2. Contents
Introduction
Anatomy of Nerve
Types of nerve fibers
Nerve morphology
Nerve injury : Classification
Physiology of nerve injury
Terminology
Nerve degeneration and regeneration
Diagnostic evaluation
Medical management of nerve injury
Surgical management of nerve injury
References
2
3. Introduction
The term “Nerve” is often used erroneously to
describe what infact is a bundle of nerve fibers.
The actual nerve fiber or axon is an anatomic process
of a single nerve cell.
Nerve fiber is the functional component of peripheral
nerve responsible for transmitting stimuli.
3
4. “
”
• The nerve fiber is composed of an axon, a Schwann cell and a
myelin sheath in myelinated nerve fibers.
• The Axon is an extension of a neuron and can be characterized
by morphology, conduction velocity and function
4
5. Many procedures performed routinely by oral and maxillofacial surgeons run
the risk of injury to one or the other nerves.
The neuropathic responses to nerve injury is very essential because the goal
of micro reconstruction is to prevent or reverse these conditions.
We have entered an era where artificial intelligence is becoming reality, an
era where the transmission of information is performed by systems that are
actually smaller that the axons required in biological systems.
The application of electrical technology to biological system is immense.
5
6. The major impediment to the clinical application is the inability
to understand and control the biological systems in man
completely.
However, attempting to understand the peripheral nerve, and
particularly the injured peripheral nerve is essential to surgeons
if the potentials of new technology are to be incorporated
successfully into clinical practice. Hence in order to understand
the neuropathic response to nerve injury, it is necessary to have a
clear mental image of normal nerve morphology.
6
7. NERVE
Nerves are solid white cords made up of bundles of axons. Each nerve fibre is
known as an axon and each axon is bound together by fibrous tissue into small
bundles.
7
8. PARTS OF NEURON
The cell body (soma) contains the nucleus and is the metabolic center of the neuron.
Neurons have several processes called dendrites that extend outward from the cell body and arborize extensively.
Particularly in the cerebral and cerebellar cortex, the dendrites have small knobby projections called dendritic spines.
A typical neuron also has a long fibrous axon that originates from a somewhat thickened area of the cell body, the axon hillock.
The first portion of the axon is called the initial segment.
The axon divides into presynaptic terminals, each ending in a number of synaptic knobs which are also called terminal buttons
or boutons.
They contain granules or vesicles in which the synaptic transmitters secreted by the nerves are stored.
8
9. Based on the number of
processes that emanate from
their cell body, neurons can be
classified as unipolar ,
bipolar , Pseudo-unipolar
and multipolar.
9
10. AXON
An axon is a direct extension of a cell body.
The most important component of the peripheral nerve is the nerve fibre that
transmits the stimuli. All other components of the nerve simply provide the
optimal conditions for the nerve fibre to function.
10
11. Nerve morphology
The nerve trunk is composed of four connective
tissue sheath. They are as follows from outside
inward,
1) Mesoneurium
2) Epineurium
3) Perineurium
4) Endoneurium
11
12. MESONEURIUM :
Is a connective tissue sheath that suspends the nerve
trunk within the soft tissue, contains the segmental
blood supply of the nerve and is continuous with the
second layer – the epineurium.
EPINEURIUM :
Is the loose connective tissue sheath that defines the
nerve trunk and protects it against mechanical stress.
It is composed of longitudinally oriented collagen
fibres that resist both compressive forces and stretch.
Nerve trunks are fairly mobile except where branches
and blood vessels enter the epineural sheath.
12
13. The PERINEURIUM delineates the fascicles.
In a living nerve, perineurium is a white glistening layer
devoid of blood vessels.
This is a continuation of the pia-arachnoid mater of the central
nervous system. It is composed of two layers: an outer layer of
dense connective tissue with collagen arranged perpendicular
to the longitudinal axis of the nerve and an inner cellular layer
made of a multiple-layered continuous sheets of flat squamous
cells ( perineurial epithelium ).
The perineurial epithelium form lamellae that vary with the
diameter of the fascicle. Larger the fascicle, the greater the
number of lamellae.
Blood vessels transverse the perineurium to connect the vasa
nervosum and endoneurial capillaries. 13
14. The perineurium has the following functions:
Act as diffusion barrier – prevents certain molecules from penetrating the
perineurial and blood-brain barrier, thus it regulates the composition of the
endoneurial fluid.
Active transport of certain molecules.
Maintains positive pressure inside the fascicle.
Gives structural support to the enclosed neural tissue.
Nerve conduction disturbances may result if the perineurium is breached. It also
occurs following intrafascicular fibrosis as a sequelae to raise in intrafascicular
haemorrhage and oedema.
14
15. ENDONEURIUM
The endoneurium surrounds the individual nerve fibre and their
schwann cells.
Endoneurium and perineurium together give elasticity to the nerve.
Endoneurium is composed of two layers: an outer layer of collagen
fibres and endoneurial fibroblasts and an internal layer of basal lamina
and endoneurial capillaries.
The capillaries of the endoneurial space are connected to vasa
nervosum through the perineurium.
The endothelium of the intrafascicular capillaries (endoneurial
capillaries) act as a blood nerve barrier, and together with the barrier
function of the perineurium they regulate the intrafascicular
environment.
The endoneurial capillaries are more resistant to compression injury
than the epineurial blood vessels. 15
16. Each individual nerve fibre and their
Schwann cell are surrounded by
endoneurium.
Group of nerve fibres – fasciculi
Each fasciculi is surrounded by
perineurium
Group of fasciculi forms a nerve trunk
Fascicules are surrounded by epineurium.
