• The spinal cord

• The spinal nerve, which contains fibres belonging to one segment

• In the brachial and sacral area, and distal from the spinal ganglion, the different spinal nerves form a nerve plexus, from which originate the large multifascicular nerve trunks

• Further distally the trunks split into peripheral nerves, with motor, sensory or combined function.

Roots

The course of the spinal nerve within the spinal canal, from the emergence of the rootlets at the anterior and posterior aspect of the spinal cord to the outer border of the foramen, is called the intraspinal root (Fig. 2.4).⁷ Being inside the meningeal membranes of the spinal cord, the posterior and anterior roots are devoid of the elaborate epineural and perineural membranes that are characteristic of peripheral nerves.

Proximally, the rootlets float freely within the cerebrospinal fluid which is the main source of their metabolic needs. In this intrathecal part of the intraspinal root, the rootlets are held together by the endoneurium which is more loosely arranged than is typically seen in peripheral nerves.⁸ Further distally, the nerve root becomes enclosed in the dural sheath – a tubular prolongation of the dura. In this dural investment the nerves do not lie freely but are bound by the arachnoid membrane (Fig. 2.5).^9,10 This area is known as the extrathecal part of the intraspinal nerve root – that length of the root and the dural sleeve between the main dural sac and the exit from the foramen. The extrathecal portion is short in the cervical region but becomes longer with the increasing obliquity of the intraspinal roots in the thoracolumbar and lumbar regions.

Distal to the posterior root ganglion, at the level of the foramen, the posterior and anterior roots are fused into one single bundle. Here the nerve root becomes extraspinal. The tissue of the epidural pouch becomes more condensed and blends with the epineurium of the extraspinal nerve root.

The segment of the spinal root which is liable to compression, whether by a disc protrusion, an osteophytic outgrowth or a narrow lateral recess, is the extrathecal part of the intraspinal root. To understand the symptom of a compression or inflammation of this part of the peripheral nerve system, it is necessary to recognize the importance of the dural investment – the nerve root sheath. The dural sheath has considerable sensitivity:¹¹ it has many nociceptive nerve endings, especially at the anterior aspect where it receives its innervation from the sinuvertebral nerve belonging to the same segment.^12–14 Pain arising from the dural sheath is segmental and obeys the rules of segmental reference of pain (see Ch. 1). There is no evidence that root pain arises from involvement of the axons. For example, pressure at the extraspinal nerve root, which misses the nerve root sleeve, as happens in some types of spondylolytic compression, causes not pain but only paraesthesia and neurological deficit.

From a clinical point of view, it is important to consider this structural duality: the outer investment is responsible for segmental pain, whereas the parenchymatous content is responsible for the paraesthesia and the conduction deficits.

Nerve plexus and nerve trunk

Immediately distal to the foramen, the single fasciculus of the extraspinal root is enclosed in a thin, but strong, perineurial sheath, external to which is the epineurial areolar connective tissue. Within a few millimetres of its formation, the single fasciculus of the spinal nerve divides into several bundles which form the plexuses. Motor and sensory fibres of one nerve root mix, and more distally there is a redistribution of the fasciculi of various consecutive nerve roots.¹⁵ The brachial plexus is thus formed of the anterior rami of roots C5–T2, and the sacral plexus of the roots L2–S5. Distally, the fasciculi continue in the large nerve trunks of the limbs.

The fasciculi of plexus and trunks do not differ significantly from those of the roots or the peripheral nerves. The connective support tissue, however, has some anatomical particularities. Because the monofascicular spinal nerve changes into a multifascicular structure, there is an increased amount of epineurial tissue, forming a protective packing for the nerve tissue. The perineurium is also reinforced by elastin fibres. The fasciculi have an undulating course, whereas the collagen fibres run more longitudinally. This structure ensures that the nerve fibres are protected from mechanical deformation (compression and elongation) during normal movements of the limbs.¹⁶ Although the epi- and perineurium contain nociceptive nerve endings, these seem to be relatively insensitive.¹⁷

Small peripheral nerve

A small peripheral nerve is the distal termination of a branching nerve trunk. The nerve ending is often monofascicular. The epineurium is then fused with the perineurium. Peripheral nerves can either have only a motor or a sensory function, or both can be combined. They all have nociceptive nerve endings in their supporting connective tissue.

Nociceptive pain

Peripheral nociceptors in the connective tissue of the peripheral nerves are stimulated, and via Ad and C fibres of the nervi nervorum conducted to the spinal cord and thence to the pain projection areas in the cortex.¹⁸ There are indications that most of the pain that stems from direct irritation of the peripheral nervous system is of nociceptive origin.^19,20 ‘Nerve pain’ thus behaves identically to other peripheral pain,²¹ obeys exactly the rules of referred pain and is not to be distinguished from pain of ligamentous, tendinous or arthrogenic origin (see Ch. 1).

