The Laryngoscope
Lippincott Williams & Wilkins, Inc., Philadelphia
© 2002 The American Laryngological,
Rhinological and Otological Society, Inc.
Letter to the Editor
Laryngeal Manifestations of Speech Dysfluency: A
Topical Anesthesia Treatment Approach
topical lidocaine was administered using a 5-cc syringe at-
tached to a 1.5-in 21-g needle. The injection induced a reflex-
ive cough that distributed the anesthetic solution over the
subglottal, glottal, and supraglottal mucosal mechanorecep-
tors. Immediately postinjection a 15-minute series of easy
voice onset exercises were used.
Dear Editor:
Stuttering is a developmental disorder that usually
begins in childhood. Its cause is unclear in most cases.
Specific focus on the role of the larynx during stuttering
has demonstrated cocontraction and spasmodic bursts
of antagonistic (abductor/adductor) laryngeal muscles
and excessive supraglottal activity. Similar findings
have been demonstrated in patients with spasmodic
dysphonia. Consequently, experimental use of Botox in-
jections into the vocal folds of stutterers with hyperki-
netic laryngeal signs have been shown to result in fewer
dysfluencies and overall improvements in speech rate
and intelligibility.1 The purposes of this case study were
to describe the aberrant phonation subsystem features
exhibited by a patient with an adventitious dysfluency
disorder, and the unique laryngeal treatment technique
used to resolve this condition.
RESULTS
Within 15 minutes postinjection the patient was dys-
fluent less than 15% of the time and speaking rate was 82
syllables per minute. Without further intervention, dys-
fluency dropped to less than 10% and speaking rate in-
creased to 127 syllables per minute at the 1-week follow-
up. At 1-, 6-, and 12-month follow-up examinations both
speech fluency and speaking rate were within normal
limits, without evidence of relapse.
DISCUSSION
The larynx contains numerous mechano- and stretch
receptors located within its mucosal linings, intrinsic
muscles, and joints that provide continuous sensory feed-
back to the lower brainstem through the internal and
recurrent laryngeal nerves. These communications form a
sensorimotor laryngeal feedback loop that influences pre-
phonatory vocal fold “set-points” such as vocal fold posi-
tion, length, and muscular tension. Both neurologic and
psychologic traumatic events may potentially disrupt the
physiological preparedness of this complex system. It has
been well documented that stuttering may be partially
attributable to excessive tension and cocontraction of la-
ryngeal muscle antagonists.1 Such pathophysiology has
also been observed in patients with MTD whose voice
symptoms dramatically improved after topical laryngeal
anesthesia.2 For the current patient, this treatment tech-
nique resulted in quick and substantial speech fluency
gains.
SUBJECT
The patient is a 38-year-old man with no previous
speech, language, or hearing difficulties. Four weeks after a
motor vehicle accident, he developed severe speech dysflu-
ency, which persisted for 4 months despite traditional speech
therapy. All consultations yielded the diagnosis of psycho-
genic stuttering, prompting referral to our office. Detailed
analyses in our speech physiology laboratory revealed that
the patient was dysfluent on approximately 50% of all words
uttered, with an associated slow speaking rate of 69 syllables
per minute (less than half normal). Experimental use of a
transcervical electrolarynx (EL) promptly resulted in 100%
speech fluency and a normal speaking rate. Laryngeal artic-
ulatory biomechanics, through videoendoscopic examina-
tion, revealed unremarkable anatomy but intermittent su-
praglottal sphincteric contractions, shimmying of the
aryepiglottic folds, and dyssynchronous true vocal fold move-
ment patterns. When aided by use of the EL, these patho-
physiological features subsided.
The mechanism of action of topical lidocaine in these
cases remains unclear, although it is possible that this
treatment served to disrupt the sensory arm of the afore-
mentioned feedback loop. The probable physiological ef-
fect was a sensory “trick,” which facilitated automatic
rebalancing of prephonatory set points by anesthetically
stifling the hyperfunctional larynx. Whether developmen-
tal stutterers or others with adventitious fluency disor-
ders would respond as favorably to this treatment regimen
requires further investigation. We suggest that dysfluent
patients who are refractory to speech therapy might also
benefit from appraisal of laryngeal anatomy and physiol-
ogy. If a potential trigger is identified during these exam-
inations, the lidocaine technique may be a reasonable
CLINICAL DIAGNOSIS AND TREATMENT
All test results suggested that the dysfluency disorder
might, at least in part, be attributable to the observed aber-
rant laryngeal behaviors. We recently reported success in
treating patients with muscle tension dysphonias (MTD),
who struggled with similar laryngeal signs, using topical
anesthesia of the larynx.2 This experience prompted exper-
imental application of the same technique with the current
patient. A transcricothyroid membrane injection of 4 cc 4%
Laryngoscope 112: May 2002
936
Letter to the Editor
Feist