Epineurium :
Epifasciculae layer (surrounds the entire
nerve trunk)
Interfasciculae layer (which occupies the
space among the fascicles). 16
17. Five types of fascicular pattern
Monofascicular pattern : The nerve consists of one large fascicle (Ex. Facial nerve at stylomastoid
foramen).
Oligofascicular pattern : (With few large fascicules 2-5). There is only minimal epineural tissue between
fascicles (fascicular co-aptation can be achieved).
Oligofascicular pattern (with more than 5 fascicules). Fascicular co-aptation cannot be guaranteed.
Polyfascicular pattern (with group arrangement). The nerve consist of many fascicules of different sizes
arranged in groups (inferior alveolar and lingual nerve).
Polyfascicular pattern (without group arrangement) Nerve with an abundant area of interfascicular tissue
are more capable of withstanding compressive forces.
17
19. Schwann cells are pluripotential cells and have a variety of functions
essential to the function of the nerve. It forms myelin and supplies the
axon with essential metabolites. Schwann cells are the cellular components
most sensitive to ischaemia and irradiation.
19
20. NERVE FIBERS
The nerve fiber is the functional unit of the peripheral nerve responsible for transmitting
stimuli.
The nerve fiber is comprised of many different types of axons of diverse diameter, Schwann
cells and a myelin sheath in myelinated nerve fibres.
The axon is a long projection from the soma ( cell body of neuron ), which can extend for
several distance.
It is bounded by a semipermeable membrane the axolemma.
This is surrounded by basement membrane, which in turn, is encircled by a layer of myelin
sheath usually.
20
21. The myelin sheath is formed by Schwann cells.
This is covered by a layer of connective tissue (endoneurium).
The axon can be characterised by morphology, conduction velocity and
function.
The conduction velocity is approximately proportional to the square root of
fiber diameter.
21
23. Nerve fibers are classified as A, B (myelinated) and C (unmyelinated) groups.
“A” group is further classified as
1) A- alpha
2) A- beta
3) A – gamma
4) A- delta
ERLANGER AND GASSER’S CLASSIFICATION
23
26. Monofascicular pattern one large fascicle. E.g. Intra-cranial part of facial nerve.
Oligofascicular pattern 2 – 10 fascicles.
Polyfascicular pattern > 10 fascicles. E.g. Inferior alveolar nerve, Lingual nerve.
( 18 – 21 fascicles )
BASED ON THE NUMBER OF FASCICLES
26
27. CAUSES OF NERVE INJURY
Central Disease
This may produce impaired sensation. Usually motor nerves are affected.
E.g. : Tabes dorsalis
Syrniogomyelia – disease of the spinal cord in which longitudinal cavities form within
the cord in the cervical region. It is likely to damage the motor nerve cells and nerve
fibers that transmit sensation of pain and temperature.
Multiple sclerosis and
Bulbar paralysis
27
28. Local conditions
Fracture of the middle face.
Eg.
1. Lefort III and its variations which frequently cause the shearing off or impingement of
the optic nerve resulting in temporary or permanent blindness. It can occur in any
fracture that can cause compression of the nerve.
2. Fracture of the mandible involving the mandibular canal or mental foramen.
3. Operative injuries : Usually due to surgical removal of impacted teeth, sulcus
extension and alveloplasty, Caldwell luc.
4. Accidental injuries : While excising large cysts and tumours.
5. Sclerosis following dental infection.
6. Implant surgery with impingement of the neuro vascular bundle by endosseous
fixtures. Transossoeus wire fixation, plates and screws.
7. Tumours involving the nerves.
28
29. ETIOLOGY OF PERIPHERAL NERVE INJURIES
Peripheral nerve may be injured as a result of
Metabolic or collagen diseases.
Malignancies.
Endogenous or exogenous toxins.
Thermal, mechanical or chemical injuries.
Mechanical injuries to peripheral nerves are most common. Among this lacerating wounds
resulting from road traffic accidents, interpersonal violence including stabs, war injuries such
as bullet injuries are more common. Iatrogenic nerve injuries are very common in
maxillofacial region. Branches of trigeminal and facial nerve are the nerves commonly injured
in maxillofacial region.
29
32. NEUROPRAXIA
It is a mere conduction block resulting from a mild insult to the nerve trunk. There is
no axonal degeneration. Sensory recovery is complete and occurs in a matter of hours to
several days. The magnitude of sensory deficit is usually mild and consists of a
paresthesia with some level of stimulus detection.
32
33. AXONOTMESIS
It is a more severe injury than neuropraxia, afferent fibres undergo degeneration but the nerve trunk is grossly intact with
variable degree of tissue injury. Though the axons are damaged there is no disruption of the endoneural sheath, perineurium
or epineurium.
Recovery is good but incomplete, can start form 2-4 months to about 12 months. The psychophysical response to an
axonotmesis is an initial anesthesia and tinel’s sign, followed by paresthesia as recovery begins. Tinel’s sign is a painful,
electric shock like sensation elicited by tapping directly over the cutaneous distribution of the injured nerve. If the distal
aspect of the nerve is percussed progressively proximally the level at which the sign is first elicited marks the most distal part
of small fibre regeneration.
33
34. NEUROTMESIS
Severe disruption of the connective tissue components of the nerve trunk.
Sensory recovery is not to be expected when the nerve courses through soft
tissue. But those within a canal may show some degree of sensory recovery
because of the guiding influence of the canal.
There is cross-shunting of the axons as they enter the distal endoneural tubes
and there is inaccurate localization of cutaneous stimuli.
