1

Axillary Nerve-Anatomy
Arises from posterior cord of brachial plexus and runs
alongside radial N behind Axillary A, separating the latter form
subscapularis muscle on the floor. At lower border of muscle, it
leaves radial N and turns posteriorly with the posterior humeral
circumflex artery through quadrangular space to posterior
aspect of humerus, where it divides into anterior and posterior
branches.
Posterior branch supplies to teres minor and posterior part of
deltoid before it curves around the posterior border of deltoid
to supply the skin over lower half of deltoid (upper lateral
cutaneous nerve of arm). The anterior branch proceeds
laterally and anteriorly beneath the deltoid and in contact with
surgical neck of humerus about 2 inches below upper
attachment of deltoid giving off numerous twigs to the muscle
throughout its course.

Axillary N injury-Clinical picture

Injury to main nerve in axilla or at surgical neck produces
complete paralysis of deltoid with loss of abduction and
anesthesia of small patch of skin over lower half of deltoid
(regimental badge area). First 20º to 30º abduction is initiated
by rotator cuff, chiefly supraspinatus. Occasionally, with
complete RD and atrophy of deltoid, the supraspinatus may
hypertrophy in compensation and restore abduction.
When the anterior branch is interrupted, the muscle anterior
the point is paralyzed. Partial muscle paralysis is frequently
compensated by hypertrophy of supraspinatus and activity of
pectoralis major, especially with arm above the horizontal
plane.

Axillary N injury-Treatment
Prophylaxis consists of avoiding unnecessary extension of
operative incisions and rough handling of deltoid muscle. If the
nerve is contused, spontaneous regeneration may take place in
4-6 months, during which time deltoid must be relaxed on
abduction splint and light massage and electric stimulation
given.
Daily active exercises are done to strengthen cuff muscles.
Operative repair of this nerve is exceedingly difficult and
frequently impossible. Conservative treatment is advised
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unless damage to main large nerve is evident. Operative

exposures of shoulder should avoid muscle splitting incisions. If
unavoidable, incision should be confined to anterior third of
deltoid and not beyond 1 ½ inches distal to AC joint.

Axillary N injury-Arthrodesis
Complete deltoid paralysis, when not compensated by other
muscle action, requires arthrodesis of shoulder. Trapezius and
serratus anterior will raise the arm effectively.

Axillary N injury-Harmon Operation

When anterior portion of deltoid is paralyzed, muscle may be
seriously weakened, particularly in forward flexion and humeral
head may dislocate or subluxate anteriorly. This is corrected by
transposing the posterior origin of functioning muscle to new
anterior position.

Axillary N injury-Trapezius T Transplant

Trapezius muscle insertion is transferred by fascia lata strip
extension to deltoid tubercle. Prerequisite is good power in
scapular muscles, including trapezius, serratus anterior,
pectoralis major, rhomboids and levator scapulae. Main
contraindication is subluxation of shoulder joint.

Axillary N injury-Biceps & Triceps Transplant

Tendons of short head of biceps and long head of triceps are
fixed to anterior and posterior rims of acromion.

Median N-Anatomy
Formed from lateral divisions of 5th, 6th and 7th cervical roots
and medial divisions of 8th cervical and 1st thoracic nerves.
Enters axilla lateral to Axillary artery and lies between MC N
laterally and ulnar N medially. It descends in arm with brachial
A and other nerves in a groove just medial to and slightly
behind the biceps muscle and gradually crosses over in front of
artery (rarely it crosses behind) until it lies medial to brachial A
before it reaches elbow.
No branches are given off in arm. At elbow it lies deep to
bicipital aponeuroses and median cubital vein. It enters
forearm by passing between larger humeral and smaller ulnar
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head of pronator teres, descending in medial part of forearm

between FDS and FDP muscles. Above wrist it is radial to FDS
and directly beneath PL tendon.
Then it passes beneath transverse carpal ligament and after
giving off motor branch to thenar muscle (OP, APB, superficial
head of FPB) it inclines volarward to supply by 6 terminal
branches the thumb, index, middle and ring fingers. In hand it
lies in a plane superficial to tendons and deep to superficial
vessels.
First branches arising just above elbow are to humeral head of
PT. Then below elbow, branches supply rest of PT,FCR, PL and
FDS. At upper border of PT a large interosseous branch arises,
penetrates between the pronator heads and supplies radial
portion of FDP and FPL, and then descends on the interosseous
membrane along with AIA to end in PQ.
In hand, it gives off 5 palmar digital nerves. First 3 supplies
both sides of thumb and radial half of index finger. Each of
other 2 divide at clefts distally to supply the opposing halves of
index and middle fingers and middle and ring fingers. Motor
and sensory distribution of median and ulnar N frequently
overlap. Normally median N supplies the palmar surface of
thumb, index, middle and radial half of ring fingers and dorsal
surface of distal thirds of these fingers.

