4Neurodynamics

LOUIS GIFFORD

Chapter Objectives '

Introduction

Tine Nervous System Responds to Movement

Design Features 'and Nervous System Dynamics

The Normal Nervous System as a Sensitive Tissue .

Physiological Effects of Movement on Nervous Tissue

Pathophysiology of Nerve and its Influence on-Movement: Tsleural Pathodynamics' .

From Theory to Practice: Neural Sensitivity

Final Comments -

Conclusions and Key Points

Chapter ObjectivesNeurodynamics addresses the peripheral andten-tral nervous systems in a unique way. Historically,the nervous system has been viewed as a commu-nicating and coordinating organ for the rest ofthe body. Little attention has been focused on thefact that as the body moves so the nervous systemhas to accommodate and adapt to the movementsit paradoxically produces.After reading this chapter you should be ableto: -

1 Appreciate that the nervous system moves andhas many design elements that allow this tohappen. This includes both the central nervoussystem [CNS] and the peripheral nervoussystem (PNSJ;

2 Appreciate that joint movements in one areacan have quite far-reaching mechanical effectson neural tissues;

3 Understand that neurodynarrircs looks at theeffects of movement/posture on the nervoussystem. This includes both movements andpostures that tend to compress neural tissue

159

Louis Gifford

and those that tend to elongate it. Most move-ments and postures are likely to produce com-binations of compression and elongationeffects;

4 Appreciate that neural compression and elon-gation produce.physiological effects on neuraltissue;

5 Appreciate that pathological processes in tis-sues that surround the nervous system mayhave detrimental consequences on its mechan-ical and physiological health and that altera-tions in compliance and sensitivity may be aconsequence;

6 Appreciate that the nervous system in generalis relatively insensitive, yet if it is injured orphysiologically compromised in some way ithas the potential to become an extremelyhypersensitive tissue and a potent source of

. ongoing pain;7 Have a good understanding of possible patho-

physiological processes that can underlie,enhanced neural sensitivity.

Introduction

That the nervous system moves is beyond doubt.In 1978 Alf Breig published a book called Adverse

4

Mechanical Tension in the Central Nervous Sys-tem which presented clear evidence that nervetrunks and roots7 the spinal cord and its cover-ings, as well as the brain, are capable of quiteremarkable movement. Professor Henk Verbeist,one of the world's leading neurosurgeons, wrotein the foreword to Breig's book:

In my opinion his work should not only beread by specialists in neuroscience and ortho-paedic surgery, but also by anaesthetistswhose activities regularly involve the position-ing of defenceless patients, and last but notleast by physiotherapists for reasons whichneed no further precision. [Breig, 1978]

That was back in 1978. For physiotherapy it wasnot until the late 1980s and early 1990s that thenotion that the nervous system has subtle designfeatures that allow it to move, was more widelyappreciated [Butler and Gifford, 1989; Butler, 1991].The prime purpose of the nervous system is oneof continuous communication, whatever thesituation and whatever the body happens to bedoing at the time. Thoughts about its anatomicaldesign must take into account the need for vitalelectrical and chemical processes to be able tocontinue unhindered during movement. Forinstance, observe the highly coordinated yetextreme movements of gymnasts and dancersand consider the need for the nervous systemto be able to physically adapt (Figure 4.1].

Figure 4.1 Extreme joint movement and muscle stretchrequires considerable physical adaptation of the peripheralnervous system and the neuraxis. The elongation andcompressive forces that the nervous system structures have tocope with in this gymnast are impressive.

160

Neurodynamics

In terms of gross structure the nervous systemappears as a well organized cord-like meshworkbranching away from the core central nervoussystem [CNS] structures, the brain and spinalcord. The term 'neuraxis' [Bowsher, 1988] in placeof CNS helps to focus us on this component ofthe nervous system from a biomechanical per-spective. However, Butler [1991] introduced theidea that we should consider the nervous systemas a continuum, in other words, get away from thetraditional anatomical descriptive concepts ofcentral, peripheral and autonomic nervous sys-'terns and move towards a view that the wholestructure is closely linked. In this way, the nervoussystem is unique among organs and systems inthat it has a pretty straightforward mechanical,electrical and chemical 'connectedness' [Butler,1991]. The implication is that mechanical, electricaland chemical changes in one part of the. nervoussystem may have far-reaching effects for the restof it.

Considers subject who gets nasty ca/fpa/o'in the full slump test position (se ~*' '*""'4.2). Lifting the head relieves trie

rtfie calf and allows the knee toextended without any major i

Putting the head flexion back oii {again ca uses a dramatic return ofcalfsyrrip'f&jjfts:" 'Without knowledge of structural cefff/fec-"tions and sensitivity of the nervous system

~-fit would be difficult to explain such"a clear-cut pheridn}e'nbn^in-fefms of other tissuesystems.

In a grossly mechanical sense the nervous systemcan be seen as a massive ligament or tendon that

Figure 4.2 The slump test note how release of the headflexion allows greater knee extension range. The slump test isfully described in Maitland [1986], Butler [1991] and Butler andGifford [1998]. [Adapted, with permission, from Butler, 1991,Mobilisation of the Nervous System. Churchill Livingstone,Melbourne.]

just happens to contain a system of specializedconducting and communicating cells. In thisextreme slump 'test' position [Maitland, 1986][Figure 4.2] the loss of knee extension could beanalysed in purely mechanical terms, thus, lift thehead, put some slack into the neuraxis/sciaticsystem and allow the knee to extend. In some.situations like this the nervous system may phy-sically limit movement. The reality though, is thatat any limit of range, noxious forces cause noci-ceptive messages that make most people call a haltto a movement as well as offering- up an appro-priate protective motor reflex that further pre-vents movement [Elvey, 1995; Hall et a/., 1995].Perhaps performing the slump test under a gen-eral anaesthetic would help clarify whether or notpure nerve mechanics/tension was the key limit-ing structure to this position.Clinical reality forces us to consider both

161

Louis Gifford

Figure43 Microanatomy of a peripheral nerve trunk and its components, [a] Fascicles surrounded by a multilaminated connectivetissue perineurium [p) are embedded in a loose connective tissue, the epineurium [epi). The outer layers of the epineurium arecondensed into a sheath, [b] and (c) illustrate the appearance of unmyelinated and myelinated fibres respectively. Nerve fibres aresurrounded by the endoneurial connective tissue [end]. Schw, Schwann cell; my, myelin sheath; ax, axon; nR, node of Ranvier.[Adapted, with permission, from Lundborg, G (1988) Nerve Injury and Repair, Churchill Livingstone, Edinburgh.)

(b)

mechanics and sensitivity in parallel. In order tofully appreciate this we must recognize that thenervous system consists of four major tissuetypes, the first two of which are generally givenmost attention:1 Conducting nerve Fibres, the neurones;2 CoIIagenous connective tissues whose impor-

tant protective role is the major consideration;3 Nonconducting glial cells;4 The vasculature.In the peripheral nervous system the conductingand connective tissue elements combine to formnerve trunks and nerve roots [Figure 4.3], whereas

in the CNS the major protective connective tis-sues envelope and remain external to the neuraxis[Figure 4.4].The existence of nonconducting cells in the CNS,the glial cells, was first recognized in the 1800s.For a long time these cells were considered asuninteresting putty that packs out spacesbetween the conducting cellular elements. Whatis now clear is that they have very important rolesto play that include an immunological function,reabsorption of unused transmitters and provid-ing the axons of conducting fibres with myelin[Streit and Kincaid-Colton, 1995].

Neurodynamics

Figure 4.4 Scanning electron micrograph of the lower spinalcord of a 15-month-oId child. L, denticulate ligaments thatsuspend the cord within the sub arachnoid space. D, Dura; notethe thickness and the layers. A, Arachnoid; note how it hascome away from the dorsal dura in the preparation. S, dorsalseptum. 1L, intermediate leptomeningeal layer. Note thesectioned multifascicular nerve roots within the subarachnoidspace. The pia can be seen adhering to and surrounding thecord. [From Nicholas, DS, Weller, RO, 1988, Journal ofNeurosurgery 69:276-282, with permission.)

The last tissue type of importance is the vascula-ture. The recent upsurge in interest in the detri-mental effects of ischaemia on nervous systemstructures means that more than passing atten-tion should be paid to the whereabouts of feedervessels and veins and, vitally, the important ejfectsthat movement and sustained posturing has ontheir patency. For now, consider that movementsthat compress or stretch bloodvessels will tend todecrease the lumen size and hence deprive thelocal or regional tissues of blood.

It is clear that the nervous system moves and thatits anatomy strongly reflects this to be a built-infeature of its design. In order to be complete, thenervous system has to be examined from all itsfunctional perspectives, that is, in terms of itsability to conduct and its ability to move in anormal and symptom-free way.

The Nervous System Responds toMovement

Basic Concepts} The relationship of nerve position to the axis

of a joint helps establish theeffecta movementmay have on neural tissue: Many of the mod-ern neurodynamic tests have been developedas a result of the anatomical and biomechanicalappraisal of nerve trunks in relation to theirsurrounding tissues. In particular, the relation-

ship to joint axes of movement. It is a matter ofmentally drawing the known position andcourse of a peripheral nerve on the body andthen moving the various joint componentsthat it traverses in a way that will exertincreased tension on the nerve under consid-eration. There has also been much reflectionon the literature [Butler and Gifford, 1989;Butler, 1991]. For instance: From the work of Millesi [Millesi, 1986; Mill-

esi et a/., 1990] it has been calculated thatfrom wrist and elbow flexion to wrist andelbow extension, the 'bed' of the mediannerve gets approximately 20% longer. ,

Beith eta/. [1995] have shown that the sciaticnerve bed increases in length by 8-12%during the straight leg raising [SLR]manoeuvre.

