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The peripheral sensory
innervations of the orofacial
region may be injured by
oral and maxillofacial
surgical and general dental
procedures
The goal in the early
management of nerve
injuries
is to decide as soon as
possible
which injuries will profit
from
early repair and which
INTRODUCTION
ANATOMY OF NERVE
NEURON
NERVE FIBER
CAUSES OF NERVE INJURY
Trauma.
Iatrogenic causes.
Third molar removal
Endodontic therapy
Orthognathic surgery
Injury due to adjacent acute
lesions.
Temporomandibular joint
arthroscopy
Systemic disease states such as diabetic
trigeminal
VULNERABILITY OF NERVES
TO INJURIES
•
•Lingual nerve
•
Inferior Alveolar
nerve
Mental
nerve
Infra orbital N – fracture
of infra orbital rim
Facial N-
penetrating injury,
parotid / TMJ surgeries
Auriculo temporal N- TMJ
surgeries
NERVE RESPONSE TO INJURY
Nerve injury
Increased metabolic phase with increase RNA production and breakdown of Nissl
substance
Edema and cellular debri at site of injury
Proliferation of phagocytes and macrophages
Axonal sprouts within days from the proximal nerve stump
Proliferation and high level of Schwann cell activity
Laying down of new myelin, plus nerve growth factor production
SEDDON (1943) CLASSIFICATION
SUNDERLAND CLASSIFICATION (1951)
SYMPTOMATIC CLASSIFICATION
ANATOMIC CLASSIFICATION
HISTOPATHOLOGIC CLASSIFICATION
PATHOPHYSIOLOGIC CLASSIFICATION
CLASSIFICATION OF NERVE INJURIES
SEDDON (1943) CLASSIFICATION
AXONOTMESIS
NEUROPRAXIA
NEUROTMESIS
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.
Surgical intervention not necessary
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.
NEUROTMESIS
Severe disruption of the connective tissue components of the
nerve trunk.
soft tissue. But those within a canal may show some degree of
sensory recovery because of the guiding influence of the canal.
Sensory recovery is not to be expected when the nerve courses
through
Surgery usually required
FIRST DEGREE INJURY
SECOND DEGREE INJURY
THIRD DEGREE INJURY
FOURTH DEGREE INJURY
FIFTH DEGREE INJURY
SIXTH DEGREE INJURY
( Dellon and
Mackinnon)
SUNDERLAND CLASSIFICATION
Based on the Degree of Tissue
Injury
SYMPTOMATIC CLASSIFICATION
P ARESTHESIA : It is an alteration on
sensibility in which there is abnormal
stimulus perception and detection that
may be perceived as unpleasant but
not painful.
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
unpredictabl
e.
HYPERALGESIA
HYPERESTHESIA
HYPOESTHESIA
HYPOALGESIA
SYMPTOMATIC CLASSIFICATION
ALLODYNIA
SYANATHESIA
PROTOPATHIA
HYPERPATHIA
DYSESTHESIA
SYMPTOMATIC CLASSIFICATION
ANATOMIC CLASSIFICATION
Increased endoneural fluid
pressure Ischemia
SOFT TISSUE NERVE INJURY
INTRAOSSEOUS NERVE INJURY
Compression
Edem
a
Nerve fibre
dysfunction
HISTOPATHOLOGI
C
CLASSIFICATIO
N
PATHOPHYSIOLOGI
C CLASSIFICATION
Neurom
a
Stretch injury
Transaction,
Laceration,
Rupture and Avulsion.
