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Author: admin | 27.03.2014 | Category: Tinnitus Causes And Treatments

Disorders of peripheral nerve function can be categorized in terms of the site of the primary disturbance. Peripheral neuropathy characteristically causes predominantly distal muscle weakness—with or without atrophy—or sensory changes and signs of autonomic malfunction, either alone or in combination. Mononeuropathies—common conditions include median nerve compression due to carpal tunnel syndrome, and damage to the ulnar nerve at the elbow and the common peroneal nerve at the fibular head.
The peripheral nerves consist of bundles (fascicles) of unmyelinated and myelinated axons that have their cell bodies in the anterior horns of the spinal cord, dorsal root ganglia, or autonomic ganglia. All nerve fibres, whether myelinated or unmyelinated, are closely related to satellite cells, the cells of Schwann.
Generalized axonal neuropathies often lead to a selective degeneration of the distal portion of the fibres, which then extend proximally. Other neuropathies primarily affect the myelin, either directly, or through interference with Schwann cell function.
Finally, in other neuropathies the nerve fibres may be secondarily damaged by processes that primarily affect the connective tissues of nerves or of the vasa nervorum.
Peripheral neuropathies may be divided into two broad categories depending on the distribution of the involvement. Second, there may be a diffuse and bilaterally symmetrical disturbance of function which can be designated polyneuropathy. Weakness or paralysis may be due to either conduction block in the motor nerve fibres or axonal degeneration. In generalized symmetrical polyneuropathies, the muscle weakness and wasting are commonly peripheral in distribution and begin in the lower limbs. Loss of the tendon reflexes is a frequent accompaniment of a peripheral neuropathy, and usually first affects the ankle jerks. Sensory symptoms and sensory loss in symmetrical polyneuropathies are usually distal in distribution, giving rise to the ‘glove-and-stocking’ pattern of involvement.
Spontaneous pains of an aching or lancinating character may complicate a number of generalized polyneuropathies. Disturbances of autonomic function are occasionally the primary abnormality in a peripheral neuropathy, as in rare syndromes of primary autoimmune autonomic neuropathy and familial dysautonomia. The history and physical examination frequently indicate that the disturbance has affected the peripheral nerves.
Examination of the cerebrospinal fluid may be helpful in the diagnosis of the cause of a peripheral neuropathy. Nerve biopsy is rarely required in establishing the existence of a peripheral neuropathy, but may be of diagnostic value in establishing the cause, especially in vasculitis and other multifocal inflammatory disorders and in amyloid. The serratus anterior acts as a fixator of the scapula, holding the scapula against the chest wall when forward pressure is exerted by the arm. The brachial plexus may be affected by intrinsic lesions, neoplastic infiltration, penetrating wounds of the neck, in fractures and dislocations of the shoulder and clavicle, as a result of traction on the arm, or by pressure from an aneurysm or a cervical rib. This condition has been described under a variety of terms, including ‘idiopathic brachial plexus neuropathy’ and ‘paralytic brachial neuritis’. The disorder develops acutely with intense pain in the shoulder region which may take some weeks to subside completely, although generally it ceases after a few days.
The pattern of muscle involvement and sensory disturbances suggests that neuralgic amyotrophy affects the brachial plexus in a patchy manner. Brachial plexus damage may occur as a sequel to radiotherapy for breast carcinoma or tumours in the neck.
Traction on the arm may result in damage to the plexus itself or may lead to avulsion of the spinal roots from the cord. In severe traction lesions, commonly encountered in current medical practice as a result of motorcycle or aircraft accidents, the whole of the plexus may be damaged.
Selective damage to the upper portion of the plexus (C5 and C6 roots or upper trunk) results in paralysis of deltoid, biceps, brachialis, brachioradialis, and sometimes supraspinatus, infraspinatus, and subscapularis.
When the spinal roots are avulsed from the cord, regeneration is impossible and intractable spontaneous pain may be a highly troublesome sequel. The contribution of the eighth cervical and first thoracic roots to the brachial plexus may be damaged by angulation over an abnormal rib or, more usually, a fibrous band arising from the seventh cervical vertebra and attached to the first rib.
Damage to the lower part of the brachial plexus leads to weakness and wasting of the small hand muscles, and of the medial forearm wrist and finger flexors.
Tumours may arise locally in the brachial plexus, such as a neurofibroma in neurofibromatosis type I (von Recklinghausen’s disease) or a solitary schwannoma, or the plexus may be invaded by tumours arising in other structures. The long course of the radial nerve and its position in relation to the humerus make this nerve unusually susceptible to external compression.
The nerve may be injured in wounds of the axilla so that the paralysis includes triceps, resulting in loss of extension at the elbow.