34
35. Based on the Degree of Tissue
Injury
FIRST DEGREE INJURY
SECOND DEGREE INJURY
THIRD DEGREE INJURY
FOURTH DEGREE INJURY
FIFTH DEGREE INJURY
SIXTH DEGREE INJURY
SUNDERLAND CLASSIFICATION
35
36. FIRST DEGREE INJURY - NEUROPRAXIA
It is characterized by a conduction block.
Complete and rapid return of function or sensation, no degeneration of axon.
There are 3 types of First degree nerve injuries.
1) First degree type I injury
2) First degree type II injury
3) First degree type III injury
36
37. FIRST DEGREE TYPE I INJURY
Occurs as a result of nerve trunk manipulation, mild
traction, compression that would occur during SSRO,
inferior alveolar nerve repositioning or lingual nerve
manipulation during sialedenectomy of the sublingual
or submandibular gland. There is rapid return of
normal function and sensation within 24 hours
following the restoration of circulation.
The mechanism of conduction block is believed to be
anoxia from interruption of segmental as epineural
blood vessels.
37
38. FIRST DEGREE TYPE II INJURY
Results form moderate manipulation,
traction, or compression of nerve.
Normal sensation and function return
in 1 week.
Cause : Inter fascicular edema from
trauma of sufficient magnitude to
injure the endoneural capillaries.
38
39. FIRST DEGREE TYPE III INJURY
Severe nerve manipulation, traction or
compression. Pressure on the nerve causes
segmental demyelination or mechanical
disruption of the myelin sheath.
Recovery : 1-2 months.
Microreconstructive surgery is not indicated
for first degree injury unless persistant
foreign body irritant is present.
39
40. SECOND DEGREE INJURY - AXONOTMESIS
Axonal injury with subsequent degeneration and
regeneration. Traction and compression causes
ischaemia, intrafascicular oedema or demyelination.
Micro reconstruction - Contraindicated
Decompression - may be done
40
41. THIRD DEGREE INJURY - NEUROTEMESIS
The infrafascicular tissue components, the axons
and endoneurium are damaged. There is some
degree of intrafascicular fibrosis blocking the path
of regenerating axons. Therefore poor sensory
recovery with some degree of persistant
paresthesia, syneasthesia, and increased 2 point
discrimination.
The incidence of neuroma in continuity is low
because the perineurium and epineurium remains
intact.
Reconstruction – indicated. 41
42. FOURTH DEGREE INJURY
Fascicular disruption is characteristic. The
perineurium, endoneurium and axon are damaged.
Since only the epineurium is intact the incidence of
sensory impairment is high because of extensive
internal fibrosis.
Prognosis – Poor. Signs same as above
Surgical intervention is necessary.
Cause : Traction, compression, injection, and chemical
(eugenol).
42
43. FIFTH DEGREE INJURY
Transection or rupture of the entire nerve trunk.
Intraosseous fifth degree injury may undergo
spontaneous recovery of some degree if the canal is
intact.
Soft tissue fifth degree injury – poor prognosis. This
requires surgical adaptation and co-aptation. It could
be due to laceration, avulsion or chemical injury.
Incidence of fibrosis and amputation neuroma is high.
43
44. SIXTH DEGREE INJURY
It is combination of first to fifth degree of injuries. Within the same nerve
trunk some fascicules may exhibit normal function and others may have
varying degree of nerve injury.
44
46. Type A : Due to intraneural circulatory arrest or metabolic block with no nerve fibre
pathology. This is immediately reversible. Managed by therapies that improve circulation
like, decompression, or the use of agents to decrease oedema, or reverse vasospasm.
Type B : Intraneural edema resulting in increased endoneurial fluid pressure with no nerve
fibre pathology. Reversible in days or weeks. Therapies to reduce edema and increase
venous return are most appropriate.
PHYSIOLOGIC CONDUCTION BLOCK
CLASSIFICATION
46
47. Patients with sensory disturbances following nerve injury present with subjective
symptoms like anesthesia, paresthesia, dysesthesia.
Anesthesia : Complete absence of any stimulus detection, perception including
mechano receptors or nociceptive stimuli. This is usually due to severe injury of the
nerve interrupting the integrity of the axons. Sensory recovery is slow and
unpredictable.
SYMPTOMATIC CLASSIFICATION
47
48. Acute or early repair is indicated for -
o Observed transaction injuries of nerve located within soft tissue.
o Within the bony canal when the canal has been disrupted.
o Anesthesia that persists for 3 months which shows high index of suspicion for severe
nerve injury and poor prognosis.
Eg. Crush injury in soft tissue or canal.
o Presence of foreign body irritant, showing poor prognosis.
Eg. Endosseous implant compressing the inferior alveolar nerve.
Paresthesia : It is an alteration on sensibility in which there is abnormal stimulus
perception and detection that may be perceived as unpleasant but not painful.
48
49. Stimulus detection - Normal
- Increased
- Decreased
It may affect mechanoreception or nociception.
Increased pressure and touch stimuli detection – HYPERESTHESIA
Decreased pressure and touch stimuli detection – HYPOESTHESIA
Decreased nociceptive stimuli detection – HYPOALGESIA
Increased nociceptive stimuli detection – HYPERALGESIA
49
50. Some patients may given additional complaints like numbness, tingling, itching,
swollen, tight, heavy, drawing, feeling. This is due to conduction disturbances,
ischaemia and alteration in protein transport along the axons to the peripheral receptors.
It need not be form disruption of the axons. Difficulty in accurately and quickly
localizing the point of stimulus application – SYANATHESIA
This is due to misdirection of axons during the process of regeneration and is a common
finding following neuroraphy.