Chemical injury
•
•
•
•
• Fibrosi
s
•Compression
DIAGNOSIS
The purpose of nerve injury examination
Outline the area of sensory deficit
Quantify the magnitude and character of the defect
Record it for comparison in an objective manner with the
results of subsequent
evaluations
Three levels of testing are
recommended
Level A - evaluation of direction, two point
discrimination Level B - contact detection
Level C - pain sensitivity
Level A : Direction discrimination/ Two point
discrimination
Soft brush 15 trials on affected and control
site Testing A alpha/beta fibres
•
•
Two-point
Brush directional
Discrimination
Level B - Estimating the threshold for
contact
(Contact/touch discrimination)
•
•
•
The detection threshold in units of force is determined for
the control and test site
Von Frey monofilaments are marked with the log of 10
times the force required to bend the monofilament . The
practitioner applies or pretends to apply the filament until
it just begins to bend
Evaulates A beta fibers
Level C ; quantifying pain sensitivity using
thermal/mechanical
stimulation
•A 22 g needle applied quickly and firmly enough to the tissue
to draw a small drop of blood
•Evaluates A Delta/C fibers
Pin pressure nociceptive
discrimination
THERMAL
DISCRIMINATION
•Warmth sensation A-delta fibers
•Cold sensation C-fibers
•Thermodes and Minnesota Thermal
Disks (MTD), ice, ethyl chloride
sprays, acetone and water.
•Cotton swab saturated with either
ethyl chloride or acetone .
•Minnesota thermal disks (MTD)
The progression of regenerating sensory dendrites can be
followed
down the nerve by eliciting TINEL’S SIGN
A tingling sensation elicited by percussion over the nerve
VISUAL ANALOG SCALE.
The MCGILL PAIN QUESTIONNAIRE (MPQ)
oSensory class
oAffective
oEvaluative class
MANAGEMENT OF NERVE INJURIES
C. NON SURGICAL TREATMENT
A. MICROSURGICAL OPERATIONS FOR REPAIR
Transoral/transcervical
exposure
Microdisection
External neurolysis(decompression)
Internal neurolysis (to eliminate epineural fibrosis)
Resection of the injured nerve segment (when a neuroma or
extensive fibrosis is present)
Approximation of proximal and distal stumps
Neurorrhaphy (Suturing) usually at the level of the epineurium
Grafting
B.ABLATIVE NERVE PROCEDURES
Observed Nerve Injury
Indications For Surgical
Repair
Presence on Paraneural Foreign
Bodies
Unchanging Anesthesia or
dysfunctional after 3-6 -12 mos
following injury
Unrealistic patient expectations
Contraindications For Surgical
Repair
Signs of improving neurosensory function based on
Patient acceptance of existing impaired function and
discomfort levels
Signs of central sensitization (spreading regional
dysesthesia, hyperalgesia)
Deafferenation pain unrelieved by local blocks
Clinical signs of autonomic derangement (burning ,
errythema, swelling)
Extremes of age and systemic or neuropathic disease
serial examinations
Excessive time since original nerve injury
ACUTE NERVE INJURY
PATIENT CARE
Primary goal is to remove sources of ongoing or secondary
nerve
injury to create a tissue environment for optimal nerve
recovery and to prevent secondary neuropathic sensitization
MANAGEMENT OF SPECIFIC OBSERVED
NERVE INJURY ETIOLOGIES
Compressive injury (root
tip/implant)
Immediate decompression
Serial Neurosensory evaluations
Chemical Injury
Immediate debridement
Serial neurosensory evaluations
Transectio
n
Allow time for nerve stump to define extent of
injury
Immediate primary anastomosis if witnessed and surgeon
experienced
Delayed anastamosis
Avulsive Injury
Delay repair 2 to 3 weeks
TIMING OF NERVE INJURY REPAIR
Delayed primary repair : 14 to 21
days
Primary : Repair is completed within hours of
injury
Secondary : More than 3 weeks following
injury
If a nerve injury is witnessed, immediate repair
preferred
Axonal regeneration is optimal in first 3 weeks
Avoid neuroma formation and restrictive secondary scarring
If injury is not witnessed
Serial Clinical Neurosensory Testing
Controversy regarding timing of repair
DECOMPRESSION/EXTERNAL
NEUROLYSIS
NEUROMA RESECTION
Mobilized nerve is inspected for discontinuity and
amputation
neuroma
Level of lesion is identified by magnification and
transillumination
• Note nerve opacity and loss of surface microvasculature
Injury zone is resected with beaver blade 3 mm proximal
and
distal to neuroma
•Submit to pathology
•
Tissue stumps trimmed and prepped for nerve
repair
INTERNAL NEUROLYSIS
Epifascicular
neurotomy
•
•
•
Epifascicular neurectomy
Interfascicular
epinerectomy
NEURORRHAPHY
The trigeminal nerve is
repaired using epineurial
sutures, not perineurial
sutures.