Many muscles not supplied by the radial nerve work at a disadvantage when the wrist and finger extensors are paralysed. A lesion of the posterior interosseus nerve gives rise to weakness confined to abduction and extension of the thumb, and extension of the fingers and extensor carpi ulnaris. This nerve is rarely damaged alone, but may be involved in injuries to the brachial plexus. The median nerve arises from the medial and lateral cords of the brachial plexus and descends with the brachial artery through the upper arm, entering the forearm deep to the bicipital aponeurosis. The median nerve may be injured in the region of the elbow or compressed at the level of the pronator teres muscle. Complete lesions of the median nerve at the elbow give rise to paralysis of pronator teres, the radial flexor of the wrist, the long finger flexors except the ulnar half of the deep flexor, most of the muscles of the thenar eminence, and the two radial lumbricals. Sensory loss is evident over the lateral three and a half digits and the lateral aspect of the palm, although individual variations occur. After a total transection of the nerve in the region of the elbow, even with a satisfactory surgical repair, recovery is slow and rarely complete, particularly with respect to the innervation of the hand. With partial lesions of the median nerve in the arm or forearm, causalgia may be a troublesome consequence. The superficial situation of the median nerve at the wrist renders it liable to injury as a result of lacerations sustained by falling against a window with the hand outstretched or in suicide attempts. Much the most common lesion at this site is the carpal tunnel syndrome, in which the median nerve is compressed as it passes deep to the flexor retinaculum.
The symptoms are usually characteristic, with abnormal signs not being found except in advanced cases. Carpal tunnel syndrome is much more common in women than men and its lifetime prevalence is 10%.
The ulnar nerve arises from the medial cord of the plexus, usually with a contribution from the lateral cord. In the upper arm, branches arise that supply flexor carpi ulnaris and the medial part of flexor digitorum profundus. Total paralysis from lesions at this level, including the branches to flexor carpi ulnaris and flexor digitorum profundus, gives rise to wasting along the medial side of the forearm flexor mass. In the hand, there is wasting of the hypothenar muscles, interossei, and the medial part of the thenar eminence. The ulnar nerve may be damaged by dislocations or fracture dislocations at the elbow and is sometimes compressed in individuals who habitually lean on their elbows.
If the nerve is compressed in the cubital tunnel, exploration and decompression by slitting the aponeurosis may suffice. Damage to the nerve at the wrist will spare the dorsal branch, so that cutaneous sensation over the dorsum of the hand and fingers is spared. It is not always easy on clinical grounds to decide whether the lesion is at the elbow or the wrist.
This nerve arises from the lumbar plexus, crosses the iliac fossa between psoas and iliacus, and enters the thigh deep to the middle of the inguinal ligament.
Damage to the femoral nerve causes weakness of knee extension, wasting of quadriceps, loss of the knee jerk, and sensory impairment over the front of the thigh and in the distribution of the saphenous nerve.
The femoral nerve may be injured in fractures of the pelvis or femur, in dislocations of the hip, and at times during operations on the pelvis or hip. The nerve emerges from the lateral border of psoas, crosses the lateral wall of the pelvis, and enters the thigh through the obturator foramen where it supplies gracilis, adductor longus and brevis, adductor magnus, obturator externus, and sometimes also pectineus, and the skin over the lower medial aspect of the thigh.
Damage to the obturator nerve results in weakness of adduction and internal rotation at the hip, pain in the groin, and sensory impairment on the medial part of the thigh. This nerve arises from the lumbar plexus, passes obliquely across iliacus and enters the thigh under the lateral part of the inguinal ligament. Meralgia paraesthetica is an entrapment neuropathy resulting from compression of this nerve as it passes under the inguinal ligament. The sciatic nerve may be involved in pelvic tumours and can be injured by fractures of the pelvis or femur or during hip replacement operations.
After separating from the peroneal division of the sciatic nerve in the lower thigh, this nerve passes through the popliteal fossa and enters the calf deep to gastrocnemius through the fibrous arch of soleus. When the nerve is interrupted, the patient is unable to plantarflex or invert the foot, flex the toes, or stand on the ball of the foot. The tibial nerve is very occasionally compressed under the flexor retinaculum (tarsal tunnel syndrome), usually precipitated by osteoarthritis or post-traumatic deformities at the ankle, or tenosynovitis.
Morton’s metatarsalgia is a syndrome of severe lancinating pain, usually in one of the web spaces at the base of the toes, especially the third web space.
After separating from the tibial division of the sciatic nerve in the lower part of the thigh, the common peroneal nerve descends through the popliteal fossa, winds around the neck of the fibula, and divides into its superficial and deep branches. Damage to the common peroneal nerve is more frequent than injury to its two branches because of its vulnerable superficial position at the neck of the fibula. The common peroneal nerve may be compressed at the neck of the fibula by habitually sitting with the legs crossed, prolonged squatting, pressure during sleep or while anaesthetized, and various other events. This arises from the sciatic nerve and descends to the back of the calf, winds around to the lateral side of the ankle, and reaches the lateral border of the foot.
Diagnosis of both localized and generalized neuropathies may be confirmed by nerve conduction studies of motor and sensory fibres.
The fascicles are surrounded by a lamellated cellular sheath, the perineurium, which provides a diffusion barrier that separates the intrafascicular or endoneurial compartment from the extracellular tissues. They may provide metabolic support for the axons, which often extend for very considerable distances from their perikarya. Synthesized materials are then transported down the axons to the termination of the fibres by an active transport system. Conditions that lead to the death of the neuron as a whole, with the loss of the cell body and the axon, are categorized as neuronopathies.
