SPINAL SYMPTOMS: NECK PAIN AND BACKACHE

John Paul Leach

INTRODUCTION

Neck pain and backache are common causes of selfreferral in primary care, but are much less frequent visitors to neurology outpatients, being seen mainly in orthopaedic clinics. Almost anyone over the age of 40 years will be able to give a history of back or neck pain at some point in their lives, as it would appear that one of the flaws inherent in the design of the human spine is the frequency with which it will produce pain, stiffness, and a general creaking as age advances. Among men over the age of 50 years, 90% will display radiographic evidence of degenerative changes.

As a result of the profusion of frequent, often nonspecific symptoms, spinal disease is one of the few areas in clinical neurology where history taking seems secondary to examination in terms of importance. Since neck and back pain are common enough to be almost physiological states, the role of the neurologist is to determine which patients warrant further investigation and which require reassurance alone.

Most cases of neck and back pain will have no demonstrable neurological deficit. Localization of spinal pathology on the basis of neurological findings can be challenging, despite the common anatomy (a bundle of nerves and nerve roots encased in a segmented bony canal) (148). The patterns of deficit caused by cervical, thoracic, and lumbar spinal disease are different, and here will be addressed as upper (cervical and thoracic) and lower (lumbar and sacral) spinal syndromes.

CLINICAL ASSESSMENT

While patients’ histories may dwell on limb symptoms and localized pain, care should be taken to elicit any complaint of sphincter disturbance or truncal sensory disturbance. General examination is absolutely essential as this may identify features suggesting generalized conditions in which the spinal cord may be secondarily involved, e.g. neurofibromatosis, adrenal insufficiency, or primary neoplasm. Such findings expand the differential diagnosis of underlying spinal pathology. As with all patients referred for an opinion, while the emphasis is on possible spinal disease, a full neurological examination is mandatory.

Cranial nerve examination

In patients with arm and/or leg symptoms, cranial nerve examination may seem irrelevant. However, it

may provide vital clues to multilevel neurological disease, or the intracranial masquerading as spinal pathology. Abnormal eye movements, fundal changes, pupillary abnormalities, and lower cranial nerve/cerebellar signs should be particularly sought. Subtle eye movement disorders may betray the existence of multiple sclerosis presenting with myelopathy, while cerebellar ataxia suggests posterior fossa disease. Horner’s syndrome can be a helpful localizing sign, ipsilateral to weakness at the cervical level while contralateral at the cranial level.

Upper limb examination

If there is significant cervical root compression, motor system examination may show signs of lower motor neurone (LMN) involvement (wasting, weakness, poor reflexes) which will vary with the level of the lesion (Table 55).

Sensory examination can help elucidate the level (149) although it should be stressed that it is motor involvement (weakness and wasting) and radiology

148 Diagram of sagittal spinal cord, illustrating nerve roots in relation to vertebral bodies.

that will motivate the surgeon when to operate. Any lesion above C8 may be associated with some evidence of upper motor neurone (UMN) dysfunction in one or both arms. In general, the higher the cervical lesion, the more probable that there will be UMN signs in the arms, often with a clear reflex level (absent or reduced at the level, and brisk below the level).

Lower limb examination

Assessment of lower limbs in patients with upper spinal cord lesions will show UMN signs. These take the form of brisk reflexes, spread of reflexes both above and below the tested level, clonus with increased tone, and extensor plantar responses. It would seem logical (although not definitive) that patients with cervical vertebral problems will be more likely to experience lumbar spine disease. Widespread spinal degenerative disease is one of the recognized causes of mixed UMN and LMN signs.

An additional test of lower spine function involves stretch testing to indicate nerve root compression/ irritation. The commonest such test is straight leg raising. This involves an assessment of the discomfort and pain induced by hip flexion, when the knee is either flexed or fully extended. When the leg is raised and the knee extended, stretching of the nerve roots will cause a shooting pain in the distribution of the affected nerve roots. This pain will not occur (or will be much less) when the knee is flexed during leg raising.

