• Routine imaging early on in the course of low back pain is of no benefit [1]. An MRI scan can detect spinal metastases in patients with normal plain X-rays or CT scan [2]. A nuclear bone scan can also detect metastases in the vertebral column before cord compression but MRI is superior [3].

• In most patients with low back pain, symptoms resolve without surgical intervention:

• Physical therapy and non-steroidal anti-inflammatory drugs (NSAIDs) are the cornerstones of non-surgical treatment [4].

• Superficial heat is the only therapy with good evidence of efficacy for treatment of acute low back pain.

• Bed rest is often advocated for the treatment of acute low back pain but continuing ordinary activity may lead to a more rapid recovery [5].

• There is conflicting evidence of efficacy for spinal manipulation in low back pain [6, 7].

• Massage and acupuncture are better than no treatment but have not been compared to conventional treatment.

TREATMENT OF CHRONIC BACK PAIN

Chronic back pain can be very difficult to treat. Although there is limited evidence for the efficacy of aquatic exercises [8], this author¹ has seen numerous patients return to a normal life once they began swimming on a regular basis, at least three times per week and 20 minutes at a time.

Note: A randomised study detected higher ambulation rates in patients with malignant spinal cord compression (MSCC) who received high-dose dexamethasone before radiotherapy (RT) compared with patients who did not receive corticosteroids before RT (81% v 63% at 3 months, respectively; P = 0.046).

¹ Personal observations.

PROBLEMS IN THE UPPER LEG

Painless numbness

MERALGIA PARAESTHETICA

Meralgia paraesthetica is very common, particularly in patients who are overweight. It is essentially about the only cause of numbness in the thigh or upper leg because compression of the sensory nerve roots in the upper lumbar (L2–3) spine is very rare.

Symptoms:

• Symptoms may be intermittent initially, but subsequently the patient may develop permanently altered sensation.

• Symptoms vary from a mildly altered sensation over the anterolateral aspect of the thigh, often only noticed when the patient touches the thigh or clothes brush up against the thigh, to a more marked alteration in sensation with persistent numbness within the distribution of the lateral cutaneous nerve of the thigh but not always involving the entire extent.

• Some patients complain of pain and others may experience dysaesthesia, an unpleasant sensation when the skin is touched. This condition is due to compression of the lateral cutaneous nerve of the thigh beneath the inguinal ligament just medial to the anterior superior iliac spine and pressure over this point is often associated with tenderness.

• The presence of weakness or an altered knee reflex excludes the diagnosis.

• The condition may be unilateral or bilateral.

Examination: The simplest test is to stroke the skin over the lateral aspect of the thigh and, if there is altered sensation, test in all directions, mapping out the exact pattern and sensory loss. The patient is then shown Figure 12.1 and immediately identifies the problem.

FIGURE 12.1 The area of sensation supplied by the lateral cutaneous nerve of the thigh Reproduced from Aids to the Examination of the Peripheral Nervous System. 4th edn, Brain, 2000, WB Saunders, Figure 78. p 50.

Another diagnostic test is to inject local anaesthetic in the region of the lateral cutaneous nerve beneath the inguinal ligament; a transient resolution of symptoms is considered diagnostic [9].

MANAGEMENT of MERALGIA PARAESTHETICA

Once the benign nature of the condition is explained, the great majority of patients do not request any specific treatment. In a number of patients the problem may resolve spontaneously [9]. Patients with pain or dysaesthesia may respond to a corticosteroid injection and, if that fails, decompression of the nerve or avulsion of the nerve (neurectomy) [10]. This latter procedure will replace dysaesthesia with permanent numbness. Regardless of the treatment chosen most patients remain free of symptoms following treatment [9, 11].

Pain and weakness in the upper leg

DIABETIC AMYOTROPHY/FEMORAL AMYOTROPHY/LUMBOSACRAL NEURITIS

The clinical features of lumbosacral neuritis, femoral amyotrophy and diabetic amyotrophy are virtually identical, except for the presence of diabetes.

Symptoms:

• Increasingly severe pain in the buttocks, hips and thighs developing over hours to days is the initial presenting symptom. It is most often unilateral but, as in brachial neuritis, the contralateral side may be involved, usually within 1–2 weeks.

• In addition to the pain, severe weakness and subsequently marked wasting of the quadriceps muscles occurs with or without parasthaesia in the anterior aspect of the thigh and at times the shin. The weakness can be so severe to render the patient unable to walk.

• Sensory symptoms are usually minimal.

• Weight loss is not uncommon [12].

Examination: The examination reveals weakness of hip flexion and knee extension with an absent knee-jerk. Although it may occur at any age, lumbosacral neuritis is more common in the middle-aged to elderly [13].

The aetiology of these conditions is uncertain but it is thought to be based on an inflammatory vasculitis [12, 14].