The consequence is a selective demyelination with relative preservation of axonal integrity. Initially, the newly formed myelin segments are short and thin, which results in an abnormally slow conduction velocity. The first category comprises lesions of isolated peripheral nerves or nerve roots termed ‘mononeuropathy’ or multiple isolated lesions termed multiple mononeuropathy or multifocal neuropathy.
When such a process affects the spinal roots, or affects the roots as well as the peripheral nerve trunks, the term ‘polyradiculoneuropathy’ is more appropriate. Conduction block is related to demyelination with preservation of axonal continuity (neurapraxia). This results in bilateral foot drop and a ‘steppage’ gait in which an affected individual lifts the feet to an abnormal extent to avoid catching the toes on the ground.
They are usually of a tingling nature (‘pins and needles’), but, especially in ‘small fibre’ neuropathies, may involve thermal sensations, most often with a burning quality. Severe paroxysms of lancinating pain occur in trigeminal neuralgia in which the lesion is at or close to the point of entry of the sensory roots into the pons. It is best performed in centres with special expertise in nerve biopsy because it is an invasive procedure that cannot easily be repeated. When the diaphragm is totally paralysed, the normal protrusion of the upper abdomen during inspiration is lost, or is replaced by retraction (paradoxical movement). The left phrenic nerve then crosses the aortic arch, runs anterior to the root of the lung along the left side of the pericardial sac, and passes to the diaphragm. It is involved in forward movement of the shoulder, as in a rapier thrust, and in elevation of the arm, when it rotates the scapula. It may follow immunizing procedures, in particular the administration of antitetanus serum or operations, or occur without a recognizable antecedent event.
Paralysis of the muscles of the shoulder girdle becomes evident within a day or two of the onset of the pain, sometimes also of the arms or of the diaphragm. If the roots are avulsed, sensory nerve action potentials from affected fingers will be preserved despite total anaesthesia, and the histamine flare response will be preserved in anaesthetized skin. With forcible downward displacement of the shoulder, as when someone is thrown forwards and the shoulder strikes against an obstacle, only the upper part of the plexus, involving the contribution from the fifth and sixth cervical nerve roots, may be damaged.
If the roots are avulsed from the cord, the rhomboids, serratus anterior, levator scapulae, and the scalene muscles will be affected. Where the injury is distal to the dorsal root ganglia, lesions of the upper portion of the brachial plexus recover more satisfactorily than lower plexus lesions. The subclavian artery may be affected by cervical ribs, giving rise to aneurysmal dilatation and vascular symptoms such as Raynaud’s phenomenon and embolic phenomena, but the simultaneous occurrence of both neural and vascular phenomena is rare.
Occasionally, there is selective wasting of the thenar pad in the hand, mimicking to some extent the appearance of carpal tunnel syndrome. The most common is involvement of the lower part of the plexus by an apical carcinoma of the lung (Pancoast’s tumour), which gives rise to wasting and weakness of the small hand muscles and of the medial forearm wrist and finger flexors, pain and sensory loss affecting the medial border of the forearm and hand, and cervical sympathetic paralysis. The most frequent type of injury is compression of the nerve in the middle third of the arm against the humerus. Supinator is spared, together with brachioradialis and the radial wrist extensors, and there is no sensory loss.
It supplies deltoid and teres minor and the skin over deltoid through the upper lateral brachial cutaneous nerve. It supplies coracobrachialis, biceps, and brachialis, and the skin over the lateral aspect of the forearm through the lateral cutaneous nerve of the forearm.
In brief, there is an inability to flex the index finger and the distal phalanx of the thumb, flexion of the middle finger is weak, and opposition of the thumb is defective.
There is almost complete anaesthesia over the two terminal phalanges of the index and middle fingers.

The skin in the distribution of the median nerve tends to become reddened, dry, and atrophic. It may also be damaged as an occupational hazard by individuals who exert repeated pressure on the butt of the hand. The usual presentation is with acroparaesthesiae, which consist of numbness, tingling, and burning sensations felt in the hand and fingers; the pain sometimes radiates up the forearm as far as the elbow or even as high as the shoulder or root of the neck. At times percussion over the carpal tunnel may elicit Tinel’s sign, or symptoms may be provoked by hyperextension of the wrist or sustained flexion (Phalen’s sign). It descends in the medial side of the upper arm, passes around the elbow in the ulnar groove, and enters the forearm under an aponeurotic band between the humeral and ulnar heads of flexor carpi ulnaris. In the forearm, the dorsal branch arises, winds around the ulna and supplies the skin over the dorsal aspect of the hand and the medial one and a half fingers. Movements of abduction and adduction of the fingers are weak, as is adduction of the extended thumb against the palm. Entrapment may occur in the cubital tunnel as the nerve underlies the aponeurotic band between the two heads of flexor carpi ulnaris.