Table 55 Reflexes and roots

loss occurs when the cord is compressed from without (150).

When there are symptoms suspicious of spinal disease with accompanying neurological symptoms, the main questions to be addressed are:

At what level in the neuraxis is the lesion? (Use of cord and radicular signs.)

Where is the lesion: intramedullary, extramedullary intradural or extradural (see page 207)?

What is the lesion (see page 209)?

Lesion level localization

This may be ascertained by differentiating the cord or nerve roots signs. The constellation of symptoms will vary depending on the region affected. In upper spinal disease (cervical and thoracic spine), the spinal cord or nerve roots may be affected.

At upper levels, therefore, the potential effects are:

Upper motor problems in the legs.

Lower motor neurone problems in the arms.

Truncal sensory level changes.

Sphincter disturbance.

Horner’s syndrome (with cervical lesions).

The spinal cord finishes at approximately L1 level. As a result, neurological effects of lumbar or sacral spine disease almost exclusively involve a radicular pattern.

Pressure on the lower spinal cord and cauda equina causes:

150 Diagram of cauda equina lesions, illustrating the affected saddle area.

LMN problems in the legs, with clinical features dependent on the particular roots affected.

Truncal or sacral sensory level changes.

Sphincter disturbance.

Cord involvement will cause LMN lesions at the level of the lesion, with UMN signs below. Involvement of the cauda equina (i.e. below the level of L1) will cause only LMN symptoms.

Localization by cord symptoms

A lesion produces neurological deficit at or below its level. Sometimes, however, a lesion may be at a higher level than is apparent clinically, i.e. a sensory level suggesting a thoracic level may be being produced by a cervical lesion ( a ‘dropped level’). At the level of the lesion, motor signs may be of a LMN type, given the direct destructive effect on anterior horn cells. Sensory signs may be soft or absent, but there may be a band of dysaesthesia round the truncal circumference at the level of spinal involvement. Below the lesion, sensory changes will usually become more likely and more severe. Motor signs will be of UMN type below the level of any spinal lesion.

Bladder symptoms only occur where the cord is affected bilaterally. Such cord lesions will initially leave an atonic bladder, with absence of sensation of fullness. With time, the bladder begins to undergo

Table 56 Pitfalls in root/peripheral nerve lesion differentiation

L5–S1 versus peroneal nerve:

Both will cause weakness of ankle dorsiflexion and sensory changes over anterior shin and foot

Peroneal nerve lesion may be associated with Tinel’s sign round the fibular neck

L5–S1 lesion may cause reduced ankle jerk and weakness of foot inversion (and possibly a positive straight leg raising test)

C8–T1 versus ulnar nerve

Both will cause weakness of intrinsic muscles of the hand

Isolated ulnar lesions should cause only hypothenar eminence and interossei wasting. Sensory changes are usually confined to the hand

C8–T1 lesions may cause wasting also at the thenar eminence and may have associated sensory change along the medial border of the forearm

reflex emptying causing urinary urgency and urge incontinence. In general, a hypertonic bladder indicates a UMN lesion, e.g. a lesion affecting the spinal cord or brain.

Autonomic fibres in the cervical cord supply sympathetic function which can be clinically assessed by checking sweating in limbs, trunk, and face. Another measure of spinal sympathetic function is the presence or absence of a Horner’s syndrome. There will sometimes be a localized pain or even tenderness overlying cord pathologies which can help with localization.

Localization by radicular symptoms

Radicular localization can be done on the basis of sensory or motor changes. Knowledge of the basic dermatomal pattern (see below) will allow inference to be drawn on the level of involvement. Sensory change is usually a subjective electric shock-like pain along the affected dermatome, although more chronic lesions

can lead to numbness in the affected area. Motor changes will usually involve reduction or loss of the relevant reflexes on the affected side (Table 55).