As long as 100 years ago it was consideredself-evident that the length of a nerve mustundergo changes during joint movementand that these changes create intraneuraltension when a nerve's length is increased[Dyck, 1984; Beith eta/., 1995].

A key consideration is the position of thenerve in relation to the axis of movement of

Louis Gifford

Figure 4.5 Diagram of a nerve as it traverses a joint while Jointis in neutral position. Arrows indicate length of nerve bed atlevel of joint, (a) Neutral position - nerve is slack, [b] Angulatedposition - nerve bed has elongated, causing nerve to belengthened and bent across joint. [Reproduced from ShaddockM, 1995, Physiotherapy-Si (1J: 9-16, with permission.)

(b)

the adjacent joint (Figure 4.5]. Thus duringelbow flexion the ulnar nerve at the elbowwill tend to elongate and the median and radialnerves on the ventral aspect of the joint willtend to shorten; buckle and be compressed.End range neurodynamic tests like the SLR andthe upper limb tension tests (ULTTJ must beconsidered in terms of rather gross elongationeffects of whole nerve trunks, plexi and nerveroots with further possible repercussions inthe neuraxis. What must be emphasized isthat even localized joint movements will havequite marked effects on adjacent neural tissues.

2 Sliding, elongation and compression: In orderto adapt to body movements the nervoussystem is known to slide over adjacent tissue,elongate and be compressed. For example:

Normal nerve roots are known to be com-pressed by spinal extension due to thedecrease in size of the intervertebral fora-men (Yoo eta/., 1992; Farmer and Wisneski,1994).At the wrist the median nerve can be simul-taneously compressed and elongated in thecarpal tunnel during wrist and finger exten-sion [LaBan eta/., 1989; Yoshioka eta/., 1993).The median nerve in the upper limb of nor-mal volunteers has been shown to slide anaverage of 7.4 mm during movements of thewrist alone (McLellan and Swash, 1976).-

The fundamental physiological effects of "sliding, elongation and compression due v 'to normal movements are that they will |load the nervous system and hence causean increase of pressure within it. Changes ;in pressure cause changes in circulation 'and prolonged changes in circulation arelikely to have detrimental effects on a tis-

*!s

Anatomical and attachment considerations Inneurodynamics: Concepts of nervous systemmovement must embrace the fact that itsstructure; its attachments and the interfacingstructures around it, are continuously chan-ging and very variable from one site to thenext. The implications of this are-that simplemovement of one part of it does not have auniform spread of effects throughout thewhole, as it would if one considered the per-ipheral nerves and neuraxis as a homogenousstring-like structure of uniform thickness and

64

Neurodynamics

elasticity and having no attachments to neigh-bouring tissues. The reality is that the nervoussystem gets ever thinner and more branchingas it reaches towards its target tissues and it hasvarying amounts of connective tissue withinand around it. It has considerable attachmentsto adjacent tissues that may prevent dispersalof forces further proximally or distally and ithas contracting and moving structures aroundit that may have varying effects on neural loaddissemination [Sunderland, 1978].Thus,"the effects of joint movement have non-uniform effects on the nervous system [Shack-lock, 1995]. For example:

Full spinal flexion induces a 15% dural strainat Ll-2 whereas at L5, strain approaches30% [Louis, 1981]. Further, the load on thenervous system will be greatest in the neuraltissue adjacent to the site of joint movement[Shacklock, 1995].

Ankle plantar flexion - inversion will pro-duce quite a marked effect on the tensionand movement of the superficial peronealnerve as it courses over the anterior aspectof the ankle and foot. This is very easy todemonstrate on a thin foot [Figure .4.6].Proximal movement and tension repercus-sions of ankle plantar flexion inversion onthe peroneal nerve tract have been observedas far as the thigh [Borges ef a/., 1981].

Smith [1956] in monkeys and Breig andTroup [1979] observing fresh human cada-vers, have demonstrated that ankle dorsi-flexion with the leg and trunk in a neutralposition can have mechanical influences asfar afield as the lumbosacral nerve roots.Performing the same movement in a SLRmay have tension repercussions as far asthe cerebellum [Smith, 1956].

Figure 4.6 Demonstrating the superficial peroneal nerve onthe dorsum of the foot. [From Butler and Gifford, 1998, TheDynamic Nervous System. Adelaide, NOI Press, with .permission.]

It seems that movements of one part of the bodycan have quite far-reaching repercussions for thenervous system elsewhere. This biomechanicalconsideration can be utilized in managementapproaches. For instance it may be desirable tophysically influence nerve roots in a pain-free waypost laminectomy. Moving the lumbar spine andhips as in performing SLR may be far too noxious,but moving the foot or knee may be toleratedwell. One of the uses of this knowledge of thenervous system is that it can easily be influencedfrom a distance. It is also often worth giving someconsideration to the order or sequence that testsand movements are performed in.A key principle is that the greatest effect of a jointmovement on a nerve will occur in the part of thenerve that is immediately adjacent to the jointbeing moved [Shacklock, 1995].Thus ankle plantar flexion inversion will have mostphysical effect on the peroneal nerve over thedorsum of the ankle and less and less higher upthe leg. Alterations of sequencing can be usefulclinically when trying to localize tension to aparticular segment of nerve trunk [Shacklock,1995; Butler and Gifford, 1998].

165

Louis Gifford

It is now worth taking a more focused look at afew specific anatomical sites that illustrate somemajor neurodynamic principles and relate them tothe pathological state.

The Effects of Movement andSustained Posture on thePeripheral Nervous SystemTrunk, head and limb movements and posturesproduce compression and elongation effects onthe peripheral nervous system.

COMPRESSION

Nerves get relatively compressed when the cross-sectional area of the surrounding interface mate-rial diminishes in size. To demonstrate this, con-sider three anatomical zones that are commonlyimplicated in pain states associated with the ner-vous system. The first two zones relate to nerveroots, the third to a nerve trunk.

1 The L5-S1 nerve roots in the radicular canal;

2 The nerve roots generally in the intervertebralforamen [IVFJ;

3 The median nerve in the carpal tunnel.

15SI Nerve Roots in the 'Radicular CanalThe L5-S1 roots are special because they cause agreat many problems. It is not surprising that theyhave unique features and relationships that makethem vulnerable to compressive distress and con-sequently the nerve root pain of sciatica.

Normal Anatomy/'Biomechanics Anatomically thelumbar spinal canal contains only the peripheralnerve roots of the cauda equina encased in theirdural sac [Figure 4.7]. [The cord terminates atapproximately Ll-2.] From the point at whichthey emerge from the spinal cord to their exit inthe IVF the lumbosacral nerve roots may be aslong as 16 cm [Grieve, 1988]. The next importantanatomical consideration is that nerve roots arepositioned more centrally in the spinal canalwhen they emerge from the cord but, as theydescend towards their exiting foramen, theycourse more and more laterally into less andless space [Figure 4.7] [Wall et a/., 1990].

Figure 4.7ab Dural sac contents at L2-3 and L45 levels, [a) Diagrammatic representation of contents of lumbar dural sac at theL2-3 level, [b) Diagrammatic representation of contents of lumbarduralsacatthe upper L45 level. [Adapted from Wall et al.,1990,Spine IS [12): 1244-1247, with permission.)

Neurodynamics

Figure 4.8 Diagrammatic representation of lumbar dura! sac nerve root anatomical relations and vulnerable zones. A, L4 root isless vulnerable to facet impingement here because the root exits the dural sac below the disc/facet level. B, 15 root vulnerable instanding/extension here - from superior facet of LS coming down on it and from disc bulging backwards. C, SI root vulnerable instanding/extension here - from superior facet of SI coming down on it and from disc bulging backwards. D, L5 and SI roots canboth be influenced by movement-related compressive effects in this zone, especially if degenerate changes have caused narrowing offoramen and spinal canal. Line of section refers to Figures 4.9 and 4.10. [From Butler and Gifford, 1998, The Dynamic NervousSystem, Adelaide, NO1 Press, with permission.]

Dural sac

Before emerging at the Sl-2 intervertebral fora-men the SI nerve root lies in the lateral recess or'radicular canal' medial to the articular pillar ofSI [Figure 4.8].Just above this it travels over the back of the LS 'disc where it is in close relation to the overlyingsuperior facet of SI.The salient feature is that the nerve root isisolated in its own dural sleeve having left thedural sac just above to the L5-S1 disc (Figure4.8]. A similar situation occurs with the L5 rootat the L4-5 disc level.

Note how the more rostral roots leave thedural sac just below the disc level.

The significance of this is that the two Isolated7roots (L5 and SI] are particularly vulnerable tocompression effects within the lateral recessesof the spinal canal during movements of thespine.

Penning [1992] has convincingly shown that at thelevel of the disc/superior facet the size of thelateral recess is movement and posture depen-dent. For instance in standing, and increasinglyin extension, the combined effects of the back-

167

Louis Gifford

Figure 4.9 [a] Horizontal section through L5-S1 disc in neutral position non-weight-bearing. [Line of section in Figure 4.8.] Imageof vertebral arch of L5 is in background, [b] Horizontal section through LSSI disc in upright or extended position. [Line of sectionin Figure 4.8.] Image of vertebral arch of LS is in background. Note how the contents of the spinal canal, the SI facet and the L5-S1disc move [arrows] to relatively compress the dural sac, the SI root and surrounding tissues [adipose tissue and venous plexus].(From Butler and Gifford, 1998, The Dynamic Nervous System, Adelaide, NOI Press, with permission.]

1_5 vertical arch Sacral rootsin dural sac

Left superior" facet of S1

Left S1 rootin lateral recess

Intervertebralforamen

Right superiorfacet of S1

Right S1 rootin lateral recess

Venousplexus

Left superiorfacet of S1

Intervertebralforamen

(b)

Right superiorfacet of S1

168

Neurodynamics

ward bulging disc and the forward-moving super-ior articular facet significantly reduces the size ofthe recess [Figure 4.9a,b]. The major effects of thisin the normal spine are a modest squashing of thedense venous plexus surrounding the root and amedial sliding of the root. However, it has beensuggested that this medial sliding may be stronglycurtailed due to ligamentous distal fixation of theroot in the intervertebral foramen [Spencer et al,1983].

