By Andrea Bianchino, student of
The voice is a place of communication and creativity, the meeting point of inner life and the external world. It is also a fine and complex human phenomenon whose physical aspects can be understood using scientific devices. However, its grey areas are rooted in the chasm of the individual’s emotions and can only be known by crossing the threshold of the irrational. Everybody’s inner wounds can be limitless and deep. Only a few can process their pain, sublimating it into creative power and regenerative potential. Others, instead, easily fall prey to their emotions, so they end up boycotting themselves. Their failure to overcome their psychological issues may find expression in their voice. Therefore, voice disorders can either be organic and functional or psychic.
When a voice disorder has a psychic origin (Psychogenic Dysphonia) it is hard to diagnose. By and large, it is a stable picture of voice alteration that does not find a precise or sufficient aetiology for its expression in the physical and biochemical situation of the patient. It is expressed in different forms – aphonia, use of falsetto and modification of the vocal tract postures. Patients with Psychogenic Dysphonia are always unaware that their symptom is self-induced, even though they sometimes take into the analytical setting their interpretation of the symptom’s psychosomatic evolution and origin.
A particularly emotional moment in people’s lives can cause distraught, which increases respiratory activity and muscular tension (also on a laryngeal level). When discomfort or painful sensations are experienced at the same time, for example when a traumatic event is taking place (e.g., drowning), the difficulty in making sounds can become a symbolic behaviour expressing a psychic conflict. In other words, the larynx and the voice become the organ and the function authorized to convey an emotional conflict through a dysfunction (i.e., dysphonia), or a prohibition (i.e., aphonia or mutism). The interplay of the above-mentioned elements makes it difficult to establish whether the treatment should be physical, psychological or both.
Psychogenic disorders of the voice have not been adequately studied. Most of the research has been carried out by speech therapists and ENTs. No data have been provided by psychologists and neuroscientists. The cost and availability of functional neuroimaging (i.e., fMRI, SPECT, PET, EEG), together with the amount of time required to collect the data necessary to create a clinically useful sample, hinder the use of functional neuroimaging. There have been few validated reports about the correlation between psychometric tools and functional neurology. Therefore, in the present article, psychogenic dysphonia, its symptoms, diagnosis and prognosis, are tackled by resorting to a multidisciplinary approach.
Psychogenic dysphonia may present a number of symptoms. The voice can be harsh, breathy or whispered, it can be euphonic but interspersed with abrupt shifts into falsetto or be produced continuously altering its register1-8. It can also appear as accompanied by phonatory fatigue leading to aphonia and mutism, thereby involving the articulatory function. The clinical picture may appear abruptly or follow an inflammatory episode, it can set in after an episode of dysphonia-aphonia or after alternating episodes of the latter and normal voice1-3.
The duration of the disorder can vary a lot and may be described as a transient episode in the anamnesis during an examination following a relapse. It can go on for a few days9,10 and it can disappear spontaneously before it is even possible to deploy any therapeutical device/strategy.
Most patients seek medical attention after a few weeks dysphonia has set in, and they can only be treated after being entrusted to a speech therapist1-3. Half of these cases present further symptoms that cannot be interpreted according to an organicist model. The most frequent and relevant among such symptoms is phonatory fatigue, together with breathlessness, pharyngolaryngeal paraesthesia, sensation of lump in the throat, mouth dryness, neck pain and respiratory difficulty4-8.
At the onset of a symptom, the patient frequently reports sometimes an inflammatory episode (real or alleged) other times a negative event (illness, surgery, death of a close relative) or, eventually, difficulty in communication within their relationships. Only seldom are these symptoms spontaneously connected by the patients with psychological problems1-3. In any case, the existence of traumatic events commonly emerges in a more or less conscious way during the course of speech therapy.
Le Huche (1994) described two vocal quality types: complete and incomplete aphonia. In complete aphonia, the voice is only whispered, sometimes with sporadic and instantaneous high- frequency sound emissions. Incomplete aphonia is instead characterised by moments of whispered voice abruptly alternating with moments of normal voice production1-3,11. Moreover, it shoes a continuum of vocal alterations spanning from a completely whispered voice to a scarcely intense one, no matter whether high or low-pitched. All these variations convey a sense of fatigue and sound unnatural1-3.
