This document discusses peripheral nerve injuries. It begins by describing the structure and components of peripheral nerves. It then discusses the signs and symptoms of different types of peripheral nerve injuries like radial nerve, ulnar nerve and median nerve palsies. The document also covers the pathophysiology of nerve injury including Wallerian degeneration. It describes the diagnostic tools like electrodiagnostic studies and various treatment options for peripheral nerve injuries including nerve repair techniques.

1. Nerve Injuries
DrSeeyan Shah
PG Resident,
Deptt ofOrthopaedics,
GMC Srinagar.

2. • Peripheral nerves comprise important connection between CNS and
peripheral body.
• In human body there are 43 pairs of peripheral nerves.
• The concept that nerve function can be restored has been known
since long, possibly the initial description was given by Paul of Aegina
(625–690 AD) who recommended approximation of nerve cut ends
along with wound closure.
• This was later refined by eminent surgeons of the time to introduce
concepts of epineural repair (Hueter, 1871) and secondary nerve
repair (Nelaton, 1864).

3. STRUCTURE OF A PERIPHERAL NERVE:
A typical mixed spinal nerve has three distinct components:
• Motor
• Sensory
• Sympathetic

4. • The upper four cervical anterior rami form the cervical plexus
• The lower four cervical and first thoracic anterior rami form the brachial plexus.
• The first three and a part of the fourth lumbar anterior rami form the lumbar
plexus.
• The sacral anterior rami along with the fifth lumbar and a part of the fourth join
to form the lumbosacral plexus.

5. MICROSCOPIC ANATOMY
Each nerve fiber, or axon, is a direct
extension of a dorsal root ganglion cell
(sensory), an anterior horn cell (motor),
or a postganglionic sympathetic nerve
cell, and it is either myelinated or
unmyelinated.

8. BIOMECHANICAL PROPERTIES OF PERIPHERAL
NERVE:
• The capacity of nerve to change its length, commonly measured as percent
change in length or strain. More than 8% elongation (limited traction) of nerve
will diminish its microcirculation which, if persistent, will damage the nerve while
more than 15% elongation (extreme stretch/ traction) will disrupt axons.
• The capacity to tolerate increases in pressure or compression from the
surrounding interfacing tissue. In general, pressures more than 30 mm Hg cause
paresthesias and praxia while pressures more than 60 mm Hg cause complete
blockade of conduction.
• Compression for 15 minutes produces numbness and tingling while pain
sensitivity is lost after 30 minutes. Motor weakness is demonstrable after 45
minutes.
• The capacity of the nerve to slide or glide relative to the surrounding interfacing
tissue.

9. Peripheral Nerves and distribution:

11. Origin, course and distribution of Radial nerve

16. PERIPHERAL NERVE INJURY:
Causes:
• Stretching
• Ischemia (transient or complete)
• Compression
• Crush, traction (pulling)
• Laceration (traction to cause nerve discontinuity)
• Cut (say iatrogenic)
• Burning (say by cautery)

17. Pathophysiology:
• The process of degeneration and regeneration (Wallerian degeneration)—
Wallerian degeneration (WD) is also called anterograde degeneration, named
after Augustus Volney Waller, an English neurophysiologist (1816–1870).
The sequence of events can be summarized as follows:
• After injury to axon, the axons may remain intact for days. The Na+/Ca++ pump
and the Na+/K+ ATPase remain functional. The lag between injury and
degeneration may range from 24 hours to few days.
• Phase of granular disintegration (24–72 hours): Activation of ubiquitin-
proteasome system (UPS) and calcium-dependent proteases. Large influx of Ca++
ions leading to Disruption of mitochondrial oxidative phosphorylation; Excessive
formation of free radicals; Activation of calpains, calcium-activated neutral
cysteine proteases causing cytoskeletal breakdown

18. • By 72–96 hours the myelin lamellae are disrupted into small fragments known as myelin
ovoids.
• Within 96 hours after the injury, the Schwann cells from neurolemma synthesize growth
factors which attract axonal sprouts to the distal end of the severed.
• There is increased neuronal permeability by the breakdown of blood-neuron barrier.
• Myelin and axonal debris are removed by resident and newly recruited inflammatory cells
(monocytes/ macrophages) and microglia (in the CNS) and by Schwann cells (in PNS).
• The neurolemma of axons (the outermost layer of the neuron made of Schwann cells)
does not degenerate and remains as a hollow tube.
• If an axon sprout reaches the tube, it grows into it and advances about 1 mm/day (3
cm/month, Steindler).

