NERVE INJURIES AND ITS MANAGEMENT
Injuries to the peripheral branches of the fifth (Trigeminal) and the seventh (Facial) cranial nerves are ever-present risks during surgical procedures performed in the oral cavity and associated maxillofacial region. Trauma is also a major cause for these type of nerve injuries. The resulting loss of sensory or motor function in an area of the body that is highly visible and in which important functions are located can be distressing or even devastating in those patients where spontaneous recovery does not occur.
Contrary to previous opinion, nerve injuries do not always heal spontaneously. Besides traumatic nerve injuries, there is an increase in iatrogenic causes with wider use of orthognathic and reconstructive surgical procedures. Unlike the other soft tissue injuries and skeletal injuries, the nerve injury is often left undetected at the initial phase of injury which result in troublesome patient suffering.
Advances in microsurgical technique that has evolved over the past 30 years have made it possible for surgical repair of the injured maxillofacial peripheral nerve in a predictable fashion when done in a timely fashion.
The knowledge of the internal structure of a nerve is essential in understanding the pathophysiological mechanisms of nerve injuries and in evaluating various methods of their surgical repair. There is no anatomic or physiologic distinction between a motor or sensory nerve. Moreover, a sensory nerve is often used as an autogenous nerve graft in the surgical repair of facial nerve.
The anatomic structure of a nerve is similar to the structure of the telephone cable. The axon, which transmits electrical impulse is the functional unit of the nerve. The nerve trunk comprises of four connective tissue sheaths. These are the mesoneurium, epineurium, perineurium and endoneurium. The axons are surrounded by a layer of connective tissue endoneurium. A number of axons are grouped into fascicles which are in turn surrounded by perineurium. A nerve might contain one or more fascicles. The fascicles are covered by epineurium and mesoneurium.
The mesoneurium is a connective tissue sheath that suspends the nerve tissue within the soft tissue. It contains the segmental blood supply of the nerve and it is continuous with the epineurium.
The epineurium is the loose connective tissue that defines the nerve trunk and protects the nerve against mechanical stress. It is composed of longitudinal oriented collagen bundles which resists both compressive and stretch forces. They occupy 22% – 88% of the cross-sectional diameter of the nerve. Nerves with an abundant cross-sectional area of epineurium are more capable of withstanding compressive forces than tensile forces. The inferior alveolar nerve and lingual nerve have little intra neural epineurium, so these nerves can’t resist prolonged retraction (Compressive force ). Epineurium has epifascicular layer that surrounds the entire trunk and lies superficial to the fascicles, and an interfascicular layer that occupies the area among the fascicles. The vasa nervosum, the longitudinal blood vessels course through the epineurium and give off branches that penetrate the perineurium to connect with the endoneurial capillaries. The epineurial blood vessels are more susceptible to compression than endoneurial vessels. Compression or excessive dissection of the nerve trunk can result in epineural oedema that may lead to epineural fibrosis. Epineurium also contains the lymphatic vessels which are not found within the fascicles.
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. 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.
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. During degeneration the endoneurial space is filled with schwann cells that clean up the myelin and axonal debris. The schwann cells line up to form Büngner bands during the process of regeneration. The endoneurial sheath with prolonged denervation may become collagenized and shrink. Damage to the endoneurium and endoneurial vessels results in solid fibrotic fascicles that prevent regeneration of the axons in spite of intact remnants of fascicular pattern.
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. 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. Based on this Erlanger and Gasser (1937) classified axons into A, B and C. A group is subdivided into alpha (α), beta (β), gamma (γ) and delta (δ).
Classification of axons — Erlanger & Gasser 1937
A α Afferents for muscle spindle: the anulospiral end organ and golgi tendon organs.
A β Flower spray, touch sensation, pressure & vibratory sensation.
A γ Motor fibers to muscle spindle
A δ Large sensory fibres : Temperature and first or fast pain.
B Autonomic fibres : Sympathetic preganglionic fibers.
C Unmyelinated fibres Temperature, second or slow pain and sympathetic efferents
Lloyd in 1943 classified axons based on the size.
Classification of axons Lloyd 1943
Group I A a 7 – 16 m m. diameter. 70 – 120m/sec.
Group II A b 6 – 8 m m. 30 – 70 m/sec.
Group III A d 2.5 – 4 m m.
Group IV C and B fibres Smaller diameter, C fibers -1m m. 0.5 – 2 m/sec.
Size of axons in decreasing order
A a > A b > A g > A d > B > C
A rough estimate on the conduction velocity of the axon can be calculated by multiplying the fiber diameter by 6. Thus a 15m m. nerve fibre conducts impulse at 90 m/s.
The Schwann cells are pluripotential cells that has a variety of functions essential for nerve function. They play an important role in providing essential metabolites to the axon. They ensheath both myelinated or unmyelinated axons. It surrounds several unmyelinated axons to form well-defined units that are inter-spread among myelinated fibers in a fascicle. In myelinated nerve fibers multiple layers of the cell membrane are wrapped around a single axon to form a myelin sheath over a definite segment of axon. The node of Ranvier is 0.3 – 2 m m unmyelinated internode segment is responsible for saltatory conduction of nerve impulse. The myelin sheath is axon dependant but the schwann cell is not. If the axons degenerates so does the myelin sheath, but the schwann cells survives. All schwann cells are covered with a basement membrane that distinguishes them from fibroblasts, macrophages and mast cells. The axons determine to a large extent the role of schwann cell in myelination process. by a layer of fibroblasts . schwann cells are the most sensitive component to ischemia and irradiation.
The nerve fiber are classified based on the number of fascicles into three fascicular patterns: monofascicular, oligofascicular and polyfascicular.
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 )
The monofascicular pattern is composed of one large fascicle surrounded by concentric layers of perineurium and epifascicular epineurium. The intra cranial course of facial nerve has monofascicular pattern.
The oligofascicular pattern is characterised by two to ten fascicles. All fascicles in oligofascicular pattern are of equal size.
The polyfascicular pattern consists of greater than ten fascicles of different sizes with a prevalence of smaller fascicles. Both inferior alveolar nerve and lingual nerve are polyfascicular, they may contain as many as 18 – 21 fascicles. Polyfascicular nerves are better able to withstand stretch than monofascicular or oligofascicular nerves. The polyfascicular pattern has a large amount of nonfascicular tissue ( epifascicular and interfascicular epineurium ), which increases the malalignment of fascicles during coaptation and epineural fibrosis following injury.
Historical Background of nerve repair .
The first written description of peripheral nervous system is found in the writings of Hippocrates (460 – 370BC) although it is not certain that he differentiated between tendon and nerve. Galen (130-200AD) has first to study the effects of transection of peripheral nerve.
One of earliest report of nerve repair was by Paget 1847 in which he reported complete recovery of function. Hoffmann and Tinel (1915) reported tingling sensations perceived by patients at increasingly distal point along the trunk of a regenerating nerve. This sign of nerve regeneration is later known as Tinel’s sign.
Waller and Young 1942 described the characteristic changes seen in the axon distal to the injury. Highly differential function of a single nerve was extensively studied by Erlanger and Gasser (1944), using this they explained compound action potential, nerve fibre conduction and refractory period. Using these concepts Hodes, Larrabee and German (1948) developed application of electrophysiology for clinical nerve testing.
