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Thread: Peripheral nerve lesions

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    Post Peripheral nerve lesions

    Structure
    4.1 Anatomical structure of peripheral nerves
    4.2 Types of nerve injury
    4.3 Clinical features
    4.4 Management
    4.5 Axillary nerve lesion
    4.6 Ulnar nerve lesions
    4.7 Median nerve lesions
    4.8 Radial nerve lesions
    4.9 Femoral nerve lesions
    4.10 Sciatic nerve lesions
    4.11 Common Peroneal nerve lesions
    4.12 Polyneuropathies (polyneuritis)
    4.13 Guillain-Barre syndrome


    4.1 Anatomical structure of peripheral nerves

    A spinal nerve is formed by the union of a ventral nerve root and a dorsal nerve root and then, after emerging from the intervertebral foramen, it divides into a dorsal ramus and a ventral ramus. The dorsal rami are generally smaller than the ventral rami and supply the muscles and skin of the posterior region of the neck and trunk. Because of their position and the manner in which they supply structures they are not as often damaged as the ventral rami. So the lesions discussed in this chapter concern peripheral nerves formed by the ventral rami. The ventral rami form nerves passing to the upper and lower limbs and the anterolateral aspects of the trunk. Those in the upper cervical region unite to form the cervical plexus and those in the lower cervical region plus the first thoracic ramus unite to form the brachial plexus. The plexuses then divide into nerves which supply the head, neck and upper limbs. In the lumbar and sacral regions the rami form the lumbar and sacral plexuses which then supply the lower part of the trunk and the lower limbs. The rami in the thoracic region run separately and are segmentally arranged in their supply to tne upper and lateral aspects of the thorax.

    The fibres forming a peripheral nerve are derived from the somatic and autonomic nervous systems. They are divided into three classes according to their size and rate of conduction. Class A are the largest, fastest conducting and are comprised of somatic efferent and afferent fibres. Class B are myelinated preganglionic autonomic fibres. Class C are nonmyelinated slow-conducting autonomic and sensory fibres.

    A peripheral nerve comprises nerve fibres arranged in bundles called fasciculi. Each fasciculus may contain anything from a few fibres to hundreds depending on the size of the nerve and the structures that it supplies. Likewise the number of fasciculi forming a nerve vary in size and number. Each fasciculus is surrounded by a connective tissue sheath of perineurium, and extending between the nerve fibres is a rather more delicate connective tissue called endoneurium. Binding the fasciculi together is a more fibrous connective tissue called the epineurium.

    In both myelinated and non-myelinated fibres there are a large number of Schwann cells which surround the axon, or in some instances a number of axons may be invaginated in the Schwann cells. In the myelinated fibres there is an extension of the Schwann cell cytoplasm - the myelin sheath - which wraps itself round the axon. The nodes of Ranvier are gaps between adjacent Schwann cells and these occur at regular intervals along the fibre. The axolemma is exposed at the nodes of Ranvier and it is this arrangement that allows the fast conduction that occurs as the impulse leaps from node to node by saltatory conduction.

    4.2 Types of nerve injury

    These will depend on the nature and degree of the initial trauma.

    Compression injury of a nerve

    The pressure on a nerve can be brief, prolonged or intermittent and may be classified as a neuropraxia or an axonotmesis.

    Neuropraxia - This is due to a brief intermittent or possibly longer pressure which causes minimal or no structural damage and recovery should occur within a few weeks.

    Axonotmesis - Prolonged or chronic recurrent pressure may cause degeneration of the nerve. Recovery will take considerably longer as the nerve fibre (or fibres) has to grow from just above the lesion to its destination. Sometimes stretching of a nerve causes disruption of the axon and consequent degeneration. The chances of recovery are much greater with an axonotmesis than with a severed nerve because the nerve sheath is intact.

    Severance of a nerve - neurotmesis

    This occurs when the axon, Schwann cell and myelin sheath are severed, and degeneration takes place.

    Mixed lesions

    As a nerve consists of many fibres damage can consist of a mixture of the above types of lesions, which may make diagnosis and treatment more difficult.

    Pathological changes

    Brief pressure on a nerve resulting in a loss of conduction is due to ischaemia and is rapidly reversible. For example, sitting with one leg crossed over the other for a short period may result in a temporary loss of conduction in the common peroneal nerve.

    A longer term compression injury may result in a mechanical displacement of the nodes of Ranvier with stretching of the paranodal myelin. Provided that the pressure is released before any structural changes have taken place recovery will occur in a few weeks.

    Sometimes pressure may be intermittent and result in a niixed segmental demyelination and remyelination. This type of lesion can affect the ulnar nerve at the elbow, or the median nerve as it passes through the carpal tunnel.

    Severance of a nerve may be partial or complete. In either case those nerve fibres that are severed will undergo Wallerian degeneration.

    Wallerian degeneration

    The changes take place in the nerve fibres from the point of severance distally to the effector or receptor organ and proximally to the node of Ranvier above the incision. Although the initial degeneration starts at the site of the lesion subsequent changes occur simultaneously down the length of the nerve fibre. Recent studies have shown that the sequence of events occurs more quickly than was previously described. Originally it was thought that there was biochemical stability for at least a week after the disruption of the fibres. Now it has been shown that there is an increase in the concentration of hydrolytic enzymes within 12 hours of the injury which is associated with the loss of the basic protein from the sheath.

