INTRODUCTION
An attempt to briefly summarise past and more recent work on nerve injury makes for some untidy bedfellows, because the field is a very large one and interesting de
velopments occur neither in step with each other nor side
by-side.
Comparatively little is known about the pathophysio
logy of nerve root compression. III .. Few clinical/experi
mental studies of root compression have been reported, mOSt studies having concentrated on peripheral nerves, and thus the knowledge of the relative amountS of damage to myelin and axon of the nerve root is somewhat limited.
Surgical biopsies of compressed roots are rarely per
formed. I n many decompression procedures, care is taken not to incise the d ura, so that the root is not even visualised.
As nerves and roots are structurally similar it seems reasonable to draw some inferences from clinical con
sequences of traumatic injury to peripheral nerve, and reports of experimental injury of nerves. The inferences should not be carried too far, since irritant and compres
sive effeclS on peripheral nerves are nor quite the same as when spinal nerve roots suffer the same interference, also spinal roots themselves appear to have different resp(»Jses to experimental compression, and to stimulation. For example:
1. During Frykholm's operations192 on the cervical spine under local anaesthesia:
a. the dorsal root was stimulated, and the patient reported a 'neuralgic' pain in the dermatome dis
tribution
b. if the ventral, motor root was stimulated, the patient reported a deep 'boring' myalgic pain, situated more proximally in the muscles which were painful and tender preoperatively.
2. I n the region of the intervertebral foramen, spinal nerve roots with motor and sensory fibres of the somatic nervous system have extensive connections, via white and grey rami communicantes, with the autonomic nervous system, the whole forming Stillwell's paravertebral plexus.l m Peripheral nerves carry only a few autonomic nerve fibres because these have already separated to pass down the limb in the coats of the arteries. Proximal mech
anical pressure on radicular nerves has a greater effect therefore on the autonomic nervous system than does dis
tal pressure on peripheral nerve trunks.l lsob The cold sciatic leg is much more common than similar distal tem
perature changes in the carpal tunnel syndrome, for example.
3. Axons compressed close to their parent neurone cell suffer a greater risk of the cell being damaged than when pressure is remote. Entrapment neuropathy at the wrist can lead to a permanent loss of power in the thenar muscles, but it is unlikely to lead to permanent damage of posterior root-ganglion cells, whereas compression at the intervertebral foramen may well cause permanent damage in the posterior ganglion cells.
4. As will be seen, there are differences in the behaviour of peripheral nerves and spinal rootS subjected to the same experimental injury. 1 I12
'In these matters it should be noted that damage to sen
sory nerve fibres is not necessarily painful' (Sunderland, 1978). ""
While lesions of trespass upon spinal cord and nerve roots remain the prime concern for those handling com
mon vertebral joint problems, the study of compressive effects on peripheral nerves remains of value and interest.
Sunderland's ( 1 968)"" authoritative and extensive review indicates that experimental findings are sometimes contradictory, as are the interpretations of findings, e.g.
the different susceptibilities of the different diameter fibres, the time needed for a complete compressive block and the most important cause of it.
Susceptibility to stress
That peripheral nerves tolerate without pain the stresses and strains of normal free active and passive movements, of a wide range, indicate that nerves enjoy protective fibres within the funiculi, the nerve fibres themselves are the last to suffer tension when stretching is applied.
3. The perineurim imparts elasticity to the nerve trunk and gives it tensile strength.
4. The large amount of epineurial connective tissue,
providing a loose matrix for the funiculi, has a cushioning effect.
Nerve roots differ from peripheral nerves-the nerve fibres are arranged in parallel bundles which are loosely supported by endoneurial tissue alone ,; they are more vulnerable to stretch since they lack the tensile strength of peripheral nerves. Without epineurial packing they are also susceptible to compression, and the semiosseous con
fines of the intervertebral foramen are an added potential danger.
Traction on peripheral nerves during neck, trunk and limb movementS will transmit tension to the nerve roots, and cause 'piston-Iike' movements of the roO[ complex within the foramen, but a degree of protection from over
stretching by transmitted forces is provided, i.e. : I . Traction pulls the entire root/dura complex out
wards, the cone-shaped dural funnel thus plugging the foramen and resisting further lateral movement.
2. Since relatively large upper limb movementS are likely to greatly stress cervical nerve roots, those of C4 to C7 are firmly attached, by slips of prevertebral fascia and from musculotendinous attachments, to the 'gutter' of the cervical transverse process.
3. The elastic properties of nerve roots allow accommo
dation of tension to a degree, but this is limited. Nerve roots will fail under a given tension before peripheral nerves.
Conversely, there are several factors which may lower (he threshold of neroe fibres for the point at which abnormal
3. Damaged nerve fibres are more susceptible to mech
anical deformation, and to ischaemia.