Regardless of the vocal quality produced, all the subjects with psychogenic dysphonia present a great tension of the extrinsic laryngeal musculature12, a common denominator of all functional dysphonia forms. However, in the psychogenic type, this common trait assumes a severity that equals the seriousness of the symptoms. The external inspection of the neck is quasi-negative. However, palpation may reveal some hypertonicity of the extrinsic and para-cervical laryngeal muscles generated by the recruitment of the intrinsic musculature in the attempt to provide additional forces meant to compensate for the imbalance between vocal necessities and potentialities of the subject1-3.
The evaluation of muscle tension includes:13
– Identification of the location of the thyroid shield in the neck and palpation of its excursion during swallowing (high laryngeal anchoring and poor mobility are indirect signs of tension in the suprahyoid muscles).
– Palpation of the suprahyoid muscles with light digital pressure in the submental region up to the hyoid bone, both at rest and during phonation.
– Acupressure pain in the major horns of the hyoid bone, pain in the thyroid cartilage’s edge, in its upper horns, posterior edges and anteriorly to the sternocleidomastoid muscle14-18 (Aronson’s sign).
– Palpation of the sternocleidomastoid muscle.
– Palpation of the thyrohyoid space and, if needed, manoeuvre to lower the larynx according to Aronson.
Aronson’s manoeuvre is accomplished by placing the thumb and index finger on the upper edge of the thyroid cartilage, anteriorly to its upper horns, and gently moving the larynx downwards with small laterocaudal movements until the increase of the thyrohyoid space is felt and improvement of the vocal quality is perceived when the patient is producing a prolonged vowel.
Before proceeding further ahead it will be worth mentioning that literature on the same subject does not provide as much contribution to the instrumental assessment of the voice, because presently it is not yet possible to depict a spectrographic or electroglottographic portrait typical of psychogenic dysphonia1-3.
The variability of the symptomatology negatively conditions the possibility of defining an electrophysiological regulation in psychogenic voice disorders20,21. Likewise, there is no regulation for the electromyographic investigation, which is in any case frequently performed for medico-legal purposes to rule out any neuromuscular pathology affecting the vocal organ1-3,21,22.
The hypertonicity of the extrinsic and para-cervical laryngeal muscles leads to the lifting of the larynx (followed by the weakening of the thyroarytenoid muscle), to poor flexibility in the laterolateral movements and to lack of control of the thyroid shield tilt both during phonation and direct manipulation1-3.
During the examination it is important to proceed both with the endoscopic investigation by stroboscopy and by perceptive evaluation of the signal. Spectral and acoustic analysis programs can also be used, since they can corroborate symptoms’ objectivity. To this purpose, using a flexible trans-nasal fiberscope while the patient is producing posterior vowels is highly recommended. Anterior vowels (such as /ī/) favour instead examination with rigid optics. In fact, despite the forward movement of the epiglottis and the rising of the larynx that anterior vowels cause, they also facilitate chordal adduction. Therefore, in the case of a patient with severe phonasthenia, just to mention an example, they could produce confusing results.
Instrumental semiotics could resort to electromyography, but this test is often rejected as particularly invasive. Usually, the test performed is therefore a general neurological examination in which particular care is devoted to cranial nerves and reflex functions (pharyngeal and swallowing reflexes). Laryngeal inspection, still necessary, points out a normal morphology and no pathologies in the vocal folds. Sometimes it is possible to detect a mild inflammation of the vocal folds’ free edge, but this proves inconsistent with the severity of the symptoms1-3,11.
Other important characteristics of which the patient is not always aware, because they are experienced as different from pure phonation, are the presence of a cough or sonorous laughter1-3. When these signs are present, they signal psychogenic dysphonia. Another rarely detectable yet very specific sign was investigated by Formigoni et al.2. It is the normalization of the quality and intensity of the voice when patients are exposed to a masking noise interfering with their auditory monitoring system to the point that they lose control of their voice (Lombard’s test)1-3,11.
Neurogenic forms of dysphonia caused by paralysis or paresis may mimic psychogenic forms of dysphonia. In this case, it is useful to perform a spectrographic test to ascertain the nature and the frequential positioning of the inter-harmonic noise.
As for the perceptive analysis, it is important to consider all aspects that are inconsistent with organic pathology, e.g., the appearance of brief episodes of physiological phonation when the constant control needed for the symptom production fails unexpectedly.
Euphonia is often present after a prolonged silence when the patient, at the very beginning of voice production is not yet able to use the acoustic feedback and can only rely on proprioception. Other times it is possible to detect other symptoms that are always incompatible with organic dysphonias: greater sonority at the end of a phrase in breathy voices, glottal sound onsets alternating with breathy ones, symptoms of phonasthenia alternating with hard attacks without signs of supraglottic hypertonia, erratic nasalization of a phoneme followed by normal production of oral consonants. Euphonia during non-communicative voice production as while yawning, sighing or spontaneously laughing may signal a psychogenic substratum.
