Peripheral Nerve injuries

Submitted By:- Manmeet kaur

 Formation of a peripheral nerve
• The dorsal and ventral nerve roots arising from the spinal
cord comes together and join at the level of intervertebal
foramina to form the spinal nerve.
• In our body there are 31 pairs of spinal nerves(8 cervical,
12 thoracic, 5 lumbar, 5 sacral , 1 coccygeal). The 12
thoracic spinal nerves provide myotomal and dermatomal
supply to each intercostal segment. The remaining 19
nerves are instrumental in forming four plexuses.
• Each spinal nerve has three components:- sympathetic,
motor and sensory. The sympathetic components of 31
spinal nerves leaves along the 14 motor roots.
• Each spinal nerve divides into a large
anterior ramus and posterior ramus. The
anterior rami form a group known as a
plexus. Each plexus integrate and gives
rise to an individual peripheral nerve.
 Structure of the peripheral nerve
• Each peripheral nerve is composed of compact group
of individual nerve fibres, each with an individual
neurolemmal tube. The nerve fibre is enclosed in a
collagen connective tissue covering known as
endoneurium.
• The number of nerve fibres with endoneurium are
bound together by a fibrous tissue covering called
perineurium.
• A group of nerve fibers with their endoneurium and
perineurium sheaths together is known as faciculus. A
number of such faciculus enclosed by a tough tissue
sheath called epineurium. Each peripheral nerve is
an individual compact bundle of such fasciculi
• Each nerve fascicle contain schwann cells,
fibrocytes, axons, myelin sheaths, collagen
fibrils, endoneurium and blood vessels.
• the diameter of the axon of PN varies
between 1 and 20 microns. The junction
between each schwann cell is called is
called a node of ranvier where the axon
remain insulated.
 Classification of peripheral nerve
injuries
A. Seddon’s classification:- According to this
classification, the severity of injuries to the nerve
is divided into three classes:
1. Neurapraxia:- Axon are intact. Spontaneous
recovery is complete.
2. Axonotmesis:- Axons divided. Connective tissue
intact. Wallerian degeneration occurs. Axon then
regenerate slowly.
3. Neurotmesis:- Whole nerve severed. Recovery
may occur if cut ends are apposed.
 Neurapraxia
• It is the contusion of the nerve
only; the axon are in continuity
and therefore wallerian
degeneration does not occur.