50
51. PROTOPATHIA : Inability to distinguish between two distinctively different stimuli like sharp
and dull.
DYSESTHESIA : It is an alteration in sensibility in which there is abnormal stimulus detection
and perception that may be perceived as unpleasant and painful. All features of paresthesia
present but also has pain which maybe spontaneous or triggered.
ALLODYNIA : It is a specific type of dysesthesia characterized by sharp first pain perception
elicited by light touch stimulus.
HYPERPATHIA : Another type of dysesthesia characterized by dull second pain elicited by
pressure stimulus. The pain lingers even after the stimulus has been removed.
51
52. INTRAOSSEOUS :
Osseous canals provide protection from mechanical trauma unless the integrity of the canal
is breached. Osseous canal predisposes the enclosed nerve trunk to compartment
syndrome which starts as a cascade of events in the acute phase ;
• Compression
• Edema
• Increased endoneural fluid pressure
• Ischemia
• Nerve fibre disfunction
ANATOMIC CLASSIFICATION
52
53. Chronic effects of compression are ;
• Fibroblast invasion
• Scarring
• Fibre deformation and degeneration
• Nerve fibre dysfunction
Surgical intervention is not necessary if canal is intact and nerve is intact and nerve is not
compressed. Chemical injuries are unique and generally require acute surgical
intervention to remove or neutralize the agent.
53
54. Soft tissues :
Nerves on soft tissues are not offered protection from mechanical trauma that their intraossoeus
counter pats are offered.
Lacerations and transactions of nerves located within soft tissues are more likely to form
neuromas (symptomatic / asymptomatic) and are less likely to undergo spontaneous regeneration
because of the formation of scar tissue between the injured ends.
The lingual nerve because of its close proximity to the lingual cortex of the mandible seems to be
very susceptible to injury.
Injuries resulting in anesthesia should be explored as easily as feasible to determine the type of
injury and repair it.
Dysasthesia depending on the response to non-surgical therapy should be explored and repaired
early to prevent the development of chronic pain and optimize favourable recovery.
54
55. Neuromas : Are disorganized attempts at regeneration resulting in a haphazard
and random micro sprouting of axons that fail to enter the distal nerve stump and
migrate along the endoneural tubes.
Amputation : Is a knobly disorganized mass of axons and collagen associated
with proximal nerve stump and completely separated form the distal stump. This
type of neuroma is a result of Sunderland 5th degree of injury.
HISTOPATHOLOGIC CLASSIFICATION
55
56. Fibrosis :
Various degree of reaction fibrosis occur following trauma to a nerve. They have been
classified by Millesi.
Type A fibrosis : involves the epifascicular epineurium and has a good prognosis.
Type B fibrosis : involves the interfascicular epineurium and prognosis is guarded.
Type C Fibrosis : It extends into the endoneurium and has a poor prognosis. It requires
excision of the scarred segment and graft reconstruction.
Type N fibrosis : Is a Sunderland 4th degree injury in which the epineurium maintains
continuity and is infiltrated by a neuroma.
Type S fibrosis : Is also a Sunderland 4th degree injury that is maintained only by a scar
tissue.
56
57. COMPRESSION :
Compression injury to a peripheral nerve may produce a neuropathic pain syndrome.
The acute response of compression is inflammatory edema.
This leads to connective tissue changes that include perineural and epineural thickening.
The next stage is localized nerve fibre changes.
Some fibre within the nerve will function normally while others undergo segmental demyelination. As the
degree of compression increases wallerian degeneration will be apparent.
The peripheral fascicles may be affected while the central ones may be spared.
The mechanism of compression injury includes both material deforming forces and ischemic factors.
PATHOPHYSIOLOGIC CLASSIFICATION
57
58. COMPARTMENT SYNDROME
The nerve injury associated with compartment syndrome is similar to that seen with nerve
compression except that the effects are largely due to ischemia of the nerve caused by
diminished flow within the compartment.
The syndrome applies to inferior alveolar nerve, descending palatine, infra orbital.
Increased venous pressure results from increased local tissue pressure, such as from
inflammation and edema of the nerve track. This leads to a decreased blood flow and
decreased oxygenation to the nerve.
Clinically the first sign is abnormal vibration and touch perception.
Management : Immediate decompression and use of anti-inflammatory drugs to alleviate
inflammation and edema.
58
59. STRETCH OR TRACTION INJURY
Stretch or traction injury is a 3 dimensional injury pattern.
Degree of injury is not only from fascicle to fascicle but also along the length of the nerve
longitudinally.
Therefore stretch injuries mandates surgical exploration of a considerable length of the nerve so as
not to miss a damaged tissue.
The sequence of changes associated with nerve stretch is not completely understood. Sunderland
feels the sequence of tissue rupture begin from within without.
• Axonal rupture (2nd degree injury)
• 3rd (3rd degree injury)
• 4th (4th degree injury)
• 5th (5th degree injury)
Hafteck concluded that epineurium is the 1st to rupture, perineurium, axons and finally
endoneurium. 59
60. TRANSITION, LACERATION, RUPTURE AND AVULSION
They constitute a Sunderland 5th degree injury.
Recovery is dependent on the approximation and co-aptation of the nerve
ends with out tension.
Transection and laceration are generally associated with less tissue
destruction then rupture or avulsion injuries.
Surgical reconstruction of intraosseous nerves should be developed with
canal intact.
Surgical reconstruction of soft tissue nerves should be performed early
because the prognosis is poor.
