Nerve injury classification
|Category||Degree of injury|
|First-degree conduction block||Second-degree axonal continuity||Third-degree endoneural tubule||Fourth-degree funiculus||Fifth-degree complete nerve trunk|
|Complete <2 wks||Complete or mild||Residual deficit||Some spontaneous recovery that is rarely useful||If untreated rare, and residual deficit if treated|
|Does not occur||6-21 d, often >14 d||6-21 d, often <14 d||100% by 3-5 d|
|Normal||There is a >50% chance of an incomplete recovery when the ENOG response is reduced by ≥90%||100% denervation by 3-5 d|
|Absent pathological spontaneous activity||Pathologic spontaneous activity is present after 14-21 d, which heralds a high probability (80%+) of an incomplete recovery|
|Volitional responses can be intact, reduced or, absent. Early intact volitional responses at multiple sites or improvement in the firing pattern suggest a good outcome. Absent (or minimal) volitional predicts a poor recovery||No volitional activity|
- •First-degree injury (neuropraxia): first-degree injuries are the result of a conduction block, which is typically secondary to nerve compression or ischemia. In this category, injury may result in some form of localized damage to the myelin sheath. However, there is no axonal degeneration so that the axonoplasmic continuity remains intact distal to the lesion. Therefore, neuropraxic injuries will continue to conduct a neural impulse if an electrical stimulus is delivered at a point distal to the site of lesion. This is the basic premise on which ENOG testing is based. Recovery from this type of injury is spontaneous and complete.
- •Second-degree injury (axonotmesis): in this degree of injury, there is a complete interruption of both the axon and the axoplasm contained within the axon. However, there is preservation of the endoneural tubule. Anterograde axonal degeneration (called Wallerian degeneration) occurs; this results in the peripheral end organ being isolated from its corresponding neuron. This loss of nerve supply to the end organ is referred to as denervation. Because the endoneurium remains intact, the axon can regenerate toward its original end organ through the intact tubule. This leads to a better prognosis in terms of recovering motor function following the injury.
- •Third-degree injury (neurotmesis): this type of injury involves damage to the endoneural tube and its contents. Retrograde disturbances are more significant because regeneration can now occur across disrupted endoneural tubules. Axons may reach functionally related end organs or they may enter totally foreign endoneurial tubes. This results in internal disorganization because some axons do not regenerate to their original end organs. The resulting abnormal healing creates a distorted and less efficient firing pattern, with the clinical manifestations of synkinesis and/or contracture. Synkinesis is the involuntary contraction of an erroneously reinnervated muscle during a contraction of the normally reinnervated muscle.
- •Fourth-degree injury (neurotmesis): fourth-degree injuries involve damage to the funiculus and its contents. The entire funiculus is involved, and all bundles are breached. Funicular bundles become so disorganized that they are no longer distinguishable from the surrounding connective tissues of the epineurium. Large numbers of regenerating axons escape and infiltrate foreign tubes. Some spontaneous recovery can occur, but it is of little functional value.
- •Fifth-degree injury (neurotmesis, complete nerve transection): a fifth-degree injury involves transection of the entire nerve trunk. The majority of axons do not reach their designated funiculi or endoneural tubule because of the separation of the nerve ends and scarring. Recovery will not occur without surgical intervention, and complete restoration of function is impossible even if the nerve ends are repaired.
- •Mixed injuries: it is entirely possible that the degree of injury can be unevenly distributed across a nerve fiber. This results in different axons, endoneural tubes, and funiculi being at various stages of injury at the same time. Fifth-degree injuries by definition cannot coexist with lesser degree injures. It is possible to have a partial transection, although injuries severe enough to partially transect a nerve will most likely leave a significant injury in any nontransected fibers. Mixed injures can muddy the diagnostic waters and make it difficult for any objective measure to make a clear and definitive differentiation regarding the specific degree of injury.