The foundation for current science of peripheral nerve surgery was probably laid by Seddon (1948) with innumerable battle casualties. He reported multiple papers on peripheral nerve injuries in all levels. He published nerve grafting techniques (1963), the effect of ischemia on peripheral nerves (Seddon and Holmes 1945) and measured rate of nerve regeneration after repair (Seddon, Medanour and Smith 1943). Another British worker Wardhall published large follow up study of peripheral nerve regeneration 1948, where 83% patients recovered some sensory and motor function after peripheral nerve graft. De Medinaceli 1972 elucidated the role of extracellular calcium in signalling messages to the cell body from the site of injury. Lundborg et al in late 1970s and early 1980s showed that nerve fiber will across a 1-cm space devoid of supporting basal lamina or Schwann cell. He elaborated the presence of neurotrophic factors in nerve regeneration.
It was the incorporation of operating microscope by Millesi and his improved microsuture technique in 1970, that establishes the scientific basis for effective nerve anastomosis and grafting. Applications of techniques that have been developed largely for injuries to arm, and hand to the maxillofacial region has been reported by Hansamen 1973 and Hansamen and Samii 1974. Doi and Kuwata (1984) described transfer of microvascularised nerve graft for reconstruction of large nerve defect. Extensive studies of neurosensory disturbances following trauma and operative procedures such as tooth extraction, orthognathic surgery and rigid internal fixation of fractures are reported in late 1980 and early 1990.
Peszkowski (1986) studied the neuromas of lingual and inferior alveolar nerves and argued that injury during tooth extraction and 3rd molar surgery is the commonest etiologic factor for these. Charles C. Alling (1986) studied the sensory disturbances of inferior alveolar and lingual nerves following 3rd molar surgery, About 13% of disorders of lingual nerve persisted for more than one year, where as for inferior alveolar nerve this value is only 3.5%. Nestor D Karas (1990) reported long term study of neurosensory disturbance following various orthognathic surgical procedures. 90% of the sensory deficits where recovered during first post operative year. Similar study also reported by Schultze – Mosque in 1993, Sorren Hillerup (1994).
Etiology of Peripheral nerve injuries
Peripheral nerve may be injured as a result of
- Metabolic or collagen diseases.
- 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.
Injury to inferior alveolar nerve may result from
- Third molar removal.
- Mandibular molar endodontics.
- Endosteal implant placement.
- Orthognathic surgical procedures.
- Visor osteotomies.
- Mandibular ramus osteotomies.
- Mandibular body osteotomies
- Sagittal split osteotomy.
- Cyst or tumour removal.
- Mandibular resection and
- Fractures of the mandibular body and angle region.
The lingual nerve may be injured during
- Third molar removal
- Sialoadenectomy of sublingual and submandibular glands.
- Iatrogenic instrumentation of the floor of the mouth.
- Sulculoplasties of the lingual vestibule.
- Tumour removal.
- Mandibular ramus osteotomies.
The infra orbital nerve is infrequently injured but may be involved in
- Le Fort I, II and III osteotomies.
- Orbital osteotomies.
- Caldwell Luc procedures
- Fractures of midface and orbit.
Injuries to the other branches of trigeminal nerve are rare. Third molar surgery is commonest cause of lingual and inferior alveolar nerves (Alling CC 1986) out of these lingual nerve injury is more common when lingual split technique is used. Various orthognathic surgical procedures can cause nerve injury, out of this major role is for sagittal split ramus osteotomy. The reported incidence of inferior alveolar nerve injury following this is 54-90%. Use of plates and screws for fixation of fractures also lead to injury to inferior alveolar and infra orbital nerves.
The facial nerve might be injured following :
- Facial trauma ( lacerations & fractures ).
- Orthognathic surgical procedures.
- Temporomandibular joint arthrotomy and arthroscopy.
- Parotid gland surgery.
- Facial aesthetic surgery.
Jones K James (1992) studied the incidence of facial nerve injury in various orthognathic surgical procedures. He concluded that facial nerve injury in orthognathic surgical procedures are rare. In a smaller number of cases bilateral intraoral subcondylar osteotomies or sagittal split osteotomies can cause facial nerve injury, mostly by blind and traction injuries by putting retractors posterior to ramus. Nerve transection is rare. Surgical approach to parotid gland, TMJ and mandible are frequent cause of iatrogenic facial nerve injury. In parotid and TMJ surgeries the main trunk of facial nerve is at risk and the marginal mandibular branch damage is more probable during submandibular incisions. Another cause of facial nerve injury is fractures of mandibular condyle which penetrates the parotid gland.
Classification of Peripheral Nerve Injury
The appropriate and logical management of nerve injuries is based on the accurate description and classification of the injury. A variety of classification have been proposed. To be useful, a classification of peripheral nerve injury should be simple, should correlate the degree of injury with symptomatology and underlying pathology, and should offer prognostic information to determine if and when operative intervention is needed or when spontaneous recovery is probable. There is no entirely a satisfactory classification for nerve injury. Although classifications based on the degree of local nerve injury are of some use, they do not take into account the time between injury and operation nor the sequential changes that might occur in the nerve cell body, motor end plate or target organ.
Seddon 1943 — Classification of nerve injury
Seddon in 1943 introduced a classification of nerve injuries based on the three fundamental types of nerve fiber injury. It is less complicated and most used today. In this nerve injuries are classified into neurapraxia, axonotmesis and neurotmesis.
Neuropraxia Local conduction block at the site of injury without Wallerian degeneration
Axonotmesis Complete interruption of axon and myelin sheath with preservation of connective tissue stroma
Neurotmesis Complete anatomic severance of the nerve
Neurapraxia is a mild form of nerve injury and denotes a localised conduction block along a nerve. Axonal continuity is maintained and nerve conduction proximal and distal to the point of injury is preserved. Recovery is rapid and restoration is normal function occurs with few days or weeks. (Simpson 1970, Spencer 1977, Horn and Crempley 1984, Castaldo 1984).
Axonotmesis is more serious and denotes sufficient damage to disrupt the continuity of axon within the connective tissue of the peripheral nerve. There will be complete conduction block and distal axon degeneration (Wallerian degeneration). Prognosis remains good because of continuity of supporting connective tissue, schwann cells and basement membrane. Spontaneous regeneration with full functional recovery can be expected.
The most severe injury occurs in neurotmesis, complete anatomic severance of peripheral nerve occurs and no recovery is expected without surgical coaptation of the ends of fibers. There is distal degeneration as well as some degree of proximal degeneration.
Sunderland 1951 — Classification of nerve injury
Sunderland 1951, proposed a classification based on five degrees of increasing severity. It is based on the anatomy of the peripheral nerve and on the degree of injury to neural elements and connective tissue structures, the endoneurium, perineurium, and epineurium. Like Seddon’s classification it tries to correlate the degree of damage with clinical symptomatology. Clinically distinction between one grade and other is not possible.
The first degree injury in the Sunderland classification is the same as neurapraxia in the Seddon’s classification. Axonal conduction is temporarily blocked and all tissue components of the nerve trunk are intact. It may be as a result of ischaemia or mechanical demyelination. There are three types of first degree nerve injury based on the proposed mechanism of conduction block.
First degree, type I injury results from nerve trunk manipulation, mild traction or mild compression such as that might occur during sagittal split ramus osteotomy, inferior alveolar nerve repositioning, or lingual nerve manipulation during sialadenectomy of the sublingual or submandibular gland. The mechanism of conduction block is presumed to be anoxia from the interruption of the segmental or epineural blood vessels, but there is no axonal degeneration or demyelination. Normal function returns within several hours ( 24 hrs.) following the restoration of circulation.
First degree, type II injury results from moderate manipulation, traction or compression of a nerve. This conduction block is as a result of intrafascicular oedema following injury to endoneurial vessels. Normal function returns within 1 –2 days following the resolution of intrafascicular oedema, which generally occurs within 1 week after nerve injury.
