NERVE INJURIES - GENERAL PRINCIPLES

Anatomy

Clinical diagnosis of
nerve injuries

Aftertreatment

Neuronal
degeneration and
regeneration
Diagnostic tests

Classification of
nerve injuries

Aetiology of
peripheral nerve
injuries

Early management
of nerve injuries

Techniques of
nerve repair

Factors affecting
outcome after nerve
repair

1. Anatomy [Also See Nervous System]

Of spinal nerves

Each segmental spinal nerve is formed by union of the dorsal/sensory root with the
ventral/motor root at or before the intervertebral foramen
In the thoracic segments, these mixed spinal nerves maintain their autonomy, providing
sensation and motor function to one intercostal segment
In all other areas (cervical, lumbar and sacral regions, plexuses are formed which provide
a limb or special body segment without retaining the primitive myomeric pattern

Components of a mixed spinal nerve

Motor

The cell bodies are in the anterior horn cells and innervate skeletal muscle.

Sensory

Cell bodies lie within the dorsal root ganglia. The fibres arise in the pain , thermal, tactile and
stretch receptors.
Proprioception, fine touch and vibration from extremities and trunk
These fibres pass cephalad in the dorsal columns and do not synapse until reaching the
cervicomedullary junction.
Pathway for pressure and crude touch from extremities and trunk

These fibres enter, synapse and cross and ascend into the contralateral ventral spinothalamic
tract.
Pain and temperature
These fibres synapse in the spnal cord, and cross to ascend in the lateral spinothalamic tract.
There is some area of neuronal overlap explained by branches that ascend or descend via the
dorsolateral column/fasciculus of Lissauer.

Sympathetic

The sympathetic component of all 31 spinal nerves leaves the spinal cord along only 14 motor
roots (from T1 to L2). Between T1 and L2 there are white rami containing sympathetic fibres to
the ganglions of the sympathetic chain. Synapses occur somewhere along the sympathetic chain
and then postganglionic fibres reenter the mixed spinal nerves through grey rami.

Gross anatomy of a spinal nerve

Divides into an anterior and posterior primary ramus after leaving the intervertbral foramen.
Posterior primary ramus supplies the paraspinal musculature and the skin along the posterior
aspect of the trunk neck and head
Anterior primary ramus supplies everything else, and form plexuses
Dermatome- The area of skin supplied by a single spinal root.

Microscopic anatomy

Sensory and motor nerves contain both unmyelinated and myelinated fibres at a ratio of 4:1.
The blood supply to the peripheral nerve enters through the mesoneurium. This blood supply is
both extrinsic/segmental and intrinsic/longitudinal within the epineurium, perineurium and
endoneurium.
Perineurium

surrounds each fascicle or funicle (bunch of sheathed axons)

it is a cellular layer with tight junctions between cells enclosing the perineurial space
(within the perineurium)

Epineurium

= anything outside the perineurium which is not nerve fibre or blood vessel
mainly collagen

strongest supporting structure of the nerve

Endoneurium

= collagen surrounding nerve fibres.

The arrangement of the fascicles in the proximal aspect of perpheral nerves is more complex
than in the distal end of the nerve.

2. Neuronal Degeneration and regeneration

1. Retraction
2. Inflammation
3. Degeneration
Any part of a neuron detached from its nucleus degenerates and is destroyed by phagocytosis.
Secondary or Wallerian degeneration

Degeneration distal to the point of injury.

The fundamental concept of wallerian degeneration is that survival of nerve fibres occurs
only if they remain connected to the cell body.

commences 2 to 3 days after injury

o

the distal segment begins to fragment.

Cell body

swells

migration of nucleus to periphery of cell

chromatolysis (basophilia)

Activation of Schwann cells close to the injury site

By 7 days the Schwann cells are mitosing & phagocytosing cellular & myelin debris

By 25-30 days the axonal debris is cleared.

Schwann cells occupy the empty endoneurial tubes forming the 'bands of von Bungner'

The bands act as sprouts (neurites) of regenerating axons ('pioneering axons') down the
endoneurial tubes -> Regeneration.

Primary or retrograde or traumatic degeneration

Degeneration proximal to the point of detachment

only as far as the next proximal Node of Ranvier.