|Nerve axon||Extension of the neuron that contains axoplasm and is responsible for transduction of electrical impulses away from the cell body.|
|Endoneurium||Contains the axon. It is a single layer of Schwann cells and an inner layer of connective tissue called neurilemma. It serves as a protective sheath for myelinated nerve cells.|
|Perineurium||Connective tissue that bundles together a number of endoneural tubes to form the funiculus.|
|Epineurium||Funiculus bundles are held together by areolar connective tissue, which is more compressed at the surface. The bundles gradually become intermingled as fibers ascend along the nerve.|
|High pass filter||20 Hz|
|Low pass filter||1000 Hz|
|ENOG stimulator setup|
|Stimulus range||0-30 mA|
|Pulse||(1) A single triggered pulse or
(2) Continuous pulse train at a frequency of 3 Hz
Interpretation of ENOG
Prognostic value of ENOG
|Facial nerve branch||Recording location|
|Temporal branch||Frontalis muscle|
|Zygomatic branch||Orbicularis oculi|
|Buccal branch||(1) Nasolabial fold (levator labi alaque nasi/levator labii superioris)
(2) Orbicularis oris
|Marginal mandibular branch||Chin: (mentalis/depressor anguli oris/depressor labi inferioris)|
|Recording window||2 s|
|High pass filter||20 Hz|
|Low pass filter||3000 Hz.|
|Electrode type||Concentric needle (preferred), monopolar electrodes can be used|
|Recording electrode||A disposable 25-mm 30-ga concentric EMG electrode|
Interpretation of EMG
Prognostic value of EMG
Timing considerations for ENOG and EMG evaluations
- 1ENOG should never be performed before 3 days postinjury. Abnormal ENOG responses rely on the onset of Wallerian degeneration, which requires a minimum of 72 hours to occur.
- 2Early signs of denervation on ENOG are a poor prognostic sign because they herald a more severe nerve injury.
- 3EMG can be performed at any time after the injury. Early responses, especially at multiple locations, are a positive indicator for recovery and help to rule out a complete nerve transection.
- 4EMG's prognostic value improves when testing can be deferred until 10 to 14 days after the onset of injury. This will allow signs of abnormal healing/abnormal resting potentials to occur. However, at least in the case where a facial nerve decompression is being considered, delaying treatment may be detrimental to the patient's ability to recover.
|Onset of injury||If the face is immediately weak at the time of trauma, this is concerning for severe injury. Later onset is more favorable than early onset.|
|0-3 d||ENOG will always be normal (unless injury is distal to point of stimulation).
Presence of any volitional activity on EMG can rule out a complete nerve transection.
Volitional responses at multiple sites are a positive sign.
|3-5 d||Evidence of Wallerian degeneration (via ENOG) in this early stage after injury is concerning for a possible fifth-degree injury (complete transection).|
|6-14 d||Evidence of onset of Wallerian degeneration (via ENOG) in this time frame is suggestive of a grade 3-4 injury. The cut off for surgical decompression in idiopathic facial weakness is of 12-14 d.|
|14-21 d||Evidence of later onset Wallerian degeneration on ENOG suggest 2nd degree injury.
EMG can now be evaluated for presence of abnormal spontaneous activity (which suggests a second-degree or worse injury and a less satisfactory outcome).
|8-24 mon||EMG can be used to monitor for improved volitional responses and to help determine the patient's candidacy for a dynamic facial reanimation procedure.|
Idiopathic facial weakness
- 1Primary facial nerve repair or cable graft is indicated in the presence of a confirmed fifth-degree injury. The best indicator of this is a complete facial paralysis at the time of injury. However, many patients are unconscious at the time injury and may be poor historians while recovering. Other signs to support a nerve transection include the early onset of Wallerian degeneration as indicated by ENOG and absent volitional activity on EMG at all recording sites.
- 2Decompression should be considered in the context of ≥90% degradation on ENOG, especially when onset of denervation is <14 days. This can be further supported by completely absent volitional EMG, volitional EMG at only one recording site, or signs of abnormal resting potentials. Surgeons also have the opportunity to explore and decompress the facial nerve and then convert to a nerve graft if their intraoperative findings reveal a complete nerve section.
- 3Observation and medical management: patients with an ongoing negative ENOG (<90% degeneration) are suspected to have a first-degree injury and will be expected to recover. In our facility, patients with volitional EMG at 2 or more recording sites are observed for 8 months or up to a year and typically recover to acceptable levels.
- 4Facial reanimation procedures: a complete discussion of these surgeries is beyond the scope of this manuscript. In general, facial reanimation procedures are a last resort when it is felt that the native facial nerve will not provide effective facial movement. It is generally agreed that the native facial musculature requires some type of innervation, either from the native facial nerve or a donor nerve, within 18 to 24 months of injury to prevent relatively irreversible atrophy and fibrosis.
|Good outcome indicators||Bad outcome indicators|
|Normal ENOG after 14-21 d||Weakness at time of trauma|
|Late onset of Wallerian degeneration||Early onset Wallerian degeneration|
|Normal resting potentials on EMG after 14-21 d||Progressive decay of ENOG ≥90% amplitude reduction|
|Volitional EMG and a normal interference pattern||Abnormal spontaneous activity on EMG after 10-21 d|
|Improving volitional EMG||No volitional EMG or EMG at only 1 recording site|
|Volitional EMG recorded at 2+ sites (4-5 better)|
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