1st degree Corresponds to Seddon’s neurapraxia
Type I Conduction block due to anoxia from interruption of the segmental or epineural blood vessels, but there is no axonal degeneration or demyelination. Resulting from nerve trunk manipulation, mild traction or mild compression. Recovery is rapid following restoration of sensation.
Type II Conduction block due to intrafascicular oedema following rupture of endoneurial capillaries as a result of trauma of sufficient magnitude. Recovery of senses within 1 – 2 days following resolution in the intrafascicular oedema.
Type III Segmental demyelination or mechanical disruption of the myelin sheaths following severe manipulation, traction or compression. Recovery takes 1 – 2 months
2nd degree Axon and myelin are interrupted, but the endoneural sheath and other supporting connective tissue stroma including epineurium and perineurium are preserved. Wallerian degeneration distal to the lesion and complete loss of motor, sensory and autonomic innervation.
3rd degree Disruption of axon, myelin sheath; damage to internal structures of the fascicles with loss of endoneural integrity. Epineurium and perineurium are preserved
4th degree Interruption of all neural and supporting connective tissue stroma, except for epineurium. The fascicular pattern is lost, and the nerve may appear as a thin strand of connective or as a neuroma in continuity.
5th degree Loss of continuity of nerve trunk with complete loss of motor, sensory and autonomic function. Pathologic overgrowth of regenerating axons might result in neuroma formation.
6th degree Mixed combinations of previous five levels of injury. (Added lately by MacKinnon & Dellon 1988.)
First degree, type III injury is as a result of segmental demyelination or mechanical disruption of the myelin as a result of severe manipulation, traction or compression. Sensory and functional recovery is complete within 1 – 2 months after nerve injury.
Electrophysiologically, the conduction block in first degree injury is confined to the injured area, distal conduction is normal. Microreconstructive surgery is not indicated unless there is a foreign body irritant.
The second and third degree injury overlap with Seddon’s axonotmesis. In second degree injury the afferent and efferent axons are damaged along with myelin sheath and they undergo degeneration and regeneration. The remaining component of the nerve trunk (epineurium, perineurium & endoneurium) remain intact. Axonal interruption results in wallerian degeneration distal to the lesion and complete loss of motor , sensory and autonomic innervation. The signs and symptoms are generalised paresthesia with localised anaesthesia. Surgical intervention is not usually required unless there is a foreign body irritant. Recovery usually takes months or years.
The third degree injury is characterised by damage to the intrafascicular components, the axon and the endoneurium. There is wallerian degeneration distal to the lesion. There is usually intrafascicular fibrosis blocking the path of the regenerating axons. Clinically, there is complete loss of motor function, sensory and autonomic function distal to the lesion with electrophysiologic evidence of denervation. Recovery is poor, usually delayed and incomplete depending on the severity of intrafascicular. The incidence of neuroma –in-continuity is low as the perineurium and epineurium are intact with this degree of injury.
The fourth and fifth degree injury corresponds to Seddon’s neurotemesis. The fourth degree injury involves interruptions of all neural and supporting connective tissue except for the epineurium. The fascicular pattern is lost , and the nerve may appear as a thinned strand of connective tissue or as a neuroma-in-continuity. Regenerating axons enter grossly disrupted intrafascicular planes with few, if any, fibers reaching the distal trunk. There is complete motor loss, sensory and autonomic loss. Surgical repair is mandatory and often requires nerve grafts.
The fifth degree injury consists of complete loss of continuity of the nerve trunk involved with complete motor, sensory and autonomic dysfunction distal to the injury. Pathologically, outgrowth of regenerating axons in the proximal stump results in neuroma formation. A few axons reach the distal stump, but this is usually not associated with any functional recovery. Intraosseous fifth degree injury may show spontaneous recovery of some degree of sensibility if the canal is intact. Soft tissue fifth degree injury have poor prognosis for recovery and hey require surgical adaptation and coaptation. There is usually some residual disability even after surgical correction.
The sixth degree injury was added by MacKinnon and Dellon (1988 ) to describe a mixed combination of five degrees of injury, within the same nerve trunk.
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
2 Lesion in continuity
- Injury to examination interval < 3 months
- Injury to examination interval > 3 months
3 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.
Patients with sensory disturbances following nerve injury present with subjective complaints of numbness. This can be broadly classified into anaesthesia, paresthesia, and dyesthesia
Anaesthesia. Complete loss any stimulus detection and perception including mechanoreceptors and nociceptor stimuli.
Paresthesia. Alteration in sensibility with abnormal or normal stimulus detection and perception which may be perceived as unpleasant but not painful.
Dyesthesia. Alteration in sensibility with abnormal stimulus detection and perception which may be perceived as unpleasant and painful. Types : Allodynia, Hyperpathia.
Nerve injuries can be classified anatomically as intraosseous or soft tissue injury. The management of and prognosis of the injured nerves contained within osseous canal is different from that for the injured nerve lying in soft tissue.
Intraosseous nerve injury
Soft tissue nerve injury
Osseous canals provide protection from mechanical trauma unless the integrity of the canal is breached. Conversely, the closed space of the osseous canal predisposes the enclosed nerve trunk to compartment syndrome, which starts as a cascade of events following acute phase of trauma. Compression causing increased vascular permeability, resulting in oedema and increased endoneurial pressure, producing ischaemia and nerve function dysfunction. The chronic effects of compression also results in nerve dysfunction due fibroblast invasion producing scarring and fiber deformation – degeneration. Generally no surgical intervention is required for mechanical injuries if the canal remains intact and the nerve is not compressed by foreign body or there is no oedema within the canal. The prognosis for nerve function recovery without any surgical intervention is good. Foreign bodies such as implants, tooth fragments, bone fragments should be removed early to alleviate the compression and prevent the unfavourable cascade resulting from compression.
Nerves located within soft tissue are not afforded the protection from mechanical trauma. Lacerations and trasections of the nerves located in soft tissue are more likely to form neuromas and are less likely to undergo spontaneous regeneration because of the formation of scar tissue between the injured ends.
Features / Effects of Peripheral nerve injury
Following peripheral nerve injury the motor function, sensory and autonomic function of the nerve is disrupted resulting in their dysfunction.
When a peripheral nerve is severed at a given level all motor functions of nerve distal to injury is lost. All muscles supplied by that nerve becomes paralysed and atonic. Significant electromyographic changes are not apparent for 8-14 days. Spontaneous fibrillation on needle insertion is evident 2-4 weeks, this coincide with onset of atrophic changes within muscle fibers. Atrophy of muscle fibers progress rapidly to 50-70% in following 2 months. Then continues at slower rate. Striations and motor and plate configuration will retain for more than 12, months, by that time empty endoneurial tube will shrink to 1/3rd of its original size. Complete disruption of muscle fibers may not occur till 3 years.
In cases of facial nerve injuries total paralysis of facial muscles is not often evident. There are reports of many cases in which despite deep lacerations of parotid gland and definite damage to facial nerve branches no traumatic paresis was not seen or any immediate facial paralysis were recorded. The reason for such an observation include nerve’s Strong resistance to mechanical damage, due to its considerable longitudinal elasticity and Existences of anastomosis between facial nerve branches from opposite side. When the total severance of main trunk occurs, complete paralysis of affected side will result.
Sensory loss usually follow a definite anatomic pattern, although the factor of over lap from adjacent nerves may cause confusion. After severance of a peripheral sensory nerve only a small area of complete sensory loss is found. This area is supplied exclusively by this nerve and is called autonomous zone or isolated zone for that nerve. A some what larger area of tactile or thermal anaesthesia is readily delineated and correspond more closely to gross anatomic distribution of nerve. This larger areas is known as intermediate zone.
The autonomous zone becomes smaller within first few days or weeks after injury long before regeneration is possible. Livingston believed this is caused by in growth of adjacent nerves, to autonomous area. This phenomenon gives a false impression of nerve regeneration.
