Nerve compression syndrome

NERVE COMPRESSION SYNDROME OF UPPER AND LOWER LIMB NERVES
THE MAJOR NERVES - MEDIAN, ULANR, RADIAL SUPRASPINATUS AND LOWER LIMB NERVES

1. NERVE COMPRESSION SYNDROME By : Vaibhav Mittal .

2. INTRODUCTION AND GENERAL FEATURES

3. 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

4. INTRODUCTION The nerve is injured by 1. chronic direct compression, 2. angulations 3. stretching forces causing mechanical damage to the nerve.

5. Anatomy

6. Anatomy

7. Anatomy

8. 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.

9. 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 .

10. 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.

11. Peripheral nerve

12. PATHOPHYSIOLOGY

13. 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

14. 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’.

15. Double Crush Syndrome

16. 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.

17. Classification of nerve injuries Seddon 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 disrupted 4.Spontaneous recovery cannot be expected unless surgically intervened

18. 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.

19. CLINICAL SCENARIO Either or all Pain Numbness Tingling Burning Weakness Muscle wasting(severe cases) in respective anatomical areas

20. Evalution History Physical examinations Investigations

21. 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.

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

23. INVESTIGATIONS MOTOR EXAMINATION

24. SENSORY EXAMINATIONS MODALITY TEST : pain, temperature, touch, pressure, vibration FUNCTIONAL TEST : ability of the patient to perform fine apprehensive task with the discriminative levels. OBJECTIVE TEST : tinels test, sweat test, skin resistance test, wrinkle test.

25. Tinels test

26. electromyography

27. 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.

28. Nerve conduction study

29. 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.

30. 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.

31. 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.

32. 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.

33. Treatment Conservative surgical

34. Conservative CONSERVATIVE TREATMENTS GENERAL MEASURES SPLINTS MEDICATIONS LOCAL INJECTION/BLOCKS PHISIOTHERAPY AND PHYSIOTHERAPY DEVICES

35. SURGICAL MANAGEMENT Removing the offending structure Release/decompression/exploration Neuroma excision Nerve resection Nerve repair Nerve grafting Nerve or muscle transfer

36. 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

37. SUPRASCAPULAR NERVE ENTRAPMENT

38. 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

39. ETIOLOGY : compression due to ganglion cyst, chondrosarcoma , ewings sarcoma, metastasis. Scapular frcatures Traction – forcible depression of shoulder, repeated ext rotation of shoulders, sustained adduction.

40. 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 .

41. 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

42. Suprascapular notch With the patient prone, make an incision parallel to and about 3 cm superior to the scapular spine Suprascapular artery is above and suprascapular nerve is beneath ligament Elevate the trapezius subperiosteally, and expose the supraspinatus muscle. ■ Identify the nerve by elevating the supraspinatus muscle and dissecting superior and inferior to the muscle. ■ Identify the suprascapular notch, and release the transverse ligament.

43. MEDIAN NERVE ENTRAPMENTS carpal tunnel syndrome anterior interosseous syndrome pronator syndrome

44. CARPAL TUNNEL SYNDROME

45. CARPAL TUNNEL SYNDROME Is a cylindrical cavity connecting the volar forearm with the palm boundaries 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

46. MEDIAN NERVE – MOTOR INNERVATION: 1 st and the 2 nd lumbricals Muscles of thenar eminence: Opponens pollicis brevis 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.

47. 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).

48. 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).

49. 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.

50. 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.

51. 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.

52. 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.

53. DURKAN TEST: The doctor presses over the carpal tunnel for 30 seconds to produce tingling or shock in the median nerve. HAND ELEVATION TEST: The patient raises his or her hand overhead for 2 minutes to produce symptoms of CTS.

54. 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 :

55. Evaluation History Physical examination Nerve Conduction Study

56. CONSERVATIVE TREATMENTS GENERAL MEASURES WRIST SPLINTS ORAL MEDICATIONS LOCAL INJECTION ULTRASOUND THERAPY Predicting the Outcome of Conservative Treatment SURGERY

57. 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

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

59. 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

60. 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

61. 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

62. Open release Endoscopic release

63. 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.

64. 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.

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

66. 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

67. 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 : Thickened fascia between deep and superficial head of PT. Tendinous origin of deep head of PT and FDS. An accessory tendon of FPL ( GANTZER’S MUSCLE ) Thrombosed ulnar collateral vessels. Volkmanns ischemia.

68. 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.

69. SPINNERS SIGN POSITIVE CANNOT MAKE THIS POSITION

70. TREATMENT INITIALLY: CONSERVATIVE SURGICAL: INDICATIONS No resolution of symptoms Severe symptoms SURGICAL EXPLORATION: Identification & division of the offending structure.

71. ULNAR NERVE ENTRAPMENT

72. Ulnar nerve gets entrapped at 2 common sites: At the elbow (cubital tunnel syndrome) Guyon’s canal (ulnar tunnel syndrome)

73. 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.

74. 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.

75. 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

76. 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

77. 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.

78. 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

79. 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

80. 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.

81. 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.

82. RADIAL NERVE ENTRAPMENTS POSTERIOR INTEROSSEOUS NERVE SYNDROME RADIAL TUNNEL SYNDROME WARTENBERG’S SYNDROME

83. 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

84. 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.

85. RADIAL TUNNEL SYNDROME The PIN passes between the 2 heads of the supinator muscle in the radial tunnel. Boundaries of radial tunnel Medial: biceps tendon Lateral : brachioradialis & extensor carpi radialis longus & brevis tendons Roof: brachioradialis floor :deep head of the supinator

86. 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.

87. 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

88. FINKELSTEIN TEST

89. LOWER LIMB

90. SCIATIC NERVE

91. LATERAL FEMORAL CUTANEOUS NERVE / MERALGIA PARASTHETICA I t 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.

92. PERONEAL NEUROPATHY

93. 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.

94. 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)

95. Differential diagnosis Sciatic neuropathy L5 radiculopathy Investigations EMG and NCS MRI’s in slowly progressing to check for masses

96. 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

97. TARSAL TUNNEL SYNDROME

98. 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

99. 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.

100. 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

101. 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 .

102. MORTONS NEUROMA

103. MORTON’S NEUROMA (INTERDIGITAL NEUROPATHY) Compression of the Plantar digital nerves in the space between the metatarsal heads Usually 3 rd space followed by 2 nd and rarely 1 st or 4 th 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

104. 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

105. 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)

106. THANK YOU…