20. FACTORS AFFECTING WALLERIAN DEGENERATION:
• Rapid Wallerian degeneration requires the prodegenerative
molecules SARM1 (sterile a and HEAT/ Armadillo motif containing
protein 1) and PHR1 (PAMHighwire-Rpm-1 ubiquitin ligase).
• Nicotinamide mononucleotide adenylyltransferase 2 (NMNAT2) is
essential for axon growth and survival. Its loss from injured axons may
activate Wallerian degeneration.
WALLARIAN DEGENERATION: It is the reactive
change of a nerve to injury whereby distal stump is
cleared of axoplasm and myelin along with
regenerative changes in proximal stump

21. CLASSIFICATION:

23. CLINICAL FEATURES:
• Motor: Flaccid, atrophic paralysis of the muscles in its typical innervation
area. Assess the pinch strength, grip strength, individual muscle function.
• Loss of all sensation, including proprioception, in the skin areas distal to
the lesion. Assess the sensations by static and moving two-point
discrimination (innervation density), vibrometer (more sensitive than two-
point discrimination) and Semmes-Weinstein monofilaments (pressure
thresholds)
• There is a loss of both superficial and deep reflexes.
• In early stage fibrillations and fasciculations are present.
• Tinel’s sign (Tinel’s-Hoffmann sign):

24. Radial nerve:
• Complete palsy (very high): Triceps paralysed (injury in axillary
region)
• High: Triceps and often anconeus preserved but rest all paralysed
(injury around radial groove till it pierces septum).
• Low: BR and ECRL preserved (posterior interosseous nerve (PIN)
palsy; ECRB in 58 per cent cases is supplied by PIN so it may also be
spared in some cases).
Palsy:
1. Inability to extend fingers (1,2,3,4,5) {low} and wrist {low+high}
2. Inability to stabilize the wrist (wrist drop) and thumb (radial
abduction of thumb) {low+high}
3. Loss of grip strength (accessory forearm flexion) {High}
4. Accessory forearm supination {Very High}
5. Sensory loss (radial 2/3 dorsal sensation)

26. Ulnar nerve:
• low ulnar nerve palsy: Anatomically – distal to olecranon fossa. Clinically –
involvement of intrinsic hand muscles
• high ulnar nerve palsy: Anatomically – proximal to ulnar fossa. Clinically;
involvement of ulnar half of FDP and Flexor carpi ulnaris.
Palsy:
1. Loss of grip strength (impairment of power grip > precise grasp) {High}
2. Flexion of distal phalanx 4,5 {High}
3. Digital balance 4,5 {High}
4. Loss of finger function (flexion (partial), adduction, abduction) {High+Low}
5. Loss of thumb adduction and weakness of thumb flexion {High+Low}
6. Sensory loss (medial 1½ digits – Low; Ulnar 1/3 volar – High)

27. • Froment’s sign: Paralysis of 1st dorsal and 2nd palmar inter-osseous muscle
with Adductor pollicis paralysis. Patient flexes thumb as a
trick/compensatory maneuver.
• Card test: To test palmar interossei
• Wartenberg sign: EDM unopposed by 3rd palmar interossei.
• Jeanne’s sign: Loss of key pinch (Adductor pollicis)
• Duchenne’s sign: loss of MCP flexion
• Pitres-stut sign: Inability to cross fingers e.g. IF on MF tests P1D2.
• Pitres-stut test: Inability to radial and ulnar deviate MF.
• Masse’s sign: Wasting and loss of metacarpal arch.
• Pollock sign: Inability to flex DIP of RF and LF (paralysis of ulnar half of FDP)
• Wasting in 1st web space (Ist dorsal interosseous)
• Impairment of precision grip.
Tests:

29. Median nerve:
• Low median nerve palsy typically is defined by involvement around
wrist (carpal tunnel). Motor loss to OP, APB, FPB, 1st and 2nd
lumbrical with variable loss of palmar cutaneous sensation.
• High median nerve palsy in addition has motor loss to FDS, radial half
of FDP, and thumb long flexor (FPL), weakness of pronation (pronator
quadratus)
Palsy:
1. Loss of thumb opposition, finger stabilization 1,2 {Low+High}
2. Weakness of wrist and partial loss of finger flexion 2,3; complete for
1 {High}
3. Forearm pronation {High}
4. Sensory loss (Radial volar 2/3 hand)

30. Signs: Pointing index, ape thumb deformity (adducted thumb) – Simian
‘hand’, thenar wasting, sensory deficit.
Tests:
• Clasp test: Ask patient to clasp both hands – IF remains extended
• Pen test
• Loss of opposition
• Kiloh-Nevin sign: Ask patient to form ‘O’ with IF and thumb using tips
– patient will extend DIP of IF and IP of thumb making peacock’s eye
instead.

32. Sciatic nerve:
1. Equinus deformity of the foot
2. Clawing of the toes
3. Atrophy of the muscles innervated by the nerve
4. Profound weakness of flexion of the knee
5. Inability to dorsiflex the foot or extend the toes
6. Inability to plantar-flex and evert the foot
7. Inability to flex the toes
8. When the peroneal part is involved, the sensory loss is primarily over the
lateral aspect of the leg and dorsum of the foot. When the tibial nerve is
involved, the sensory deficit is primarily over the plantar aspect of the
foot.