The sensory modalities are affected in the order of decreasing frequency as follows. Proprioception, touch, temperature, and pain. Sympathetic fibers are most resistant to lower degrees of nerve injuries.
Interruption of peripheral nerve is followed by loss of sweating and of pilomotor response and by vasomotor paralysis in the autonomous zone. The area of Unhydrosis usually corresponds to but may be slightly larger than the sensory defect. Vasodilation occurs in higher degree injuries and the area affected at first warmer and pinker than the adjacent area. After 2-3 weeks the affected area becomes colder and skin may become pale, cyanotic and mottled. This changes may extend even beyond the maximal zone of injured nerve.
The motor sensory and autonomic deficit make the affected region liable to injury. In order to protect the tissue from damage and to reduce atrophic changes various therapeutic measures are suggested. These include massage, oedema control, skin care, splinting, and regular physiotherapy with muscle stimulation and biofeed back. (Chin and Ishi 1986).
Wound Healing in Peripheral nerves -Regeneration and Degeneration
When a nerve is injured there are responses that occur distal to the injury, at the site of injury, proximal to the injury and within the central nervous system.
The neuron undergoes hypertrophic changes beginning on the third or fourth day following injury to the axon and peaks between the tenth and twelfth day. Neuronal RNA content increases, and synthesis of glycoprotiens increase. This preparatory period last for 24 hours. The neuron enters anabolic proteosynthetic phase with an increase in RNA content, this is maintained as long as the nerve is in active regeneration. The hypertrophic changes are more pronounced in more proximal location of the nerve injury. Nerve repair should ideally be done 14 –21 days after injury to take into account the cells metabolic response.
Proximal nerve trunk.
One hour after injury there is marked swelling on the proximal segment as far as 1 cm. The cross sectional area of the nerve increases to three times normal size and this swelling persists for 1 week or more. On the 2nd or 4th day there is clear demarcation of the proximal nerve stump. Proximal to nerve injury the axon undergo limited degeneration up to the last preserved internode. By seventh day there is vigorous sprouting of axons from the proximal stump. Regeneration is by sprouting of newly formed neurofibrills out of the proximal axon. This sprout is known as growth cone Ramon and Cajol (1928). Tennyson (1970) studied this growth cone, electron microscopically and demonstrated multiple cytoplasmic process called filopodia that protrude and retract in an ameboid manner which direct the growth of cone. Letourneau (1981) explained that a large number of filopodia extend from the surface of growth cone and sensed by this they will attach to the Schwann cell membrane and will pull the growth cone forwards. The direction of filopodia is controlled by some neutrotrophic factors. ( Laminin and type 4 collagen – secreted by Schwann cells).Each axon may have as many as 50 collateral sprouts. Axon buds begin advancing across the point of injury 14 to 21 days after injury. They cross the point of injury by 28th day and by 42nd day a considerable amount of axons occupy distal segment. The delay in crossing the site is greater for more proximal injuries and in blast injuries because of the local inflammatory response. When one sprout establishes contact with target organs (Muscle spindle, sensory organs etc.) the axon gets matured while others disintegrate. Some sprout may be branch or grow back on themselves in an arbitrary manner. The manner of myelination of new growing sprout is determined by the original proximal axon and not by the end organ.
The direction and shape of growth cone are influenced by mechanical factors along its path. Impermeable scar causes a change in direction of growth of advancing axon or cause it to branch (Büngner 1984) . In ideal situations the growth cone will enter the distal stump where longitudinally arranged Schawnn cell will direct it to end organ.
Site of injury:
Within hours of injury there is proliferation of macrophages, perineural fibroblasts, schwann cells and epineural fibroblasts. There is cellular proliferation in the proximal and distal stumps . Schwann cell is most active by 7th day. Schwann cells are responsible of debridement by phagocytic function. Schwann cell response is dependant on the amount of injury. Tubules ( Bands of Büngner ) composed of schwann cells and surrounded by collagen guide the axons towards the distal nerve trunk. The mesenchymal and neuroectodermal scar remains after the debridement by Schwann cells. This tissue is not longitudinally arranged and the axonal regeneration may be twisted and resulting in a neuroma.
Distal nerve trunk :
The distal nerve trunk undergoes wallerian degeneration in preparation for the arrival of sprouting axons. A reactive schwannoma may form from the proliferating supportive elements and block the neurotization. Wallerian degeneration is initiated because all distal neural elements die. By 7th post injury day most of the distal neural elements break down. Majority of the cellular debris are phagocytosed by 21st day by the Schwann cells. Within 42nd day debridement is complete and part of the fascicular anatomy persist. The endoneurial tube either shrinks or collapse and some are obliterated as a result of active cellular proliferation and abundant collagen deposition. The diameter of the endoneurial tubes shrink by 50% at 3 months postinjury and may be only 10% to 25% of their original diameter by 12 months. The entire distal nerve shrinks ( distal atrophy) and in time the shrinkage becomes irreversible. Collagen accumulated during the repair process does not diminish when reinnervation occurs, unlike the collagen of cutaneous skin. The metabolic activity of the schwann cells in the distal stump increases with the arrival of sprouting axons. New myelin is deposited around the sprouting axon which is never as good as the original one. The size of the axon is diminished with shorter nodes of Ranvier resulting in slower conduction of impulse.
Rate of regeneration of axons
Axonal regeneration occurs in following stages.
- Initial delay : the time required for axons to sprout and advance as far as the lesion site. It is usually 2-3 weeks.
- Site delay : the time required for axons to cross the lesion site or anastomosis. This is for 1- 2
- Outgrowth period : the time during which axons transverse the distal nerve stump by following the basement membranes of the schwann cells that had supported the original nerve fibers. This is inversely proportional to length of the distal stump.
- Terminal delay : the period that begins with axonal reconnection at an appropriate end organ, includes the recovery of fiber diameter and the reversal of end-organ atrophy, and ends with recovery of function.
The rate of growth of axon depend on a number of factors. Average growth rate through a scar tissue is 0.25mm/day). After entering the endoneurial tube the rate of growth varies from 1.0 – 8.5 mm/day. The rate of nerve regeneration is inversely proportional to the distance from the cell body (Tinnel 1971). Clinically the advancement of growth cone can be detected by Tinel’s signs in which taping on growth cone or proximal stump will elicit paresthesia or muscle twitching. Sunderland 1968 reported regeneration rates of nerve at various regions which are sustained a second degree crush injury. This is 8mm or more/day in upper arm, 6mm in proximal forearm, 1-2mm in wrist, 1-1.5mm in hand. Ferxis 1988 reported that the rate of nerve regeneration through non vascularised nerve graft is 3-4mm/day.
Neuropathic events following nerve injury.
There are four basic types of neuropathy ( pathological changes ) seen after a nerve injury. Collateral macrosprouting, peripheral neuroma, cervical sympathetic pathosis and central pathosis. These are clinically manifested as anaesthesia dolorosa, causalgia or sympathetically maintained pain, allodynia and hyperpathia. The incidence of chronic pain following peripheral nerve injury range from 2.5 to 60 %.
Collateral Macrosprouting :
Collateral macrosprouting from the injured or from the adjacent uninjured nerves will produce a dyesthetic pattern due to neuroma like collaterals invading the injured zone. This is traumatic collateral macrosprouting. If inferior alveolar nerve is injured, adjacent nerves such as the cervical cutaneous branches, the mylohyoid nerve, long buccal nerve or the contralateral mental nerve might send branches into the uninjured zone. This can be verified by blockage of the inferior alveolar nerve which will not eliminate pain. The possible collateral branches to be blocked for pain relief. Microreconstructive surgery is not effective unless the collateral branches are addressed.