Neurorrhaphy is the act of
nerve suturing for both direct
and gap repairs.
NERVE GRAFTS
When neurorrhaphy is not
possible without tension and
a
nerve gap exists, an
interpositional graft must be
considered for indirect
neurorrhaphy.
To repair the trigeminal, the
sural nerve is most commonly
used
ENTUBULATION
An emerging technology
Attempt to avoid donor site
morbidity
NON SURGICAL TREATMENT
Indications
Metabolic neuropathy
Atypical pain that does not conform to
anatomic
distribution of peripheral nerves
Centrally mediated
pain
ROLE OF VITB12 IN NERVE
INJURY
•Vit b12- reactive oxygen scavenger
neuroprotective function
anti- apoptic and anti-necrotic effect
•It increases the regeneration of axons
•Vitamins may have synergistic effects that
cause production of endogenous neurotropic
factors, which enhance peripheral nerve
repair.
RECENT RESEARCH ON NON
SURGICAL TREATMENT
• LASER
• ULTRASOUND
• ELECTROMAGNETIC STIMULATION
CONCLUSION
Comprehensive evaluation or documentation
of injury is required to determine the most
appropriate timing and method of
intervention. Accurate diagnosis and timely
intervention are critical in achieving
acceptable outcomes.
REFERENCES
Peterson’s Principles of Oral and Maxillofacial Surgery
Oral and Maxillofacial Trauma, Vol.2, 2nd Edn., Raymond J. Fonseca.
Atlas of the Oral and Maxillofacial Surgery, Clin of N.A. Sept. 2001
LaBanc JP, Epker BN, Jones DL, et al: Nerve sharing by an interpositional sural
nerve
graft between the greater auricular and inferior alveolar nerve to restore lower
lip
sensation. J Oral Maxillofac Surg 45:621, 1987.
Wolford LM, Cottrell DA, LaBanc JP: Infraorbital nerve sharingto restore
sensibility
to the lower lip: Case report. J Oral Maxillofac Surg 53:594, 1995).
Eppley BL, Snyders RV: Microanatomic analysis of the trigeminal nerve and
potential

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Nerve injuries seen in oral and maxillofacial surgery

  • 1.
  • 2. The peripheral sensory innervations of the orofacial region may be injured by oral and maxillofacial surgical and general dental procedures The goal in the early management of nerve injuries is to decide as soon as possible which injuries will profit from early repair and which INTRODUCTION
  • 6. CAUSES OF NERVE INJURY Trauma. Iatrogenic causes. Third molar removal Endodontic therapy Orthognathic surgery Injury due to adjacent acute lesions. Temporomandibular joint arthroscopy Systemic disease states such as diabetic trigeminal
  • 7. VULNERABILITY OF NERVES TO INJURIES • •Lingual nerve • Inferior Alveolar nerve Mental nerve
  • 8. Infra orbital N – fracture of infra orbital rim Facial N- penetrating injury, parotid / TMJ surgeries Auriculo temporal N- TMJ surgeries
  • 9. NERVE RESPONSE TO INJURY Nerve injury Increased metabolic phase with increase RNA production and breakdown of Nissl substance Edema and cellular debri at site of injury Proliferation of phagocytes and macrophages Axonal sprouts within days from the proximal nerve stump Proliferation and high level of Schwann cell activity Laying down of new myelin, plus nerve growth factor production
  • 10. SEDDON (1943) CLASSIFICATION SUNDERLAND CLASSIFICATION (1951) SYMPTOMATIC CLASSIFICATION ANATOMIC CLASSIFICATION HISTOPATHOLOGIC CLASSIFICATION PATHOPHYSIOLOGIC CLASSIFICATION CLASSIFICATION OF NERVE INJURIES
  • 12. 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. Surgical intervention not necessary
  • 13. 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.
