Entrapment neuropathy

Entrapment Neuropathies
PRESENTER : DR SAI SHASHIDHAR
MODERATOR : DR DEEPTHI MADAM
CHAIR PERSON : DR SARATH SIR

Introduction
• Entrapment neuropathy is defined as : pressure or pressure induced injury to a
segment of a peripheral nerve secondary to anatomic structures or pathologic
processes.
• Result of mechanical dynamic compression of a short segment of a nerve that
passes through a specific site fibro-osseous tunnel or an opening in fibrous or
muscular tissue.

• Symptoms usually begin insidiously and progress slowly.
• Earliest symptoms to occur : tingling and neuropathic pain
• Followed by reduced sensation or complete numbness
• Muscle weakness is noticed later, followed by muscle atrophy
• Diagnosis-combination of history, examination, electrodiagnostic studies, MRI and
high-resolution ultrasonography (US)

Compression of a peripheral nerve predominantly affects the nerve in
three ways:
• Hampering the intraneural blood flow and hence transport of oxygen and
nutrients: Venous blood flow is reduced at 20–30 mm Hg. Frank ischemia
develops at pressures of 60–80 mm Hg. Reduction in the blood flow interferes
with maintenance of neural myelination and frequent compression episodes or
prolonged compression is known to cause demyelination.
• Direct injury to axons also causes nerve dysfunction.
• Interfering with the axoplasmic flow altering the dispersion of metabolites
within nerve: Axonal flow reduces by pressures as low as 50 mm Hg and complete
conduction loss occurs at pressures of 130–150 mm Hg.

Pathophysiology of effect of compression on nerve:
Often mild pressure reduces epineural blood flow
edema and fibrosis in sub-endoneurial space and the synovium
increases pressure on other fibers
further increase in pressure due to lost axoplasmic flow
Axonal damage

Upper limb
Median nerve
1. CTS
2. Pronater syndrome
3. AIN syndrome
Ulnar nerve
1.Cubital tunnel syndrome
2.Guyon’s canal
Radial nerve
1.Radial tunnel syndrome
2.PIN syndrome
3.Wartenberg syndrome
Lower limb
Meralgia
parasthetica
Common
peroneal
entrapment
Tarsel tunnel
syndrome
Piriformis
syndrome

CARPAL TUNNEL SYNDROME
The carpal tunnel is formed by
• Dorsally : Carpal bones forming an arch
• Volar aspect : Transverse carpal ligament (TCL).
• Medially it is attached to the pisiform and the
hook of the hamate and
• Laterally to the tubercle of the scaphoid and the
trapezium’s crest.

Ten structures from the volar forearm
pass through the carpal tunnel :
• Eight flexor tendons to the fingers
FDS & FDP
• Flexor pollicis longus
• The median nerve.

• The depth of the tunnel varies from 10 mm to 13 mm.
• In the carpal tunnel the most common location of compression is 1 cm distal to
proximal border of ligament which corresponds to the thickest part of the
ligament.
• Normal pressure within the carpal tunnel measures 2.5 mm Hg.
• An external compression of 20–30 mm Hg reduces the venule flow in the
epineurium and the nerve gets edematous, and a pressure of greater than 30 mm
Hg diminishes the nerve conduction.

Clinical features :
• The most common symptom is “nocturnal acroparesthesia,” consisting of a
painful tingling and numbness in the thumb and one of the radial digits, which
may even disturb sleep.
• Thenar atrophy is a late sign often in neglected cases over a long duration of
disease and patients often report less pain by this time!
• Tinel sign
• Phalen’s test

Clinical grading of CTS severity :
• Mild : numbness, tingling, or discomfort but no sensory loss or weakness, no
sleep disruption, and no difficulty with hand function or interference with ADLs.
• Moderate : sensory loss, nocturnal symptoms occasionally disrupt sleep.
Symptoms may interfere slightly , but the patient should be able to perform all
ADLs.
• Severe : weakness, symptoms are disabling and prevent the patient from carrying
out one or more ADLs. Nocturnal symptoms routinely disrupt sleep.

Provocative tests for CTS :
• TINEL’S SIGN
• PHALEN’S TEST
• DURKAN’S TEST
Sensitive tests :
• WEBER 2 POINT DISCRIMINATION TEST
• SEMMES WEINSTEIN MONOFILAMENT TESTS

• Tinel’s sign : An electric shock like or tingling sensation is felt in the
distribution of median nerve after a firm but gentle tap on the median nerve at
the TCL region.

• Phalen’s wrist hyperflexion test :
Paresthesia in the median nerve
distribution on flexion of the wrist for 60
seconds
• Reverse Phalen’s test : has also been
found positive and useful but in moderate
to advanced compression predominantly.

• Durkan’s test : Direct median nerve compression at TCL for 30 seconds also elicits
similar response in a patient with CTS. More sensitive test.

• Semmes-Weinstein monofilament test : The most sensitive test for detecting early CTS.
These threshold tests reflect both sensory changes and decreases in sensory nerve function
quite reliably and early.

Diagnostic Studies :
Electrodiagnostic Testing : The goals of an electrodiagnostic examination are basically to:
• Localization of lesion
• Evidence of reinnervation or of ongoing axonal loss
• Type of fibers involved motor, sensory fibers, or both
• Define the extent of injury to neural tissue (axon loss, demyelination)
• Defining degree of axonal loss, the continuity of axon.

Types of Nerve Injury
Neurapraxia(1st degree)-brief or mild compression on the nerve that distorts the
myelin, resulting in segmental demyelination but leaving the axons intact
Axonotmesis-Axonal damage that results in wallerian degeneration; distal to
the injury, the axons and their investing myelin sheath degenerate
2nd –Degree- Axonal loss is associated with intact endoneurial tubes as well as
intact perineurium and epineurium
3rd Degree- Axons and endoneurium are damaged while leaving the
perineurium and epineurium intact.
4th –Degree- Axons, endoneurium, and perineurium are disrupted, but the
epineurium is intact
Neurotmesis(5th -degree)-complete disruption of the nerve and all
supporting structures.