60
61. CHEMICAL INJURY
They are most often the result of endodontic therapy, dry socket packing, or
chemical neurolysis.
Offending agents : Eugenol, alcohol, phenol etc. The intraoral response following
exposure to a chemical is inflammation. This in turn way initiate a compartment
syndrome for intraosseous nerves. The severity of fibrosis and nerve fibre
dysfunction will depend on the duration of exposure, depth of intraneural
penetration, and toxicity of the chemical.
Management : First identify the chemical and determine its neurotoxicity.
Surgical reconstruction should be delayed because of the variability and
unpredictability of the injury pattern.
61
62. NERVE INFECTION INJURY
Needle penetration of a nerve trunk causes minimal nerve injury and results in no long lasting alterations.
But the intraneural injection of drugs and chemicals does result in severe and irreversible changes in the
nerve.
The fascicular architecture is disrupted by scarring and fibrosis that prevents axonal regeneration beyond the
point of scaring.
Therefore there remains a conduction block that is reversible only through surgical repair. Extrafascicular
injection of substances will cause injury.
In injection injury the patient will C/O severe, immediate pain that radiates into the sensory field of the nerve
being blocked.
Any symptoms of paresthesia when injecting should alert the surgeon that the needle may have penetrated
the nerve. It should be withdrawn until the paresthesia has subsided.
62
63. INTRA-OPERATIVE GRADING OF PERIPHERAL
NERVE LESIONS - GENTILI 1985
Gentili et al 1985, graded intraoperative findings of nerve injuries into three groups based on the
fascicular pattern and the time interval between the injury and surgical intervention.
Divided peripheral nerve
Injury to examination interval < 3 weeks
Injury to examination interval > 3 weeks
Lesion in continuity
Injury to examination interval < 3 months
Injury to examination interval > 3 months
Mixed 1 and 2
Group I lesion includes lesion associated with gross anatomic disruption of the nerve. Group 2 include
lesions in continuity. Group 3 includes mixed type of lesions.
63
64. ROLE OF VITAMIN B12 IN NERVE INJURY
Vitamin B12 is a scavenger of the reactive oxygen species and has a neuroprotective
function owing to its anti-apoptotic and anti-necrotic effects on neurons .
Vitamin B12increases the regeneration of axons and the metabolic pathway of vitamin
B12 is closely related to neuronal survival and repair after injury.
These vitamins may have synergistic effects that cause production of endogenous
neurotropic factors, which enhance peripheral nerve repair.
64
65. NEUROMA FORMATION
Neuromas result from the abnormal regeneration of sprouting axons.
A nerve swelling is formed at the proximal end of the injured nerve.
It consists of random proliferating proximal axonal sprouts and scar tissue deposited by
fibroblasts.
65
66. The most widely held theory behind neuroma formation is that axon fascicles escape
out of a damaged perineurium.
An intact perineurium is hypothesized to be an impenetrable barrier to axons.
However, when the perineurium is damaged, either through sharp laceration or stretch,
sprouting axons escape into the extraendoneurial environment.
The unorganized proliferation of axons into the extraendoneurial environment in
conjunction with scar tissue deposition by fibroblasts results in neuroma formation.
66
67. PHYSIOLOGY OF NERVE INJURY
When a nerve is injured there are
1) responses distal to injury
2) at the site of injury
3) proximal to site of injury
4) within central nervous system.
In neuron, hypertrophic changes begin on 3rd or 4th day following the injury. The neuron begins an anabolic
proteosynthesis that is maintained as long as there is active regenerative efforts.
67
68. Nerve repair should ideally be done 14 – 21 days after injury to take
full advantage of the cell’s metabolic response.
After regeneration is complete and conduction-maturation has
occurred, the neuron returns to normal size and electrical activity.
68
69. CHANGES IN PROXIMAL NERVE TRUNK :
There is marked swelling in the nerve proximally 1 hour after the
laceration.
2nd -3rd day : Demarcation of proximal nerve stump.
7th day : Vigorous sprouting of axons. Each axon may have as many as
50 collateral sprouts.
Axon buds begins advancing across the point of injury on 14th -21st
day.
28th day : Axons cross the point of injury.
42nd day: Sizeable number of axons occupy the distal segment.
The delay in crossing the site of injury is greater for more proximal
injuries and in blast injuries because of local inflammatory response.
69
70. CHANGES IN SITE OF INJURY :
Within hours of injury, there is proliferation of macrophages, perineural
fibroblasts, Schwann cells and epineural fibroblasts.
3rd day : Cellular proliferation in proximal and distal stumps of nearly all
elements.
7th day : The Schwann cell is the most active cell. It assumes a phagocytic
function of debridement.
Schwann cell response is propotional to the severity of injury.
Mesenchymal and neuroectodermal scar remains after Schwann cell debridement
is complete.
70
71. CHANGES IN DISTAL NERVE TRUNK :
The distal nerve trunk undergoes Wallerian degeneration in
preparation for the arrival of sprouting axons. It is initiated because all
distal neural elements die.
Collagen accumulated during repair process does not diminish when
re- innervation occurs, unlike collagen remodeling in cutaneous
wounds.
Axonal numbers decrease during regeneration, and in the healed nerve
there are fewer than the normal number of axons.
The rate of axon regeneration varies during the process of repair. 71
72. DIAGNOSTIC EVALUATION
The purpose of diagnostic evaluation is to check if there exists a sensory
disturbance, to assess if micro-reconstructive surgery is required and to
monitor its recovery following surgery.
72
73. 1) HISTORY :
Ask the patient to describe the symptoms of his/her sensory disturbance, including the affected area.