Median N-Clinical Picture

Above elbow results in loss of flexion of thumb, index, and
middle finger, wrist flexion is weak and deviates ulnar side
from unopposed action of FCU, pronation is weak or absent,
thumb is in a position at the side of hand and cannot be
brought into opposition, upper forearm and thenar area are
atrophied, loss of sensation in volar aspect of thumb, index,
middle and radial half of ring finger.
Appearance of hand is similar to flat hand of monkey and is
called simian hand. Trophic changes occur at distal end of
index finger, which becomes thin and conical. Lesions at wrist
occur from accidental cuts by knives or broken dishes or
suicide attempts. It may be compressed against non yielding
TCL by a dislocates lunate or by strongly grasping an object
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particularly with wrist in flexion, whereby flexor tendons are

strongly displaced volarly.
Inflammatory synovial swelling due to RA or neoplasm
encroaches on carpal tunnel and constricts the nerve. Lesions
at carpal tunnel affects short abductors (inability to abduct)
opponens, superficial part of short flexors (FPB) and lumbricals
to index and middle fingers. Loss of sensation is same as in
higher lesions.
Partial N injury or irritation is most common cause of
causalgia. Severe burning pain in extremity and hand,
aggravated by physical or emotional stimuli. Hand is initially
swollen, red, warm, perspiring and hyper esthetic. Gradually
skin becomes thinned, glossy, cold, cyanotic and dry. The hand
is held fixed with fingers extended and thumb adducted and
joints may ankylose in this position. Pain becomes extremely
distressing . Keeping the part moist seems to reduce the
symptoms temporarily.

Median N-Treatment
In nerve suture, better results are obtained from early
intervention. Late repair leads to partial restoration,
particularly of sensation and paraesthesia. Nerve should be
explored and ends obtained and sutured in exact rotary
apposition. Gaps can be overcome in palm by flexing MCP joint.
Above wrist the nerve is freed and wrist is flexed. If elbow is
also flexed and nerve is gently pulled distally, a 3 ½ inch gap
can be overcome.
For larger gaps, dissect the nerve in upper arm and reroute it
superficial to elbow structures by detaching humeral head of
PT. A plaster cast maintains flexion of joints and later very
gradual extension is obtained over period of 1 month. If graft is
needed, Sural N may be used.
At exploratory operation in causalgia states, nerve displays a
lesion in continuity (intraneural scarring). Complete division of
nerve rarely causes causalgia. Treatment consists of
sympathectomy, preceded by procaine block of 2nd thoracic
ganglion. Complete anhidrosis and increase in warmth of hand
after 10 min of block. Pain is relieved for 1 to 3 hours. A
preganglionic sympathectomy is most effective. The white rami
communicates to 2nd and 3rd thoracic ganglia and sympathetic
trunk below 3rd are divided.
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Radial N-Anatomy
It is continuation of posterior cord formed by posterior
divisions of brachial plexus. In axilla it lies directly behind
Axillary A and runs on a floor formed by subscapularis muscle
proximally and latissimus dorsi and teres major distally. Axillary
(circumflex) N which originates form posterior cord, descends
alongside radial N, then leaves it at lower border of
subscapularis, where it passes backwards through
quadrangular space.
Beyond TM, it proceeds posterior to humerus by entering
interval between long and medial heads of triceps and
reaching spiral groove. It passes around back of humerus to
lateral side, where it pierces LIMS to reach anterior aspect of
arm. Here it lies in interval between brachialis medially and
brachioradialis and ECRL laterally.
At this level it gives off branches to lateral half of brachialis,
all of brachioradialis, ECRL and PIN. It then continues distally in
forearm under cover of BR till about 2” above wrist. It then
pierces deep fascia and turns laterally and dorsally, crossing
superficial to APL and EPB tendons and reaching dorsum of
hand where it supplies digital branches of sensation to dorsum
of thumb, index, middle and ring finger as far as MP.
In spiral groove radial N gives off posterior and lower lateral
cutaneous nerves of arm, posterior cutaneous nerve of
forearm, and muscular branches to triceps and anconeus.
PIN arises form radial N at level of lateral epicondyle. It
descends under cover of BR and gives branches to ECRB and
supinator. Then it penetrates supinator and passes obliquely
around lateral aspect of shaft to reach back of forearm and
travels distally of surface of APL under cover of EDL.
Then it lies on IM under cover of EPL and proceeds distally to
supply wrist joint. In back of forearm it supplies remainder of
extensor muscles and APL. Thus it supplies all muscles on
lateral and dorsal aspect of forearm except the BR and ECRL
which are supplied directly by radial N.