MANAGEMENT of DIABETIC AMYOTROPHY/FEMORAL AMYOTROPHY/LUMBOSACRAL NEURITIS

Although the condition may resolve spontaneously after many months or years, immunomodulatory therapy, including corticosteroids or even cytotoxic drugs, may shorten the duration of the illness. Intravenous immunoglobulin has also been recommended and several case reports describe apparent dramatic responses [15, 16].

At this point in time there are no randomised controlled trials to guide therapy but, in the absence of specific therapy, significant disability persists for months or years.

POLYMYALGIA RHEUMATICA

Polymyalgia rheumatica is a condition seen in middle-aged to elderly patients.

In both lumbosacral neuritis and polymyalgia rheumatica there is constant pain. The worsening of pain with movement of the hips is seen only in polymyalgia and the presence of severe weakness and sensory disturbance occurs only in lumbosacral neuritis.

Symptoms: It presents with aching and stiffness predominantly affecting the shoulders but in 50–70% of cases may also affect the hips [17]. The condition is thought to relate to synovitis of the proximal joints and extra-articular synovial structures. The pain is constant day and night, as opposed to osteoarthritis of the hips where the pain mainly occurs on weight bearing. It often radiates to the knee and is exacerbated by movement of the hip joints. Although initially it may be unilateral, almost invariably patients develop bilateral symptoms.

A low-grade fever, fatigue and anorexia may occur in as many as 40% of patients and the presence of high spiking fevers should alert the clinician to the possibility of an associated giant-cell arteritis affecting the aorta and major branches. This can result in constant headaches, scalp tenderness and jaw claudication (see Chapter 9, ‘Headache and facial pain’, for further discussion).

Examination: The examination reveals restricted active and passive movement of the hips but in the absence of any joint swelling.

MANAGEMENT of POLYMYALGIA RHEUMATICA

In patients with polymyalgia rheumatica the erythrocyte sedimentation rate is invariably raised and corticosteroids are the treatment of choice. Doses as little as 10–20 mg/day almost invariably lead to a rapid resolution of the aching and stiffness within days and a rapid response at this low dose is considered diagnostic.

Occasional patients may require higher doses for longer periods [17]. If the patient fails to respond to 30 mg of prednisolone within 1 week the diagnosis should be questioned.

Early cessation of steroids may lead to a relapse and treatment at a low dose should be continued for 1–2 years [18]. Methotrexate has been shown in a randomised controlled trial to be an effective steroid-sparing agent.

Unfortunately, side effects of steroids in this group are common.

DRUG-INDUCED MUSCLE PAIN AND/OR WEAKNESS

A large number of pharmaceutical agents, including lipid lowering agents, NSAIDs, antineoplastic drugs and even over-the-counter essential amino acids, such as L-tryptophan, can result in myalgia or even myositis causing muscle pain, cramps, swelling, tenderness and weakness [19, 20]. This list is almost certain to enlarge with the advent of new therapeutic agents.

In any patient presenting with myalgia or muscle weakness a detailed list of drugs used should be obtained and each drug should be checked to see if it has been reported to cause myalgia or myositis. Some drugs produce a pure muscle disorder; others are associated with a neuropathy. The pharmacy department of the public hospital is a very useful resource, as is the patient’s own pharmacist.

Weakness in the upper leg

POLYMYOSITIS/DERMATOMYOSITIS

Inflammatory disorders of muscle, including polymyositis, dermatomyositis and inclusion body myositis, are extremely rare and most general practitioners are unlikely to encounter a case during their working career.

Patients present with the insidious onset of proximal weakness in the legs in the absence of sensory disturbance. The weakness is bilateral but may be asymmetrical. Pain in the muscles occurs in approximately 50% of cases but, as opposed to the above two conditions, is rarely severe. Dysphagia, neck weakness and impaired respiratory function may occur [21]. Inclusion body myositis affects the long flexors of the fingers and, in the lower limbs, the extensor muscles of the knees and hip flexors, resulting in significant proximal weakness. In this latter condition the knee reflex is often absent, whereas in polymyositis and dermatomyositis the reflexes are preserved.

MANAGEMENT of MYOSITIS

Most patients will have an elevated creatinine phosphate kinase (CPK), but a normal CPK does not exclude the diagnosis. The nerve conduction studies (NCS) should be normal, but electromyography may demonstrate a typical myopathic pattern associated with fibrillation potentials and positive sharp waves indicating an inflammatory muscle disorder. Magnetic resonance imaging, contrast-enhanced ultrasound and positron emission tomography can demonstrate abnormalities in muscles in patients with inflammatory myositis and can help determine the site for the definitive diagnostic test, a muscle biopsy [22].