Neuromas are characterised by disorganised microsprouting and formation of disorganised mass of collagen and randomly oriented small neural fascicles. Many factors may detract the growth cone from establishing continuity to end organ. This may be scar tissue or foreign bodies between the proximal and distal axon terminals. In such situations the growth cone may continue the proliferate at the site of injury in an aimless manner and a tumour of small nerve fiber or a neuroma forms. The growth of neuroma depends on local factors such as nerve growth factor, a substance secreted by fibroblasts (McCarthy 1990), local infection, foreign body, or repeated irritation from pressure or friction. (Herudon 1982) These factors will tend to increase the size of neuroma.
Peripheral neuromas can be classified into : amputation or stump neuroma, central or neuroma in continuity and eccentric neuromas.
The amputation or stump neuroma is a knobby, disorganised mass of axons and collagen associated with the proximal nerve stump and completely separated from the distal nerve stump. This type of neuroma is the result of Sunderland’s fifth degree injury.
The central or neuroma in continuity is a fusiform expansion or fibrotic narrowing of the nerve with variable degrees of fascicular disruption and disorganisation. There is no breach in epineurium. This type of neuroma is as a result of Sunderland’s fourth degree or fifth degree injury in which the continuity between the proximal and the distal stump has been re-established.
There are two types of eccentric neuroma: lateral exophytic and stellate neuroma. The lateral exophytic neuroma is an outgrowth of axons and collagen forming a terminal knob like bulb in an otherwise intact nerve. Here only a few superficial fascicles are disrupted owing to an incomplete transection of the nerve or from a poor coaptation of the distal and proximal nerve stumps. There is recognisable breach of epineurium at the site of lateral exophytic neuroma. The Stellate neuroma has two or more branches ending in the adjacent soft tissue or mucosa. In contrast to lateral exophytic neuroma, the epineurium is intact and the branches end in soft tissue. These type of neuroma is seen with inferior alveolar nerve in the third molar region where the branches are seen penetrating the cortical plates to end in the adjacent soft tissue. If stellate neuroma is symptomatic it is necessary to ligate theses branches.
The fibers of neuroma rarely matures and get myelinated. They will be having a low threshold for stimulation, and will result in intermittent pain and bizarre paresthesia. This phenomenon is explained as artificial synapses by Wall 1974 in an attempt to explain the trigeminal neuralgia. It is estimated that as few as 7% (Wilson 1981) or as many as 30% of neuromas are painful. Handrous 1982. Mactren and Peckock 1972 stated that there is no relation between size and configuration of neuroma and the presence of symptoms. Wilson 1981 explained that painful neuromas are tend to be large and soft where as asymptomatic neuromas are likely to have a firm fibrous outer capsule and are smaller in size. John M Greg 1990 studied the neuromas histologically and found that painful neuromas are framed of mechanosensitive A δ fibers. M J Peszkowski (1990) studied the intraosseous oral traumatic neuromas. Tooth extraction was frequent cause of developing neuroma.
There are various degree of reactive fibrosis that occur following trauma to a nerve. These have been classified by Millesi et al into type A, B, C, N and S. Type A fibrosis involves epifascicular epineurium and is associated with good prognosis for recovery. Type B fibrosis involves intrafascicular epineurium. The prognosis is guarded and depends on the original damage. Internal neurolysis is indicated for type A and B fibrosis. Type C fibrosis extends into endoneurium and has poor prognosis. Type C requires excision of the fibrosed segment and neurorrhaphy or nerve graft reconstruction. Type N is associated with Sunderland’s fourth degree injury in which epineurium is intact and it is infiltrated by neuroma. Type S is associated with fourth degree injury and the intervening tissue is only by a scar. It requires scar excision and neurorrhaphy or graft reconstruction.
Classification of nerve injuries by location of fibrosis Millesi et al 1989.
Depends on original damage
In a Sunderland class IV injury, the epineural connective tissue that maintains continuity can be infiltrated by neuroma
Continuity in class IV injury maintained only by scar tissue.
Grade A, B & C are used in combination with Sunderland’s classification : I A & I B; II A & II B and III A, III B & III C.
Grade C fibrosis occurs only with class III injury.
Cervical Autonomic pathosis :
This involves collateral macrosprouting from the cervical sympathetic branches into the injured nerve. This results in signs and symptoms of Causalgia or Sympathetically maintained pain. It is diagnosed by blockage of the sympathetic ganglion.
Causalgia or sympathetically maintained pain has clinical feature of burning pain, allodynia and hyperpathia following nerve injury. The onset might be immediate or delayed. It is characterised by spontaneous pain described as constant, burning and exacerbated by light touch, stress, temperature change or movement of the involved part. Associated symptoms include atrophy of skin appendages, secondary atrophic changes in bones, joint and muscles.
A wide variety of theories have been propounded for explaining the mechanism of Causalgia. The theory proposed by Roberts 1986 explains the mechanism of SMP. This is due to chain of events which render the sympathetic efferents capable of driving the neurons that are part of the central afferent nociceptive pathway. Activity of the A δ and C nociceptive stimulus to the trigeminal nucleus and dorsal horn stimulates wide dynamic range ( WDR ) neurons. WDR neurons receive both nociceptive and mechanoreceptor inputs. The sensitised WDR neurons are activated by A fibers to cause a painful sensation. The diagnosis of Causalgia or sympathetically maintained pain is by sympathetic blockade ( stellate ganglion blockade in case of face ). This condition is minimally improved by microneurosurgical technique. This condition is best treated by sympathectomy.
Central Pathosis :
Following peripheral nerve injury there are central anatomical degenerative changes that may result in central hyperactivity. Inputs reach the injured receptive sites in the brain stem from the adjacent uninjured neurons. Depending on the age of the patient, location of the lesion and metabolic status of the injured nerve certain ganglion cells will die. Degenerative changes are also seen in the brain stem as granular degeneration and cell loss. These changes can result in deafferentation and central pain.
Post traumatic neuralgias
During regeneration of a sensory nerve, gradual return of sensory function is experienced that is functional and tolerable in quantity. But in some patients these become pathologic and intolerable and are referred to as post traumatic neuralgias. Abnormalities in nerve regeneration is the explained mechanism of this neuralgia. The predominant among these are anaesthesia dolorosa, neuralgiform pain and causalgia.
Anaesthesia dolorosa occurs in 3-15% of cases. It is a constant, boring, penetrating or grinding type of pain, experienced in the centre of autonomous zone of injured nerve. Patient experience this sensation in tissue which is other wise unresponsive to any other sensory stimulation. The neural mechanism for this is explained to be situated in Central nervous system. Therefore local surgical management is of little use in controlling this.
Triggered neuralgiform pain may be experienced within first week following injury and continue for few weeks. The pain is like classic trigeminal neuralgia, fine tactile or mild heat stimulation evoke brief hyperanaesthesia, and sharp tingling or stabbing pain, it is explained as a result of nerve inflammation, caused by foreign bodies, mobile fragments etc. It can also be caused by painful neuromas surgical exploration of the injury site is indicated in this case to get rid of foreign bodies, bony spicules, or for treatment of neuroma.
Diagnostic evaluation of nerve injury
The purpose of diagnostic evaluation is to:
- Document whether or not a sensory disturbance exists.
- Quantitate the sensory disturbance, monitor the progress of recovery.
- Determine whether or not microreconstructive surgery may be needed and
- To monitor the progress of sensory recovery following microreconstructive surgery.
This includes a properly taken thorough history, clinical evaluation and some diagnostic testing as nerve blocks and electrophysiological testing of nerve and muscles. The basic clinical examination involves testing for motor function, sensory function and autonomic function.