Conversely, the presence of sonority in induced coughing in a subject with aphonia does not signal psychogenic dysphonia. Coughing recruits the stabilizing function of the larynx through thoracic fixation. Therefore, it does not only require the adduction of the intrinsic system (thyroarytenoid, cricoarytenoid and interarytenoid muscles) but can also be accompanied by postural raising of the glottic plane, forward movement of the tongue, which provide extra adduction and allow to overcome even severe phonasthenia. However, the cough test is almost always positive, even though it is not pathognomonic of the psychogenic aetiology and shows normal sonority. Its importance is therefore limited to psychogenic forms expressed through non-hyperkinetic aphonia and non-pressed whispered voice.
In these forms, there is no hypertonia of the supraglottic structures but only a transglottic air leak, which demonstrates that unlike organic dysphonia, which is always accompanied by a hypertonic compensation attempt, in this case, the psyche unconsciously excludes the use of the glottis.
Since psychogenic dysphonia is the symptom of an inner malaise, voice alterations are frequently accompanied by mannerisms, i.e. stylized and stereotyped brief mimic, postural and respiratory actions which are iterated in particular situations. They can be classified as follows4,6,8:
– Vocal mannerisms: vocalised interjections, (in speech, moaning, sighing, and prosodic intonation) inconsistent with the communicative needs, inspiratory sounds, insistent and unmotivated raclage, inspiratory phonation.
– Phonoarticulatory mannerisms: alterations of phoneme production consisting of excessive emphasis on distinctive traits, hyper-labialization, excess or reduction of the articulatory force, rhinolalia, hypo-articulation of the tongue, etc.
– Linguistic mannerisms: linguistic stereotypes, expression unrelated to the meaning conveyed by the speech, repetitions of the adverb ‘no’ or others like ‘so’, ‘naturally’, ‘sure thing’, repetition of phrases meant to coordinate thoughts, e.g., ‘just, ‘well’, ‘I mean’ etc.
– Facial expression mannerisms: excessive articulation of facial expression, rolling of the eyes, eyelid closure, unmotivated lateralization of labial articulation.
– Postural mannerisms: rotation or inclination of the head, protrusion of the jaw, alterations in vertical alignment, lifting of the shoulders and exaggerated gesticulation.
– Functional mannerisms: forced and repetitive swallowing, unmotivated cough, regularly and periodically repeated raclage in significant communicative situations.
Other signs of discomfort may concern involuntary and rapid movements of the face and body muscles (blinking, eyelid tremor, orbicular contracture, excessive stabilization of the jaw with reduced oral opening, excessive postural rigidity or emphasis and excessive self-solicitation through self-referential gestures such as stroking one’s own face, rubbing one’s limb against the other, etc.)1-8.
The absence of objective organic pathologies, the subject’s denial of their psychic disturbance, the coexistence of vocal alterations of dysfunctional origin, the presence, even in healthy subjects, of small alterations of the vocal apparatus, the small epidemiological incidence and the lack of a method for the ENT and speech therapist to relate to psychic pain, can make the diagnosis of psychogenic pathology very complex.
The diagnosis of psychogenic dysphonia is often linked mainly to an immediate perceptual assessment that occurs during the first meeting with the patient: the qualitative characteristics of their voice, phonation fatigue and attitude towards one’s disorder are unequivocal.
Laryngeal dynamics are still a subject of scientific discourse. Some scholars (Luchinger and Arnold23) describe distinct pictures of marked chordal hypotonia associated with laryngeal vestibule hypertonia and concealment of the glottic plane. These scholars divide psychogenic dysphonia in hypo and hyperkinetic types. Others9,14-18,24-26, in a number of works, describe it as an anomalous behaviour of the vocal cords that oscillates between the most disparate functional pictures: hyperadduction of the false cords of medium or tight degree (sphincter) with or without concomitant hyperadduction of the true vocal folds; initial hyperadduction of the vocal folds with displacement and subsequent inter-medialization without effective vibration; hypo- adduction of the vocal cords with marked glottic ovality; tremors of the folds during the abduction. However, some authors14,21,25,27 also underline that what can be observed often varies remarkably not only from examination to examination (even when performed after short intervals of time) but also during the span of time of one examination.