• It is relatively mild injury

typically caused by moderate
compression such as that
caused by tourniquet, slight
stretching.
• Complete recovery occur within
3-6weeks.
 Axonotmesis
• The axon are damaged but the endoneurial
tube remains intact. Wallerian degeneration
occur in distal segment of the injured nerve.
• Intact epineurium, perineurium and
endoneurium guide the regeneration axons to
their appropriate connection.
• Partial to complete recovery may occur within
3-6 months(eg. Fractures and dislocation).
 Neurotmesis
• The nerve either completely cut or
disorganized to an extent where spontaneous
recovery is impossible. wallerian degeneration
sets in early and the neural elements mingles
with the fibrous elementsto form the
neuroma,which needs surgery
• The prognosis of recovery is poor ( eg. Cut
injury and open lacerated wound, severe
crush injury
B. Sunderland classification:-
According to this nerve injuries are
classified into five grades in an ascending
order depending upon the extent of injury to
the axon, endoneurium,perineurium, entire
nerve trunk, myelin,motar march,tinel sign
and overall prognosis of recovery.
 Aetiology
• Direct injury:- fractures and dislocations alone account
for over 40-50%. Sharp cuts, piercing innuries, nerve
entrapment between the fractured bony ends at the
time of a fracture.
• General cause:- metabolic diseases, collagen disease,
infection, excessive cooling, excessive heating,
neurotoxic drugs like tetracycline,quinifine, radiation
therapy for cancer , carelessely given intramuscular
injections directmy piercing the nerve, excessive
traction or a friction of the nerve (eg. Skeletal or pin
traction), prolonged ischemia and electric shock.
• Late cause:- compressive pathology due
to growing tumour, excessive callus,
malunion, fibrosis, adhesions.
 Clinical features
■ Early signs:-
• Pain due to injury may be present with stiffness of the adjacent
joint.
• Setting in of paresis or paralysis of the muscles innervated by
the injured nerve.
• Loss of skin sensation to touch, pain, temperature, and
steriognosis.
If the motor supply remains intact, the perception of joint position
, joint movement , deep pressure and vibration will be perserved.
• Anaesthetic skin area which feeds cool and dry.
• Presence of tinel’s sign.
■ late signs:-
• Muscle paresis gradually progress to paralysis.
• Deep tendon reflexes are reduced or lost.
• Trophic changes like dry, thin and glossy skin,
nails appearing brittle, hair fall, even bones
develop a tendency for osteoporosis.
• Typical deforming attitude , related to muscular
imbalances due to paralysis gradually setting in.
• Atrophy of the muscles of innervation.
Steps in the evaluation and diagnosis
of PN injury
1. History:- emphasis is needed on three factors;
each is directly related toh the prognosis.
• When? – how long back?
• How? – injury type: cut, laceration,blunt injury, non
traumatic?
• What happened following imjury? For example:-
□ the presence of excessive bleedinv indicates
associated vascular injury, the onset of numbness
indicates break in the continuity of the nerve.
□ the earlier treatment and its response.
2. Extensive motor and sensory evaluation:-
• Motor evaluation: critical evaluation of the
strength and other muscle functions.
• Supplementary action of the projected
tendon, eg. Projection of the tendon of
abduction pollicis brevis into the terminal
phalanx produces strong extension of the
terminal IP joint of the thumb ( in the
presence of radial nerve lesion ).
 Spot diagnosis( by testing motor
status)
Simple and specific physical examination
greatly helps in the spontaneous diagnosis
of the injured peripheral nerve.
■ indentation of the injured peripheral nerve
by simple observation and clinical
examination
1. Clinical motor test of the muscles
inervated by the respective PN.
2. Localized atrophy of the muscle
innervated by a relevant injured PN.
Axillary nerve Flattening of the shoulder contour
due to paralysis of deltoid
Median nerve Flattening of the muscles of the
thenar eminence
Ulnar nerve Flattening of the muscles of the
hypothenar eminence
Femoral nerve Wasting over the anterior thigh
above knee
Posterior tibial Wasting over the calf on the
nerve posterior aspect of the leg
3. Typically abnormal postural attitued as a
result of paralysis of the muscle group
innervated by the injured peripheral nerve.
Brachial plexus Waiter’s or policeman’s
tip
Thoracodorsal Winging of scapula
Radial nerve Wrist drop
Ulnar nerve Ulnar claw hand
Median nerve Medial claw hand
Median+Ulnar True claw hand involving
nerve all the four fingers
4. Susceptible area of the limb where the
nerve lies superficially between the skin and
the bone.
Radial nerve Laterally winding over the spiral groove
over the midshaft area of humerus
Median nerve Palmar aspect of the forearm just proximal
to the wrist joint