    The myelin sheath breaks down into fatty droplets within the Schwann cell cytoplasm. These droplets are subsequently extruded into the endoneurial space and phagocytosed by macrophages. As this process occurs the Schwann cells begin to proliferate, especially around the gap produced when there is severance of the nerve. The axon breaks down and the debris is removed. These changes take place within 14-21 days after the injury, and the end result is an empty endoneurial tube with the proliferating Schwann cells.

    Changes occur in the cell body of the neuron and can be seen as a reduction in the number of Nissl granules and a movement of the nucleoli towards the periphery of the nucleus. However, provided that the cell is not destroyed these changes are reversible and are linked with the subsequent regrowth of the axon.

    Regeneration

    Regrowth of the axon will take place down the endoneurial tube provided that it is intact. However, when there is severance of the nerve, and consequently a gap in the tube at the site of the lesion, regeneration is unlikely to be successful unless the nerve is sutured. The proliferation of the Schwann cells, which occurs down the length of the tube and particularly at the point of severance, helps to guide the axon down the tube and they may bridge the gap if the disruption is not too severe. The stump of the axon develops a swelling and from this a number of fibres grow into the surrounding tissue. One of these may enter and grow down the empty neural tube, if there is good apposition, whilst the others will eventually disappear. Thus it can be seen why an axonotmesis has a good chance of recovery. But the chance of obtaining good apposition of the fibre relative to an empty neural tube following severance of the nerve is not good, although recent advances in microsurgery have improved the level of recovery. Also the degree of recovery will depend on the type of neurons in the nerve fibre. Mixed nerves, containing afferent and efferent fibres, are a greater problem than those containing only one type of fibre. For example, a fibre from a sensory neuron could grow down an endoneurial tube which terminates on an effector organ and so be useless, and similarly a fibre from a motor neuron would be useless in growing to a receptor organ. Another factor that could stop regeneration is the presence of scar tissue which could block the pathway of the growing axon. If the nerve is severed a long way from some of the muscles that it innervates then degeneration of the muscle fibres may take place before the regenerating nerve reaches the end organ. This could occur with a lesion of the sciatic nerve when the motor fibres that supply the intrinsic muscles of the foot are severed. Lesions of a nerve fibre close to the cell body may result in irreversible damage to the cell, and then regeneration will not occur.

    During regeneration the axon will grow at the rate of 1-2 mm a day, although the rate will tend to be a little slower as it extends further away from the cell body. Thus it is possible to measure the length of the nerve from the lesion and estimate the time that it will take for the fibre to grow down the tube and when some recovery might be expected. Before function can recur the myelin sheath and nodes of Ranvier must be re-formed. Also the axon and myelin sheath need to recover sufficient diameter for transmission to take place. So any calculations of recovery time must take all of these factors into account.

    4.3 Clinical features

    The severity of these will depend on the extent of the neurological damage and upon the type of lesion.

    Somatic motor function Paralysis

    The extent of the paralysis will depend on which nerves have been damaged. A lesion of the median

    nerve in the axilla would result in paralysis of all the muscles supplied by the median below the level of the lesion. However, it would be less if the median nerve were severed at the wrist or only a branch of the nerve affected. The paralysis may be partial, as for example when some of the fibres to a muscle are intact but others are damaged, resulting in muscle weakness. Paralysis of muscles will result in the loss of tendon reflexes.

    Weak muscles

    A neuropraxia may sometimes cause a weakness of muscles rather than a paralysis. When some muscles which work as part of a group are paralysed then the other muscles may become weak because they are unable to function normally. This may apply to movements of a whole limb when activity is impossible because of the paralysis of one or more groups of muscles.

    As regeneration of a nerve occurs and contraction of a muscle becomes possible there will be a period of muscle weakness until it can be strengthened to full power again.

    Somatic sensory function

    If somatic afferent nerve fibres are damaged then the modalities of pain, touch, pressure and temperature may be affected. There is a considerable overlap in the sensory distribution of nerves and so the area of sensory loss may not be as large as anticipated.

    Anaesthesia - This is a loss of sensation in the area affected which can cause considerable disturbance of function depending on the area affected and the extent of the anaesthesia. The hand is a particular problem and may suffer further injury if the patient is not made fully aware of the difficulties arising from the sensory loss.

    Dysaesthesia - Incomplete lesions may lead to a disturbance in sensation, resulting in numbness and tingling. During re-innervation there is initially a hypersensitivity (hyperaesthesia) which gradually returns to a more normal sensation.

    Analgesia - Complete lesions affecting fibres giving sensations of pain may result in analgesia.

    Hyperpathia - Pain is a feature in some lesions, especially if it is an incomplete lesion. Sometimes pain can be very acute, particularly if sympathetic fibres are involved (causalgia).

    Autonomic disturbances

    These result in the loss of the normal function of sweating, and the skin becomes dry and scaly. The local circulation is affected partly by interference with the sympathetic innervation of blood vessels and partly because of the loss of normal movement.

    These disturbances may result in the development of trophic lesions although these may also develop as the result of damage to an anaesthetic area.

