the other dimensions, though smallest in the stenotic group. were less in those with sciatica than in the normals. Comparable results came from Roberts6 who showed that the mid-sagittal diameter and the interpedicular distance were unaffected by hypertrophic osteoarthrosis but that the pedicles were shorter in operated cases of cauda equina syndrome. He also showed by cadaveric dissection that the thecal sac was disproportionately affected by the size and shape of the canal. With a trefoil-shaped canal the theta was markedly narrowed and displaced anteromedially. Ultrasonic scanning of the mid-sagittal diameter permitted ;I measurement at about IS” to the sagittal plane. In ;I series of studies from Doncaster it has been shown that this dimension is related not only to the severity of symptoms. signs and operative findings of disc prolapse’.“” hut also to the severity of chronic back pain in general’. Though there has been discussion about t hc origin of the ultrasonic echoes with this tcchniquc”‘. the rcpeafability of the measurement” and the consistency of the results provides a strong confirmation of the radiographic studies. However, ultrasonic measurement, because of i;s angle to the sagiltal plane. appears to reflect not only the midsagittal diameter itself but may be influenced by facetal hypertrophy. More recent work has shown first, the correlation between radiographic measurements from plain films and osteological measurements and secondly, that the various dimensions of the canal are not all dependent variables. those in the transverse plane being independent of those in the sagittal”. Thus narrowing of the interfacetal diameter can arise independently of midsagittal narrowness. Figure I6 shows the five measurements which can be made. The pedicular length, the interpedicular distance and the mid-sagittal diameter are genetically determined and they are relatively insusceptible to hypertrophic osteoarthrosis and show comparatively fewer age-related changes. The interfacetal distance, on the other hand, is highly susceptible to hypertrophy of the

Troup: Lumbar spinal canal

41

Pedicular length

lnterpedicular distance

Foraminal A P

Mid-sagittal diameter

Fig. 16. Measurements of the size and shape of the lumbar canal and foramina from plain radiographs: mid-sagittal diameter, pedicular length and AP foraminal distance from the lateral view; and interfacetal distance and interpedicular distance from the AP view.

process and the AP foraminal distance is reduced by hypertrophy of the inferoposterior margins of the vertebral body. The interfacetal distance, particularly at Sl, was found to be significantly less in cases of disc prolapse compared with less severe cases of lumbar disorder”. And in a study of the relation between lumbar mobility and radiographic measurement it was found that in males, restricted mobility was associated with narrowing of the AP foraminal distance but in females, it was associated with narrowing of the interfacetal distances74. Thus males and females appear to be more susceptible to diminution in space in the diameters, AP foraminal and interfacetal respectively, in which they are normally narrower than the opposite sex. articular

Discussion

The diagnostic interpretation of symptoms and clinical signs of lumbosacral radiculopathy depends. with few exceptions, on an understanding of the movements of, and forces applied to, the lumbar spinal canal in the course of the patient’s normal activities and during the clinical examination. This is complemented by plain radiographs which give a picture of the size and shape of the lumbar spinal canal and foramina, and thus of potential sources of angulation or compression. What the radiographs cannot show is the extent of soft tissue hypertrophy superimposed upon the bony changes; though where bony hypertrophy is indicated, some soft tissue encroachment is likely. It would, however, be over confident to claim that the picture is complete. More elegant and precise clinical methods will supersede. Doubts on the interpretation of tension signs remain. For example, some patients with severely limited SLR can sit, apparently without undue distress, on the examination couch with their hips flexed and knees more or less fully extended. This is sometimes taken to be one of the non-organic clinical signs, suggesting an exaggerated response to the SLR test. But not uncommonly it is found in patients in whom operative findings are positive and for whom a genuine explanation must be sought, Where tension