Ulnar nerve Over the medial epicondyle of the

humerus

Axillary nerve Close to the fibrous septa in the axilla

Common Winding course over the fibular head and

peroneal nerve neck
 5. Site of injury to the bone and the joint where
damage expected to a particular peripheral nerve.
Fracture of the clavicle Brachial plexus injury
Fracture of the proximal humerus Axillary nerve injury
Fracture of the midshaft of the Radial nerve injury
humerus
Posterior dislocation of the elbow Radial nerve
Monteggia fracture Posterior interosseous
nerve
Fracture of the medial epicondyle Ulnar nerve
Posterior dislocation of the hip Sciatic nerve
Anterior dislocation of the hip Femoral nerve
Dislocation of the knee joint Common peroneal nerve
Fracture of the neck of the fibula Lateral popliteal nerve
 Testing sensory status
• Sensory status testing give a profile of the
sensory pathways.
■ sensory pathway:- The sensory pathways
can be divided into four components:-
1. The receptor field
2. The conducting line – axon
3. The central conduit – the spinal cord
4. The central decoding apparatus – cerebral
cortex.
 Early tests
• There are six sensory tests:-
1. Vibratory test
2. Pseudomotor activity test
3. Two – point discrimination test
4. Von frey pressure test
5. Pickup test
6. Pin – prick test
1. Vibratory test:- This is done with A turning fork with
stimulus of either 30cps or 256cps. Its stimulates
the quickly responding fibres. It should be done
early to know the extent and prognosis of the lesion.
2. Pseudomotor activity test:- Sweating In the area
supplied by PN is one of the initial tests indicative of
regeneration, whereas dryness of the skin over the
distribution of a peripheral nerve indicates severe
laceration.
3. Two – point discrimination test:- It can be done
with an ordinary paper clip, with the patient
observing and then with the eyes closed. Ten
separate stimuli are given; seven correct responses
are essential to adequate conduction.
4. Von frey pressure test:- This test is a pressure test to
detect the perception of light touch. The hand should
marked into seven zones. The monofilament of a horse
hair of varying thickness and stiffness id placed and
pressed on the ares under the examinationuntil its bends,
the examiner can judge the force of pressure required to
evoke response.
5. Pickup test:-It is important as it combines sensibility
and sensory input with motion. The blindfolded patient is
given nine object of different shapes and sizes. He is
instructed to pick up one object at a time and place it into a
small container. Time taken to perform this is compared
with the contralateral normal limb. It usually take 5-8s for a
young adult male.
6. Pin – prick test:- This test is commonly
used to assess the sensation of pain. The
patient is blind folded and is asked to count
the pricks applied intermittently.
 Special investigations
• Electrodiagnostic tests
• Electromyography
• Nerve conduction velocity studies
• Stength – duration curves (SD curves)
 Electromyography
• It is the most important test to
distinguish between:-
1. The presence or absence of
nerve injury.
2. When present, whether the
nerve injury is complete or
incomplete.
3. Whether the regeneration of
the injured nerve is taking
place or not.
 EMG characteristics of normally innervated
muscles and denervated muscle by
electromyography
Normal innervated muscle Denervated muscle

• At rest: no electrical activity At rest: show denervation potenti

• At weak voluntary attempt: als, spontaneous electrical activity
displays only a single motor unit by 1-2 weeks after injury
action potential
• During the attempted strong If these denervation potentials fail
voluntary muscle contraction to appear by 3 weeks after muscle
number of motor unit Firing denervation, it indicates good
simultaneously are super-imposed prognosis of recovery.
Giving rise to the interference
pattern of Motor action potentials
Nerve conduction velocity studies
■ Motor NCV:- The nerve to be studied is stimulated at
two levels and the latent period between the application of
the stimulus and the ensuring muscular contraction is
determined.
• The distance between two levels(D) is measured.
• The stimulating electrode is applied directly at the point
over the nerve trunk. The response is picked up bye the
second electrode placed over the muscle to stimulated.
• The precise value of NCV i calculated by dividing the
difference between the proximal and diatal stimulation in
mm.
NCV= D/PL – DL
■ sensory NCV :-
• Determined by Stimulating a point over the
skin or a digit with the action potentials picked
up bye electrodes along the course of tge
nerve at two different points.
• The sensory NCV is calculated by the same
method as motor NCV.
• However, the conduction of the sensory
impulses is much faster than the motor nerve
conduction.
 Stength – duration curve
• A curve plotted between the strength
current and the varying durations ( ranging
from 0.01 to 800 ms ) of.
• The nerve is stimulated at the motor point
to elicit minimal muscular contraction.
• The SD curve provides objective evidence
of the integrity of the nerve.
 Additional tests
• Vascular test:- A strong association exist between
vascularity and nerve conduction. Entire physiologic
function including that of all motor and sensory end
organs is involved distally. It is done by palpating distal
pulses or plethysmography msy be used to assess
pulse volume.
• Blood flow detection test:- By doppler test.
• Skin resistance test:- Sympathetic nerve involvement
gives arise to dry and glossy skin. In partial lessions,
vasomotor changes like cynosis, excessive sweating
may occur. Trophic changes may be present.
• Sweat test:- The presence of excessive
sweating over the area of skin within the
autonomous zone of the injured nerve
indicates only patial interruption in the
conduction of impulses and a good
prignosis.
• Tinel’s sign:- A simple clinical test that
helps in the diagnosis as well as prognosis
of the injured nerve.
 Treatment planning
• After confirmed diagnosis, while planning
the methodology of treatment, due
emphasis must be given to certain factors
directly influencing the prognosis of
recovery
• Due to the muktifactorial dependency of
the recovery, only the general plan of
treatment forms the basic procedure of
treatment.
 Orthropaedic management
The standard orthopaedic management of fracture is applied.
Most of the time, the nerve injury is associated with a fracture.
• Bone and vascular repair take precedence over the repair of
the nerve.
• Primary nerve repair:- carried out within 6- h only when
open wound is clean. The cut end of nerve trunk are
brought close and suture are applied with a fine silk
material. The sutured nerve is immobilized and protected
from tension or stretches by orthosis.
• If wound is contaminated the suture are applied between 7
and 18 days, only after ensuring proper wound care.
• Secondary repair:- By 18 days to 3
weeks in certain situation like;
○ Failure of the conservative treatment.
○ Symptoms of definite nerve irritation.
○ No symptoms of recovery.
○ Poor general condition of patient.
Surgical methods of nerve repair