4. Toxic or metabolic neuropathies, and intercurrent infections, render the nerve more likely to suffer from a traumatic or ischaemic event.
Axonal transport
Those neurones with long axonal processes, which depend upon components manufactured in the cytoplasm, allow the study of traffic which moves within them. '07'
Transfer of substances underlies trophic and other long-term influences of peripheral neurones on the meta
bolism, function, development and growth of the st.ructure innervated.
Orthograde transneuronal movement of biochemical substances, proceeding from the anterior horn cell along the axon into the fibres of muscle, has been demon
strated by radioactive isotope tracing methods (Korr.
1967). ,N
The most extensively studied are the labelled proteins, some of which move slowly at about I mm a day (slow
PATHOLOGICAL CHANGES--GENERAL 9S
transport) while others move considerably more quickly (fast transport).
Ochs (1 975)'" showed that the characteristic outflow is graphically seen as a crest of advancing activity followed by a plateau, typically with less activity in it compared to the crest. The crest advances at a linear rate down the fibre, and in a large number of experiments the rate deter
mined was 410 mm per day. The rate is independent of nerve size, i.e. diameter of myelinated fibres or unmyeli
nated fibres, and for a given neurone, the rate of transfer of all molecules is always the same. A range of soluble pro
teins, polypeptides and particulates are carried down, as are glycoproteins, glycolipids and phosphatidyl-cholinc, together with catecholamines and enzymes related to their synthesis.
I t is common knowledge that effector cells have im
portant influences on the innervating neurones, and Thoenen ( 1 978) "" describes the evidence that retrograde axonal transport is linked to subcellular structures which are similar to those associated with orthograde transport.
Among the many experiments described were those in which transplants, pre incubated in a medium containing nerve growth factor (NGF) become more densely and more rapidly innervated by adrenergic fibres than without preincubation. Preincubation in a medium containing antibodies to NGF markedly impaired the reinnervation of the transplanted tissue. These and other observations provide support for the hypothesis that NGF might act as a macromolecular messenger between effector organs and their innervating neurones.
A1buqerque et al. ( 1974)" have demonstrated that the important trophic action which nerves have on striated muscle is in fact related to axonal transport.
Some of the molecules delivered by axoplasmic transport are needed for transmitter metabolism and for trophic action on in
nervatedcells . . . . With the present state of knowledge, the impact that nerve compression, stretching, angulation or other deforma
tions may have on the neurochemistry of axonal transport is not known but can reasonably be inferred to be significant. [Samson, 1978) 1078
SjOstrand (1978)"" mentions that a local supply of energy is needed to fuel the axonal transport, which is partially or completely blocked by local ischaemia or compression.
In nerves which had been subjected to local compres
sion, an acute accumulation oflabelled proteins was found in the region of the compression.
A 2-hour compression with pressures as low as 50 mmHg (6.67 kPa) caused blockage of fast transport, which was reversible within 24 hours. Reversal of trans
POrt blockage usually occurred within 3 days after com
pression at 200mmHg (26.66 kPa) for 2 hours and within 7 days after compression at 400 mmHg (53.33 kPa) for 2 hours.
96 COMMON VERTEBRAL JOINT PROBLEMS
SjOstrand'''' has suggested that conduction block, transport impairment and intraneural oedema may differ in their reversibility, also that orthograde and retrograde transport may also be differentially affected by nerve in
jury.
Haldeman and Meyer ( 1970)'" mention that the recorded study of peripheral nerve compression or con
striction is more than 1 00 years old.
Waller ( 1 862)''''' described the effects of compression on the radial, median and ulnar nerves of his own arm.
He did not refer to the mechanism by which these experi
ments disturbed nerve conduction, perhaps because it appeared self-evident that the conduction block was due to simple pressure. That this was apparently not so was demonstrated by Grundfest ( 1936)'" who found that a pressure of I 000 atmospheres ( 1 01,325 kPa) was necessary to completely block nerve conduction ; hence the until recently prevailing view that the clinical consequences of compression or stretching of nerves were due mainly to obliteration of the vasa nervorum. '0)7
There is a list of more than 50 reports of investigation into conduction block, ischaemia and posrischaemic para
esthesiae, indicating the importance of these abnormal processes and their prime interest for clinicians. Severe and prolonged compression blocks the nerves' blood supply and produces other damage ; it then loses its ability to conduct impulses. Prolonged inflammation appears to produce the same effect. Temporary compression will produce temporary loss of conduction, from minutes to days according to the degree and duration of compression.
Intermittent compression or mechanical irritation may lead to inflammatory changes, with space-occupying effects produced by oedema and thus some or all of the changes and clinical features following inflammation.