Diagnostic criteria for carpal tunnel syndrome (CTS) on
electrodiagnostic study :
Evidence of sensory nerve fiber compression
• Delayed or absent motor nerve sensory action potential (SAP), > 3.4 ms
• Increased median-to-ulnar latency difference of the fourth finger SAP (and 0.5ms)
Evidence of motor nerve fiber compression
• Prolonged distal motor latency (> 4.2 ms)
• Denervation signs in the abductor pollicis brevis muscle

Electrodiagnostic grading
• Mild : Prolonged (relative or absolute) sensory latencies with normal motor
studies. No evidence for axon loss.
• Moderate : Abnormal median sensory latencies and relative or absolute
prolongation of median motor distal latency. No evidence of axon loss.
• Severe : Evidence of axon loss

Radiographs in standard AP and lateral and carpal tunnel view are ordered but are
helpful only to identify and study cause of CTS due to:
• Trauma
• Arthritis
• Degenerative cases may show calcification at the carpal region in carpal tunnel view.

Magnetic resonance imaging (MRI) and ultrasonography :
• Measurements of the canal size.
• Flattening of the nerve at the level of hook of hamate is a usual finding.
• Cross-sectional diameter ratio of median nerve : In normal individuals it should be
one, an increase in the diameter is diagnostic. It is checked at the level of pisiform
to distal radius.
• Fatty infiltration of median nerve
• Bursitis and
• Demonstration of neuroma or other space occupying lesions.
• Incomplete resection of ligament.

TREATMENT
• Nonsurgical measures
• Steroid injections
• Surgical CTR including endoscopic methods.
The decision for specific modality relies on severity of nerve
involvement judged by clinical examination and electrophysiological studies,
chronicity of symptoms and individual patient choices.

Nonsurgical Measures
Splinting :
• Wrist immobilization in night and intermittently
during day time.
• The position of splint is debatable, it has been
demonstrated that the pressure is lowest 2˚ ± 9˚ of
extension and 2˚ ± 6˚ of ulnar deviation.
Oral Medications :
• Anti-inflammatory medications like nonsteroidal anti-inflammatory drugs (NSAIDs) and
supplementation with pyridoxine (B6) and methylcobalamin for its neurotropic action.
• Oral steroids and diuretics to lower the interstitial fluid pressure.

Local Corticosteroid Injections

Surgical Release
• Open release
• Limited open method
• Endoscopic methods
Choice of method of release is mainly surgeon dependent and
comfort of the Surgeon.

OPEN RELEASE
• It is the most common used method for carpal tunnel decompression.
• Various authors have described different incisions although the shape of incisions varies , they
commonly involve similar deep dissection releasing palmar fascia and carpal ligament
longitudinally.
• The cutaneous incision line is ulnarly located with respect to the thenar crease and is located 2
mm ulnarly to the fourth ray.
• It is important to keep the superficial and the deep dissection lateral so as to prevent injury to
motor branch and palmar cutaneous nerve of median nerve.

Principles for the nerve release are as follows :
• Care is taken to prevent laceration to motor branch and palmar cutaneous branch of median
nerve.
• Internal neurolysis, epineurotomy and tenosynovectomy often initially performed commonly
leads to skin adhesions, neurodermodesis phenomenon, algoparesthesias. Hence internal
neurolysis has been definitively abandoned.
• The sectioning of the TCL is performed in layers and is kept along the 4th ray.
• While sectioning the midpalmar adipose tissue one should also be extremely careful not to injure
the superficial vascular arch.
• In majority of cases there is hourglass constriction in the median nerve at the level of hook of
hamate while occasionally there is marked compression of the nerve with ecchymosis.

Limited open carpal tunnel release: Limited-incision CTR
• Limited-incision CTR techniques similar to endoscopic surgery were developed to
Decrease palmar discomfort and
Hasten the return to activities.
• A “palm-only” less than 2 cm mini-incision is used to release the transverse carpal
ligament. Some authors have recommended both proximal and distal release.

Endoscopic Technique
• In an attempt to reduce the complications of open release like scar tenderness and prolonged
healing time endoscopic procedures were developed.
• Both single and dual portals have been described. In single portal technique a portal placed
midway between flexor carpi ulnaris (FCU) and flexor carpi radialis (FCR). With wrist extended
and endoscopic blade assembly aligned to ring finger distal edge of ligament is identified and
sectioned from distal to proximal in controlled fashion.
Contraindications of endoscopic
procedures include:
• Proliferative synovitis
• Stiffness of wrist joint
• Space occupying lesions in the tunnel
that obliterate the view of canal.

Complications of Surgical Procedures
• Motor and/or palmar cutaneous branch injuries
• Hypertrophic scar formation and scar tenderness
• Pillar pain
• Injury to superficial palmar arch (more with
endoscopic release)
• Tendon adhesions
• Infection
• Incomplete CTR
• Wound hematoma
• Reflex sympathetic dystrophy
• Weak grip strength
• Finger stiffness
• Laceration of ulnar artery (more
with endoscopic release)
• Recurrence 7–20%
• Transient paresthesias (more with
endoscopic release).

ANTERIOR INTEROSSEOUS NERVE (AIN) COMPRESSIVE NEUROPATHY
(ANTERIOR INTEROSSEOUS NERVE SYNDROME) :
• It is a compressive neuropathy involving the anterior interosseous nerve (AIN)
manifesting as isolated motor deficit of muscles innervated by the nerve without
any sensory symptoms.
• Has two specific presentations:
• An acute self-resolving nontraumatic, inflammatory syndrome
• A chronic often traumatic compression that needs release commonly.

• The AIN arises from the posterolateral part of median
nerve beneath the fibrous arch of FDS, approximately 4
cm distal to medial epicondyle.
• AIN is terminal motor branch of median nerve. AIN has
motor innervation only (no sensory).
• It lies between flexor digitorum profundus (FDP) and
flexor pollicis longus (FPL) on the interosseous membrane.
• The following are the muscle it innervates:
• Flexor pollicis longus
• Radial half of FDP (to index and middle finger)
• Few branches to PT
• Terminally to pronator quadratus.

The potential sites of AIN entrapment in elbow and forearm are as follows :
• The most common site and cause is where the nerve
passes between the two heads of PT. The tendinous edge
promulgating as a fibrous band of deep head of PT
(underside of the humeral origin)
• Flexor digitorum profundus arcade
• Edge of lacertus fibrosus
• Thrombosed ulnar radial or ulnar collateral vessels
crossing the nerve near its origin.

Etiology
• Spontaneous compression
• Anatomic variations
• Trauma : supracondylar fractures (usually traction injury)
• Infections
• Iatrogenic cause : venipuncture, catheterization in cubital fossa.
• Compartment syndrome
• Volkmann ischemic contracture (VIC).

