1 Chronic lumbar ligamentous strain

This term is one of many used to describe the condition of persistent backache without demonstrable pathology. The condition is common in unskilled manual workers of both sexes and tends to recur with physical activity and to be work related. Depressive illness is a common association. The onset of the pain may also be dated from a specific injury, occasionally from an operation or from a past medical illness. The pain is diffuse, radiates widely but usually without definite anatomical features and tends to be worse on stooping and lifting. Usually, clinical examination yields no abnormal objective physical signs. Pain on straight leg-raising is variable. In nearly half the patients presenting with chronic back pain, a precise pathological diagnosis is not possible. In contrast to the diffuse pain of chronic back strain, patients with focal pathology usually have more localised pain at or near the site of the lesion. X-rays, CT and MRI are normal or a minor degree of spondylosis is seen. A rehabilitative approach is generally recommended, and often helpful.

A history of pain after lifting at work is common with chronic and recurring back pain. The WorkCover context complicates the situation considerably. Most patients still get better with rest, gentle activity and time. In those cases that pass into chronic pain, the significance of neurosis or malingering in the pathogenesis of this litigation-linked condition can rarely be determined with absolute assurance. True malingering in the sense of complete fabrication of a set of symptoms and signs is uncommon; exaggeration of symptoms and signs in the absence of demonstrable organic disease and persistence of symptoms and signs while litigation is pending is common.

2 Degenerative disc disease, spondylosis and osteoarthritis

With disc degeneration, especially following recurrent disc prolapse, gradual flattening of the disc and displacement of the posterior facet joints occur, eventually gives rise to osteoarthritis in those joints (Fig 5.2). A past history of lumbar pain is common, with subsequent recurrent attacks of pain over a period of several years. The onset of such attacks is often related to exertional trauma, such as repetitive bending or lifting a weight, or strain from sitting in an uncomfortable position during a long journey. Sciatic radiation of the pain to the buttock and sometimes down the backs of the legs, on one or both sides, is common. With the development of osteoarthritis of the facet joints, pain becomes constant and nocturnal. On examination, tender areas may be felt over the spine. There is limitation of all lumbar spine movements and residual neurological signs of disc prolapse, such as an absent ankle jerk, may be present. Most instances of chronic recurring back pain fall into this category; however, it is surprising how many patients have minimal symtoms despite impressive changes on scans.

Figure 5.2 Pathological sequence in degenerative back disease

A: normal lumbar vertebrae and disc; B: herniation of the nucleus pulposus; C: disc space degeneration and flattening with early osteoarthritis of the facet joint; D: advanced lumbar degenerative spine disease with facet joint osteophyte formation and compression of the nerve root. Forward slip and arthritis may also lead to narrowing of the spinal canal.

3 Spondylolisthesis

This term refers to displacement of one vertebra upon its neighbour. The two most common forms are lytic and degenerative. The lytic form occurs most commonly at L5/S1 due to lysis of the pars interarticularis of L5, allowing anterior displacement of L5 on S1. The posterior elements of L5 do not migrate forward. Therefore, there is no narrowing of the spinal canal, neither centrally nor in its lateral recesses. However, vertical narrowing of the foramen may occur as the condition progresses, which may lead to L5 nerve root impingement. The cause of the spondylolisthesis is debated, and may include non-union of the adjacent growth centres or stress fractures in early to mid-childhood.

The degenerative form of spondylolisthesis occurs as a late outcome of spondylosis, with a decline in structural integrity resulting in a ‘slip’. Since the centre of gravity of the body tends to lie anterior to the spinal column, the upper vertebra tends to slide forwards on the lower one, although the reverse may occur. There may be associated scoliosis. The slip may be stable or unstable, which has significant bearing on the symptoms. In this form of spondylolisthesis, the posterior elements migrate forwards, resulting in canal stenosis between the lower edge of the upper lamina and the upper edge of the lower vertebral body. This can lead to severe neurological symptoms or signs.