Histologically identical to Wallerian degeneration

4. Regeneration

Axonal sprouting can occur within 24 hrs of injury. All sprouts are unmyelinated to begin
with.
If the sprouts manage to make distal connections then nerve fibre maturation occurs, with
increase in axon & myelin thickness.

Neurites which fail to make distant connections die back & are lost to the regenerative
process.

If the perineurium is not disrupted then the axons will be guided along their original
pathway (1mm/day)

If the perineurium is disrupted there are neurotrophic substances (NGF - nerve growth
factors) which attract the neurites to nerve tissue.

The critical gap over which this does not occur is 2mm.

Neuromas form when neurites migrate aimlessly across a large gap. They can be stump
neuromas or neuromas in continuity.

4. Classification of nerve injuries

Seddon Classification
Neuropraxia (nerve, non-action)

usually compression injury

local conduction block & demyelination

thick myelinated nerves mainly affected

heals by Schwann cell repair of demyelination - takes several weeks or months

Axonotmesis (cylinder, cutting)

usually traction injury, but may occur after severe compression

Wallerian degeneration occurs

endoneurial tubes are intact -> no miswiring & good regeneration

limiting factor is the distance of regeneration required

worse with proximal injuries

sensory recovery is better (sensory receptors survive longer than motor units)

Neurotmesis (nerve, cutting)

complete severance of the nerve trunk

no recovery unless repair undertaken

lots of miswiring of organs

reduced mass of innervation

Sunderland Classification

accounts for the injuries between an axonotmesis & neurotmesis

based on involvement of the perineurium

Degree of
injury

Degree of
injury

Mye
lin

Ax
on

Endoneuri
um

Sunderlan
d, 1978

Seddon,
1943

1st degree

Neuroprax
ia

+/-

11

Axonotme
sis

111

Axonotme
sis

1V

Axonotme
sis

Perineuri
um

Epineuri
um

Tinel
sign
pres
ent

Tinel
sign
progress
es
distally

Neurotme
sis

Mckinnon & Dellon (1988) added a 6th degree injury = neuroma-in-continuity, where a nerve
has had a disordered self-repair with a lateral neuroma. There is a mixture of injuries, when a
nerve is partly severed and the remaining trunk sustains a 1 st, 2nd 3rd or 4th degree injury.
Complex regional pain syndrome

Pain, swelling, discoloration, hyperhydrosis, osteoporosis, resulting from an abnormal

and prolonged response from the sympathetic nervous system.
3% of major nerve injuries

5. Aetiology of Peripheral nerve injuries

Can be due to metabolic, collagen disease, malignancy, toxins, thermal or mechanical

injury, but only mechanical causes mentioned here.
Mechanical causes producing primary injury include laceration, fracture, fracture
manipulation, gunshot wound
Secondary injury can be due to infection, scarring, callus, vascular complications, eg. AV
malformation, aneurysm, ischaemia

6.Clinical diagnosis of nerve injury and assessment post injury

Requires thorough knowledge of the anatomy of nerves.
Motor function
Visible fibrillation of muscle
Power loss (MRC):
0 Total paralysis
1 Muscle flicker
2 muscle contraction
3 muscle contraction against gravity
4 muscle contraction against gravity and resistance
5 normal muscle contraction compared to other side
Must have full passive range of motion of joint
Muscle wasting

50-70% muscle atrophy after 2 months

Striations and motor end plates retained for approx 12 months

Method for assessing the the return of muscle function after nerve injuries (British
Research Council)

M0 No contraction
M1 Return of perceptible contraction in proximal muscles
M2 Return of perceptible contraction in both proximal and distal muscles
M3 Return of prox. and distal muscle power enough to allow the major muscle groups to
act against resistance
M4 Return of function as in stage 3 but synergistic and independent movements are
possible
M5 Complete recovery

Sensation
Sharp pin to assess pain, cotton wool to assess light touch, tips of a paper clip to assess
two point discrimination.
Normal 2 point discrimination in the hand:

There is an area of complete sensory loss ' the autonomous zone', which gets smaller
even before fibres can regenerate (? Due to increased function of anastomotic branches
from adjacent nerves)
A larger area of reduced sensation surrounds this = 'the intermediate zone'
When a nerve is intact and the surrounding nerves are blocked, an area of sensibility
larger than the gross anatomical distribution of the nerve occurs = ' the maximal zone'