When it is suspected that the nerve has been subjected to repeated compression at the elbow, surgical transposition to the front of the medial epicondyle should be considered.
A lesion just proximal to the wrist will give rise to sensory impairment on the palmar aspect of the hand and fingers alone, and weakness of all the ulnar-innervated intrinsic hand muscles. Compression of the nerve in the cubital tunnel, for example, may spare the branches to flexor carpi ulnaris and flexor digitorum profundus. The plexus may be involved in pelvic malignancy, such as from carcinoma of the uterine cervix, bladder, prostate, or rectum, or be the site of a local neural tumour.
In the iliac fossa it supplies iliacus and, in the thigh, pectineus, sartorius, and quadriceps femoris, and anterior cutaneous branches to the front of the thigh. With a proximal lesion, there may also be weakness of hip flexion from paralysis of iliacus.
The nerve may be involved in pelvic fractures, hip and pelvic surgery, and neoplastic infiltration, and can be damaged by the fetal head or forceps during parturition. It is composed of the tibial and peroneal divisions which are usually bound together within a common sheath, the tibial division lying medially. Walking is possible, but the patient cannot stand on the toes or the heel of the affected foot and the ankle is unstable. After the radial and ulnar, it is implicated in gunshot wounds more frequently than any other nerve. It descends through the calf to the medial side of the ankle, passes beneath the flexor retinaculum, and divides into the medial and lateral plantar nerves. Burning pain and tingling paraesthesiae occur in the sole, usually after prolonged standing or walking. The superficial peroneal nerve passes down in front of the fibula, supplies peroneus longus and brevis, and emerges in the lower leg, supplying the skin on the lateral aspect of the lower leg. It gives rise to foot drop, with paralysis both of dorsiflexion and eversion at the ankle and of toe extension. It can be damaged by traction caused by fractures of the tibia and fibula, and is sometimes damaged by ischaemia in the anterior tibial compartment syndrome. Simple investigations for diabetes mellitus, B12 deficiency and common medical causes are sufficient for the diagnosis of many cases. Peripheral nerve trunks usually consist of several fascicles bound together by the mainly collagenous epineurial connective tissue. In myelinated fibres, the myelin segments are derived by the spiralling of the surface membrane of Schwann cells around the axons.
This pattern is seen in many toxic neuropathies and neuropathies due to nutritional deficiency.
This may be restricted to the region of the nodes of Ranvier (paranodal demyelination) or involve whole internodal segments (segmental demyelination) with consequent conduction block.
The lesions in a widespread multifocal neuropathy may summate to produce a symmetrical disturbance, but the history or a careful examination may indicate the involvement of individual nerves. In general terms, polyneuropathies result from causes that act diffusely on the peripheral nervous system, such as metabolic disturbances, toxic agents, deficiency states, and some autoimmune disorders. Involvement of the upper limbs begins with weakness and wasting of the small hand muscles, and usually weakness of the finger and wrist extensors, before the forearm flexor muscles. Causalgia constitutes a particularly troublesome painful syndrome, most often after injuries of the median nerve, lower trunk of the brachial plexus, or tibial nerve. Conduction may be examined in motor and sensory nerve fibres, and can give evidence of both localized and generalized neuropathies. Also, special processing and staining techniques are necessary to avoid fixation artefacts and provide high-quality immunohistochemistry, morphology, and electron microscopy.
Radiographically, paralysis may be detected by unilateral or bilateral elevation of the diaphragm in a chest radiograph and its failure to descend on inspiration.
When serratus anterior is paralysed in isolation, the position of the scapula is almost normal at rest but, if the extended arm is pushed forward against resistance, ‘winging’ of the scapula becomes more evident.
It can occur on a genetic basis as an autosomal dominant disorder, hereditary neuralgic amyotrophy, with variable penetrance. It can be difficult to distinguish from tumour recurrence but is less likely to be painful.
This follows from the fact that the nerve fibres are interrupted proximal to the dorsal root ganglia and therefore the peripheral sensory axons do not degenerate.
This may also be encountered as a birth injury from traction on the head, or on the trunk in a breech presentation (Erb’s palsy), and rarely in anaesthetized patients during surgery or in individuals carrying heavy rucksacks.
The arm hangs at the side, internally rotated at the shoulder, with the elbow extended and the forearm pronated in the ‘waiter’s tip’ position. Numbness, pain, and paraesthesiae occur along the inner border of the forearm and hand, extending into the medial two fingers. Other tumours that may invade the brachial plexus include carcinoma of the breast and malignant lymphomas affecting the lymph glands in the root of the neck.
In the upper arm, it supplies triceps and anconeus, and the skin on the back of the arm, just above the elbow through the posterior cutaneous nerve of the arm.
This is encountered as ‘Saturday night palsy’ in which an individual falls asleep when intoxicated with the upper arm over the arm of a chair. Owing to the flexed position of the wrist, gripping is impaired, but, if the power of the wrist and finger flexors is tested with the wrist extended, it can be shown to be normal. It may be damaged in injuries to the shoulder and the chief symptom is an almost complete inability to raise the arm at the shoulder.