Corticosteroids are the cornerstone of treatment, unfortunately often associated with significant side effects. Other immunomodulatory drugs, such as azathioprine, methotrexate, cyclosporine, cyclophosphamide, interferon, intravenous immunoglobulin and plasma exchange, are often used as steroid-sparing agents despite the lack of good evidence regarding the effectiveness of any of these treatments [23]. Apart from exercise there is no specific treatment for inclusion body myositis at the time of writing this text.

MUSCLE WEAKNESS DUE TO ENDOCRINE DYSFUNCTION

Hyperthyroidism, hypothyroidism and Addison’s disease may all present with muscle weakness. Usually there are associated manifestations to point to the underlying endocrine disorder. Hyperthyroidism may also present with periodic paralysis [24] or rhabdomyolysis [25] and hypothyroidism may present with muscle hypertrophy [26].

The weakness will resolve with correction of the endocrine disturbance.

PERIPHERAL NEUROPATHY

Certain peripheral neuropathies such acute and chronic inflammatory demyelinating peripheral neuropathy and the IgG- and IgA-related peripheral neuropathies can result in significant proximal weakness in the lower limbs. However, this rarely occurs in isolation and these patients usually present with generalised weakness affecting the proximal lower limbs and the distal upper limbs and neck weakness with or without respiratory muscle weakness. Peripheral neuropathy is discussed in more detail later in this chapter.

PROBLEMS IN THE LOWER LEGS AND FEET

Unpleasant sensations in the feet

In the lower leg and feet patients can experience unpleasant sensations at rest that can cause difficulty walking or unpleasant sensation at rest improved by walking or, in fact, that can be improved by walking. Figure 12.2 shows an approach to patients with discomfort or unpleasant sensation in their feet. Erythromelalgia and painful legs moving toes are extremely rare.

FIGURE 12.2 Suggested approach to pain in the feet

There are many non-neurological causes of pain in the feet where pain is either exacerbated or precipitated by weight bearing and/or walking. These include osteoarthritis in the ankle or joints of the feet, a calcaneal spur and plantar fasciitis. The neurological causes of pain in the feet that can result in difficulty walking due to pain include Morton’s neuroma or metatarsalgia and tarsal tunnel syndrome. All will have pain with weight bearing, but there are subtle differences in the nature of the pain and the presence of altered sensation that occurs with the neurological causes to help differentiate the various entities.

UNPLEASANT SENSATIONS AT REST THAT DO NOT CAUSE DIFFICULTY WALKING

Restless legs syndrome (RLS) and burning feet are the two common conditions that cause unpleasant sensations in the feet and lower legs. They do not interfere with walking; in fact, the symptoms improve with walking with RLS and walking on a cold surface with burning feet.

Restless legs syndrome: Restless legs syndrome [27–31] is common, affecting 5% of the population. However, many patients complain that most doctors do not seem to be aware of the entity or know much about it. A more appropriate term is restless limbs syndrome because in more severe cases it can also affect the upper limbs and, rarely, symptoms may be confined to the upper limbs.

The essential features of RLS are:

• Patients develop symptoms when they are not moving, such as prolonged sitting at the dinner table, on an aeroplane or in a lecture or movie.

• Symptoms are particularly severe in bed at night.

• Patients find it very difficult to describe the nature of the symptoms except to say that they are unpleasant.²

• Patients cannot keep their limbs still because of this unpleasant sensation that feels deep inside the limb, not over the surface or affecting just the skin.

• The pain is in the feet, shins, calves and often seems to cross joints but is not confined to the joints.

• Symptoms persist on and off for hours until patients are forced to be up and about.

• Both legs are usually affected although the symptoms can be either confined to or more severe in one leg.

• Patients invariably pace the floor at night to obtain relief but, unlike burning feet syndrome, they do not need to walk on cold surfaces and the symptoms are not relieved by moving the feet to where the sheets are colder.

• There are no symptoms during the day unless the patient sits down.

• Sleep is disturbed whether the patient is sleeping at night or during the day.

• The neurological examination of the affected limbs should be completely normal, although sometimes this condition is associated with a peripheral neuropathy, so patients should be examined specifically looking for absent ankle reflexes, weakness of dorsiflexion of the toes and feet and possible peripheral sensory loss affecting the toes and distal aspect of the feet.

The condition can occur at any age although most patients will have experienced their first symptom before the age of 30. The symptoms are more marked in the presence of renal failure, iron deficiency and pregnancy. It is important to test for iron deficiency and impaired renal function.

The aetiology of RLS is unclear although there is a genetic factor with autosomal dominant and autosomal recessive inheritance. As it is predominantly inherited as an autosomal dominant condition, a positive family history can be obtained in up to 90% of patients with detailed questioning, although the patient may not be aware of the specific name but can recall their parents or grandparents pacing the floor at night. Other patients will initially say that there is no other family member affected but, when sent away to enquire, discover one or more relatives who have the condition. In many but not all patients there is involuntary jerking of the limbs referred to as myoclonus. The symptoms of RLS increase in severity with increasing age and duration of the disease.