Sensibility recovery sequence:

1. Pain and temperature
2. Pseudomotor function
3. Touch (Semmes-Weinstein monofilaments: protective sensation present if able to feel
5.07 Semmes-Weinstein filament)
4. Perception of 30 Hz vibration (tested over bony prominences with a tuning fork)
5. Perception of moving touch
6. Perception of constant touch
7. Perception of 256Hz vibration
8. Stereognosis (test with heptagonal UK 50 pence coin)

Sensation assessment after peripheral nerve injury - British Medical Research Society

S0 Absence of sensibility in the autonomous area

S1 Recovery of deep cutaneous pain in the autonomous area
S2 Return of some degree of superficial cutaneous pain and touch in the autonomous
area
S3 Return of superficial cutaneous pain and touch throughout the autonomous area, with
disappearance of any previous over response
S4 As for 3 but also some recovery of two point discrimination in the autonomous area
S5 Complete recovery

The best correlator of eventual function is return of 2 point discrimination (as emphasised
by Moberg, 1995)

Autonomic function

There is loss of sweating , the pilomotor response and vasomotor action when a
peripheral nerve is disrupted.
Pilomotor - The wrinkle test is a useful objective test - Denervated skin does not wrinkle
in water
Vasomotor - Initially there may be vasodilatation in a complete lesion, pinkness for 2-3
weeks. Then coldness paleness, mottled. This may spread to more than the anatomical
area of skin supplied by the nerve.
Atrophy of fingers and nails can occur.
Test sweating:
1. by rubbing smooth pen against side of finger (if finger moves with pen = sweating
present)
2. Ninhydrin print test - applying nihydrin to sweat turns it purple (Moberg, 1995)
3. Look through the +20 lens of an opthalmoscope to see the beads of sweat
4. Dust the extremity with quinizarin powder. Sweating turns the powder purple
5. Absence of sweating causes an increased resistance to an electric current

If sweating still present this suggests that the nerve damage is incomplete

Hoffmann-Tinel Sign (1917)

Gentle percussion with the finger along the course of the injured nerve will produce a
transient tingling sensation in the distribution of the injured nerve, persisting for several
seconds.
Start distally and proceed proximally
A positive Tinel sign is evidence of regenerating axonal sprouts which have not
completed myelinisation are progressing.
A distally advancing Tinel sign should be present in Sunderland 11 and 111 injuries
A type 1 injury (neuropraxia) should not produce any Tinel's sign as no new regeneration
should need to occur
Type 1V and V injuries do not produce an advancing Tinel sign unless repaired

A progressing Tinel's sign is encouraging but does not necessarily mean complete
recovery.

Reflexes

Complete severance of either the efferent or afferent nerve in a reflex abolishes that
reflex. However, the reflex can be lost even in partial injury and is not a good guide of
injury severity

7. Diagnostic tests
Nerve conduction studies

Evaluation of peripheral nerves & their sensory & motor responses anywhere along their
course
Stimulation of a peripheral nerve should evoke a contraction in the muscles it supplies
(seen, palpated or measured electromyographically)
Latency (t)= time between onset of stimulus & the response
Amplitude = size of response
Nerve Conduction Velocity (V) = d / t (d = distance between stimulating & recording
electrodes)
Motor Nerve:
o Recording electrode (cathode) placed over a muscle supplied by the nerve (over
the 'motor point' = region where the nerve enters the muscle)
o Indifferent electrode is placed a few centimeters away
o Ground electrode placed over an inactive muscle nearby
o Stimulation site is where the nerve is superficial (eg. elbow)
o Stimulator is turned on until a clearly defined CMAP (compound motor action
potential) appears = 'threshold'
o Stimulus is increased by 50% to 'supramaximal' ensuring complete activation of
the muscle.
o A second stimulator is added, distal to the first stimulator & closer to the
recording electrode. The segment velocity between the 2 stimulation sites is
calculated:
V(motor) = [d1-d2]/ [t1-t2] (where V(motor) = segment velocity in motor fibres; d1
is distance betw. first (proximal) stimulation site & recording cathode; d 2
is distance betw. second (distal) stimulation site & recording cathode; t1 is
latency betw. first (proximal) stimulation site & recording cathode; t 2 is
distance betw. second (distal) stimulation site & recording cathode)