Radial N-Clinical Picture

If radial N is interrupted at axilla where it is usually involved
by direct compression such as arm resting over back of chair
(Saturday night palsy), the extensors of elbow, extensors and
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supinator of forearm, extensors of wrist, extensors of MCP

joints of fingers and extensor and long abductor of thumb are
paralyzed. A strip of posterior and posterolateral surface of
arm, posterior third of forearm and autonomous zone on
dorsum of hand over 1st IO web space are anesthetic.
Patient holds extremity at side, elbow is slightly flexed,
forearm is pronated, hand dropped at wrist and fingers are
dropped at MCP joints. Thumb is turned forwards into palm and
interferes with flexion of fingers. Patient cannot make fist
because wrist drop tenses the extensors of fingers and thereby
opposes their flexion.
Involvement of nerve in spiral groove may be caused by sharp
jagged edge of # bone or may be delayed by callus formation
and incarceration of nerve. Here it permits function of triceps
and anconeus and preserves sensation at back of arm and
forearm.
Injury to radial N between BR and brachialis involves BR and
ECRL. But the brachialis which has dual nerve supply may
continue to function.
If injury is at level of radius where PIN encircles the bone 1
finger breadth below the head of radius, these muscles escape.
Beyond this level supinator brevis is permitted to function,
whereas wrist drop, finger drop at MCP joints and thumb rolled
forward into palm are the deformities.
EPL, EPB & APL gain their branches of supply little more
distally than EDC, ECRL & ECRB so it is possible to have thumb
alone involved by properly placed point of trauma. When
superficial radial N alone is severed, loss is restricted to
sensation in autonomous zone. This area is main site of pain
when a causalgia state results form incomplete lesions of
superficial radial.
Partial paralysis of one or several muscles and
hypoesthesia or hyperesthesia rather than anesthesia
indicate that the nerve lesion is incomplete and
continuity of the nerve is preserved.
Examination of extension of fingers should be limited to MCP
joints only as lumbricals supplied by median and ulnar nerves
extend the IP joints.
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Automatic movements at wrist like extension due to finger

flexion leading to extensor tendon tightening should not be
interpreted as preservation of movements.

Radial N - Treatment
Regardless of level, affected muscles should be kept relaxed
by supportive splints and their tone maintained by galvanic
stimulation and light massage until nerve regenerates. Anterior
moulded splint counteracts wrist drop and should extend
beyond MCP joints to support PP. An additional extension from
splint holds thumb in complete extension and dorsal abduction.
If paralysis is immediate and complete, nerve should be
explored and sutured promptly. Good results are proportionate
to early repair. Nothing is lost by early exploration and finding
the nerve intact.
Gaps between nerve ends may be overcome by flexing the
elbow, externally rotating and adducting the arm and by
freeing various branches. If distance is extensive, nerve may
be transposed anteriorly. Shortening of humerus is sometimes
justified to aid approximation.
Compression injuries are generally temporary and almost
complete restoration of function is the rule.
Possibility of complete nerve tears and their serious
implications certainly warrant operative exposure of # site,
whereupon both nerve and bone injuries can be dealt with at
the same time.
Following complete cut of nerve, NCV begins to slow after 2-3
days and is maximum at 2 weeks. Therefore within 24-48 hours
eliciting this findings justifies surgical exploration. If no
conduction impairment develops by 1 week, nerve interruption
is physiological (neuropraxia) and non surgical treatment is
pursued. During this period electrical stimulation, heat and
massage to maintain tone, splinting to relax affected muscles
and range of motion exercises are started.
When causalgia occurs, an incomplete nerve lesion should be
suspected, the nerve explored, neuroma if any should be
resected, if necessary by removal of portion of nerve, F/B re
approximation, or adhesions if any are freed.
The Tinel sign may reveal the exact site of initiation of pain
impulses.
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Radial N - Prognosis
Prognosis of radial N repair is usually very good. Failure of
some portion to regenerate necessitates tendon
transplantations.
Triceps paralysis needs no compensation other than that
provided by gravity.
Supination of forearm may be restored by osteotomy of radius
and by rotating the distal fragment. Tubby operation
transplants the insertion of PT from volar to dorsal aspects of
radius.