In the case of the paradoxical and adaptive mutation, as Italian scholar Magnani5 has defined them, subjective symptoms include a sense of tension in the neck, constriction, difficulty swallowing and air hunger. Vocal symptoms relate to fatigue, difficulty in managing the voice in noisy environments, higher than normal frequency phonation according to sex and age, transglottal air leak, loss of glottal timbre, tense quality of the voice, untimely chordal abduction, reduction of intensity dynamics and vocal breaks4-8. Objective signs include phonation during laryngeal elevation, accompanied by different degrees of thyroid tilt, reduced amplitude of phonoarticulation movements due to stabilization of the mandible at the cranial base and scarce mobility on palpation of both the hyoid bone and of the thyroid shield. These symptoms must be distinguished from the phases of the physiological vocal change. Initially, there is a perceptively apparent decrease in the average F0 in conversation (due to the increase of the chordal mass and the maturation of the adductor muscles), tone darkening obtained using resonators (lengthening of the vocal tract) and supraglottic air leak (adduction deficit)4-8. When voice mutation reaches its acme, it presents vocal instability, register breaks and shifts into falsetto because neuromuscular coordination can prove difficult on the dimensionally and histologically new structure that has developed4-8.
Upon inspection, the paradoxical voice change shows mandibular stabilization during mouth opening, reduction of articulatory movements and postural alteration resulting in positioning the head either forward or upwards. On palpation, it reveals a reduction in the mobility of the glottic plane (which is elevated at the onset of phonation), cranial stabilization of the hyoid bone, reduction of the thyrohyoid space and reduced laryngeal descent during inspiration. The high-pitched quality of the voice in the male voice change does not necessarily signal discomfort and it is obtained to counteract the perception of vocal maturation, it is often resorted to for the sole purpose of stabilizing the functioning of the adductor system. Therefore, it is not appropriate to interpret as psychogenic all the forms of the extremely high-pitched voice of a child who does not wish to become and adult4-7.
When the above pathology occurs in the adult patient as a physical decompensation, the subject’s suffering is caused by the unreliability of their voice rather than by its quality, to which they have long been accustomed. Their request to recover their health may not concern, in fact, the return to an average F0 suitable for conversation according to gender and age and to adequate management of the resonators.
Differentially diagnosing an adaptive form from a paradoxical one is very complex, especially because the discomfort that the patient with the paradoxical form felt as a pre-adolescent has long been resolved and what the clinician can observe during the examination is often due only to the postural alteration and phonasthenia, now lacking dysphoric correlates, In other words, the clinician is faced with what remains, that is the consequences of a malaise that is no longer there4-6,8. The patient, however, although no longer suffering as during their adolescence, experiences their vocal image with discomfort and a certain degree of secondary suffering, both for their high-pitched voice quality, which does not match their age and physical appearance and for the ineffectiveness of their asthenic voice4-6, 8.
The differential diagnosis of psychogenic clinical pictures is achieved after comparison with pathologies that can perceptually mimic the acoustic manifestation of psychogenic dysphonia. Such pathologies are the following1-8:
Phonasthenia: condition of the subject where the voice is characterized by a tired, energy- deprived and difficult production, poor timbre, intense air leak, reduced frequency and intensity modulation. Phonasthenia is often concomitant with hyperventilation, which helps sustain phonation. It is also accompanied by a decrease in the maximum phonatory time which, in turn, brings about a decrease in the duration of phrases. Phonasthenia is a pathology that can have a multifactorial aetiology and is often determined by surmenage leading to fatigue of the thyroarytenoid muscle and adduction deficit6,8.
Sulcus: this is an invagination of the chordal mucosa near Reinke’s space and can involve the epithelium up to the vocalis muscle. Perceptually speaking, the item presents dispersion of transglottic flow due to adductor incapacity and intensity deficit. Mechanically speaking, phonation takes place using postural falsetto or it is based on the stable hypertonia of the cricothyroid muscle. In this pathology, modulation is difficult. The frequency shift towards high notes requires massive air leaks and signals energy dispersion. Dynamics are lost and the phonatory duration decreases due to the increase of the transglottic flow and the reduction of glottal resistance. The spoken voice is usually characterized by a light timbre. Chronic stabilization of the falsetto attitude can lead to contraction deficit of the thyroarytenoid muscle and consequent phonasthenia6,8.