Pathological Anatomy/Biomechanics Pathological encroachment of the radicular canal area by aprotruding disc or as a result of degenerativefacet enlargement and flaval ligament thickeningmay have dire compressive consequences instanding and extension [Figure 4.10]. This maygo a long way to explaining why so manypatients with sciatic nerve root distribution,symptoms so often dislike standing for long,

especially standing upright and extending, andprefer to be in varying degrees of flexion.

The important point is that we so often think ofpathology affecting the root at the 1VF, yet itshould be apparent that if we follow the L5-S1roots upwards there is a second zone where theyare also vulnerable to compressive 'subarticular'forces [Vanderlinden, 1984].Degenerative changes, congenially limited radi-cular canal size and nerve root anomalies [Grieve,1988] are important factors to consider whenassessing any contributing factors to a disorder.

Nerve Roots and the Intervertebral ForamenAccordingto Hoyland eta/. [1989] the roots of thelumbar spine occupy the upper pole of the fora-men, above the disc, and occupy a maximum of.35% of the area of the IVF. These workers foundthat the average area occupied by the root was

Figure 4.10 Degenerate changes: horizontal section through LS-SI disc in upright or extended position. [Line of section in Figure4.8J Image of vertebral arch of LS is in background. Note how the thickened spinal canal contents, SI facet and LS-SI disc move[arrows] to compress the dural sac, the SI root and surrounding tissues [venous plexus and adipose tissue]. [From Butler and Gifford,1998, The Dynamic Nervous System, Adelaide, NOI Press, with permission.]

Left superiorfacet of S1

Intervertebralforamen

Right superiorfacet of 81

169

Louis Gifford

21% and that it ranged from as low as 2%. The restof the apparantly ample space is mainly occupiedby adipose tissue, radicular arteries and a venousplexus meshwork. Hoyland et a/. [1989] stressedthat relatively few of the cadavers they studiedshowed evidence of direct compression of thenerve roots by the disc. They highlighted thefact that the disc protrusions they observedmore frequently compressed and severely dis-torted the venous plexus situated predominantlyin the lower pole of the IVF overlying the discprotrusion. The pathophysiological importanceof this observation is supported -by Jayson[1992] who noted that careful examination ofradiculograms in patients with disc prolapse oftenshowed dilated veins and swelling of the nerveroot indicating the presence of oedema. Unfortu-nately observing dissected cadavers does not takeinto consideration the effect of posture- andmovement on the discsuperior facetrootstructure relationship in this area.

Dorsal Root Ganglion The position of the dorsalroot ganglion [DRG] relative to the IVF is ofsome interest as this structure is recognized bysome as a key player in the generation of radi-cular pain [Howe et a/., 1977; Devor and Rappa-port,1990; Devor, 1994]. The reason for this-isthat the DRG is normally exquisitely mechano-sensitive, yet the rest of the root tissue proxi-mally and distally is relatively insensitive unless itis in an inflamed state [Garfin eta/., 1991; Kuslicheta/., 1991]. The clinical implication of this is thatsymptoms of nerve root compression may onlyoccur if the DRG gets compressed, or the adja-cent insensitive areas of the root becomeinflamed a process that does not invariablyhappen, and if it does, takes time to build up. Itis very tempting to argue that sciatic pain thatoccurs at the instant of injury must be the result

Figure 4.11 Variation in anatomical position of the dorsal rootganglion. Classification according to Sato and Kikuchi [1993].[Adapted from Sato and Kikuchi, 1993, Spine 18 [15]: 2246-22S1, with permission.]

i Intraforaminaltype

\l canalExtraforaminal _/ : _ jtype

of DRG compression since normal nerve roottakes time to become inflamed and generatepain.It seems likely that some people may be moreprone to DRG compression. A recent cadaverstudy by Sato and Kikuchi [1993] revealed thatthe position of the ganglion relative to the fora-men was remarkably variable. They classified theposiiton of the DRG as being either located medi-ally [spinal canal type], within the foramen, orextraforaminal [see Figure 4.11] and found thatthe extraforaminal type was the least likely tosuffer adverse pathological compression. As faras the 15 ganglion was concerned, it appearedmore vulnerable if it was situated more proximallySato and Kikuchi [1993] interestingly noted'indentations' on the ganglia due to impingementby the disc and adjacent superior facet in elderlyspecimens which showed space encroachingpathology [enlarged degenerate facets and bulg-ing disc material]. The authors made no commentas to whether the ganglia were physically pinchedby these structures when they dissected them [adissected out lumbar spine is likely to be in aneutral position and not subjected to anycompressive forces that would alter the relevant

170

Neurodynamics

Figure 4.12 Diagram of lumbar nerve root dynamics in the intervertebrai foramen, [a] Flexion: posterior wall of disc annulus isstretched and tightened, the body of the vertebra above moves forwards and away from the root and the superior facet movesbackwards in relation to the root. The intervertebrai foramen area thus enlarges, [b] Extension: the opposite occurs; note how the.disc bulges into the foramen/ the facet tip and the posterior rim of the vertebra above come close together and the nerve getsrelatively compressed by this pincer mechanism. (From Penning, 1992, Clinical Biomechanics 7 [1]: 3-17, with permission.]

structures position and shape]. According to Pen-ning's [1992] findings, it is reasonable to assumethat standing postures and extension movement?:would dramatically decrease the already patholo-gically limited space in the foramen and evenphysically pinch the ganglion/root there [Figure4.12].Thus the-" dorsal root ganglion/nerve root in theIVF can be compressed in the 'jaws' formed by thetip of the superior facet behind and the bulgingdisc and the inferior rim of the adjacent vertebralbody in front. The fundamental movements toconsider are those that tend to 'close' the IVF7i.e. going to standing'[since erect standing com-presses and causes the disc to bulge], extensionand movements towards the side under consid-eration [Panjabi et a/., 1983]. This principle alsoapplies to the cervical spine [Yoo et a!., 1992;Farmer and Wisneski, 1994] and more than likelyin the thoracic spine, judging by clinical findings.

The Carpal TunnelSince the carpal tunnel contains the median nerveto the 'hand, as well as nine flexor tendons, it has

little room for intrusions. Thus any process thattends to cause narrowing of the space, or anincrease in the size of the contents, will increasethe tissue pressure in the tunnel.Normal pressure in the carpal tunnel is around 2.5mmHg, in wrist flexion the pressure increases toabout 30 mmHg, a pressure which correspondswell to the critical pressure known to induce thefirst changes in intraneural microcirculation andaxonal transport [see below] [Gelberman et a/.,1981].Movements of the wrist alter the size of the carpaltunnel. For example, Yoshioka et ai [1993] haveshown that in wrist flexion the carpal tunnel gets16% smaller at the pisiform level. It is hardly

- surprising that sustained wrist flex-ton begins tocause hand paraesthesia in many who are other-wise normal.

SLIDING AND ELONGATION

Nerves get relatively elongated by limb and trunkmovements that increase the length of their nerve

171

Louis Gilford

Figure 4.13 Anterolateral view of right sacral plexus androots L4 and LS as they emerge from their intervertebralforamen. Paper markers 1 cm long have been sutured to thenerves. In [a] with the trunk in neutral and hip in flexion theneural structures are relatively slack and the markers lie within(L4) and just distal [LSJ to the intervertebral foramen. In [b) theright knee has been extended into the straight leg raiseposition and the amount of root movement relative to theforamen is clear. [From Breig, A, 1978, Adverse Mechanical

Tens/on in the Central Nervous System, Almqvist and Wiksell,Stockholm, with permission.]

[a]

Cb]

beds [i.e. the tissues which surround them andwhich they lie in]. They adapt to this in two ways:

1 By sliding;2 By elongation.

The remarkable movement of the L4and L5 spinalnerves during the SLR manoeuvre is shown inFigure 4.13. The SI nerve root complex has beenreported to slide as much as 10 mm [Goddard andReid; 1965] and tension transmitted as far rostrallyas the mid brain [Smith, 1956]. An important prin-ciple to consider with regard to neurodynamics isthat in some situations more sliding of a nerve willoccur, yet in others more tensioning and elonga-tion will occur, and that what occurs when, is likelyto be hugely variable between individuals.Examination of fresh cadavers [Goddard and Reid,1965] has revealed that during straight leg raising,when the heel is only 5 cm above the horizontal,movement/sliding of the nerve at the greatersciatic notch has already begun. The movementspreads proximally the more the leg is lifted anddoes not start to affect the nerve roots in the IVFuntil around 35 of SLR. As the leg raising con-tinues so the sliding effect diminishes and thetension/elongation effects grow, so that by 70there is little sliding and the adaptation has to beborne by the intrinsic elastic capabilities of thenerve. Considerable stresses are imparted onnerve roots during spinal movements. Forinstance, Louis [1981] calculated that during flex-ion greatest strain [16%] was taken by the SI nerveroot.