Radial N - Treatment
Extension and abduction of thumb which stabilizes the thumb
at CMC joint is necessary for proper apposition. FCR may be
transplanted to APL and EPL and EPB.
FCU is transferred to EDC.
If no tendons are available, dorsiflexion of wrist is provided by
arthrodesis of wrist or by cutting tendons of EDC and
tenodesing the proximal ends of distal segment to dorsum of
radius.
Active flexion at MCP joints thereby tightens these tenodesed
tendons and automatically dorsiflexes the wrist. The CMC joint
of thumb may also be stabilized by arthrodesis.

Ulnar N - Anatomy
Largest branch of medial cord, arising under cover of PMn,
and descending along medial side of Axillary A and proximal
half of brachial A. At middle of humerus it leaves brachial A
and in company with UCA it passes backwards through the
MIMS to posterior aspect of arm. Then it descends along medial
head of triceps to back of medial epicondyle and passes
between heads of FCU to enter forearm. Under cover of FCU
(which it supplies) it lies on FDP (supplies its medial half) and is
immediately lateral to ulnar A.
Near pisiform bone it emerges through deep fascia lateral to
FCU and descends anterior to FR, where it divides into
superficial and deep branches. Deep branch passes medial to
hook of hamate and along with deep branch of ulnar A, enters
interval between ADM and FDM to gain the deep area of palm.
It supplies to hypothenar muscles and turns laterally across
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palm deep to flexor tendons giving off 3 branches, each of

which runs distally in front of IS, supplying the interosseous
muscles.
Medial 2 branches also medial 2 lumbricals muscles. At lateral
side of palm, main deep branch of ulnar N ends by breaking up
into nerves of supply to adductor pollicis and 1st dorsal IM.
Superficial branch of ulnar N runs under PB, which it supplies,
and then divides into 2 digital branches, which provide
sensation to palmar aspect of little and ulnar half of ring finger.
Dorsal branch arises at middle of forearm and descends with
parent nerve to carpus, where it becomes superficial and
inclines backwards to gain to dorsum of hand. Here it divides
into 2 dorsal digital nerves, which supply skin of medial third of
back of hand and little finger and ulnar half of ring finger as far
as second phalanx.

Ulnar N – Clinical picture

If FCU is paralyzed, on attempting flexion at wrist, hand
deviates radially, S/O interruption of ulnar N above elbow.
Otherwise ulnar N paralysis leads to extension of ring and
little fingers at MCP joints and flexion at IP joints, because of
lack of lumbricals. When lesion is sufficiently low in forearm,
FDP is spared and unopposed by intrinsic, exerts strong flexion
on DP, clawing of ring and little fingers is pronounced.
When FCU and ulnar portion of FDP are paralyzed by a high
lesion, atrophy over ulnar aspect of forearm is very apparent.
Flexion of DP of ring and little finger is lost. Demonstrated best
by placing hand palm down where inability of little finger to
scratch the surface of table is evident.
Hypothenar eminence is thinned and hollowing of IS suggests
atrophy of interosseous. Abduction and adduction of fingers is
lost to great extent. Index and middle finger may still abduct
because their lumbricals innervations is through median N.
Pinch between thumb and index finger normally depends on
ability to stabilize MCP joint in flexion (adductors and flexor
brevis) so that action is strong and apposed fingers form letter
O. in ulnar paralysis, PP is hyper extended, IP joint of thumb
hyper flexes and pinch is weak. Failure of stabilization at CMC
joint by APL will likewise interfere with pinch.
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Inability of thumb to scrape across distal palm suggests loss of