4 Osteoporosis

This condition is most common in elderly women; gonadal involution is the most important causal factor. Longstanding steroid therapy is an important cause, while nutritional problems may also contribute. Fractures, especially crush fractures of the vertebrae, can occur with minimal trauma. Trabecular bone stiffness varies with the cube of its density — there is almost 50% loss in strength with 30% decrease in the density. Vertebral compression fractures lead to backache, kyphosis and shortening in height. Plain X-ray reveals loss of bone density, wedging or biconcave indentation of vertebrae. Bone densitometry is a more sensitive and effective method of quantifying change in bone mineral density.

5 Secondary carcinoma of the vertebral body

The most common tumours of the vertebral bodies are metastatic lesions arising from tumours of the lung, breast, prostate, thyroid or kidney. The predominant symptom of localised destruction of the vertebral body is constant pain that steadily increases in severity. There may be associated neurological disorders because of involvement of the spinal cord or nerve roots. Plain X-ray may reveal osteolytic or osteosclerotic vertebral destruction by tumour, with preservation of an adjacent normal intervertebral disc (Fig 5.3). Metastases from carcinoma of the prostate are more commonly osteosclerotic. Considerable destruction of bone substance is necessary before radiological signs occur; X-rays are thus commonly negative in the presence of metastases. CT is more sensitive and MRI better again. Bone scans can be diagnostic. Furthermore, focal metastatic deposits can be difficult to differentiate from localised Paget’s disease.

Figure 5.3 Verterbral collapse

A: infection — the vertebral body appears intact because the infection usually lies adjacent to the disc; B: metastatic disease of vertebra leads to collapse with apparent preservation of the adjacent disc. Both conditions lead to kyphosis.

6 Spinal infection

Bacterial infections can occur in the discs of the spine, resulting in discitis. The patient can present in an acute septic state or with acute progressive back pain without overt features of sepsis. Subacute and chronic forms also occur, with gradual progression being a typical feature. Nocturnal pain may be prominent. The infection may spread, resulting in an epidural abscess that can cause rapidly progressive neurological damage. Paraspinal myositis with abscess formation may also occur. MRI, FBE, ESR and CRP may be diagnostic. Plain X-ray and CT may be falsely reassuring until late in the disease. Bone scan is useful if MRI is not available.

Tuberculosis of the spine is less common than in the past but should not be forgotten in the differential diagnosis of chronic back pain.

7 Referred pain

Abdominal and thoracic causes of back pain must not be forgotten. Patients with conditions as wide-ranging as lung carcinoma, pancreatitis, gallstones, abdominal aneurysms, gynaecological problems and rectal carcinoma can, on occasions, present with back pain as the major symptom. This will only be picked up by attention to associated symptoms and careful physical examination.

8 Less common causes

These include Paget’s disease, ankylosing spondylitis, tuberculosis and osteomyelitis.

Paget’s disease can cause back pain in older patients. The bones most commonly affected are the pelvis, vertebra, femur, tibia and skull. There may be a history of an increase in hat size. Most cases of Paget’s disease are asymptomatic. On X-ray the features are thickening and reduced density of the cortex, coarsening of the bony trabeculae and, later, a general increase in density of the affected bones.

Ankylosing spondylitis is an insidious, chronic inflammatory disorder of the spine and sacroiliac joints characterised by pain and stiffness with increasing lumbar kyphosis. The condition often starts in the sacroiliac joints and is manifest early by local tenderness of these joints. In the early phase, differential diagnosis can be difficult. Sciatica is a common symptom. On plain X-ray the earliest sign is osseous erosion at the anterior aspects of the vertebral bodies followed by a reparative process that leads to prominence of the anterior corners — ‘squaring off’. Erosion and fuzziness of the sacroiliac joints is also common. End-stage disease with bridging syndesmophytes gives rise to the characteristic picture of a bamboo spine.

History

Symptoms of neurological disease in the limbs include paralysis, clumsiness, movement disorder, anaesthesia (to pain, light touch and temperature) and paraesthesia. The full characterisation of these disorders lies outside the range of this book, and readers are referred to neurological texts.