Traction, of insufficient force to disrupt the nerve, will cause irritation and consequent neuritis. " sob
Sunderland ( 1 968)"" refers to the three fundamental types of peripheral nerve injury, in which:
1 . There is temporary interruption of conduction with
out loss of axonal continuity between neurone and end
organ.
2. The axon is severed or axonal mechanisms are so dis
organised that the distal axon does not survive, neither for a variable distance does the proximal axon. The endoneurial sheath is preserved unthreatened by the in
jury reaction and the ensuing Wallerian degeneration.
3. The fibres are severed or the wall of the endoneurial tube and its contents are so disorganised that the normal architecture of the fibre is completely destroyed.
Compressive injury to nerve results iU lwo distinct pathologi
cal processes :99'
1. Relatively low-intensity trauma (pressures between 1 50-1000mmHg) (20-U3.33 kPa) causes segmental demyelination. Electrical studies demonstrate slowing of
conduction velocity (partial conduction block) in the in
jured segment. Distal to the injury, conduction velocity and neuromuscular function are preserved. For restora
tion of full normal function, only myelin resynthesis in the injured section is needed ; this is ordinarily rapid and complete.
2. With more severe trauma, Waller ian degeneration occurs. Distally, the nerve becomes electrically inexcit
able, and the myoneural junction and sensory end-organs degenerate. For the restoration of full function, neurones must synthesise large quantities of axonal Structure pro
teins, axons must sprout through the distal nerve segments to re-establish synaptic contact with muscle and finally these axons must be remyelinated. This complex regenerative process is usually incomplete and unsatisfac
tory especially in the adult.
Denny-Brown and Brenner ( 1944)'" applied compres
sion of 1 70-430 g by a spring clip to a peripheral nerve for two hours, and reported intermittent loss of myelin at the nodes of Ranvier in the compressed area. There was transient paralysis of 5-18 days, but this was not associ
ated with any gross defects of sensation, and the distal por
tion of the nerve did not degenerate. Despite the recovery of motor conduction within a few days, res(Qration of mye
lin was only slight at two months, and remained in
complete at six months. The authors regarded the effects of compression to be due entirely to changes produced in the axoplasm rather than due to the selective con
sequences of pressure on fibres of different sizes.
Barlow and Pochin ( 1948)" showed that repeated ischaemia reveals a reduction in the degree of recovery of nerve, e.g. after cuff occlusion of a human arm for 2S minutes, sensation and motor power will return to normal.
For some hours afterwards, however, a second occlusion will produce earlier development of sensory and motor changes. Thus repeated pressures increase the vulner
ability of peripheral nerves, although cumulative effects only appear if the periods of relief are small in comparison to the periods of occlusion.
Haldeman and Meyer (1970)'" used different tech
niques to compress the frog peroneal nerve and showed that there are two mechanisms involved in the blocking of nerves by constriction and pressure. The techniques were :
1 . A single loop of surgical cotton (0.25 mm) was tied loosely around the nerve, and weights which created ten
sions of 40, 60 and 80 g were applied to pull the cotton more tightly around the nerve.
2. A 2-3 mm wide plastic strip was placed around the nerve, and weights to effect a constriction exerting 40 g and 80 g were applied. The responses of alpha and beta fibres, to a stimulus applied at a frequency of one impulse every 4 seconds, were noted. Decreasing amplitudes of the spike potential were expressed as percentages of the maximum :
I . With the 0.25 1//1// cons t r;ct;oll, recordings were as follows :
Tablr 5.1
40 g 60 g
Time Alpha Beta Time
(minutes) (n II of maximum) (minutes)
0 100 100 0
1.0 85 80
3 71 65 2
6 56 35 5
18 46 20 8
20
36 44 10
45 43 10 45
60
Release Release
5 46 35 5
30 44 65 30
At 40g cOllStricrio" the spike decreases rapidly for 1 5 minutes, and then much more slowly. The slow-conduct
ing gamma fibres stopped conducring almost at once, within 1 minute, and are nOt recorded.
The beta spike virtually disappeared after 1 8 minutes.
After this, the alpha spike continued slowly decreasing.
On release, the alpha response was virtually unchanged at 30 minutes ; the beta spike had increased to about half its normal amplitude, its responses being roughly similar to those of an unconstricted nerve after 75 minutes of the steadily repetitive stimulation described above.
At 60g cotlStriction, the amplitude of responses has diminished more quickly and to a greater degree ; release of constriction had little effecL effecL
At 80g c011striclioll, twitching was observed as the spike potential began immediately to decrease to virtual dis
appearance at I ! minutes. Similar constriction in anaes
thetised experimental animals produced paralysis which still persisted at 60 days, when the spike potential remained absent and typical Wallerian degeneration was evident distal to the constriction. There is a puzzling dis
crepancy between the effects of compression by a spring clip'" and by constriction by a single, 0.25 mm wide loop of surgical cotton, and the authors refer to this when com
paring their findings with those of other reports. 81, 84, L6L,
1 302 The second method of constriction was varied to
resemble more closely the techniques of previous investi
gators.
