Laryngology Seminar
Muscular Tension Dysphonia
R3 陳佳弘 2002/05/08
INTRODUCTION
muscular tension dysphonia (MTD) (Morrison & Rammage, 1983)
other terms: vocal hyperfunction (Froeschels, 1952); vocal fatigue (Sander &
Ripoich, 1983); hyperkinetic dysphonia; myasthenia larynges; laryngeal
tension-fatigue syndrome (Koufman & Blalock, 1988)
functional dysphonia (FD): absence of mucosal or neurogenic disease of the
larynx; exclusion of organic disease;
fluctuant course
more than 40% of dysphonic p’ts have no identifiable organic or mucosal disease
more than 50% of FD: due to vocal abuse or misuse
ETIOLOGY & PATHOPHYSIOLOGY
excessive or “imbalanced” activity of intrinsic and extrinsic muscles
normal phonation: contraction of lateral cricoarytenoid (LCA) and interarytenoid
mm.; relaxation of posterior cricoarytenoid (PCA) m.
in MTD, contraction of LCA and interarytenoid mm.; without adequate
relaxation of PCA m. compensated by tightening of thyroarytenoid m. 
apposition of vocal folds (VFs)  convex reverse bowing of the glottic aperture
+ posterior glottic chink
sources of excessive muscle activity:
 psychological, and/or personality factors;
 technical misuse + extraordinary voice demands;
 learned adaptation following URI;
 compensation of underlying disease
phonotrauma: heat dispersing and shearing force during high-frequency vibration
SYMPTOMATOLOGY
neck or shoulder stiffness; excessive vocal effort, vocal fatigue, intensified with
extended vocal use.
EXAMINATION
physical Examination
 focal palpation: 1) extent of laryngeal elevation, 2) focal tenderness or tender
trigger points, 3) voice effect of applying downward pressure over the
superior border of the thyroid lamina, 4) extent of sustained voice
improvement following circumlaryngeal massage
 pressure 1) over the major horns of the hyoid bone, 2) over the superior cornu
of the thyroid cartilage, and 3) along the anterior border of the SCM m. and
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into the suprahyoid musculature, the posterior belly of the digastric m.
Laryngoscopic features:
plica ventricularis, anteroposterior compression, posterior glottic chink, and hard
glottal attack
Videostrobolaryngoscopy
abnormal findings on the vocal folds (89.7%), especially during vibration
uneven VF mucus surface (83%); vessel dilatation or neovascularization on the
surface of vocal folds (53.8%), abnormal glottal closure (43.5%), and bilateral
vibratory asymmetry(8.6%). multiple: 73.8% (Hsiao)
Morrison-Rammage classification of MTD (1986)
Sama A: laryngeal isometry (37%); lateral supraglottic pressure (60%) in the
dysphonics; less frequent: glottic lateral contraction, incomplete adduction, and
bowing
1) MR 1 (laryngeal isometric): generalized tension in all the laryngeal muscles; an
open posterior chink due to persistent PCA m. pull during phonation.
2) MR 2 (lateral hypercontraction): lateral compression of larynx; tense-sounding
voice; high laryngeal resistance forces; “vocal fatigue”; may be triggered by an
infection or chronic reflux; “habituated hoarseness” (Koufman 1982);
generalized postural misuse and tension
subtype 2a: glottic contraction;
subtype 2b: supraglottic adduction/squeezing, approximation of false VF during
phonation; “plica ventricularis”; psychologically based
3) MR 3 (anterior-posterior supraglottic contraction): technical misuse; a petiole of
epiglottis moved toward the arytenoids during phonation
“Bogart-Bacall” syndrome: tension-fatigue dysphonia (Koufman 1982);
reduced A-P diameter; compression  dropped voice pitch
4) MR 4 (conversion dysphonia): psychological; generalized hypertonicity; highpitched, squeaky, or breathy, “la belle indifference”.
VFs are away from the midline during phonation but function well for other types
of vegetative phonation, e.g. cough, laughter.
5) MR 5 (psychological dysphonia with bowed VFs)
excluding senile atrophy or sulcus vocalis; “habituated hoarseness” following a
trigger.
6) MR 6 (adolescent transitional dysphonia)
perpetuated falsetto; tension at the posterior glottis; high larynx; tight neck
Van Lawrence Fibreoptic features of vocal hyperfunction (1987)
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


common features in the dysphonics: harsh approximation of arytenoids,
decreased vocal length visibility, excessive vertical movement, and
anteroposterior compression (40-50%).
vestibular fold and lateral compression: less (25–40%).
the prevalence of Van Lawrence features in control subjects: similarly high.
In the nondysphonics (Sama A et al)

features of hyperfunction: also prevalent in the nondysphonics; cannot
distinguish between patients with FD

