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Nerve injury

NERVE INJURY

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Nerve injury

  1. 1. NERVE INJURIES 1 DR. SWATI SAHU ORAL & MAXILLOFACIAL SURGERY
  2. 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. 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. 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. 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. 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. 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. 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. 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. 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. 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. 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. 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. 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. 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. 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. 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
  18. 18. 18
  19. 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. 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. 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
  22. 22.  22
  23. 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
  24. 24. 24
  25. 25. LLOYD CLASSIFICATION (1943) 25
  26. 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. 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. 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. 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
  30. 30.  SEDDON (1943) CLASSIFICATION  SUNDERLAND CLASSIFICATION  PHYSIOLOGIC CONDUCTION BLOCK  SYMPTOMATIC CLASSIFICATION  ANATOMIC CLASSIFICATION  HISTOPATHOLOGIC CLASSIFICATION  PATHOPHYSIOLOGIC CLASSIFICATION 30
  31. 31.  NEUROPRAXIA  AXONOTMESIS  NEUROTMESIS SEDDON (1943) CLASSIFICATION 31
  32. 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. 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. 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. 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. 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. 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. 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. 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. 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. 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. 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. 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. 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
  45. 45. 45
  46. 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. 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. 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. 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. 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. 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. 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. 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. 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. 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. 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. 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. 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. 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. 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. 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. 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. 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. 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. 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. 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. 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. 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. 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. 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. 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. 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. 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. 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
  75. 75. 2) CLINICAL EXAMINATION : 75
  76. 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. 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. 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. 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. 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
  81. 81. 81
  82. 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. 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. 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. 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
  86. 86. 86
  87. 87. 87
  88. 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. 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. 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
  91. 91. 91
  92. 92. 92
  93. 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
  94. 94. SURGICAL MANAGEMENT OF NERVE INJURY SURGICAL EXPLORATION EXPOSURE COAPTATION NERVE GRAFTING ENTUBATION APPROXIMATION NEURORRAPHY NERVE STUMP PREPERATION NEUROLYSIS 94
  95. 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. 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
  97. 97. 97
  98. 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. 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. 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
  101. 101. 101
  102. 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. 103.  With any neuroma, the clinical appearance of neuronal edema or atrophy is less than the internal fascicular changes. 103
  104. 104.  Failure to resect enough nerve tissue to reach normal fascicles results in a failure of neurosensory recovery. 104
  105. 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. 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. 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. 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. 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. 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. 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. 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. 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. 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
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  116. 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. 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. 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. 118
  119. 119. Thank you!!!!!! 119

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