Examination

The aim on examination is to determine the site of a neurological lesion by evaluating disordered function. Dysfunction is manifest by abnormalities in one or more of the five major components of the nervous system: the lower motor neurone (including the peripheral nerve), the upper motor neurone, the extrapyramidal system, the cerebellum and the sensory system.

The upper motor neurone consists of the motor cells of the cerebral cortex and their axons contained within the corticospinal tracts, terminating in the contralateral motor neurone cells of the brain and spinal cord after decussating in the pyramids. Damage to the upper motor neurone leads to a volitional paralysis of the muscle groups that corresponds to the site of the cortical damage. Muscle tone and reflexes may be lost initially. Subsequently, spasticity develops, tendon reflexes increase and the plantar response — also known as the Babinski reflex — becomes extensor. Muscle wasting is not marked in patients with upper motor neurone lesions.

The lower motor neurone extends from the motor neurone cell to voluntary muscle fibres. Acute focal damage to a peripheral nerve or its motor neurone cells produces paralysis characterised by loss of tone, voluntary movement and reflexes. Wasting is marked and rapid. Chronic conditions affecting the lower motor neurone and peripheral nerves may be slowly progressive and are often associated with fine, twitching muscle movements (‘fasciculations’).

The extrapyramidal system also links the cerebral cortex with the lower motor neurone via the basal ganglia and brain stem. Lesions in this system produce rigidity and tremor. This is the system most often affected in Parkinson’s disease.

The cerebellum is concerned with control of rhythm and posture. The features of cerebellar dysfunction include ataxia, slurred speech, intention tremor, poor coordination, hypotonia and nystagmus.

Sensory dysfunction is of two types: superficial sensation, including disorders of light touch, pain and temperature, and deep sensation, including joint position, vibration and deep pain sense. Superficial sensations are mainly carried in the spinothalamic tracts of the contralateral side to the sensory cortex. The fibres cross within a few spinal levels of their entry into the spinal cord. Deep sensation afferent fibres are located mainly in the posterior spinal cord columns and pass on the same side up to the medulla, where they cross and pass to the thalamus, finally also terminating in the sensory cortex. This helps explain the ipsilateral loss of vibration sense and the contralateral loss of temperature sensation in a person with a hemisection of the spinal cord.

Neurological examination of the limbs commences with inspection and proceeds to assessment of motor nerve function, sensory nerve function and reflex functions. Assessment of gait and of other coordinated movements is an important component of the examination.

2 Sensory nerve function

Testing of superficial touch, pain and temperature sensation is followed by assessment of position and vibration sense and by discriminatory sensation (Fig 5.4). Light touch is tested using a wisp of cotton wool, pain is tested by the response to pin prick and cortical sensory discrimination by the ability to differentiate between pressure from the pointed end and the blunt head of a pin. Temperature is tested by asking the patient to differentiate between tubes of warm and cold water. Areas of diminished sensation are mapped out and compared with the normal sensory dermatomes. The reproducibility of clinical findings should be checked. Variable results can occur due to ‘hysterical’ or factitious sensory loss or to loss of concentration — the patient’s tolerance and cooperation are particularly labile at extremes of pain, age and intellect. Glove-and-stocking loss of pain sensation in the lower limbs with normal motor function is typical of the peripheral neuropathy associated with diabetes. Deep sensation is tested by vibration and position sense; the former using a tuning fork applied to the medial malleolus and the latter by identifying the position of the moved great toe with the eyes closed.

Figure 5.4 Sensory dermatomes of the body

Upper limb nerve palsies

Median, ulnar, radial and axillary nerves, brachial plexus.

Lower limb nerve palsies

Common peroneal, posterior tibial, sciatic and femoral nerves, lumbosacral plexus.

Common causes

Lesions at the wrist — carpal tunnel syndrome. This is the most common peripheral nerve lesion in current practice. The patient typically presents with a chronic history of episodic, poorly localised pain in the wrist and forearm and numbness in the hand. Many patients identify the involvement of the thumb index, middle and ring fingers, but it is very frequent that the ‘whole hand’ is numb. Symptoms typically manifest at night, or during the day with prolonged holding of the telephone or reading materials, driving or prolonged use of the hands. In advanced cases, sensory or motor disturbance can be identified on examination.