1. Nerve suture ( neurorrhaphy ) and nerve

grafting
(a)Epineural repair:-Carried out by suturing
the epineurium.
(b)Fascicular repair:- After excising the
epineurium,the fasiscles are separated.
Then tge fascicles of both the nerve ends
are matched together and sutured using
microsurgical techniques.
(C) Both epineural and perineural repair:- when the
approximation of the cuts ends of the nerve becomes difficult due
to the neuroma is carried out, followed by adequate mobilization
of the nerve to gain a shortened length; then suturing is carried
out by;
1. Immobilizing the joint close to the course of the nerve in slight
flexion. Sutures are applied only after gaining adequate length
for suturing. Eg. anterior transposition of the ulnar nerve when
injured behind the medial epicondyle of the humerus.
2. Sacrificing the unimportant branches of the nerve hampering
the nerve mobilization.
(D) Nerve grafting:- when
the gap between the cut
ends is 10cm or more, it is
bridged over by nerve
grafts obtained generally
from the sural nerve or the
lateral cutaneous nerve of
the thigh.
(E) Decompression of the
nerve:- Median nerve
compressed in the
muscular or fibro- osseous
tunnel is decompressed
surgically.
2. Neurolysis:- sometimes the continuity of
the nerve is well maintained but its
conductivity is hampered due to its
entrapment with the scar formation, fibrosis
and excessive callus formation.
■ The fibrosis may be:-
• external- formed outside the nerve trunk.
• Internal – formed within the nerve trunk.
Reconstruction surgical procedures

By 18 months, the conduction of impulses

across the injured nerve completely stops,
indicating complete nerve degeneration. This
requires reconstructive surgical interventions
like;
• Tendon transfer
• Joint stabilization( arthrodesis) in a
functional position to facilitate and restore
functional tasks.
 Physiotherapy management
Physiotherapy has a most significant role in the
management of all type of peripheral nerve lesions;
■ During early stage (first 3 weeks)
1. Control of pain:-
• Relaxed totally supported positioning of affected limb with
suitable orthosis.
• TENS over area nearest to intact sensorium.
• Recommended standard orthoses like aeroplane splint
for brachial plexus injury, static cock up splint for radial
nerve injury.
2. To control oedema:-
• Limb elevation with supportive orthosis.
• Repetitive active, assisted or passive full ROM
movements go distal joints.
• Gentle effleurage.
• Compressive elastic bandage.
3. Assist in early detection of possible nerve injury, and the
prevention of expected complications due to injury and
treatment or skeletal pin traction or accidental nerve injury
during surgery.
• Identification of paretic or paralysed muscle and
baseline motor and sensory evaluation.
• Mapping the area of parasthesia and its protection when
present. The patient should be instructed thoroughly
how to protect these areas.
■ Three weeks onwards( recovery stage)
(a)Responding cases:-
• Graded active assisted exercise programme.
• Motor sensory; re-education training , progressive
functional restoration with resistive mode
(b) Non- responding cases:-
• Electro diagnostic tests.
• Use special techniques to restore neuromuscular
functions.( e.g. PNF technique)
• Sensory re-education
• Persistence to perform lost motor control by
audiovisual enforcement and biofeedback with
stimulation ( electric) of EMG
■ Late stage
• Alternate route of guiding a patient to facilitate functional
tasks like; hypertrophy of muscle group which can
compensate for the permanently paralysed muscle( e.g.
Use of long head of biceps to achieve shoulder
abduction in absence of deltoid).
• Static or dynamic orthosis to assist stabilizing the joint
for functional use.
• Cock – up splint with locking system to lock in extension
for a stronger grip or release.
• Altering the biomechanics of the body to assist functional
activity (e.g. Shoulder girdle elevation synchronized with
trunk lateral flexion to the opposite side to facilitate
elbow, wrist and hand function in the absence of
shoulder abduction.
Injuries to the major peripheral nerves