The motor function is evaluated by testing the motor power of the associated muscle.
The neurosensory testing involves: static light touch, brush directional discrimination, two-point discrimination, pin pressure nociceptive discrimination and thermal discrimination. The area of sensory disturbance is mapped first by brushing from the unaffected area to affected area. Then the above test are performed both on the unaffected side and the area mapped with sensory disturbance. Static light touch is tested with Weinstein-Semmes filaments or with Von Frey hairs. This assess the integrity of the Merkel Cell and Ruffini endings innervated by A β fibers. Brush directional discrimination tests the proprioception and it tests the integrity of A α and A β fibers. Two point discrimination is a test of tactilegnosis and it assess the quantity and density of functional sensory receptors and afferent fibers. If sharp points are used then A δ and C fibers are evaluated, if blunt points are used then A α fibers are assessed. Pin pressure nociceptive assess the free nerve endings and the small A δ and C fibers. Thermal discrimination is a useful adjunctive test of sensation. Warmth sensation is attributed to A δ fibers and cold sensation is attributed to C fibers.
Diagnostic nerve blocks are important part of the diagnostic evaluation when pain is the symptom. Post traumatic pain may be due to nerve compression, neuroma, anaesthesia dolorosa, causalgia, sympathetic nervous system irritation, central pain etc. the purpose of diagnostic nerve block is to aid in determining the mechanism of pain, identifying the pain pathway, and to help to determine the prognosis for decreasing or eliminating the pain.
Electrophysiological testing of the peripheral nerve injury is an indispensable addition to clinical evaluation of peripheral nerve injury. It provides new and corroborative information about the nature of an injury and can aid in predicting outcome and timing of recovery during the follow up of an acute injury. The studies mainly involve electromyographic( EMG ) and electroneurographic studies. EMG studies are done to evaluate the motor function. Electroneurographic studies ( Trigeminal Sensory Evoked Response testing) are of limited use in maxillofacial region due to minimal amplitude of the response than the brain electrical activity.
Algorithm for managing nerve injuries.
The essential feature of the algorithm for management of nerve injury is serial diagnostic evaluations and to classify the injury as observed or unobserved. Treatment of the observed injury may be initiated immediately, whereas the unobserved may need to be monitored for a period of time before definite treatment is initiated. The timing of nerve repair may be classified as primary, delayed primary and secondary. Primary nerve repairs are completed within hours of injury, delayed primary repairs 14 to 21 days after injury and secondary repairs are done 3 weeks after injury.
An observed nerve injury is any injury or wound that provides direct access to and visualisation of the nerve without extensive surgical dissection. The transected observed nerve is repaired primarily while observed compression or stretch injury is managed by decompression and alleviation of stretch to prevent ischaemia. The unobserved nerve injury requires long follow up because the exact anatomical nature of the injury usually is not known. Microreconstructive surgery for unobserved nerve injury are indicated for painful conditions, prevention of avoidable posttraumatic sensory disturbances and anaesthesia. Microreconstructive surgery are contraindicated in anaesthesia dolorosa, sympathetically maintained pain, deafferentation, atypical facial pain and most instances paresthesia.
NERVE REPAIR (NEURORRHAPHY)
Jabaley 1984 described the ideal nerve repair. This would be with alignment of fascicles that would be perfect at axonal level, without use of sutures. The stumps should be bonded with a non-inflammatory tissue glue. Epineurium soft tissue should not be interposed between the stump ends and perfect coaptation would preclude tension free, the nerve will heal in a viable vascular bed without foreign body reaction. Although this ideal situation is not possible, this principle should remain the goal to strive for.
There are few micro surgical procedures which are generally used for the treatment of maxillofacial nerve injuries. These are nerve anastomosis (Neurorrhaphy) nerve grafting, nerve decompression and neurotization.
Indication for Surgical Correction
(Philip E Write 1992)
In the presence of traumatic peripheral nerve deficit exploration of nerve is indicated.
(1) When a sharp injury has obviously divided a nerve. In such case exploration
can be for diagnostic or therapeutic purpose. Neurorrhaphy may done at the
time of exploration or later.
(2) In abraded, avulsed or blasted wounds exploration is done to identify the
condition of nerve and the ends are marked with sutures for later repair.
(3) When a nerve deficit follows a blunt or closed trauma no clinical evidence of
regeneration has occurred after an appropriate time.
(4) When a nerve deficit follows a penetrating wound such as low velocity gunshot,
the part is observed for evidence of regeneration for an appropriate time. Then
if evidence of regeneration is absent, exploration is indicated.
Factors influencing regeneration after neurorrhaphy:
The following factors seem to influence nerves regeneration:
- Age:- Better axonal regeneration and functional recovery is seem in younger individuals (Onne 1972) Black and Lasek (1974) showed that the rate
of regeneration declines with increasing age.
- Timing:- Nerve injury can be primary or secondary. The Primary repair is that
which is done up 48 hours after injury. Early secondary repair are
those accomplished within first 3-6 weeks following injury and late
secondary repair are those performed after 3 month (McCarthy 1990).
There is no absolute rules with regard to the timing of nerve repair, and it should be decided after considering the nature of injury, condition of patient and status of associated injuries. It is generally accepted that clean transected injuries are repaired primary. In cases of severe injuries secondary repair is recommended because viable and non viable nerve tissues can be better designated (Buske 1972) Experimental finding showed better results with primary reconstruction Branch 1972, Peakock 1984).
Advantages of Primary repair are: It allows
– Early correction of sensory and motor defect.
– Better functional nerve regeneration (Peacock 1984)
– Fascicles can be identified by electrical stimulation (up to 4 days).
-Less time consuming.
– Degeneration of distal stump is less.
– Chance of secondary deformity resulting from long term denervation is less.
Daker 1972 recommended a short delay for nerve repair is consideration of metabolic response of cell body to injury cell showed peak metabolic regeneration activity after 2 weeks.
Horn and Crumely 1984 advocated a longer delay because
- The state of nerve can be better defined in relation to surrounding tissue.
- Intraneural scarring is more apparent in proximal and distal stumps, and this
facilitate more accurate debridment.
- The epineurium is thicker at this time yielding a more accurate repair.
- (4) The surgery can be planned to proceed in an unhurried elective manner.
- Proper facilities can be made available,
Young in (1944) described few disadvantages of delaying the repair.
- The longer the delay the greater is the distal endoneurial Shrinkage (due to collagen deposit an the schwamn cell sheath) which prevents successful re-entry.
- Prolonged delay may arrest maturation of regenerating axon and the nerves never attain the pre-injury
- Longer period of denervation causes atrophy of and organ. In such cases renervation is difficult. McQuarrie (1986) recommended a definitive delay in bullet injuries, because the bullet is unlikely to have transected the nerve. The injury sustained will be at all the degree. The delay will help to resolve Ist and 2nd degree injuries. The injured and functional fascicles can be identified and the treatment can be better planned. According to him for low velocity bullets 8-10 weeks delay is probably sufficient and for high velocity bullets 12-16 weeks delay is required.
Time factors should be taken seriously. As the time passes the degenerative changes are proceeding. Considering all options, early repair should be performed if damage to neural elements can be identified, contamination and associated trauma are minimal and a well trained surgical team is available (McCarthy 1990).
- Gap between the Nerve Ends:-
Nerves, as in the case of vessels will retract or severe. If the cut is sharp the cut ends will retract slightly. In high velocity, injuries excessive loss of nerve tissue create larger gaps. Millesi (1981) recommended that if the gap is less than 2.5cm direct end to end coaptation can be done. Larger gaps required grafting.