On examination, the thenar eminence may be flattened due to wasting of the abductor and flexor pollicis brevis and opponens pollicis. The shaft of the first metacarpal bone becomes visible as the mound of the thumb muscles wastes; the weakened thumb drifts laterally to lie in the plane of the other fingers beside the index (‘simian hand’). The radial two lumbricals are also paralysed. Advanced sensory and autonomic losses may cause the radial three and a half digits to become dry and glossy with trophic changes.

Motor loss is best tested by asking the patient to abduct the thumb against resistance at right angles to the plane of the palm while keeping the thumb within the radial margin of the index finger as the movement proceeds (palmar abduction). The patient presses the thumb upwards against the examiner’s finger or a pencil. Weakness is seen and felt. The patient attempts to compensate by radial abduction of the thumb away from the side of the hand, a movement performed by muscles innervated by the radial nerve. Palmar abduction tests the competence of abductor pollicis brevis (APB) that is almost invariably supplied by the median nerve. Opposition of the thumb to the other fingers is also impaired. The loss of the short abductor, flexor and opponens causes the thumb component of this complex movement to be deficient. The thumb is brought straight across the palm and flexed, to lie against the radial side of the base of the little finger (‘pseudo-opposition’). In carpal tunnel syndrome, the motor branches of the median nerve in the forearm are spared (see next).

Anaesthesia or hypoaesthesia to touch (cotton wool) and pain (pin-prick) occurs in severe cases over the volar aspect of the radial three and a half digits, extending onto the dorsum of the fingertips. The area of the pulp of the index finger is virtually always supplied by the median nerve. The sensation in the palm of the hand is spared because the palmar cutaneous branch arises from the median nerve proximal to the carpal tunnel.

Provocative tests, such as percussing over the median nerve in the wrist or palm with a finger and producing paraesthesia over the median nerve distribution (Tinel’s sign), then placing the wrist in full flexion by putting the dorsum of one hand against the dorsum of the other and eliciting paraesthesia or the symptoms of carpal tunnel syndrome (Phalen’s test), may be used to confirm the diagnosis. Nerve conduction studies should be performed.

The most common causes of carpal tunnel syndrome may be remembered with the mnemonic ‘PRAGMATIC’ — Pregnancy, Rheumatoid arthritis, degenerative Arthritis, Growth hormone abnormalities (acromegaly), Metabolic abnormality (diabetes mellitus, gout and hypothyroidism), Alcoholism, Trauma, Idiopathic and Connective tissue disorders (amyloidosis). Of this, the majority are idiopathic, presumably due to a combination of a congenitally small canal with superadded thickening of tendons and joint structures due to usage over many years. There may be a family history. Repetitive overuse is accepted as a cause.

If the site of the median nerve lesion lies in the forearm, the motor branches of the median nerve in the forearm may be involved. These supply the wrist flexors (apart from flexor carpi ulnaris) and all of the long flexors of the first three digits (i.e. all of the flexor digitorum superficialis and flexor pollicis longus, and half of flexor digitorum profundus).

The ability of the patient to flex the end joint of the thumb and index finger against resistance (Fig 5.5) helps to determine that the level of median nerve involvement must be above the wrist — these muscles always being supplied by the median nerve — motor supply by the anterior interosseous nerve branch. A lesion in the forearm above the origin of the anterior interosseous nerve branch causes paralysis of these long flexors in addition to the two radial lumbricals. It also gives the sensory changes associated with a median nerve lesion. The deformity of the ‘pointing’ index and middle fingers, which are extended relative to the other fingers (signe de cardinal), and an inability to make the an ‘OK’ sign demonstrate the absence of tip–tip pinch with this nerve lesion.

Figure 5.5 Median nerve lesions

The long flexor of the thumb is tested by flexion of the distal interphalangeal joint against resistance.

