The joints of the lower cervical segment consist of the interbody joint anteriorly and the two zygapophyseal joints posteriorly. The interbody joint is made up of the intervertebral joint and the uncovertebral joints. When stacked, the joints can be considered to form three pillars in a triangular formation, the vertebral bodies and uncinate processes forming the anterior column and the two articular pillars formed by the zygapophyseal joints arranged posteriorly (Mercer & Bogduk 1999).

The intervertebral joint is a symphysis formed between the relatively avascular intervertebral disc and the adjacent vertebral bodies. The disc contributes to mobility and, as it ages, assists the uncovertebral joints in providing translatory glide to the movements of flexion and extension (see below).

The uncovertebral joints (joints of Luschka) are formed between the unciform processes and corresponding facets on the vertebral body above (Fig. 8.3), though their existence has been challenged (Mercer & Bogduk 1999). They may be true synovial joints or adventitious fibrous joints which have developed through clefts or fissures in the lateral corners of the annulus fibrosis of the intervertebral disc originally described by Hurbert von Luschka in 1858 (Prescher 1998). These fissures are absent in young children and appear to develop in conjunction with the development of the unciform process.

Once formed, the fissures in the annulus develop a pseudocapsule in which vascularized synovial folds have been seen. Prescher (1998) relates the development of these fissures and the uncovertebral ‘joint’ to the development of the cervical lordosis resulting in a change in configuration and the magnitude of the loads transmitted through the cervical spine. This results in strong shear forces being transmitted through the intervertebral disc, particularly during rotation and side flexion. C3–C5 are the most loaded segments and it is at these levels that the fissures in the disc first appear.

The uncovertebral joints also contribute to mobility by providing a translatory gliding component to flexion and extension as well as stabilizing the spine by limiting the amount of side flexion. The gliding component produces shear which extends horizontal fissuring of the disc medially from the uncovertebral joints. This, together with the degenerative process, may eventually produce a bipartite disc (see below) (Taylor & Twomey 1994, Mercer & Bogduk 1999).

The position of the uncovertebral joints gives bony protection to the nerve root from posterolateral disc displacement. As synovial ‘joints’, degenerative changes can have an effect on the uncovertebral joints. Osteophyte formation on the uncinate process occurs predominantly in the lower cervical segments. Posterior osteophytes can encroach on the intervertebral canal leading to compression of the emerging spinal nerve root, whereas anterior osteophytes may compress the vertebral artery.

The zygapophyseal joints are synovial plane joints with relatively lax fibrous capsules to facilitate movement. The articular facets are angled at approximately 45° to the vertical so that side flexion and rotation of the lower cervical spine occur as a coupled movement. This angle of inclination adds to the component of translatory glide during flexion and extension (Taylor & Twomey 1994).

A number of intra-articular structures have been described, particularly vascular synovial folds, similar to the alar folds of the knee, as well as fat pads and meniscoid structures. All are highly innervated and can be a potential source of pain (Taylor & Twomey 1994, Oliver & Middleditch 2006). As synovial joints, the zygapophyseal joints are prone to degenerative changes and, being placed near the exiting nerve root, osteophyte formation may affect the size of the intervertebral foramen.

Orthopaedic medicine treatment was traditionally based on the discal model, but it should be remembered that any structure that receives a nerve supply can be a potential source of pain. Since the cervical spine is made up of individual motion segments, a lesion of one part of the segment will tend to influence the rest of that segment. Similarly, treatment directed to one part of a segment will affect the segment as a whole.

There are six cervical discs which facilitate and restrain movement as well as transmit load from one vertebral body to the next (Fig. 8.4). Cervical discs are approximately 5 mm thick (Palastanga et al 2006) and the thinnest of all the intervertebral discs. Each forms part of the anterior wall of the intervertebral foramen and is thicker anteriorly, contributing to the cervical lordosis. The intervertebral disc consists of an annulus fibrosus, nucleus pulposus, and transitional superior and inferior vertebral end-plates.

The difference in function between the lumbar and cervical spine and the traditionally accepted view that cervical discs are smaller versions of lumbar discs does not hold true. Mercer & Bogduk (1999) acknowledged this in their investigation of the form of the human adult intervertebral cervical disc and its ligaments. At birth the nucleus consists of no more than 25% of the entire disc and it undergoes rapid degeneration with age so that, by the age of 30, the nucleus is undistinguishable as such.