signs on both cervical flexion and SLR are positive, there is likely to be adhesion of the root in or near the foramen. If tension above and below the site of adhesion is equalized, the adhesion site itself will not be distrained or only minimally. This, at any rate, appears to be the explanation but, like any other hypothesis. it remains to be tested; although it would be unethical to do so at operation and difficult at post mortem. It is not, unhappily, always possible to validate a clinical sign with cadaveric observations, study it epidemiologically and complete the picture by assessing its predictive value. Two, at any rate. of the SLR qualifying tests have been so validated, as well as limitation of SLR itself44,64. To a great extent it is necessary to rely on one’s powers of observation, test them with reasonable scientific rigour whenever possible. but above all be aware of the underlying biomechanits. Lastly it has to be appreciated that one pathological factor in the biomechanics of the spinal canal remains unexplored: the temporal factor. Neural tissues, judging by some of the earlier studies quoted, can withstand a considerable mechanical insult and yet recover their function. Unless the insults are repeated. local inflammatory reaction and endoneurial oedema may be minimal. If, on the other hand, a mechanical encroachment is slow and insidious there may be time for adaptation, both structurally and functionally. At autopsy, it is not uncommon to find canal and foramina hypertrophically narrowed to the point that the nerve roots are positively ribbon-like, with no evidence that the individual was seriously disabled by it. What have to be studied in some depth are the rates of onset of these mechanical insults; the concomitant states of irritability and oedema; together with the immediate and eventual neurological function. Acknowledgements

My thanks to Professor Alf Breig and to his publishers, Almqvist & Wiksell International, for permission to reproduce Figures 2, 67A, 123, 134, 136, 137, 138 and 140 from the book ‘Adverse Mechanical Tension in the Central Nervous System’; and to Dr Tom Reilly, and

42

C/in. Biomech.

1986; 1: No 1

his publisher, for permission to reproduce Figures 2513 and 2574 from my chapter in his book ‘Sports Injuries and Sports Fitness’, London: Faber and Faber Ltd 1981.

References 1 timone

I. The importance of the sagittal diameters of the :ervical spine in relation to spondylosis and myelopathy. J 3one Joint Surg 1974; 56B: 30-6 2 Veidlinger OF, Colwill, JC, Smyth HS, Turner D. Cervical myelopathy and its relation to cervical stenosis. spine 1981; 6: 550-2 3 Gdwards WC, LaRocca SH. The developmental ;egmentai sagittal diameter in combined cervical and umbar spondylosis. Spine 1985; 10: 42-9 4 Eismont FJ, Clifford S, Goldberg M, Green B. Cervical ;agittal spinal canal size in spinal injury. Spine 1984; 9: 563-6 5 Baddeley H. Radiology of lumbar spinal stenosis. In: layson MIV. ed. The lumbar spine and back pain. London: Sector Publishing Co. 1976, pp. 151-71 Roberts GM. Lumbar stenosis. University of London. 1978. MD Thesis Porter RW, Hibbert C, Wellman P. Backache and the lumbar spinal canal. Spine 1980; 5: 99-105 Macdonald EB, Porter RW, Hibbert C, Hart J. The relationship between spinal canal diameter and back pain in coal miners. J Occup Med 1984; 26: 23-8 9 Dyck P, Doyle JB. “Bicycle test” of van Gelderen in diagnosis of intermittent cauda equina compression syndrome: case report. J Neurosurg 1977; 46: 667-70. 10 Dyck P, Pheasant HC, Doyle JB. Rieder JJ. Intermittent cauda equina compression syndrome: its diagnosis and treatment. Spine 1977; 2: 75-81 11 Breig A. Biomechanics of the central nervous system. Stockholm: Almqvist and Wiksell, 1960. 12 Breig A. Adverse mechanical tension in the central nervous system: Relief by functional neurosurgery. Stockholm: Almqvist & Wiksell International, 1978 13 Breig A, Troup JDG. Focal intramedullary tension in patients with cord lesion and its surgical relief by spinal cord relaxation. Lancet 1984; 1: 739-40 14 Colachis SC, Strohm BR. Radiographic studies of spinal motion in normal subjects: flexion and hyperextension. Arch Phys Med Rehabil 1965; 46: 753-60 15 Penning L. Functional pathology of the cervical spine. Amsterdam: Excerpta Medica, 1968 16 Lysell E. Motion in the cervical spine: an experimental study on autopsy specimens. Acta Orthop Stand 1969. Supplementum 123 17 Bhalla SK, Simmons EH. Normal ranges of intervertebral joint motion of the cervical spine. Can J Surg 1969; 12: 181-7 18 Colachis SC, Strohm BR, Ganter EL. Cervical spine motion in normal women: radiographic effect of cervical collars. Arch Phys Med Rehabill973; 54: 161-9 19 Loebl WY. Regional rotation of the spine. Rheumatol Rehabill973; 12: 223 20 Babin E, Capesius P. Etude radiologique des dimensions du canal rachidien cervical et de leurs variations au tours des Cpreuves fonctionelles. Ann Radio1 1976; 19: 457-62 21 Kadir N, Grayson MF, Goldberg AAJ, Swain MC. A new neck goniometer. Rheumatol Rehabil 1981; 20: 219-26 22 Jirout J. The mobility of the cervical spinal cord under normal conditions. Br J Radio1 1959; 32: 744-51 23 Edgar MA, Nundy A. Innervation of the spinal dura mater. J Neurol Neurosurg Psychiatr 1966; 29: 530-4 24 Cyriax J. Perineuritis. Br Med J 1942; 1: 578-80