Paresis or paralysis of the vocal cords: these pathologies can be congenital or acquired, unilateral or bilateral and can be linked to brain diseases or damage of the vagus nerve (whose function, among others, is to keep the larynx open) or the recurrent nerve (inferior laryngeal nerve), i.e., the branch of the vagus nerve that innervates all intrinsic muscles of the larynx except the cricothyroid muscle. Unilateral paralysis is often a consequence of esophageal, cardiovascular or mediastinal surgery. The involvement of both vocal cords is instead more frequently linked to congenital diseases of the central nervous system or trauma. In some cases, it is not possible to identify the cause of the paralysis, which can also depend on viral agents (idiopathic forms). Phonation mode is falsetto or functional hypertonia either of the cricothyroid muscle or of the supraglottic tract. If not compensated for by the contralateral chord or by assuming a paramedian position, it presents flow dispersion associated with air leakage and laryngeal elevation. It comes across with difficult modulation in terms of intensity and frequency, it can present diplophonia, lightening of timbre and interharmonic noise6,8.
Neurogenic pathologies: these are several pathologies that can indirectly affect the larynx either by central or peripheral affection. They have accompanying neurological signs such as dysphagia, tremor, loss of oral coordination, pharyngeal sensitivity deficit etc. The differential diagnosis must also distinguish them from the hypokinetic dysarthria of parkinsonism, in whose early form the monotone and breathy voice may not be accompanied by its other characteristic manifestations (articulatory and prosodic alterations). Mixed dysarthria due to degenerative diseases, such as amyotrophic lateral sclerosis, can begin with a breathy and gurgling voice alternating with a tense voice before hypernasality and other disorders, both articulatory and prosodic, become detectable6,8. Very breathy voice or aphonia: first of all, it is necessary to rule out lesions of the recurrent and the superior laryngeal nerves through indirect laryngoscopy or laryngo-stroboscopy. Insignificant laryngeal objectivity and a breathy voice must make the clinician suspect myasthenia gravis, especially if progressive vocal decay appears during a prolonged sound emission often associated with increased nasality and articulatory alterations1-3. Laryngeal dystonia, voice tremor and spasmodic dysphonia, which also need a differential diagnosis, since they all show clinical and semiotic aspects very similar to psychogenic dysphonia. In these cases, the instrumental evaluation of the voice, the perceptual analysis, the clinician’s experience and a neurological evaluation are of the essence for the differential diagnosis1-3. There are conditions affecting other organs that may eventually affect the voice. To achieve differential diagnosis such pathologies must be excluded too – hypothyroidism, diabetes, eating disorders, allergies, iatrogenic pathologies due to medications and deficiency diseases (vitamins, amino acids, etc.).
A strained or harsh voice, not secondary to laryngeal pathology or destructive surgery performed on the larynx, may suggest spasmodic dysphonia due to pseudobulbar, ataxic or choreic dysarthria, especially if sudden increases in the intensity and frequency of the F0 alternate with tremor or a monotone voice. However, vocal alterations in these clinical pictures are often accompanied by other articulatory or motor signs typical of the primary pathology1-3.
The diagnosis of conversion dysphonia may also involve mutism, which is the maximum disability limit reached in the case of voice conversion disorder. In this case, patients cannot produce a breathy voice nor articulate words; other times, articulation, is not accompanied by expiratory airflow. These patients often communicate with the help of a notepad and a pencil, but then they involuntarily reveal a normal vocal ability showing a sonorous cough (cough test). Writing relieves a person of the emotional aspects entailed in voice production and makes it difficult to infer the emotional status of the subject. These patients often present with chronic stress, indifference to the symptom (typical of somatization disorders), other manifestations of conversion, poor sexual identification, suffocated anger, immaturity, dependence, neurotic adaptability to life, and mild or moderate depression. Although these individuals are different from each other, each of their stories is underpinned by common denominators:
– The conflict between what they would like to express and what they are allowed to – anger, fear or remorse;
– Failure to communicate something important to someone;
– Fear and shame in expressing one’s feelings through conventional speech and language14-18.
A study carried out by Aronson et al.,18 compared patients with mutism and aphonia with patients suffering from various forms of dysphonia to determine their aetiological differences or similarities in their symptoms. He pointed out that in terms of personality, history of the disease and clinical criteria relating to the conversion reaction, the group of dysphonic subjects was not essentially different from the group of patients with mutism and aphonia18.
As in cases of mutism, patients with aphonia or dysphonia have medical histories showing both acute and chronic emotional distress, loss of voice with symbolic meaning, indifference towards their vocal incapacitation and the presence of conversion reactions both in other areas of their bodies and in different moments of their lives. Additional reports in this study are emotional immaturity, neurotic adaptation to life, and mild to moderate depression.
