Peripheral Nerve Disorders pdf - D. Jamal

DR. JAMAL AL-SAIDY

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Peripheral Nerve Disorders

Nerve Structure And Function



Peripheral nerves are bundles of axons conducting efferent (motor) impulses from

cells in the anterior horn of the spinal cord to the muscles, and afferent (sensory)
impulses from peripheral receptors via cells in the posterior root ganglia to the
cord.



They also convey sudomotor and vasomotor fibres from ganglion cells in the

sympathetic chain.



Some nerves are predominantly motor, some predominantly sensory; the larger

trunks are mixed.



Each axon is, in reality, an extension or elongated process of a nerve cell, or

neuron.



In the peripheral nerves, all motor axons and the large sensory axons serving

touch, pain and proprioception are coated with myelin, a multilayered lipoprotein
membrane derived from the accompanying Schwann cells.



Every few millimetres the myelin sheath is interrupted, leaving short segments of

bare axon called the nodes of Ranvier.



Depletion of the myelin sheath causes slowing – and eventually complete

blocking – of axonal conduction.



Outside the Schwann cell membrane the axon is covered by a connective tissue

stocking, the endoneurium.



The axons that make up a nerve are separated into bundles (fascicles) by fairly

dense membranous tissue, the perineurium.



The groups of fascicles that make up a nerve trunk are enclosed in an even thicker

connective tissue coat, the epineurium.



The nerve is richly supplied by blood vessels that run longitudinally in the

epineurium before penetrating the various layers to become the endoneurial
capillaries.



The tiny blood vessels have their own sympathetic nerve supply coming from the

parent nerve, and stimulation of these fibres (causing intraneural vasoconstriction)
may be important in conditions such as reflex sympathetic dystrophy and other
unusual pain syndromes.

Pathology



Nerves can be injured by :



ischaemia,



compression,



traction,



laceration



burning.



Damage varies in severity from transient and quickly recoverable loss of function
to complete interruption and degeneration :-

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M.B.CH.B…F.I.C.M.S

TYPES

Transient Ischaemia



Acute nerve compression causes numbness and tingling within 15
minutes, loss of pain sensibility after 30 minutes and muscle weakness
after 45 minutes.



Relief of compression is followed by intense paraesthesiae lasting up to 5
minutes (the familiar ‘pins and needles’ after a limb ‘goes to sleep’);
feeling is restored within 30 seconds and full muscle power after about 10
minutes.



These changes are due to transient endoneurial anoxia and they leave no
trace of nerve damage.

Neurapraxia



Seddon (1942) coined the term ‘neurapraxia’ to describe a reversible
physiological nerve conduction block in which there is loss of some types
of sensation and muscle power followed by spontaneous recovery after a
few days or weeks. It is due to mechanical pressure causing segmental
demyelination and is seen typically in ‘crutch palsy’, pressure paralysis in
states of drunkenness (‘Saturday night palsy’) and the milder types of
tourniquet palsy.

Axonotmesis

 This is a more severe form of nerve injury, seen typically after closed

fractures and dislocations. The term means, literally, axonal interruption.
There is loss of conduction but the nerve is in continuity and the neural
tubes are intact. Distal to the lesion, and for a few millimetres retrograde,
axons disintegrate and are resorbed by phagocytes. This wallerian
degeneration (named after the physiologist, Augustus Waller, who
described the process in 1851).

 The axonal processes grow at a speed of 1–2 mm per day.

Neurotmesis

 In Seddon’s original classification, neurotmesis meant division of the

nerve trunk, such as may occur in an open wound, recovery will not occur.

 Regenerating fibres mingle with proliferating Schwann cells and

fibroblasts in a jumbled knot, or ‘neuroma’, at the site of injury.

The ‘Double Crush’ Phenomenon

There is convincing evidence that proximal compression of a peripheral nerve renders it
more susceptible to the effects of a second, more peripheral injury. This may explain why
peripheral entrapment syndromes are often associated with cervical or lumbar
spondylosis. A similar type of ‘sensitization’ is seen in patients with peripheral
neuropathy due to diabetes or alcoholism.