Conditions that may be confused with restless leg syndrome include peripheral vascular disease (PVD) and two very rare conditions, akathisia and a curious entity called painful legs and moving toes.

MANAGEMENT of RESTLESS LEGS SYNDROME

Exclude iron deficiency and renal failure.

Abstinence from alcohol, caffeine, nicotine and drugs that may exacerbate the problem is advocated [32].

A number of treatments have been recommended:

• Some patients can minimise their symptoms by either exercising just before retiring to bed or by running several kilometres each day. In most patients such exercise is not practical and drug therapy is necessary [30].

• Levodopa is considered the treatment of choice [30, 33].

• Other medications include benzodiazepines such as clonazepam [34], the dopamine agonists pramipexol [35] and ropinerole [36], rotigotine transdermal patches [37], in severe cases opiates such as oxycodone [38] and in very severe cases methadone [39].

Note: Methadone has not been studied in randomised controlled trials; the evidence is based on a case series.³

³ Personal observations in several patients suffering from very severe restless legs syndrome is that methadone has provided significant benefit, although tachyphylaxis has occurred, requiring increased doses. Methadone is approved for the treatment of severe RLS by the Australian Pharmaceutical Benefits Scheme on an authority preseription.

The characteristic feature of PVD is exercise-induced leg pain relieved by rest but occasionally it can cause pain at rest. The symptoms are confined to the lower limbs and upper limb symptoms would exclude this diagnosis. The pain is usually in the feet and calves; very rarely, buttock pain can occur due to involvement of the internal iliac artery. The peripheral pulses will be difficult to palpate with PVD.

Akathisia: Akathisia consists of an inner sense of restlessness with a desire to move not just the limbs but the entire body. It is only seen in patients who have been exposed to dopamine antagonists. Whereas the unpleasant sensations associated with RLS are alleviated by walking or moving the limbs, patients with akathisia cannot obtain relief with movement.

Painful legs and moving toes: Painful legs and moving toes may develop in the setting of spinal cord and cauda equina trauma, lumbar root lesions, injuries to bony or soft tissues of the feet and peripheral neuropathy; in some patients it is idiopathic [40]. It is not familial and is not thought to be related to RLS.

It consists of continuous or semi-continuous involuntary writhing movements of the toes associated with pain in the affected extremity [41]. Symptoms may begin on one side and become bilateral; movements may be momentarily suppressed by voluntary action or exacerbated by changing posture [40]. Pain preceding the movements was most commonly burning in nature. Movements consisted of flexion/extension, abduction/adduction and fanning or clawing of toes/fingers and sometimes the foot or hand [42]. Surface electromyography (EMG) showed movements suggestive of both chorea and dystonia. Movements are partially suppressible and diminished but still apparent during light sleep.

Gamma-aminobutyric acid (GABAergic) agents are most effective in controlling the pain and the movements [42].

Burning feet syndrome: Patients complain of an unpleasant burning sensation involving mainly the soles of the feet and occasionally the dorsal aspect of the feet and the legs below the knees that predominantly occurs in bed at night. They prefer to remove the bed covers, move their feet to where the sheets are colder or walk on cold surfaces to obtain some relief.

This differs from RLS where relief is obtained simply by walking on any surface. In some patients burning feet occurs in the setting of a distal sensory peripheral neuropathy; in most patients, the examination does not reveal any abnormality in the peripheral pulses or the skin and there are no abnormal neurological signs.

The aetiology of the syndrome is thought to be a small fibre neuropathy, and reduced intraepidermal nerve fibre density has been demonstrated on skin biopsy [43]. It has been reported in:

• diabetes mellitus or impaired glucose tolerance detected by oral glucose tolerance testing [44]

• hypothyroidism [45]

• HIV [46]

• vitamin B deficiency such as thiamine (B1), riboflavin (B2), nicotinic acid (B3), pantothenic acid (B5) and cyanocobalamin (B12)

Note: Vitamin B deficiency may cause burning feet syndrome that will respond to replacement therapy, but the evidence for this is poor [47].

MANAGEMENT of BURNING FEET SYNDROME

Cold soaks

One of the most effective treatments for significant burning, prickling and tingling in the feet that is present mainly at night is to use cold foot soaks [47].

• Use cold tap water in a basin and leave the feet in it for 20 minutes.

• Take them out and dry them very thoroughly and use a lotion such as Vaseline Intensive Care massaged into the feet. Often this is needed a couple of times a day to gain good relief.

• In addition a tricyclic antidepressant, such as amitriptyline or nortriptyline, at night can be used [48], starting with a small dosage and gradually building up to 50–75 mg.

With a combination of foot soaking and amitriptyline you can get the vast majority of patients under control.