Clinical Presentation
Symptoms:
• Motor deficits only : Patient with complete AIN palsy loses motor function of all the 4
muscles supplied by AIN. The patient is unable to flex the interphalangeal (IP) joint of the
thumb and the distal interphalangeal (DIP) joint of the index and long fingers. A typical
pinch attitude occurs where patient is unable to make a ring by bringing together the tips
of thumb and index finger and rather it transforms into a “Peacock’s eye”.
On physical examination there is specifically:
• Patient is unable to make the OK sign which tests for weakness of FDP and FPL. There
may be weakness of grip and pinch, specifically thumb, index and middle finger flexion.

Diagnostic studies :
• Sensory and motor nerve conduction studies of the median nerve are usually
normal.
• EMG Reveal abnormalities in the FPL, FDP index and middle finger and pronator
quadratus muscles (in 85% patients). Can define the severity of involvement and
can also rule out more proximal lesion.
• MR imaging- signal intensity changes related to muscle denervation,FDP,FPL, and
pronator quadratus muscles.
• US-limited for the evaluation-because of the small size of the nerve and relatively
deep location.

TREATMENT
• Nonoperative treatment is commonly effective for acute onset lesions while long
standing ones do not always improve with these measures.
• Empirically observation rest and splinting in supination help if no organic lesion for
compression is identified. Spontaneous recovery usually occurs within 3 to 12 months.
• Systemic disorders should be corrected (diabetes mellitus, alcoholism and
hypothyroidism). Additional vitamins like pyridoxine 100 mg for a few weeks (6–8 weeks)
may be given.
• Operative indication is needed for surgical decompression of AIN in case nonoperative
measures fail or if the cause of nerve compression is evident (supracondylar spur,
forearm mass).
• The cause of compression should be relieved and surgical decompression is done by a
long incision beginning 5 cm proximal to elbow near the supracondylar spur to medially
along the biceps tendon in forearm and further 5 cm into forearm. The nerve is
decompressed all along.

• Cutaneous nerves should be preserved
• Nerve should be isolated from the brachial vessels and released from
compressive lesions
• Excise the supracondylar spur and fibrous bands (ligament of struthers, pronator
band, lacertus fibrosus, etc.)
• Preserve the branches to PT
• Interfascicular neurolysis may be necessary in some long-standing cases
(resection and anastomosis is not recommended).

PRONATOR SYNDROME
It is a compression of median nerve between the two heads of pronator muscle at the level of
elbow joint.
The potential sites of entrapment include:
• Fibrous bands between ulnar and humeral heads of PT where the median nerve passes most
common cause of compression.
• Thickened or tight bicipital aponeurosis (lacertus fibrosus)
• Supracondylar process: Present in 1% of population. It is a residual osseous structure on
distal humerus that gives rise to ligament of Struthers (this structure is different from arcade of
Struthers which is a site of ulnar compression neuropathy in cubital tunnel syndrome). The ligament
travels from tip of supracondylar process to medial epicondyle. The site is a rare point for
compression.
• Flexor digitorum superficialis (FDS) aponeurotic arch
• Honeymoon paralysis: This is a transient compression of median nerve at elbow due to
prolonged compression on forearm.
• Other uncommon causes of compression include: Compression due to casting (iatrogenic),
hypertrophic PT, or its high origin especially the humeral head, an anomalous insertion of the
coracobrachialis muscle.

Symptoms:
• Insidious onset of aching pain in the volar aspect of the proximal forearm and the distal
arm. Pain is increased by exertion, excessive use of extremity and forceful pronation.
• Paresthesias and hypoesthesias similar to CTS is present but the difference being that it is
more severe with pronation and supinatioin rather than wrist flexion and also sensory
loss over the distribution of palmar cutaneous branch of median nerve.
Physical examination:
• Tenderness on the median nerve in the proximal forearm
• Weakness of the muscles supplied by median nerve
• Provocative tests are specific for different sites of entrapment

• Positive Tinel’s sign in the proximal anterior forearm that is usually present only
after 4–5 months of compression
• Resisted elbow flexion with forearm in supination (compression at bicipital
aponeurosis)
• Direct pressure over proximal pronator muscle increases paresthesias
• Resisted forearm pronation with elbow flexed and gradually extended
(compression at two heads of PT)
• Resisted contraction of FDS to middle finger.
Diagnostic Studies
• Radiographs: It may reveal supracondylar process
• Electromyogram and NCV: To exclude other sites of nerve entrapment.

Differential Diagnosis
• Carpal tunnel syndrome:
– Absence of pain over proximal volar forearm
– Absence of sensory disturbances over the distribution of palmar cutaneous branch of the
median nerve
– Phalen’s/Durkans positive
• Cervical radiculopathy : Pain localized in the C6 and C7 dermatomes with weakness of biceps and
diminished biceps reflex.
• Thoracic-outlet syndrome : Symptoms in C8 and T1 distribution
• Medial epicondylitis.

Treatment
“Nonoperative” is effective in 50% of patients.
• The typical nonoperative treatment comprises rest, splinting and NSAIDs for 3–6
months but effect may be seen up to a year or later.
• Patients experiencing progressive symptoms and also in patients with less than
satisfactory control of the symptoms operative treatment is indicated.
“Operative treatment” involves surgical decompression of median nerve. Typically
the decompression of nerve is done simultaneously at all the possible compression
sites. The operative treatment is effective in 90% patients.

CUBITAL TUNNEL SYNDROME
It is a compressive neuropathy of the ulnar nerve.
Anatomy of cubital tunnel : The cubital tunnel is a
fibroosseous tunnel that connects the extensor surface of
the upper brachium to the flexor surface of antibrachium.
Roof : Formed by Osborne’s fascia and Osborne’s ligament
(fibrous band from the medial epicondyle to the
olecranon).
Floor : Formed by ulnar groove of the medial epicondyle
anteriorly in its first two parts with the posterior and
oblique portions of the ulnar collateral ligament and elbow
joint capsule in the third part.
Walls : Formed by medial epicondyle and olecranon.