It should be noted, though, that cadaver observa-tions must be interpreted with caution since closescrutiny of nerve trunks and roots reveals quitemarked attachment tissues that often stronglyanchor the nerve to the surrounding interfacingtissues [e.g. see Spencer eta/., 1983]. These tissuesmay well be dissected away during exposure ofthe nerve and hence give a false representationof the amount of movement available$e\th eta/.,1995]. For example, Lombard! et al. [1984] havecriticized the notion that the L5 nerve root slips

172

Neurodynamics

in and out of the IVF during SLR since it issecurely bound to the side of the body of SI.There is ample evidence that upper limb nervetrunks slide and move. For instance, the ulnarnerve migrates proximally during elbow flexion(MacnicoL 1980], extension of the index fingerhas been shown to move the median nerve in thecarpal tunnel 4 mm distally [LaBan etal, 1989] andwrist and finger extension will pull the mediannerve in the upper arm downwards by an averageof 7.4 mm (McLellan and Swash, 1976]. This lastresult was achieved on normals by inserting fineneedles into their median nerves that protrudedout of the skin! The excursion of the nerve wascalculated by observing the amount of movementproduced by the tip of the needle.In summary, the nervous system is capable ofquite remarkable adaptations in response to the

body's movement and postural demands. Periph-eral nerve roots and nerve trunks are being.con-'tinuously squashed and stretched and insituations where there is relatively little room orwhere they are anatomically tethered they arevulnerable to adverse forces and pathologicaltissue encroachment.

The Effect of Movement on theNeuraxisEVIDENCE FOR DYNAMIC EFFECTS DUE TOSPINAL MOVEMENT

The neuraxis is housed in the spinal canal andcranium. Since the spinal canal increases in lengthby 5-9 cm from full extension to full flexion[Breig, 1978; Louis, 1981; Inman and Saunders,1942] there are quite marked physical effects on

Figure 4.14 Normal deformation of the dura, cord and nerve roots in the cervical canal in the cadaver due to full extension [left]and flexion [right] of the cervical spine. A total laminectomy has been performed and the dura opened and retracted although stillable to transmit tension. In cervical extension, the nervous system is slack, the root sleeves have lost contact with the pedicles [lowerarrows] and the nerve roots with the inner surfaces of the dural sleeves [upper arrows]. In flexion, the nervous system including thedura mater has been stretched and moved in relation to surrounding structures. Note change in shape of the blood vessels. [FromBreig, A, 1978, Adverse Mechanical Tension in the Central Nervous System. Almqvist and Wiksell, Stockholm, with permission.]

173

Louis Gifford

the connective tissue sheaths and the cord andbrain structures themselves. Most lengtheningoccurs in the most mobile cervical and lumbarregions [28 mm each] and least in the thoracicregion [3 mm) [Louis, 1981]. The dynamic adapta-tions of the cervical cord and roots can be seen inthe dissection photograph [Figure 4.14). Figure4.15 illustrates the effects of flexionextensionon the brainstem. Further examples include:

Neck flexion causing the floor of the fourthventricle to elongate;

The thoracic cord decreasing its diameter dur-ing spinal flexion [Breig71978);

The folding and straightening of individual neu-rones in the dorsal column tracts'of the cordduring flexion and extension [Breig, 1978; But-ler, 1991). This emphasizes the need for physicaladaptations to movement right down to.thecellular level.

During spinal flexion the key considerations arethat the whole neuraxis contained in the spinalcanal tends to move anteriorly, elongate alongits entire length and slide relative to the canalinterface [see Shacklock eta/., 1994).

MOVEMENTS OF NEURAXIS RELATIVE TOTHE SPINAL CANAL

Butler [1991) first brought more widespread atten-tion to the fact that movements of the neuraxisrelative to the surrounding tissues was not at alluniform and not necessarily in directions onewould expect. For instance, during flexion ofthe monkey spine the dura at the level of L4moves 3 mm caudally yet at L5 it moves 3 mmrostrally. In the neck the dura at C5 tends to movecaudally and at C6-7 rostrally. In the thoracicregion the dura above and below T6 tends tomove away from it [Louis, 1981).

Figure 4.1S The remarkable movement of the brain stem in extension [a] and flexion [b] is illustrated by reference to the markers.Marked changes in tension of the eleventh cranial nerve (spinal accessory] can also be seen anterior to the cord/brainstem as itpasses up from its origins on the cord to exit through the jugular foramen on the upper right of the picture. [From Breig, A, 1978,Adverse Mechanical Tension in the Central Nervous System. Almqvist and Wiksell, Stockholm, with permission.]

[a) --. [b)

Neurodynamics

Effects on Nerve RootsThese relative movements will have repercus-sions for the tension and angulation of thenerve roots as they leave the dura and asthey exit in the 1VF. For example, in flexion,nerve roots above L4 will tend to be angledmore horizontally and those below more verti-cally. Further, any deviations from such 'normal'movement adaptations, due to for instanceabnormal tethering following injury, may haveserious mechanical overload repercussions atlocal and distant sites which may already besomewhat vulnerable. These thoughts havebeen used to hypothesize why symptoms oftenspread or jump to remote sites [Butler, 1991].For example, it is not uncommon for pain fromwhiplash injuries to appear in the midthoracicand lumbar regions long after the event.

EFFECTS OF SPINAL EXTENSION During spinal extension the whole canal short-

ens causingthe neuraxis to slacken and increasein cross-sectional area. Observable folds can beseen in the cervical dural sac in extension.

In the lumbar spine in particular, the spinal canal' gets smaller in diameter in extension due to theposterior bulging of the discs and the forwardbulging of the interflaval fat pad and the liga-mentum flavum. This effect increases greatly inthe presence of degenerative encroachment[Penning, 1992; Penning and Wilmink, 1981].

This may be a reason why lumbar extensioncauses an increase in lumbar cerebrospinal fluidpressure [Hanai eta/.71985].

Zones of the spinal canal where there is relativelylittle space, like C5 compared to Cl or C2 [Figure4.16], may be significantly more vulnerable to:1 Pathological encroachment;2 The addition of movements into extension.

Figure4.16 The changing spaces available for the neuraxis andmeninges in the cervical spinal canal at C1[A], C2[B], C3[C) andC5[D]. LF, ligamentum flavum; UJ, uncovertebral Joint. -[Reproduced from Parke, WW, 1988, Spine 13:831-837, withpermission. Lippincott Raven Publishers, Philadelphia.]

Think how common it is for the elderly degen-erate spine to become relatively flexed. One wayof viewing this is to see it as an adaptive processthat helps maintain the least possible pressure onthe threatened neuraxis and its peripheral rootsand trunks.

SIDE FLEXION AND GRAVITY Side flexion of the spine tends to produce slack-ening on the concave side and tightening on theconvex side, and gravity displaces the spinal canalstructures downwards [see Breig, 1978; Shacklocket al., 1994].When interpreting symptom responses it iswise to consider the relative flexion/extension

175

Louis Gifford

position of the spine as well as compressioneffects in the canal and IVF. It is apparent that itis not easy to find a position where there isn'tsome degree of mechanical impact on any onepart of the nervous system. Knowledge of neu-rodynamic influences does help rationalize thedifficulties patients have in finding relief whenconfronted by neurogenic pain.

Design Features and NervousSystem-DynamicsSince it seems well established that movement ofthe nervous system occurs it is pertinent to high-light a few anatomical features that add weight tothe notion of it having this dynamic capacity.

Neurones, Fascicles and Plexi Neurones, the individual nerve fibres, tend to

run an undulatory course within the fascicles ofperipheral nerves and within the tracts of thespinal cord [Breig, 1978].

If a nerve fibre is stretched the myelin sheathlamellae slide on each other and little clefts[incisures of SchmidtLantermann] in the mye-lin part to accommodate the increased stress[Friede and Samorajski, 1969].

The fascicles that contain the nerve fibres arecapable of sliding within their epineurial sheaths

Figure 4.17 The fascicular branching in themusculocutaneous nerve. [Redrawn/ with permission, fromSunderland, S, 1978, Nerves and Nerve Injuries. ChurchillLivingstone, Edinburgh.)

Figure 4.18 The brachial plexus as a force distributor. Tensionon one trunk will be distributed throughout the whole plexus.(From Butler, DS, 1991, Mobilisation of the Nervous System,Churchill Livingstone, Melbourne, with permission.]

as well as following an undulating and branch-ing course [Figure 4.17] that appears geared to afunction of load dispersal.

The reason for the complex branching of thevarious peripheral nerve plexi may relate toload dispersal [Figure 4.18] [Butler, 1991].

Connective TissueThe peripheral and central nervous system con-tains connective tissue with viscoelastic proper-ties, similar to ligaments and tendons [Bora et a/.,1980; Kwan et a/., 1992; Sunderland and Bradley1961a,b]. These tissues serve to allow and controlnerve trunk motion in parallel with a protectiverole when forces reach physiological limits. Itappears that in regions where the nervous systemis more vulnerable to injury there is a higherdensity of connective tissue.

Clinical Example

size of the superficial- peroneal nervedveif- the top of the foot [Figure 4.6} isquite remarkable when one. considersthat it has only a relatively small dermal

Neurodynamics

1 innervation field to reach that is very doseby. Its size here has to be considered Interms of its obvious vulnerability to-'injury:

: andtherefore its need for a relatively large' connective tissue protection component. '.

Other examples are the sciatic nerve at the but-tock where it gets compressed in sitting. Here itcontains in the region of 80% connective tissue[Sunderland, 1978]. The peroneal nerve at the headof the fibula contains 17% more connective tissuethan the same nerve a few centimetres proximallyin the relatively sheltered area of the poplitealfossa [Sunderland and Bradley/1949]. Sunderland[1978] also demonstrated how the number offascicles in vulnerable areas tends to increase inparallel with the increase in connective tissue, yetanother mechanism thought to afford -betterprotection to the nerve fibres from 'adversecompression.Inside the spinal canal attention is focused on thetough dura mater connective tissue covering. Thisstructure is particularly strong and well designedto cope with longitudinal forces [see Butler, 1991and Shacklock et al, 1994 for good overviews ofthe neuraxis connective tissues].

Blood SupplyThere are many dynamic design features in thenervous system. It is designed to elongate andrecoil and it is designed to cope with intermittentcompression and distortion. During all this itmust still continue to conduct and connect phy-siologically to its target organs and tissues - acondition only possible if adequate blood supplyis provided. Although only accounting for 2% ofthe body mass the nervous system requires 20%of the available oxygen [Domisse, 1994].