    Contractures

    Contractures of muscle may occur as the result of an imbalance between normal and paralysed groups. Muscles that are paralysed for a prolonged period may undergo fibrous degeneration. Contractures can occur because of damage to soft-tissue structures or because adhesions develop in tendon sheaths or around joints.

    Prognosis

    The outlook following a neuropraxia is good, and there should be full recovery, which is usually within a few weeks but occasionally may take longer. The prognosis for an axonotmesis is also quite good although full function is not always achieved. A neurotmesis is quite a different problem, and the prognosis depends on many factors; for example:

    1. There may be associated injuries, and treating the nerve lesion may not be the first priority.

    2. There may be infection.

    3. If the nerve ends are clean and in good apposition then the results of surgery are likely to be better.

    4. The results after a mixed nerve lesion are not as good as with an unmixed nerve.

    5. If the lesion is close to the effector and/or receptor organs the result is likely to be better.

    6. The age and general health of the patient.

    Even if all the factors are favourable to recovery it is unusual to obtain better than a 60% recovery.

    4.4 Management

    This will depend on the cause of the injury and the type of the lesion. Often there are associated injuries of bones, joints, and/or soft tissues, so the surgeon may have to deal with a complex situation in which the nerve injury is only one of a number of injuries. This chapter is dealing with peripheral nerve lesions, and so other injuries will be alluded to only when they are the cause of the lesion or they have a specific effect on the total management.

    Diagnosis

    If paralysis of muscles supplied by a particular nerve has occurred it is important to ascertain the type of nerve lesion so that suitable treatment may be arranged. In some cases where there is a wound or surgical intervention is required, because of a fracture or other damage, the surgeon will be able to see whether there is an neurotmesis. Otherwise electromyographic tests can be used to find out whether the nerve is conducting. Sensory testing will be carried out to discover the degree of sensory impairment.

    Treatment

    Once the type of lesion has been confirmed then treatment can be arranged. Neither a neuropraxia nor an axonotmesis will require surgical intervention unless there is a need to relieve pressure on the nerve. A neurotmesis will need to be sutured if there is to be any chance of recovery.

    There must be an integrated plan of treatment and all the health care professionals in the team must have regular discussions so that progress is carefully monitored. Whenever possible and appropriate the patient should be involved as a member of the team, or if not one of the members of the team should have a counselling role.

    Physiotherapy management

    Neuropraxia

    This may not require any treatment as recovery is likely to occur with in a few weeks. However, a patient may need advice on carrying out as much movement of the limb as possible and reassurance about the gradual recovery of normal function. Occasionally with an apparent neuropraxia a few fibres may be more extensively damaged (axonotmesis) with resulting degeneration, and then more treatment may be required.

    Axonotmesis and neurotmesis

    Assessment

    The initial assessment is very important in determining management. The physiotherapist needs to know the history, the likely prognosis, the proposed medical or surgical management, and how much detail has been explained to the patient. If the nerve has been sutured, following a neurotmesis, it must not be stretched for 2-3 weeks and so it may not be possible to carry out a full assessment.

    During the subjective examination the physiotherapist can assess the reaction of the patient to the injury and their motivation towards recovery. An assessment will be made of the problems as seen by the patient in relation to the activities of daily living, their occupation and leisure activities. This will be linked with the problems as seen by the physiotherapist following the physical examination and taken into account in formulating the treatment programme.

    If only some of the muscles in a group action are paralysed then the movement may be produced but with reduced power. Some patients adapt quickly to a loss of movement and may perform trick movements, whilst others may have more disability than the loss of muscle power would seem to indicate. The latter may be due to sensory loss, and it is important to check the extent of this very carefully.

    An examination of the sensory modalities will reveal which modalities are altered by the lesion. Areas of anaesthesia can be shown on a diagram of the limb or body. When an area of anaesthesia is present the test should start in this area and move towards the normal part (Tinel’s test), otherwise once the patient has felt touch in a normal area they may imagine that they can feel it in the anaesthetized part. There may be areas of

    The examiner should note alterations in the colour and text ire of the skin, loss of muscle bulk and any deformities.

    Functional loss will depend on the extent of the lesion and the particular muscle groups affected. For example, a lesion of the radial nerve will allow very little use of the hand even though the flexors and intrinsic muscles are still innervated.

    Electrical tests

    The use of electromyographic tests for diagnosis has already been mentioned. The physiotherapist may also use forms of modified direct current to test nerve/muscle reactions. If there is a normal nerve conduction to a muscle then the electric impulse will stimulate the nerve directly. A strength-duration curve may be plotted on a graph by starting with a long duration pulse and using the minimum intensity of current to produce a response (rheobase) and then gradually decreasing the duration of the pulse until a response can no longer be obtained. A chronaxie is the minimum duration of impulse that will produce a response with a current of double the rheobase.

    Denervated muscle can be stimulated directly but the shorter the pulse the greater is the intensity needed to produce a contraction. Eventually the pulse is too short to produce a response regardless of the intensity of the current and the graph shows complete reaction of degeneration. Sometimes a variable number of nerve fibres supplying a muscle have escaped damage whilst others have been severed. When this happens the strength-duration curve shows a combination of a normal curve and that of degeneration. If more nerve fibres become degenerated the ’kink’ in the curve will move to the left. As the nerve starts to regenerate and some nerve fibres are remyelinated a similar curve showing partial innervation will develop, and the ’kink’ in the curve will move to the right.