  • 14. NEUROTMESIS Severe disruption of the connective tissue components of the nerve trunk. soft tissue. But those within a canal may show some degree of sensory recovery because of the guiding influence of the canal. Sensory recovery is not to be expected when the nerve courses through Surgery usually required
  • 15. FIRST DEGREE INJURY SECOND DEGREE INJURY THIRD DEGREE INJURY FOURTH DEGREE INJURY FIFTH DEGREE INJURY SIXTH DEGREE INJURY ( Dellon and Mackinnon) SUNDERLAND CLASSIFICATION Based on the Degree of Tissue Injury
  • 16. SYMPTOMATIC CLASSIFICATION P ARESTHESIA : It is an alteration on sensibility in which there is abnormal stimulus perception and detection that may be perceived as unpleasant but not painful. 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 unpredictabl e.
  • 19. ANATOMIC CLASSIFICATION Increased endoneural fluid pressure Ischemia SOFT TISSUE NERVE INJURY INTRAOSSEOUS NERVE INJURY Compression Edem a Nerve fibre dysfunction
  • 21. DIAGNOSIS The purpose of nerve injury examination Outline the area of sensory deficit Quantify the magnitude and character of the defect Record it for comparison in an objective manner with the results of subsequent evaluations
  • 22. Three levels of testing are recommended Level A - evaluation of direction, two point discrimination Level B - contact detection Level C - pain sensitivity
  • 23. Level A : Direction discrimination/ Two point discrimination Soft brush 15 trials on affected and control site Testing A alpha/beta fibres • • Two-point Brush directional Discrimination
  • 24. Level B - Estimating the threshold for contact (Contact/touch discrimination) • • • The detection threshold in units of force is determined for the control and test site Von Frey monofilaments are marked with the log of 10 times the force required to bend the monofilament . The practitioner applies or pretends to apply the filament until it just begins to bend Evaulates A beta fibers
  • 25. Level C ; quantifying pain sensitivity using thermal/mechanical stimulation •A 22 g needle applied quickly and firmly enough to the tissue to draw a small drop of blood •Evaluates A Delta/C fibers Pin pressure nociceptive discrimination
  • 26. THERMAL DISCRIMINATION •Warmth sensation A-delta fibers •Cold sensation C-fibers •Thermodes and Minnesota Thermal Disks (MTD), ice, ethyl chloride sprays, acetone and water. •Cotton swab saturated with either ethyl chloride or acetone . •Minnesota thermal disks (MTD)
  • 27. The progression of regenerating sensory dendrites can be followed down the nerve by eliciting TINEL’S SIGN A tingling sensation elicited by percussion over the nerve
  • 28. VISUAL ANALOG SCALE. The MCGILL PAIN QUESTIONNAIRE (MPQ) oSensory class oAffective oEvaluative class
  • 29. MANAGEMENT OF NERVE INJURIES C. NON SURGICAL TREATMENT A. MICROSURGICAL OPERATIONS FOR REPAIR Transoral/transcervical exposure Microdisection External neurolysis(decompression) Internal neurolysis (to eliminate epineural fibrosis) Resection of the injured nerve segment (when a neuroma or extensive fibrosis is present) Approximation of proximal and distal stumps Neurorrhaphy (Suturing) usually at the level of the epineurium Grafting B.ABLATIVE NERVE PROCEDURES
  • 30. Observed Nerve Injury Indications For Surgical Repair Presence on Paraneural Foreign Bodies Unchanging Anesthesia or dysfunctional after 3-6 -12 mos following injury Unrealistic patient expectations Contraindications For Surgical Repair Signs of improving neurosensory function based on Patient acceptance of existing impaired function and discomfort levels Signs of central sensitization (spreading regional dysesthesia, hyperalgesia) Deafferenation pain unrelieved by local blocks Clinical signs of autonomic derangement (burning , errythema, swelling) Extremes of age and systemic or neuropathic disease serial examinations Excessive time since original nerve injury