Maintaining an adequate blood supply, whateverthe posture or movement, is imperative forthemetabolic demands of normal neural function. Itis hardly surprising therefore that the blood ves-sels appear relatively slack and coiled, followmeandering courses along and within nerves,and enter the domain of the nervous system inzones where the system is relatively fixed in rela-tionship to its adjacent structures [see Breig, 1978;Lundborg, 1988; Parke and Watanabe, 1985]. Forexample, major feeder vessels enter the cervicalcord between C5 and C7 - a region that doesmove in relation to the interface, but relativelylittle, due to the fixation effect of the brachialplexus and the strong tethering of these lowercervical nerve roots to the gutters on the trans-verse processes just distal to the IVF [Sunderland,1974; Butler, 1991]. Even though there is gooddesign for continuous adequate blood supply,no matter what the posture or position, thereare still plenty of opportunities that lead to itscompromise [see below].

The Normal Nervous System as aSensitive Tissue

Generally, tissues that are most likely to beexposed to extreme physical stress are likely tohave a good sensory innervation - compare themechanical sensitivity of the contents of the gutto the sensitivity of the skin or the' musculoskel-etal system for instance. Further, any tissue that isweakened or vulnerable following injury requiresa greatly enhanced sensory mechanism to Jielpprotect it from further damage and to promoteappropriate behaviour for it to recover [seeChapter 5]. Coupled with a good sensory relayis a good reflex system, and in many higher

177

Louis Gifford

vertebrates, an active consciousness that providesthe background for appropriate adaptive action/behaviour.The normal nervous system copes with physio-logical movements in a remarkably silent way;however, extreme ranges of movement anddirect forces often endanger neural tissue. Thenervous system has the means to respond via itsown sensory system, just as the heart has itsown blood supply so the nervous system hasits own nerve supply. The innervation is speci-fically to the protective connective tissues ofthe peripheral and central nervous systems [seeButler, 1991, Shacklock et a/., 1994, for goodoverviews].It is well known that brain tissue itself is mechani-cally insensitive and that normal peripheral nervefibres will only modestly respond to intensephysical probing [Melzack and Wall, 1996]. Infact there are many who report that peripheralnerve trunks are more or less insensitive tomechanical pressure and manipulation [e.g.Kuslich et a/., 1991; Howe et a/., 1977]. However,anyone who has spent time learning to palpateperipheral nerves will know that some nerves arefar more sensitive than others and that where anyone nerve is sensitive depends on its anatomicalsite [Butler and Gifford, 1998]. For example, avulnerable nerve like the superficial peroneal onthe foot [Figure 4.6], is pretty insensitive - youhave to tap it or 'twang' it vigorously to get amodest tingling in its distal innervation field.Compare that to palpating the ulnar nerve atthe elbow or the tibia! nerve just behind themedial malleolus; in both cases gentle palpatorypressure reveals a rather sickening 'nervy' discom-fort.The important practical point is that peripheralnerves are variably sensitive - depending on the

anatomic site and depending on the individual.Some people's nerves have great sensitivity overothers.

Senstitivity to Stretch /ElongationWe should also consider sensitivity to stretch/elongation. Again there is great variability in sen-sitivity and some people have far more slack intheir nervous systems than others.

Try this: place your arm down by yourside, extend your elbow hard and keep itextended hard, extend your wrist with'your fingers as -straight as you can. Now_depress your shoulder slowly and focus on 'what you feel in your hand and arm. Manyof you will get a deep generalized achei M l y ' 'm

in u'nff' the h'ari&r^dWng-neck' sideaway nopjfiall^'JM^ea'ses thegift further, 'hfjj: -'go qftefttlly.

who have good.-nTpBilify-of 'theirften',haye-e'xi-iieme m'oBility ofitheir

systems -and may -get very littlemanoeuvre like this; ethers will

easily get .many of -the symptoms'described and more. Note that since thesymptoms can be changedjn the forearm/hand with scapular depression and neckmovement, the assamption is- that neuraltissue is responsible [see Ghapter 6]. It isargued that fascia and vaseulature that alsotraverse these regions are unlikely to pro-duce such 'nerv/ sensations as deep dif-fuse ache and paraesthesia in such a clear-cut way.

Neurodynamics

Type of SensitivityThere are two significant issues with regards tosensitivity:

1 Mechanical sensitivity;2 Sensitivity to ischaemia.

Mechanical sensitivityThis exists through

Mechanical stimulation of mechanically sensi-tive nerve endings in the protective connectivetissue layers of the nerve;

Mechanical sensitivity of the nerve fibres[neurones] themselves.

Nerve fibre axons are generally considered to-bedesigned to convey impulses not generate them -nerve impulses traditionally originate from theends of nerves that reside in target tissues, notmid-axon somewhere. Impulses that do originatemid-axon are said to be 'ectopic' [see Chapter 5]and if derived from afferent fibres may cause thegeneration of odd sensations hence pins andneedles-are commonly felt when nerve trunks thatsupply cutaneous sensation are firmly tapped.Sensitivity to ischaemia or to blood loss, i.e.'Ischaemosensitivit/ [Butler and Gifford, 1998].Falling asleep with your arms above your headand later waking up with a numb and tinglingarm that does not respond to demands for move-ment is an extreme example that is not uncom-mon. Holding continuous pressure on theanterior wrist over the carpal tunnel produces a

' slowly building paraesthesia in many otherwiseasymptomatic subjects. The fact that symptomsare not immediate suggests loss of blood supplyto the underlying median nerve as a likely mechan-ism. Some people are more susceptible thanothers and they often find constant end-rangepositions in bed [wrist flexion for example] or

during the day [crossed leg sitting] a commonsource of irritation by way of numbness and

'pins and needles type sensations.When individual nerve fibres are deprived of cir-culation their function is impaired and many ofthe large metaboiically demanding A|3 sensoryfibres begin to fire ectopicaily - hence pins andneedles if they innervate skin. Ectopically firingsensory fibres [due to mechanical force or loss ofblood] that innervate deeper tissues, like muscle,may produce incongruent sensations that relateto their innervated tissues. Thus persistent pres-sure over the radial nerve in the radial groove mayproduce deep aching sensations vaguely in theforearm muscles as well as paraesthesia in theskin over the back of the lateral hand. These areasrelate to the muscles and skin innervated by theradial nerve.Although not proven, it seems that nerve trunkmechanosensitivity in the normal physiologicalstate depends firstly on vulnerability and secondlyon design that includes connective tissue densityas well as specialized local innervation character-istics, and the senstivity of the contained nervefibres themselves [Lundborg, 1988]. Thus, manynerves are in extremely vulnerable places near thesurface of the skin, like the many little geniculatenerves on the side of the knee, the superficialperoneal nerve on top of the foot and the radialnerve in the radial groove on the lateral aspect ofthe humerus. These nerves seem particularlyinsensitive to palpation and are probably hugelyadapted to cope by consisting of large quantitiesof protective connective tissue [Sunderland, 1978].By contrast, some superficially placed nervetrunks are remarkably mechanosensitive [Butler,1991], the ulnar nerve at the elbow, the mediannerve in the axilla and just distally, and the proximalcords of the brachial plexus in the supra clavicular

179

Louis Gifford

fossa are examples. It appears that these nerves areless well endowed with connective tissue, haverelatively exposed nerve fibres and are hencemore sensitive (Butler, 1991]. To a degree, theseareas are situated in regions less likely to bedirectly injured in the rough and tumble of dailylife. Deeper nerves often reside in zones prone topressure changes with normal movements andpostures, and seem to cope in a remarkablyrestrained and silent way. For example, nerve rootsin the intervertebral foramen and the mediannerve in the carpal tunnel get squashed andstretched all the time yet we are totally unawareof it unless pathological changes cause them tobecome acutely ischaemosensitive or mechano-sensitive.

Physiological Effects of Movementon Nervous Tissue

The Importance of BloodThe importance of an uninterrupted blood supplyto the nervous system has already been discussed.Like all other cells, neurones require blood fortheir metabolic demands, but in particular forpowering axoplasmic transport and impulse gen-eration and conduction [Lundborg and Dahlin,1996; Lundborg, 1988]. Loss of conduction dueto ischaemia is most notable by the appearance ofparaesthesia, numbness and weakness as whenyou fall asleep with your arms above your head.

AXOPLASMIC FLOW OR TRANSPORT

Many neurones in the peripheral nervous systemare unique in that they are extemely long cells, forexample an individual nerve cell from the foot tothe spinal cord may be 1 metre long. To put this in

perspective, consider if this neurone's cell bodywas increased in size to 100 cm in diameter, itwould have an axon diameter of 10 cm and a lengthof around 10 kilometres (Rydevik eta/., 1984].The viability of any cell is largely dependent on theactivities of the nucleus and cell body and itsability to communicate with the rest of the cel-lular constituents.In neurones the specialized flow of cytoplasmfrom the cell body to its distant peripheral sitesand back is termed axoplasmic flow..This flow ofneurochemicals and cellular structural compo-nents within the axoplasm is essential not onlyfor the health and functioning of the cell itself, butalso for the health of the tissues that the cellinnervates. The nonmyelinated afferent C fibresare now thought to have a particularly importantrole to play in the maintenance of their targettissues' health and in aiding any healing processvia a direct chemical contribution to the inflam-matory cascade (see Chapter 5]. Importantly, neu-rones are not just designated to an impulse-conducting role, many also have the ability tochemically sample the tissues they innervate andrelay these chemicals as a type of'messenger' backto their nucleus and cell bodies (Donnerer et ai,1992]. The nucelus/cell body then alters its activ-ity to produce a specific chemical response that istransported back to the target tissues in order torebalance the trophic disturbance that wasdetected earlier (Donnerer et a/., 1992; Heller eta/., 1994; McMahon and Koltzenburg, 1994]. Inthis way the nerve cell is constantly monitoringthe health of its target tissues, responding to anyabnormality and as a result helping to maintaintissue viability. The implications of this are thatanything that disturbs the bidirectional axoplas-mic flow between cell body and the axon and itsterminals will have repercussions for the health of

Neurodynamics

the nerve cell itself as well as the target tissues itsupplies. If the loss of communication is severeenough the distal axon undergoes Walleriandegeneration or the whole cell may even die(Devon 1994).