thumb adductors. Instead it comes forward into opposed
position. Another test is failure to resist attempts to extract a
sheet of paper held between apposed sides of thumb and
index finger. Trophic changes in ring and little fingers reflect
sensory loss. Very frequently innervations form median N
preserves function of intrinsic and thumb adductors. Fibers
innervating these muscles proceed distally in median N to
distal 3rd of forearm and by a connecting branch enter ulnar N.
in such case a high ulnar lesion fails to eliminate intrinsic
action.

Ulnar N –Treatment
Repair should be done with care. Nerve contains both motor
and sensory fibers. Gaps are overcome by flexing wrist and
elbow. Nerve at elbow may be transposed anteriorly, and
branches freed, permitting mobilization distally. Recovery of
function requires > year in following order, forearm muscles,
sensations, hypothenar muscles, interossei and thumb
adductors.
During this period, hand is splinted with MCP joint in flexion
and IP joint in extension to keep paralyzed muscles relaxed and
prevent joint contractures.
When ulnar N paralysis is permanent, tendon transplantation
is the treatment of choice.

Ulnar N –Repair of clawed fingers

Claw hand is due to intrinsic muscle paralysis while long
extensors and flexors are still functioning. Loss of flexor power
on PP allows extensors to pull PP into hyperextension, tension
on long flexors pull DP into flexion, unopposed by lost
extension of intrinsic.
Extension of distal 2 phalanges takes place synergistically by
long extensors and intrinsic. Action of long extensors is lost
when PP is hyper extended. Any procedure that prevents
hyperextension of PP preserves extension of distal 2 phalanges
and eliminates claw deformity.
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Bunnell Technique : Transplants multiple slips of sublimis

through lumbrical canals into aponeurotic expansion. This
procedure is not effective in claw hand of long standing in
which patient has developed habit of flexing wrist to extend DP
automatically, thereby rendering the sublimis ineffective.
Fowler Technique : Splits EIP and EDQ into 2 strands each,
next each individual slip is passed through IOS anterior to
TMCL and inserted into aponeuroses.
Riordan technique : Tenodesis procedure. Half of ECRL & ECU
is separated and each half is split longitudinally into 2 slips and
then each slip is passed and attached into aponeuroses.
Tendon should be under tension so as to obtain restriction of
extension.
Post operatively wrist is in dorsiflexion, MCP joints in flexion
and distal 2 joints in extension.

Ulnar N –Restoration of thumb adduction and arches

When grasping small round objects, hand cups into arch and
enables fingers to converge during flexion, thus strength of
grasp is obtained. These arches are produced mainly by thenar
and hypothenar muscles. They are reduced considerably in
ulnar paralysis and completely flattened in combined ulnar and
median paralysis. It is essential to restore functions of pinch
and grasp.
Tendon Loop operation : EIP is removed just before its
insertion and is prolonged by tendon graft around ulnar border
of hand, placed volar to hypothenars and beneath finger
flexors and inserted into ulnar side of base of PP of thumb. The
distal remaining stump of tendon is attached to EI to avoid
adduction and rotation deformity of index finger. This
procedure only adduction and is suitable only in pure ulnar
paralysis.
Tendon T Operation : Provides strong adduction to both thumb
and index finger and reforms arches. Tendon graft is placed
transversely across palm beneath flexor tendons and is
attached to neck of 5th MC and ulnar side of base of PP of
thumb. To its centre is attached motor tendon, usually one of
sublimis. Contraction of motor tendon pulls on cross member
and apposes thumb and index finger. This is more suitable
when median N is also involved with ulnar N and it becomes
necessary to correct thumb opposition also.
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Compression of Ulnar N at elbow