Flexion at the elbow is still possible by brachioradialis, but is weak, and sensation may be impaired along the radial border of the forearm. It supplies all the muscles in the anterior aspect of the forearm except flexor carpi ulnaris and the medial half of flexor digitorum profundus. The appearance of the hand has been described as simian; it shows ulnar deviation, the index and middle fingers are more extended than normal, and the thumb lies in the same plane as the fingers. Paralysis of the wrist flexors is evident when attempts are made to flex against resistance. This degree of sensory loss, combined with the motor deficit, renders the thumb and index fingers almost useless and makes paralysis of the median the most serious single nerve lesion in the upper limb.
The pulp of the affected fingers becomes atrophic and ulceration occasionally develops in the tip of the index finger.
The paraesthesiae are sometimes restricted to the radial fingers, but may affect all the digits because some fibres from the median nerve are distributed to the fifth finger through communication with the ulnar nerve in the palm. It may develop as a consequence of involvement of the wrist joint in rheumatoid arthritis or osteoarthritis, or deformity related to an old fracture. It then runs superficial to flexor digitorum profundus to the wrist and enters the hand between the pisiform bone and the hook of the hamate, superficial to flexor retinaculum. In the hand, a superficial branch supplies palmaris brevis and the skin over the medial aspect of the palm and the medial one and half fingers. If the proximal portions of these fingers are held immobilized, flexion of the terminal phalanges is not possible. Sensory loss affects the dorsal and palmar aspects of the medial side of the hand and the medial one and a half fingers.
This is most likely to occur in those performing heavy manual work or if there is an excessive carrying angle at the elbow, as may occur after a previous malunited supracondylar fracture of the humerus (‘tardy ulnar palsy’). Decompression of the nerve is the safer operation because transposition puts the blood supply of the nerve at risk.
A slightly more distal lesion spares the superficial branch of the nerve and therefore produces no sensory deficit. In these circumstances, nerve conduction studies may be helpful, as they may in distinguishing between lesions of the ulnar nerve and damage to the eighth cervical and first thoracic spinal roots.
It may be compressed by a haematoma in patients receiving anticoagulant therapy or who have haemophilia, or be involved in fractures of the pelvis.
The continuation of the femoral nerve is the saphenous nerve, which supplies the skin over the medial aspect of the lower leg as far as the medial malleolus.
It is commonly involved in large psoas muscle haematomas in individuals with haemophilia and in diabetic amyotrophy.
The symptoms consist of numbness in the territory of the nerve, combined with tingling or burning paraesthesiae provoked by prolonged standing or after excessive walking. It descends through the posterior aspect of the thigh, initially deep to gluteus maximus, and supplies semitendinosus, semimembranosus, and the long head of biceps through its peroneal division. It supplies popliteus, all the muscles of the calf, and, through the plantar nerves, the small muscles of the sole of the foot and sensation to the sole.
It crosses the extensor retinaculum and supplies the skin on the dorsum of the foot and the second to fifth toes.
Cutaneous sensation is impaired over the lateral aspect of the lower leg and ankle, and on the dorsum of the foot.
Paralysis caused by external pressure frequently gives rise to a local conduction block with satisfactory recovery within a few weeks. Sensory impairment occasionally results from pressure on the nerve as it lies in a superficial situation in the back of the calf.
Cerebrospinal fluid examination, may be useful—especially in suspected inflammatory demyelinating polyradiculopathy. The nutrient vessels connect with a longitudinal anastomotic network of arterioles and venules in the epineurium.
The axon is exposed at the nodes of Ranvier, which represent the gaps between adjacent myelin segments. The system is bidirectional: there is also a retrograde system transporting materials, including neurotrophic factors, back from the periphery to the cell body. A selective effect on axonal conduction is seen in poisoning with tetrodotoxin, which blocks the sodium channels at the nodes. In these conditions, the axonal breakdown may result either from interference with enzymes involved in glycolysis which provide the metabolic energy for axonal transport mechanisms, or from cofactor deficiency or inactivation. The selective myelin damage may occur, for example, as the result of a cell-mediated attack on myelin by sensitized mononuclear cells, which is a possible explanation for the acute inflammatory demyelinating polyradiculoneuropathy (AIDP) form of Guillain–Barre syndrome.
Isolated or multiple isolated peripheral nerve lesions arise from conditions that produce localized damage, such as mechanical injury, nerve entrapment, thermal, electrical, or radiation injury, vascular causes, granulomatous, neoplastic, or other infiltrations, and nerve tumours.