Motor nerve conduction test for Ulnar

nerve above & below elbow

Motor nerve conduction test for

Ulnar nerve at wrist using ADM (from
TeleEMG)

Sensory Nerve:
o CNAP (compound nerve action potential) is measured (lower amplitude than
CMAP)
o a uniquely sensory nerve must be chosen for the stimulation site
o V(sensory) = d / t (where V(sensory) is the segment velocity in sensory fibres; d is
distance betw. stimulation site & recording cathode; t is the average latency betw.
stimulus & CNAP)

Sensory nerve conduction test for

Ulnar nerve across the wrist (from
TeleEMG)

Collision Studies
Timing of NCS:
o Immediately after section of a peripheral nerve, stimulation distally will elicit a
normal response for 18-72 hrs until wallerian degeneration occurs.
o Absence of distal nerve motor conduction (CMAP) after 3-7 days excludes a
neuropraxia type injury.
o Absence of sensory conduction (CNAP) after 7-10 days excludes a neuropraxia
type injury.
o Therefore the ideal time for NCS after injury is 10-14 days after injury to
discern neuropraxia from axonotmesis / neurotmesis.
o Neuropraxia will improve (incr. velocity & decr. latency) with repeated tests, while
axonotmesis & neurotmasis will deteriorate

Somatosensory Evoked Potentials (SSEP) = stimulate peripheral sensory nerves & measure
on the scalp. For study of brachial plexus & spinal cord monitoring.

Electromyography

A needle electrode in the muscle is used to record motor unit activity at rest and on
attempted contraction of the muscle
Normal EMG shows no muscle activity at rest and a characteristic pattern on voluntary
contraction
Normal EMG

Immediately after nerve section, EMG will be normal, although there will be no muscle
response after stimulation of the nerve proximal to the nerve injury (CMAP)
Within Between 5 and 14 days positive sharp waves consistent with denervation

Positive sharp waves of Denervation

At between 15 and 30 days, spontaneous denervation fibrillation potentials are present

Denervation fibrillation potentials

If denervation fibrillation potentials are not present by the end of the 2 nd week this
is a good prognostic sign.
Evidence of reinnervation is when highly polyphasic motor unit potentials are
detected at attempts at voluntary activity
Denervation fibrillations in a muscle only tell you that the muscle is not innervated. It does
not determine whether the injury is 2nd 3rd or 4th degree.
Reinnervation potentials by the same token can be restored after regeneration of only a
few motor fibres and does not necessarily mean a good return to voluntary motor control

EMG Findings in Specific Conditions:

Condition

Insertional
Activity *

Rest
Activity
**

Fibrillation
s ***

Sharp
Wave
s

Potentials++

Interferenc
e

Normal

Normal

Silent

No

No

Biphasic &
triphasic

Complete

Neuropraxia

Normal

Silent

No

No

No

None

Axonotmesis

Increased

Increase
d

Yes

Yes

Large &
longer
polyphasic

None

Neurotmesis

Increased

Increase
d

Yes

Yes

Large &
longer
polyphasic

None

Axonal
Neuropathy

Increased

Increase
d

Yes

Yes

Demyelinating
Neuropathy

Normal

Silent

No

No

Yes

Incomplete

Anterior Horn
Disease

Increased

Increase
d

Yes

Yes

Large
polyphasic

Incomplete

Myopathy

Increased

Silent

Yes

Yes

Small
polyphasic

Early

Incomplete

* Insertional Activity = needle is inserted into muscle or moved within muscle, there is a
single burst of activity that usually lasts 300 to 500 ms; thought to result from mechanical
stimulation or injury of the muscle fibers
** Rest Activity = differentiates neuropathic muscle atrophy from myopathic atrophy
*** Fibrillations - are action potentials that arise spontaneously from single muscle
fibers; usually occur rhythmically and are though to be due oscillations of the resting

membrane potential in denervated muscles. Appears 3 - 5 weeks after the nerve lesion.
Preceded by Positive Sharp Waves.
++
Potentials - number of phases (? action potentials); indicates collateral axonal
sprouting; polyphasic = > 4 phases