• Median nerve
• Ulnar nerve
• Radial nerve
• Femoral nerve
• Obturator nerve
• Sciatic nerve
• Common peroneal nerve
 Median nerve( nerve roots C5- T1)
• A mixed nerve derived from the C5 to T1 nerve roots via medial and lateral
cords of brachial plexus
• Common sites of injury- a sharp cut close to the wrist and cubital fossa.
Anatomy
• Course and innervation:- In the arm, it runs close to the brachial artery and
has no supply. It enters the forearm between The two heads of pronator
teres, supplies the pronator teres and give branches to Palmaris longus,
flexor carpi radialis and flexor digitorum superficialis. Then it give a
muscular branch to the anterior interosseous nerve which supplies the
flexor digitorum profundus l and ll, flexor pollicis longus and pronator
quadratus.
• Proximal to carpel tunnel, it gives a sensory branch, plamar cutaneous,
supplying the thenar eminence descends down and passes through the
carpal tunnel
• In the hand , it supplies the abductor pollicis brevis, flexor pollicis brevis,
opponens pollicis, lumbricals l and ll and digital to 1,2,3 and half of the
fourth digit.
• Deformities:-
○ Ape thumb:- There is wasting of thenar
muscles and thumb lies adduction and in
plane of palm of hand.
○ Simian hand:- In this deformity; the plane of
the thumb is much more in line with the palm,
with wasting of the thenar and hypothenar
muscles. This deformity occur due to
combined median and ulnar nerve palsy.
 Treatment
• Fresh injuries are treated by nerve repair.
• Chronic injuries require excision of neuroma followed
by nerve grafting.
• In injuries beyond repair, tendon transfer procedure are
performed to improve function. Brand’s oppenensplasty
is done using the tendon of flexor digitorum sublimis of
the ring finger in median nerve palsy to restore
opposition of the thumb.
• In simian hand hand, oppenensplasty is done using the
tendon of the extensor indicis proprius to restore
opposition.
 Compressive lesion of the median
nerve
• Carpal Tunnel syndrome:- Carpal tunnel is the
overcrowded fibro- osseous canal formed
between three carpal bones( scaphoid,
trapezoid, hamate) and the transverse carpal
ligament.
○ The median nerve and the nine tendons of
digital flexor pass through this 2- 2.5 cm tunnel.
○ Therefore, any bony or soft – tissue pathology to
its precipitates compressive forces over the
median nerve passing through it.
 Aetiology
• Occupational overuse of wrist joint, [Link]
keyboards.
• Malunited colles fracture, RA or OA.
• Ganglia or haematoma at the wrist.
• Connective tissue disorder
• Endocrine disorders like hypothyroidism,menopause.
• Metabolic cause like gout.
• Pregnancy.
• Growth hormone abnormality.
 Clinical features
• Pain and discomfort at the wrist during movements or
even at rest.
• Burning , aching , warmth, parasthesia in the hand and
wrist in the distribution of median nerve; relieved by
shaking hands.
• Vasomotor symptoms life swelling, cold, dry, and shiny
skin.
• Motor weakness of opponens, flexor pollicis brevis result
in difficulty in making circle with thumb or index finger
due to the paralysis of abductor pollicis brevis, causing
difficulty in gripping a cylindrical objects, e.g. Bottle
• Loss of true opposition.
• Late stage muscular atrophy- thenar muscle of hand.
Symptom provocative motor tests
1. Phalen’s test
2. Modified phalen’s
test
3. Reverse phalen’s
test
4. Tourniquet sign
5. Bilateral arm
percussion test
6. Vibratory test
 Treatment
■ conservative:-
• Treatment of the relevant causative factor which has
precipitated the syndrome.
• A simple splint that blocks movement at the wrist is adequate
to avoid compressive stretches to the carpal hand.
• Non steroidal anti- inflammatory drugs agent.
• Pain free relaxed passive or speedy active movements are
encouraged by removing the splint.
• Cryotherapy, TENS over the palmar aspect of wrist.
• Local corticosteroid injection may be given only after
confirming the absence of sensory deficit.
■ Surgical :- surgical release of the median
nerve may have to be undertaken by
division of carpal flexor retinaculum and
transverse carpal ligament either by open
surgery or by endoscopic surgery.
 Anterior interosseous syndrome
Rare pain in the forearm and elbow because the
sensory fibres from the wrist and the carpal bones
travel in the anterior nerve.
Indentifying signs:-
• Muscles of innervation; flexor pollicis longus, flexor
digitorum profundus l and ll, pronator quadratus.
• Functional difficulty in using hand like picking up a
cup, tearing a paper, using spoon and fork.
• Motor weakness- performing forearm pronation
against resistance.
Ulnar nerve( nerve roots C8 – T1)
• Course and branches of ulnar nerve:-
 Deformity
Deformities due to lesion of ulnar nerve:-
• Ulnar claw hand:- It result in hyperextension at the MP
joint due to paralysis of lumbricals and unopposed action of
extensor digitorum communis, where as intact flexor
produces flexion at both the IP joints of the ring and little
hand finger.
• Median claw hand:- The deformity is similar to the ulnar
claw hand but instead of ring and little finger, the clawing
appears at index and middle finger.
• The true claw hand:- A combined lesion of both the ulnar
and median nerve result in a true hand, where clawing is
present in all four finger.
 Clinical tests for ulnar nerve injury
• Froment’ sign
• Card test ( a test for palmar interossei )
• Egawa test ( a test for dorsal interossei )
Compressive lesion of the ulnar nerve