Pathophysiology
• The shape of the cubital tunnel changes with elbow movements. As the elbow flexes
the cubital tunnel converts from a round configuration to a flattened triangle
(reducing the cross-sectional area by approximately 55%).
• Medial epicondyle is a fixed structure while for each 45˚ of forward flexion the
olecranon moves forward some 5 mm.
• The combination of the above two of these phenomenon produces an elongation
stretch of approximately 47 mm on the ulnar nerve from full extension to full flexion.
• There is increase in the cubital tunnel pressure from 9 mm Hg to 63 mm Hg with full
flexion that substantially increased to 209 mm Hg with FCU contraction. The pressure
increase can be partly dissipated by division of Osborne’s fascia.

Most common site for ulnar nerve compression is
• Between the two heads of FCU/aponeurosis (most
common site) followed by
• Arcade of Struthers : In up to 70% of the population, a
band of fascia extends from the medial head of the
triceps (8 to 10 cm proximal to the medial epicondyle)
to the medial intermuscular septum (arcade of
Struthers). This may be a source of entrapment of the
ulnar nerve followed by
• Hiatus in medial intermuscular septum where the
ulnar nerve pierces the septum to enter posterior
compartment followed by
• Location between Osborne’s ligament and medial
collateral ligament (MCL).
Less common sites of compression include : Medial head of triceps, Medial epicondyle, Fascial
bands within FCU, Proximal edge of the FDS aponeurosis.

Extrinsic and miscellaneous causes :
• Fractures and nonunions
• Cubitus varus or valgus deformities (Tardy ulnar nerve palsy)
• Osteophytes in the cubital tunnel
• Heterotopic ossification
• Tumors, cysts and medial epicondylitis
• Burns
• Iatrogenic : Fixation of intercondylar fractures and medial epicondyle fractures in
malposition reducing the tunnel volume. Radial head excision produces lateral instability
and tardy ulnar like phenomenon.

Symptoms:
• Sensory symptoms of small finger, ulnar half of ring finger, and ulnar dorsal hand (it is localizing
sign that can exclude a compression in Guyon’s canal)
• Night symptoms: Due to flexion of the arm while sleeping, may even awaken the patient from
sleep.
On Physical examination:
• Inspection and palpation
• Atrophy of first web space and the interosseous muscles.
• Clawing of the ring and fifth finger. The clawing is due to loss of intrinsic muscles especially the
lumbricals that produce extension at the interphalangeal joint (IP) joint so there is flexion at the
IP joints
• MCP joint hyperextension.
• Subluxation of ulnar nerve on the medial epicondyle during flexion of elbow.

Sensory examination : Hypoesthesia in ulnar one and half digits and dorsal ulnar half of hand:
The latter is a localizing sign of high ulnar nerve palsy.
Motor testing : Reduced strength/paralysis of deep head flexor pollicis brevis (FPB), adductor
pollicis, all hypothenar muscles, 4th and 5th lumbricals and interossei. The following signs can be
elicited utilizing this knowledge in a classic case.
• Weak grasp: Because of loss of flexion power of metacarpophalangeal joint (MP) joint
• Weak pinch: Because of loss of adduction of thumb (as much as 70% of pinch strength is lost)
Froment sign :
Compensatory flexion of thumb IP joint by FPL (supplied
by AIN) during key pinch. It compensates for the loss of
(MCP) flexion by adductor pollicis supplied by ulnar
nerve.
Adductor pollicis muscle normally acts as a MCP flexor,
first metacarpal adductor, and IP extensor.

Bunnell’s O’test : Hyperextension at MP
joint and hyperflexion of IP joint making an
“O” when the patient is asked to make pulp
to pulp contact of thumb and index finger .
Earle and Valstou (cross your
finger test) : Inability to cross the
middle over index (testing volar
interossei of first and dorsal
interossei of second) or vice versa.

Jeanne sign: Compensatory thumb MCP hyperextension and thumb adduction by EPL
supplied by radial nerve during key pinch. The EPL compensates for loss of IP extension and
thumb adduction by adductor pollicis supplied by ulnar nerve

Wartenberg sign: Persistent abduction and extension of small finger during attempted
adduction, occurring secondary to weak third palmar interosseous and small finger
lumbrical.

Extrinsic weakness
• Pollock’s test : Loss of flexion of distal IP joint of the ring and little finger—due to
weakness of two ulnar FDPs
• Bowden and Napier : Partial loss of wrist flexion with inability to perform power grip
with a neutral wrist (due to paralysis of the flexor carpi ulnaris)
• Conversion of “X” crease to “Y” pattern of intersected crease: Normally the little and
ring fingers are flexed fully into the palm on closing the fist to give an X configuration to
the folded creases of the little finger. Loss of DIP flexion in ulnar nerve palsy converts the
X configuration to a Y.

Provocative tests :
• Positive Tinel’s sign over cubital tunnel
• Elbow flexion test: An elbow flexion of more than 60 seconds reproduces symptoms
• Direct compression of cubital tunnel exacerbates symptoms.
Electromyogram/nerve conduction velocity :
• Nerve conduction velocity less than 48 m/s or difference on two sides of more than 10
m/s is suggestive.
• Distal motor and sensory latencies higher than normal or unobtainable.
• Low amplitudes (less than 50%) of sensory nerve action potentials and compound
muscle action potentials.
• A B
• A B

Diagnosis
• Pain on pressing on the ulnar nerve at the elbow
• A Tinel’s sign over the ulnar nerve as it passes beneath the area of entrapment
• Subluxation of the nerve
• Sensory loss over ulnar half of dorsum of hand
• Extrinsic and intrinsic weakness
• Reproduction of symptoms by holding the elbow fully flexed.
• Cervical spondylosis
• Thoracic outlet syndrome
• Ulnar nerve entrapment at Guyon’s canal
• Double crush phenomenon

Treatment
Nonoperative treatment involves NSAIDs, activity modification and night-time
elbow extension splinting.
Operative : The interventions can be grouped into three categories as follows:
1. In situ nerve decompression (simple decompression).
2. Anterior transposition (subcutaneous, intramuscular or submuscular).
3. Medial epicondylectomy.

Decompression of Cubital Tunnel
Indications of simple decompression are:
• Mild symptoms and a short history
• Nonsubluxating nerve and symptoms not associated with varus or valgus deformity
• No prior evidence of injury or degenerative changes that distort anatomy
• Compression localized to be due to Osborne’s fascia.
This is done through medial approach under tourniquet control.
This open release of cubital tunnel is performed through an incision 5–10 cm long
beginning proximally.
One should avoid opening the nerve too much proximally as it may lead to ulnar nerve
subluxation.
The procedure can also be performed in endoscopic assistance.