- The level of Injury :-
The more proximal the injury the more incomplete is the overall return of function especially in more distal structures. This is because
(a) Proximal injuries require a greater percentage of total cell mass.
(b) Regenerating axon has to pass a longer distance to reach the end organ.
(c) The fascicular topography of nerve is more complicated proximally.
- Type of Nerve:
Repair of a pure sensory or pure motor nerve achieve a higher percentage of functional recovery than a mixed nerve.
- Cause of nerve injury and associated injuries:
The less a nerve is traumatised the greater is likelihood of functional recovery. In simple clean lacerations the extend of tissue damage and necrosis is less. In such cases faster regeneration and better functional recovery is expected. In high velocity injuries and avulsion injuries, greater amount of nerve tissue is lost and nerve injury will be mixed In such cases regeneration potential is less. In severe injuries necrosis of surrounding tissue occurs. The level of contamination and subsequent ischemia may lead to infection and scar formation in such cases regeneration will be incomplete.
The other factors influencing are presence of neurotrophic substances in tissue bed and finally the precision of repair which is related to experience and technique of surgeon.
End to End Anastamosis:
This the simplest and most commoly performed nerve repair. This is indicated for simple transections without considerable loss of nerve tissue so that the transected ends can be brought together without tension. For achieving this after planned and adequate exposure of the area the nerve is freed proximally and distally and the ends are brought together and sutured. Suturing can be done over perineurium or epineurium depending on requirement.
At the onset of nerve exploration, wide exposure of proximal and distal stump is essential. Dissection should begin at non injured region, tissue are retracted away from nerve. It is done by putting a longitudinal incision on the normal appearing nerve. Using a microscisors the epineurium is dissected off towards the lesion.
It is usually white in colour, composed of several layers of lose connective tissue and contain longitudinally oriented blood vessels. Uninjured fascicles should be identified and preserved. Before the nerve is raised from the bed marking suture are put on the perineurium at 12 and 6 ‘O clock position to avoid rotational defect.
Epineural repair is the conventional method of surgical coaptation of peripheral nerve. Its advantage is short execution time, simplicity and need for minimal magnification. The intraneural contents are not disturbed and there is not intra neural suture foreign body. This technique is applicable to primary and secondary repair and is easily to perform.
After adequate exposure of proximal and distal stumps the intraneural and perineural scar tissue should be removed from the injured site and a fresh face of cut end should be obtained to maintain a uniform fascicle length. This will help correct approximation. Excessive neural tissue should not be removed of because this will lead to tension at the nerve is approximated. To achieve this nerve is held with a nerve holding forceps and cut (Neurotomy) is done with a micro blade. Use of scissors will produce more crush injury (Mayer 1980) sectioning starts at the centre of injury end proceed proximally and distally 1mm intervals until the fascicular structure is identified an d relatively free of scar.
Up on transecting a nerve or fascicle, axoplasm will sweep out and collect at the end. Excessive axoplasmic outflow will interfere with accurate coaptation. Therefore as a rule, the nerve section should not be done until the last possible moment when the surgeon is prepared to perform suturing. Bleeding should be controlled with bipolar microcoagulator and damp sponge pressure.
After the nerve ends are make lying without tension opposite each other the magnification is increased to 16x and 10-0 nylon sutures are carefully placed in epineurium. Before placement of first suture fascicular bundles are matched by noting features such as position of longitudinal vessels. First suture tie is trimmed long and can be used for retracting. The second suture is placed 180 o from the first and then at 90o to right and left depending on size of nerve. The number of sutures should be kept minimum. Buckling of nerve ends caused by in appropriately large suture ties should be avoided since this leads to wasteful regeneration and neuroma formation.
If the gap is so large that first 10-0 suture does not hold the nerves together, then a 8-0 suture can be used and it can be replaced at the end of the procedure. If the nerve gap is more than 2.5cm after mobilisation nerve grafting is indicated (Williams 1975).
Cause of failures of epineural repair are lack of accurate coaptation of corresponding fascicles, gapping, over riding, buckling of fascicles.
Perineural (Fascicular) Repair:
This implies the surgical manipulation of corresponding fascicles in the proximal and distal stumps to achieve optimum alignment. Identification of corresponding fascicle can be done by intra-operative electro-diagnosis or histochemical identification and this is easy at distal portions of a nerve owing to fascicular homogeneity.
For perineural repair, after exposing the injured nerve, the epineurium is stripped away to expose the underlying fascicles. Fascicular groups are carefully isolated making sure to observe and maintain the integrity of perineurium which is normally glistening white and devoid of blood vessels. Intact fascicles if any should not be disturbed. After careful matching the sutures are placed under high magnification. Suture is placed to inner epineurium which is adherent to perineurium. Care is taken to avoid placing sutures within endoneurium and to avoid a rotational deformity. Usually only two sutures are required to complete each coaptation. Any number of fascicles can be coapted in this manner, but each carries the potential of further intraneural foreign suture materials and subsequent fibrosis.
Millesi (1975) described various “Septa” which separate various fascicular groups. These Septa can be sutured and thus groups of fascicles can be coapted instead of individual fascicles. This help to reduce amount of suture foreign body within nerve. The most frequent indication of epineural repair is reconstruction of partially severed nerves.
The Disadvantages are
– Intra neural fibrosis by increased dissection and foreign materials.
– The Technique is tedious and time consuming (Urbanic 1984 and Orgel 1987).
When a nerve is partially severed and if some fascicles are intact partial neurorrhaphy is indicated. For this after adequate exposure of nerve longitudinal incision is made along epineurium for several centimetres. Then the intact fascicles are dissected out for equal distance on both sides. Then the ends of severed fascicles are brought together and sutured. Epineural sutures are adequate. If not possible perineural sutures are put in each fascicles. The intact fascicles are then put as a loop. Cinching of this should be avoided by adequate relief of epineurium. Care should be taken to preserve the integrity of intact fascicles.
Effect of Tension:- Tension at the site of nerve coaptation invites connective tissue proliferation and subsequent scar formation. As scar tissue matures it has a tendency to constrict, there by compressing any regenerating axon (Daniel and Terziz 1977).
Millesi (1975) studied the effects of tension on 252 nerve repair in 146 animals and observed that connective tissue proliferation and length of resulting scar between the two ends of the coapted nerve were directly related to the amount of tension. The major source of connective tissue out growth was epineurium and the proliferation of the scar begins at the suture line and displaced the suture inwards. In such cases the cross sectional area for nerve regeneration is decreased.
On the basis of these findings, placement of a nerve graft is believed to be indicated for any nerve defect exceeding 2 to 2.5cm (Moniem 1952) amd Milles 1987)
Nerve grafting is indicated in cases of neurotmesis where
- Reanastomosis can not be done without tension
- Neurotemesis and axonotemesis injuries that have resulted in pain and poor return of sensitivity
- There is evidence of symptomatic neuroma.
Usually the donor nerves are taken from .
– Sural nerve, the branch of peroneal nerve.
– The medical antebrachial cutaneous nerve.
– Lateral antibrachial cutaneous nerve
– Lateral and posterior nerve of thigh
– Great auricular nerve.
Hiroyasher Noma (1986) recommended that the great auricular nerve is ideal donor nerve for reconstruction of lingual and inferior alveolar nerve because It is superficial, having equal diameter, sensory defect is less when compared to sural nerve where the lateral part of sole loses sensation.
Suzanne E MacKinnon (1994) in a histologic comparison study of fascicular pattern of sural nerve and medial antebrachial cutaneous nerve conclude that MACN is more suitable for grafting the defects of inferior alveolar and lingual nerves than sural nerve.