Classification Of Nerve Injuries

Seddon’s description of the three different types of nerve injury (neurapraxia,
axonotmesis and neurotmesis) served as a useful classification for many years.
Increasingly, however, it has been recognized that many cases fall into an area

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somewhere between axonotmesis and neurotmesis. Therefore, following Sunderland
(1978), a more practical classification is offered here:

First degree injury

This embraces transient ischaemia and neurapraxia, the effects of which
are reversible.

II.

Second degree injury

This corresponds to Seddon’s axonotmesis. Axonal degeneration takes

place but, because the endoneurium is preserved, regeneration can lead to
complete, or near complete, recovery without the need for intervention.

III.

Third degree injury

This is worse than axonotmesis. The endoneurium is disrupted but the
perineurial sheaths are intact and internal damage is limited.

IV.

Fourth degree injury

Only the epineurium is intact. The nerve trunk is still in continuity but
internal damage is severe. Recovery is unlikely; the injured segment
should be excised and the nerve repaired or grafted.

Fifth degree injury

The nerve is divided and will have to be repaired.

Clinical Features

 Acute nerve injuries



are easily missed, especially if associated with fractures or dislocations.



Always test for nerve injuries following any significant trauma.



If a nerve injury is present, it is crucial also to look for an accompanying

vascular injury.



Ask the patient if there is numbness, paraesthesia or muscle weakness in

the related area.



Then examine the injured limb systematically for signs of abnormal

posture (e.g. a wrist drop in radial nerve palsy), weak-ness in specific
muscle groups and changes in sensibility.



The neurological examination must be repeated at intervals so as not to

miss signs which appear hours after the original injury, or following
manipulation or operation.

 In chronic nerve injuries



The anaesthetic skin may be smooth and shiny, with evidence of

diminished sensibility such as cigarette burns of the thumb in median
nerve palsy or foot ulcers with sciatic nerve palsy.



Muscle groups will be wasted.



Postural deformities may become fixed.

Motor Power Is Graded : -

0   No contraction.
1   A flicker of activity.
2   Muscle contraction but unable to overcome gravity.

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3   Contraction able to overcome gravity.
4   Contraction against resistance.
5   Normal power.

Principles Of Treatment

Nerve exploration
 Closed low energy injuries usually recover spontaneously.
 Exploration is indicated:

(1) if the nerve was seen to be divided and needs to be repaired
(2) if the type of injury (e.g. a knife wound or a high energy injury)
suggests that the nerve has been divided or severely damaged.
(3) if recovery is inappropriately delayed and the diagnosis is in doubt.

 Vascular injuries, unstable fractures, contaminated soft tissues and tendon

divisions should be dealt with before the nerve lesion.

Primary repair
  A divided nerve is best repaired as soon as this can be done safely.
   Primary suture at the time of wound toilet has considerable advantages.:z
Delayed repair
  Late repair, i.e. weeks or months after the injury, may be indicated because:

(1) a closed injury was left alone but shows no sign of recovery at the
expected time;
(2) the diagnosis was missed and the patient presents late
(3) primary repair has failed.

Nerve grafting
 Free autogenous nerve grafts can be used to bridge gaps too large for direct

suture.

 The sural nerve is most commonly used; up to 40 cm can be obtained from each

leg.

Nerve transfer
 The spinal accessory nerve can be transferred to the suprascapular nerve.
 intercostal nerves can be transferred to the musculocutaneous nerve.

Care of paralysed parts
 While recovery is awaited the skin must be protected from friction damage and

burns.

 The joints should be moved through their full range twice daily to prevent

stiffness.

 ‘Dynamic’ splints may be helpful.

Tendon transfers
 Motor recovery may not occur if the axons, regenerating at about 1 mm per day,

do not reach the muscle within 18–24 months of injury.

 In such circumstances, tendon transfers should be considered.

DR. JAMAL AL-SAIDY

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PROGNOSIS



Type of lesion Neurapraxia always recovers fully; axonotmesis may or may not;

neurotmesis will not unless the nerve is repaired.



Level of lesion The higher the lesion, the worse the prognosis.



Type of nerve Purely motor or purely sensory nerves recover better than mixed

nerves, because there is less likelihood of axonal confusion.



Size of gap Above the critical resection length, suture is not successful.



Age Children do better than adults. Old people do poorly.



Delay in suture This is a most important adverse factor. The best results are

obtained with early nerve repair. After a few months, recovery following suture
becomes progressively less likely.



