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d. Compression

e. Ligation

3. Based on the extent of injury:

a. Type I or segmental

b. Type II or global

Segmental or Type I injury is rapid in onset, more severe and slower to recover. It could be due to traction,
cauterization, ligation, or compression around the nerve. Global or Type II injury is more gradual in onset,
[14]
milder, and more likely to recover rapidly. It is usually due to traction .

The vast majority (> 70%) of nerve injuries are traction or stretch related. Majority of traction-related
[11]
injuries are transient and most recover with time. Dionigi et al. reported that, of all etiologies resulting in
RLN paralysis, thermal, clamping, and transection are the most severe resulting in permanent palsy in 28%,
50%, and 100% or patients, respectively.

PHYSIOLOGY OF THE NERVE AND BASIS OF IONM
RLN is a mixed motor and sensory nerve; the motor component supplies the intrinsic muscles of the larynx
resulting in normal vocal cord movement. The nerve fibers when stimulated release a compound action
potential (CAP), which is a sum of impulses of the nerve fibers. The CAP traverses through the nerve
resulting in a waveform recordable by placing electrodes at muscle end plates. This is recorded as
electromyography (EMG) potentials or compound muscle action potentials (CMAP). Thus, IONM is an
[9]
EMG recording of CMAP .
Intraoperatively, a neural insult results in ischemia of the vasa nervosum when more than 5% of the nerve is
stretched, resulting in neuropraxia [9,15] . This progresses to reduction in recruitment of functional nerve fibers
[16]
resulting in decrease in amplitude . Further insult causes loss of myelin sheaths and axonotmesis resulting
in an increase in latency . More than 50% reduction in amplitude and 10% increase in latency is considered
[9]
significant with respect to loss of nerve function, especially if these combined events occur for 40 s or
longer . However, these events are reversible if the offending maneuver is altered (release of traction, etc.).
[17]
Non-recovery of the amplitude within 20 min, however, portends a high risk for postoperative vocal cord
palsy .
[18]

[19]
Physiologically, Wallerian degeneration of the distal segment after the neural insult sets in 48-72 h . Thus,
the nerve segment distal to the site of injury continues to generate a response on stimulation
intraoperatively . This has implications on monitoring the post dissection response (R2), as described in
[20]
subsequent sections.

LEARNING CURVE
While understanding neurophysiology is essential for interpretation of the findings of IONM, the
experience of the operating team contributes to overcoming problem issues, thus helping identification of
impending injuries and aiding crucial intraoperative decisions. This in turn has a bearing on patient
counseling with regards the possibilities of change in operative plans. Most authors who have examined the