The diagnosis of psychogenic dysphonia can have a great impact on the emotional sphere of a subject. Especially in cases of conversion, the diagnosis is never a process based only on signs and symptoms but is also filtered through the interpretation of the clinician. Therefore, it is necessary to be linguistically cautious and not to ‘sentence’ the patient with a disorder4,6,7. The clinician should perform a detailed analysis of both the old and recent history of the patient, then proceed with a perceptual evaluation, inspection and palpatory assessment of the larynx and the cervical district, then with the screening of the predominant symptoms, an endoscopic examination and finally, if necessary, a spectro-acoustic analysis and electromyography. Having excluded objective pathologies through the collected signs and symptoms, both organic and dysfunctional, one can then proceed with the interpretation of the collected data, the psychiatric consultation and with sharing their conclusion4,6,7.
The diagnosis is not only achieved because no dysfunctional and/or organic causes have been identified, but rather because the histories of the patients have been interpreted and their psychic disorders or inner sufferings have been acknowledged4,6,7. For this purpose, a narrative approach to the patient is necessary one in which the specialist bends down and put themselves on the same level as the patients. Not looking down on them but rather sharing the same perspective. This attitude shows that the clinician is not only interested in signs and symptoms, but rather in the patient as a person, as the bearer of a story of illness. During an examination, this behaviour does not exclude the search for objective signs, nor does it neglect the value of medical evidence. It rather repositions the doctor and the patient on the same level and provides them with a shared meaning of what is happening.
In conclusion, the laryngological diagnosis is carried out on the exclusion of causal organic pathologies and the anamnestic interpretation, while the psychiatric diagnosis is formulated on the recognition of signs of mental illness. During the first medical examination, it is already possible to pursue both behavioural and emotional therapeutic results, (the examination is but the first step in the therapeutic process) through manipulation manoeuvres. The relevant literature reports different interpretations of this idea from different schools. The pragmatic manoeuvres of manually lowering the larynx and of exerting pressure on the cricothyroid space can in a short time (20-30 minutes) bring the patient back to a normal voice. As already explained, even Lombard’s deafening test gives an immediate sign of functional recovery of the voice since, due to the abrupt noise suppression, the patient emits an acceptable voice. However, some rehabilitation schools of thought believe that it is not advantageous to suppress the symptom and revitalize the speech function before the triggering cause has been dealt with, since a relapse may occur. In addition, the therapeutic strategies deployed may surprise patients, frighten them or even hurt their modesty. Certainly, in the diagnostic act these manoeuvres do not resolve the problem, or rather, they simply mask a discomfort that may resurface in a different form (symptom substitution).
Finally, it is also worth evaluating both the biochemical effects on the microscopic structure and the organ’s biological functions induced by exogenous factors such as drugs, vitamin deficiencies and comorbidities. In the anamnesis, thence in the diagnosis, it is essential to focus not only on any biochemical causes that can give a paradoxically negative clinical picture in anatomical terms but also on tangible internal problems of the speech apparatus. Some of the symptoms described by patients may be the consequence of drug use, concomitant systemic diseases and possible lack of organic catalysts with bio-regulatory functions.
The rehabilitation perspective can follow different procedures and lines of thought. It is possible to distinguish five trends inevitably reflected in both evaluation and rehabilitation.
The first is the aetiology-oriented approach, which considers many alterations of the voice as the consequences of behaviours that damage the laryngeal structures. The elimination of such behaviours produces improvement in speech and a very low relapse rate. Once the behaviours that damage the voice have been identified, the elimination of triggering factors is encouraged, and new behaviours are adopted, to re-establish the instrument’s physiology. However, this does not eliminate the real cause of dysphonia, which can therefore resurface.
The second is the psychogenic approach. This approach tries to associate the disturbance with the underlying emotional cause of the behaviour producing the voice disturbance. The psychogenic approach to voice problems, initiated by Aronson25, encourages the identification and elimination of emotional and psychosocial problems associated with the initiation or maintenance of the vocal problem. It also highlights that understanding the emotional history on which dysphonia is based can inform the clinician about the components of the subject’s emotional behaviour and argues that if the emotional or psychological component is removed, the vocal problem should disappear. The criticism of this type of rehabilitation approach is that the understanding of the subject’s emotional dynamics does not guarantee healthy vocal production. Furthermore, patients can become anxious and fear that they would not be able to achieve better vocal production16.