The use of visual analog scales, lists of verbal descriptors- E.g.., McGill Pain Questionnaire is used
in describing the magnitude and nature of sensory disturbance.
The MCGILL PAIN QUESTIONNAIRE (MPQ) may be used to assess pain and altered sensation,
and it is a useful tool for monitoring progression of neurosensory recovery.
The MPQ uses three classes of descriptive words to assess the level of dysfunction and interference
with activity:
o Sensory class (temporal, spatial, thermal, punctate, incisive, constrictive, traction pressure)
o Affective class (tension, fear, autonomic properties, punishment)
o Evaluative class (patient perception)
73
74. Perhaps the simplest and most reliable measure of subjective patient assessment is the
use of a VISUAL ANALOG SCALE.
Generally, this is a 10 cm five-degree scale, with a degree marked every 2.5 cm.
This is a useful tool for monitoring subjective improvement.
74
76. BRUSH DIRECTIONAL DISCRIMINATION :
This is a test of tactile-gnosis which assesses the quantity and density of functional sensory receptors and afferent fibers.
Brush-stroke directional discrimination is performed with a fine sable or camel hair brush.
The brush is stroked gently across the area of involvement at a constant rate, and the patient is asked to indicate the direction
of movement (ie, to the left or right) and the correct number of patient statements out of 10 is recorded.
If sharp points are used, the small myelinated A-delta and unmyelinated C-afferent fibers of 0.5 to 7 um diameter are
assessed.
If blunt points are used , the larger myelinated A-alpha afferent fibers of 5-15 um diameter are assessed.
76
77. TWO POINT DISCRIMINATION :
It is measured with any instrument with which the distance between two points can be
altered.
ECG calipers or Boley gauge can be used for this test. Both ascending and descending
trails are performed.
The test is performed with patient’s eye closed and with the 2 points essentially touching
so that the patient is able to discriminate only one point.
The distance between 2 points are increased in 2 mm increments until the patient is able
to discriminate between two distinct and separate points in at least four of five intervals.
77
78. STATIC LIGHT TOUCH DETECTION :
It assess the integrity of the Merkel cell and Ruffini
ending which are innervated by myelinated afferent axons
of 5-15 um in diameter ( A-beta).
It is performed using Weinstein-Semmes filaments,
which are nylon filaments of identical lengths but
variable diameter mounted in plastic handles.
The patient closes his eyes to eliminate visual cues and is
instructed to say “touch” whenever he feels a light touch
to face and to point out the exact spot where he felt the
touch.
78
79. PIN PRESSURE NOCICEPTION :
This test assess the free nerve endings and the small A-delta and C-
fibers that innervate the free endings responsible for nociception.
A pressure algesimeter is used. It is made from a number 4 Taylor’s
needle and an orthodontic strain gauge.
The needle is applied perpendicular to the skin of affected area and
force is increased over 1-2 secs until desired level is reached.
The same force is applied to the affected region and the patient is asked
to choose one of the four objectives (touch , pricking, stinging,
stabbing) that best describes his perception of sensation.
Then a set of paired stimuli are applied, the first in the affected area and
the second in the unaffected area. The patient is asked to rate the second
stimulus with that of first.
79
80. THERMAL DISCRIMINATION :
A simple thermal test can be performed using a cotton swab saturated with ethyl
chloride or acetone. It is applied to skin and patient is asked to mark on a visual
analog scale, the magnitude of temperature perceived and if the stimulus was
painful or uncomfortable.
Special instruments like Minnesota thermal disks (MTD) can also be used.
Other diagnostic methods include Diagnostic nerve blocks, Trigeminal sensory
evoked response testing (TSER) etc.
80
82. 3. ASSESSMENT OF TASTE SENSATION
It is performed as either whole-mouth or localized testing.
Solutions such as 1 M sodium chloride (salt), 1 M sucrose (sweet), 0.4 M acetic acid (sour), and 0.1 M quinine
(bitter) may be used.
There are many difficulties with taste assessment in the patient with a lingual nerve injury.
The perception of taste alteration is extremely variable and has little correlation with the degree of lingual nerve
injury.
For example, a patient with a fourth- or fifth-degree lingual nerve injury may not report any taste alteration
subjectively but may test abnormally with different solutions.
The complex sense of taste is mediated not only by the chorda tympani branch of the facial nerve but also through
feedback mechanisms in the nasopharynx, oropharynx, and hypopharynx, as well as the nucleus tractus solitarious
in the brainstem. 82
83. Diagnostic nerve blocks can be a useful component of the patient evaluation when dysesthesia
or unpleasant sensations predominate the clinical scenario.
The primary purpose of the diagnostic block is to localize the source of pain and determine the
prognosis for recovery following either pharmacologic or surgical therapy.
The preferred local anesthetic solution is of a low concentration (eg, 0.25% lidocaine) to
selectively block the smaller A delta and C fibers while not affecting the larger myelinated
fibers.
83
4. DIAGNOSTIC NERVE BLOCKS
84. If the low concentration fails to relieve the pain, a higher concentration is used in the same location.
Diagnostic blocks begin peripherally and proceed centrally with constant reassessment of the area
of involvement both objectively and subjectively.
If patients present with symptoms consistent with sympathetically mediated pain or causalgia, a
stellate ganglion block may be performed.
These symptoms indicate a problem not amenable to peripheral microneurosurgery.
Other pain syndromes that generally are not relieved with diagnostic nerve blocks include
anesthesia dolorosa and deafferentation pain; these also are not managed surgically but,
rather, pharmacologically.
