Nerve compression syndrome

NERVE COMPRESSION SYNDROME

By : Vaibhav Mittal.

INTRODUCTION AND

GENERAL FEATURES

DEFINITION

• Nerve compression syndrome/ compression neuropathy/ Entrapment Neuropathy is defined as: Pressure or Pressure induced injury to a segment of a peripheral nerve secondary to anatomical or pathological structures

INTRODUCTION• The nerve is injured by 1. chronic direct compression, 2. angulations 3. stretching forces

causing mechanical damage to the nerve.

Anatomy

Anatomy

Anatomy

Micro anatomy• Each nerve fiber, or axon, is a direct extension of a dorsal

root ganglion cell (sensory), an anterior horn cell (motor), or a postganglionic sympathetic nerve cell, and it is either myelinated or unmyelinated.

• Sensory and motor nerves contain both unmyelinated and myelinated fibers in a ratio of 4 to 1

• In the unmyelinated or sparsely myelinated fibers several axons are wrapped by a single Schwann cell. In the more heavily myelinated fibers the Schwann cell by rotation forms a multilaminated structure that encloses a myelin sheath about a single axon.

• The segment of myelinated nerve fiber enclosed by a single Schwann cell is referred to as an in-ternode and varies in length between 0.1 and 1.8 mm with the more heavily myelinated fibers having the longer internodes

• The point at which one Schwann cell ends and the next begins is relatively sparse in myelin and is called the nodal gap, or node of Ranvier .

• The axon with its Schwann cell and myelin sheath is in turn surrounded by a veil of delicate fibrous tissue called the endoneurium. Seen longitudinally, the endoneurium forms a tube encircling individually the Schwann cell sheaths that cluster together to form a fascicle (or funicle as termed by Sunderland). Each fascicle or separate group of sheathed axons is in turn surrounded by a denser layer of perineurium.

• The entire group of fascicles with their surrounding perineurium is encased as a mixed spinal or peripheral nerve in a denser epineurium

• The blood supply to the peripheral nerve enters through the mesoneurium, which is loose connective tissue extending from the epineurium to the surrounding tissues.

• There is both an extrinsic (segmental) as well as an intrinsic (longitudinal) blood supply to each nerve.

• The intrinsic blood supply that runs longitudinally within the epineurium, perineurium, and endoneurium is fairly extensive and allows surgical mobilization without complete devascularization over variable lengths of nerves.

Peripheral nerve

PATHOPHYSIOLOGY

PATHOPHYISOLOGY• Focal slowing of Nerve conduction is the principal

electrophysiological feature of entrapment neuropathy

• Mild degrees of pressure(suprasystolic) applied to the nerve for short periods produce reversible dysfunction d/t ischemia(entrapped nerve more sensitive to ischemia than normal nerve)

• Acute ischemia may be responsible for paresthesias and dysethesias

• Prolonged ischemia may l/t neural tissue infarction• Epineurium protects against compression• Epineurium and perineurium protect against stretch

COMPRESSION

Compromised

intraneural circulation

Reduced axoplasmic

flow Hypoxia

and altered microvascul

ar permiability

Subperineural edema &

EXACERBATI

ON OF ORIGINAL

COMPRESSIONCONT OF

VICIOUS CYCLE

PERSISTENT EDEMA + ANOXIA/HYPOXIA

FIBROSIS

IMPAIRMENT OF

SUPPLY

DEFICIENCY OF VITAL NUTRIENT

SFUNCTION

AL IMPAIRMEN

T

PERMANENT IMPAIRMENT

OF FUNCTION IF

LEFT UNTREATED

Double Crush and multiple crush syndromes

• A proximal level of nerve compression could cause more distal sites to be susceptible to compression.

• The summation of compression along the nerve would result in alterations of axoplasmic flow

• The possibility of a distal site of compression making the more proximal nerve susceptible to secondary compression: A reverse double crush.

• Systemic diseases such as obesity, diabetes, thyroid disease, alcoholism, rheumatoid arthritis and neuropatthies lower the threshold for the occurrence of a nerve compression and alter axoplasmic transport rendering that nerve more susceptible to develop compression neuropathy and act as a ‘crush’.