Isolated nerve lesions may sometimes be superimposed on a symmetrical polyneuropathy, as a consequence, for example, of pressure lesions in a patient confined to bed. At times, a symmetrical involvement of the proximal limb muscles occurs in peripheral nerve disorders, e.g. It is a severe persistent pain, often with a burning quality, which may be aggravated by emotional factors. Severely reduced conduction velocity may occur as a result of segmental demyelination or because of conduction in regenerating axons of small calibre after axonal degeneration. The protein concentration is also usually increased in Guillain–Barre syndrome, especially after the first week, whereas the cell count remains normal or only shows a small number of lymphocytes. The phrenic nerve may be involved in its course through the neck or thorax by wounds or tumours such as bronchial carcinoma, and it is sometimes affected in idiopathic brachial plexus neuropathy (neuralgic amyotrophy). This is often caused by mutations in the gene encoding septin-9, a cytoskeletal filament-forming protein involved in the mitotic spindle. More distal upper limb muscles may at times be affected, as may the phrenic nerve and, occasionally, the recurrent laryngeal nerve. Corticosteroids do not appear to influence the initial pain but may improve the ultimate outcome but this needs confirmation with a randomized controlled trial which is now in progress. Selective injury to the lower part of the plexus involving the contributions from the eighth cervical and first thoracic nerve roots occurs as a result of traction with the arm extended, as when an individual falls from a height and tries to save himself by hanging on to a ledge. In Erb’s form of birth injury, weakness of abduction at the shoulder and flexion at the elbow often persist, although there may be little residual sensory loss. The pain tends to be provoked by carrying heavy articles with the hand on the affected side. The lateral aspect of the lower part of the upper arm is supplied by the lower lateral brachial cutaneous branch and the dorsal aspect of the forearm, by the posterior cutaneous nerve of the forearm. Triceps is spared, but brachioradialis, supinator, and all the forearm extensor muscles are paralysed.
The action of the interossei in abducting and adducting the fingers is also feeble when the wrist is flexed, but full power is demonstrable if these muscles are tested with the hand resting flat on a table so that the fingers are maintained in extension.
This is formed by a sharp band of fibrous tissue, which binds together the superficial and deep heads of the supinator muscle as they arise from the lateral epicondyle of the humerus and lateral border of the radius. The main trunk of the nerve supplies pronator teres, flexor carpi radialis, palmaris longus, and flexor digitorum superficialis.
The tendon of flexor carpi ulnaris stands out alone and the hand goes into ulnar deviation. Upon this may be superimposed severe paroxysms of pain provoked by either touching or jarring the limb or emotional distress. The attacks of pain and paraesthesiae are most common at night and often wake the patient from sleep.
Predisposing causes are pregnancy, obesity, myxoedema, acromegaly, and infiltration of the flexor retinaculum in primary and hereditary amyloidosis. After penetrating the hypothenar muscles, its deep branch crosses the palm and ends in flexor pollicis brevis.

The deep branch, after supplying the hypothenar muscles, innervates interossei, the third and fourth lumbricals, adductor pollicis, and part of flexor pollicis brevis.
When the hand is flexed to the ulnar side against resistance, the tendon of flexor carpi ulnaris is not palpable. The medial wall of the cubital tunnel is formed by the elbow joint; osteoarthritis of the elbow can lead to osteophytic encroachment on the tunnel and compression of the ulnar nerve.
Finally, damage to the deep palmar branch spares the hypothenar muscles, but causes weakness of the other ulnar-innervated small hand muscles.
The lumbosacral cord may be compressed against the rim of the pelvis by the fetal head during parturition, with consequent weakness of the anterior tibial and peroneal muscles, and sensory impairment in the distribution of the fourth and fifth lumbar dermatomes.
Owing to the rapid dispersion of the branches in the thigh, partial lesions are common from wounds at this site.
It separates into the tibial and common peroneal nerves in the lower thigh, which supply all the muscles below the knee, and both nerves contribute to the formation of the sural nerve. Incomplete lesions of the nerve may be caused by pressure of the nerve against the hard edge of a chair in individuals who fall asleep while intoxicated. Careful examination may demonstrate wasting of the intrinsic muscles in the medial aspect of the foot, and sensory impairment over the sole. The deep peroneal branch continues to wind around the fibula, pierces the anterior intermuscular septum, and descends on the anterior interosseous membrane. This nerve is the one most commonly chosen on the rare occasions when a nerve biopsy is needed. When the diagnosis is not revealed by simple tests an extensive range of investigations for rare causes may be needed. This, in turn, communicates through perforating vessels with a longitudinal, intrafascicular, capillary anastomotic network. Conduction in unmyelinated axons takes place by the spread of a continuous wave of depolarization, the action potential, which migrates along the axolemma. The retrograde system may be involved in the regulation of protein synthesis in the cell body and probably carries the signal for chromatolysis, which follows transection. As the enzymes are synthesized in the cell bodies and then transported down the axons, the further the distance from the cell body the greater the likelihood of metabolic insufficiency occurring.
Another instance is in diphtheritic neuropathy where the demyelination is secondary to an interference with Schwann cell protein metabolism. In certain peripheral nerve disorders, there is an abnormal susceptibility to pressure lesions. In the first, the impairment predominantly affects the sensations of joint position, vibration and light touch, corresponding to a predominant loss of function in the larger myelinated nerve fibres. Painful stimuli may give rise to an excessive or hyperpathic response, in which a mildly painful stimulus, e.g. The cell count is usually increased in neuropathies associated with HIV infection and in Lyme disease. The nerve to serratus anterior may be involved in penetrating wounds, but usually in association with damage to the brachial plexus. It may also occur as a birth injury following traction with the arm extended (Klumpke’s paralysis), but is less common than upper plexus damage. Muscular branches of the radial nerve innervate brachioradialis and extensor carpi radialis longus and brevis.