    If the muscle tissue degenerates to fibrous tissue there will be no response to any type of electrical stimulation, which is known as the absolute reaction of degeneration.

    Electrical tests are not carried out for the first week or two as the changes of degeneration may not be complete and the tests could give a false picture of the changes.

    Once the examination has been carried out and the findings have been considered, a plan of treatment can be arranged. The goals must be realistic and take into account the future needs of the patient. For example, paralysis of the muscles in the dominant hand might mean the loss of livelihood to a patient unless a good recovery is achieved. The level of recovery needed will vary according to the occupation, as some patients may undertake their type of work with an incomplete recovery whereas others such as concert pianists could not continue to play to the standard required. The problem of waiting several months to know how much recovery they will achieve may be very difficult for a patient to cope with and the therapist will have to consider this aspect in management.





    Principles of treatment

    Initial care during stage of paralysis

    There are certain basic aims of treatment and these can be modified or altered depending on the specific lesion and the assessment of the individual patient.

    To prevent or reduce oedema

    The patient must be shown how to position the limb, particularly when at rest, and be given general advice on preventing oedema. There may be a problem if there are other associated injuries that prevent suitable positioning and movement.

    Movement is very important because of the pumping action of the muscles on the vessels and the active movement of joints, which stretches and compresses vessels thus maintaining an adequate circulation. If this is not possible passive movements will help to maintain the circulation. Massage may be given to reduce the oedema, ideally with the limb in the elevated position.

    To maintain the circulation in the affected area

    A slowing of the circulation will reduce the effective supply of nutrition to the tissues and removal of waste products. Active movements are the best means of preventing this slowing but passive movements and massage will help if there is paralysis.

    To prevent contractures

    It is essential to prevent the development of any contractures which would impede recovery. Passive movements must be carried out to maintain the full range of joint movements and to maintain the full length of muscles. The latter is particularly important when muscles work over more than one joint as the muscles must be stretched over both joints at the same time. Passive movements must be carried out daily as stiffness can develop very quickly. A patient may be able to carry out their own passive movements, or they may be performed by a relative, but the physiotherapist must ensure that full movements and full stretch of muscles is being maintained.

    To maintain activity and power of unaffected muscles

    The patient must be encouraged to use the unaffected muscles in the limb. If this is not possible because of the paralysis the physiotherapist may be able to facilitate movement by supporting the limb, or functional splinting may allow movements to occur.

    At one time electrical stimulation in the form of interrupted direct current was used to try to prevent muscle fibrosis and maintain contractility. However, recovery seemed to be as good using the other techniques described and so this was no longer used. Recent research has shown that there may be some value in using some of the new current forms, such as pulsed electromagnetic energy, and some authorities advocate the use of this.

    To maintain function

    As indicated above the patient must be encouraged to use the limb as much as possible. The use of well-designed and well-applied lively splints (functional splints) may allow some functional activity.

    To look after areas where there is any sensory disturbance

    The patient must be told how to care for areas of anaesthesia. If a lesion of the skin and soft tissues occurs it may be difficult to heal and will impede recovery.

    Stage of recovery

    In a mixed nerve the recovery programme will include both motor and sensory re-education. Depending on the particular nerve and the extent of the sensory and motor loss the re-education can be equally important, especially in the case of the hand.

    Muscle re-education

    During the performance of passive movements before any recovery occurs it is useful for the patient to think about the movement provided that it does not cause too much anxiety. It is difficult to predict the recovery time exactly for the reasons given above, but as the anticipated time approaches it is useful to start using methods of initiating a contraction. When a successful outcome is doubtful the physiotherapist must be careful not to raise the hopes of the patient too high.

    Initiation of a contraction

    There are many techniques that can be used to try to stimulate a contraction. As some of these depend on sensory stimulation this may be part of the sensory re-education.

    A muscle works in a number of ways - as an agonist, or fixator, or synergist - and attempts should be made to use it in all of these actions. During recovery a muscle may work as a fixator or synergist before it will work as an agonist. A muscle may work with one group of muscles to produce one movement and with another group to produce a different action. For example, the extensor carpi ulnaris will work with the flexor carpi ulnaris to produce ulnar deviation and with the extensor carpi radialis longus and brevis to produce wrist extension. Thus all actions should be attempted when trying to initiate a contraction. It is also important to try to irradiate impulses to the affected muscles by demanding maximal effort from normal muscles that work with them. For example, to stimulate the finger flexors using the eating pattern maximal resistance could be given to the elbow and shoulder components (flexor adduction lateral rotation pattern - proprioceptive neuromuscular facilitation (PNF) technique).

    Other methods of initiating a contraction include a quick stretch, tendon tapping, brief ice or quick brushing.


    Muscle strengthening

    Once there is a flicker of contraction recorded as grade 1 on the MRC scale then the muscles can be strengthened through the grades of this scale. Once there is a perceptible contraction the number of these must be counted and gradually progressed. As free movement becomes possible the number of movements, firstly with gravity and later against gravity, must be recorded and progressed. Maximal effort must be demanded if an effective programme of recovery is to be achieved. The muscles should be worked in all their actions.