25 Tanz SS. Motion of the lumbar spine: a roentgenographic study. Am J Roentgen01 1953; 69: 399-412 26 Jirout J. Mobility of the thoracic spinal cord under normal conditions. Acta Radio1 (Diagn) 1963; 1: 729-35 27 Bakke SN. Rontgenologische Beobachtungen iiber Bewegungen der Wirbelsaule. Acta Radio1 1931; Supplementum 13 28 Alvik I. Tuberculosis of the spine. II. The mobility of the lumbar spine after tuberculous spondylitis. Acta Chir Stand 1949: Suonlementum 141 29 Begg C, Faicondr MA. Plain radiography in intraspinal protrusion of lumbar intervertebral discs: a correlation with operative findings. Br J Surg 1949; 36: 225-39 30 Allbrook DB. Movements of the lumbar spinal column. J Bone Joint Surg 1954; 39B: 339-45 31 Schalimtzek M. Functional roentgen of degenerated and normal intervertebral disks of the lumbar spine. Acta Radio1 1954; Supplementum 116: 300-6 32 Jonck LM. Niekerk JM van. A roentgenological study of the motion of the lumbar spine of the Bantu. S Afr J Lab Clin Med 1961: 7: 67-71 33 Twomey LT. The effect of age on the range of motion of the lumbar region. Aust J Physiotherapy 1979; 25: 257-63 34 Taylor JF, Twomeg LT. Sagittal and horizontal plane movement of the human lumbar vertebral column in cadavers and in the living. Rheumatol Rehabil 1980; 19: 223-32 35 Day MH. The anatomy of the lumbosacral plexus with particular reference to the blood supply. University of London 1962; PhD thesis 36 Breig A. Marions 0. Biomechanics of the lumbosacral nerve roots. Acta Radio1 (Diagn) 1963: 1: 1141-60 37 Sunderland S. Meningeal-neural relations in the intervertebral foramen. J Neurosurg 1974; 40: 756-63 38 Sunderland S. Mechanisms of cervical nerve root avulsion in injuries of the neck and shoulder. J Neurosurg 1974; 41: 705-14 39 inman VT. Saunders JBdeCM. The clinico-anatomical aspects of the lumbosacral region. Radiology 1942; 38: 669-78 40 Falconer MA. McGeorge M, Begg AC. Observations on the cause and mechanism of symptom production in sciatica and low back pain. J Neural Neurosurg _ Psychiatr 1948; 11: 13-26 41 Woodhall B. Haves GJ. The well lee raisine test of Fajerstajn in thehiagnosis of rupturid inteyvertebral disc. J Bone Joint Surg 19.50; 32A: 786-92 32 Charnley J. Orthopaedic signs in the diagnosis of disc protrusion with special reference to the-straight leg raising test. Lancet 1951; 1: 186-92 43 Goddard MD, Reid JD. Movements induced by straight leg raising in the lumbosacral roots, nerves and plexus, and in the intrapelvic section of the sciatic nerve. J Neural Neurosurg Psychiatr 1965; 28: 12-8 44 Breig A. Troup JDG. Biomechanical considerations in the straight-leg-raising test: cadaveric and clinical studies of the effects of medial hip rotation. Spine 1979; 4: 242-50 45 Sugiura K. Yoshida T. Katoh S, Mimatsu M. A study on tension signs in lumbar disc hernia. Int Orthop 1979; 3: 225-8 46 Golub BS, Silverman P. Transforaminal ligaments of the lumbar spine. J Bone Joint Surg 1969; 51A: 947-56 47 Rydevik B, Brown MD, Lundborg G. Pathoanatomy and pathophysiology of nerve root compression. Spine 1984; 9: 7-15 48 Denny-Brown D, Brenner C. The effect of percussion of nerve. J Neurol Neurosurg Psychiatr 1944; 7: 76-95 49 Causey G. The effect of pressure on conduction and nerve fibre size. J Anat 1950; 84: 65 50 Denny-Brown D, Brenner C. Paralysis of nerve induced by direct pressure and by tourniquet. Arch Neurol Psychiatr 1944; 51: 1-26