84
85. MANAGEMENT OF NERVE INJURY
The management of trigeminal nerve injuries is based upon the
progressive monitoring of sensory recovery and early recognition
of traumatic neuropathic conditions.
CLASSIFICATION OF THE INJURY :
Observed • Treatment initiated immediately
Unobserved
• Monitored for a definitive period
followed by treatment
85
88. Timing of nerve injury repair
Primary : Repair is completed
within hours of injury
Delayed primary repair : 14
to 21 days
Secondary : More than 3
weeks following injury
88
89. MEDICAL MANAGEMENT OF NERVE INJURY
Nerve blocks, analgesics and transcutaneous nerve stimulation (30 mins per day at
maximum tolerable intensity for 3 weeks) .
If pain does not subside after 3-4 weeks of treatment, then microsurgical exploration
and repair must be considered.
89
90. Line of treatment for post-traumatic pain is use of various pharmacologic agents such as
FLUPHENAZINE (1 mg TDS) , AMYTRYPTLIN (75 mg HS), DOXEPIN (25 mg
TDS), CARBAMAZEPINE(up to 100 mg per day), BACLOFEN (up to 80 mg per
day).
If the pain is determined to be of sympathetic origin, then treatment options include
serial stellate ganglion block( 1 block, 5 days/ week for 3-4 weeks).
90
93. PRINCIPLES OF NERVE REPAIR
Hanno Millessi pioneered nerve repair techniques emphasizing a tension free repair.
The basic principles of nerve repair are,
1) Quantitative pre-operative assessment of motor and sensory systems
2) Microsurgical techniques that include magnification, instrumentation, microsutures.
3) Tension-free repair
4) If tension free repair is not possible then use of an interpositional nerve graft.
5) Early protected range of movement to allow gliding.
6) Occupational and physical therapy to maintain range of motion and assist in post operative sensory and
motor rehabilitation to maximize the clinical outcome.
93
95. EXPOSURE
Surgical access to the lingual or IAN maybe accomplished transfacially or
transorally.
The transfacial approach affords wide exposure and access; however, it
necessitates a facial incision with subsequent scar formation.
The intraoral approach provides a more difficult surgical access and requires more
diligence in microsurgery in the posterior regions of the oral cavity, but it avoids a
facial incision.
The decision regarding surgical access depends on an individual patient’s anatomy,
the site of nerve injury, planned surgical procedures, patient preference, and
surgeon’s skill and experience. 95
96. NEUROLYSIS
EXTERNAL NEUROLYSIS –
Microdissection of the nerve once exposed involves liberation of the nerve from the
surrounding tissues to facilitate inspection.
For the lingual nerve this procedure may involve the release of the nerve from a lateral
adhesive neuroma in the area of the lingual plate in the third molar region, whereas for the
IAN a corticotomy is generally required for external neurolysis.
Several techniques have been described for lateral decortication in the area of the third molar
for IAN exposure, and these range from a simple nerve transpositioning to a modified buccal
corticotomy or a unilateral sagittal split ramus osteotomy
96
98. The location of the injury and the surgeon’s preference frequently dictate the specific approach
used.
The lingual nerve is usually exposed via a modified incision used for third molar surgery with a
sulcular lingual extension .
98
99. For the infraorbital nerve, external neurolysis may be performed secondary to
reduction and fixation of a displaced zygomaticomaxillary complex fracture impinging
on the neurovascular bundle at the infraorbital foramen.
It has been suggested that external neurolysis may provide definitive treatment for a
nerve injury if the nerve compression is < 25% of the normal diameter, if the
paresthesia is of short duration (< 6 mo), and if there is no evidence of neuroma
formation.
99
100. INTERNAL NEUROLYSIS –
The term internal neurolysis refers to surgical manipulations within the epineurium to prepare
the nerve for repair.
Sophisticated maneuvers may compromise repair by unnecessary removal of tissue and
induction of cicatrix formation owing to excessive manipulation.
Several types of internal neurolysis have been described, including epifascicular
epineurotomy, epifascicular epineurectomy, and interfascicular epineurectomy .
The first two prepare the epineurium for repair; any interfascicular surgery may cause further
fascicular disruption and scarring.
Extensive internal neurolysis procedures should be used with caution.
100
102. NERVE STUMP PREPARATION
Perhaps the most critical portion of the surgical
procedure involves the inspection of the
proximal and distal nerve stumps via
magnification.
The preparation of the nerve stumps follows
exposure; there may already be an existing
discontinuity from a transection injury.
When a neuroma is present, meticulous
excision is required.
102
103. With any neuroma, the clinical appearance of neuronal edema or atrophy is less than the
internal fascicular changes.
103
104. Failure to resect enough nerve tissue to reach normal fascicles results in a failure of
neurosensory recovery.
104
105. Once the nerve is divided, if necessary, into proximal and distal stumps, care must be
taken to resect small (1 mm) portions of the nerve trunk in both directions until healthy
glistening white mushrooming fascicles are seen to herniate through the edges of the
epineurium.
105
106. APPROXIMATION
The trigeminal nerve is similar to other peripheral nerves in that it does not tolerate tension well;
therefore, tension-free closure is mandatory.
The deleterious effects of tension result from vascular compromise and subsequent fibrosis at
the nerve repair site.
Approximation is the act of bringing the nerve stumps into contact and assessing the degree
of tension that is present.
At the time of approximation a decision must be made regarding whether to use an
interpositional graft.
In general, mobilization with primary epineurial repair is possible for lingual nerve gaps < 10
mm and for IAN gaps < 5 mm.