Also called traumatic ulnar neuritis, tardy ulnar N palsy and
ulnar neuropathy at elbow.
Chronic repetitive blunt trauma : Ulnar N is superficial within
post condylar groove between olecrenon and medial
epicondyle. Here it is vulnerable to single, severe direct blow or
to repeated external pressures, sustained under occupational
conditions.
Post # : Nerve is held firmly within groove by firm dense
fascia. Roughening of bone due to # imposes frictional force
against gliding nerve.
Cubitus Valgus deformity : Nerve is supposedly stretched over
medial prominence at elbow. Deformity may be congenital and
associated with anterior dislocation of radial head, retarded
growth of lateral portion of lower humeral epiphyses following
trauma or infection, or mal union of #.
Arthritis of joint : OA produces irregularities of post condylar
groove or may compress nerve by prominent osteophyte or
protruding ganglion. Rheumatoid synovium may penetrate the
medial capsule and compress nerve.
Recurrent subluxation or dislocation of nerve : When fascia
covering nerve in groove is thin and lax, ulnar N moves out of
its groove onto tip of medial epicondyle when elbow is
completely flexed, returning to its normal location when elbow
is extended. Repetitive subluxation normally occurs in 16% of
population.
Acute trauma, infection : Produce scarring which can
incarcerate ulnar N.
Muscle compression : By an accessory muscle, anconeus
epitrochlearis, which bridges the groove.
Idiopathic : Not unusual.

Pathophysiology
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2 cm distal to medial epicondyle, an aponeurotic arch passes

between 2 heads of origin of FCU, one firmly attached to
medial epicondyle and other loosely attached to olecrenon,
with aponeurotic arch forming roof of cubital tunnel. Floor of
tunnel is formed by medial capsule of elbow. During flexion,
space of tunnel is diminished by tightening of aponeurotic arch
and by outward bulging of capsule.
INP is 3 times when elbow is flexed with wrist extended;
adding abduction and external rotation of arm as when placing
hand behind head, INP is 6 times that of relaxed N, such
pressures are capable of damaging nerves.
Aponeurotic arch, is slack in extension. When this is divided,
underlying N is often found flattened, and proximally it
presents a fusiform swelling.
Normally, ulnar N elongates by 5 mm during flexion and glides
freely in groove. Encroachment on groove or cubital tunnel,
produce friction, pressure and tension, which compromises IN
vascularity and results in edema and scarring.
Symptoms are highly variable, from subjective dysesthesias to
combination of sensory and motor deficit. FCU and ulnar half of
FDP are usually spared. Reason is, fibers to these muscles are
deeply situated in nerve at elbow and are generally unaffected
by external compression.

Clinical Picture
H/O Cubitus valgus deformity, severe direct trauma or
repetitive trauma to ulnar groove.
Symptoms are related to severity of involvement. Minimal
nerve irritation causes subjective dysesthesias in ulnar
distribution and sensation of clumsiness.
Moderate involvement produces pronounced subjective pain
and paraesthesia and IO weakness and atrophy. FCU & FDP to
DP of little and ring fingers are rarely affected. Nerve may be
tender and palpably enlarged at post condylar groove.
Severe N lesions are rare. Interossei are very weak and
atrophied. FCU & ulnar half of FDP are partially weakened.
Sensory loss varies from marked hypoesthesia to anesthesia.
Sweating in reduced, although hyperhydrosis is not infrequent.
Cubital tunnel syndrome caused by compression of N by
arcuate ligament is provoked by prolonged flexion attitudes of
elbow, such as during sleep. Sometimes symptoms can be
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elicited by acutely flexing elbow for about 5 minutes (elbow

flexion test).
Recurrent ulnar N subluxation at elbow are usually
asymptomatic, unless trauma is superimposed. Complete
anterior displacement is exceptional. Condition is nearly
always bilateral. Enlarged tender N can be felt to slip beneath
examining finger during flexion and extension.

Diagnosis
Traumatic ulnar neuritis at elbow must be differentiated from
ulnar N compression at wrist. Dorsal cutaneous branch of ulnar
N leaves parent N beyond elbow. So sensory impairment in
dorsal ulnar aspect of hand localizes lesion proximally.
Contrariwise, absence of this finding does not necessarily
implicate ulnar N lesion at wrist, because N may be only
partially involved at elbow.
Electro diagnostic studies will reveal slowing of conduction at
elbow, and differentiate whether N is involved proximally (at
thoracic outlet) or distally at wrist. Preoperatively it is
important to determine compressive bone lesion about ulnar
groove. In addition to routine x-rays, special view is taken to
outline groove. The externally rotated arm is placed against
cassette, while elbow is acutely flexed, and central x-ray beam
is directed vertically.