Aspirin lotion⁴

Ingredients: 1 x 300-mL pump pack of sorbolene cream; 1 x 100-tablet pack of soluble aspirin (e.g. Disprin)

To make soluble aspirin lotion for skin application:

1. Pump 20 mL (1½ teaspoons) of sorbolene cream into a wide-mouthed glass receptacle or cup.

2. In a spoon dissolve two soluble aspirin in a few drops of water.

3. When the fizzing stops, mix very thoroughly into the sorbolene using a spoon handle in a stirring/beating motion.

4. Apply and rub this cream into the affected skin 3 times a day.

Every morning make up a similar quantity freshly for each day’s use. Alternatively, aspirin tablets may be crushed to a powder and thoroughly mixed with the cream.

⁴ Aspirin lotion has been shown to be superior to oral aspirin for the burning pain of acute herpes zoster [49]. This recipe was found some years ago by the author who can no longer find the reference. It is an innocuous treatment with no side effects and has been used with apparent good effect in patients with burning feet.

Erythromelalgia: Erythromelalgia is a rare condition, of uncertain aetiology, characterised by episodic erythema, intense burning pain and warmth of the hands and/or feet. When chronic, it is associated with significant disability [50]. Severe erythromelalgia may spread up the legs and arms and even affect the ears and face. It may be unilateral or bilateral. Symptoms flare up late in the day and continue overnight.

This may not be a disease entity at all, but a syndrome of dysfunctional vascular dynamics [51]. Exposure to warmth can trigger flaring and increase its severity; symptoms are relieved by cooling in ice water. Sometimes the condition may be precipitated by immersing the affected area in hot water for 10–30 minutes [51]. Many patients have either small or large fibre neuropathy (quoted as unpublished data in the article by Kuhnert et al [52]).

Erythromelalgia can be primary or secondary. Primary erythromelalgia begins spontaneously at any age. Secondary erythromelalgia has been reported with many disorders but most often with polycythemia, thrombocythemia, neuropathies and autoimmune diseases.

UNPLEASANT SENSATIONS IN THE FEET AT REST THAT CAUSE DIFFICULTY WALKING

Tarsal tunnel syndrome: Tarsal tunnel syndrome (TTS) is a controversial entity in which the posterior tibial nerve is compressed under the flexor retinaculum in the tarsal tunnel, inferior and posterior to the medial malleolus. This is much rarer than most medical practitioners think.

The symptoms consist of:

• Tingling and numbness on the sole of the foot. If paraesthesia occurs it MUST be confined to the sole of the foot and within the distribution of either the medial and/or lateral plantar nerves (see Figure 1.21). Paraesthesia on the top of the foot excludes the diagnosis.

• Burning paraesthesia and pain described as sharp, shooting, shock-like or electric radiating either proximally or distally.

• The symptoms worsen after prolonged standing or walking [53].

• The symptoms are more intense at the end of the day.

• Symptoms do not awaken the patient from sleep and are unlike carpal tunnel.

• Rarely, pain confined to the soles of the foot may also occur at rest and in non-weight-bearing positions [54]. A positive Tinel’s sign with tapping of the nerve behind the medial malleolus producing tingling into the sole(s) would be diagnostic but is very rare. Altered sensation within the distribution of the medial and/or lateral plantar nerves is also rarely seen.

The diagnosis of TTS may be difficult as the symptoms are often vague, as are the physical findings and signs. Bilateral cases are seen occasionally. There is often a long delay in diagnosis of up to 2½ years [55].

MANAGEMENT of TARSAL TUNNEL SYNDROME

The entrapment neuropathy of TTS and its treatment are controversial. Nerve conduction studies are of uncertain value due to the lack of definitive studies [56]. Their value is in excluding peripheral neuropathy. Symptoms and signs, operative findings and response to therapy define most cases of TTS reported in the literature [56]. A variety of pathologies have been reported with MRI scans [57], although most are idiopathic in origin.

Surgery consisting of neurolysis of the tibial nerve in the tarsal tunnel and the medial, lateral plantar, calcaneal nerves in their own tunnels and immediate postoperative mobilisation of the posterior tibial nerve through ambulation can achieve a good or excellent outcome in >90% of cases [58].

Morton’s neuroma or metatarsalgia: Morton’s neuroma is entrapment of the interdigital nerve, most commonly between the 3rd and 4th and less commonly the 2nd and 3rd toes.

• Patients complain that it feels like there is a stone or pebble in their shoe.

• There is the gradual onset of pain while walking with sudden attacks of throbbing burning pain and paraesthesia, on the plantar surface of the foot localised to the web space that radiates to the corresponding toes.

• As opposed to pain of neurological origin it is not burning, shooting or associated with altered sensation.

• Pain is minimal or absent when sitting or lying as opposed to a calcaneal spur and plantar fasciitis.