106
107. COAPTATION
Coaptation is the process of aligning the proximal and distal nerve stumps into the
premorbid cross-sectional fascicular orientation.
This is a difficult maneuver with a polyfascicular nerve that has undergone any degree
of distal nerve changes in diameter or fascicular pattern.
This step is usually not performed painstakingly in trigeminal nerve repair because of
the complex polyfascicular pattern.
107
108. NEURORRAPHY
Neurorrhaphy is the act of nerve suturing
for both direct and gap repairs.
The trigeminal nerve is repaired using
epineurial sutures, not perineurial sutures.
108
109. Generally, an 8-0 monofilament nonresorbable nylon suture is chosen since a resorbable
material would invoke inflammation and disturb the area of anticipated neural healing.
At least two sutures are used per anastomosis site to prevent rotation, but not more than
three or four sutures should be used per anastomosis.
The first suture is placed on the medial side of the anastomosis since it is more difficult to
access.
The epineurium is pierced with the needle 0.5 to 1.0 mm from the edge of the nerve.
The second suture is placed 180° from the first suture, and then an assessment is made
regarding the need for more sutures.
109
110. NERVE GRAFTS
When neurorrhaphy is not possible without tension and a nerve gap exists, an
interpositional graft must be considered for indirect neurorrhaphy.
The options for autogenous nerve grafting include but are not limited to the sural nerve,
the greater auricular nerve, and possibly the medial antebrachial cutaneous nerve.
The sural nerve is the preferred nerve for grafting since it most appropriately matches
the nerve diameter and the fascicular number and pattern of the trigeminal nerve.
110
111. The area of the nerve superior to the lateral malleolus exhibits less branching than at or
below the lateral malleolus.
The sural nerve, or medial sural cutaneous nerve, is a branch of the sacral plexus (S1,
S2) and supplies sensory information to the posterior lower extremity and the
dorsolateral foot.
Sural grafts up to 20 cm in length are possible, and patients tolerate the donor site
deficit well.
111
112. The greater auricular nerve is a poor choice for trigeminal repair.
As a branch of the cervical plexus (C1, C2), the greater auricular nerve supplies
sensation to the pre- and postauricular regions, the lower third of the ear, and the skin
overlying the posteroinferior border at the angle of the mandible.
Patients are generally not amenable to sacrificing one facial region for another.
Additionally, the small diameter of the nerve makes it useful only when used as a cable
graft
112
113. The sole advantage of a greater auricular graft over a sural graft is in situations when
it can be harvested via the same incision for another procedure, such as the repair of an
extraoral mandibular fracture or management of pathology.
The basic premise with graft repair is that the graft supplies the Schwann cells and
growth factors necessary to support and encourage axonal sprouting through the graft
toward the target site.
113
114. ENTUBATION TECHNIQUES
In an attempt to avoid donor site morbidity, a variety of entubulation techniques have
been proposed to create conduits during nerve regeneration.
These conduits involve both autogenous and alloplastic materials .
The autogenous options include vein, collagen, and muscle grafts.
Alloplastic materials include polyglycolic acid,polymeric silicone,and expanded
polytetrafluoroethylene.
114
116. POSTSURGICAL MANAGEMENT
In the majority of cases, patients experience a variable period of complete anesthesia following
nerve repair.
In general, nerve regeneration progresses at approximately 1 mm/d (about 3 cm/mo) from the
cell body to the target site.
For example, with a direct IAN repair, the approximate distance from the trigeminal ganglion
to the lower lip and chin is 10 cm; therefore, complete nerve regeneration takes about 100 days
or 12 weeks following repair.
116
117. With graft repair the time frame is lengthened owing to slowed regeneration through the
graft site, but recovery is variable.
A poor outcome following microneurosurgery may preclude future surgical options;
therefore, the best chance for microneurosurgical success is at the first (and most likely,
the last) surgical intervention.
117
118. References
1) Textbook of Physiology, AK Jain, 5th edition
2) Contemporary Oral and Maxillofacial Surgery, Ellis Hupp and Tucker, 5th edition
3) Current advances in Oral Surgery, Volume III, Temperomandibular joint, William B Irby
4) Operative Oral and Maxillofacial Surgery, 2nd edition, Langdon and Patel.
5) Grabb and Smith’s Plastic Surgery, 6th edition
6) Clinical Manual of Trigeminal Neuralgia, Alan M Stiles
7) Guyton and Hall, Textbook of Medical Physiology, 10th edition
8) Ganong’s review of Medical Physiology, 23rd edition
9) Orofacial pain : A Primer, Scott S. De Rossi
10) Nerve repair, grafting, and nerve transfers, Clin Plastic Surg 30 (2003) 203-221
11) Pathophysiology of nerve injury, Clin Plastic Surg 30 (2003) 109-126
12) Evaluation of nerve-injured patient, Clin Plastic Surg 30 (2003) 127-138
13) Cranial Neuralgias, Wendy S Hupp and John Firriolo, Dent Clin N Am 57 (2013) 481-495
14) Central mechanisms of Orofacial Pain, Robert L Merrill, Dent Clin N Am 51 (2007) 45-59
15) Bailey and Love’s Short Practice of Surgery, 25th edition
16) Shafer’s Textbook of Oral Pathology, 7th edition
17) Oral and Maxillofacial Pathology, Allen and Damn, 3rd edition
18) Davidson’s Principles and Practice of Medicine, 21st edition
19) Overview of orofacial pain, Dent Clin Of N Am 51 (2007) 1-17
20) Modern Practice in Orthognathic Surgery, William Bell, WB Saunders.
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