The advantages of the procedure are as follows:
• Simple procedure and easy to perform: The aponeurosis is simply divided over the ulnar
nerve. This can also be performed under local anesthesia.
• Safe as the handling of ulnar nerve is minimal not interfering with the intrinsic and
extrinsic blood supply.
• Prompt result if the site of compression of the nerve is limited to Osborne’s fascia.
Poor results are associated with:
• Presence of intrinsic muscle atrophy
• Compression due to secondary causes (deformity at elbow (neuritis), tumors or cyst as
cause of compression, etc.).

Ulnar Nerve Decompression and Anterior Transposition
Indications
• Failed in situ release: Secondary surgery
• Intractable, long-standing ulnar neuritis localized to the elbow
• Throwing athlete
• Metabolic/granulomatous neuropathy
• Mobilization associated with nerve repair at the elbow
• Preventive
• Open reduction of intra-articular fractures
• Elbow reconstruction and arthroplasty.

The procedure can be performed in various ways :
Subcutaneous:
The nerve is transposed anteriorly beneath the skin and subcutaneous fat after releasing
the intermuscular septum proximally and freeing the nerve 6 cm proximally and 3–4 cm
distally.
The nerve is stabilized in position by suturing a flap of pronator muscle raised from the
medial epicondyle to the anterior skin flap.
This is the most commonly performed procedure and preferred for severe nerve
compressions.
Intramuscular transposition:
The nerve is placed in the groove formed by splitting the muscle.
The problem is rescarring and hence neural compression.

Submuscular :
• It places the nerve in an intermuscular
interval, where nerves normally run.
• The indication is mainly for recurrent cases.
• The flexor pronator muscle group is
transected sharply; leaving a cuff of tissue
on the medial epicondyle that is repaired
after the nerve is transposed.
• This procedure is associated with the least
recurrence rates but requires a bit more
experience.
• It is commonly preferred by the experienced
surgeons over subcutaneous transposition
for moderate nerve compressions.

Medial Epicondylectomy
• Serves to decompress the nerve and also moves it anteriorly.
• Though theoretical advantages are many but the biggest problem is of creating valgus
elbow instability.
• Only 19% of medial epicondyle can be resected without producing instability.
• So a complete epicondylectomy is to be combined with medial collateral ligament (MCL)
reconstruction/repair.
• The technique could be specifically preferred for subluxating nerves and recurrent cases
or very severe neural compression.
Complications :
• Recurrence: Often due to inadequate decompression, perineural scarring. There is higher
rate of recurrence than after CTR. This should be treated by extensive re-exploration,
microsurgical neurolysis and autogenous saphenous nerve wrapping.
• Neuroma formation.

ULNAR TUNNEL SYNDROME
• Direct compression of the ulnar nerve in the Guyon’s canal. It is also known as handlebar
palsy (seen in long distance cyclists who rest their hand on the cycle handle bar).
• The ulnar nerve in forearm lies deep to the FCU. Distally it becomes more superficial as it
crosses the myotendinous junction of FCU. Radially it is accompanied by the ulnar artery and
FCU lies on the ulnar aspect as it progresses further and enters the ulnar canal/tunnel
(Guyon’s canal).
• Guyon’s canal: It is a 4 cm long structure starting at the proximal extent of the volar carpal
ligament and ends at the arch of the hypothenar muscles.
The ulnar canal contains :
• Bifurcation of ulnar nerve: The ulnar nerve divides into the superficial sensory and deep
motor branches (Fig. 25). The deep branch supplies all the interosseous muscles and the
third and fourth lumbricals, the hypothenar muscles and some thenar muscles [the adductor
pollicis and the medial head (deep) of the FPB].
• Ulnar artery.

The various causes of ulnar tunnel syndrome include:
Anatomical (anomalies or malformations):
• Ganglion cyst: most common cause
• Fibrous bands
• Accessory flexor digiti minimi, palmaris longus and
palmaris brevis hypertrophy
• Congenital bands
• Pisiform-hamate coalition.
Traumatic
• Repetitive trauma
• Nonunion or fracture of hook of hamate
• Dislocation of pisiform
• Handlebar palsy.
Systemic
• Diabetes
• Alcoholism
• Hypothyroidism.
Others
• Ulnar artery thrombosis,
aneurysm and hemangioma
• Inflammatory arthritis
• Calcinosis (metastatic and
scleroderma)
• Pigmented villonodular synovitis
(PVNS).

• Clawing of the ring and little finger that is more pronounced than cubital tunnel
syndrome
• Weakened grasp: From loss of MP joint flexion power
• Weak pinch: From loss of thumb adduction (as much as 70% of pinch strength is lost)
• Froment sign
• Jeanne sign
• Wartenberg sign
Diagnostic Imaging
• Plain radiographs may show hook of hamate fractures or other bony
abnormalities.
• MRI is useful to evaluate ganglion cysts and other soft tissue conditions known to
produce ulnar nerve compression.
• MR angiography may additionally reveal aneurysms and thrombosis.

• Cubital tunnel syndrome (high ulnar nerve palsy) differentiate by the presence of:
– Less clawing (due to involvement of long flexors also that remain weak to
flex the joints)
– Positive elbow flexion test
– Motor deficit to ulnar-innervated extrinsic muscles
– Sensory deficit to ulnar half of dorsum of the hand
– Tinel’s sign positive at the elbow.
• Cervical spondylosis
• Thoracic outlet syndrome
• Guillain-Barré syndrome.

Treatment
Nonoperative management is indicated in mild symptoms and comprises of activity
modification, NSAIDs and splinting.
Operative treatment is needed for obvious disability due to clawed fingers, loss of power in
pinch and grasp. It is usually indicated for severe symptoms or failed nonoperative treatment.
• Local decompression: incision given in line with the radial aspect of ring finger.
Decompression is done sequentially from zone 1 to 3. Ganglions and other masses are
removed. Nonunion hook of hamate is excised. In case of arterial thrombosis or aneurysm
reconstruction with autogenous vein graft is performed especially if the thrombosis extends
beyond the common digital arteries.
• Tendon transfers: For correction of clawing and to restore power of pinch
-Lasso procedure can correct the clawing deformity
-Using the FDS of ring finger or extensor carpi radialis brevis (ECRB) to restore
power pinch.