Double Crush Syndrome

Entrapment Neuropathy in Diabetes

• DM is a significant predisposing factor for entrapment neuropathies .

• Metabolic and phenotypic abnormalities of endoneurial and

perineurial fibroblasts lies behind the vulnerability of DM patients to entrapment neuropathy.

• In contrast to angiopathies, retinopathy, and nephropathy, three representative complications of DM, mast cells do not

play significant roles in the onset or progression of the entrapment neuropathy associated with DM.

Classification of nerve injuriesSeddon Classification

Neuropraxia: 1.Minor contusion or compression with preservation of axis – cylinder of myelin sheath. 2.Impulse transmission physiologically interrupted.3.Complete recovery in a few days to weeks.

Axonotemesis : 1.More significant injury 2.Breakdown of axon and distal Wallerian degeneration but with preservation of schwann

cell & endoneurial tubes 3.Spontaneous regeneration with good functional recovery can be expected. Neurotmesis 1.More severe injury 2.Complete anatomical severance, avulsion or crushing of nerve 3.Axon, Schwann cell & endoneurial tubes are completely disrupted4.Spontaneous recovery cannot be expected unless surgically intervened

Sunderland Classification• Each degree of injury suggesting a greater anatomical disruption

with its correspondingly altered prognosis.• Anatomically various degrees (1st – 5th) represent injury to Myelin Axon Endoneurial tube & it’s content Perineurium Entire nerve trunk• Sixth degree (Mackinson) or mixed injuries occur in which a

nerve trunk is partially severed and remaining part of trunk sustains 1st to 4th degree injury.

• Mixed recovery pattern depending on degree of injury to each portion of nerve.

CLINICAL SCENARIO

Either or all• Pain• Numbness• Tingling • Burning• Weakness• Muscle wasting(severe cases) in respective anatomical areas

Evalution

• History • Physical examinations• Investigations

General conditions associated that lead to neuropathy

• Systemic • Guillain-Barre syndrome• Double crush syndrome - A proximal level of nerve compression could cause

more distal sites to be susceptible to compression.

Physical examination • Motor changes • -deformity• -loss of movements• -lagging• Sensory changes• - areas of loss of sensation• Autonomous • -vasomotor• -pilomotor• -tropic

INVESTIGATIONSMOTOR EXAMINATION

SENSORY EXAMINATIONS

1. MODALITY TEST : pain, temperature, touch, pressure, vibration

2. FUNCTIONAL TEST : ability of the patient to perform fine apprehensive task with the discriminative levels.

3. OBJECTIVE TEST : tinels test, sweat test, skin resistance test, wrinkle test.

Tinels test

electromyography

• Denervation fibrillations seen after 3 weeks of axonotemesis and neuronotemesis which are not seen in normal and neuropraxia.

• In neuropraxia minimal residual activity seen which suggest continuity of the nerve fiber.

• Earliest sign of reinnervation is low ampitude polyphasics, slow duration waves.

• High complexed poly phasic waves suggest early nerve generation.

Nerve conduction study

• Normally the speed is 50-70 meters per second• Time interval between application of stimulus

to median nerve and response as seen in abductor policis brevis is prolonged from 3 miliseconds to 7-10 miloseconds.

• Sensory conduction velocity can be measured by stimulating distally and measuring potential at wrist.

F WAVES

• To study the proximal segment late responces the F WAVEES and H REFLEXES are used.

• F wave is a long latency muscle action potential produced at the supramaximal stimulus from antidromic stimulation of mototr neurons involving the conduction to and from the spinal cord.

• It occurs at interface between the PNS and CNS.

• Properties of F waves:• Latency, chronodispersion, amplitude,

persistence, F/M ratio, F estimation[ f estimate = (2D/CV) X10 +1 +DL ]

• CLINICAL IMPORTANCE:• Absent in sedated patient• They study the entire course of nerve so they

are more reliable in neuropathies.