Associated lesions Damage to vessels, tendons and other structures makes it

more difficult to obtain recovery of a useful limb even if the nerve itself recovers.



Surgical techniques, skill, experience and suitable facilities are needed to treat

nerve injuries. If these are lacking, it is wiser to perform the essential wound toi-
let and then transfer the patient to a specialized centre.

REGIONAL SURVEY OF NERVE

INJURIES

Brachial Plexus Injuries

Pathological Anatomy

 The brachial plexus is formed by the confluence of nerve roots from C5 to T1

 It is vulnerable to injury –either a stab wound or severe traction caused by a fall

on the side of the neck or the shoulder.

 Traction injuries are generally occur in motorcycle accidents: his neck and

shoulder are wrenched apart.

 In the most severe injuries the arm is practically avulsed from the trunk, with

rupture of the subclavian artery.

 An important distinction is made between preganglionic and postganglionic

lesions.

 Avulsion of a nerve root from the spinal cord is a preganglionic lesion, i.e.

disruption proximal to the dorsal root ganglion; this cannot recover and it is
surgically irreparable.

 Rupture of a nerve root distal to the ganglion, or of a trunk or peripheral nerve, is

a postganglionic lesion, which is surgically reparable and potentially capable of
recovery.

 Brachial plexus injuries are often overshadowed by other, life-threatening trauma

which needs immediate attention. Associated injuries, such as rupture of the
subclavian or axillary artery, should be sought and attended to.

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The Level Of The Lesion

 Upper plexus injuries: the shoulder abductors and external rotators and the

forearm supinators are paralysed. Sensory loss involves the outer aspect of the
arm and forearm.

 Lower plexus injuries: are rare, the Wrist and finger flexors are weak and the

intrinsic hand muscles are paralysed. Sensation is lost in the ulnar forearm and
hand.

 Entire plexus: is damaged, the whole limb is paralysed and numb.

Management

 The patient is likely to be admitted to a general unit where fractures and other

injuries will be given priority.

 Emergency surgery is required for brachial plexus lesions associated with

penetrating wounds, vascular injury or severe (high energy) soft-tissue damage
whether open or closed.

Obstetrical Brachial Plexus Palsy

 Obstetrical palsy is caused by excessive traction on the brachial plexus during

childbirth, e.g. by pulling the baby’s head away from the shoulder or by exerting
traction with the baby’s arm in abduction.

 Three patterns are seen:

(1) upper root injury (Erb’s palsy), typically in overweight babies with
shoulder dystocia at delivery
(2) lower root injury (Klumpke’s palsy), usually after breech delivery of
smaller babies
(3) total plexus injury.

 The diagnosis is usually obvious at birth: after a difficult delivery the baby has a

floppy or flail arm. Further examination a day or two later will define the type of
brachial plexus injury.

Erb’s Palsy



is caused by injury of C5, C6 and (sometimes) C7.



The abductors and external rotators of the shoulder and the supinators are

paralysed.



The arm is held to the side, internally rotated and pronated.



There may also be loss of finger extension.



Sensation cannot be tested in a baby.

Klumpke’s Palsy

 is due to injury of C8 and T1.
 The baby lies with the arm supinated and the elbow flexed; there is loss of

intrinsic muscle power in the hand.

 Reflexes are absent and there may be a unilateral Horner’s syndrome.

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Total plexus injury

the baby’s arm is flail and pale; all finger muscles are parlysed and there may also be
vasomotor impairment and a unilateral Horner’s syndrome.

X-rays

should be obtained to exclude fractures of the shoulder or clavicle (which are not
uncommon and which can be mistaken for obstetrical palsy).

Management

Over the next few weeks one of several things may

happen.

  Paralysis may recover completely
   Many (perhaps most) of the upper root lesions recover spontaneously.
  A fairly reliable indicator is return of biceps activity by the third month.
   A total lesion may partially resolve, leaving the infant with a partial paralysis.
  Paralysis may remain unaltered This is more likely with complete lesions,

especially in the presence of a Horner’s syndrome.

 While waiting for recovery, physiotherapy is applied to keep the joints mobile.
 If there is no biceps recovery by 3 months, operative intervention should be

considered.

Long Thoracic Nerve

 The long thoracic nerve of Bell (C5, 6, 7) may be damaged in shoulder or neck

injuries (usually an axonotmesis) or during operations such as first rib resection,
transaxillary sympathectomy or radical mastectomy.