• The clue to the diagnosis is that the pain is aggravated by wearing tight shoes and may be relieved by massage to the forefoot and toes [59].

• There is a localised area of reproducible tenderness between the metatarsal heads.

It occurs most commonly in middle-aged women. Bilateral cases are seen occasionally. If the pain is severe it can create difficulties walking because of the pain, referred to as the antalgic gait. A characteristic limp, characterised by a very short stance phase, may be adopted so as to avoid pain on weight-bearing structures.

MANAGEMENT of MORTON’S NEUROMA

In patients with suspected Morton’s neuroma an ultrasound may detect an ovoid, hypoechoic mass located just proximal to the metatarsal heads in the intermetatarsal space, most often between the 2nd and 3rd or 3rd and 4th metatarsals in >90% of patients [60].

Patients should be advised about suitable footwear and possibly be given orthoses to control abnormal pronation.

Injections of local anaesthetic and hydrocortisone around the nerve or surgical excision are recommended [59] although there are no randomised trial results to support this [61].

Calcaneal spur: A calcaneal spur causes:

• sharp, stabbing chronic heel pain, particularly in overweight patients [62]

• pain that is characteristically worse in the morning

• tenderness to firm palpation at the distal aspect of the heel where the tendon inserts into the calcaneus bone.

Calcaneal spurs are seen in some patients with plantar fasciitis.

Plantar fasciitis: Plantar fasciitis is the most common cause of plantar heel pain.

SYMPTOMS:

• Pain is felt in the sole of the foot.

• Pain is worse when standing after periods of rest or on taking the first steps in the morning.

• The pain improves only to worsen again later in the day after prolonged weight bearing.

• Nocturnal pain is not a feature of plantar fasciitis.

• The pain is searing, throbbing or piercing not burning or shooting.

• There is tenderness over the origin of the plantar fascia and the anteromedial aspect of the heel.

TREATMENT for PLANTAR FASCIITIS

A variety of treatment regimens have been recommended, but there is no scientific evidence to help guide choice of a particular therapy.

• First-line treatment consists of the combination of a viscous-elastic heel pad, a stretching program, NSAIDS and a tension night splint [64].

• Extracorporeal shockwave therapy is also recommended [65].

• Combined local corticosteroid injections may be given in the form of triamcinolone 2 mL and using a peppering (injecting, withdrawing, redirecting, and reinserting without emerging from the skin) technique [66].

• Retrospective studies have claimed improvement with surgery in patients who have failed to improve with conservative measures [67].

It is more common in runners who increase the distances they run, in obesity and in those who are on their feet most of the day. The condition is self-limiting in most patients and resolves within 12 months [63].

Weakness and/or sensory loss in the lower leg

FOOT DROP

A foot drop can result from:

• an L5 radiculopathy

• a lumbosacral plexus problem

• a sciatic nerve problem

• a common peroneal nerve lesion

• a peripheral neuropathy.

A careful examination to establish the pattern of weakness can help differentiate the various causes.

Figure 12.3 lists the features that help to differentiate the various causes of a foot drop. The crucial thing to note is that the tibialis posterior and tibialis anterior muscles invert the foot at the ankle. The tibialis posterior tendon can be seen and palpated behind the medial malleolus and the tibialis anterior tendon in front of the medial malleolus (see Figure 12.4).

FIGURE 12.3 The patterns of weakness that help to differentiate the various causes of foot drop

FIGURE 12.4 Testing A dorsiflexion, B eversion and C inversion of the foot, D plantar flexion

Figure 12.4C shows both the tibialis anterior and tibialis posterior tendons contracting with inversion.

The neuroanatomy explains the signs:

• Foot drop or weakness of dorsiflexion of the foot relates to weakness of the tibialis anterior and extensor digitorum muscles. These muscles are supplied by the common peroneal nerve, the lateral branch of the sciatic nerve that arises in the popliteal fossa and traverses the neck of the fibula, a common site for compression. The 5th lumbar nerve root (L5) is the main innervation of these muscles.

• The peroneii muscles that are responsible for eversion of the foot are also innervated by the common peroneal nerve and the L5 nerve root.

• Inversion of the foot results from the combined action of the tibialis anterior and posterior muscles, both supplied by the L5 nerve root, but the tibialis posterior is supplied by the posterior tibial nerve and the tibialis anterior by the common peroneal nerve.

Common peroneal nerve lesion: This is the commonest cause of a foot drop and is related to compression of the common peroneal nerve at the neck of the fibula. Common peroneal nerve palsies are most often related to trauma or compression during surgery, in comatose patients or with prolonged squatting. Some occur for no obvious reason [68]. In the compressive group the prognosis for spontaneous recovery is excellent [68].

