Entrapment Neuropathies are largely underdiagnosed.

1. PRESENTER:Dr. Bikash Ch.Nanda
1st YEAR,PG(INTERNAL MEDICINE)
PRECEPTOR:Dr. L Ravi Kumar,MD
Asst Professor
Dept of Internal Medicine
VSS MCH Burla

2. Entrapment Neuropathy is defined as:
Pressure or Pressure induced injury to a
segment of a peripheral nerve secondary
to anatomical or pathological structures

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

7.  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

9. • Relevance
 *Epineurium protects against compression
 *Epineurium and perineurium protect against stretch
• NEUROPRAXIA:Segmental axonal conduction block
• CONDUCTION SLOWING:(in the absence of histological change)
 Myelin is slightly damaged,widening of nodal areas(NOT destruction of
 internodal segment)-longer time to activate
 Conduction is slowed,but not completely blocked
 Characteristic of Entrapment Neuropathies(Old term:Axonostenosis)


10.  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’.

12.  DM is a significant predisposing factor for entrapment
neuropathies .
TN-C(Tenascin-C) expression in the
endoneurium is closely correlated with nerve function.
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.
 Ref: Histol Histopathol (2008) 23: 157-166
http://www.hh.um.es

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

14. Electro diagnosis: mainstay
• Nerve Conduction studies(NCS)
• Electromyography(EMG)
NCS assess integrity of sensory and motor
neurons
EMG assess electrical activity of a muscle
from a needle inserted into a muscle

17. nerve Site of entrapment
Median N.(wrist)
(elbow)
Ulnar N. (wrist)
(elbow)
Lower trunk or medial cord of
branchial plexus
Suprascapular N
Post.interosseous N
Common Peroneal nerve
Lateral femoral cutaneous
(meralgia paresthetica)
Posterior tibial
Interdigital plantar (Morton
metatarsalgia)
Obturator
Carpal tunnel
Btwn heads of pronator teres
Guyon’s canal( ulnar tunnel)
Bicipital groove,cubital tunnel
Cervical rib or band at thoracic outlet
Spinoglenoid notch
Radial tunnel—at point of
entrance into supinator
Muscle (arcade of Frohse)
Fibular tunnel
Inguinal ligament
Tarsal tunnel; medial
malleolus–flexor
Retinaculum
Plantar fascia: heads of third
and fourth metatarsals
Obturator canal

19.  Median Nerve :Position and Morphology
• Round or oval at distal radius level
• Elliptical at the pisiform and hamate
• Morphology changes with flexion and extension
• Wrist flexion :elliptical shape flattens
• Wrist extension :least morphological change
• Frictional forces btwn the median N.adjacent tendons and the
transverse carpal lig compounded by morphologic changes
irritate nerve
Mechanism: demyelination f/b axonal degeneration.
Sensory and autonomic fibers affected before motor
 Epidemiology: F:M::3-10:1,Age peak 45-60yrs

20.  Aging,female,Increased BMI,Square shaped wrist,short
stature,dominant hand ,white race,caffeine,alcohol, nicotine
 Linked to body morphology,DM,thyroid disease,hereditary
neuropathies,RA,Acromegaly,Amyloidosis
 High amounts of repititive wrist movements and exposure to
vibration/cold
 Lack of aerobic exercise,preg,BF,Use of wheelchairs,walking
aids,recent menopause,renal dialysis(elbow positioning during
dialysis, upper extremity vascular-access, and underlying
disease is one cause of ulnar entrapment.)
 REF:Journal of Research in Medical Sciences Oct 2012

21.  PAIN :aching over ventral wrist extending distally
to finger and proximally to forearm
 SENSORY :hyperasthesias,parasthesias
 Mus.atrophy and weakness are late findings
 Autonomic changes:Incr sensitivity to temp
changes
 Intermittent sym and increase with
driving,reading the paper,crocheting,painting

23.  ELECTRODIAGNOSIS
• 1st LINE INVESTIGATION
• Prognosticates severity and used to follow disease process
over time
• Positive in >90 % pts. with clinical CTS
• Distal Motor latency is usually prolonged(50%)
• -stimulate the Med N> at the wrist, record at APB-latency
>3.7-4.5ms is abnormal
• Distal sensory latency is abnormal
 -Antidromic sensory study: stimulate at wrist and record at index
or middle finger,8cm distally->3.5ms
• Condn vel across carpal tunnel slowed:<41m/s