8. Early management of nerve injuries

ABCs as with any injury

Open wound with nerve injury- thorough debridement . If wound adequately clean and
general state of the patient allows, then immediate primary nerve repair is preferred
Open wound but patients general state in danger. clean wound and dress with moist
dressing, attempt repair at 3-7 days
Contaminated wounds- Thorough debridement, mark ends of nerve with a suture and
consider suturing to soft tisssue to avoid retraction. Repair the nerve when the soft
tissues have healed at 3-6 weeks post injury
A closed injury with peripheral nerve damage. Early active motion of all affected
musce groups should be started. Contractures should be prevented by passive motion.
Specific effects of electrical muscle stimulation are unclear. Dynamic and static splints
can be used intermittently.
A closed fracture associated with nerve injury. Early exploration usually avoided.
Assess progress of functional return using EMG, NCS and clinical assessment. However,
if ORIF required explore nerve too.
If nerve deficit follows manipulation and /or casting of a closed fracture. Early
exploration is favoured

9. Techniques of nerve repair (neurorrhaphy)

Epineurial

Perineurial

Epi perineurial
repair

Interfascicular nerve
grafting

Clinical evidence to support one over the other type of repair is meagre. The technique selected
depends on the experience of the surgeon.

Sunderland points out that fascicular repair is not possible in all cases, but most practical when

Fascicular groups are large enough to take sutures

Each fascicular group is made up of fibres to a partiicular branch occupying a constant
position at the nerve ends eg. In median and ulnar nerves above the wrist and radial
nerve above the elbow.

10. Aftertreatment

Opinions differ as to when joints can be moved

In upper limb, immobilise in a plaster splint or cast for 4 weeks, then replace in a plastic
splint, gradually extending the joint over 2-3 weeks
In lower limb immobilise for 6 weeks
Rigid splinting not justified if prognosis for nerve function doubtful
Dynamic splinting of distal joints with passive exercises to maintain motion whilst nerve
recovers

11. Factors influencing regeneration after nerve repair (neurorrhaphy)

Info from warzone injuries
1. Age
Worsening results with increasing age, though numbers at extremities of age are small
2. Gap between nerve ends
Nicholson, Seddon and Sakellarides noted that the upper limit of gap beyond which results will
deteriorate is 2.5 cm. Methods of closing gaps;
1.
2.
3.
4.
5.

nerve mobilisation
nerve transposition
joint flexion
nerve grafts
bone shortening

3. Delay between injury and repair

Delay affects motor recovery more than sensory recovery (due to the survival time of
striated muscle.
Satisfactory reinnervation of muscle can occur after denervation of 12 mnths
Little evidence about sensory function return in relation to delay, but sensation can
improve in as late a repair as 2 years.

Kleinert et al feel that a delayed repair of between 7 and 18 days is best for return of
satifactory function. Reasonable approach is immediate repair if conditions allow and
before 6 weeks in extensive soft tissue contusion, contamination, crushing.

4. Level of injury

The more proximal the lesion, the more incomplete the recovery. Boswick et al reviewed
102 peripheral nerve injuries in 81 patients. 87% of those injuries below the elbow gained
protective sensation. 14% regained normal 2 point discrimination.

5. Condition of nerve ending The better the condition the more improvement

Further Reading:

TOP

Review of Orthopaedics - Mark Miller

Sciences Basic to Orthopaedics - Sean Hughes & Ian McCarthy; WB Saunders, 1998.
TeleEMG - http://www.teleemg.com/

SYLLABUS
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JB, LF - Updated on:

