The human voice is acutely responsive to changes in emotional state, and the larynx plays a prominent role as an instrument for the expression of intense emotions such as fear, anger, grief, and joy. Consequently, many regard the voice as a sensitive barometer of emotions and the larynx as the control valve that regulates the release of these emotions (Aronson, 1990). Furthermore, the voice is one of the most individual and characteristic expressions of a person—a “mirror of personality.” Thus, when the voice becomes disordered, it is not uncommon for clinicians to suggest personality traits, psychological factors, or emotional or inhibitory processes as primary causal mechanisms. This is especially true in the case of functional dysphonia or aphonia, in which no visible structural or neurological laryngeal pathology exists to explain the partial or complete loss of voice.

Functional dysphonia, which may account for more than 10% of cases referred to multidisciplinary voice clinics, occurs predominantly in women, commonly follows upper respiratory infection symptoms, and varies in its response to treatment (Bridger and Epstein, 1983; Schalen and Andersson, 1992). The term functional implies a voice disturbance of physiological function rather than anatomical structure. In clinical circles, functional is usually contrasted with organic and often carries the added meaning of psychogenic. Stress, emotion, and psychological conflict are frequently presumed to cause or exacerbate functional symptoms.

Some confusion surrounds the diagnostic category of functional dysphonia because it includes an array of medically unexplained voice disorders: psychogenic, conversion, hysterical, tension-fatigue syndrome, hyperkinetic, muscle misuse, and muscle tension dysphonia. Although each diagnostic label implies some degree of etiologic heterogeneity, whether these disorders are qualitatively different and etiologically distinct remains unclear. When applied clinically, these various labels frequently reflect clinician supposition, bias, or preference. Voice disorder taxonomies have yet to be adequately operationalized; consequently, diagnostic categories often lack clear thresholds or discrete boundaries to determine patient inclusion or exclusion. To improve precision, some clinicians prefer the term psychogenic voice disorder, to put the emphasis on the psychological origins of the disorder. According to Aronson (1990), a psychogenic voice disorder is synonymous with a functional one but offers the clinician the advantage of stating confidently, after an exploration of its causes, that the voice disorder is a manifestation of one or more forms of psychological disequilibrium. At the purely phenomenological level there may be little difference between functional and psychogenic voice disorders. Therefore, in this discussion, the terms functional and psychogenic will be used synonymously, which reflects current trends in the clinical literature (nosological imprecision notwithstanding).

In clinical practice, “psychogenic voice disorder” should not be a default diagnosis for a voice problem of undetermined cause. Rather, at least three criteria should be met before such a diagnosis is offered: symptom psychogenicity, symptom incongruity, and symptom reversibility (Sapir, 1995). Symptom psychogenicity refers to the finding that the voice disorder is logically linked in time of onset, course, and severity to an identifiable psychological antecedent, such as a stressful life event or interpersonal conflict. Such information is acquired through a complete case history and psychosocial interview. Symptom incongruity refers to the observation that the vocal symptoms are physiologically incompatible with existing or suspected disease, are internally inconsistent, and are incongruent with other speech and language characteristics. An often cited example of symptom incongruity is complete aphonia (whispered speech) in a patient who has a normal throat clear, cough, laugh, or hum, whereby the presence of such normal nonspeech vocalization is at odds with assumptions regarding neural integrity and function of the laryngeal system. Finally, symptom reversibility refers to complete, sustained amelioration of the voice disorder with short-term voice therapy (usually one or two sessions) or through psychological abreaction. Furthermore, maintaining the voice improvement requires no compensatory effort on the part of the patient. In general, psychogenic dysphonia may be suspected when strong evidence exists for symptom incongruity and symptom psychogenicity, but it is confirmed only when there is unmistakable evidence of symptom reversibility.

A wide array of psychopathological processes contributing to voice symptom formation in functional dysphonia have been proposed. These mechanisms include, but are not limited to, conversion reaction, hysteria, hypochondriasis, anxiety, depression and various personality dispositions or emotional stresses or conflicts that induce laryngeal musculoskeletal tension. Roy and Bless (2000) provide a more complete exploration of the putative psychological and personality processes involved in functional dysphonia, as well as related research.

The dominant psychological explanation for dysphonia unaccounted for by pathological findings is the concept of conversion disorder. According to the DSM-IV, conversion disorder involves unexplained symptoms or deficits affecting voluntary motor or sensory function that suggest a neurological or other general medical condition (American Psychiatric Association, 1994). The conversion symptom represents an unconscious simulation of illness that ostensibly prevents conscious awareness of emotional conflict or stress, thereby displacing the mental conflict and reducing anxiety. When the laryngeal system is involved, the condition is referred to as conversion dysphonia or aphonia. In aphonia, patients lose their voice suddenly and completely and articulate in a whisper. The whisper may be pure, harsh, or sharp, with occasional high-pitched squeaklike traces of phonation. In dysphonia, phonation is preserved but disturbed in quality, pitch, or loudness. Myriad dysphonia types are encountered, including hoarseness (with or without strain), breathiness, and high-pitched falsetto, as well as voice and pitch breaks that vary in consistency and severity.

In conversion voice disorders, psychological factors are judged to be associated with the voice symptoms because conflicts or other stressors precede the onset or exacerbation of the dysphonia. In short, patients convert intrapsychic distress into a voice symptom. The voice loss, whether partial or complete, is also often interpreted to have symbolic meaning. Primary or secondary gains are thought to play an important role in maintaining and reinforcing the conversion disorder. Primary gain refers to anxiety alleviation accomplished by preventing the psychological conflict from entering conscious awareness. Secondary gain refers to the avoidance of an undesirable activity or responsibility and the extra attention or support conferred on the patient.