34. DIAGNOSIS OF NERVE INJURY:
• Clinical examination
• High-resolution ultrasound and MRI
• Electrodiagnostic studies: Electrodiagnostic studies (EDS) comprise
of:
1. Electromyography (EMG)
2. Nerve conduction studies (NCS)
3. Strength-duration curve.

35. Electromyography (EMG)
Normal muscle is electrically silent
on EMG (embryonic muscle show
fibrillation till 6 weeks of foetal
life).
Denervated muscle starts showing
fibrillation potential by 18-21 days
(three weeks). If renervation occurs
fibrillation potential decreases and
motor unit action potential (MUAP)
of low magnitude appear.
Giant MUAP are seen in a partially
denervated muscle which is
additionally reinnervated by nearby
nerve.

36. Nerve conduction studies (NCS)
Normal conduction velocity about
50 m/sec (slightly more in sensory
nerves), demyelization reduces
speed; unmyelinated fibers have
about 10 m/sec of conduction
velocity. Sunderland type I injury
may show delay at the site of injury
but otherwise NCS and EMG is
normal.

37. Strength-duration curve
• A graph plotting the intensity
of electrical stimulus to the
length of time it must flow to
produce response
• Rheobase is the minimal
amount of stimulus strength
that will produce a response
when applied indefinitely
(practically a few milli-
seconds).
• Chronaxie is the stimulation
duration that yields a response
when stimulus strength is set
to exactly 2 × rheobase

38. MANAGEMENT:
Management of a clinically identified nerve injury depends on the :
• Type of injury (classification, complete/incomplete)
• Associated injuries (fracture/crush/open injury/head injury)
• Level of injury (stronger repair needed at mobile regions)
• Availability of facilities and expertise
• Duration of presentation

39. GENERAL CONSIDERATIONS OF TREATMENT OF NERVE INJURIES
• Appropriate actions to prevent cardiopulmonary failure and shock should be
taken and systemic antibiotics and tetanus prophylaxis should be provided.
• Injury to the peripheral nerve should be evaluated and the specific nerve deficit
should be assessed carefully.
• An open wound in which a peripheral nerve has been injured should be cleansed
and debrided thoroughly of any foreign material and necrotic tissue, using local,
regional, or general anesthesia.
• Immediate primary repair of the nerve is preferred. If the general medical
condition of the patient does not permit, prefer to perform the neurorrhaphy
during the first 3 to 7 days after injury.
• If the ends of the nerve can be identified, they are marked with sutures, such as
Prolene or stainless steel, which can be easily identified later.
• After the initial pain has subsided and the wound has healed, early active motion
of all joints of the involved extremity should be started.
• Dynamic and static splinting to support joints and to prevent contractures should
be used intermittently.

40. FACTORS THAT INFLUENCE REGENERATION AFTER
NEURORRHAPHY
• AGE: Neurorrhaphies are more successful in children than in adults and are more likely to fail in
elderly patients.
• GAP BETWEEN NERVE ENDS: Recovery is slightly better when the gap is relatively small.
• DELAY BETWEEN TIME OF INJURY AND REPAIR: About 1% of recoverable nerve function is lost for
each week of delay after 3 weeks postinjury.
• LEVEL OF INJURY: The more proximal the injury, the more incomplete the overall return of motor
and sensory function.
• CONDITION OF NERVE ENDS: Meticulous handling of the nerve ends, asepsis, care with nerve
mobilization, preservation of neural blood supply, avoidance of tension, and provision of a
suitable bed with minimal scar all exert favorable influences on nerve regeneration.

41. INDICATIONS FOR PRIMARY OPEN EXPLORATION AND REPAIR OF
A NERVE:
• Nerve injury secondary to manipulation of fracture (absolute indication) that was
previously absent.
• Open fractures
• Fractures in which satisfactory alignment is not possible by closed methods
• Fractures with associated vascular injury.
• Patients with multiple trauma.
• When a sharp injury has obviously divided a nerve, early exploration is indicated for
diagnostic, therapeutic, and prognostic purposes.
• When abrading, avulsing, or blasting wounds have rendered the condition of the nerve
unknown.
• When a nerve deficit follows blunt or closed trauma and no clinical or electrical evidence
of regeneration has occurred after an appropriate time
• When a nerve deficit follows a penetrating wound.