60% of the nondysphonics demonstrate one or more of the features
classically associated with FD

50% of the control population did demonstrate abnormal vocal technique
Koufman’s diagnostic criteria for six types of functional voice disorders
Electromyography (EMG)
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


Stemple (1980): biofeedback
Milutinovic (1988): 2-4-fold increase of EMG activity (7/11)
Hocevar-Boltezar (1998): 6-8-fold increase of EMG activity and/or an
alternation of the EMG activity level in the perioral (upper lip; m. orbicularis
oris)& supralaryngeal (m. thyrohyoideus, m. omohyoideus, m.
sternohyoideus, platysma) muscles before and during phonation (7/11);
excessive tension of both the internal and external laryngeal mm.
TREATMENT
Topical lidocaine injection

3 cc of 4% lidocaine using 25-gauge needle (Dworkin)

abrupt cough reactions; a sensation of laryngeal/ tracheal numbness; slight
difficulty with dry swallows

persistently high-pitched shrill vocal quality was converted to near normal
voice patterns within 15 mins after transcricothyroid membrane injection

break the perverse cycle of hyperactive glottal and supraglottal muscle
contractions

sensorimotor mechanism of action
Manual laryngeal tension reduction in diagnosis and management (Roy)
A. Medial suprahyoid musculature is
palpated at rest and during upward pitch
glide maneuvers. Focal sites of tenderness
and taut bands signal excessive muscle
activity
B. Signs of excess laryngeal tension are
assayed by 1) evaluating presence of focal
sites of pain or nodularity, 2) determining
size of thyrohyoid space, and 3) observing
voice effect of downward traction over
superior border of thyroid lamina and
during circumlaryngeal massage
C. Larynx is compressed by exerting
anterior-to-posterior pressure over inferior
border of hyoid bone
D. Manual tension reduction procedure
(circurmlaryngeal massage) with hand
configuration and placement. Pressure is
applied in circular motion over tips of
hyoid bone and within thyrohyoid space.
Procedure is repeated over posterior
borders of thyroid cartilage and larynx is
gently pulled downward.
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Voice therapy
effective in 69% of the p’ts
failure: continued tobacco use, noncompliance, premature termination of therapy
1) progressive relaxation: (Jacobson, 1938)
alternatively tensing and relaxing all the muscles from the scalp to the toes
2) chewing exercise (Froeschels, 1952)
ask p’ts to image they are chewing food (Wilson)
3) yawn-sigh approach (Boone)
a. eliminate abusive vocal initiations and to reduce tension of the larynx.
b. “yawn”: expand the pharynx and stretch extrinsic laryngeal muscles 
lowering the larynx position, forward placement of the tongue a slight
opening between the vocal folds, and dilated pharynx
c. “sigh”: produce a sustained inhalation.
d. maximum power transfer theorem: the vocal tract input impedance was
calculated [Sondhi and Schroeter (1987), Titze and Story (1997)]
 a wide epilarynx tube (laryngeal vestibule) matches well with low glottal
resistance
e.
f.
g.
provide relief from laryngeal tension--> appreciate the sensation of
laryngeal relaxation
replace the sigh with words beginning with /h/ such as "hi", "hey", "home",
"happy".
produce phrases/sentences following the yawn, "Hi, how are you?", "He has
hairy hands!"
4) biofeedback training: Stemple (1980)
EMG biofeedback permitting p’ts to monitor the electric activities of their
muscle & to exert some control.
Other treatment modalities
1) role of microsurgery for hypertrophy of the ventricular folds: three stages
(Kosokovic, 1973)

stage I: reversible histological changes: and quick success in V/T

stage II: reversible histological changes; prolonged and persistent V/T

stage III: irreversible histological changes (connective hyperplasia)
2) laser therapy of dysphonia plica ventricularis: carbon dioxide laser for excision
of the hypertrophied false VFs
3) botulinum toxin injection into the false vocal folds followed by speech therapy
(Kendall 1997)
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REFERENCE
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functional dysphonia. Laryngoscope. 2001 Mar;111(3):458-63.
2. Hsiao TY, Liu CM, Hsu CJ, Lee SY, Lin KN. Vocal fold abnormalities in
laryngeal tension-fatigue syndrome. J Formos Med Assoc. 2001 Dec;100(12):83740.
3. Roy N, Ford CN, Bless DM. Muscle tension dysphonia and spasmodic dysphonia:
the role of manual laryngeal tension reduction in diagnosis and management. Ann
Otol Rhinol Laryngol. 1996 Nov;105(11):851-6.
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power transfer theorem to a low dimensional phonation model. J Acoust Soc Am.
2002 Jan;111(1 Pt 1):367-76.
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