• Slowing of the proxiaml Fwave conduction in comparison the distal seen in GBS

• Absent F waves and normal M wave shows nerve block.

• Fwave chronodispersion is prolongated in polyneuropathies.

• F waves are absent in cases of spinal shock.• All features of Fwaves are increased in patients with

long standing spasticity or upper motor neuron syndromes.

Treatment

• Conservative • surgical

Conservative

• CONSERVATIVE TREATMENTS– GENERAL MEASURES– SPLINTS– MEDICATIONS– LOCAL INJECTION/BLOCKS– PHISIOTHERAPY AND PHYSIOTHERAPY DEVICES

SURGICAL MANAGEMENT

• Removing the offending structure• Release/decompression/exploration• Neuroma excision• Nerve resection• Nerve repair• Nerve grafting• Nerve or muscle transfer

SPECIFIC ENTRAPMENT SYNDROMES

• UPPER LIMB A)MEDIAN NERVE -CARPAL TUNNEL SYNDROME - ANTERIOR INTEROSSEOUS SYNDROME - PRONATOR SYNDROME B)ULNAR NERVE -AT ELBOW -AT GUYON’S CANAL C)RADIAL NERVE - RADIAL TUNNEL -WARTENBERG’S SYNDROME

• LOWER LIMB A) SCIATIC NERVE - PYRIFORMIS SYNDROME B)PERONEAL NERVE -TARSAL TUNNEL SYNDROME C) LATERAL FEMORAL CUTANEOUS NERVE - MERALGIA PARASTHETICA

SUPRASCAPULAR NERVE ENTRAPMENT

SUPRASCAPULAR NERVE ENTRAPMENT

• Throwers, other overhead athletes and weight-lifters

• Arises from superior trunk of brachial plexus

• Innervates supraspinatus and infraspinatus

• Compression most commonly suprascapular or spinoglenoid notch

ETIOLOGY : • compression due to ganglion cyst,

chondrosarcoma, ewings sarcoma, metastasis.• Scapular frcatures• Traction – forcible depression of shoulder,

repeated ext rotation of shoulders, sustained adduction.

Predisposing factors:• Deep scapular notch• Hypertrophy of transverse scapular ligament,

spinoglenoid ligament.Clinics:• Dull ache in post. Shoulder which aggrevates on

shoulder adduction and external rotation.• Pain over scapular notch, atropy of infraspinatus,

weakness of externl rotation and adbuction.

• MRI may exclude rotator cuff tears, demonstrate atrophy and/or reveal a ganglion or space-occupying lesion- if present, strongly consider surgical excision

• NCS/EMG may assist with the diagnosis• Typically begin with non-operative mgmt.

TREATMENT : • Rest from repetitive hyperabduction

• NSAIDs and corticosteroid injections considered

• Nonresponders may benefit from a spinoglenoid notchplasty, transverse scapular ligament release, nerve decompression or surgical exploration

Suprascapular notch

With the patient prone, make an incision parallel to andabout 3 cm superior to the scapular spine

Suprascapularartery is above and suprascapularnerve is beneath ligament

Elevate the trapezius subperiosteally, and expose thesupraspinatus muscle.

■ Identify the nerve by elevating the supraspinatusmuscle and dissecting superior and inferior to themuscle.

■ Identify the suprascapular notch, and release the transverseligament.

MEDIAN NERVE ENTRAPMENTS•carpal tunnel syndrome• anterior interosseous syndrome• pronator syndrome

CARPAL TUNNEL SYNDROME

CARPAL TUNNEL SYNDROMEIs a cylindrical cavity connecting the volar forearm with the palmboundaries– It is bounded by bones on 3 sides and a fibrous

sheath(flexor retinaculum)on one side• floor : formed by transverse arch of carpal bones• Medially : hook of hamate, triquetrum, pisiform• Laterally : scaphoid, trapizium, fibro osseous flexor

carpi radialis sheath• Roof : transverse carpal ligament, deep forearm

fascia proximally, aponeurosis between thenar and hypothenar muscles distally

MEDIAN NERVE – MOTOR INNERVATION:

1st and the 2nd lumbricals

Muscles of thenar eminence: 1. Opponens pollicis brevis2. Flexor pollicis brevis

SENSORY INNERVATION:

Skin of the palmar side of the thumb, index and middle finger.