The patient invariably awakens, steps out of bed and almost falls because of weakness of dorsiflexion of the foot. The neurological signs are listed in Figure 12.3. The area of sensory loss is small (between the 1st and 2nd toes on the dorsal aspect of the foot) if only the deep peroneal nerve is affected and more extensive (dorsum of foot and lateral aspect of distal half of lower leg) if the superficial peroneal nerve is also affected (see Figure 1.19).

Sciatic nerve lesion: Sciatic nerve lesions are very rare and usually result from posterior dislocation fracture of the hip or as a complication of total hip joint replacement. It has also been reported as a complication following coronary artery bypass surgery when patients were sat upright while still unconscious [69].

The neurological signs are listed in Figure 12.3. As opposed to an L5 radiculopathy, hip extension and abduction are normal and the sensory loss involves the L5 and S1 dermatomes and is over the lateral aspect of the shin, dorsum of the foot, the lateral aspect of the foot on both the dorsal and plantar surfaces and also over the calf.

L5 radiculopathy: Lumbar nerve root compression is a common cause of leg pain with or without a foot drop and occasionally patients present with a painless radiculopathy [70]. The neurological signs are listed in Figure 12.3. If sensory loss occurs, it is within the distribution of the 5th lumbar nerve root (see Figure 1.22).

Peripheral neuropathy: The list of causes of peripheral neuropathy is long and well beyond the scope of this book. Readers are referred to more definitive texts [71].

Earlier in this chapter we referred to significant hip flexion weakness related to the inflammatory demyelinating and IgA- and IgG-related peripheral neuropathies.

Other causes of peripheral neuropathy more typically present with weakness and/or sensory loss commencing in the toes and ascending up the foot and leg as the condition worsens. These neuropathies are often referred to as length dependent (because the abnormalities appear first in the longest nerves). The commonest are those related to alcohol, where weakness predominates, and diabetes, where distal symmetrical stocking distribution sensory loss is the main clinical feature.

Vitamin B₁₂ deficiency is very rare, easily diagnosed and readily treatable so it should always be considered. In B₁₂ deficiency the clinical picture is dominated by signs related to subacute combined degeneration of the spinal cord with marked vibration and proprioceptive loss in the limbs, resulting in significant ataxia and clumsiness exacerbated with eye closure or in the dark. Similar signs occur in paraneoplastic and Sjögren’s related neuropathy as well as Friedreich’s ataxia. The paraprotein related neuropathy with IgM is predominantly a length-dependent one with distal sensory loss and paraesthesia/dysaesthesia.

There are a variety of ways to classify the peripheral neuropathies:

• One way is to differentiate between single nerves being affected, referred to as mononeuropathy, multiple single nerves, the mononeuropathy multiplex, or diffuse involvement of the peripheral nervous system. In this section the peripheral neuropathies with diffuse involvement are discussed.

• A second way to characterise these neuropathies is the rapidity with which they develop, differentiating acute with onset over days to weeks, subacute with onset over months and chronic with onset over years.

• Nerve conduction studies are used to classify whether the peripheral neuropathy is axonal (affecting the axons) or whether it is demyelinating (affecting the myelin) and, in the case of demyelinating neuropathies, whether there is uniform slowing or conduction block (see additional information in Table 12.1 below).

TABLE 12.1

Features on NCS and EMG of demyelinating versus axonal neuropathies

	Demyelinating	Axonal
Amplitude of motor response	Normal or mildly reduced	Markedly reduced
Conduction velocity	Very slow	Normal or mildly reduced
Conduction block	Yes	No
Temporal dispersion^∗	Present	Absent
Distal motor latency	Prolonged	Not prolonged
Absent response	No	Possible
f-wave latencies	Prolonged	Not prolonged
EMG	No denervation	Denervation

^∗The term ‘temporal dispersion’ is where the proximal response (the site of stimulation is further up the arm or leg) is substantially lower in amplitude and of longer duration than the distal response.EMG – electromyography; NCS – nerve conduction studies.

Most neuropathies are mixed axonal and demyelinating.

DIABETES AND THE PERIPHERAL NERVOUS SYSTEM: There are a number of peripheral nerve lesions that occur in the setting of diabetes.

• Acute neuropathies

• Diabetic amyotrophy with proximal weakness and pain in the legs

• Third nerve palsy, usually not involving the pupil

• Truncal neuropathy with pain radiating around the lateral chest and abdominal wall toward the mid-line with sensory loss extending laterally from the mid-line anteriorly

• Chronic neuropathies

• Distal sensory loss to pain and temperature that gradually ascends up the toes, feet and legs with increasing duration of diabetes

• Autonomic neuropathy with postural hypotension, anhidrosis, nocturnal diarrhoea, hypothermia, dry eyes and mouth, impotence in males and bladder atony

• Chronic proximal motor neuropathy

MANAGEMENT of PATIENTS with SUSPECTED PERIPHERAL NEUROPATHY

If a patient is suspected of having a peripheral neuropathy the initial investigation should be NCS and EMG (see Table 12.1). This will confirm the presence of peripheral neuropathy and should help characterise whether it is axonal, demyelinating or mixed axonal and demyelinating. The presence of conduction block on NCS indicates a demyelinating neuropathy in keeping with the acute and chronic inflammatory demyelinating neuropathies (AIDP, CIDP) or multifocal motor neuropathy with conduction block. If a peripheral neuropathy is confirmed, the following screening investigations would be appropriate:

• random blood glucose

• vitamin B₁₂

• immunoglobulin quantitation and protein electrophoresis

• Bence–Jones proteins.