RADIAL TUNNEL SYNDROME (RTS, SUPINATOR SYNDROME)
• It is a compressive neuropathy of the radial nerve main trunk in the proximal forearm
before/at/just after it splits into main trunk posterior interosseous neuropathy (PIN) and
the minor trunk (sensory branch) which results in refractory lateral elbow and forearm
symptoms (both sensory and motor).
• Compression of only sensory nerve [radial sensory nerve, (RSN)] is called Wartenberg
syndrome, while that of only motor component (PIN only is called PIN compression
palsy) and are distinct entities.
• Radial tunnel syndrome is possibly a misnomer and not a true representative of the
compressive neuropathies for following reasons:
-Prominent focal tenderness
-Normal neurologic function
-No confirmatory electrodiagnostic evidence of nerve dysfunction.

• The radial tunnel (approximately 5 cm in length)
originates near the level of the radiocapitellar
joint where the nerve lies against the joint
capsule continuing further to the distal border
of supinator.
• The boundaries of the tunnel are as follows:
Medially : brachialis muscle proximally and the
biceps tendon distally
Roof and lateral : ECRL and the ECRB
Floor : Capsule of radiocapitellar joint.

Etiology of Nerve Compression
• Repetitive pronosupination movements as in industrial workers causing microtrauma
• Monteggia fracture dislocation, radial head fracture (with or without dislocation)
• Lesions compressing the nerve in the tunnel like ganglion, neuromas and lipomas
• Rheumatoid synovitis of radiocapitellar joint
• Iatrogenic while surgery on radial head/neck or replacement.

There are commonly mentioned five potential sites of
compression as follows:
1. Between the brachialis and BR
2. “Leash of Henry” are recurrent radial vessels that fan out
across the PIN at the level of the radial neck causing
3. Distal border of supinator muscle at its edge
4. At the origin of ECRB or fibrous bands within ECRB
5. “Arcade of Frohse” that lies at the proximal edge of the
superficial portion of the supinator.

Clinical presentation
• The main complaint is pain in the forearm and wrist distal to the lateral epicondyle about
4–5 cm in the region of the mobile wad, the ECRL, ECRB and BR and over the course of
the radial nerve down the forearm
• The location of pain varies with the site of nerve compression—pain just distal to the
lateral epicondyle of the elbow is due to compression at arcade of Frohse.
• The various characteristics of pain in PIN compression include:
-Presence of night pain and pain at rest
-Pain increases with activities requiring wrist extension and forearm pronation.
• (Quick examination finding to identify PIN compression) Patient has pain and inability to
extend the middle finger against resistance with elbow extended and forearm pronated
with wrist neutral.

• There is tenderness over the region of the PIN in forearm 4–5 cm distal to lateral
epicondyle as elicited by rolling fingers perpendicular to the PIN course over extensor
muscles. Maximal site of tenderness in radial tunnel verses on the ECRB differentiates
from tennis elbow.
• Tinel’s sign may elicit tingling along the course of sensory branch of radial nerve
(uncommon).
• Weakness of wrist extension: The patient is unable to extend wrist in ulnar deviation
– The wrist will extend with radial deviation due to intact ECRL supplied by radial
nerve but not in ulnar deviation (paralyzed/weak ECU supplied by PIN).
• Provocative tests :
– Painful resisted supination: Compression at the Arcade of Frohse.
– Painful resisted middle finger extension test : Compression at ECRB and BR.

• Tennis elbow (co-exists in 5% cases) :
– Maximal tenderness at the ECRB
– Pain with resisted wrist extension in radial deviation at the ECRB.
• Posterior interosseous nerve syndrome (only motor symptoms no sensory involvement)
• Cervical spondylosis and radiculopathy
• Ganglion cyst of proximal radioulnar joint
• Intra-articular elbow pathology

Diagnosis of Radial Tunnel Syndrome
• Pain in lateral elbow and forearm (absent in PIN compression syndrome)
• Paresthesias : Numbness and/or tingling that also impairs the patient’s fine motor
control of affected digits
• Weakness of pinch and grip
• Weakness of finger MCP joints
• Positive provocative maneuvers.

TREATMENT
• Conservative and rehabilitative treatment comprises of activity modification, stretching,
splinting, medications (NSAIDs, neurotropic vitamins and limited use of corticosteroids).
• Local corticosteroid injection is given to facilitate the rehabilitation and improve
symptoms.
• “Surgical decompression” is typically indicated for:
-Symptoms that persist for greater than 3 months of nonoperative treatment or
patients with worsening neurology identified in the first three weeks.
-The other definitive indication is a compressive mass detected on imaging.

TECHNIQUE
• The radial tunnel can be approached both anteriorly and posteriorly.
• The Volar approach is between the BR and biceps and is most popular.
• The Dorsal approach between ECRB and EDC, between BR and ECRL, Transmuscular BR-
splitting.
• By any method it is imperative to decompress with sequential release of:
Fibrous bands connecting brachialis and BR
Leash of Henry (ligate and cut)
Fibrous edge of ECRB
Arcade of Frohse (most important structure to be released)
Distal edge of supinator
Release superficial radiocapitellar joint superficial bands.

WARTENBERG SYNDROME
• Cheiralgia paresthetica, hand cuff neuropathy/neuropraxia, wristlet watch neuritis: It is
the compressive neuropathy of the superficial radial sensory nerve (RSN).
• Pathoanatomy of nerve compression : During forearm pronation there is a scissoring
action of BR and ECRL tendons which may cause superficial radial nerve (SRN)
compression.
• Etiological causes :
– Trauma (Colles’ fracture and stretch injuries by bony spike)
– Diabetes
– Lipoma
– Operative scars
– Brachioradialis anatomic variations.

Clinical presentation
• The patient should be evaluated for any history of forearm fractures, trauma, wearing
tight handcuffs, bracelets, tight wrist band, wristwatch band or plaster cast.
• The symptoms include an ill-defined pain over dorsoradial hand with reluctant to wear
watch, paresthesias and numbness over dorsoradial forearm.
• Repetitive wrist flexion and ulnar deviation aggravates the symptoms and motor
symptoms are conspicuously absent.
• On examination:
– Tinel’s sign positivity is the most common finding, over the superficial sensory radial
nerve. It can be positive at the exit point of the nerve from forearm fascia (8–9 cm from
radial styloid) or over the radial styloid or over both.
– Dellon’s provocative test is positive: Increased symptoms on wrist flexion, ulnar
deviation and pronation for 1 minute.
– Finkelstein test is positive in 96% of cases because of traction on the nerve.