■ Tardy ulnar nerve palsy:- The major

cause is the repetitive friction or compression
of ulnar nerve in the cubital tunnel in
situations like the following:
• Cubitus valgus deformity.
• Tension over the supracondylar grove or
cubital tunnel or repetitive friction due to
overuse. E.g. Ganglia, excessive formation
and malunion.
 Clinical features
• Motor paralysis of muscle supplied by nerve,
sensory tingling and numbness in the 4th and 5th
finger with wasting, proximally radiating pain.
■ Diagnostic motor test:- The elbow joints are
held in complete flexion with wrist extended fully.
In a positive test, by 3min, the symptoms of pain,
tingling and pins and needles begin to appear in
the distribution of ulnar nerve, which appear on
extending the elbow
 Treatment
• NSAID, wrist with elbow in extension.
• Local US exposure and orthosis.
• Release of entrapment by medial
epicondylectomy.
• Anterior transposition of ulnar nerve.
 Claw hand
• Claw hand presents a typical deformity with
hyperextension of the MP joints and flexion of the IP joint.
■ Clinical features:-
• Finger loss the stabilizing effect, resulting in a whether
grasp, pinch , as well as grip.
• Loss of sensation on the skin along the distribution of
involved peripheral nerve.
• Wasting and weakness of intrinsic muscle of hand,
resulting in wasting at the intermetacarpal spaces of
dorsum of the hand.
• Wasting of thenar and hypothenar muscles.
 Treatment
• The treatment is centred on controlling the
hyperextension at the MP joint to facilitate
the functions if the finger movements.
• Active method is by surgically transferring
the tendon whenever its fulfil the required
criteria.
 Radial nerve( C5 – T1 nerve roots )
• Course and innervation of radial nerve:-
 Deformities
• Total wrist drop:- Simultaneous extension
at the wrist , finger and the thumb is lost due
to the loss of finger and thumb extensor.
• Hitchhiker’ sign:- Inability to extend the IP
joint of the thumb due to paralysis of the
extensor pollicis longus and brevis is the
only clinical sign to suspect radial nerve
lesion during the early stage of injury.
 Treatment
In closed injury:-
• Cock – up splint. Initially static and at the later stage,
dynamic.
• Full ROM passive movements to the wrist , fingers and the
thumb.
• Progress to active assisted movements, self – efforts , EMG
biofeedback or initiating contraction with PNF technique by
using stretch reflex.
In open fracture:- Nerve repair procedure along with the
reduction of a fracture.
• late and non recovered lesions:- Surgical procedure like
tendon transfer and wrist joint arthrodesis.
 Compressive lesions of the radial
nerve
The common site of compressive lesion could be:-
1. Lesion in axilla:- Either due to crutch pressure or during
sleep. Crutch palsy, involves triceps and all distal muscles
innervated by the radial nerve.
2. Retrohumeral lesion:- A lesion at posterior aspect close to
the spiral groove of the humerus.
• Saturday night palsy:- Sustained compression due to
malpositioning of the arm during the sleep , during general
anaesthesia or tourniquet application.
• Motor weakness:- All the extensor of the wrist, finger and
thumb.
• Sensory:- Over the dorsum of the thumb.
3. Lesion at the proximal forearm:- Involves the posterior
interosseous nerve.
• Motor:- Weakness of the wrist and MCP joint Extensors,
extension at the IP joints is preserved as the intrinsic
supplied by median and ulnar nerve ate spared.
4. Lesion at distal forearm:-
• Superficial cutaneous radial nerve entrapment:- A nerve may
entrapped due to compression by tight cast , a tight band of
a wrist watch or handcuff. It result in altered sensorium over
the small area of dorsum of thumb web.
• Usually a surgical release of radial nerve at the elbow is
indicated.
 Treatment
• Static or dynamic cock- up splint.
• Full ROM passive movements to the
wrist and hand joints.
• Educate patient on assisted active
movements of wrist , finger and thumb
extension , elbow flexion in supination
and forearm supination
• PNF, biofeedback sessions.
Surgery:- When recovery does not take
place by 18 weeks , surgical exploration
and repair, release or reconstructive
procedure is the only alternative.
Peripheral nerve of the lower limb