Half the ring finger and nail bed of these fingers.

Signs and symptoms

• Tingling• Numbness or discomfort in the

lateral 3 1/2 fingers• Intermittent pain in the distribution

of the median nerve• Symptoms gets aggravated at

night.• To relieve the symptoms, patients

often “flick” their wrist as if shaking down a thermometer (flick sign).

MOTOR CHANGES:

Apelike thumb deformity

Loss of opposition of thumb

Index and middle finger lag behind when making the fist.

SENSORY CHANGES:

Loss of sensation of lateral 3 1/2 digits including the nail bed and distal phalanges on dorsum of hand (An important point to remember for Carpal tunnel syndrome is that there is no sensory loss over the thenar eminence in Carpal tunnel syndrome because the branch of median nerve that innervates it (palmar cutaneous branch) passes superficial to Carpal tunnel and not through it).

VASOMOTOR CHANGES:

• Skin area with sensory loss is warmer• Dry skin

TROPHIC CHANGES:

• Long standing cases leads to dry and scaly skin• Nail crack easily• Atrophy of the pulp of the fingers.

Physical Assessment Tests: • Less sensitivity to pain where the median nerve runs to the

fingers• Thumb weakness• Inability to tell the difference between one and two sharp

points on the fingertips• Flick Signal. The patient is asked, "What do you do when

your symptoms are worse?" If the patient responds with a motion that resembles

shaking a thermometer, the doctor can strongly suspect carpal tunnel.

PHALEN’S TEST:

The patient rests the elbows on a table

The wrists dangle( flexion) with fingers pointing down and the backs of the hands pressed together.

POSITIVE: If symptoms develop within a minute, CTS is indicated.

• TINEL’S SIGN TEST: In the Tinel's sign test,

the doctor taps over the median nerve to produce a tingling or mild shock sensation.

o DURKAN TEST:

The doctor presses over the carpal tunnel for 30 seconds to produce tingling or shock in the median nerve.

o HAND ELEVATION TEST:

The patient raises his or her hand overhead for 2 minutes to produce symptoms of CTS.

• Torniquet test: Torniquet inflated above systolic for one minute

intensifies the symptoms• Carpal compression test: Pressure with both the thumbs to the median

nerve in the carpal tunnel for 30 sec will aggravate the symptoms

• Tests for sensations :

Evaluation

• History• Physical examination• Nerve Conduction Study

• CONSERVATIVE TREATMENTS– GENERAL MEASURES– WRIST SPLINTS– ORAL MEDICATIONS– LOCAL INJECTION– ULTRASOUND THERAPY– Predicting the Outcome of Conservative

Treatment• SURGERY

• Avoid repetitive wrist and hand motions that may exacerbate symptoms or make symptom relief difficult to achieve.

• Not use vibratory tools• Ergonomic measures to relieve symptoms

depending on the motion that needs to be minimized

splintss

Probably most effective when it is applied within three months of the onset of symptoms

• Nonsteroidal anti-inflammatory drugs (NSAIDs)

• pyridoxine (vitamin B6)• Orally administered corticosteroids

– Prednisolone– 20 mg per day for two weeks– followed by 10 mg per day for two weeks

• Splinting is generally recommended after local corticosteroid injection.

• If the first injection is successful, a repeat injection can be considered after a few months

• Surgery should be considered if a patient needs more than two injections

Surgical management

• Should be considered in patients with symptoms that do not respond to conservative measures and in patients with severe nerve entrapment as evidenced by nerve conduction studies,thenar atrophy, or motor weakness.

• It is important to note that surgery may be effective even if a patient has normal nerve conduction studies

• Open release • Endoscopic release

• Transverse incision proximal to the anterior wrist crease between flexor carpi ulnaris and flexor carpi radialis tendons. Distal longitudinal incision made between proximal palmar crease and 1 cm distal to hamate hook in line with radial border of ring finger.