 However, serratus anterior palsy is also seen after comparatively benign events,

such as carrying loads on the shoulder, and even viral illnesses or toxoid
injections.

Clinical Features

  Paralysis of serratus anterior is the commonest cause of winging of the scapula.
  The patient may complainof aching and weakness on lifting the arm.
  Examination shows little abnormality until the arm is elevated in flexion or

abduction.

 The classic test for winging is to have the patient pushing forwards against the

wall or thrusting the shoulder forwards against resistance.

Treatment

 Except after direct injury or division, the nerve usually recovers spontaneously,

though this may take a year or longer.

 Persistent winging of the scapula occasionally requires operative stabilization by

transferring pectoralis minor or major to the lower part of the scapula.

Spinal Accessory Nerve

 The spinal accessory nerve (C2–6) supplies the sternomastoid muscle and then

runs obliquely across the posterior triangle of the neck to innervate the upper half
of the trapezius.

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 Because of its superficial course, it is easily injured in stab wounds and operations

in the posterior triangle of the neck (e.g. lymph node biopsy).

 It is occasionally injured in whiplash injuries.

Clinical Features

 Following an open wound or operation, the patient complains of severe pain and

‘stiffness’ of the shoulder.

 Examination reveals asymmetry or drooping of the shoulder, reduced ability to

hitch or hunch the shoulder and weakness on abduction of the arm.

 Often the true nature of the problem is not appreciated and diagnosis is delayed

for weeks or months. In late cases there may be wasting of the trapezius.

Treatment

 Stab injuries and surgical injuries should be explored immediately and the nerve

repaired.

 If the exact cause of injury is uncertain, it is prudent to wait for about 8 weeks for

signs of recovery.

Axillary Nerve

 The axillary nerve (C5, 6) arises from the posterior cord of the brachial plexus.
 Runs along subscapularis and across the axilla just inferior to the shoulder joint. It

emerges behind the humerus, deep to the deltoid.

 The landmark is 5 cm below the tip of the acromion.
 More often it is injured during shoulder dislocation or fractures of the humeral

neck.

 Iatrogenic injuries occur in transaxillary operations on the shoulder and with

lateral deltoid-splitting incisions.

Clinical Features

  The patient complains of shoulder ‘weakness’, and the deltoid is wasted.
  Although abduction can be initiated (by supraspinatus), it cannot be maintained.
  Retropulsion (extension of the shoulder with the arm abducted to 90 degrees) is

impossible.

 Careful testing will reveal a small area of numbness over the deltoid (the

‘sergeant’s patch’).

Treatment

 Nerve injury associated with fractures or dislocations recovers spontaneously in

about 80 per cent of cases.

 If the deltoid shows no sign of recovery by 8 weeks, EMG should be performed;

if the tests suggest denervation then the nerve should be explored.

DR. JAMAL AL-SAIDY

M.B.CH.B…F.I.C.M.S

Radial Nerve

The radial nerve may be injured at the elbow, in the upper arm or in the axilla.

Clinical Features

 Low lesions :

  usually due to fractures or dislocations at the elbow
   local wound
  Iatrogenic lesions of the posterior interosseous nerve where it winds

through the supinator muscle are sometimes seen after operations on the
proximal end of the radius.

 The patient complains of clumsiness and, on testing, cannot extend the

metacarpophalangeal joints of the hand.

 In the thumb there is also weakness of extension and retroposition.
 Wrist extension is preserved because the branch to the extensor carpi

radialis longus arises proximal to the elbow.

 High lesions

 occur with fractures of the humerus or after prolonged tourniquet

pressure.

 There is an obvious wrist drop, due to weakness of the radial extensors of

the wrist, as well as inability to extend the metacarpophalangeal joints or
elevate the thumb.

 Sensory loss is limited to a small patch on the dorsum around the

anatomical snuffbox.

 Very high lesions

 may be caused by trauma or operations around the shoulder.
 More often, though, they are due to chronic compression in the axilla;

this is seen in drink and drug addicts who fall into a stupor with the arm
dangling over the back of a chair (‘Saturday night palsy’) or in thin
elderly patients using crutches (‘crutch palsy’).

 In addition to weakness of the wrist and hand, the triceps is paralysed and

the triceps reflex is absent.