24. SPECIAL:
• Hoffman Tinel,Phalen,Reverse Phalen,carpal
compression test,square wrist sign
• USG more cost effective and non invasive-may
detect minute details which Electrophysiology may
miss
• Lacks standardisation
• REF:J Korean Neurosurg Soc. Feb 2013; 53(2): 132–135

25.  Physical therapy-
• Aerobic exercise,Modalities(iontophoresis,phonophoresis,ultrasound)
 Occupational therapy
• Work site ergonomic assessment (posture)
• Wrist-hand orthosis(worn at night for 3-4 wks)
• Stretching/strengthening
 Pharmacotherapy:
• NSAIDS,diuretics,steroids,Vit B6/12-no proven benefit,reduce
caffeine,nicotine,alcohol intake
• Local 40mg methyl pred inj results in significant improvement in mild CTS
REF:Clin neurophysiol 2012 Apr;123(4):838- 41. doi: 10.1016/j.
 Surgery-release of transverse carpal lig
• Indicated for failure of conservative care or severe category at presentation
• Open vs endoscopic
REF:EURA MEDICOPHYS 2007;43:327-32

26.  In CTS, steroid injections (such as cortisone or prednisolone) shrink the swollen
tissues and relieve pressure on the nerve. they offer short-term symptom relief in a
majority of CTS patients. However, in about half of cases, symptoms return within 12
months. Generally a second injection does not provide any added benefit.
 Another concern with the use of these injections in moderate or severe disease is that
nerve damage may occur even while symptoms are improving.
 Corticosteroid injections are helpful for pregnant patients, as their symptoms often go
away within 6 - 12 months after pregnancy.
 Most doctors limit steroid injections to about three per year, because they can cause
complications, such as weakened or ruptured tendons, nerve irritation, or more
widespread side effects.
 Low-Dose Oral Corticosteroids. A short course (1 - 2 weeks) of oral corticosteroid
medicines may provide relief for some people, but the relief does not usually last.
Long-term use of these medications can cause serious side effects.

Source: Carpal tunnel syndrome
University of Maryland Medical Center

27. USG guided percutaneous
injection,hydrodissection, and fenestration
• An extension of blind steroid injection with advantage
of safety,accuarcy of medication
placement,effectiveness,non invasiveness,ease of
performance and lower cost than open surgical
release
REF: Vol.10,No.3,2010,Journal of Applied
research

29.  Site of compression essentially same for both Pronator
syndrome(PS) and AIN
 PS:Vague volar forearm pain,Median nerve
parasthesias,minimum motor findings
 AIN:Pure motor palsy of any or all three 1.FPL,2.FDP
of index and middle fingers,3.PQ.
 Surgical indications for nerve decompression include
persistent symptoms for >6 months in patients with PS
or for a minimum of 12 months with no signs of motor
improvement in those with AIN syndrome

31. MECHANISM
Repititive bending or leaning on elbow for
long periods
Fluid build up in the elbow
Trauma
• All of these cause narrowing and constriction of
the nerve

32. Aching pain on the inside of elbow
Numbness, tingling ring and index finger
esp when bending the elbow
Weakening of grip,difficulty in finger
coordination,muscle wasting- when more
severe compression

35.  In situ or simple decompression
Incising the aponeurotic arch between the
olecranon and medial epicondyle if
conservative treatment fails
In situ decompression is simple and does not influence the blood
supply of the ulnar nerve
Second, it is also effective because it addresses the primary focus
of the lesion, the cubital tunnel.
Third, it has lower rate of postoperative complications and more
opportunities for quicker rehabilitations
Simple decompression, however, is not appropriate in a poor bed,
severe cubitus valgus, or a subluxing nerve

38. Typically in cycling,wt lifters,jackhammers
 Seen also in hook of hamate compression of
ulnar nerve at Guyon’s canal
 Symptoms may be motor or sensory
• Feeling of pins and needles in the ring and little
fingers, which is often noticed in the early morning
• This may progress to a burning pain in the wrist and
hand followed by decreased sensation in the ring and
little fingers.
• The hand may become clumsy when the muscles
controlled by the ulnar nerve become weak.