Median nerve lesions above the wrist are relatively uncommon. The sites for compression above the wrist include the bicipital aponeurosis, the deep head of the pronator teres and the origin of the flexor digitorum superficialis. Two further sites, located just proximal to the elbow and which may provoke discussion regarding the evolution of the forearm musculature, are the supracondylar process and the ligament of Struthers. Provocative tests include resisted elbow flexion with forearm supination (bicipital aponeurosis), resisted forearm pronation with the elbow extended (pronator teres) and isolated long finger proximal interphalangeal joint flexion (origin of the flexor digitorum superficialis).

The anterior interosseous nerve proper may also be compressed. Sites for compression of the anterior interosseous nerve (motor involvement without sensory involvement) include fibrous bands within the pronator teres, the flexor digitorum superficialis arcade, the edge of the lacertus fibrosus and an enlarged bicipital bursa.

Common causes

At the wrist. The ulnar nerve can be compressed in Guyon’s canal as it travels across the wrist joint between the volar carpal ligament and the transverse carpal ligament. The findings may be pure motor, pure sensory or mixed, depending on the site of the lesion, as the nerve branches into a deep motor and a more superficial sensory branch. Major motor loss as well as sensory loss may occur to the ulnar one and a half digits. The small muscles of the hand that are paralysed are those of the hypothenar eminence (abductor, flexor and opponens digiti minimi), all the interossei muscles, the two ulnar lumbricals and the adductor pollicis, and the deep head of flexor pollicis brevis. A characteristic deformity ensues. The motor loss causes the deformity of ulnar claw hand (main-en-griffe). The little and ring fingers are held in hyperextension at the metacarpophalangeal joints and flexed at the interphalangeal joints. The little and ring fingers are also twisted and bowed away from the other fingers. The claw deformity results from loss of lumbrical and interossei function (which normally flex the metacarpophalangeal joints and extend the distal joints of the fingers) and the unopposed action of the extensor digitorum communis on the metacarpophalangeal joints. The functioning two radial lumbricals prevent clawing of the index and middle fingers. If both median and ulnar nerves are severed at the wrist, a complete claw hand occurs. Other striking signs are the trophic changes affecting the skin of the ring and little fingers, the flattened hypothenar eminence, the guttering between the metacarpals due to wasting of the interossei and the marked wasting of the web between the thumb and index finger due to wasting of the first dorsal interosseous muscle and adductor pollicis.

Confirmation that the motor disability is due to an ulnar nerve lesion is given by the sensory loss over the ulnar aspect of the palmar and dorsal surfaces of hand and of the ulnar one and a half digits. The area of sensory loss always present in ulnar nerve injury is to the pulp of the little finger. With lesions at or below the level of the wrist joint, the sensation to the dorsal aspect of the ulnar one and a half digits is spared because the dorsal cutaneous branch of the ulnar nerve arises proximal to the wrist joint.

Additional tests of loss of motor function include:

Figure 5.6 Ulnar nerve lesion

The little finger is abducted away from the other fingers against resistance.

Figure 5.7 Ulnar nerve lesion — Froment’s sign

On the side that the adductor pollicis is weak, the patient can only hold the card by flexing the terminal joint of the thumb.

Lesions at the elbow or forearm. The ulnar nerve has no branches in the upper arm. Cubital tunnel syndrome is due to compression of the ulnar nerve in the vicinity of the elbow. Potential sites for compression include between the two heads of the flexor carpi ulnaris, the arcade of Struthers, the fascia of Osborne (between the medial epicondyle and the olecranon), the fibres within the flexor carpi ulnaris and the anconeus muscle. As the ulnar nerve in the forearm supplies the flexor carpi ulnaris and the ulnar two tendons of the flexor digitorum profundus, involvement of these muscles indicates a lesion in or above the forearm.

Flexor digitorum profundus to the little finger is always supplied by the ulnar nerve and is tested by flexion of the end joint of the little finger. Flexor carpi ulnaris flexes and adducts the wrist.

Combined median and ulnar palsies are usually due to an obvious wrist wound and result in a complete claw hand, with sensory loss affecting all five digits. Tendon injuries are commonly associated. It is always important to separate the effects of tendon and other injuries when assessing traumatic nerve palsies. Other causes of finger deformities are illustrated in Figure 5.8.

