Voice disorders associated with hyperfunction 119

MTD Type 2 denotes medial compression of the true vocal folds and/or
ventricular folds (Morrison and Rammage, 1994). Again, Morrison and
Rammage associate this pattern of muscular tension with poor vocal
technique and psychogenic factors. A distinction is made between hyper-
adduction at the glottic and supraglottic levels, with the former being
linked primarily to vocal misuse and the latter to ‘unresolved psycho-
logical conflict’. Morrison and Rammage list normal appearing vocal folds,
erythema or diffuse thickening of vocal fold mucosa, an increased closed
phase of vocal fold vibration and reduced amplitude and mucosal wave as
the possible signs of MTD Type 2 at the glottic level. The resulting voice
features are said to include harshness, vocal fatigue and throat discomfort.
MTD Type 2 at the supraglottic level is described as involving compression
of the ventricular folds over either tightly adducted true vocal folds or over
incompletely adducted true vocal folds where there would be a gap
between the membranous and cartilagenous glottis. The former pattern is
said to result in a ‘high-pitched squeaky voice’ whereas the latter is associ-
ated with a breathy voice or a ‘tense whisper’.
MTD Type 3 with anteroposterior supraglottic contraction refers to the
use of a laryngeal posture where the distance between the epiglottis and
the arytenoid cartilages is reduced. Morrison and Rammage (1994)
attribute this pattern of hyperfunction to poor vocal technique, ‘tense
pharyngolaryngeal postures’, and/or an attempt to produce a particular
resonance quality (e.g. the ‘Bogart–Bacall’ syndrome described by
Koufman and Blalock, 1982). They also state that MTD Type 3 involves
phonation in the low part of the speaker’s dynamic range and is associated
with vocal fatigue, particularly at low pitches.
This classification of muscular tension dysphonias developed by Morrison
and Rammage (1994) has received some support from clinical investigations
of subjects with hyperfunctionally related voice disorders, empirical studies
of subjects simulating muscular tension in the larynx and experiments on
human cadaver larynges (e.g. Belisle and Morrison, 1983; Morrison et al.,
1983; Rammage, 1992). Because they describe the physiology underlying
each of the three types of MTD, Morrison and Rammage’s work also provides
a possible framework for objective physiological assessment of vocal hyper-
function using techniques such as laryngeal videoendoscopy. Unfortunately,
empirical evidence for the validity of their classification scheme is not
complete and further research will be required to test the many proposals
made by Morrison and Rammage concerning causality and the physiological
and perceptual correlates of muscular tension dysphonia.
The notion that vocal hyperfunction may be reflected in either hyperad-
duction of the vocal folds or incomplete adduction has also been incorpo-
rated in a theoretical framework proposed by Hillman et al. (1989). Hillman
et al. have postulated that vocal hyperfunction which leads to vocal fatigue