    Once external resistance to movement can be used a form of progressive resistance exercise can be used either by manual resistance (PNF) or by the use of weights. If weights are used there is some controversy as to the most suitable programme. Some authorities recommend one maximum contraction per treatment as being the most effective whereas others advocate a 10-repetition maximum.

    It is necessary to remember that endurance is an important part of functional activity, and reeducation of this factor demands a high-repetition, low-resistance scheme.

    The strength and endurance required will differ from one patient to another depending on their occupation, leisure activities and age. Usually younger patients will rehabilitate more quickly than older patients.

    Muscle coordination

    Movement must be smooth and well coordinated to allow normal function.

    Functional activities

    The level of normal functional activitiy regained will depend on the extent of the recovery. When this is full the patient should be able to resume their normal occupation and leisure activities. However, if recovery is limited a careful asessment must be made to see whether the patient is capable of their original employment and other activities. If their previous employment is not possible then the patient must be counselled and an assessment made for a change of occupation if this is practical.

    Following suture of the nerve

    The rehabilitation programme will have to be modified for the first 2-3 weeks following the suture as the nerve must not be stretched. In some instances a splint may be applied to prevent movement.

    Minimal or no recovery after the lesion

    The physiotherapist must try to achieve optimum function. Sometimes functional splinting may help to give a reasonable level of activity. However, a number of patients do not like appliances and would prefer to manage without. The surgeon may consider further surgery to try to improve function.

    Specific lesions of nerves

    Upper extremity

    4.5 Axillary nerve lesion

    This is not a common lesion but it can occur associated with injuries around the shoulder, in particular a dislocated shoulder or a fracture of the surgical neck of the humerus. Usually the type of lesion is a neuropraxia or axonotmesis rather than a neurotmesis, as the nerve is likely to be stretched or compressed by the lesion rather than severed.

    Sensory re-education

    Some of this is integrally linked with motor re-education, as mentioned above. However, specific attempts can be made to stimulate sensation particularly in lesions affecting the hand. The techniques will depend on the modality that is being re-educated. For example, the patient may try to identify different objects by shape and texture with their eyes closed. If proprioception is affected the patient can try to identify the position of the limb or part of the limb, again with the eyes closed.

    Clinical features

    The main functional disability due to the nerve lesion is the inability to abduct the arm because of paralysis of the deltoid. A number of patients will develop a trick movement, enabling them to lift the arm up.

    The muscle will waste. This can be observed by the loss of contour over the shoulder which is normally provided by the bulk of the deltoid. The sensory loss is minimal because of the overlap of sensory supply, but there is a small area of anaesthesia over the lower part of the muscle.



    Specific points of management

    The orthopaedic surgeon will reduce the dislocation; or if the associated injury is a fracture of the surgical neck this will be managed. Usually these injuries do not require open surgery anc so the nerve will not be examined, but intervenvlon will probably not be required if the lesion is a neuropraxia or an axonotmesis.

    Physiotherapy

    Passive abduction of the shoulder should be carried out with care, because of the associated injury, as soon as the surgeon permits it. The physiotherapist must ascertain that there is a full range of other movements, particularly lateral rotation.

    If the lesion is a neuropraxia recovery should occur within a few weeks although progress may be a little slower than following an uncomplicated dislocation. Following an axonotmesis progress will be much slower because of the nerve degeneration. It is essential to keep full passive movements until the nerve regenerates and the muscle can be strengthened.

    It should be remembered that many of the patients with these injuries are older and so there is a greater danger of a stiff shoulder developing.

    4.6 Ulnar nerve lesion

    The nerve may be injured in the axilla by pressure such as that caused by falling asleep with the arm over the back of a chair or, in patients using axillary crutches, by the pressure of the crutch. Occasionally there could be injury due to a wound. At the elbow the nerve could be stretched or torn when a fracture or dislocation takes place. Later, following these injuries the nerve could be compressed by scar tissue or callus formation. Injury at the wrist usually occurs as the result of direct trauma caused by a cut or wound.

    Clinical features

    Lesion in the forearm or above - This will cause paralysis of the flexor carpi ulnaris and the medial half of the flexor profundus digitorum. This will result in weakening of ulnar deviation and the loss of flexion of the terminal phalanges of the third and fourth fingers. In the hand there will be paralysis of the following small muscles: abductor digiti minimi, flexor digiti minimi, opponens digiti minimi, the interossei, the third and fourth lumbricals, adductor pollicis and usually flexor pollicis brevis. This results in a loss of the ability to abduct and adduct the fingers, and to flex the third and fourth fingers at the meta carpo phalangeal joints while the interphalangeal joints are extended. This disability severely limits the use of the hand, particularly in a power grip. The loss of the adductor pollicis and flexor pollicis brevis will weaken the pinch grip.

    The sensory loss will depend on the level of the lesion: if it is at the elbow the palmar cutaneous, the dorsal cutaneous and the superficial terminal branches will all be affected. This will give an area of anaesthesia on the ulnar side of the hand, on both palmar and dorsal aspects, and on the little, ring and part of the middle fingers.

    If the lesion is at the wrist the paralysis will affect only the muscles in the hand, and the sensory loss may affect only the fingers unless the injury has also severed the dorsal and palmar cutaneous nerves.

