The protective function of the larynx may be viewed
neurophysiologically by examining the glot tic closure
reflex. This simple reflex produces protective laryngeal
closure during deglutition. Of note is the fact that this
reflex is absent or diminished in newborn animals,
whose central and peripheral nervous systems are not
fully developed. In adult animals, electrostimulation of
the superior laryngeal nerve (SLN) produces a low-threshold evoked action potential in the adductor branches of the recurrent laryngeal nerve (RLN). In humans, the threshold of the adductor reflex measures 0.5 V and has a latency of 25 ms, indicating that this is a polysynaptic brain stem reflex, a view supported by appropriate calculations of latency measures.

Unlike common animal models, however, human
subjects do not have a crossed adductor reflex; i.e.,
stimulation of one SLN does not produce simultaneous
action po- tentials in the contralateral adductor
musculature. Thus, unilateral SLN dysfunction or
injury in humans may result in a failure to activate the
ipsilateral cord, a condition predisposing to aspiration
despite a functional RLN on both sides.
In healthy subjects, sphincteric closure of the upper
airway produced by bilateral SLN stimulation results
in protective adduction of three muscular tiers
within the laryngeal framework. The highest level of
closure occurs at the aryepiglottic folds, which contain
the most superior division of the thyroarytenoid
(TA) muscle. With reflex contraction of these fibers,
the aryepiglottic folds approximate to cover the superior
inlet of the larynx. At this level the anterior
gap is filled by the epiglottic tubercle, completing the
first of three sphincteric tiers of protection. A me-
chanical phenomenon protects the airway during reflexive
swallow. The forward posture of the tongue and
coupling of the base of tongue, hyoid bone, and
thyroid cartilage position the larynx in a
superior-anterior posture during reflexive swallow.

The second tier of protection occurs at the level of
the false cords, consisting of bilateral folds that form
the superior aspect of the laryngeal ventricles.
Laterally, along each fold are fibers of the. A muscle
that are capable of bringing the folds together in a
reflex response to SLN stimulation.

The third tier of protection occurs at the level of
the true vocal cords, which in humans are shelflike,
with slightly upturned free edges. The inferior division
of the TA muscle forms the bulk of each shelf,
producing the potential for strong reflex protective
closure. In conjunction with the passive valvular ef –
fect caused by the upturned borders of the cord margin,
the true cords represent the most effective of the
three barriers to aspiration.
Although classically the glottic closure reflex may
be elicited by direct SLN stimulation, other sensory
stimuli can also cause this basic reflex response. For
example, stimulation of all major cranial afferent
nerves produces strong laryngeal adductor responses,
as does stimulation of other special sensory and
spinal somatosensory nerves. In cats, reflex action
potentials in the adductor branch of the RLN can be
elicited by electrostimulation of the optic, acoustic,
chorda tympani, trigeminal, splanchnic, vagus, radial,
and even intercostal nerves. In humans, the afferent
input from a tight posterior nasal pack in the
nasopharynx is thought to cause inspiratory dyspnea
by inducing the glottic closure reflex. The suscep-
tibility of this reflex response to such diverse sensory
input is unique and emphasizes its primitive role in
protecting the lower airway from potentially noxious
When exaggerated, the glottic closure reflex produces
laryngospasm, a condition in which closure is sustained
even after the withdrawal of a noxious glottic or
supraglottic stimulus. An understanding of laryngeal
spasm has important clinical ramifications, particularly
during induction of general anesthesia.
Neurophysiologic studies of laryngeal spasm have
shown prolonged adductor spike activity in the RLN.
This spike activity characteristically has no precise
temporal relation (Le., latency) to its initiating
stimulus. Afferent stimuli capable of
producing laryngospasm are conducted solely by the
SLN. Although other afferents may elicit simple glottic
closure, they do not produce the adductor afterdischarge
activity that is characteristic of laryngospasm.
In experimentally induced laryngospasm, the char –
acteristic output of the brain stem adductor
mo-toneuron aggregate is sfcrongly modified by the
level of barbiturate administration. The
deeper the anesthesia, the smaller the number of
afterdis-charges elicited by repetitive SLN stimulation.
This response is not surprising because barbiturates
both increase the refractory period of active
motoneurons and impair their synaptic
transmission. This explains the markedly impaired
motor output elicited by repetitive SLN stimulation
during deep barbiturate anesthesia.
Hypoventilation is another cause of depressed adductor
motor function. A possible mechanism is
suggested by the fact that hypoxia preferentially
abol-ishes postsynaptic potentials.’W/Ioreover,
postsynaptic recovery lags behind presynaptic
recovery, depressing all reflex neural
activity, hypoventilation, therefore, understandably
impairs the output of brain stem adductor neurons in
response to repetitive SLN stimulation.
These experimental
data are consistent with the clinical observation that
laryngospasm occurs more often in well-ventilated
than in cyanotic patients, the spasm often breaking
spontaneously as the patient becomes increasingly
Finally, it should be recognized that SLN stimulation
not only excites the adductor response, but also
inhibits medullary inspiratory neurons. This action
results in decreased laryngeal abductor function as
well as diminished phrenic nerve activity, causing reflex
apnea. This is just one of the many examples of
close coordination between respiration and laryngeal
function, in this case, preventing inspiration or expiration
against a closed glottis.



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