Neuropathic pain

This type of pain, also called ‘de-afferentation or neuralgic pain’ is less common than nociceptive pain and results from prolonged damage to peripheral nerve tissue, such as avulsion, dissection or amputation.²² The pain is felt in the anaesthetic area, is continuous and burning and is independent of posture or movement, although local pressure can increase the pain considerably.²³

Chronic damage or formation of scar tissue seems to provoke pain mechanisms without involvement of peripheral nociception. Also, the formation of a neuroma leads to increased sensitivity and spontaneous pain.²⁴ Research on experimental neuromata has shown that regenerating axons have a spontaneous excitability and an increased sensitivity to mechanical stimuli. An action potential in one axon probably leads to an impulse in a nearby axon. This mechanism of ‘cross-talking fibres’ accounts for the repetitive train of action potentials in a bundle of regenerating axons.²⁵ A small stimulus thus leads to a self-perpetuating series of action potentials, and excessive and long-standing pain.²⁶

Another mechanism that may account for neuropathic pain is the loss of inhibitory effects of the large diameter mechanoreceptor afferents in a traumatized nerve. This leads to a relative increase of the activity from the small nociceptive afferents, and thus an opening of the gate at the dorsal horn.²⁷ (see Ch. 1).

Superficial dysaesthetic pain

This type of pain is also rare, and is typical of diffuse polyneuritis, for example in diabetes,²⁸ vitamin B₁ deficiency or chemical irritation. Damage to small C fibres leads to sprouting of small offshoots in the regenerating axons. This leads to increased excitability, which results in unpleasant painful sensations during normal stroking of the skin (allodynia).²⁹ The patient also complains of a burning feeling and ‘electrical sensations’ when the skin is gently touched (dysaesthesia), and there is also some analgesia (see Box 2.1 for an overview of neurogenic pain).

Pain

The pain mechanism in entrapment phenomena is usually nociceptive: free nerve endings in the connective tissue of the nerve or in the dural investment of the nerve root are depolarized by application of mechanical forces or after exposure to irritating chemical substances, released from inflamed tissues.³¹ The pain stems from irritation of the support tissue enclosing the nerve fibres and only exceptionally does it result from pathological processes in the nerve tissue itself (neuropathic and dysaesthetic pain). This has the following clinical consequences.

The pain will depend largely on the density of the nociceptive receptors in the support elements. It follows that the intensity of the pain depends not only on the intensity of compression but also on the localization along the course of the peripheral nerve. Pressure on a nerve root, for instance, will be more painful than an equal degree of force applied on a nerve plexus.

Because an external force acts first on the outer supporting structures of the nerve, pain will usually be the first symptom and it sometimes appears before involvement of the parenchyma is present. A chronic but moderate pressure that is insufficient to impair conduction solely influences the outer structures and results in pain only. It is thus possible to have a completely normal examination of the peripheral nervous system, even though the patient does have nerve compression.³²

Paraesthesia

Pins and needles are pathognomonic of involvement of the peripheral nervous system in that the sensation cannot be produced in any way other than compression or inflammation of nerve tissue.³³ Paraesthesiae are always felt in the cutaneous area supplied by the nerve tissue involved and distal to the site of the lesion. It is therefore extremely important to ascertain the precise site of the symptom, in that this helps to determine the site of compression.

Provocation of pins and needles by movements (distant movements or local pressure) or by stroking over the affected skin demonstrates an external origin for the symptoms. In primary afflictions of the peripheral nerve (neuritis), the pins and needles come and go spontaneously and movements do not influence them.

Loss of function

The epineurium and perineurium initially buffer the fasciculi from constrictive effects, but with a greater amount of compression, structural changes of the elements within the endoneurium follow.³⁴ Recent research has demonstrated that the intraradicular oedema caused by alteration of the blood–nerve barrier is the most important factor in the nerve root dysfunction of chronic compression.^35,36

Sometimes only the Schwann cells are affected, without damage to the axons. Destruction of the myelin sheath then results in loss of conduction. This type of lesion (lesion of Schwann cells without lesion of the axon fibre) is termed ‘neuropraxis’. If the compression has been only temporary, recovery of the Schwann cells will not take more than 2 weeks. This is the type of lesion responsible for the ‘Saturday night palsy’ seen after prolonged pressure on the radial nerve, or the ‘gardener’s palsy’ seen after prolonged traction on the peroneal nerve.

If considerable compression is maintained for a longer period, atrophy of the nerve tissue occurs and is followed by Wallerian degeneration of the distal part of the axon. Oedema, cellular proliferation and ingrowth of connective tissue also follows.³⁷ If the compression is maintained for long periods, fibrotic degeneration appears at the site of the lesion, which makes recovery most unlikely.³⁸

Small peripheral nerves

Pressure on a small peripheral sensory nerve results in pain, paraesthesia and numbness. Pain is usually moderate and the main symptom is numbness. Together with some paraesthesia, these symptoms occupy the appropriate area of supply, which is usually well defined with clear-cut borders. The patient can tell precisely where the cutaneous analgesia is felt and where sensation is still normal. The centre of the region is often completely anaesthetic. A typical example is ‘meralgia paraesthetica’, which results from compression of the lateral cutaneous femoral nerve of the thigh.