The structure of the annulus fibrosus, described by Mercer & Bogduk (1999), is different anteriorly and posteriorly (Fig. 8.5). The anterolateral annulus forms a crescent shape when viewed from above, thicker in the median plane and thinner laterally, tapering out to the unciform processes. It forms a dense, anterior interosseous ligament. The fibres arise from the superior surface of the lower vertebra, fanning out in an alar fashion laterally, but in the midline form a tightly interwoven pattern with fibres from opposite sides, not the true laminate structure as seen in the lumbar spine. A distance of 2–3 mm from the surface of the anterior annulus, collagen fibres have been found embedded with proteoglycans and forming a fibrocartilaginous mass which has a pearly appearance and the consistency of soap.

On a deeper plane, the fibrocartilaginous mass becomes more homogeneous and less laminated, forming what the authors interpret as the nucleus of the disc. Clefts, presumably the uncovertebral ‘joints’, are seen to extend into the fibrocartilaginous core laterally at the uncovertebral region, partially into the core in younger patients but totally transecting the posterior two-thirds of the disc in older specimens (bipartite disc). Covering the clefts in the uncovertebral region is thin periosteofascial tissue, the annular fibres being deficient here.

The posterior annulus demonstrates different features to the anterior annulus. It consists of a thin layer of one set of vertically oriented collagen fibres, not more than 1 mm thick, passing between adjacent vertebrae and extending out as far as the unciform process on each side where no oblique posterior annular fibres were found. Deep to this is the fibrocartilaginous core. It would appear that the deep layer of the posterior longitudinal ligament, with short fibres spanning each intervertebral joint, compensates for the lack of annular fibres in the posterior part of the disc, supporting the nucleus posteriorly. Posterolaterally the alar fibres of the posterior longitudinal ligament alone contain the nucleus and these may become torn or stretched by a bulging disc, or nuclear material may herniate under or through them.

Cyriax (1982) stated that ‘from a clinical point of view nuclear protrusions form only a small minority of cervical disc displacements’. He postulated that a true nuclear disc lesion occurs only in adolescents and young adults, presenting as an acute torticollis. His hypothesis would seem to be substantiated by Taylor & Twomey (1994) who suggested that early degeneration of the cervical nucleus makes nuclear protrusion in the cervical spine unlikely, unless precipitated by severe trauma. A central bar-like protrusion of the annulus was more likely to occur in the cervical spine. This appeared to be refuted by the work of Mercer & Bogduk (1999) described above, given the relatively deficient posterior cervical annulus identified. Perhaps, like lumbar discs, herniated cervical discs may consist of degenerate nuclear material. Posterolateral herniation of the disc could be possible through the weak supporting alar fibres of the posterior longitudinal ligament in the uncovertebral region. Indeed, one specimen from the Mercer & Bogduk study (1999) illustrates a disc bulge and a herniation, both below their respective alar fibres.

The position of the uncovertebral joints and the large vertebral canal in the cervical spine may both also exert a protective influence on disc movement. Degenerate cervical discs may prolapse directly posteriorly, encroaching on the dura through the posterior longitudinal ligament, rather than laterally at the uncovertebral region, to affect the dural nerve root sleeve and underlying nerve root in the intervertebral canal. Alternatively, discal material may be reflected posterolaterally in the vertebral canal by the stronger median part of the posterior longitudinal ligament to cause unilateral pressure on the dura.

The triangular vertebral canal is at its largest in the cervical spine and, even though the cervical cord is enlarged in this region, there may be room for a prolapse to be accommodated. Posterolateral prolapse through the weaker alar portion in the uncovertebral region may encroach on the dural nerve root sleeve and underlying nerve root. However, it would seem that only a very large posterolateral prolapse would be able to compress the nerve root at the same level, unless there is canal stenosis caused by osteophyte formation, an infolding ligamentum flavum or congenital factors.

Since the extent of pain referral is thought to be related to the amount of pressure on the dural nerve root sleeve (Mooney & Robertson 1976), brachial pain is not as commonly associated with cervical disc lesions as sciatica is with lumbar disc lesions. Dural pressure due to a cervical disc tends to produce central or unilateral scapular pain.

It is assumed that cervical discs are innervated in a similar way to lumbar discs, since no studies have refuted this as yet. Bogduk (1994a) acknowledged the paucity of data on cervical discs but claimed that the few studies that had been done had been positive, demonstrating that the cervical discs do have an innervation. In that respect, the data on cervical discs are in accord with those on lumbar discs. At least the outer third and possibly the outer half of the annulus fibrosis receives a nerve supply from branches of a posterior longitudinal plexus, derived from the cervical sinuvertebral nerves, as well as from a similar plexus formed from cervical sympathetic trunks and the vertebral nerves, and from penetrating branches from the vertebral nerve (Bogduk 1994a). Mendel et al (1992) found evidence of nerve fibres and mechanoreceptors in the posterolateral region of the annulus.