Differential Diagnosis :
• De Quervain’s tenosynovitis:
– No increase in pain on wrist pronation
– The symptoms are present with activity while in patients with RSN syndrome, the
symptoms are also present at rest
• Lateral antebrachial cutaneous nerve neuritis
• Intersection syndrome.
Treatment :
• Nonoperative management : Rest, activity modification, NSAIDs and wrist splints.
• Additional modalities for peripheral nerve stimulation like pulsed low-intensity infrared
laser or local ultrasonics may be selectively provided.
• Surgical decompression (done only after 6–8 months of aggressive treatment) is done via
longitudinal incision volar to Tinel’s sign (to protect the lateral antebrachial cutaneous
nerve).

POSTERIOR INTEROSSEOUS NERVE COMPRESSION SYNDROME
• It is a compressive neuropathy involving the posterior interosseous branch of the radial
nerve (PIN) with only motor dysfunction and no sensory dysfunction.
Clinical presentation :
• The patients typically present with dropped fingers and thumb. ECRL is preserved as it
receives supply along with BR before the nerve enters radial tunnel.
• Predominant involvement of medial branch may cause weakness of the ECU, extensor
digitorum communis and extensor digiti minimi
• Predominant compression of lateral branch may cause weakness of the EPB, APL,
extensor indicis proprius and EPL.

Etiology :
• Lipomas
• Synovial chondromatosis
• Ganglia from anterior capsule of radioulnar joint.
• Septic arthritis of elbow
• Pannus in rheumatoid arthritis
• Fibrous bands in muscle or anterior to capsule
• Cervical radiculopathy at C6–7 with predominant motor symptoms
• Brachial plexopathy (partial involvement)

Treatment
• The management is essentially same as that for the RTS except that the NSAIDs may not
be needed due to absence of pain.
• Nonoperative management is done for 4–6 months followed by surgical release of the
nerve if there are no improvement or neurology progresses.
• Surgical release is also indicated in delayed cases with evident atrophy of muscles at
presentation.

PIRIFORMIS SYNDROME(DEEP GLUTEAL SYNDROME, PELVIC
OUTLET SYNDROME, INFRAPIRIFORM FORAMEN SYNDROME)
• It is a painful neuromuscular disorder that
occurs when the piriformis muscle irritates
and/or compresses the proximal sciatic
nerve.
• The piriformis muscle is a flat pyramid-
shaped muscle originates from anterior
surface of the sacral 2nd–4th vertebrae,
sacrotuberous ligament, and the roof
(superior margin) of sciatic notch.
• Muscle then passes through the greater
sciatic foramen and inserts onto the
posteromedial region of greater trochanter
near the piriformis fossa.

Symptoms:
• Deep, boring, ill-defined buttock pain or
posterolateral thigh pain that may be
referred along the course of the sciatic
nerve also.
• Pain and paresthesia in the lower back,
groin region, perineum, buttocks, hip,
posterior region of the thigh (saddle
region), calf, foot (outer border), even in
the rectum (during defecation).
• Aggravated by sitting, walking, climbing
stairs, or performing squats.
• Sitting intolerance, especially on hard
surfaces.

• Piriformis sign: On gross inspection, the
patient may hold the leg in an externally
rotated position while lying supine.
• The Freiberg test is a passive stretch test
and causes pain with internal rotation during
thigh extension.

• The FADIR test (Lasegue’s sign,
piriformis test): Eliciting pain with flexion,
adduction and internal rotation at hip.
• Beatty maneuver: Patient lies on the
uninvolved side and abducts the involved
thigh upward causing contraction of the
ipsilateral piriformis muscle causing pain.

• Sacroiliac joint dysfunction.
• Prolapsed intervertebral disc (PIVD) and spinal lesions.
• Femoroacetabular impingement and acetabular labrum tears.
• Post laminectomy syndrome.
• Vascular compression of sciatic nerve.
• Posterior facet syndrome of lower lumbar vertebrae.
• Pelvis fractures and pseudo fractures.

TREATMENT
• Combination of NSAIDs, muscle relaxants.
• The physical therapy comprises of stretching
with hip internal rotation with adduction and
flexion, myofascial therapy, massage, hip
muscle strengthening, sacroiliac manipulation,
ice and hydrotherapy, and possibly
acupuncture.
• Trigger point injections like the lidocaine
hydrochloride, steroids, botulinum toxin type
A may be used in those patients that fail
conservative treatment for 1–2 months.

Meralgia Paresthetica
• It is a clinical condition that includes pain and
dysesthesia in the anterolateral thigh associated
with lateral femoral cutaneous nerve
compression.
• The lateral femoral cutaneous nerve is a pure
sensory nerve vulnerable to compression as it
passes from the lumbosacral plexus towards the
inguinal ligament and into the subcutaneous
tissue of the anterior thigh.
• This condition is also known as Bernhardt Roth
syndrome, lateral femoral cutaneous nerve
syndrome, or lateral femoral cutaneous
neuralgia.

• The LFCN is derived from a combination of lumbar nerve
roots (posterior divisions of L2/L3 spinal nerves).
• It emerges from the lateral aspect of the psoas muscle,
passes under the iliac fascia, then crosses the anterior
surface of the iliacus muscle as it travels toward the anterior
superior iliac spine.
• It then passes under, through, or above the inguinal ligament
and divides distally into the anterior and posterior divisions.
• The anterior branch provides sensory innervation of the
anterior thigh to the knee, while the posterior branch
provides innervation from the lateral thigh to the greater
trochanter.

ETIOLOGY
MECHANICAL:
• External direct pressure from tight
seat belts, belts, or restrictive
clothing.
• Increased intra-abdominal pressure
from obesity.
• Pregnancy.
• Tumors.
• Degenerative defects of the pubic
symphysis.
SYSTEMIC :
• Diabetes mellitus
• Lead poisoning,
• Alcohol use disorder
• Hypothyroidism

C/F :
• Causalgia or burning pain, paresthesias , and hypesthesia over the upper lateral thigh,
repeated rub their outer thigh causing hair loss over the area.
• Unilateral.
• Onset is usually subacute over days to weeks.
• Symptoms may be associated with prolonged hip extension, such as walking or rising
from a seated position or prolonged standing which is relieved by hip flexion movements
such as sitting.