Troup:

51 Denny-Brown D. Docherty MM. Effect of transient stretching of peripheral nerve. Arch Nemo1 Psychiatr 1945; 54: 116-29 52 Lundborg G. Ischemic nerve injury: experimental studies on intraneural microvascular pathophysiology and nerve function in a limb subjected to temporary circulatory arrest. Stand J Plast Reconstr Surg 1970; Supplementum 6 53 Blower PW. Neurologic patterns in unilateral sciatica: a prospective study of 100 new cases. Spine 1981; 6: 175-9 54 Denny-Brown D. Paper read at joint discussion on the causation and treatment of interstitial neuritis. Proc SOC Med 1933; 26: 1399-1403 55 Edgar MA. The role of the spinal dura mater in the clinical presentation of lumbar disc prolapse. University of Cambridge, MChir thesis, 1975 56 Lasegue C. Considerations sur la sciatique. Arch GCn Med 1864; 2: 558-80 57 Fajersztajn J. Uber das gekreuzte Ischiasphanomen. Wien Klin Wochenschr 1901; 14: 41-7 58 Dyck P. Lumbar nerve root: the enigmatic eponyms. Spine 1984; 9: 3-6 59 Deutsch F. cited by Alexander W. Neuralgic und Neuritis: specielle Pathologie und Therapie. Band I. Nervenkrankheiten. Berlin, Wien: Urban und Schwarzenberg 1924; 341608 60 Troup JDG. Straight-leg-raising (SLR) and the qualifying tests for increased root tension. Spine 1981; 6: 526-7 61 Troup JDG, Martin JW, Lloyd DCEF. Back pain in industry: a prospective survey. Spine 1981; 6: 61-9 62 Hudgins WR. The crossed straight leg raising test: a diagnostic sign of herniated disc. J Occup Med 1979; 21: 407-8 63 Macnab I. Backache. Baltimore: Williams & Wilkins Company 1977; 125-7

A TEXTBOOK

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canal

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64 Lloyd DCEF, Troup JDG. Recurrent back pain and its prediction. J Sot Occup Med 1983; 33: 66-74 65 Dyck P. The femoral nerve traction test with lumbar disc protrusions. Surg Neural 1976; 6: 163-6 66 Nachlas IW. The knee-flexion test for pathology in the lumbosacral and sacroiliac joints. J Bone Joint Surg 1936; 18: 724-S 67 Herron LD, Pheasant HC. Prone knee-flexion: provocation testing for lumbar disc protrusion. Spine 1980; 5: 65-7 68 Jones RAC, Thomson JLG. The narrow lumbar canal: a clinical and radiological review. J Bone Joint Surg 1968; 50B: 595-605 69 Porter RW, Wicks M, Ottewell D. Measurement of the spinal canal by diagnostic ultrasound. J Bone Joint Surg 1978; 60B: 481-4 70 Kadziolka R, Asztely M, Hanai K, Hansson T, Nachemson A. Ultrasonic measurement of the lumbar spinal canal: the origin and precision of recorded echoes. J Bone Joint Surg 1981; 63B: 504-7 71 Hibbert CS, Delaygue C, McGlen B, Porter RW. Measurement of the lumbar spinal canal by diagnostic ultrasound. Br J Radio1 1981; 54: 905-7 72 Leiviska T, Videman T, Nurminen T. Troup JDG. Radiographic versus bony measurements of the spinal canal at lumbar vertebrae L3-L5 and their relations to age and body stature. Acta Radio1 (Diagn) 1985; 26: 403-11 73 Heliovaara M, Vanharanta H, Korpi J, Troup JDG. Herniated lumbar disc syndrome and vertebral canals. (Submitted for publication) 74 Vanharanta H, Korpi J, Heliovaara M. Troup JDG. Radiographic measurements of lumbar spinal canal size and their relation to back mobility. Spine 1985; 10: 461-6

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