    Specific points of management

    If scar tissue or callus formation is causing pressure at the elbow this will be dealt with by the surgeon and there should be a full recovery unless the pressure has been prolonged.

    Lesions resulting in a neurotmesis will need to be sutured. When degeneration of the nerve has caused paralysis of the muscles in the hand a functional splint may be given to the patient. This comprises a light padded bar across the dorsal aspect of the proximal phalanges of the third and fourth fingers and a similar one over the upper end of the metacarpals. These are attached to another padded bar in the palm of the hand by a small spring which pulls the metacarpophalangeal joints into flexion but allows the patient to extend the joints.


    Physiotherapy

    The paralysis will impede most activities of the hand, which will be particularly incapacitating if it is the dominant hand. The functional splint described above may allow reasonable use of the hand if the patient is encouraged and taught how to use it.

    The sensory loss can cause problems and the patient must be warned to be careful of activities using the ulnar side of the hand, for example taking something out of the oven.

    If the nerve has to be sutured at the elbow this will not normally interfere with treatment to the hand. However, a lesion at the wrist may require a modified treatment in the early stage to avoid stretching the nerve. There will probably be damage to other structures, possibly the median nerve and/or flexor tendons, which will complicate the rehabilitation.
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    4.7 Median nerve lesions

    The median nerve can be damaged in any part of its course but the commonest lesions are in the region of the wrist. Lacerations in this area that cause a lesion of the nerve are often combined with a lesion of the ulnar nerve and damage to the flexor tendons. The other type of lesion is a compression of median nerve in the carpal tunnel.


    Laceration at the wrist causing a neurotmesis

    Clinical features

    The muscles paralysed are those of the thenar eminence, abductor pollicis brevis and opponens pollicis (the flexor pollicis brevis is usually supplied by the ulnar nerve), and the first two lumbricals. As a result of this the thumb lies back on the same plane as the fingers, producing the deformity known as the monkey hand (main en singe).

    The sensory loss gives anaesthesia of the lateral side of the palm of the hand and the palmar surface of u.e thumb, index, middle and half the ring fingers. Sometimes there is a disturbance rather than a loss of sensation which may cause hyperaesthesia and pain.

    Trophic changes are often apparent in this lesion which may be due to the large number of vasomotor fibres in the nerve and in part may be due to damage to the area because of the lack of sensation.

    Specific points of management

    The nerve will be sutured and the wrist maintained in flexion for approximately 3 weeks. Following this the patient will be supplied with a lively splint to keep the thumb in partial opposition which should enable the patient to use the hand. The splint consists of a strap round the wrist and another round the proximal part of the thumb. The two bands are connected by an elastic band which pulls the thumb into partial opposition and yet allows the patient to extend and abduct the thumb.

    Physiotherapy

    Passive movements must be given to all movements of the thumb. The patient may be taught to do the movements but care must be taken that they are properly carried out.

    The patient must be given instructions about the care of areas of anaesthesia. When a lively splint is fitted the patient can be encouraged to use the hand as much as possible. Motor and sensory reeducation must be given to try to regain normal function.

    Carpal tunnel compression

    This may occur in women in the fourth or fifth decade and may be the result of soft-tissue changes, particularly swelling of synovial sheaths. It is also a complication that occurs with rheumatoid arthritis.

    Clinical feature
    The early problems may be largely sensory, with pain and tingling in the area of sensory supply. Later there may be an area of anaesthesia and paralysis of the muscles mentioned under laceration at the wrist.

    Management

    Surgical division of the flexor retinaculum will give relief of compression. This is usually followed by complete recovery of sensation and almost full function.

    4.8 Radial nerve lesions

    Lesions in the axilla may be due to compression or, more rarely, a wound. Pressure can be ’caused by falling asleep with the arm over the back of a chair, or in the case of patients using axillary crutches it may be due to incorrect use of the crutches.

    Fractures of the mid-shaft of the humerus may cause a lesion of the nerve because of its position in the humeral sulcus. This could be a neurotmesis, axonotmesis or neuropraxia. A neuropraxia is sometimes a late complication following this fracture if there is a lot of callus formation.

    Supracondylar fractures of the humerus or fracture dislocations of the elbow may injure the radial nerve.

    Clinical features

    A lesion of the nerve below the axilla will result in paralysis of the following muscles: brachioradialis, extensors carpi radialis longus and brevis, supinator, extensor digitorum, extensor digiti minimi, extensor carpi ulnaris, extensor pollicis longus, extensor indicis, abductor pollicis longus and extensor pollicis brevis. The main problem is the inability to extend the wrist and fingers. The loss of the synergistic action of the wrist extensors prevents the patient using the finger flexors adequately to grip. If the lesion is in the axilla there may be a slight weakness of the triceps.

    The sensory loss causes minimal disability in this lesion as the area of anaesthesia would be on the dorsal aspect of the hand apart from a tiny area on the anterolateral side of the thenar eminence.


    Specific points of management

    If the injury results in a neurotmesis the nerve will have to be sutured. A lively splint will be fitted when possible to allow functional use of the hand. This comprises a leather (or other suitable material) support for the forearm incorporating a metal bar on the lateral side. This has a spring hinge at the wrist and a horizontal bar which goes across the palm to keep the wrist in extension. Thus the patient can use the finger flexors but also can actively flex the wrist.