Surgical exploration and decompression should be performed if the palsy lasts more than 12?weeks. Through the anterior interosseus branch, it also supplies the lateral aspect of flexor digitorum profundus, flexor pollicis longus, and pronator quadratus. A twin study has shown a strong genetic component to the development of carpal tunnel syndrome. In the cubital tunnel syndrome, the ulnar nerve is often palpably enlarged in the ulnar groove and for a short distance proximally. Lesions at the wrist or in the hand are usually the result of compression by ganglia or by repeated occupational trauma. The nerve to quadriceps is most often injured, and the resulting paralysis causes considerable difficulty in walking because the knee cannot be locked in extension and gives way, especially when descending stairs.
The skin is completely anaesthetized over the entire foot except for the medial border which is supplied by the saphenous nerve. Similar lesions may occur in people with diabetes, in whom the peripheral nerves are more susceptible to pressure neuropathy. Injury to the distal portion of the nerve by a penetrating injury or deep wound of the calf gives rise to paralysis of the intrinsic muscles of the foot but spares the muscles acting at the ankle. It innervates tibialis anterior, extensor digitorum longus, extensor hallucis longus, and peroneus tertius. Nerve biopsy is rarely required and is principally useful for the detection of vasculitis which cannot be diagnosed in any less invasive way. This anastomotic system is extremely efficient: experimentally it is very difficult to produce ischaemia of nerve trunks by ligation of nutrient vessels.
In myelinated fibres, because of the high electrical resistance of the lipid in the myelin lamellae, the generation of the action potential is restricted to the nodes of Ranvier.
This probably accounts for the distal distribution of many such neuropathies, because longer axons will be more vulnerable.
Local compression by a tourniquet also gives rise to selective damage to myelin through mechanical effects, although more severe pressure causes axonal interruption. If axonal interruption takes place, axonal degeneration occurs below the site of interruption. Fasciculation due to spontaneous contraction of isolated motor units is most often a feature of anterior horn cell disease but may be encountered in peripheral neuropathies, as may muscle cramps.
Loss of joint position sensation may cause sensory ataxia, which can resemble that in cerebellar disease. Sensory loss affects the lateral aspect of the shoulder and upper arm and the radial border of the forearm. Nerve conduction studies are helpful when there are difficulties in distinguishing a cervical rib syndrome from a lesion of the ulnar or median nerves on clinical grounds.
Commonly the lesion consists of a localized conduction block so that muscle wasting does not occur and a muscle response can be obtained on electrical stimulation of the nerve below the level of the lesion. The main trunk passes deep to the flexor retinaculum of the wrist and its recurrent muscular branch supplies abductor pollicis brevis and opponens pollicis, and contributes to the innervation of flexor pollicis brevis. The hand tends to feel numb and useless on waking in the morning but recovers after it has been used for some minutes.
Paralysis of interossei and the medial two lumbricals gives rise to the ‘claw-hand’ deformity.
Damage to the deep palmar branch, for example, may be caused by firm pressure in the palm from a screwdriver or drill.
Orthoses are often tried and decompressive operations or excision of the neuroma is commonly recommended without adequate evidence to determine which is the best treatment.
It passes deep to the extensor retinaculum after which it supplies extensor digitorum brevis and the skin of the adjacent sides of the first and second toes. The occurrence of an ischaemic neuropathy therefore implies widespread vascular insufficiency. Conduction is therefore saltatory, jumping from one node to the next by local currents that traverse the axon and the extracellular tissue fluid. In diffuse demyelinating neuropathies, the distribution of the clinical effects, as for distal axonal neuropathies, is often maximal peripherally. Postural tremor, mainly affecting the upper limbs and resembling essential tremor, may be seen in patients with chronic demyelinating polyneuropathies with slow conduction velocity. With repeated stimulation at the same site, the pain that is felt may spread widely and reach an intolerable intensity. Serratus anterior weakness is a common component of idiopathic brachial plexus neuropathy (neuralgic amyotrophy) and it is not infrequently encountered as an isolated and unexplained lesion. Selective paralysis of the lower brachial plexus (C8, T1) results in paralysis of all the intrinsic hand muscles and a consequent claw-hand deformity, weakness of the medial finger and wrist flexors, and sensory loss along the medial border of the forearm and hand and over the medial two fingers. Early recognition and the application of measures to reduce the risk of joint contractures are important.
Surgical removal of the rib or fibrous band often leads to abolition of the pain and paraesthesiae, but recovery of power in the small hand muscles is usually disappointing.
It descends along the radial border of the forearm and supplies the skin over the dorsum of the hand and the thumb, index, and middle fingers. It also supplies the lateral two lumbrical muscles, the skin of the lateral aspect of the palm, and the lateral three and a half digits over their palmar aspects and terminal parts of their dorsal aspects. Flexion at the metacarpophalangeal joints is possible in all fingers, including the index, and flexion at these joints with extension at the interphalangeal joints is accomplished by interossei and the lumbricals.