Differentiation of radicular symptoms from peripheral nerve-related symptoms can only be done when there is a knowledge of the characteristic patterns of innervation of each of the peripheral nerves and the functions supplied by each spinal root. This can be difficult, however, and some characteristic pitfalls are listed (Table 56). Direct pressure on the sacral roots by a lumbar or sacral lesion causes a LMN bladder, with loss of sensation of fullness and an atonic overfilling bladder.

Lesion anatomical localization

The extent and pattern of involvement of the spinal cord in disease may result in characteristic patterns of deficit, which can give further clues to the nature of the pathological process (151).

Sensory deficit

‘Suspended’ sensory loss

Useful localizing features (if present)

Loss of pain, temperature and light touch below a specific dermatome level (may spare sacral sensation)

Loss of all modalities at one or several dermatome levels

Loss of pain and temperature below a specific dermatome level

Loss of proprioception and ‘discriminatory’ touch up to similar level and limb weakness

Bilateral loss of all modalities.

Bilateral leg weakness

Bilateral loss of pain and temperature. Preservation of proprioception and ‘discriminatory’ sensation

151

Lesion site

CONTRALATERAL

SPINOTHALAMIC

TRACT LESION

(Partial spinothalamic tract lesion)

BROWN-SÉQUARD SYNDROME

(Partial cord lesion)

COMPLETE CORD LESION

CENTRAL CORD LESION

Brown-Séquard syndrome

Lesions affecting one or other half of the spinal cord will cause UMN weakness and spasticity below the lesion. There occurs typically a mixed bilateral sensory deficit of spinothalamic loss (pain and temperature) below and contralateral to the lesion, and dorsal columnar loss (proprioception and vibration) below and ipsilateral to the lesion (152).

Complete transverse lesions

These result in bilateral UMN weakness and spasticity below the lesion. There may be LMN signs at the level of the lesion which can help in localization. Corticospinal, spinothalamic, and dorsal column tracts are affected (153). All modalities are affected (there may frequently be sphincter involvement, and sometimes Lhermitte’s sign).

Central cord lesions

Earliest motor effects of central cord lesions will involve anterior horn cells at the levels of the lesion, with a resultant LMN lesion pattern. Later, with further expansion, the corticospinal tracts can be involved and can cause caudal UMN signs. Early decussation near the point of entry by spinothalamic fibres means that more rostral fibres layers tend to be more centrally placed in the cord. This explains why central cord lesions may therefore spare spinothalamic fibres below the level of the lesion (sacral or abdominal pinprick) (154). Central cord lesions which extend anteriorly may also affect second order spinothalamic fibres as they decussate in front of the anterior ventral commissure.

153

Tumour

Impairment of all sensory modalities up to the level of the lesion

Bladder

dilated

Limbs flaccid

152 Diagram of an incomplete lateral compressive lesion, with the attendant pattern of sensory impairment.

153 Diagram of a complete extrinsic spinal cord lesion, with attendant clinical features.

Anterior spinal cord

Thrombosis of the anterior spinal artery damages anterior spinal cord only. The effects on corticospinal tracts leave bilateral spasticity and weakness below the lesion with, sometimes, LMN weakness at the level of the lesion. There is a dissociated sensory loss, i.e. there is a bilateral decrease in pinprick and temperature sensation with sparing of light touch, joint position sense, and vibration sense. This is because of selective damage to the spinothalamic tracts: dorsal column sensation is supplied by the posterior spinal arteries, and is therefore unaffected.

Nature of the lesion

The nature of onset and rate of progression will suggest the nature of the lesion; for example, vascular lesions will occur abruptly, while demyelinating lesions may demonstrate a more subacute onset. Metastatic lesions will usually be slowly progressive,

154

CENTRAL CORD LESION

‘CAPE’ sensory deficit

Sacral sparing

154 Diagram of a central cord lesion, with sensory findings.

and may cause pain secondary to local destruction. Pathologies around the spinal cord may be referred to as either intrinsic to the spinal cord (intramedullary) or extrinsic to the cord (extramedullary) (Table 57). Extramedullary lesions may in turn be intradural or extradural.