    Physiotherapy

    Passive movements are very important in this lesion both to maintain joint range and muscle length. A number of the muscles work over more than one joint and must be fully stretched otherwise it may be difficult to gain good function even if regeneration of the nerve occurs. If the patient is going to do their own passive movements these points must be emphasized, and the physiotherapist must see that they are being carried out properly.

    Re-education will be related mainly to motor function.

    The above lesions are those that are most commonly seen. Any others will demand basic principles of management and any specific points depending on the lesion. It is worth mentioning three other lesions, but details of management will not be given here:

    1. Brachial plexus lesion - These are usually traction injuries or may be caused by a wound. There may be damage to all the roots of the plexus: C5, C6, Cl, C8, and Tl.

    2. Erb’s palsy - Usually this is the result of a birth injury and damages the fibres of the 5th and 6th cervical nerves.

    3. Klumpke’s paralysis - This may be caused by sudden traction or possibly a birth injury and damages fibres from C8 and Tl. Birth injuries are not as common now with better obstetric

    4.9 Femoral nerve lesions

    This nerve is seldom damaged but if it were, the result would be a paralysis of the quadriceps and anaesthesia over most of the anterior aspect of the thigh and the medial side of the lower leg and foot.

    4.10 Sciatic nerve

    It is fortunate that the whole nerve is seldom injured, as the resulting functional loss is so considerable. Occasionally it may be damaged as the result of a traumatic posterior dislocation of the hip joint. If the whole nerve is damaged the paralysis will affect the hamstrings and all the muscles of the lower leg and foot. There will be a sensory loss of the whole of the lower leg and foot except for the Medial side.

    4.11 Common peroneal nerve

    This is the most commonly injured of the nerves in the leg and usually occurs as the result of injury round the neck of the fibula. The lesion may occur as a complication of fractures of the neck of the fibula or lateral tibial condyle, or there may be compression by splints or plaster of Paris. The injury may affect the common peroneal or one of the two branches. The deep peroneal nerve is the most likely to be damaged.


    Clinical features

    If the common peroneal nerve is damaged there will be paralysis of the tibialis anterior, extensor hallucis longus, extensor digitorum, peroneus longus, peroneus brevis and peroneus tertius. This will give a loss of dorsiflexion, extension of the toes and eversion. Inversion will be weak because of the paralysis of the tibialis anterior. Hence the patient will tend to drag the foot when walking and to avoid this usually flexes the hip and knee, thus giving a high-stepping gait. The sensory loss is over the lateral side of the lower leg and the dorsum of the foot, but this does not cause any functional disability.

    When only the deep peroneal nerve is damaged the peroneus longus and brevis are not paralysed and so eversion can occur in the plantar flexed position. The functional disability in walking will be the same as with the common peroneal lesion. The sensory loss is much less, only affecting the web between the big toe and second toe.

    Specific points of management

    It is important that a patient is carefully watched after the application of a splint or plaster so that any loss of toe extension can be seen or any altered sensation on the dorsal aspect of the toes noted. If any loss is observed then the pressure can be relieved and there should be full recovery. If the trauma has caused a neurotmesis then this will be sutured. Following this the patient may be supplied with a light-weight plastic splint which prevents the foot dropping into plantar flexion. This can be worn inside the shoe, the splint passing from the sole of the foot under the heel and up the back of the calf where it may be kept in place with straps and Velcro fastenings. A splint may be necessary at night to stop the foot falling into plantar flexion for a prolonged period which could result in a contracture of the calf muscles.

    Physiotherapy

    A neuropraxia may not require any treatment, but when there is degeneration of the nerve it is important to keep full-range passive movements especially of dorsiflexion. If the patient is able to walk this will help to keep a stretch on the tendo-calcaneum.

    During the stage of paralysis the physiotherapist must ensure that the patient walks as well as the disability allows, particularly when the patient is wearing a splint to keep the foot in dorsiflexion.

    As regeneration occurs the muscles must be strengthened and normal function regained. The extent of re-education will depend on the needs of the patient both at work and for leisure activities.

    4.12 Polyneuropathies (polyneuritis)

    As the name implies this disorder results in a widespread dysfunction of the peripheral nerves and affects both somatic and visceral systems. There are a number of known causes but some causal agents are unknown particularly in the neuropathies produced by metabolic defects. Direct infection is rare but indirect infection such as occurs in the Landry-Guillain-Barre syndrome is relatively common. This is a post-infective polyneuropathy and seems to be the result of an autoimmune response following a viral infection or an allergen. Metabolic causes include toxic substances, such as some of the heavy metals; one of the side-effects of some drugs can be a polyneuropathy; lack of certain vitamins such as B] and B12; and some endocrine disorders, the most common of which is diabetes. Vascular disorders such as atheroma can lead to a polyneuropathy because of the upset in blood supply to the nerve fibres. Collagen disorders, for example reheumatoid arthritis and polyarteritis nodosa, can develop a polyneuropathy. There are also genetic disorders, for example peroneal muscular dystrophy.