Treatment

 Open injuries should be explored and the nerve repaired or grafted as soon as

possible.

 Closed injuries are usually first or second degree lesions, and function eventually

returns.

 In patients with fractures of the humerus it is important to examine for a radial

nerve injury on admission, before treatment and again after manipulation or
internal fixation.

 If the palsy is present on admission, one can afford to wait for 12 weeks to see if

it starts to recover.

 If it does not, then EMG should be performed; if this shows denervation potentials

and no active potentials then a neurapraxia is excluded and the nerve should be
explored.

 If it is certain that there was no nerve injury on admission, and the signs appear

only after manipulation or internal fixation, then the chances of an iatropathic

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injury are high and the nerve should be explored and – if necessary – repaired or
grafted without delay.

 While recovery is awaited, the small joints of the hand must be put through a full

range of passive movements.

 The wrist is splinted in extension to ‘avoided fixed contractures.
 If recovery does not occur, the disability can be largely overcome by tendon

transfers: pronator teres to the short radial extensor of the wrist, flexor carpi
radialis to the long finger extensors and palmaris longus to the long thumb
abductor.

Ulnar Nerve

Injuries of the ulnar nerve are usually either near the wrist or near the elbow, although
open wounds may damage it at any level.
Clinical Features

 Low lesions

  are often caused by cuts on shattered glass.
  There is numbness of the ulnar one and a half fingers.
  The hand assumes a typical posture in repose – the claw hand deformity –

with hyperextension of the metacarpophalangeal joints of the ring and
little fingers, due to weakness of the intrinsic muscles.

 Hypothenar and interosseous wasting may be obvious.
 Finger abduction is weak and this, together with the loss of thumb

adduction, makes pinch difficult.The patient is asked to grip a sheet of
paper forcefully between thumbs and index fingers while the examiner
tries to pull it away; powerful flexion of the thumb interphalangeal joint
signals weakness of adductor pollicis and first dorsal interosseous with
overcompensation by the flexor pollicis longus (Froment’s sign).

 High lesions

 occur with elbow fractures or dislocations.
 The hand is not markedly deformed because the ulnar half of flexor

digitorum profundus is paralysed and the fingers are therefore less
‘clawed’ (the ‘high ulnar paradox’).

 Otherwise, motor and sensory loss are the same as in low lesions.

 ‘Ulnar neuritis’

 may be caused by compression or entrapment of the nerve in the medial

epicondylar (cubital) tunnel, especially where there is severe valgus
deformity of the elbow or prolonged pressure on the elbows in
anaesthetized or bed-ridden patients.

Treatment

 Exploration and suture of a divided nerve are well worthwhile, and

anterior transposition at the elbow permits closure of gaps up to 5 cm.

  While recovery is awaited, the skin should be protected from burns.
  Hand physiotherapy keeps the hand supple and useful.
  Tendon transfers.

DR. JAMAL AL-SAIDY

M.B.CH.B…F.I.C.M.S

Median Nerve

The median nerve is most commonly injured near the wrist or high up in the forearm.
Clinical Features

 Low lesions

 may be caused by cuts in front of the wrist or by carpal dislocations.
 The patient is unable to abduct the thumb, and sensation is lost over the

radial three and a half digits.

 In longstanding cases the thenar eminence is wasted and trophic changes

may be seen.

 High lesions

 are generally due to forearm fractures or elbow dislocation, but stabs and

gunshot wounds may damage the nerve at any level.

 The signs are the same as those of low lesions but, in addition, the long

flexors to the thumb, index and middle fingers, the radial wrist flexors and
the forearm pronator muscles are all paralysed.

 Typically the hand is held with the ulnar fingers flexed and the index

straight (the ‘pointing sign’).

 Also, because the thumb and index flexors are deficient, there is a

characteristic pinch defect.

Lumbosacral Plexus

  The plexus may be injured by massive pelvic trauma.
  These lesions are usually incomplete and often missed.
  The patient may complain of no more than patchy muscle weakness and some

difficulty with micturition.

 Sensation is diminished in the perineum or in one or more of the lower limb

dermatomes.

 Some patients, however, have significant problems with incontinence, impotence

and neurogenic pain.

 Plexus injuries should always be sought in patients with fractures of the pelvis.

Femoral Nerve

The femoral nerve may be injured by a gunshot wound, by pressure or traction during an
operation or by bleeding into the thigh.