Nerve trunk/plexus

Minor and intermittent pressure on a nerve trunk or a plexus causes paraesthesia and numbness. Sudden and serious tissue damage may provoke neuropathic pain. Constant pressure on a nerve trunk leading to parenchymatous damage does not usually provoke pain nor paraesthesia but only loss of motor and sensory function.

If the pressure is intermittent, a neurological deficit does not appear, even after many years. Paraesthesiae do not appear during the time of compression but only when the pressure on the nerve trunk has been released. It is common knowledge that pressure on the sciatic nerve while sitting causes only vague analgesia in the affected area or no symptoms at all. The shower of pins and needles then only appears when the subject relieves the pressure by standing up. The interval between the cessation of the pressure and the onset of the tingling depends on the duration of the compression: the longer the pressure is applied, the longer is the interval between the relief of pressure and onset of symptoms.

There is also a relation between the duration of compression and the duration of paraesthesia. Thus, after 15 minutes of pressure, the pins and needles appear 20–60 seconds after the release and last only 1 or 2 minutes. After release from 15 hours’ compression, paraesthesiae will probably appear only after an interval of some hours, then persist for 1 to 2 hours before recovering spontaneously. Cyriax³⁹ calls this strange and hitherto unexplained phenomenon the ‘release phenomenon’ (see his p. 37). Lundburg and Rydevik have demonstrated that fluctuations in membrane permeability of the structures within the endoneurium are more noticeable when compression on the nerve trunk is released and oedema appears, than during the compression of the nerve and its supplying blood vessels.⁴⁰ This might explain the release phenomenon.

Another characteristic of paraesthesia induced by compression at the level of the plexus is that active movements of the limb or the digits, or stroking over the analgesic area of skin usually brings on or increases the pins and needles. It is a common experience that the paraesthesia in the feet that comes on after relieving pressure on the sciatic nerve increases when the subject walks around or stamps the feet on the ground.

Paraesthesia and numbness are usually felt in the distal part of the cutaneous area supplied by the compressed plexus or nerve, no matter at what point in its course the compression occurs. The lesion lies proximal to the upper edge of the paraesthetic area but not always close to it. Therefore it must not be thought that, if movement of the foot provokes the pins and needles, the lesion lies in the ankle or foot. Clinical examination must include the entire length of the nerve involved.

The release phenomenon is typical of compression of the sacral plexus and the nerve trunks of the lower limb. The phenomenon is also provoked by compression at the brachial plexus (thoracic outlet syndrome) but ceases to operate when a nerve trunk distally to the thoracic outlet is compressed. It is a curious clinical fact that pressure on a nerve in the upper limb only provokes paraesthesia during the moment of compression. Pins and needles in the two ulnar fingers, caused by compression of the ulnar nerve at the elbow, immediately stop when the compression is released. Similarly, in carpal tunnel syndrome, the paraesthesiae are felt during the moment of compression.

Compression of the nerve root

Pressure on the extrathecal intraspinal nerve root results in a typical set of symptoms (pain and paraesthesia) and signs (motor and sensory deficit) strictly related to the segment involved. Contrary to the pins and needles brought on by the release of pressure on a nerve trunk, the paraesthesiae only appear during the period of compression, and cease immediately thereafter.

The sequence of appearance of pain, paraesthesia and deficit and their mutual interrelation have important clinical significance and are often of considerable help in the diagnosis of nerve root compression.

Spinal cord

Pressure on the anterior aspect of the spinal cord results, inter alia, in bilateral paraesthesia. Pain is absent if the compression is slowly progressive, but dural pain may accompany the paraesthesia if the compression is sudden. The main cause of spinal cord compression is spinal stenosis at the cervical or thoracic level. When the cord is compressed over the thoracic region, the paraesthesiae are felt only in the limbs. In compression at the cervical level, pins and needles will be present in all limbs or in the lower limbs only. The paraesthesiae are usually bilateral and extend beyond the borders of the areas of the cutaneous innervation of any spinal nerve, nerve trunk or peripheral nerve. For instance, the patient may complain of pins and needles in both hands and forearms at both aspects or in both legs from the knees to all the toes.

The symptoms are provoked neither by movements of the limbs nor by stroking the skin. Neck flexion is the only way to bring on the pins and needles (L’Hermitte’s sign). Together with the extrasegmental and bilateral distribution of the painless paraesthesiae, positive neck flexion provides the clue to the diagnosis of incipient spinal cord compression.

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