    The method of onset will vary depending on the cause, and so an infective or post-infective polyneuropathy will have an acute or subacute onset. Some metabolic disorders may give an acute or subacute onset although endocrine disturbances such as diabetes tend to be more chronic. Vascular and collagen diseases usually have an insidious development.

    Pathology

    Depending on the cause of the condition there are two different pathological processes that can take place:

    1. Axonal degeneration - The nerve cell body and the axon are affected, and the process is similar to Wallerian degeneration. If regeneration occurs it is not complete and recovery is slow. Axonal degeneration tends to occur in neuropathies with the following causes: poisons, nutritional deficiences, ischaemia.

    2. Segmental demyelination - This affects the Schwann cell, resulting in a demyelination. Recovery is more likely to occur in this type of lesion and if it does it happens quickly and is usually complete. This type of process may occur with a diabetic neuropathy and the GuillainBarre syndrome.

    Clinical features

    An early feature is often sensory with the patient complaining of pain, tingling, and numbness, which usually occur in the hands and feet. Muscle weakness and/or paralysis occurs mainly in the limbs, and the lower more than the upper limbs. It is more marked distally than proximally and often results in a foot drop or wrist drop.

    Contractures develop early and there may be fibrous adhesions. Loss of proprioception gives an ataxia which can be observed if the patient has some active movement, and is particularly marked in the lower limbs giving the patient a high-stepping gait.

    The tendon reflexes will be decreased or lost. Trophic changes may lead to the skin appearing red and shiny, and there may be increased sweating and oedema. Sometimes there can be cardiac involvement resulting in cardiac arrhythmia.

    Some of the cranial nerves can be affected in certain neuropathies.

    4.13 Guillain-Barre syndrome

    Usually this has an acute onset although sometimes it is subacute, and the patient may have a fever. The paralysis starts distally and moves proximally. Also it may affect the trunk and head muscles. Respiratory and bulbar paralysis may be a complication of this condition.

    Sensory changes are variable and may be severe, with hyperalgia and hyperaesthesia, or there may be some cases with no sensory disturbance.

    Management

    This will depend on the cause of the neuropathy. Improved safety precautions in industry have decreased the incidence of cases due to heavy metals or chemicals. Careful testing of drugs should reduce side-effects such as polyneuropathy. Polyneuropathies resulting from vitamin deficiencies may recover or the progress be halted if the deficiency is remedied. Polyneuropathies from vascular or collagen diseases are unlikely to recover although drug therapy may slow the progress of the disease. Patients with the Guillain-Barre syndrome will usually recover fully although the rate of recovery may be slow. Nevertheless there can be fatalities with this syndrome particularly when there is an epidemic. Some of these patients with respiratory and bulbar problems will have to be treated in an intensive care unit.

    Physiotherapy

    In cases where there is little chance of recovery the main objective is to retain as much function as possible. It is important to prevent the development of contractures, and so passive movements to maintain joint range and muscle length must be given regularly. These are necessary to assist the circulation as deep vein thrombosis can be a complication particularly with loss of movement and the effect of the muscle pump. The patient probably cannot perform his own passive movements and if not it may be possible to teach a relative to do them. The patient must be taught correct positioning and support for sitting and lying and the importance of moving to prevent any pressure sores. The patient or relatives) must be taught to look for any evidence of pressure causing reddening of the skin.

    Light-weight splints may be given to keep the correct position of joints, and in some cases to assist function, but these must be padded and care must be taken to see that that they do not cause pressure sores.

    Pain and hyperaesthesia may present a problem in performing passive movements; consequently techniques and positioning may have to be modified. If analgesics a^e given to relieve pain, treatment should be carried out when relief of pain has occurred, if possible.

    When recovery is occurring re-education of sensory and motor function should be carried out using the appropriate techniques. Coordination exercises may be given if the patient is ataxic.

    Patients must be helped to gain their maximum potential, both psychologically and physically.

    Physiotherapy in the intensive therapy unit

    Physiotherapy in the intensive therapy unit will be similar to that described elsewhere. Apart from respiratory care particular attention must be given to passive movements and maintaining a good functional position of the joints. Pain and hyperaesthesia may be a problem as mentioned above in treatment for general polyneuropathies. Both nursing and physiotherapy staff will be concerned in the prevention of pressure sores.

    Once the patient recovers sufficiently to leave the intensive therapy unit recovery may begin, and the physiotherapist will be concerned with motor and sensory (if needed) re-education. This progress is likely to be slow, and it is important that the patient is aware of this as he is likely to become depressed and frustrated unless sufficient counseling and support is given by the professionals concerned. Improvements must be carefully charted so that the patient and therapist are aware of the points of recovery.
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    I must thank you for your nice and useful post in this forum.
    Main motto of our learning should be "Learn to Serve and Share". So let me also share something.

    Types of symptoms of nerve lesions can be broadly divided into:
    1. Positive Symptoms: This means the symptoms which should not be present normally are present. Eg. Fibrillation and fasciculation
    2. Negative symptoms: This means symptoms which should normally be present are absent. Eg. Loss of tone

    The concept of this classification was given by Hugling Jackson.

    The symptoms like fasciculation and fibrillation are commonly referred to as Dancing of a dying nerve.

    On the other hand the symptoms like tingling are referred to as weeping of a dying nerve

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