Clinical Features



Quadriceps action is lacking and the patient is unable to extend the knee
actively.



There is numbness of the anterior thigh and medial aspect of the leg.



The knee reflex is depressed.



Severe neurogenic pain is common.

Treatment

 This is a fairly disabling lesion and, where possible, counter-measures should

be undertaken.

DR. JAMAL AL-SAIDY

M.B.CH.B…F.I.C.M.S

 A thigh haematoma may need to be evacuated.
 A clean cut of the nerve may be treated successfully by suturing or grafting

but results are disappointing.

 The alternative would be a caliper to stabilize the knee, or tendon transfers of

hamstrings to quadriceps.

Sciatic Nerve

 Division of the main sciatic nerve is rare except in gunshot wounds.
 Traction lesions may occur with traumatic hip dislocations and with pelvic

fractures.

 Intraneural haemorrhage in patients receiving anticoagulants is a rare cause of

intense pain and partial loss of function.

 Iatropathic lesions are sometimes discovered after total hip replacement.

Clinical features

 In a complete lesion the hamstrings and all muscles below the knee are

paralysed.

 The ankle jerk is absent.
 Sensation is lost below the knee, except on the medial side of the leg

which is supplied by the saphenous branch of the femoral nerve.

 The patient walks with a drop foot and a high-stepping gait to avoid

dragging the insensitive foot on the ground.

 Electrodiagnostic studies will help to establish the level of the injury.
 In late cases the limb is wasted, with fixed deformities of the foot and

trophic ulcers on the sole.

Treatment

 If the nerve is known to be divided, suture or nerve grafting should be

attempted

 While recovery is awaited, a below-knee drop-foot splint is fitted.
 Great care is taken to avoid damaging the insensitive skin and to prevent

trophic ulcers.

 Sometimes can be managed by transferring tibialis posterior to the front in

order to counteract the drop foot.

 If there is no recovery whatever, amputation may be preferable to a flail,

deformed, insensitive limb.

Peroneal Nerves

Injuries may affect either the common peroneal (lateral popliteal) nerve or one of its
branches, the deep or superficial peroneal nerves.
Clinical features

 The common peroneal nerve is often damaged at the level of the fibular neck

by severe traction when the knee is forced into varus (e.g. in lateral ligament
injuries and fractures around the knee, or during operative correction of gross
valgus deformities), or by pressure from a splint or a plaster cast, from lying
with the leg externally rotated, by skin traction or by wounds.

 The patient has a drop foot and can neither dorsiflex nor evert the foot.

DR. JAMAL AL-SAIDY

M.B.CH.B…F.I.C.M.S

 He or she walks with a high-stepping gait to avoid catching the toes.
 Sensation is lost over the front and outer half of the leg and the dorsum of the

foot.

 Pain may be significant.

Treatment

 Direct injuries of the common peroneal nerve and its branches should be

explored and repaired or grafted wherever possible. As usual, the earlier
the repair, the better the result.

 While recovery is awaited a splint may be worn to control ankle weakness.
 Pain may be relieved and drop foot is improved in almost 50 per cent of

patients, especially those who are operated on early.

 If there is no recovery, the disability can be minimized by tibialis

posterior tendon transfer or by hind-foot stabilization; the alternative is a
permanent splint.

Tibial Nerves

The tibial (medial popliteal) nerve is rarely injured except in open wounds. The distal
part (posterior tibial nerve) is sometimes involved in injuries around the ankle.

Clinical features



The patient is unable to plantarflex the ankle or flex the toes.



Sensation is absent over the sole and part of the calf.



Because both the long flexors and the intrinsic muscles are involved, there is
not much clawing.



With time the calf and foot become atrophic and pressure ulcers may appear
on the sole.

Treatment



A complete nerve division should be sutured as soon as possible.



A peculiarity of the tibial nerve is that injury or repair (especially delayed
repair) may be followed by causalgia.



While recovery is awaited, a suitable orthosis is worn (to prevent excessive
dorsiflexion) and the sole is protected against pressure ulceration.



In suitable cases, weakness of plantar flexion can be treated by hindfoot
fusion or transfer of the tibialis anterior to the back of the foot.

Thank You

DR. JAMAL AL-SAIDY

M.B.CH……..F.L . M. S