Prognosis
Depends largely on degree of N involvement and time interval
between onset of symptoms and surgical intervention. In
minimal involvement, anterior transposition of N leads to
immediate relief of local discomfort and peripheral
paraesthesia. With moderate sensory and motor impairment,
following surgery, hand becomes stronger, but variable
weakness and sensory impairment persist in some. In
advanced paralysis, surgery results in partial recovery of motor
power in some but sensory recovery is better, normal function
is never regained.
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After 1 year, only about 1/4th of patients will achieve

satisfactory recovery after anterior transposition and
improvement after simple aponeurotic release is poor.
Muscle power continue to improve over 6 months to year.
Long flexor muscles recover more completely than intrinsic.
Variable sensory deficit often persists. Complete recovery is
rarely attained if course exceeds 3 months and chances are
poor when symptoms have existed for 1 year.

Treatment
Nerve must be transposed anteriorly. Sites of potential kinking
should receive proper attention. MIMS extending proximally
from epicondyle must be adequately resected. Aponeurotic
band is released. N should not be laid in groove cut in muscle,
because scarring and IMS become adherent to N. Origin of
common flexor pronator tendon should be elevated, the N
placed beneath the muscle mass, and tendon origin restored.
Occasionally, it may be possible to remove local compressing
lesion like ganglion or osteophyte without need for anterior
transposition.

Ulnar N compression at wrist

Ulnar N courses through tunnel anterior to FR just lateral to
pisiform, then divides into superficial (mainly sensory) and
deep branch as it proceeds distally. Floor of narrow canal is
formed by ligaments between pisiform, triquetrum and
hamate. Because of limited diameter, it is vulnerable to lesions
that encroach on canal (OA osteophyte, ganglion, rheumatoid
pannus). When N is compressed proximal to point of
bifurcation, both sensory and intrinsic muscle deficit results.
As dorsal branch leaves ulnar N proximal to wrist, sensation to
medial third of back of hand and entire dorsal surface of little
and ulnar half of ring finger as far as MP is preserved. When N
compression is within tunnel distal to bifurcation, only deep
branch is affected, hypothenars are often spared, and intrinsic
muscles denervated. FDP to little and ring fingers and FCU is
unaffected.

Ulnar N compression at wrist-Anatomy

Ulnar A and N enter hand through triangular space (Guyon’s
canal), which is bordered medially and proximally by FCU and
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pisiform, anteriorly by thin VCL blended with tendinous

insertion of FCU and posteriorly by TCL overlying pisotriquetral
joint. Distal to Guyon’s canal, under cover of PB muscle, nerve
divides into superficial and deep branches.
Superficial branch supplies overlying muscle and passes
through fat pad, courses distally and SC to provide sensory
innervations to ulnar side of palm.
Deep branch passes lateral to pisiform, then medial to hook of
hamate, where it makes an abrupt turn as it dips between
origins of ADM & FDM. It enters narrow fibro-osseous tunnel
that is bounded proximally by pisohamate ligament.
Before it passes into this extremely narrow tunnel, deep
palmar branch supplies motor N to hypothenar muscles; then
passes through opponens and turns laterally under cover of
deep flexor tendons along line of deep palmar arch and
supplies branches to interossei, 3rd & 4th lumbricals, adductor
pollicis and deep part of FPB. As deep branch passes across
palm, it lies in close relationship to proximal end of MC,
providing hard surface against which nerve may be
compressed.
Within Guyon’s canal, ulnar N lies medially and ulnar A lies
laterally, and remainder of space is occupied by fat globules.
Beyond narrow rigid fibro-osseous canal as nerve courses deep
in palm, nerve is most often damaged by penetrating injury.
Motor fibers are posterior and sensory fibers are anterior.
Theoretically, if N is compressed posteriorly, motor weakness
should prevail over sensory loss. However, this is not the
clinical situation, because both motor and sensory deficits
develop concomitantly. Because dorsal cutaneous branch
leaves main N 6 to 8 cm proximal to wrist, an injury beyond
this level spares the dorsal ulnar distribution.