POSTURE AND MOVEMENT EFFECTS ONCIRCULATION TO NERVE

Axoplasmic flow is particularly sensitive tochanges in circulation [Okabe and Hirokawa,1989], and circulation to and within nerve tissuesis influenced by changes in pressure produced bypostures and movements of the interfacingtissues.Circulation to a nerve, like any other tissue, isdependent on a pressure gradient existingbetween the incoming arterial supply and the out-going venous return [Sunderland, 1978]. Thus agreater pressure is required at the arterial side inorder to push blood flow through the nerve andout into the veins. Further, any changes in pres-sure around the veins or nerve will upset thisgradient and will cause back-pressures that leadto vascular stasis and ischaemia/hypoxia.Pressure changes that influence circulation tonerve can be brought about by relative compres-sion or elongation of nerve tissue. The influencesof pressure changes produced by wrist flexion onthe contents of the carpal tunnel have alreadybeen noted. Olmarker's group (Olmarker et a/.,1989) have found that pressures as low as 5-10mmHg can stop venular blood flow in the lumbar.nerve roots of pigs, pressures probably easilyachieved at the IVF and radicular canal due tocompression during normal extension or perhapseven during prolonged standing.When elongation forces are applied to a periph-eral nerve the supply vessels tend to straighten upand narrow; the intraneural vessels similarly

unfold, stretch and reduce their lumens, and theintraneural pressure steadily increases the morethe nerve is stretched [Pechan and Julis, 1975). Inthe rabbit peripheral nerve, venous return startsto decline at 8% elongation and by 15%, arterial,capillary and venous flow is completely occluded.If we consider that the length of the nerve bed ofthe median nerve can increase by as much as 20%in full arm, hand and finger extension, it is notsurprising that many of us get building ischaemia-related neural responses when maintaining thesepositions.

It is important to understand that thenervous system is designed to accom-modate to continuous pressurizing andstretching forces and that recoveryafter short-term modest loading is ^normal. \ the nervous system does seem to

find unacceptable is ongoing adversephysical stress - it far prefers move-ment.' Long-term increased pressuresand stretching that many of our rela-tively static lives foist upon the nervoussystem may welt be quietly damaging itmore than it otherwise should be.Pechan and Julis [1975] showed thatmere elbow flexion doubles the pres-sure in the ulnar nerve when comparedto elbow extension.Dahlin and McLean (1986) showed thatmodest prolonged pressures on rabbit

andtime of "pressure.

181

Louis Gifford

AxoQlasm tends to increase, its. viseos-^If^'enves.are not moved (Safer etal,1977]; it thus gets thicker, less fluid-and its flow properties will be compro-,mised at the expense of the health of- -the nerve and its target tissues. By con- '., trast movement will enhance its flowproperties and hence nerve and tissue-health.

Many of the features discussed may also be perti-nent to the neuraxis. For example, the longitudi-nal stress imparted during spinal flexion mayincrease the pressure within the cord since itdecreases its diameter in flexion [Breig, 1978].Longitudinal vessels may be narrowed - [Figure4.14] and movements of the limbs may influencefeeder vessel lumens by directly or indirectly pull-ing or angulating them. Adequate cerebrospinalfluid circulation in the subarachnoid space.'of the.cord and brain is maintained by movement andsince much nutritional delivery is via this route itunderlines yet again the importance of regularmovement for adequate neural health andfunction.The student is reminded that far more can beachieved in tissue physiological terms by thepatient performing simple uncomplicated activemovements than can be achieved by purely passivetechniques.

Pathophysiology of Nerve and itsInfluence on Movement: 'NeuralPathodynamics7

Pathodynamics: IntegratingPathomechanics andPathophysiologySo far the emphasis has been on the influence andinteraction of mechanical forces on the physiol-ogy of the nervous system. Shacklock's [1995]timely introduction of the term 'neurodynamics'has helped focus attention away from puremechanics [Butler and Gifford, 1989] and towardsa perspective that powerfully includes the insepar-able influences of mechanics and physiology oneach other. Further, in order to emphasizethoughts of pathophysiology and pathomecha-nics when injury or disease occurs Shacklock hasintroduced the term 'neural pathodynamics'[Shacklock, 1995].Many pain states that physiotherapists encounterare the result of some mechanical event whichvaries from the extreme of sudden insult tomore minor sustained and prolonged adversepressures or tensions of some kind. Adversemechanical events lead to burgeoning pathophy-siological responses, typically inflammation, heal-ing and repair plus or minus a pain state, whichtaken as a whole, is the body's means of restoringfunction. That full or perfect repair in many of themore complex and metabolically sluggish tissuesof the body can be achieved has to be questionedsince most adult musculoskeletal tissues repair byscar tissue formation not regeneration [Butler andGifford, 1998]. Thus, it is to be expected that as aresult of physiological reparative processes

182

Neurodynamics

[pathophysiology/pathobiology], some mechan-ical dysfunction [pathomechanics] will inevitablyoccur during the later stages of healing and muchmay well remain permanently. Inevitably thismeans that tissues in the functional proximity ofa given lesion will have to adapt accordingly andmay well predispose the individual to furtherproblems later on. It has to be assumed that if arepaired tissue is mechanically compromised it willalso be physiologically compromised in some waytoo. For example; a tissue that remains scarredafter healing may have a less than perfect vascu-[ature and this could have futher negative conse-quences. In considering pain states local adversephysiology must be interpreted in terms of con-tinued effects on the firing and sensitivity ofsensory nerve endings in the neural connectivetissues and on any local damaged nerve fibres.

Pain Mechanisms Relating toInjury of Nervous TissueThe nervous system is a special tissue in that itmust be considered as having two distinctly sepa-rate mechanisms that cause pain when it is physi-

: cally injured [see Chapter 5 for review ofmechanisms]:1 A nociceptive mechanism, which is due to

injury and/or stimulation of the sensory end-ings of nerve fibres in its connective tissues; forexample/ injured and inflamed dura, in thespinal canal, or perineurium in a peripheralnerve trunk.

2 A neurogenic mechanism, which is due toinjury and alteration of sensitivity of the con-ducting fibres themselves. 'Peripheral neuro-genic mechanism^ consider abnormalresponsivity of peripheral neurones, and 'centalneurogenic mechanism^ consider lesions in

the central nervous system as well as abnorm-alities of information processing [see Chapter 5for expanded discussion] [Devor, 1996].

Clinically, the fact that several different mechan-isms of pain production can operate when thenervous system is injured may in part accountfor the very complex pain patterns, pain qualitiesand pain behaviour that is so often seen.

Injuring ForcesPeripheral nerve trunks and roots can be injuredand hence become pain sensitive as a result ofdirect mechanical force or as a result of alterationsin pressure around the nerve. The key to under-standing the influences of alterations in pressure[vascular factors] and direct mechanical injuryreally revolves around a consideration of lengthof time of the forces involved. As a generalization,sudden high forces cannot be tolerated well bythe nervous system and, like any other tissue, leadto injury, inflammation, healing and repair plus orminus a pain state. More sustained forces can betolerated surprisingly well, especially if the load isdispersed over a wide area. Long-term focalincreases in pressure may not be tolerated with-out some expense. Alteration of normal circula-tion by pressure change may lead to degenerativechanges in nerve tissue without necessarily anyinflammation [Olmarker et ai, 1995] and moreimportantly without necessarily_any pain. This isa rather 'occult' form of pathophysiology that isprobably quietly accumulating in all of us as weprogress through life.

SUDDEN MECHANICAL FORCE

Sudden mechanical force considers adversestretching/compression of nerve, for example:

183

Louis Gifford

Sudden twisting of an ankle which may injurethe superficial peroneal nerve over the ankle[Nitz et a/., 1985] or as far proximally as thelower part of the thigh [Nobel, 1966];

Any sudden direct physical force on nerve7 forexample an injury to the radial nerve following afracture dislocation of the radial head;

A whiplash involves huge forces that may wellrip and squash many major or minor nervetrunks and plexi [Jeffreys; 1980], as well as thecord [McMillan and Silver, 1987] and brain [LaRocca, 1978].

ONGOING MECHANICAL FORCE

As already discussed, ongoing mechanical forcesresult in the disruption of the subtle pressuregradient required to maintain adequate vascularsupply to nerves. The spectrum of physical fac-tors that can influence supply range from'normalpostural forces and ongoing inactivity to patho-logical intrusions such as disc protrusions, osteo-phytes, thickened ligamentous, muscular andtendinous tissues, scar tissue, oedema and inflam-matory exudate and haematoma [Butler, 1991; But-ler and Gifford, 1998].Local pressure changes affecting the immediatenerve may not be the sole influencing factors.Thus, consideration of vascular 'control systems'focuses attention on sympathetic tone to supplyvessels if tone is increased the tissues in thesupply field will suffer. There is also the possibilityof pathologies in more remote regions adverselyinfluencing the supply of blood to the area. Thiscould range from heart disease [LaBan and Weso-lowski, 1988] to localized adverse pressures onsupply vessels due to for instance sustained pos-tures, tight muscles, scar tissue, tumours orsimple swelling.