The third is the symptomatic approach, which was codified by Daniel Boone28. The author argued that direct modification of semi-proper or altered symptoms, components and/or parameters of the voice was the way to perform voice rehabilitation. This type of approach caresses the idea that it is necessary to alter and change the symptoms, or even make them disappear, regardless of what happens in the physiology of the patient. Most forms of dysphonia are caused by malmenage and surmenage. In cases of dysfunctional dysphonia, the direct modification of symptoms can offer immediate results, but these are generally transient because they come from a practical aspect, namely the execution of voice gestures, rather than from a long-lasting learning approach28,29. Therefore, patients become experts at performing vocal exercises, but do not generalize and cannot utilise the skills acquired during therapy in everyday life.
The fourth type of approach is the physiological one. It is the most recent trend followed to tackle dysphonia and it is used in all countries where the science and practice of the voice is very advanced. In the United States it has been in use for 35-40 years. This approach focuses on reshaping the physiology of the voice. Just like the symptomatic approach, it works on the systems involved in voice production, but with an opposite focus, namely interaction. It does not work in a segmented or sequenced way, it does not tackle symptoms, but rather the physiology underlying the symptoms.
Let’s suppose that a patient has impaired breathing, a constricted larynx with obvious palpable, visible and audible tension, or that they have a breathy or raspy voice; these symptoms originate from the altered balance of their voice production system as a whole. Once the correct interaction between the parts of the system has been re-established, breathing, tone and intensity will normalise and the hard sound onset will disappear. In other words, physiologic therapy tackles the same parameters as symptomatic therapy but with an overall view, a dissimilar perspective and a different philosophy of vocal rehabilitation.
The fifth therapeutical approach is Eclectic Vocal Therapy. It recommends combining all the above approaches in order to produce vocal change. The greatest advantage of this therapeutic philosophy is its large number of resources available for the treatment of dysphonia, but it can confuse the scarcely expert therapist. In addition, the patient may be bombarded by an excessive number of techniques and approaches without obtaining a good result or obtaining it after an excessive and unnecessary number of therapy sessions30.
Most voice therapists resort to the eclectic approach, but other peculiar choices can be made according to the pathology, aetiology, context and type of patient. The choice of the suitable rehabilitation approach is not only a matter of taste and style, it involves ethical issues.
The relevant literature suggests that the therapy for treating psychogenic problems of the voice should turn to both a symptomatic approach carried out by the speech therapist and to a psychological approach. Historically speaking, both have been influenced by the prevailing doctrines and by the differences in the cultural and experiential backgrounds of the scholars who followed them.
The most recent contributions in the literature recommend symptom-centered rehabilitation work but they do not always agree on priorities in the therapeutic management of the patient. Some authors17,31-33 see the speech therapist as the person who should take over the treatment and decide whether the vocal therapy can or cannot go on without the contribution of the psychotherapist. Others23,34-36, instead, prefer a combined treatment in which the speech therapist and the psychotherapist tackle the vocal pathology collaboratively, though independently from each other, thus achieving together the final solution to the problem.
In the author’s opinion, assessing who comes first or whose prerogative it is to treat a patient is not an essential matter. It is instead seminal to keep in mind that the sensation of not being able to produce a better voice is experienced by patients as real, and, in this respect, they should be supported and guided with exercises for the control of pneumo-phono-articulatory coordination and for the de-contraction of the laryngeal extrinsic muscles. At the same time, it is necessary to deal with their new voice until they are convinced that they can produce more voice than they think.
Therefore, both the therapeutic gesture of the clinician and the work of the speech therapist must be used to reassure the patient about the inorganic (therefore not final) nature of their illness by guiding them indirectly and with due verbal caution towards a functional-psychological interpretation of their problem.
Most authors agree that after the resolution of dysphonia the displacement of conversion symptoms to other organs rarely occurs. Conversely, there is no agreement on the incidence of relapses in the same patients. With or without the involvement of a psychotherapist, psychogenic dysphonia therapy is in any case a journey into the symptom meant to make patients aware of what is happening to them and to teach them how to master the physiological mechanisms of phonation.
Tackling symptoms manually can be the first step towards their exploration. The manual therapy performed by the speech therapist, namely the circumlaryngeal massage by Aronson, is useful for the treatment of hyper-functional dysphonia, in which one can observe a growth of the intrinsic and extrinsic muscles of the larynx and even the involvement of the pharyngeal constrictors and neck muscles. This manoeuvre aims to briefly interfere with the bad motor patterns acquired over time, remove tension in the tense laryngeal and pharyngeal muscles thus improving their flexibility, correct any asymmetry, diminish phonatory fatigue, encourage a correct neuro-muscular pattern, make the sensation of cricopharyngeal bar disappear and improve swallowing. The removal of tension may be obtained through passive stretching (the patient breathes normally) or dynamic stretching (voice exercises and swallowing).
