ELECTRICAL PACING OF THE
PARALYZED LARYNX
WITH AN IMPLANTABLE DEVICE
D.Zealear, C.Billante, M.Courey,
R.Ossoff, J.Netterville
Department of Otolaryngology,
MCN S2100,
ABSTRACT
Electrical stimulation of the vocal fold
opening muscles, paced with inspiration, offers a physiologic approach to
restore ventilation in case of bilateral laryngeal paralysis. This study presents the results of the first
clinical trial of laryngeal pacing in the
INTRODUCTION:
Bilateral vocal fold paralysis
(BVFP) is a serious and often life-threatening clinical problem. Surgical techniques such as laser
arytenoidectomy can be performed to enlarge the embarrassed airway. However, these procedures sacrifice voice and
airway protection to restore ventilation.
They also ignore the long-term effects of atrophy on vocal fold mass and
position. A new, more physiologic
approach termed laryngeal pacing has been studied in animal models.1-3 It involves electrical stimulation of the
posterior cricoarytenoid (PCA) muscle to restore ventilation with
inspiration. During noninspiratory
phases, the vocal folds passively relax to the midline to allow for normal
voicing and airway protection. Recently,
the efficacy of laryngeal pacing was directly demonstrated in the human
patient. An external pacing circuit and
percutaneous needle electrodes were used to deliver stimuli to the abductor
muscles.4
In view of the feasibility of this
treatment using an external device, preliminary trials with an implantable
device have been undertaken by Medtronic, Inc. in a phase I multi-institutional
FDA study. To date, seven patients have
been implanted worldwide with this laryngeal pacemaker. The present report describes the results of
the first implantation in the
METHODS:
The patient was a 63-year-old female
with an eighteen month history of BVFP following thyroidectomy. She was tracheotomized two months later. At
the initial visit, she was unable to tolerate closure of the tracheotomy tube
for more than a few seconds. The general
innervation status of laryngeal muscles was assessed by means of percutaneous
needle electromyography. The Itrel II
device was then implanted. An incision
was made in the neck and the electrode inserted into a subperichondrial pocket
between the PCA muscle and its cartilage.
The electrode lead was brought subcutaneously to a second incision where
the implantable pulse generator (IPG) was positioned. After implantation, the IPG could be programmed through the skin by an external
transmitter to change stimulus parameters.
In monthly post-operative sessions with the patient, an effective
stimulus paradigm was derived, the magnitude of stimulated vocal fold abduction
and ventilation measured, and the effect of stimulation on voice production
assessed. The primary goal of the study
was to determine whether the device could restore ventilation through the mouth
equal to that through the tracheotomy without disturbing voice. If so, mouth ventilation would be deemed
sufficient to permit removal of the tracheotomy, i.e. decannulation.
RESULTS:
As often observed in patients with
BVFP following thyroidectomy, all laryngeal muscles had some reinnervation as
shown electromyographically. However,
the reinnervation was faulty as indicated by the inappropriate firing patterns
of motor units. Both the inadequacy and
synkinetic nature of reinnervation likely accounted for the vocal fold
immobility.
In post-operative sessions, it was
determined that a 1.5 second train of 1 millisecond pulses delivered at a frequency of 40 hertz and amplitude of 2-6
volts effectively produced a dynamic airway.
One and a half seconds of stimulated abduction allowed sufficient air
exchange with each breath. The device
was set to deliver twelve stimuli every minute to match the patient's
respiratory rate at a moderate level of activity. (This device in its present
form is not synchronized with respiration). The ideal stimulus amplitude was
one that evoked maximum vocal fold opening without inducing discomfort or
nociception. At this amplitude, the
patient could feel the stimulus, which provided a signal to inspire.
FIGURE 1
Figure 1 is a
histogram of the static and stimulated airway measurements in post-operative
sessions. In the initial sessions, a
stimulated opening of 2.5 mm was obtained which was significantly larger than
the .5 mm static airway. Stimulated
abduction increased further to 4 mm with the identification of optimal stimulus
parameters. At 6.5 months, the loss in
abduction was attributed to a slight shift in electrode position less favorable
for PCA activation. It was hypothesized
that the shift could have also caused greater recruitment of nearby nerves
supplying adductor (closing) muscles, which antagonized glottal opening. In order to nullify the antagonistic
response, a short-acting neuromuscular blocking agent, pancuronium bromide
(PB), was injected into the ipsilateral thyroarytenoid muscle. Within ten minutes, dynamic abduction was
restored to a level greater than that observed in previous sessions. The success with PB provided a rationale for injection of
botulinum toxin (Botox or "B").
As shown in subsequent sessions, the stimulated abduction following
Botox treatment was maintained at a higher level. Repeated injections of Botox over the next
nine months not only maximized the dynamic airway (7.0 mm), but directly
enlarged the passive airway (2.5 mm).
The device malfunction at 10 months
was due to the loss of an electrode channel.
Since the electrode had only two channels, the stainless steel case was
made to serve as the second channel, and the highest level of abduction was
regained.
FIGURE 2
Figure 2 summarizes the ventilation
data, graphically illustrating the flow rate of inspired air measured at each
session. Air flow through the mouth with
the device on (filled circles) was always greater than with the device off
(filled squares). This finding was not
unexpected since the device was observed endoscopically to produce vocal fold
abduction. However prior to Botox administration,
mouth breathing with the device on was dramatically less than trach breathing
(open circles). Air exchange was so
limited that the patient could not tolerate trach closure for more than a few
minutes. This inadequacy in ventilation
was surprising and appeared inconsistent with the relatively large glottal
opening viewed endoscopically during stimulation. The explanation lay in the fact that the
patient's glottis in the "off " phase was so constricted that air
exchange during expiration was severely compromised. Following Botox therapy, the static airway
increased sufficiently to allow normal volume exchange during both inspiration
and expiration with the device either on or off (not shown). The volume of air
that could be passed through the mouth equaled that which could be passed
through the tracheotomy. For the first
time since her tracheotomy, the patient could sit quietly with her stoma closed
for many hours. Furthermore, when the
device was activated the patient could engage in more demanding levels of
activity such as standing or walking. As
shown in figure 2, the airflow during stimulated abduction was sufficient to
support this higher level of activity, while airflow through the passive glottis
was not (11-16 months) Flow rates with
dynamic opening approached 1.6 liters per second characteristic of that through
the trach site. With the device on, the
patient kept the trach closed 24 hours a day.
Subsequently, two months after completion of the study, the patient was
decannulated.
The patient's voice before
implantation was hyperfunctional, and rated as moderately rough and
strained. Following implantation of the
Itrel II, there was no effect of chronic PCA stimulation on voice quality over
a six month period of electrical pacing.
With subsequent repeated botox injections into both vocal folds, the
passive glottis enlarged and the patient's voice quality improved to near
normal.
DISCUSSION:
The results of this study
demonstrate the merit of laryngeal pacing as a new treatment approach. The optimum stimulus parameters for PCA
activation were identified. Using this
paradigm, electrical pacing restored
vocal fold movement with a peak glottal opening as large as 7 mm. Once the passive airway had been enlarged
with Botox to permit expiration, ventilation through the mouth was also
recovered. An inspiratory airflow of 1.6
liters per second allowed the patient to engage in normal everyday activity,
sufficient for her eventual decannulation.
The fact that chronic electrical pacing caused no disturbance of voice
further validated the physiologic nature of this treatment. The improvement in ventilation with null
effect on voice attest to the significant advantage of laryngeal pacing over conventional
surgical therapies for BVFP.
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SUPPORTED BY NIH
Grant 2R01 DC01149