The Repercussions of NeuralIschaemiaLoss of blood to a nerve results in local hypoxic orischaemic conditions [Figure 4.19]. This in itselfmay cause nerve fibres to start to fire ectopicallyand produce abnormal sensations that includeparaesthesias, numbness and pain depending onthe type of fibre affected and the central nervoussystem processing of the abnormal impulse dis-charges that are generated. Continuing hypoxialeads to plasma leakage from the endothelial wallsof capillaries within the nerve itself [Lundborg,1988; Lundborg and Dahlin, 1996]. This intraneuraloedema formation leads to a further increase inpressure within the nerve that adds to the prob-lems of inadequate circulation. The nerve mayeven swell proximally or distally. The end result,originally proposed by Sunderland [1976], is thatthis protein-rich oedema promotes the formationof fibrosis both around the fascicles and withinthem. This must have detrimental affects on thenormal mechanics and physiology of the connec-tive tissue as well as on the health of the nervefibres themselves.It is easy to see how local loss of circulation canlead to dysfunction and damage to nerve fibresand even to their death (jayson, 1992]. Ratherpuzzlingly, this may or may not lead to a pain state.Examination of lumbar nerve roots post mortemoften reveals quite severe nerve fibre damage andfibrosis yet the patients' medical records make nomention of back-related pain problems [Hoylandet a/., 1989]. On the other hand, conditions likethose describe must surely be adequate to pro-duce or predispose to a neurogenic pain state.Ultimately, or at least from a purely tissue-basedperspective, it depends on whether the physio-logical changes are enough to sensitize and fire

184

Neurodynamics

Figure 4.19 Pathobiological effects of compression on nerve.

Intraneural plasma leakage

Intraneural oedema

Fibre dysfunction

Nerve fibre damage, dysfunction, deathLeads to development of ectopic impulse generating sites(peripheral neurogenic pain mechanism)

Input from afferent fibres in neural connective tissues(nociceptive pain mechanism).

Sickneuro'n

Repercussions elsewhere: nerve, target tissues, central nervous system

nociceptors or create ectopic impulse generatingsites in damaged nerve fibres (Hasue, 1993]. The

other perspective to consider is that many of usmay actually have many nociceptors and ectopicimpulse-generating sites firing, but our CNSchooses to pay no attention to the activity.

The Importance of InflammationInflammation, or at least the presence of irritativechemicals, may be a vital determinant as towhether or not a neuropathy is painful. Theremay be a marked difference in the chemical envir-onment of a nerve that is being slowly com-pressed by developing degenerative invasion andone where inflammation has occurred due to a

more acute injury or where local interfacing tissuehas been damaged and becomes inflamed.'Disc disruption is a powerful example of the manydiverse influences on a nerve tissue.

Any disc protrusion may mechanically damagethe adjacent nerve root - compression of thedorsal root ganglion is likely to be immediatelysymptomatic since it is normallly mechanosen-sitive- Neural connective tissue may bedamaged [perineurium, dura] which leads toan inflammatory response in this tissue andmore than likely a pain state.

The protrusion, even without contacting thenerve root tissue, may increase the pressurearound the nerve and cause an increase invenous pressure. This may be sufficient to

185

Louis Gifford

produce ischaemic conditions both around andwithin the nerve a situation that has thepotential to lead to inflammation within thenerve [Hoyland et al, 1989], or more likely tooedema and fibrosis in and around the nerve asdescribed above [Cooper et a/., 1995].

The disc injury itself may precipitate inflamma-tion in the immediate environment of thenerve. Leakage of nuclear fluid is thought tocreate an inflammatory response [McCarron etal, 1987; Saal, 1995], and chemicals so producedmay get rapidly transported into the localnerve'[Byrod eta/., 1995] and thus produce anintraneural pain-generating environment[Olmarker eta/., 1993,1994].

As a result of possibly profound intraneuralphysiological changes, nerve fibres' becomedamaged and develop abnormal ectopicimpulse generating sites that can be responsiblefor ongoing and often very disturbing painstates [see Hasue, 1993, for useful summary].-

In summary,

9 Acute disc injury has many potential repercus-sions when creating a pain state - from noci-ceptive mechanisms in damaged tissues of thedisc and adjacent tissue, to peripheral neuro-genic mechanisms as a result of direct or indir-ect nerve root irritation and damage [seeChapter 5]. The mechanisms are complex andmay develop over time which warns cliniciansto progress cautiously with very early manage-ment of low back disorders.

Physiotherapists should be aware that discinjury related pain and therapy is more complexthan discs mechanically 'going ouf and being'put back'. Appreciation of the complexity andtiming of the recovery process and the condi-tions that enhance the natural resolution argu-ably promote a rehabilitative physiotherapy

approach coupled with a more rational use ofthe best that modern medicine can offer.

Implications of Peripheral NervePathophysiologyThe wider implications of any nerve injury seemquite daunting [Figure 4.19]: Impulse barrages from ectopic impulse gener-

ating sites are potent modulators of centralnervous system sensitivity [Chapter 5].

Damage in one area of a nerve has been shownto influence the sensitivity and health of distalor proximal areas on the involved and relatednerve trunks [Mackinnon, 1992]. Thus healthyneurones effectively become 'sick neurones'and their seemingly malevolent influences canspread.

Loss of, or poor communication, between theneurone nucleus and its target tissues may havedire consequences for target tissue health [seeabove].

Nerve contraction, loss of elasticity or any tether-ing as a result of pathophysiological processesmay have far-reaching adverse mechanical influ-ences on related tissues. For example, it is easy tovisualize how a tethered, fibrous and inelastic seg-ment of a peripheral nerve trunk would put morestrain on its proximal and distal segments duringmovements that stretched it. Adverse mechanicaltension in one area may thus lead to pathophy-siological processes with the potential to becomethe source of symptoms at distant sites [Breig,1978; Butler and Gifford, 1989,1998; Butler, 1991].Thus, it is not uncommon to find that following asingle neuropathy other pain states later crop upin 'neural!/ related areas. For instance, carpaltunnel syndrome has been strongly related tonerve injury in the neck.

186

Neurodynamics

Upton and McComas [1973] found approxi-mately 80% of patients with carpal tunnel syn-drome or lesions of the ulnar nerve at the elbowhad neural lesions in the neck. These authorstermed the phenomenon 'double crush' syn-drome, i.e. where a proximal nerve compressionpredisposes a nerve to pathology distally.

The literature also describes reversed doublecrush [Lundborg, 1988] and multiple crush syn-dromes [Mackinnon, 1992] that really highlighthow the health of a whole nerve can be affectedby modest forces that start in one area. Spread-ing of symptoms and signs is very common inchronic pain development.

Mechanical injury and changes in pressures andcirculation to the spinal cord, brain and its liningconnective tissues are less easy to study [Butler,1991] than the peripheral nervous system. There isno reason not to assume that issues similar tothose that influence peripheral nerves could oper-ate in the CNS [see Butler, 1991; Butler and Gilford,1998].

From Theory to Practice:Neural Sensitivity

Pathological MechanosensitivityClinically, mechanosensitivity can be seen as animmediate symptom response that bears a directrelationship with a physical force. Nerves can beinfluenced mechanically by any movement, staticmuscular contractions, even the pulsating ofarteries if extremely sensitive [Butler, 1991; Butlerand Gifford, 1998].It may make clinical analysis easier to think interms of movements that mechanically stretchnerves - as in the neural tension or 'neurody-

namic' tests [Shacklock, 1995], and those whichcompress nerves - as in the closing of the inter-vertebral foramina in spinal extension or ipsilat-eral rotation/side-flexion movements, or thecompression of the median nerve in the carpaltunnel by wrist flexion or extension.Butler [1996] has used the terms: 'Container dependent' for symptoms evoked

by compressive effects; 'Neural dependent' for symptoms evoked by

neural elongation/neurodynamic tests like theslump, SLR and ULTT [see Chapter 6].

Analysis of symptom-provocative postures andmovements with these thoughts in mind is oftenvery useful.The frequent straightforward link between a per-formed movement or posture and symptomreproduction are often complicated by the factthat impulse discharges from ectopic impulsegenerators in mechanosensitive segments ofnerve respond in a great variety of ways [Devor,1994; Butler and Gifford, 1998]. For example: You do a test, it hurts for a couple of seconds

and then disappears, you repeat the test andnothing happens. Five minutes later you repeatthe test and it responds again, and so on.

A test may produce a fleeting symptom imme-diately tension or compression is applied andthen again when the force is removed, therebeing no response when the- force is main-tained.

A test may produce a response in parallel withthe force applied but continue long after thetest force is removed.

Odd and clinically frustrating reactivity like thismakes one suspect a peripheral neurogenic painmechanism [see Chapter 5].

187

Louis Gifford

Pathological IschaemosensitivityFurther evidence of sensitivity is found when adelay and then a slow build-up and spread ofsymptoms is produced. This may be an indicatorthat the nerve is more ischaemosensitive thanmechanosensitive, especially when the test per-formed could well be adversely influencing thepressure in the nerve or the circulation to it(Butler and Gifford, 1998]. A classic example is an acute or subacute cervi-

cal or lumbar nerve root problem where sus-tained rotation towards the side of pain is atfirst symptom free but then after a few secondsa slow build-up of discomfort occurs that fre-quently spreads down the arm/leg to producedistal paraesthesia.

Carpal tunnel syndrome symptoms are- oftenheightened by Phalen's test. Here, sustainedwrist flexion slowly produces an increase andspread of symptoms.

Further Considerations -Many peripheral nerve problems are far frompredictable, are ongoing in nature or occur spon-taneously often with agonizing ferocity that canbe very worrying to the patient. There are manypossible explanations that can be derived fromcurrent tissue pathophysiological knowledge.For example:

A consideration of mechanisms that produce'ectopic pacemaker' capability must beincluded [see Chapter 5).