Butcher and colleagues (Butcher et al., 1987; Butcher, Elias, and Raven, 1993; Butcher, 1995) have argued that there is little research evidence that conversion disorder is the most common cause of functional voice loss. Butcher advised that the conversion label should be reserved for cases of aphonia in which lack of concern and motivation to improve the voice coexists with clear evidence of a temporally linked psychosocial stressor. In the place of conversion, Butcher (1995) offered two alternative models to account for psychogenic voice loss. Both models minimized the role of primary and secondary gain in maintaining the voice disorder. The first was a slightly reformulated psychoanalytic model that stated, “if predisposed by social and cultural bias as well as early learning experiences, and then exposed to interpersonal difficulties that stimulate internal conflict, particularly in situations involving conflict over self-expression or voicing feelings, intrapsychic conflict or stress becomes channeled into musculoskeletal tension, which physically inhibits voice production” (p. 472). The second model, based on cognitive-behavioral principles, stated that “life stresses and interpersonal problems in an individual predisposed to having difficulties expressing feelings or views would produce involuntary anxiety symptoms and musculoskeletal tension, which would center on and inhibit voice production” (p. 473). Both models clearly emphasized the inhibitory effects of excess laryngeal muscle tension on voice production, although through slightly different causal mechanisms.

Recently, Roy and Bless (2000) proposed a theory that links personality to the development of functional dysphonia. The “trait theory of functional dysphonia” shares Butcher's (1995) theme of inhibitory laryngeal behavior but attributes this muscularly inhibited voice production to specific personality types. In brief, the authors speculate that the combination of personality traits such as introversion and neuroticism (trait anxiety) and constraint leads to predictable and conditioned laryngeal inhibitory responses to certain environmental signals or cues. For instance, when undesirable punishing or frustrating outcomes have been paired with previous attempts to speak out, this can lead to muscularly inhibited voice. The authors contend that this conflict between laryngeal inhibition and activation (with origins in personality and nervous system functioning) results in elevated laryngeal tension states and can give rise to incomplete or disordered vocalization in a structurally and neurologically intact larynx.

As is apparent from the foregoing discussion, the exquisite sensitivity and prolonged hypercontraction of the intrinsic and extrinsic laryngeal muscles in response to stress, anxiety, depression, and inhibited emotional expression is frequently cited as the common denominator underlying the majority of functional voice problems. Nichol, Morrison, and Rammage (1993) proposed that excess muscle tension arises from overactivity of autonomic and voluntary nervous systems in individuals who are unduly aroused and anxious. They added that such overactivity leads to hypertonicity of the intrinsic and extrinsic laryngeal muscles, resulting in muscle tension dysphonias sometimes associated with adjustment or anxiety disorders, or with certain personality trait disturbances.

Finally, some researchers have noted that their “psychogenic dysphonia and aphonia” patients had an abnormally high number of reported allergy, asthma, or upper respiratory infection symptoms, suggesting a link between psychological factors and respiratory and phonatory disorders (Milutinovic, 1991; Schalen and Andersson, 1992). They have speculated that organic changes in the larynx, pharynx, and nose facilitate the appearance of a functional voice problem; that is, these changes direct the somatization of psychodynamic conflict. Likewise, Rammage, Nichol, and Morrison (1987) proposed that a relatively minor organic change such as edema, infection, or reflux laryngitis may trigger functional misuse, particularly if the individual is exceedingly anxious about his or her voice or health. In a similar vein, the same authors felt that anticipation of poor voice production in hypochondriacal, dependent, or obsessive-compulsive individuals leads to excessive vigilance over sensations arising from the throat (larynx) and respiratory system that may lead to altered voice production.

Research evidence to support the various psychological y et al. (1997). The empirical literature evaluating the functional dysphonia–psychology relationship is characterized by divergent results regarding the freqmechanisms offered to explain functional voice problems has seldom been provided. A complete review of the relevant findings and interpretations is provided in Rouency and degree of specific personality traits (Aronson, Peterson, and Litin, 1966; Kinzl, Biebl, and Rauchegger, 1988; Gerritsma, 1991; Roy, Bless, and Heisey, 2000a, 2000b), conversion reaction (House and Andrews, 1987; Roy et al., 1997), and psychopathological symptoms such as depression and anxiety (Aronson, Peterson, and Litin, 1966; Pfau, 1975; House and Andrews, 1987; Gerritsma, 1991; Roy et al., 1997; White, Deary, and Wilson, 1997; Roy, Bless, and Heisey, 2000a, 2000b). Despite methodological differences, these studies have identified a general trend toward elevated levels of (1) state and trait anxiety, (2) depression, (3) somatic preoccupation or complaints, and (4) introversion in the functional dysphonia population. Patients have been described as inhibited, stress reactive, socially anxious, nonassertive, and with a tendency toward restraint (Friedl, Friedrich, and Egger, 1990; Gerritsma, 1991; Roy, Bless, and Heisey, 2000a, 2000b).

In conclusion, the larynx can be a site of neuromuscular tension arising from stress, emotional inhibition, fear or threat, communication breakdown, and certain personality types. This tension can produce severely disordered voice in the context of a structurally normal larynx. Although the precise mechanisms underlying and maintaining psychogenic voice problems remain unclear, the voice disorder is a powerful reminder of the intimate relationship between mind and body.

See also psychogenic voice disorders: direct therapy.