ANTERIOR INTEROSSEOUS SYNDROME&

PRONATOR SYNDROME

Site of compression essentially same for both Pronator syndrome(PS) and Ant. Int. nerve

• Laceratus pronatus• Between superficial and deep head of

pronator teres.• Beneath FDS arch.

Pronator syndrome :• Proximal• sensory involvement• Vague volar forearm pain,• Median nerve parasthesias,minimum motor

findings.

differential diagnosis of sites of compression

PROVOCATIVE TESTS• Flexion of elbow against resistance between 120-135

degrees – struthers ligament• Flexion of elbow with forearm pronation -- lacertus fibrosus• Pronation against resistance combined with wrist flexion - 2 heads of pronator teres• Resisted flexion of FDS of middle finger - musculotendinous arch of FDS

Anterior interosseous syndrome/ kiloh nevin syndrome

• Arises from posterior surface of the median nerve 5-8 cm distal to the

• Major branch supplying FDP, FPL, PQ.• Etiology :1. Thickened fascia between deep and superficial head of

PT.2. Tendinous origin of deep head of PT and FDS.3. An accessory tendon of FPL ( GANTZER’S MUSCLE )4. Thrombosed ulnar collateral vessels.5. Volkmanns ischemia.

• Clinics:• Acute pain in proxiaml forearm.• No sensory deficits seen usually.• Loss of pinching position due to absence of

pinching of DIP of index finger and interphalangeal joint of thumb.( SPINNERS SIGN )

• Deterioration of handwriting.• Weakness FDP, FPL, PQ.

SPINNERS SIGN POSITIVECANNOT MAKE THIS POSITION

TREATMENT• INITIALLY: CONSERVATIVE• SURGICAL: INDICATIONS

No resolution of symptomsSevere symptoms

• SURGICAL EXPLORATION: Identification & division of the offending structure.

ULNAR NERVE ENTRAPMENT

• Ulnar nerve gets entrapped at 2 common sites:

At the elbow (cubital tunnel syndrome)

Guyon’s canal (ulnar tunnel syndrome)

CUBITAL TUNNEL SYNDROME• Second commonest nerve entrapment of the upper limb• ANATOMY: CUBITAL TUNNEL

Starts at the groove between the olecranon & the medial epicondyle.

Tunnel is formed by a fibrous arch connecting the 2 heads of the flexor carpi ulnaris & lies just distal to the medial epicondyle.

CAUSES OF ENTRAPMENT• ARCADE OF STRUTHER’S: Formed by superficial muscle

fibres of the medial head of triceps attaching to the medial epicondyle ridge by a thickened condensation of fascia.

• Tight fascial band over the cubital tunnel.• Medial head of triceps• Aponeurosis of flexor carpi ulnaris• Recurrent subluxation of ulnar nerve, results in neuritis.• Osteophytic spurs• Cubitus valgus following supra condylar fracture.

CLINICAL FEATURES• Numbness involving the little finger & the ulnar half of the

ring finger.• Hand weakness & clumsiness• Tenderness over the ulnar nerve at the elbow.• Tinel’s sign is positive: exacerbation of paraesthesia’s with

light percussion over the ulnar nerve.• Advanced cases : clawing of the ring & little fingers

TREATMENT

• NON OPERATIVE: Early stages

Activity modification

Immobilization of the elbow in 30 degrees of extension, followed by

periods of mobilization with elbow padding.

• SURGICAL:

Decompression of the nerve by dividing of the basic offending

structure.

Anterior transposition of the ulnar nerve

Medial epicondylectomy

GUYON’S CANAL• Ulnar nerve is compressed as it passes through

GUYON’S canal in the wrist.• Less common than entrapment of the ulnar nerve at the

elbow.

ANATOMY:GUYON’S CANAL– ROOF: composed of palmar carpal ligament blending into the

FCU tendon attaching to the pisiform & the pisiohamate ligaments.