Figure 5.8 Causes of finger deformities and clawing

A: normal finger; B: claw hand (ulnar nerve or T1 lesion); C: Volkmann’s ischaemic contracture; D: intrinsic plus hand; E: Dupuytren’s contracture

Common causes

Upper arm. Considerable motor loss may occur with compression neurapraxia in the spiral grove or distal third humeral shaft fractures. The long extensors of the wrist, fingers and thumb (extensor digitorum, extensor pollicis longus and brevis, abductor pollicis longus, extensor carpi radialis longus and brevis, extensor carpi ulnaris) are affected. Wrist and finger drop follows; the patient is unable to extend the hand and fingers against gravity. Extension of the metacarpophalangeal joint of the thumb is paralysed and radial abduction of the thumb metacarpal is deficient. Brachioradialis can be tested by flexing the pronated forearm at the elbow against resistance. Supinator is also paralysed but the biceps maintain the action of supination in flexion. The radial nerve’s branches to the long and lateral heads of the triceps arise in the axilla; the action of the triceps is therefore usually spared in radial nerve lesions caused by injuries of the arm. Anaesthesia is often minor and restricted to a small area over the anatomical snuff box but can extend more widely over the radial aspect of the forearm and hand.

The radial nerve may also be compressed in the vicinity of the elbow. It may be idiopathic or secondary to compression from mass lesions (lipoma, ganglia), bicipital tendon bursitis or injury from trauma (fractures with dislocations of the radial head) or surgery. A posterior interosseous nerve syndrome is heralded by a deep aching pain in the forearm with weakness of the wrist and digital extensors soon following. In complete paralysis there is still weak extensor strength because the extensor carpi radialis longus in innervated above the elbow. Sensation to the radial dorsum of the hand is normal. It may be differentiated from a lesion in the upper arm by the presence of brachioradialis and extensor carpi radialis longus function.

Common causes

Dislocation of the shoulder. The most common cause of axillary nerve palsy is anterior shoulder dislocation. Motor loss causes weakness or failure of arm abduction with atrophy of the cowl of the deltoid muscle, making the bony prominences of the shoulder more prominent. The deltoid is tested by palpating the muscle during isometric contraction or by abduction of the arm above the head, which cannot be performed with complete deltoid paralysis. Sensory loss involves a small patch over the lateral aspect of the shoulder.

Common causes

Brachial plexus lesions are often traction injuries and may involve the whole plexus or, more commonly, its upper or lower components. Lesions near the spinal column or of the roots and trunks present as root lesions involving the C5–T1 dermatomes and myotomes. If the whole plexus is involved in a severe traction injury, there is flaccid paralysis of the whole arm, which hangs limply from the shoulder. The arm is areflexic and anaesthetic from the upper arm or shoulder. Major trophic changes occur in the skin, with dryness, redness and thinning and gross atrophy of all muscle groups. Horner’s syndrome will be present with central lesions of the lower roots close to the spinal cord, due to involvement of the T1 outflow to the sympathetic trunk.

Upper plexus lesions (Erb-Duchenne palsy). This injury occurs with lateral flexion of the head and neck away from the shoulder. The upper trunk or the fifth and sixth cervical nerve roots are mostly involved. The arm hangs at the side in the ‘Porter’s tip’ position, the shoulder in adduction and internal rotation, the elbow extended, the forearm pronated and the wrist flexed. Paralysed muscles include upper arm abductors and external rotators and forearm supinators: deltoid, supraspinatus and infraspinatus, biceps, brachialis and supinator. Anaesthesia is maximal over the outer arm, forearm and hand.

Lower plexus lesions (Klumpke’s paralysis). These are due to stretching injuries to the lower trunk, as occurs with traction on an abducted arm. Compression from a cervical rib is another cause; vascular effects are also commonly present. The lesion, which is rare, affects the lower trunk or the C8 and T1 roots. The motor loss involves all small muscles of the hand, so a complete claw deformity occurs with wasting of all muscles, as for combined median and ulnar nerve lesions. The sensory loss, however, makes it clear that the lesion is in the neck and involves the trunk, as sensation is impaired over the C8–T1 area of the inner arm and forearm and over the medial aspect of the hand.