Investigations

As stated above, minor ‘wear and tear’ is seen in the majority of plain X-rays of cervical and lumbar spine in middle age. Plain X-rays of spine will be useful where there has been acute spinal trauma, but not otherwise. The imaging regime of choice is magnetic resonance imaging (MRI). This will give both axial (transverse cuts) and sagittal (longitudinal cuts) views of the affected region, which will allow a good assessment both of any spinal cord compression and any root canal stenosis that may correlate with radicular symptoms. In patients where MRI is contraindicated (e.g. patients with prostheses in situ) then computed tomography myelogram is a helpful alternative. In differentiation of peripheral nerve and root lesions, nerve conduction studies and electromyography can be useful.

SUMMARY

Minor spinal symptoms are common, neurological sequelae are not.

Imaging is best done where there is a possibility of surgery; or where symptoms or signs suggest serious neurological disease.

Table 57 Causes of spinal cord pathology

Pathology around the cord

Vertebral/spinal column disease:

Degenerative

Infiltrative (neoplastic)

Infective

Dural disease

Neoplastic

Pathology within the cord:

Inflammatory

Neoplastic (primary or secondary)

Ischaemic/haemorrhagic

Developmental (syringomyelia)

Degenerative

The patient was alert and fully orientated. Cardiovascular and respiratory examinations were normal although the patient was breathless on minimal exertion. Cranial nerve examination was unremarkable. Examination of the upper limbs revealed increased tone bilaterally, symmetrically reduced power of all movements, and brisk biceps, supinator, and triceps jerks. Sensory testing was normal. In the lower limbs, tone was increased, and there was mild weakness of all movements with increased reflexes and upgoing plantars. Examination confirmed UMN signs involving all four limbs: together with the sphincter disturbance (mid-stream specimens of urine were consistently sterile) this would immediately alert the clinician to a spinal cord lesion at the cervical level. Dyspnoea had become prominent and was another localizing symptom (muscles of respiration are supplied at C3,4, and 5 levels). Speed of onset was quicker than would be expected for a demyelinating or inflammatory lesion. (In any event, demyelination is rare at this age.) The timing of the weakness, coming immediately after a fall, was felt to be more than coincidental, and it appeared likely that there had been significant mechanical damage to the cervical spine sustained during (or perhaps contributing to) her fall. MRI of cervical spine showed there to be severe spondylitic and degenerative changes, most pronounced at higher levels (155). Referral was made to the neurosurgeons, who initially refused to offer operation in view of the risk of exacerbation. She deteriorated over the next few weeks, with increasing weakness in both arms and a worsening in respiratory function. It was decided that a conservative policy posed an unacceptably high risk to her respiratory function. Decompression was carried out in order to prevent further deterioration, but she did surprisingly well; she regained her mobility, and has now begun to mobilize outdoors with the aid of a zimmer frame.

REVISION QUESTIONS

1In cervical spine disease which of the following statements are true?

a A ‘clicking’ or ‘crunching’ sensation experienced by the patient is a symptom of serious pathology.

b Bony change on X-ray is unusual in patients of middle age.

c Cranial nerve examination can provide useful information.

d Jaw jerk is a sign of cervical myelopathy.

e Hyper-reflexia in the legs is a reliable sign of myelopathy.

2In thoracic spine disease which of the following statements are true?

a The sensory level is a reliable pointer to the level of the involvement.

b Urinary urgency and incontinence is a sign of radiculopathy.

c Loss of perianal sensation is a sign of pathology in the central cord.

d Unilateral cord pathology causes loss of pain and temperature sensation inferior and ipsilateral to the lesion.

e Anterior cord lesions cause loss of vibration and proprioception.

3In lumbar and thoracic spine disease which of the following statements are true?

a Hyper-reflexia is a common sign of lumbar spine involvement.

b A normal straight leg raising test precludes surgical intervention.

c Loss of knee jerks is a sign of L5 radiculopathy.

d Unilateral lesions commonly cause bladder symptoms.

e A lower motor neurone bladder is small and has a small residual volume when catheterized.