The cervical disc may produce either primary disc pain, pain due to the mechanical effect of secondary compression of pain-sensitive structures, or pain associated with chemical or ischaemic effects. The mechanism of pain produced by disc displacement is covered in greater detail in Chapter 13 since much of the investigative work on pain production has been performed in the lumbar region and no studies have been identified that relate to the cervical spine. If findings can be extrapolated to the cervical spine, disc material is thought to undergo a process of degradation which contributes to its herniation. The chemical mediators of inflammation may play a role in the pathophysiology of cervical radiculopathy which renders the nerve root pain-sensitive (Kang et al 1995).

There are eight cervical spinal nerves, each approximately 1 cm long. Each nerve, together with the dorsal root ganglion, occupies a large, funnel-shaped intervertebral foramen (Fig. 8.6). The spinal nerve is composed of one dorsal or posterior nerve root and one anterior or ventral nerve root, the ventral nerve root emerging more caudally from the dura mater (Tanaka et al 2000). The dorsal nerve root carries sensory fibres and the ventral nerve root, motor fibres.

The spinal nerve occupies one-fourth to one-third of the intervertebral foramen diameter and carries with it an investment of the dura mater, the dural nerve root sleeve. The dural nerve root sleeve is sensitive to pressure and produces pain in a segmental distribution. Cervical spinal nerves generally emerge horizontally and therefore the nerve roots are vulnerable to pressure only from the disc at that particular level, producing signs and symptoms in one segment only (Fig. 8.7). Indication of more than one nerve root involvement should be considered suspicious until proved otherwise.

However, Tanaka et al (2000), in a cadaver study, showed that the roots below C5 reached their intervertebral foramen with increasing obliquity making compression of more than one nerve root below this level possible. At the C7–T1 disc, 78% of specimens showed that the C8 nerve roots did not have any contact with the disc at the entrance of the intervertebral foramen, which probably accounts for the low frequency of C8 radiculopathy.

Nerve root compression was found to occur at the en-trance of the intervertebral foramen and was determined to be due to herniated discs and osteophytes in the uncovertebral region anteriorly, and to the superior articular process, ligamentum flavum and periradicular fibrous tissue posteriorly (Tanaka et al 2000). Motor impairment, therefore, is suggestive of anterior compression from a disc prolapse or degenerative changes in the uncovertebral region, whereas sensory change is indicative of compression due to changes in the posterior structures. Of course a large disc prolapse or gross degenerative change, anteriorly or posteriorly, may compress both elements of the nerve root.

After it leaves the intervertebral foramen, the spinal nerve root immediately divides into ventral and dorsal rami. The sinuvertebral nerve is a mixed sensory and sympathetic nerve, receiving origin from the ventral ramus and the grey ramus communicans of the sympathetic system (Fig. 8.8). The nerve returns through the intervertebral foramen and gives off ascending, descending and transverse branches to supply structures at, above and below the segment (Oliver & Middleditch 2006, Palastanga et al 2006, Standring 2009). The structures it supplies include the dura mater, posterior longitudinal ligament and the outer part of the annulus of the intervertebral disc (Bogduk 1994b).

Anatomically the vertebral artery is divided into the following four sections, which include two right-angled bends where it is vulnerable to internal and external factors which tend to compromise blood flow (Fig. 8.9) (Oliver & Middleditch 2006, Standring 2009):

The internal carotid artery arises from the bifurcation of the common carotid artery in the anterior cervical spine (Fig. 8.9). It supplies most of the ipsilateral cerebral hemisphere, the eye and accessory organs, the forehead and part of the nose. It ascends to enter the cranial cavity via the carotid canal and turns anteriorly to end by dividing into the anterior and middle cerebral arteries, which anastomose into the circle of Willis.

The internal carotid arteries together provide the most significant proportion of blood to the brain, 80%, compared with 20% passing through the posterior vertebral artery system. Blood flow is known to be influenced by neck movements, particularly extension and less so rotation (Rivett et al 1999, Kerry & Taylor 2006).

An understanding of the anatomy at the cervical spine, together with a detailed history and examination of the patient, will help with the selection of patients suitable for manual treatment and contribute to safe practice. The two areas of danger in this region are the cervical arteries and the spinal cord, and certain signs and symptoms will become evident on examination which would exclude some patients from manual treatment techniques.