The patient adopts a protective attitude towards the limb, so that fixation of the joints of the fingers and wrist may develop, together with atrophic changes in the skin and subcutaneous tissue. The symptoms may recur during the day after use, or at times if the patient sits with the hands immobile and hanging down. The action of these muscles is to flex the fingers at the metacarpophalangeal joints with the fingers extended at the interphalangeal joints. Here the enlargement of the nerve tends to be maximal at a little distance above the elbow. If occupational pressure is the cause, recovery follows cessation of the precipitating cause.
The anaesthesia extends upwards on the posterolateral aspect of the calf in its lower two-thirds. If the injury is distal to the origin of the branches to flexor hallucis longus and flexor digitorum longus, the lesion may escape detection because paralysis of the small foot muscles and sensory loss over the sole may be overlooked. A blood–nerve barrier, comparable to the blood–brain barrier, exists in peripheral nerves (except in the sensory and autonomic ganglia and at motor nerve terminals). In many distal axonal neuropathies that involve the peripheral nervous system, not only does the degeneration affect the distal parts of the motor and sensory axons in the periphery, but also the terminal parts of the centrally directed axons derived from the dorsal root ganglion cells degenerate. Presumably, this is a statistical effect: the longer the nerve fibre, the more likely it is to develop a region of demyelinating conduction block.
If the interruption is reversible, recovery has to take place by axonal regeneration which is often slow and incomplete. An unusual symptom encountered most often in uraemic neuropathy is that of ‘restless legs’. Cervical sympathetic paralysis, giving rise to Horner’s syndrome, is frequently associated. Surgical treatment may be considered soon after the injury in cases where the nerve roots have been avulsed. The deep branch forms the posterior interosseus nerve which winds around the lateral aspect of the radius, passes through supinator, which it supplies, and innervates extensor digitorum, extensor digiti minimi, extensor carpi ulnaris, and often extensor carpi radialis brevis, abductor pollicis longus, extensor pollicis longus and brevis, and extensor indicis.
If the proximal phalanx of the thumb is immobilized, it will be found that flexion of the terminal phalanx is abolished because of paralysis of flexor pollicis longus. Such symptoms of acroparaesthesiae may persist for many years without the appearance of symptoms of median nerve damage. In claw hand, the posture of the fingers is opposite to this, namely extension of the metacarpophalangeal joints with flexion at the interphalangeal joints.
Should improvement fail to occur after an appropriate interval, surgical exploration to establish whether a ganglion is present is merited. Rare instances of idiopathic lumbosacral plexopathy are encountered, comparable to the corresponding disorder that affects the brachial plexus.
This, together with the diffusion barrier provided by the perineurium, regulates the composition of the endoneurial connective tissue fluid and thus the ionic environment of the nerve fibres.
An important recovery mechanism in conditions in which muscles become partially denervated is reinnervation of denervated muscle fibres by collateral sprouting from the remaining intact axons. A rare manifestation of peripheral neuropathy is the occurrence of continuous repetitive discharges in motor nerve fibres, leading to generalized muscular rigidity or ‘neuromyotonia’ (Isaacs’ syndrome, continuous motor unit activity syndrome). In the second pattern of selective sensory loss, pain and temperature sensibility are predominantly affected, often associated with loss of autonomic function, corresponding to a predominant loss of small myelinated and unmyelinated axons. Affected individuals experience sensations in the feet and legs that they find difficult to describe but which are temporarily relieved by moving them. A comparable disorder can affect the lumbosacral plexus (idiopathic lumbosacral plexopathy).
At times, there is some associated axonal degeneration so that electromyographic evidence of denervation is detectable and full recovery is correspondingly delayed. Paralysis of the thenar muscles gives rise to defective abduction and opposition of the thumb.
In some patients, weakness of the thenar muscles develops, particularly of abduction of the thumb, and is associated with atrophy of the lateral aspect of the thenar eminence. Although all the interossei are paralysed, the defect is seen mainly in the ulnar fingers because the radial lumbricals supplied by the median nerve are still active.
Beyond this area of complete anaesthesia, there is a wide zone in which sensibility may be diminished.
By means of the adductor, the thumb can be drawn into the palm, but, as the radial fingers cannot be flexed or the thumb opposed, it is impossible to place the tip of the thumb on the fingers.
The long extensors of the fingers, being unopposed, overextend the proximal joints, and flexor digitorum superficialis flexes the proximal interphalangeal joints. Sweating is absent on the sole and dorsum of the foot, but is preserved on the medial side. Neuropathy from iminodipropionitrile blocks the slow axonal transport system and leads to large swellings in the proximal parts of the axons that contain aggregations of neurofilaments (proximal axonopathy).
Occasionally patients present with symptoms of median nerve deficit in the hand without attacks of acroparaesthesiae having occurred, or motor and sensory signs may be discovered incidentally in the absence of symptoms, particularly in older individuals.

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