Before measuring the length of nerve defect it should be ensured that all the injured non viable nerve tissue is removed. Adequate length of distal and proximal stumps are freed and the scar tissue is resected away.
Grafts are cut slightly longer than the defect with the surrounding tissues completely extended. A clean vertical sectioning of nerve is then made proximal and distal to injured area. Epinurectomy is not indicated because being tension free the proliferation of scar tissue will not occur before revascularisation of graft. Now the graft is interposed and epineural suturing is done with 10,0 nylon. Since there is no tension, graft will adhere to nerve tissue by fibrin clot so one or two sutures are adequate. Suture is carefully placed in inner epineural and outer perineural layer of fascicles and the epineurium graft. The polarity of the graft is not important.
The nerve graft are revascularised by direct in growth of vessels instead of the growth from transected ends. Therefore graft diameter is most important in survival. Thicker nerves show central necrosis before revascularisation (Smith 1986). The nerves graft should lie in a well vascularised viable bed devoid of infection, haematoma or foreign bodies.
Vasscularised nerves Grafts:
When the extensive nerve grafting is necessary or when the tissue bed is poorly vascularised microvascularised nerve grafting is indicated. This will assure immediate blood supply to graft so that fibrosis secondary to ischaemia is avoided and this will assure more rapid axonal regeneration (Terziz 1987). Experimental evidence suggests that regeneration proceeds in a faster rate in revascularised nerve grafts. Terziz 1988 shown that Tinel’s sign progresses in such grafts in a rate of 7-12mm per day compared to 3-4mm in conventional grafts. Fuminori (1992) showed faster return of nerve function is revascularised grafts.
Suitable nerves that may be used for vascularised nerve grafts, are the superficial radial, the Ulnar, sural, anterior tibial superficial peroneal and saphenous (Terzies 1987). These nerves have got predominant vessels supplying the perineurium which can be used for anastomosis. In this after the coaptation of nerve the nutrient vessel is microanastomosed with adjacent vessels.
Nerve Decompression (Neurolysis)
This is the procedure of releasing of nerve from surrounding scar tissue, foreign, bodies, bones or tooth fragments by micro dissection, so that pressure over the nerve is released and regeneration is facilitated. This can be internal neurolysis and external neurolysis. In external neurolysis the perineurium is carefully dissected out of scar tissue a bony fragment which is compressing the nerves. This is indicated where there is a commutation of bone across a neurovascular bundle as seen in zygomatic maxillary body fractures across inferior alveolar nerve or during complicated lover 3rd molar surgery.
Even though the nerve may be visualised with naked eye external neurolysis should be done using surgical microscope with 4x or 8x magnification in order to avoid tearing of epineurium. Attempt should be made to preserve the extrinsic arterioles that are found within the epineurium and nerve is carefully inspected for interruptions, lateral neuroma or neuroma in continuity. If there is a sign of intraneural injury internal neurolysis or nerve grafting may be required.
Internal Neurolysis: of previously injured nerves is indicated when there is incomplete return of normal sensory function with hyperesthesia or triggered pain. In internal decompression an external release is first made to visualise the nerve and a small amount of saliva or local anaesthetic solution is injected beneath epineurium with a 30 Gauge needle. Then using micro scissors epineurium is longitudinally opened to expose the fascicles. Then under 16x magnification the adhesion between the fascicles are carefully released and continuity of each fascicle is re-established. The epineurium is closed with 10-12-0 nylon.
Neurolysis procedure is having complication that it produce some amount of intra neural injury and subsequent scarring. Therefore it should be restricted to the cases where scaring due to injury is more than that expected from surgery.
Non Suture nerve repair:- Technique for the sutureless repair of nerve with and without grafting have recently shown promise for maxillofacial surgery. Mtrays 1982 described use of fibrin clot anastomosis for repair of trigeminal and facial nerve injuries. In the non suture technique the injured nerve ends are isolated from the surrounding scar and they are kept in close proximity using tubes known as nerve conduits, Various materials are described as nerve conduits.These are
– Psuedosynovial tube – (Lundborg 1980)
– Autogenous Vein – (Chiu DT 1980)
– Permanent nerve guide (Machinon 1986)
– Bio observable nerve guide ( Seckel 1984)
– Silicon tube ( Vron 1986)
– Autogenous muscle ( Glosby 1986)
– Bioresobable polyglycolic acid ( William A- Crawly 1992)
It is a technique by which the proximal portion of one nerve is anastamosed to the distal end of another nerve. This is indicated in cases where proximal segments are not accessible for microreconstruction. The greater auricular nerve, mental nerve and infra orbital nerve have been used for neurotization of inferior alveolar nerve and lingual nerve. The hypoglossal nerve and contralateral facial nerve along with nerve grafts have been used for facial nerve reconstruction.
Post Operative Care
In order to maximise the functional recovery the area of nerve repair should be protected for 7-10 days post operatively. Care is taken in wound closure and even gentle washing of skin over the repair is avoided. Skin sutures are removed at two weeks. After this physiotherapy is started and muscle stimulation is carried out. The patient should be seen for evaluation at one, 3, 6 and 12 month postoperatively. The assessment of regeneration is done by noting advancing Tinel’s sign and by electromyographic and electroneurographic studies.
Several methods are used to evaluate motor function return following peripheral nerve injury. They involve assessment of muscle strength against gravity, against gravity and graded resistance. British medical research council (BMRC) established the following system for assessing the return of motor function.
M0 – No Contraction
M1 – Return of perceptible construction in the proximal muscles.
M2 – Return of perceptible contraction in proximal and distal muscles.
M3 – Important muscles are sufficiently power full to act against resistence.
M4 – Return of function as in M3 synergetic and independent movements possible.
M5 – Complete Recovery.
The sensory return is assessed by the following:
Moving Touch, Constant touch, vibratory stimulation, pin prick and two point discrimination. Pin prick sensation is returned first, followed by low vibratory, moving touch, constant touch, then high frequency vibration. Small diameter fibers show faster degeneration. The BMRC established the following six level grading scale for sensory return.
S0 – Absence of sensibility in autonomous area.
S1 – Recovery of deep cutaneous pain sensibility within autonomous area.
S2 – Return of some degree of superficial cutaneous pain and tactile sensibility
within autonomous area.
S3 – Return of superficial cutaneous and tactile sensibility through out the
autonomous area and disappearance any pevious over response.
S3+ – Return of sensibility as on S3 and there is some recovery of two point
S4 – Complete recovery.
Sensory Reeducation and physiotherapy
Sensory reeducation and physiotherapy are extremely helpful in improving the quality of life after nerve repair. The aim of sensory reeducation is to stimulate the peripheral receptors of touch, pain and temperature which sends impulses to the brain to improve the perception of these sensations.
Understanding the clinical manifestations of peripheral and autonomic nerve injury requires a thorough knowledge of the peripheral nervous system and the musculoskeletal system. The clinical evaluation of the peripheral and autonomic nervous system injury should be carefully documented because such documentation along with electrophysiological parameters forms a baseline upon which further decision about operative and non-operative management strategies can be based.
Injuries of nerves in the maxillofacial region is of major concern when considering the functional deficit as a result of the injury. Introduction of complicated osteotomies to correct dentofacial deformities and ever increasing complex facial trauma have resulted in an increase in incidence of nerve injuries over the past few years. The results of repair of traumatically damaged nerves have improved considerably with the introduction of newer micro surgical technique, diagnostic modalities such as somotosensory evoked potential (SEP), intra operative Histochemical fascicle identification etc. Patients require constant evaluation, follow up, sensory reeducation and physiotherapy for an effective outcome following a nerve injury.
Severe to moderate nerve injury can be an injury for life, so it would be ideal to give a realistic assurance to the patient.
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