PATHOLOGICAL CHANGES--GENERAL 97
80g
Alpha Beta Time Alpha Beta
(U II of maximum) (minutes) (00 of maximum
100 100 0 100 100
0.5 35 60
1.0 8 0
1.5 2 0
67 85
53 60
42 40
30 30
12 1 5
7 8
Release
10 0
8 0 30 0 0
60 days 0 0
2. With [he 2-3 mm constriction, the effects were as follows :
Table 5.2
40g 80g
Time Alpha Beta Time Alpha Beta
(minutes) (°0 of maximum) (minutes) ("0 of maximum)
0 100 100 0 100 100
I 50 50
2 25 10
3 86 50 3 13 0
5 2 0
6 57 0
10 21 0
1 5 5 0
Release Release
2 14 10
5 28 40
15 43 60
30 57 70
45 3 0
With all 80 g compression, the spike potential reacted in much the same way as after 80 g compression with the 0.25 mm cotton. The quickly diminishing response was completely absent after 5 minutes and had not returned after 30 minutes.
WiTh the 40 g compressioll, the responses were markedly different. The spike potential diminished more rapidly than with the 0.25 mm constriction at the same pressure, being completely absent after 1 5 minutes. On release, however, recovery started almost immediately, and con
tinued for about 25 minutes, reaching to around 60 per
98 COMMON VERTEBRAL JOINT PROBLEMS
cent of its original value by 30 minutes, at which time it had levelled out to remain constant. As previously, the beta response disappeared first. It also showed the larger recovery.
CONCLUSIONS
There appear to be two mechanisms involved in nerve block by compression :
1 . The first is completely reversible and seems to leave the nerve undamaged, i.e. a reversible conduction block.
2. The second is irreversible-it disturbs nerve conti
nuity and Wallerian degeneration follows, i.e. the irrever
sible conduction block.
The nature of the mechanism involved appears depen
dent upon the nature of compression, its duration and the degree of deformity produced by it.
1 . The reversible conduction block
Depending upon the nature of the constriction, a nerve can still obtain enough oxygen, by diffusion over a dis
tance of 5 cm, to maintain almost full activity. The usual explanation of the reversible block is anoxia, based on the knowledge that a nerve deprived of oxygen ceases to con
duct in 1 6-35 minUles. Vet pressure may be applied to a nerve in such a way as to make it ischaemic, without impairing conduction ;81 although diffusion ceases at pressures in excess of 100 mmHg ( 1 3.33 kPa), when the nerve does become anoxic.
Cessation of oxygen diffusion is probably then due to a decrease in axoplasmic and endoneural fluid (produced by the more severe compression) through which oxygen can diffuse. Ifneither axons nor blood vessels are damaged during the constriction, conducting ability returns soon after compression is removed.
2. The irreversible conduction block
This is a different mechanism; the time needed to produce block with the O.25 mm cotton stricture is longer, with the same 40 g tension. The number of fibres affected depended on the degree of constriction. Moderate con
striction affected a few fibres, the others presumably being protected by the inertia of axoplasmic and endoneural fluids. With increasing stricture all fibres were blocked, and more quickly. Two months later, the nerve had not recovered conduction.
From cross-sections through the constriction it was observed that the three elements necessary for impulse conduction (intracellular fluid, extracellular fluid and an intact membrane) were all eliminated by severe con
striction. The fluids had been forced out by the pressure, which had also destroyed the axolemma and myelin sheath.
Allen (1938)" showed that while asphyxia ofa limb may cause a paralysis which is reversible, direct pressure from
a tourniquet can cause permanent loss of nerve con
duction. Vascular injury or irritation leading to traumatic arterial spasm may also produce an irreversible block.485 Alpha and bela fibres appear to act quite differently to compression and its consequences. In the reversible COtl
sen'criarl, the beta-response disappeared long before the alpha spike was eliminated, but the beta fibres were quicker to recover and did so to a greater degree. In the irreversible conscricciarl, the beta fibres were again blocked earlier, and again showed a degree of recovery. The alpha fibres showed no recovery at all.
Gelfan and Tarlov ( 1956)"" found the largest fibres most susceptible to compression and the finest relatively resistant, while anoxia blocks the smaller alpha before the
Gelfan and Tarlov ( 1956)"" found the largest fibres most susceptible to compression and the finest relatively resistant, while anoxia blocks the smaller alpha before the