EVALUATION:
• Deficiencies may be noted with pinprick, and light touch over an area over the
anterolateral thigh.
• Pelvic compression test in which the patient lies on their unaffected side, and the
examiner applies downward pressure on the patient’s ilium/pelvis for approximately 45
seconds. A test is positive if symptoms are reduced.
• Nerve blockade via injection of the lateral femoral cutaneous nerve (in which relief of
pain confirms the diagnosis) is rarely used for diagnosis to distinguish from lumbosacral
root pain.
• Electrodiagnostic studies for the LFCN indicated in the diagnosis to rule out radiculopathy
or plexopathy.
• Imaging studies such as a pelvic x-ray may be indicated if a tumor or osteoarthritis is
suspected. Likewise, an ultrasound or MRI may be ordered to investigate for a pelvic or
retroperitoneal tumor.

TREATMENT
• Self-limited condition with frequent spontaneous remission.
• Patient reassurance and ways to reduce pressure and irritation over the nerve and groin
region.
• Counseling the patient to avoid tight-fitting garments, and discussion of weight loss if
obesity is a contributing factor.
• Icing the area may be helpful in reducing local nerve irritation and inflammation of acute
symptoms.
• Medications that may be helpful include NSAIDs, topical capsaicin, lidocaine, or
tacrolimus for epidermal dysesthesia or cutaneous hypersensitivity.
• Anticonvulsants such as gabapentin, phenytoin, or carbamazepine may be helpful for
treating the patient’s neuropathic pain.
• SX: Decompression of LFCN.
• Radiofrequency nerve ablation of the LFCN, Electroacupuncture.

Tarsal Tunnel Syndrome
• It is an entrapment neuropathy that is associated with the compression of the structures
within the tarsal tunnel.
• Tarsal tunnel syndrome is sometimes referred to as tibial nerve dysfunction or posterior
tibial nerve neuralgia.

CONTENTS OF TARSAL TUNNEL :
From medial to lateral
• Tibialis posterior tendon,
• FDL tendon,
• Posterior tibial artery and vein,
• Posterior tibial nerve, and
• FHL tendon.
• The tarsal tunnel is a narrow fibro-osseous space that runs behind and inferior to the
medial malleolus. It is bounded by the
• Medial malleolus anterosuperiorly ,
• Posterior talus and calcaneus laterally,
• And is held against the bone by the flexor retinaculum which extends from the medial
malleolus to the medial calcaneus and prevents medial displacement of its contents.

• The posterior tibial nerve passes between the FDL and FHL muscles before it bifurcates in the
tarsal tunnel, forming the medial and lateral plantar nerves.
• The medial plantar nerve passes deep to the abductor hallucis and FHL muscles and provides
sensation to the medial half of the foot and first 3.5 digits and motor function to the lumbricals,
abductor hallucis, flexor digitorum brevis, and flexor hallucis brevis.
• The lateral plantar nerve passes directly through the abductor hallucis muscle belly and provides
sensory innervation of the medial calcaneus and lateral heel and motor function to the flexor
digitorum brevis, quadratus plantae, and abductor digiti minimi.
• The medial calcaneal nerve typically
branches off of the posterior tibial
nerve proximal to the tarsal tunnel
and provides sensory innervation to
the posteromedial heel.

ETIOLOGY
INTRINSIC FACTORS:
• Tendinopathy.
• Tenosynovitis.
• Perineural fibrosis.
• Osteophytes.
• Hypertrophic retinaculum.
• Space-occupying or mass effect lesions
(enlarged or varicose veins, ganglion cyst,
lipoma, neoplasm, and neuroma).
EXTRINSIC FACTORS:
• Poorly fitting shoes.
• Trauma (Ankle sprain).
• Anatomic-biomechanical abnormalities
(tarsal coalition, valgus or varus hindfoot).
• Post-surgical scarring.
• Generalized lower extremity edema.
• Systemic inflammatory arthropathies.
• Diabetes.

CLINICAL FEATURES
• Pain directly over the tarsal tunnel that radiates to the arch and plantar foot.
• Sharp shooting pain in the foot, numbness on the plantar surface, radiation of pain and
paresthesias along the distribution of the posterior tibial nerve, pain with extremes of
dorsiflexion and eversion, and a tingling or burning sensation.
• The patient may note weakness in the muscles of the foot.
• Symptoms may worsen at night, with walking or standing, or after physical activity, and
typically get better with rest.
• In chronic cases, atrophy, weakness of the intrinsic foot muscles, and contractures of the
toes may be appreciated.

EVALUATION
• Light touch and two-point discrimination should be tested. The patient may have
diminished plantar sensation in the distribution of either the medial or lateral plantar
nerve.
• Muscle strength and foot range of motion should be assessed. Strength deficits are
typically a late finding in tarsal tunnel syndrome.
• The Tinel test involves lightly tapping over the tarsal tunnel repeatedly. Pain or tingling in
the distribution of the nerve is a positive test.
• The dorsiflexion-eversion test involves passively dorsiflexing and everting the ankle to
end range of motion and holding for 10 seconds; Reproduction of symptoms is a positive
sign due to compression of the posterior tibial nerve in this position.

Tarsal Tunnel Syndrome Severity Rating Scale
• A score of 10 indicates a normal foot and 0 indicates the most symptomatic foot.

• Achilles tendonitis.
• Degenerative changes (calcaneal spurs, arthrosis of the joints of the foot).
• Inflammatory conditions of the ligaments and fascia of the foot and ankle.
• L5 and S1 nerve root compression.
• Morton metatarsalgia.
• Neurogenic intermittent claudication.
• Plantar fasciitis.
• Retrocalcaneal bursitis.

TREATMENT
CONSERVATIVE :
• Oral analgesics including acetaminophen and NSAIDs can be helpful.
• Ice application.
• Neuropathic pain medications include gabapentin, pregabalin, and tricyclic
antidepressants can be tried.
• Corticosteroid injections into the tarsal tunnel.
• Orthotic shoes, CAM (controlled, ankle, motion) walker or walking boots may be tried.
• Night splints can be tried.
SURGICAL :
• Release of the flexor retinaculum from its proximal attachment near the medial
malleolus down to the sustentaculum tali.
• Nerve decompression.

Entrapment neuropathy

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