Localisation of lesions of the brachial plexus: dermatomes and myotomes of root lesions

Nerve root dermatomes are:

Myotome segments are:

Common causes

The common peroneal nerve is rather superficial as it courses into the popliteal fossa. Furthermore, it is tethered at the neck of the fibula by deep fascia. Common peroneal nerve injury results in paralysis of the anterior and lateral compartment muscle groups, causing foot and toe drop. Extension of the great toe (EHL) is paralysed, as is eversion of the foot. Sensory loss occurs over the dorsum of the foot and toes with sparing on the medial and lateral sides; the loss extends up the anterolateral aspect of the lower leg half way to the knee.

The deep peroneal is protected in the anterior compartment of the leg; however, it is at risk from anterior compartment ischaemia in the setting of compartment syndrome.

Common causes

This is an uncommon injury in which multiple structures can be disrupted. The anatomy of the popliteal neurovascular bundle helps explain the pattern of injury. The tibial nerve may be stretched such that the gastrocnemius and soleus are paralysed. The patient cannot stand on tiptoe and the ankle jerk is absent. Paralysis of the posterior compartment muscles causes loss of active flexion of the great toe (FHL) and other toes (FDP) and some weakness of ankle flexion. Sensory loss involves the sole of the foot and the toes, as well as the back of the calf. One must be mindful that the popliteal artery may also be injured in up to a third of cases, as it is secured both proximally and distally at the adductor hiatus and the fibrous arch of the soleus respectively.

Common causes

The sciatic nerve is prone to injury with posterior fracture dislocations of the hip joint. It may also be injured with gluteal trauma, including penetrating wounds. Surgical intervention to the posterior aspect of the hip joint may be indicated in sciatic nerve dysfunction.

The sciatic nerve originates from the anterior and posterior divisions of the nerve roots L4–S3. It is one of the more frequently injured nerves in the lower limb. It may be more vulnerable because it is relatively fixed proximally and distally at the sciatic notch and the fibula head respectively. Of its two components, the peroneal component is more vulnerable at the hip level as it tends to lie more superficially and more laterally in the buttock and upper thigh.

Paralysis of the sciatic nerve causes paralysis of all muscles below the knee with flaccid paralysis of foot and ankle (FDL, FHL, EHL, EDC), and loss of sensation over the whole lower leg except for a patch extending down the inner leg to the inner aspect of the great toe supplied by the saphenous nerve. The lesion is thus a combined common peroneal and posterior tibial nerve lesion. Extension of the knee is maintained. Depending on the level of involvement, the hamstrings may retain function. The clinician should therefore test the biceps femoris (from the common peroneal) and the semitendinosus and semimembranosus (from the posterior tibial) to localise the level of involvement.

Late sciatic nerve dysfunction may also occur. Heterotopic ossification, which is common after a posterior fracture–dislocation of the hip joint, may either compress or stretch the nerve.

Common causes

The femoral nerve is formed by the posterior divisions of the anterior primary rami of nerve roots L2–L4. Gunshot injuries, lacerations and surgical procedure such as lymph node dissections, vascular bypass procedures and total hip replacements may affect the femoral nerve distal to its entry into the femoral triangle. Within the pelvis the femoral nerve may also be injured during surgical interventions close to the iliac fossa, including renal transplantation and abdominal hysterectomy.

The quadriceps femoris muscle is paralysed with weakness of hip extension and an absent knee jerk. The psoas muscle, innervated segmentally, may still provide some hip flexion. There is also a loss of sensation on the front and sides of the thigh and the inner aspect of the lower leg.

Common causes

Disc prolapses and other spinal degenerative problems are the commonest cause of neurological disturbance in the lower limbs. Tendon reflexes of the lower limb are knee jerk (L3–4) and ankle jerk (S1). The cutaneous plantar response reflex arc is also via S1. Common nerve root compression syndromes from disc protrusion are:

Wasting without sensory loss

This may be due to motor neurone disease, to a lower motor neurone lesion affecting the anterior horn or nerve root, to a purely motor peripheral neuropathy or to a myopathy. Recheck for fasciculation, whether proximal or distal muscles are most affected, whether a family history is present and whether muscle power decreases with use. Full diagnosis should be made by a neurologist.