Pathology
Ganglion produce largest number of compressive lesions at
wrist.
Often H/O blunt trauma over hypothenar area by single
severe blow from using hand as hammer or by fall on
outstretched hand or repetitive trauma. Pisiform appear to
sustain the brunt of injury, and OA changes develop at
pisotriquetral joint.
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Scarring may develop weeks to months after an injury about

hypothenar eminence, enveloping both ulnar N and ulnar A
within Guyon’s canal. At surgery, edematous fibrous tissue and
thrombosed vessels are found. They appear to constrict the
nerve, and provided that collateral circulation is adequate,
resection of scar tissue and affected segment of ulnar A and
freeing the nerve will relieve neurological symptoms.
Ulnar A because of superficial location is vulnerable to injury.
Single or repetitive blunt trauma may damage intimae,
resulting in thrombosis. Trauma also disrupts elastic fibers
resulting in progressively enlarging true aneurysm, or
penetrating injury may partially tear A, producing localized
hemorrhagic mass whose interior becomes reanalyzed,
developing a cystic, bulbous false aneurysm. Regardless of
cause, ulnar neuritis occurs, and majority of cases produce
paraesthesia and objective sensory loss.

Clinical Picture
Dependant on site and degree of injury.
2 anatomical patterns; lesion proximal to pisohamate
ligament that causes both sensory and motor involvement and
lesion deep in palm distal to pisohamate ligament that affects
interossei and ulnar lumbricals but spares hypothenar muscles
and ulnar volar sensations.
Compression at level of Guyon’s canal presents following
features :-
Compressive tissue (ganglion, RA pannus, bone fragment) is
sometimes palpable.
Sensory loss over volar ulnar distribution but spares dorsal
area except over DP.
Motor involvement affects hypothenar, ulnar 2 lumbricals and
interossei.
Clawing of little and ring fingers.
Compressive lesions that exerts pressure only on deep branch
produces purely motor weakness of interossei but spares
hypothenar muscles. Abducted attitude of little finger results
from unopposed action of ADM. Clawing of little and ring finger
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is seen sometimes. In general development and effects take

place silently i.e. without pain.
Penetrating injury within palm leads to involvement of motor
structures beyond the point of nerve interruption.
OA of pisotriquetral joint causes pain and tenderness over
pisiform, crepts and pain elicited by passively moving pisiform
bone from side to side. Active ulnar deviation and flexion of
wrist against resistance reproduce pain.
Rarely, superficial branch may sustain direct injury, leading to
pain over ulnar side of palm and ring and little fingers, where
sensory loss may be detected with no sensory loss over
proximal portion of dorsal aspect of these fingers.
Positive Tinel’s sign.
X-ray evidence of bone fragment.
Intrinsic muscles are not affected.

Diagnosis
Muscle weakness and wasting are seen but is common to
whole lot of neurological and myopathic conditions.
When symptoms suggest distal ulnar N involvement, inquire
about injury such as laceration, despite a time lapse.
Detailed sensory examination to distinguish between nerve
compression at elbow from injury to distal portion. When
sensation is lost over volar ulnar area, but intact over dorsal
ulnar area, injury is localized distal to point of origin of dorsal
sensory branch (6 to 8 cm above wrist).
Muscle examination must be detailed.
EMG studies of 1st dorsal interossei may show fibrillation
potentials S/O involvement of deep branch.
NCV studies between wrist and 1st DI or adductor pollicis, is
highly diagnostic and any delay must be clearly demonstrated
before surgical intervention. When fibrillation potentials are
already present on EMG studies, denervation is far advanced.
X-rays of wrist and hand, including special carpal tunnel and
pisiform views are necessary to determine presence of OA, #
and neoplasm.

Treatment
Immediate decompression of ulnar N is mandatory. Nerve is
isolated adjacent to FCU tendon in distal forearm and then
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freed progressively by cutting volar carpal ligament and then

fascial roof overlying interval between pisiform and hook of
hamate. Any compressive lesion is identified and removed.
When OA of pisotriquetral joint is present or pisiform is
dislocated, bone may be removed without impairing power of
wrist flexion.
When possibility of severance of deep palmar branch by
penetrating injury exists, nerve should be explored beneath
the flexor tendons in palm and repair carried out. Thrombotic
occlusion of ulnar A at wrist requires segmental arterial
resection. Aneurysm of A requires excision of aneurysmal sac.
If collateral circulation is insufficient, restoration of arterial
continuity by end to end anastomosis or a vein graft is
necessary.