– Medial wall : pisiform & pisiohamate ligament.– Lateral wall: hook of hamate & some fibres of the transverse

carpal ligament.– Ulnar nerve enters guyon’s canal accompanied by ulnar A &

Ulnar V.– Guyon’s canal lies in the space between flexor retinaculum &

volar carpal ligaments

• The anatomy of distal ulnar tunnel is divided into 3 zones.

• Zone 1:proximal to the bifurcation of the ulnar nerve &

consists of both sensory & motor fibres of the nerve.

• Zone 2: represents the motor branch of the ulnar N distal

to the bifurcation.

• Zone 3: represents the sensory branches of the ulnar

nerve beyond its bifurcation

Clinical presentations:

• ZONE 1 LESIONS : Mixed sensory & motor loss.

• ZONE 2 LESIONS : Isolated motor deficit.

• ZONE 3 LESIONS : Isolated ulnar N sensory loss.

• Common Causes in zone 1 & 2: ganglions, fractures of the hook of

hamate.

• Zone 3: ulnar artery thrombosis

OTHER CAUSES:• Malunited fracture of fourth/fifth metacarpal.• Anomalous muscles• Occupational trauma : Bicycling, videogames, computer mouse,

using palmof hand as hammer. Pizza cutter.

INVESTIGATIONS• X RAY : Oblique/carpal tunnel views

Delineate bony anatomy to diagnose hook of hamate fractures.

• MRI: Ganglia, space occupying lesions

TREATMENT• Operative release of the canal by reflecting the FCU, pisiform &

pisiohamate ligament ulnarly.• Distal deep fascia of the forearm below the wrist crease should be

released.• Resection of any space occupying lesion• Treatment of hook of hamate fractures.

RADIAL NERVE ENTRAPMENTS

• POSTERIOR INTEROSSEOUS NERVE SYNDROME

• RADIAL TUNNEL SYNDROME

• WARTENBERG’S SYNDROME

POSTERIOR INTEROSSEOUS NERVE SYNDROME

ANATOMY Proximal to the elbow joint, the radial nerve branches into the

superficial radial nerve & the PIN. The PIN travels around the radial neck and through the interval

between the 2 heads of the supinator muscle. Also called as supinator tunnel syndrome. This opening which has an overlying compressive fibrous arch is

known as arcade of frosche.

TYPES :Type 1 ; all muscle supplied by the nerve are papalysed : EDC, EIP, EDQ,

AbPL, EPB

TYPE 2: only few are paralysed

Clinical features:– Initially, presents with a dull ache in the proximal forearm.– Later, there is difficulty in extending the fingers & the thumb.– Partial wrist drop as ECRL is spared .

Etiology: Fracture of elbow, Ganglion cyst, fibroma, lipoma, VIC Proliferative synovitis (rheumatoid arthritis)

• Electro diagnostic testing may localize the site of compression.• Initially : observation & non operative treatment.• Operative methods: exploration & appropriate division of

compressing structures.

RADIAL TUNNEL SYNDROME

• The PIN passes between the 2 heads of the supinator

muscle in the radial tunnel.

• Boundaries of radial tunnelMedial: biceps tendonLateral : brachioradialis & extensor carpi radialis longus & brevis tendonsRoof: brachioradialisfloor :deep head of the supinator

• Pain is often acute & can mimic tennis elbow.

• Increased pain on resistive active forearm supination.

• Middle finger test : elbow extended and wrist

• Electrophysiological studies shows no abnormality.

• Treatment: non-operative: Activity modification, splinting,

NSAID’S & rest.

• Surgical decompression is often combined with lateral

epicondyle release.

WARTENBERG’S SYNDROME• Compression of the superficial branch of the radial nerve

can occur most commonly as it exits from beneath the brachioradialis in the forearm.

• Nerve can get trapped b/w the ECRL & the brachioradialis,( approx 7cm proximal to the radial styloid process) especially with pronation in the forearm.