40. Proper bicycle fitting, handlebar
adjustments, frequent change in hand
position, handle bar and glove padding
Wrist splints
Surgical decompression from failed non-op
mgmt., especially with structural lesions
such as hook of hamate fracture

42.  Radial nerve entrapment at one of 5 sites
 Anatomy- posterior cord to emerge between
long and lateral heads of triceps, spiral
groove of humerus proceeding medially to
laterally to emerge between brachialis and
brachioradialis on lateral elbow to enter the
radial tunnel
 Susceptible:Racquet sports, rowing and wt.
lifting

43. Sensory and motor complaints, although
typically less weakness than with Posterior
interosseous Nerve entrapment
Dull, deep lateral elbow pain
Tenderness over extensor muscle group
Pain reproduced with resisted forearm
supination with elbow flexed

44.  May mimic or coexist with lateral epicondylitis
 Rx:Conservative
neural mobilization techniques
 Neural mobilization is a manipulative
technique by which neural tissues are moved,
relative to their surroundings
 Surgery for persistent symptoms usually
involves releasing the entrapped location

46. PIN is a branch of the radial nerve,
originating in the lateral intermuscular
septum
Purely motor function
Innervates the supinator
Most common in racquet sports, bowlers,
rowers, discus throwers, golfers,
swimmers
 All involve repetitive supination and
pronation

47. Specifically, pain with resisted supination;
EMG/NCS may be helpful to differentiate
between lateral epicondylitis and PIN
Rx:minimize supination during
rehabilitation

48.  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

50.  Notch narrowing
 Ganglion cyst from intraarticular defect
• Often indicative of a labral (SLAP) tear
 Nerve kinking or traction from excessive
infraspinatus motion
 Superior or inferior (spinoglenoid) transverse
scapular ligament hypertrophy causing
compression

51. Vague posterior shoulder pain, weakness and
fatigability
• Weakness/atrophy without pain often suggests
compression at spinoglenoid notch (nerve purely
motor beyond this)
Symptoms may mimic rotator cuff pathology
or instability
 Exam reveals rotator cuff weakness and
possibly supra- and/or infraspinatus atrophy

52. Infraspinatus Atrophy

53.  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.
 Rx: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

56. Plain films may reveal a cervical rib or
exuberant callus from a clavicle/upper rib
fx
MRI and MRA can reveal brachial plexus
anatomy, subclavian vein anatomy or
vascular occlusion/compression
MRA with the arm in abduction can
demonstrate subclavian vein obstruction in
baseball pitchers

57.  Nonoperative treatment focuses on rest, stretching of the
nearby soft tissue structures and posture mechanics;
gradual improvement
 Injection of botulinum toxin into the muscles of the
thoracic outlet (scalenes, pectoralis minor, subclavius)
has potential for obtaining long-term symptom relief, but
further research is needed.
REF:Foley JM, Finlayson H, Travlos A. A review of thoracic
outlet syndrome and the possible role of botulinum toxin
in the treatment of this syndrome. Toxins (Basel). Nov
2012;4(11):1223-35. [Medline]
 Surgical treatments
• Rib resection
• Brachial plexus neurolysis and sympathectomy
• Effort thrombosis also treated with clot lysis with urokinase or heparin

59.  Mech:Compression (entrapment)may occur at the
point where it passes between the two prongs of
attachment of the inguinal ligament.
 Clinical:numbness,mild sensitivity of the skin,or
occasionally persistent burning
 Perception of touch and pinprick are reduced in the
territory of the nerve; there is no weakness of the
quadriceps or diminution of the knee jerk.
 The symptoms are characteristically worsened in
certain positions and after prolonged standing or
walking

60. Dx: The sensory response is absent in
71% of patients with meralgia paresthetica
and is prolonged in 24%
 Electromyographic test results with needle
are normal which may help to differentiate
it from an upper lumbar radiculopathy

61.  Weight loss
 Adjustment of restrictive clothing or
correction of habitual postures
Neurectomy of the nerve,
 Hydrocortisone