• The myotomal and the dermatomal

innervation of lower limb are provided by
two plexuses.
1. The lumbar plexus( derived from L1 – L4
nerve roots.)
2. The sacral plexus( derived from the L4 –
S3 nerve roots )
■ Lumbar plexus:- It give rise to two major mixed
nerves;
1. Obturator nerve:- It exist the psoas muscle
medially and supplies The adductor group of
muscle of thigh.
2. Femoral nerve:- It is formed by dorsal portion of
the anterior rami of L2 – L 4 nerve roots. It
descends down and passed between the psoas
and iliacus muscles and lies most laterally in
femoral triangle.
• Then it divide into anterior and posterior division.
The anterior division supplies the anterior thigh.
The posterior division supplies the hip and knee
joints and terminates as long cutaneous which
supplies the skin over anteromedial aspect of leg
and foot.
■ Sacral plexus:- Formed by the L4 – S3
nerve roots in front of the sacroiliac joint, it
gives two branches :-
1. Superior gluteal( L4,L5; S1) innervates
the gluteus medius , minimus and tensor
fascia lata.
2. Inferior gluteal nerve ( L5- S1 ) innervates
the gluteus maximus and sciatic nerve.
 Sciatic nerve
The longest and thickest nerve in the body, the
sciatic nerve innervates important muscle group
of lower limb. Although strong, it is highly
susceptible to injury due to its intra pelvic position.
• It emerges out of pelvic through the sciatic
notch along with superficial gluteal nerve,
inferior gluteal nerve, posterior aspect of thigh.
In the thigh, it lies at the middle of posterior
aspect of thigh, a common site of sciatic pain.
• The injury to the sciatic nerve may occur due to
traumatic or compressive pathology.
○ Proximal lesion of nerve in the pelvis or close to
sciatic notch result in:-
• Involvement of gluteal muscle and sensory loss in
distribution at posterior cutaneous of thigh.
• Weakness of hamstrings, all muscles below the knee,
sensory loss over the leg and foot below knee.
○ Distal lesion:-Behind the popliteal fossa, it divides into
two branches, the lateral popliteal or common peroneal
and the posterior tibial nerve.
 Common peroneal nerve
• The lateral trunk of sciatic nerve descends
obliquely through the popliteal fossa as lateral
cutaneous branch supplying the anterior, lateral,
posterior aspect of the leg, then it winds round
the fibular neck where it is lost superficial and
therefore common site of injury. Then it passes
through the fibular tunnel and divides into two
branches:-
1. Superficial peroneal nerve
2. Deep peroneal nerve
 Posterior tibial nerve
The medial trunk of the sciatic nerve continues posteriorly
below the popliteal fossa as a posterior tibial nerve. It
innervates:-
• Both head of gastrocnemius and soleus muscles.
• Tibialis posterior, popliteus, flexor digitorum longus,
flexor hallucis longus.
• At ankle, posterior tibial nerve divides into medial and
lateral plantar nerve after giving a branch to calcaneum.
• The medial plantar branch innervates the 1st lumbrical
and the lateral plantar branch innervates the 2nd , 3rd
and 4th lumbricals.
 Sural nerve
• It is purely a sensory nerve from S1 to S2 roots.
It is formed by joining together of two branches,
medial branch is derived from tibial and lateral
branch from peroneal nerve.
• Being deep, it is rarely injured. It may be
compressed by baker cyst, scar tissue following
fractured fifth metatarsal etc.
• It innervates the posterolateral aspect of the
distal leg, a small strip over the lateral – most
foot.
 Foot drop
• Foot drop or dropping of foot into
plantar flexio position is most common