42. To Assess the tension at suture site:
• Wilgis -> take a single suture bite with 8-0 suture and if a knot cannot
be tied without tension (or if it breaks) then there will be
unacceptable tension at suture site (or a gap >4 cms).
• Millesi ->gap of >2.5 cms after keeping the limb in functional position
indicates possibility of tension.
• Elbow flexion >90º or wrist flexion >40º required for nerve
approximation indicates tension.
• Brooks: If gap cannot be closed after mobilizing the nerve then there
is bound to be tension
NERVE REPAIR (NEURORRHAPHY)
1. Preparation of the nerve stump and approximation of
the stumps with no tension are essential.

43. 2. Consider normal excursion of the nerve when the extremity is
moving. The nerve will elongate with extension of the joints and
repair may fail, so extremity should be moved through range of
motion during repair itself.
3. Lacerated fascicles must be dissected proximally and distally
until adequate exposure is obtained for repair.
4. Epineural vessels must be preserved, because they serve as an
important guide for fascicular orientation during repair.

44. Types of nerve repair:
Depending on duration from injury:
1. Primary repair – within hours
2. Delayed primary – within 5-7 days
3. Secondary – any repair > 7 days
Depending on the technique used:
1. Epineural
2. Group fascicular
3. Individual fascicular (funicular)
4. Interfascicular nerve grafting

45. Epineural repair: The sutures are carefully placed through the
epineurium. It is useful to place all sutures through the nerve
before tying so that suture tension can be controlled

46. Group fascicular:
• Placement of one or two sutures of 10–0 suture material in the
perineurium to anastomose individual funiculi.
• Avoids lateral growth and allows best possible coaptation of the
fascicles.

47. Individual fascicular (funicular): Individual
fascicles are identified and sutured. This is more
precise but cumbersome

48. Interfascicular nerve grafting:

49. Overcome nerve gap: In general indication for a primary, direct repair of a nerve is
a defect of size approximately less than 2 cm and, if the defect is greater than 4 cm a
repair is performed with a nerve graft. For defects between 2 cm and 4 cm, direct
repair (with nerve mobilization) or grafting may be chosen on a case-by case basis.
Following in isolation or combination are often required:
1. Mobilization
2. Transposition
3. Limb positioning
4. Resection osteotomy
5. Nerve stretching and bulb suture (neuroma to glioma suture)
6. Neuromatous neurotisation (e.g., intercostal nerve for brachial plexus)
7. Nerve grafting
8. Nerve crossing (ulnar to median)
9. Addition of non-neural tubes (e.g., vein segment)

50. Mobilization limit for a nerve:
• Depends on the type of nerve but in general mobilization >6-8 cms
decreases perfusion. (about 8 per cent tension decreases venular
flow, 10-15 per cent - tension: blood flow arrest).

51. Types of nerve grafting:
1. Trunk grafting using full-thickness segment of major nerve trunk (disadvantage – central
necrosis/total graft dissolution)
2. Cable graft using multiple strands of cut nerve sewn at both ends (drawback – wastes axons and
ignores anatomic localization of function)
3. Pedicle grafting often preferred for high combined ulnar and median nerve palsy where ulnar
nerve is used as a pedicle graft to repair median nerve.
4. Interfascicular nerve graft (group fascicular nerve grafting)
5. Individual fascicular nerve grafting – often done for paucifascicular nerve, e.g., ulnar nerve at
elbow or for thin/terminal nerves, e.g., motor thenar branch of distal digital N.
6. Free vascularised nerve graft.

52. Nerve harvest for graft:
1.Autogenous:
a. Lateral cutaneous nerve of thigh
b. Medial brachial and antebrachial cutaneous nerve
c. Radial sensory nerve
d. Sural nerve (up to 40 cms of graft)
e. Lateral cutaneous nerve of forearm (up to 20 cms)
f. Terminal branch of PIN (for digital nerves)
2. Autologous vessels and muscle
3. Allograft nerve
4. Artificial conduits (veins/collagen conduits).

54. Fascicle: Termed funiculus by Sunderland it is the smallest unit of nerve
that can be manipulated surgically.
Topographic sensitivity: Reinnervation of correct muscle within motor
system or correct patch of skin in sensory system.
PARTIAL NEURORRHAPHY:
• Done in Partial severance of the larger nerves, such
as the sciatic nerve and the cords and trunks of the
brachial plexus.
• The incision is extended longitudinally in the
epineurium proximally and distally several
centimeters, as necessary. The intact funiculi are
dissected out for the same distance. The ends of
the injured part of the nerve are resected to
normal tissue. At the cut ends, an end-to-end
neurorrhaphy is performed.

55. Tinel’s sign:
• Paresthesia (fornication) experienced along the nerve distribution
(not at the percussion site) on gentle percussion from distal to
proximal over the nerve.
• Cause: Bare young hyper-excitable unmyelinated sprouts from
injured proximal end.
• Seen in: Sunderland’s grades II-V.
• Importance: Advancing Tinel’s can be used to calculate and gauge
progression of recovery.

62. Thank You