Causes include:

• In clinical practice peripheral neuropathy most commonly relates to diabetes or alcohol in Western societies; the commonest cause worldwide is leprosy.

• The other more common causes include AIDP and CIDP, neuropathy related to mononclonal gammopathies such as IgG, IgM and IgA, drug-related neuropathy, uraemia, familial neuropathy and, although relatively rare, vitamin B₁₂ deficiency should not be missed.

• There are many other causes including hereditary, toxic, metabolic, infectious (including HIV), inflammatory, ischaemic and paraneoplastic disorders. Occasionally, patients may present with a peripheral neuropathy in the setting of malignancy; more often the neuropathy appears after the diagnosis of the malignancy and the difficulty is to differentiate neuropathy related to drug therapy of the malignancy and a paraneoplastic neuropathy.

• In approximately 20% of patients a cause may not be established. A careful family history and examination of near relatives (including NCS) will detect a familial neuropathy in nearly half of the patients where the initial assessment fails to elucidate the cause.

Currently, peripheral neuropathies are classified as either demyelinating or axonal based largely on the results of NCS [72, 73].

The features on NCS and EMG of demyelinating versus axonal neuropathies are shown in Table 12.1 The term ‘temporal dispersion’ is where the proximal response (the site of stimulation is further up the arm or leg) is substantially lower in amplitude and of longer duration than the distal response and relates to differences in conduction of different fibres within the nerve. Conduction block (CB) refers to a marked reduction in the amplitude of the motor response between distal and proximal stimulation and/or prolongation of the distal motor latency, and is due to focal demyelination in the nerve. Occasionally, CB is so severe that no response can be obtained. CB cannot be diagnosed at sites where the nerve can be compressed, e.g. ulnar nerve at the elbow. The criteria for CB have varied over the years and are divided into definite or probable, based on the degree of reduction of amplitude and increase in duration of the motor response between distal versus proximal stimulation [74].

In patients with an acute onset neuropathy, e.g. AIDP, abnormalities on EMG (the study of muscle using a concentric needle electrode) are usually manifest within 7–10 days of onset of the illness but may not be evident for up to 3 weeks. When there is axonal damage, EMG demonstrates increased insertional (as the needle enters the muscle) activity, spontaneous activity in the form of fibrillation potentials and positive sharp waves (both indicative of denervation) with a reduced recruitment pattern (the diminished number of motor units recruited with voluntary contraction of the muscle is reflected in the baseline being visible between motor units). Fasciculations may be seen but are not synonymous with denervation.

Pain in the lower leg

RADICULOPATHY

Sciatica (also referred to as radiculopathy) refers to pain from compression of the nerve root, most commonly L5 or S1, less commonly L4.

Lumbar nerve root compression is a common cause of leg pain, and L5 radiculopathy accounts for 75% and L4 for 15% of these cases.

SYMPTOMS:

• These patients present with pain radiating down the back of the thigh and lateral aspect of the shin to the dorsum of the foot with an L5 radiculopathy and to the medial aspect of the lower leg with an L4 radiculopathy.

• If weakness does occur with an L5 radiculopathy, it affects dorsiflexion of the foot; inversion of the ankle is weaker than eversion as both the tibialis posterior and tibialis anterior muscles are affected; plantar flexion is normal.

• The area of sensory loss, if present, affects the lateral aspect of the shin and dorsal surface of the foot.

• A number of patients are seen with sciatic-like pain radiating from the buttock down to above the knee where no evidence of nerve root compression can be detected, and the aetiology of this pain is unclear.

MANAGEMENT of SCIATICA

Sciatica usually resolves without surgery within 12 months in 95% of patients [75]. If back pain is the major complaint and leg pain only a minor symptom then, in the absence of instability in the form of spondylolisthesis (one vertebra slips on another), back surgery is less likely to relieve symptoms and the patient may possibly best be treated conservatively with exercise and cognitive behaviour treatment [75, 76]. Even in patients with predominantly leg pain, the pain may settle with rest, NSAIDs, acetaminophen, skeletal muscle relaxants (for acute low back pain) or tricyclic antidepressants (for chronic low back pain). The anecdotal observation that oral corticosteroids appear to be of benefit has not been substantiated [77, 78].