Учебники / Voice Disorders and Their Management Freeman 2000

Appendix 6.2: Arms

Appendix 6.3: Hugs

Appendix 6.4: People waving

Appendix 6.5

dysfunction (e.g. Cooper, 1973; Herrington-Hall et al., 1988; Yiu and Ho, 1991; Fritzell, 1996). In the absence of such conversion disorders or organic conditions, the most likely aetiological candidate is vocal hyperfunction. Further, the increased prevalence rates of vocal disorders among people who have vocally demanding occupations and lifestyles indicate that hyperfunction is likely to be a common denominator (e.g. Calas et al., 1989; Sapir et al., 1990; Fritzell, 1996). Indeed, in a comparison of the vocal intensities used by teachers and nurses, Masuda et al. (1993) demonstrated that teachers spent more of their phonation time using loud speech and screaming intensities, suggesting that this hyperfunctional vocal behaviour may underlie the higher prevalence rates of voice disorders among teachers than nurses. Similarly, the disproportionate number of higher pitched voices (i.e. young children and adult females) among those with voice disorders suggests that the frequency of collision between the vocal folds is instrumental in the development of voice problems (Titze, 1994).

The typical location of pathological changes assumed to arise from vocal hyperfunction provides further support for the role of excess muscle tension and force; the common pathologies of vocal fold nodules and polyps, for example, occur in the centre of the membranous part of the vocal folds where the mechanical impact of vocal fold vibration is greatest (Hirano et al., 1983). In addition, investigations of the structural alterations to the vocal fold cover which occur in these vocal pathologies, in concert with studies of the effects of mechanical trauma on canine vocal folds, demonstrate that vocal hyperfunction is likely to cause damage to the epithelium and lamina propria of the vocal folds (e.g. Gray and Titze, 1988; Gray, 1991; Dikkers et al., 1993; Gray et al., 1993). Such damage may include loss of surface microvilli, epithelial desquamation, rupture of subepithelial blood vessels, subepithelial oedema, disruption of the basement membrane zone, and increased collagen production.

Direct evidence for the negative effects of vocal hyperfunction in humans is scarce, but a small number of experimental studies have been conducted to examine the effects of hyperfunctional vocal behaviours such as loud talking, speaking at high pitch levels, and prolonged voice use at high intensity and/or high pitch (e.g. Stone and Sharf, 1973; Gelfer et al., 1991; Scherer et al., 1991; Stemple et al., 1995b). Although such investigations have not generally simulated the vocal hyperfunction which can occur in a naturalistic environment, and although the findings are inconsistent, there is certainly some evidence that such vocal behaviours can lead to vocal fatigue and throat discomfort, alterations in glottal configuration, and negative effects on various measures of vocal quality and pitch.

The susceptibility of the human larynx to vocal hyperfunction is not surprising. To fulfil its primary biological functions of protecting the lower airways from aspiration of food, liquid and foreign bodies and of facilitating defecation, childbirth, heavy lifting and coughing, the larynx must reflexively rise in the neck and close off the airway (Brodnitz, 1959; Aronson, 1990). This reflexive pattern of closing down, or constricting, takes precedence over the phylogenetically more recent role of the larynx in speaking and singing (Boone and McFarlane, 1994). With a predilection for constriction in the vocal tract, it is no wonder that vocal hyperfunction creeps into human speech patterns so readily.

Taken together, these considerations suggest that hyperfunction or mechanical stress on the vocal mechanism will be a primary focus in the evaluation and management of clients with voice disorders.

The nature of vocal hyperfunction

The description of vocal hyperfunction as the use of excessive levels of laryngeal muscle tension, force and constriction is useful as a broad definition, but is not sufficiently specific to guide clinicians in the evaluation and treatment of hyperfunctionally related voice disorders. Specification of the types of vocal behaviours that are hyperfunctional, classification systems for differentiating the various forms of hyperfunction, and approaches to the quantitative measurement of vocal hyperfunction are also required if clinicians are to provide effective management for clients with these voice disorders.

All of the major textbooks on voice disorders outline examples of vocal behaviours which are considered to be hyperfunctional (e.g. Wilson, 1987; Aronson, 1990; Boone and McFarlane, 1994; Morrison and Rammage, 1994; Andrews, 1995; Stemple at al., 1995a; Brown et al., 1996; Colton and Casper, 1996; Dworkin and Melecca, 1997). There is considerable consistency in the examples provided in these texts and controversy as to what constitutes hyperfunctional voicing is rare. The most commonly cited hyperfunctional behaviours include:

•speaking or singing with excessive loudness levels;

•speaking or singing with excessively high or low pitch levels;

•persistent use of glottal fry in speaking;

•speaking or singing with excessive intrinsic laryngeal muscle tension and constriction (e.g. hyperadduction of the vocal folds and/or ventricular folds);

•speaking or singing with excessive extrinsic laryngeal muscle tension (e.g. holding the larynx rigidly in a raised or lowered position);

•yelling and screaming;

•speaking with hard glottal attack;

•excessive coughing and throat clearing;

•crying, laughing and sneezing with excessive laryngeal muscle tension and constriction;

•phonation during effort closure of the glottis in non-speaking activities such as weightlifting.

Whether or not hyperfunctional vocal behaviours will lead to signs of vocal dysfunction such as vocal fatigue, throat discomfort, impaired voice quality, or pathological changes such as vocal fold oedema, inflammation, nodules, polyps or haemorrhage will depend on the frequency and extent or severity of the hyperfunction. Occasional throat clearing with low levels of laryngeal muscle tension and constriction, for example, is unlikely to lead to vocal impairment or vocal fold pathology. Similarly, it is likely that some of these behaviours can be used even for long periods, without resulting in voice disorders, if the individual uses a vocal technique which protects them from vocal damage. Although there is considerable controversy surrounding the use of belting in singing (see Van Lawrence, 1979; Miles and Hollien, 1990; Schutte and Miller, 1993, for example), it is clear that some singers can employ this type of high-intensity voicing with little or no ill effect (Estill, 1988). Ethel Merman, Barbra Streisand and Liza Minelli are prime examples of singers who have maintained effective voices despite the use of very loud singing.

In addition to the use of vocal techniques which are protective, it may be that certain individuals have laryngeal structures which are less susceptible than others to the negative effects of vocal hyperfunction (Child and Johnson, 1991). We are all aware of individuals who appear to be able to use potentially hyperfunctional voicing such as loud talking, yelling and screaming without developing any vocal pathology or vocal impairment. As long as three decades ago, Arnold (1962) proposed that genetically determined cellular composition of the laryngeal mucous membranes and overall configuration of the larynx may result in differing degrees of susceptibility to pathologies such as vocal nodules and polyps. More recently, Child and Johnson (1991) have suggested that genetic differences in vocal fold histology may predispose some individuals to hyperfunctionally related voice disorders. That certain people are predisposed to voice problems related to vocal hyperfunction has received some early empirical support from the landmark work of Stephen Gray and his colleagues at the University of Iowa. Gray’s investigation of the detailed structure of the vocal folds has indicated that the make-up of the basement membrane zone between the outer epithelial layer and Reinke’s space may determine susceptibility to pathologies such as vocal nodules (Gray, 1991; Gray et al., 1993).