Causes of wasting with normal sensation

Clinical features

Common causes

A typical constellation of physical signs usually enables the diagnosis of hemiplegia or hemiparesis to be made or suspected on sight. Features are as described below; refer also to Figure 5.9.

Figure 5.9 Typical features of hemiplegia

Clinical features

Diagnostic plan

Treatment plan

Specific treatment depends upon the causative lesion. Treatment of hemiplegia involves supportive rehabilitation of the various disabilities. Rehabilitative treatment is multidisciplinary and involves medical and nursing staff, a physiotherapist, speech therapist and occupational therapist.

For patients who have made a good recovery of functions after a stroke, or those presenting with TIAs or amaurosis fugax caused by carotid artery bifurcation stenosis, invasive treatment should be offered in addition to ‘best medical management’. Best medical management comprises optimisation of atherosclerotic risk factors, antiplatelet therapy and the exclusion of important comorbidity.

Invasive treatment is offered for those patients with carotid stenosis ≥70%. Carotid endarterectomy is the gold standard in reducing the long-term risk of stroke. Recent trials have shown that carotid endarterectomy plus best medical management results in a 6 to 10 times risk reduction as compared with best medical therapy alone. Carotid stenting is a recently offered alternative therapy to carotid endarterectomy in reducing the risk of stroke. Long-term results are not available and, in general, carotid stenting is offered only to those who are at high risk of surgery, such as severe medical comorbidities, previous surgery or irradiation and difficult anatomical access.

Common causes

History, examination and clinical assessment

A history of injury, prodromal symptoms of nerve compression or back pain, other sites of neoplasms and nutritional deficiencies may help diagnosis. Prodromal urinary or bowel difficulties may also have occurred. In milder cases, clumsiness and stiffness of gait, rather than weakness is typical. With the hands, myelopathy commonly leads to complaints of clumsiness and difficulty handling small objects. Subjective sensory disturbance of the hands is commonly reported.

In chronic lesions, upper motor neurone signs are typically found in the lower limbs. In very acute pathology, flaccid weakness may be apparent and is an ominous prognostic sign. Sensation to all modalities is tested and an upper level of sensory loss noted. The sensory loss level is best elicited by testing each modality of sensation (cotton wool, pinprick, vibration sense) from below upwards and noting the level at which sensation is first appreciated on both sides. In milder cases, the sensory disturbance may be patchy and subjective. The skin is examined for neurofibromas and pigmented macules.

The patient is turned carefully to examine the back and spine for any deformity or scar and for any spinal tenderness.

The upper limbs and the cranial nerves are examined to accurately determine the level of the lesion and if other neurological deficits exist. In subtle lesions, asking the patient to undo and re-do their shirt buttons or to write is a useful sign of clumsiness of the fingers. Spreading of reflexes to the fingers is an important sign. The bladder is checked for distension or incontinence.

Hemisection of the spinal cord (Brown-Séquard syndrome)

Motor changes are all on the side of the lesion: upper motor neurone signs below the hemisection and lower motor neurone signs at the level of the lesion.

Sensory losses below the lesion are dissociated and crossed: vibration sense and proprioception (posterior columns) are lost on the same side as the lesion, pain and temperature (anterior column) loss is on the opposite side. Light touch is variably affected.

Other causes of paraplegia with dissociated sensory loss are:

Diagnostic and treatment plans

MRI is the test of choice and has supplanted other investigations. It is sensitive and specific for the diagnosis of demyelinating disorders and has supplanted the use of myelography in localising the level and cause of compression. Plain X-ray is mainly limited to the definition of instability, if suspected. If MRI is unavailable, the clinician will be forced to rely on a combination of plain X-ray, CT, isotope bone scans and myelography with post-contrast CT. Relief of incipient or progressive compression is often required, sometimes as a surgical emergency.