disability encountered of all the
peripheral nerve injurie.
Causes:-
1. At the spine:- Spina bifida, localized
spinal tumour.
2. At the hip:- Posterior dislocation and
fracture around the hip and femur and
acetabulum and deep IM injection.
3. At the thigh:- Deep IM injection.
4. At and around knee:- Fracture of the
neck of fibula, fracture of lateral
femoral or tibial condyle,knee
dialocation, lateral meniscal injury etc.
• Level of lesion:-
1. High leson:- Both common peroneal and tibial nervea
are involved, causing TRUE FOOT DROP involving all
foot muscles.
2. Low lesion:- All the extensor group of muscle of ankle
and toes including peroneus tertious are involved.
• Early detection:-
1. Common peroneal high stepping gait or toe drag.
2. Posterior tibial lesion:- Foot slap immediately followed
heel strike(calcaneus gait).
 Treatment
Early treatment:-
• first provide splint which will
maintain the foot in neutral
position.
• Orthosis could vary from static
POP posterior slab or AFO or
toe pickup orthosis.
• Depending upon the causative
factor, anti- inflammatory or
steroid agents may become
necessary.
Physiotherapy:-
• Control of pain and inflammation.
• Preventing joint stiffness due to contractures.
• Full ROMPassive movements.
• Assisted active movements.
• PNF techniqueof bilatreally symmetrical pattern combined
by strong stretch reflex at initiation of pattern or even
repetitive stretches to ankle plantar flexion stimulate the lost
muscular action of ankle and foot dorsiflexion.
• EMG biofeedback using viaual as well as auditory feedback.
• Providing the necessary ortbosis.
Surgical procedure:-
• Fixed equines due to TA
tightness :- tendo –
achilles lengthening.
• Paralysis due to
thickened and tender
nerve caused by
tuberculoid leprosy:-
peroneal nerve stripping.
• Fixed varus deformity:-
subtalar joint arthrodesis.
• Fixed varus deformity at
subtalar joint:- Triple
arthrodesis
• Tendon transfer.
Physiotherapy following surgery:-
• Initial stage ( <3 week ):- Immobilized limb and reduce pain ,
inflammation and exercise to improve function of unaffected joints.
• Intermediate stage:- Electrodiagnostic test, assisted active
exercises to affected joints related to nerve repaired without causing
stretch to repaired nerve, progress to activestrong sustained efforts.
• Late stage:- After 6 – 8 weeks ;
• Add graded resistance to muscle action of repaired nerve.
• Maintain full passive ROM of related joint.
• Initiate functional activities.
• Functional use of upper extrmity.
• Standing, balancing, gait training with or without orthosis.
Compressive lesion of the lower limbs

Meralgia paraesthetica:- occasionally the lateral

cutaneous femoral nerve of the thigh gets entrapped
at the inguinal tunnel or at the fascia medical to the
anterior superior iliac spine.
Causes:-
• Tight corset, set belt or obesity.
• Psoas abscess, retroperitoneal tumour or
pooperative scarring in the region of the iliac fossa.
• Sensory loss restricted to a small size over tge
anterolateral aspect of the thigh.
 Treatment
• Anti- inflammatory drugs.
• Local steroid infiltration. I
• Surgical decompression of latera cutaneous nerve
• Orthosis is prescribed with modifications in shoe.
• NSAIDs
• Cortisone injection
• Excellent result with surgical release of
compression. Scarred nerve excision and nerve
repair may be done.
 Physiotherapy management
• It follow the same pattern as for the foot
drop. Motor and sensory re – education
plays a major role in both the therapeutic
approaches along with extensive guidance
to the patient to prevent damage to the
anaesthetic area.