• Also called as CHEIRALGIA PARESTHETICA• PRISONERS PALSY

• HAND CUFF DISEASE

FINKELSTEIN TEST

LOWER LIMB

SCIATIC NERVE

LATERAL FEMORAL CUTANEOUS NERVE /MERALGIA PARASTHETICA

It arises from L2 and L3 nerve root levels, emerges from the lateral border of psoas muscle, crosses iliacusand then passes through a tunnel formed by a small slit in the latral end of the inguinal ligament.

Gives purely sensory supply to the antero lateral and lateral aspect of the thigh.

PERONEAL NEUROPATHY

PERONEAL NEUROPATHY AT FIBULAR HEAD

• Usually involves both deep and superficial peroneal nerves

• Therefore weakness in ankle df and eversion

• Sensory loss over dorsum of the foot and lat calf

• May be pain and Tinel’s over fib neck

• Ankle inversion spared as innervated by Tib nerve.

Causes

• Habitual leg crossing• Repetitive stretch from squatting• Cresentric band at the origin of peroneus longus

muscle, beneath which the nerve travels ( fibular tunnel syndrome )

• Ganglions, schwannomas, neurofibromas, leprosy.• Associated to ankle inversion injury including # fib

– Traction to nerve– Prolonged immobilisation (especially sedated pt’s)

• Differential diagnosis• Sciatic neuropathy• L5 radiculopathy

• Investigations • EMG and NCS• MRI’s in slowly progressing to check for

masses

Treatment • Local injection• AFO• Stretches to prevent

contractures• Gait rehab• Eliminate offending

activities ie leg crossing• Surgery rarely needed

except where extensive nerve damage or mass present

TARSAL TUNNEL SYNDROME

Tarsal tunnel syndrome• Compression of the tibial nerve

branches under the flexor retinaculum

• Pain medial ankle, burning, numbness, tingling under foot

• More common women than men

• Worst with weight bearing• Possible wasting of intrinsics in

foot• Tinel’s positive in tarsal tunnel• Reduced light touch on soles of

foot

Physical examination :• Tinel's test is performed by taping the area below the medial malleolus.

The test is positive when it results in tingling along the nerve distribution. • Alongside this test, the physiotherapist can use the “straight leg raise” test

to provoke symptoms similar to a nerve problem.• Another test that can be use is a dorsiflexion-eversion test if the test is

positive it may be due to the entrapment of the nerve in the tarsal tunnel. In this test the distal posterior tibial nerve is stretched and compressed. Diagnosis of tarsal tunnel syndrome is largely clinical. This test can only give a suspicion of tarsal tunnel syndrome.

• The dorsiflexion-eversion test and the inversion test may both increase symptoms. When performing dorsiflexion and eversion of the foot, tension is applied on the nerve. The volume of the tarsal tunnel is decreased when inversion of the foot is been performed. This shows that either of these tests can reproduce pain or increase the symptoms.

Differential diagnosis

• Plantar Fascitis– DF with eversion then SLR– Tinel’s not +ve in pf– EMG/NCS– High resolution US

• Fat pad atrophy– More pain over fat pad– Visible loss of fat pad

• Rest• NSAID’s• Steroid Injections• Heel pads• Orthoses• Stretching exercises for PF and calf• Surgical intervention : release of the flexor retinaculum

by incision behind and below medial malleoli.

MORTONS NEUROMA

MORTON’S NEUROMA(INTERDIGITAL NEUROPATHY)

• Compression of the Plantar digital nerves in the space between the metatarsal heads

• Usually 3rd space followed by 2nd and rarely 1st or 4th space

• Can give pain which is debilitating as mobility severely limited

• Pain often relieved by removing tight footwear

• May be accompanied by numbness of toes adjacent to pain

Differential diagnosis

• TTS– Can be very difficult to differentiate

• Plantar fascitis• TMT OA

– Both of these will have no neurological S&S– Also compression of the MT heads should not be

exquisitely painful

Treatment

• No good evidence• Conservative treatment helps 50%

– Insoles– Stop offending activities– Steroid inj– Alcohol inj x4– Physio (not specified)

• Surgery neurectomy/neurolysis (variable outcomes)

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