Ongoing normal or pathological pressures onsensitized nerve may be factors. Consideroedema, muscle tone, haematomas, or anypathology/defect/congenital defect that

. could occur adjacent to sensitized neural tissue

and that will put pressure on it or its vascularsupply

Many ectopic impulse generating sites haveincreased sensitivity to circulating chemicals.Thus, anxiety and 'stress' may increase pain/symptoms since ectopic sites can become sen-sitive to adrenaline and noradrenaline releasedas a result of sympathetic nervous system activ-ity (see Chapter 5 and Devor and Rappaport,1990; Devor, 1994,1996].

Neural mechanical sensitivity and ischaemosensi-tivity can be investigated by analysing pain qualityand pain behaviour, pain response to normalmovements, sustained movements and responsesto tests that attempt to focus mechanical forceson neural tissues. These include tests that have abias to elongation and tension (see Chapter 6] andto those that emphasize compression, via jointmovement or via direct 'palpator/ techniques(Butler and Slater, 1994; Butler and Gifford, 1998].

Restricted Range ofNeurodynamic Tests - A WiseStance?Physiotherapists must consider the nervous sys-tem as capable of becoming a very mechanicallysensitive system and rarely one that becomes somechanically compromised that it is physicallyresponsible for major losses of range of move-ment. It can be argued that in the majority of casesit limits range by producing pain/symptoms thatthen call a halt to movement via the active will ofthe patient and reflex protective muscular con-traction in concert.This now has support from current workreported by Elvey (1995] and Hall et al. (1995]that demonstrates increased muscle activity dur-ing straight leg raising in patients with sciatica.

188

Neurodynamics

They found that the electromyographic [EMG]activity of the hamstring muscle increases in par-allel with the pain response felt by the patient.The key point is that the nervous system/ espe-cially if it has become injured and hence sensitized,mobilizes adaptive motor protective mechanismsif it is physically challenged.A blocked straight leg raise in a subject withchronic sciatica may be a point of argument forsome, in that the block to movement can be seenas being due to. tethered and noncompliantlumbosacral nerve roots, especially if sciatic painis reproduced. The root may well be tethered andnot moving as well as it once did, but can thistethering be responsible for as much as 30-40.of loss of SLR range?Consider that: The amount of movement observed in fresh

cadavers in the lumbar nerve roots is at best10 mm [Goddard and Reid, 1965] [Figure 4.13],which is hardly enough to cause such a largeloss of range.

It seems more likely that the nervous system mayprotect itself by: Becoming mechanically sensitive; Inducing powerful protective reflexes in the

hamstrings/glutei when mechanically threa-tened;

Later, more long-term protective processesmay be added, e.g. adaptive physiological/mechanical changes in the hamstrings/glutei,the nerve root itself and other relevant tissues.

Thus, in the acute and subacute situation loss ofrange is related more to physiological processesand pain responses [sensitivity], and in the morechronic situation is related to both neural sensi-tivity and some mechanical compromise of mul-tiple tissues that includes the nerve roots.

It is complex and often difficult to sort out clini-cally The easiest way would be to place the.patientunder a general anaesthetic and observe the rangedevoid of any pain response or protective mus-cular activity. Although this is rarely feasible itdoes occasionally help to think when examininga patient, 'would this range be normal if there wasno pain?' Ultimately, the nearest we can get to theanswer comes from the highly skilled analysis ofthe 'end-feel', or the resistance felt during testingand the rate of improvement of range whenattempts are made to mobilize it. However, Butlerreports [1996] that he has had the opportunity toexamine a few apparently mechanically 'blocked'straight leg raises under general anaesthetic andwas surprised to find some quite normal in rangeand yet others that were indeed tight and blocked.

. Our thoughts must always be open.The purpose of making these points aboutmechanical block and sensitivity is that there aregreat dangers in viewing disorders labelled asneural 'tension' solely in terms of mechanicalcompromise of the nerve, and that pushing hardinto resistance at end of range is a necessaryprocedure to overcome a pain problem that pre-sents with limited range of motion of a neruody-namic test.Even if a nerve is mechanically compromised thereare many inherent dangers in strongly mobilizingit since it is likely to be far more physically vulner-able and more easily resensitized than it was beforeinjury.

Understanding Neurally Safe'Stretching7 or MobilizingIt is possible to move into tissue resistance in'neurally safe' ways.

189

Louis Gifford

Practical Jask

i with straight knees in the-staMaf^fp'r- ward-bending test and who fialj^d&yffpz torn problems at all. ^ Perform a standard SLR test and ask **

carefully about their symptoms at area- 'sonably firm end-range position the -quality and distribution of the symp- Atoms are important. In my experience >-.'there is commonly a deep diffuse zching ''sensation distributed anywhere from j.

*the back of the hip, back of thigh, back of knee into the calf, and some- '..times into the foot Get the subject to 'Ifocus on the symptoms and remember ,;them so that they can be compared.to ;the next test.

On the same leg perform hip flexion to

^ add knee extension into_,'^'desjfresistaffse 'but-do not allow it to

go to full extension. If the knee doesreach full extension take the hip intofurther hip flexion and add the kneeextension again [see Figure 4.20).Keep the knee in exactly the same posi-tion while further flexing the hip and 'ask about the area and type of response*in comparison to the first test Theclassic response _to this test is a well 'localized pulling sensation in the ham-string muscles it 'feels'muscular.

It seems that in the last position muscle tensionand a muscle tension sensation come into play farearlier than neurally related tension and symptomresponse. The concept then is to use mobilizationtechniques that tend to produce more muscletension feelings rather than neural ones.

Figure 20 Hip flexion test with knee short of full extension [see text for explanation]. [Reproduced, with permission, from Butler andGifford, 1998, TTie Dynamic Nervous System. NO1 Press, Adelaide.]

190

Neurodynamics

Practical TipsIt is quite often possible to mobilize achronic orsubacutely restpisted'SL-R'intoresistance by< going into flexion -Mt/i hipabduction ajid exflexion a^

gains in range can be made. The patientcan also perform home stretches utilizingsimilar components. For example, in sit-ting symptomatic leg forward, heel onfloor, foot in neutral, knee in 1520 offlexion, hip in abduction and modest lat-eral rotation perform gentle flexionmovements from the back and hips.

In the SLR with the knee-flexed position described 'it is often possible to see the tibial division of thesciatic nerve standing out at the back of thepopliteal fossa. It is certainly easy to palpate hereeven if it cannot be seen [Figure 4.21]. The nerve inthis position is very tight, and is a reasonableindication of quite marked dynamic changesalong the length of the nerve that probablyincludes the nerve roots. However, in terms ofsymptom response, it seems that SLR with a fullyextended knee is far more 'nerve provocative' thanwhen the knee is flexed 15-20.Hopefully this illustrates one way of addressingresistance in a neurally safer way, i.e. perform the

-restricted movement into resistance so that asensation of muscle stretch is produced [kneeslightly flexed SLR] rather than one that producesstrong neural symptoms [knee extended SLR].The essential element of safety is provided byfocused symptom enquiry and analysis andcleverly adjusting starting positions.

Figure 4.21 The tibial and common peroneal nerve at the backof the knee are sometimes very visible in the position shown inFigure 4.20. The examiner's thumb is on the lateral aspect ofthe subject's right knee. The peroneal nerve lies medial to thebiceps femoris tendon and the tibial nerve runs centrally intogastrocnemius. (Reproduced, with permission, from Butlerand Gifford, 1998 The Dynamic Nervous System, NOI Press,Adelaide.]

However, we should always be aware that symp-toms reporting by consciousness is not always asaccurate a reflection of what may be happening at.tissue level as we would wish [see Chapter 5].Restoring range of movement'Is an importanttenet of physiotherapy that should be achievedin the safest possible way. Since it is argued herethat in the majority of patients neural sensitivityissues are much more dominant than mechanicalblock to neural movement issues, it is suggestedthat physiotherapists use neurodynamic tech-niques and exercises:

191

Louis Gifford

1 With thoughts of promoting better physio-logy to help decrease sensitivity and restorerange;

2 With thoughts of slowly stretching/ elongatingrelated musculature that may be reflexly morealert, or modestly mechanically shortened, dueto the reasoning discussed above.

Final Comments

Butler and I published a paper in 1989,entitled 'Theconcept of adverse mechanical tension in thenervous system' [Butler and Gifford, 1989] whichwith hindsight viewed and addressed disorders ofthe nervous system in a predominantly mechan-istic way - just as joints and muscles were exam-ined at the time. Sensitivity of the nervous systemwas addressed by attempting to judge the irrit-ability of the system as per Maitlan'd' [Maitland71986]. This is no longer adequate. New biologicallybased knowledge now allows reasoned judge-ments to be made on the class of pain a patientmay be suffering [see Chapter 5 and Butler andGifford, 1998], and provides an understanding ofthe complex issues of sensitive neural tissues andtheir clinical correlates. For many patients, mobil-izing neural tissue may well be as appropriate asmobilizing any tissue. However, under anexpanded reasoning framework [see Chapters 5,6 and Butler and Gifford, 1998] that pays dueattention to the manual therapist's findings inrelation to the pathobiological process involvedin the patient, modern management now calls forbetter'and gentler techniques, decisions on handson or hands off, more patient self-management,empowering the patient with knowledge, andtechniques and exercises done with the fullunderstanding of the patient and therapist[see Chapter IS].

These are exciting times for physiotherapy. It isessential that clinicians take a forward step fromthe old mechanistic systems of manual therapyand integrate the pain-related sciences to providea better and safer delivery of physiotherapy whoseaims are to reduce pain, relieve suffering, restorerange and enhance overall function.

Conclusions and Key Points

The nervous system moves and this is reflectedin many of its anatomical features.

Movement of the nervous system is not at allsimple. Over and above many fundamentalgross movement features and principles thereis great variability between one individual andthe next.

The nervous system is designed to cope withremarkable elongation and compression effectsdue to posture and movement. Sudden elonga-tion or compression forces extend the nervoussystems' safety adaptations to their limits andmay easily cause injury.