62. Piriformis syndrome (false
sciatica)because instead of actual nerve
irritation, it is caused by referral pain.
caused by tight knots of contraction in the
piriformis muscle,
Sciatica refers to irritation of the sciatic
nerve, that arises from nerve roots in the
lumbar spine. The most common cause
of “true” sciatica is compression of one
or more of its component nerve roots
due to disc herniation or spinal
degeneration in the lower lumbar region

64.  During delivery as a result of compression of
the nerve between the head of the fetus and
the bony structures of the pelvis,
 As a consequence of compression of the
nerve between a tumor and the bony pelvis.
in the obturator canal during surgery or with
total hip arthroplasties.
 Malposition of the lower limb for prolonged
periods, entrapment in the adductor magnus
in athletes,

65. Clinical: difficulty with ambulation and the
development of an unstable leg.
Dx: Membrane instability (positive sharp
waves and fibrillation potentials) will occur
within 3 weeks of the nerve injury, and
needle examination should be performed
on patients with groin pain of longer than 3
months

66.  With physical therapy, cryotherapy or a
transcutaneous electrical nerve stimulation (TENS)
unit may be tried.
 "TENS" is the acronym for Transcutaneous
Electrical Nerve Stimulation. A "TENS unit" is a
pocket size, portable, battery-operated device that
sends electrical impulses to certain parts of the
body to block pain signals. The electrical currents
produced are mild, but they can prevent pain
messages from being transmitted to the brain and
may raise the level of endorphins (natural pain
killers produced by the brain).

68. habitual leg crossing,
compression of the
nerve against a bed
railing or hard mattress
in debilitated patients,
or prolonged immobility,
such as that observed
in patients under
anesthesia

70.  Mech:Thickening of the tendon sheaths,or connective tissue
or osteoarthritic changes
 Clinical: Tingling pain and burning over the sole of the foot
develop after standing or walking for a long time
 Dx: EMG and NCV testing values include the following:
 Prolonged distal motor latency: Terminal latencies of the
abductor digiti quinti muscle (lateral plantar nerve) longer than
7.0 ms are abnormal.
 Terminal latencies of the abductor hallucis muscle (medial
plantar nerve) longer than 6.2 ms are abnormal.
 Fibrillations in the abductor hallucis muscle may be present.

71. Rest, NSAIDs, corticosteroid injection
Footwear adjustments, including a medial
arch support
Surgical release ~75% success rate

73.  Mech:perineural fibrosis and nerve degeneration due to
repetitive irritation
 Incidence:occurs most frequently in women (F:M 8:1) aged
40-50 who wear high-heeled, pointed-toe shoes
 Clinical:common digital nerve to the third/fourth metatarsal
spaces is most often affected pain is only felt when the patient
wears shoes. There is localized tenderness over the site of the
neuroma
 Dx :USG is the modality of Choice
 Rx: If there is no relief from symptomatic padding then the
neuroma may be excised

74. CLASS AGENT(S) ACTION
Neurotropic Factors and
Chemoattractants
Ciliary neurotrophic
factor (CNTF)
Nerve growth factor
(NGF)
Insulin-like growth factors
(IGFs)
Brain-derived
neurotrophic factor
(BDNF)
NT-3
NT-4
Promote neuronal
survival and
regrowth
Attract and guide axon
Chemorepellent Factors Semaphorins
Netrins
Others
Selectively repel some
types of
axons
Inhibitors of Connective
Tissue
Formation
Inhibitors of fibroblasts
Collagenases
Others
Decrease fibrosis at the
site of
nerve injury to promote
axonal

76.  Hassouna H, Singh D. Morton's
metatarsalgia: pathogenesis, aetiology and
current management. Acta Orthop Belg.
2005;71(6):646-55
 Neurosurg Focus. 2009 Feb;26(2):E13. doi:
10.3171/FOC.2009.26.2.E13
 Adam’s and Victor’s Principles of neurology
 Entrapment Neuropathies John D. England,
MD

77.  Brain’s Textbook of Neurology
 Ann R Coll Surg Engl. Nov 2011;93(8):634-8.
 Sanders RJ, Hammond SL, Rao NM. Diagnosis
of thoracic outlet syndrome. J Vasc Surg. Sep
2007;46(3):601-4

78. THANK YOU