Nerve Injuries
What are nerves? Nerves are the electrical wiring system in all people that carry messages from the
brain to the rest of the body. A nerve is like an electrical cable wrapped in insulation. A ring of tissue forms
a cover to protect the nerve, just like the insulation surrounding an electrical cable (Figure 1).
Nerves serve as the wires of the body that carry information to and from the brain. Motor nerves carry
messages from the brain to muscles to make the body move. Sensory nerves carry messages to the brain
from different parts of the body to signal pain, pressure, and temperature. While the axon (nerve fiber)
carries only one type of message, either motor or sensory, most nerves in the body are made up of both.
What happens when a nerve is injured? Nerves are fragile and can be damaged by pressure, stretching,
or cutting. Injury to a nerve can stop signals to and from the brain causing muscles not to work right, and
you may lose feeling in the injured area. When a nerve is cut, both the nerve and the insulation are broken.
Pressure or stretching injuries can cause the fibers carrying the information to break and stop the nerve
from working, without damaging the cover.
When nerve fibers are cut, the end of the fiber farthest from the brain dies, while the insulation stays
healthy. The end that is closest to the brain does not die, and after some time may begin to heal. If the
insulation was not cut, new fibers may grow down the empty cover of the tissue until reaching a muscle or
sensory receptor. If both the nerve and insulation have been cut and the nerve is not fixed, the growing
nerve fibers may grow into a ball at the end of the cut, forming a nerve scar or neuroma. A neuroma can be
painful and cause an electrical feeling when touched.

How is it treated? To fix a cut nerve, the insulation around both ends of the nerve are sewn together. The
goal in fixing the nerve is to save the cover so that new fibers may heal and work again (Figure 2). If a
wound is dirty or crushed, your physician may wait to fix the nerve until the skin has healed. If there is a
space between the ends of the nerve, the doctor may need to take a piece of nerve (nerve graft) from
another part of the body to fix the injured nerve. This may cause permanent loss of feeling in the area
where the nerve graft was taken.
Once the nerve cover is fixed, the nerve generally begins to heal three or four weeks after the injury. Nerves
usually grow one inch every month depending on the patients age and other factors. This means that with
an injury to a nerve in the arm above the fingertips, it may take up to a year before feeling returns to the
fingertips. The feeling of pins and needles in the fingertips is common during the recovery process. While
this can be uncomfortable, it usually passes and is a sign of recovery.
What is my role in recovery and what kind of results can I expect? The patient must do several things
to keep up muscle activity and feeling while waiting for the nerve to heal. Your doctor may recommend
therapy to keep joints flexible. If the joints become stiff, they will not work even after muscles begin to
work again. When a sensory nerve has been injured, the patient must be extra careful not to burn or cut
fingers since there is no feeling in the affected area. After the nerve has recovered, the brain gets lazy,
and a procedure called sensory re-education may be needed to improve feeling to the hand or finger. Your
doctor will recommend the appropriate therapy based on the nature of your injury.
Factors that may affect results after nerve repair include age, the type of wound and nerve, and location of
the injury. While nerve injuries may create lasting problems for the patient, care by a physician and proper
therapy help two out of three patients return to more normal use.

Easy to remember URL is www.lingualnerve.org.

Espaol - Supported and translated by: Carballo, J. Garrido, M. &
Iglesias, E. Email
Lingual nerve injury or damage can result in anesthesia (numb
tongue), paresthesia (tingling), or dysesthesia ( pain and burning ) in
the tongue and inner mucosa of the mouth. This can be due to
complication of tooth extraction of the wisdom teeth ( third molar ) or
dental anesthetic injection (nerve block) for fillings, crowns. It result in
a chronic pain syndrome or neuropathy. If the inferior alveolar nerve is
involved, numbness of the lip may result.
Some people have injury to the inferior alveolar nerve. While this site
was created addressing lingual nerve damage, inferior alveolar nerve
damage is even more common. The injury can result in anesthesia,
paresthesia, or dysesthesia of the chin, lower lip, and the jaw. This
nerve can be injured by injection, but is more commonly injured during
wisdom tooth extraction. It can also be injured by root canal
procedures, other tooth extractions and with placement of implants.
Tooth extraction is one of the
leading causes of lingual nerve and
inferor alveolar nerve damage, usually
the third molars ( wisdom teeth). ..
.MORE

Traumatic injuries to the lingual

nerve are rare, partially due to its
protected location, to the inside of the
mandibular bone.
**********

***********
Lingual or inferior alveolar nerve
injury from injection of local
anesthetic during a dental
procedure can also happen, and
some think it is happening more
often....MORE
*************
Painful lingual (tongue) nerve or
inferior alveolar (jaw, chin, lip)
injuries are difficult to live with, and
to treat, but here is a list of
options...MORE

Choices for dental procedures with

avoidance of needles and
anesthetic injections, and the
associated complications... MORE
********
Have a question, try the discussion
board. This area has been very
successful, ask questions, share your
experience with others.. MORE