  • 31. ACUTE NERVE INJURY PATIENT CARE Primary goal is to remove sources of ongoing or secondary nerve injury to create a tissue environment for optimal nerve recovery and to prevent secondary neuropathic sensitization
  • 32. MANAGEMENT OF SPECIFIC OBSERVED NERVE INJURY ETIOLOGIES Compressive injury (root tip/implant) Immediate decompression Serial Neurosensory evaluations Chemical Injury Immediate debridement Serial neurosensory evaluations
  • 33. Transectio n Allow time for nerve stump to define extent of injury Immediate primary anastomosis if witnessed and surgeon experienced Delayed anastamosis Avulsive Injury Delay repair 2 to 3 weeks
  • 34. TIMING OF NERVE INJURY REPAIR Delayed primary repair : 14 to 21 days Primary : Repair is completed within hours of injury Secondary : More than 3 weeks following injury
  • 35. If a nerve injury is witnessed, immediate repair preferred Axonal regeneration is optimal in first 3 weeks Avoid neuroma formation and restrictive secondary scarring If injury is not witnessed Serial Clinical Neurosensory Testing Controversy regarding timing of repair
  • 37. NEUROMA RESECTION Mobilized nerve is inspected for discontinuity and amputation neuroma Level of lesion is identified by magnification and transillumination • Note nerve opacity and loss of surface microvasculature Injury zone is resected with beaver blade 3 mm proximal and distal to neuroma •Submit to pathology • Tissue stumps trimmed and prepped for nerve repair
  • 39. NEURORRHAPHY The trigeminal nerve is repaired using epineurial sutures, not perineurial sutures. Neurorrhaphy is the act of nerve suturing for both direct and gap repairs.
  • 40. NERVE GRAFTS When neurorrhaphy is not possible without tension and a nerve gap exists, an interpositional graft must be considered for indirect neurorrhaphy. To repair the trigeminal, the sural nerve is most commonly used
  • 41. ENTUBULATION An emerging technology Attempt to avoid donor site morbidity
  • 42. NON SURGICAL TREATMENT Indications Metabolic neuropathy Atypical pain that does not conform to anatomic distribution of peripheral nerves Centrally mediated pain
  • 43. ROLE OF VITB12 IN NERVE INJURY •Vit b12- reactive oxygen scavenger neuroprotective function anti- apoptic and anti-necrotic effect •It increases the regeneration of axons •Vitamins may have synergistic effects that cause production of endogenous neurotropic factors, which enhance peripheral nerve repair.
  • 44. RECENT RESEARCH ON NON SURGICAL TREATMENT • LASER • ULTRASOUND • ELECTROMAGNETIC STIMULATION
  • 45. CONCLUSION Comprehensive evaluation or documentation of injury is required to determine the most appropriate timing and method of intervention. Accurate diagnosis and timely intervention are critical in achieving acceptable outcomes.
  • 46. REFERENCES Peterson’s Principles of Oral and Maxillofacial Surgery Oral and Maxillofacial Trauma, Vol.2, 2nd Edn., Raymond J. Fonseca. Atlas of the Oral and Maxillofacial Surgery, Clin of N.A. Sept. 2001 LaBanc JP, Epker BN, Jones DL, et al: Nerve sharing by an interpositional sural nerve graft between the greater auricular and inferior alveolar nerve to restore lower lip sensation. J Oral Maxillofac Surg 45:621, 1987. Wolford LM, Cottrell DA, LaBanc JP: Infraorbital nerve sharingto restore sensibility to the lower lip: Case report. J Oral Maxillofac Surg 53:594, 1995). Eppley BL, Snyders RV: Microanatomic analysis of the trigeminal nerve and potential