Similarly, there are other causes of neck pain in which manual treatment techniques are either contra-indicated or not as appropriate. The following section will be divided into two parts. The first covers mechanical lesions, which present a set of signs and symptoms that help to establish diagnosis and to rationalize treatment programmes. The second covers the other causes of neck pain and associated signs and symptoms. On the whole, these patients are not appropriate for treatment with manual orthopaedic medicine treatment techniques and require suitable referral.

As well as being a primary source of pain, the disc, through prolapse into the vertebral or intervertebral canal, can have a secondary effect on any pain-sensitive structure lying within. This effect can be mechanical through compression and distortion, chemical through the inflammatory process and ischaemic through the pressure of oedema. For further information on these theories, the reader is referred to Chapter 13. Although the differences in the anatomy and function of the cervical and lumbar spine must be acknowledged, few studies have been unearthed to reflect patterns of radicular pain production specific to the cervical spine, although conclusions have been drawn in relation to myofascial pain patterns based on clinical observation. For the time being, cervical radicular pain patterns have been extrapolated from the lumbar model.

A central herniation of cervical disc material produces central and/or bilaterally referred symptoms. A unilateral herniation produces unilaterally referred symptoms. Reference of pain arising from compression of the central structures is characteristically multisegmental, i.e. over many segments (see Ch. 1). Involvement of the unilateral structures, dural nerve root sleeve and/or the nerve root produces segmentally referred signs and symptoms.

Since the disc degenerates early in the cervical spine, disc lesions tend to produce a pattern of symptoms which indicate a progression of the same condition. The symptoms are age-related with a pattern of increasing frequency and severity. Eventually the nerve root may become involved.

The anatomy of the zygapophyseal joint with its intra-articular structures makes it susceptible to possible mechanical derangement. It is difficult to differentiate pathology in the absence of neurological signs or symptoms, and primary disc lesions and zygapophyseal joint lesions appear to be similar in their presentation. Referral pain patterns arising from the zygapophyseal joints in symptomatic subjects have been looked at by Cooper et al (2007) who found that there was referral into the neck but minimal reference into the arm. As mentioned above, there are no similar studies for primary or secondary disc pain.

While acknowledging the zygapophyseal and other pain-sensitive somatic structures as possible causes of pain, the approach in orthopaedic medicine is traditionally based on the discal model.

Disc lesions in the cervical spine need to be reduced to prevent them contributing further to the degenerative process. A central prolapse in particular may cause osteophyte formation through ligamentous traction which may eventually threaten the spinal cord. Cyriax (1982) was emphatic in pointing out the danger of not reducing an early, minor cervical disc lesion for this reason as there comes a time when manipulation will not have an effect and a point at which it may be dangerous. Elderly patients with osteophytic cord compression often report the onset of paraesthesia associated with cervical extension and for that reason it would seem that particular attention should be paid to restoring cervical extension which would act as an indicator that reduction had been effected.

Cervical lesions produce a pattern of signs and symptoms and a set of clinical models has been established to aid diagnosis and establish treatment programmes. These are outlined later in this chapter. The models should be used as a general guide to the clinical diagnosis and treatment of cervical lesions. All show a non-capsular pattern on examination.

The following terminology will be used to describe disc lesions:

Serious, non-mechanical conditions may present with signs and symptoms similar to those of a mechanical presentation. For this reason, careful examination is necessary to eliminate serious disease which would be contraindicated for orthopaedic medicine treatment. Patients may present with local symptoms which are rarely provoked by movement or posture. On examination it may be difficult to reproduce the symptoms. Other more generalized features may also be present, such as increasing and unrelenting pain, night pain, weight loss, general malaise, fever, raised erythrocyte sedimentation rate or other symptoms, e.g. cough.

The following conditions are not serious but should be considered as part of the clinical reasoning required in differential diagnosis:

The site and spread of the symptoms give important clues to diagnosis in the cervical spine and highlight the importance of understanding the mechanisms of referred pain in a segmental or multisegmental pattern. Pain may be localized to the neck or occur in association with symptoms felt in the scapular area, chest, upper limb or head. The sole presentation of internal carotid artery dysfunction may be unilateral upper cervical or anterolateral neck pain and headache and/or sensitivity in the frontotemporal region (Kerry & Taylor 2006).

Nerve root compression in the cervical spine can only occur at the levels at which the nerve root can be compressed. In the mid and lower cervical regions the roots are under threat from the intervertebral discs, uncovertebral joints and zygapophyseal joints which form the boundaries of the intervertebral foramen. C1 and 2 nerve roots do not run in intervertebral foramina, therefore compression of these nerve roots is not the mechanism for upper cervical pain.

Headache of sudden onset may be an indication of internal carotid artery dysfunction (Taylor & Kerry 2005, Kerry & Taylor 2006).