Laryngeal manipulation finds application in musculotensive dysphonia of various etiologies (hyperkinetic or compensatory), in spasmodic dysphonia, in post phono-surgery, in dysphonia forms due to unilateral chordal paralysis and in psychogenic forms of dysphonia (including paradoxical dysphonia)11,37. At the endoscopic level, manifestations that have a manipulative indication include rigid mediolateral contraction of the glottic and/or supraglottic tract, anteroposterior glottic and/or supraglottic compression, posterior glottic fold and slanting of the vocal cords. At the palpatory level, the execution takes place on a seated patient, at vocal rest and with the back of the head supported in a neutral position. The hand of the person who performs the massage should form a horseshoe. Thumb and index finger are positioned on the greater hyoid horns, then on the superior horn of the thyroid cartilage, in the thyrohyoid space and along the anterior edge of the sternocleidomastoid muscle15,38-42.
This allows the examination of:
– The high positioning of the larynx through palpation of the thyrohyoid space (lower margin of the hyoid bone and thyroid cartilage notch;
– Working around the hyoid bone using the thumb and index finger exerting a posterior circular pressure right on the apexes of the posterior horns of the hyoid bone.
– Repeating the same manoeuvre in the thyrohyoid space and posteriorly.
– Identification of the posterior margins of the thyroid cartilage medial to the sternocleidomastoid muscle and repetition of the procedure.
It is fundamental that while these manoeuvres are being performed that the patient vocalises a sustained ‘a’ and that their breathing is calm. In itself the manoeuvre consists of11,15:
– Hyoid Pushback. During the production of sustained ‘a’, an anteroposterior pressure is exerted above and below the hyoid bone.
– Pull Down. This is performed through a downward pull on the upper edge of the thyroid cartilage lamina.
– Combined manoeuvres. Points one and two are performed together. This third point proves particularly useful in cases of non-adductive hyperfunctioning.
Evidence of the effectiveness of this treatment comes from different investigative methods, first of all from its perceptual evaluation. In the studies of Roy, Bless and Leeper40,42 96% of patients were evaluated and improvement was acknowledged. Almost two-thirds of all patients acquired a normal voice after one treatment session. A total of 68% of patients who initially responded to manual therapy reported early, partial, or severe relapses in the follow-up phase (<2 months after treatment). For some patients, greater results may be obtained when manual laryngeal techniques are combined with supportive counselling and/or more frequent clinical support. Before treatment, 88% of patients reported pain and/or tenderness in the laryngeal region during palpation. During and immediately after the manual procedure, most patients reported a gradual laryngeal pain reduction. The advantage of manual techniques cannot be isolated from other phonatory treatments. The improvement of the voice with manual circumlaryngeal therapy is correlated with the lowering of the laryngeal position and the muscle tension decrease it brings about.
In the above studies, the mechanical coupling of the supraglottic tract, articulatory structures and larynx was also investigated. It revealed that freeing the larynx and the hyoid bone could have potentially desirable effects on articulation. The techniques used seem to benefit both sub-systems, as evidenced by the improvement of conversation speed and joint flexibility. Through fMRI, the change in neural activation in response to patterns created by MTD-related stressors was evaluated39,42.
These models emphasize the inhibitory effects of laryngeal muscle activity on voice production and how life stressors or interpersonal difficulties stimulate internal conflicts which, in turn, are channelled into musculoskeletal tension. Specifically, the characters that play a fundamental role are the ‘behavioural inhibition system’ (BIS), which includes a large group of neural structures such as the cingulate cortex, amygdala, hypothalamus, and periaqueductal grey matter. The septum- hippocampal system and the amygdala also play key roles within the BIS.
Two parallel ways of voice control were considered:
– The limbic control pathway (anterior cingulate cortex ACC) – PAG – up to the motor neurons;
– The laryngeal cortical motor pathway (from the sensorimotor cortex to motor neurons);
The laryngeal motor cortex has bidirectional connections to the cingulate cortex and integrates signals from the prefrontal cortex, insula, putamen, and thalamus for voice and language. Hence, the limbic vocal pathway controls involuntary and voluntary vocalizations by playing a role in the pathogenesis of musculoskeletal disorders. The fMRI evaluation carried out before laryngeal manipulation shows increased activity, especially at the level of PAG, hypothalamus, ACC and hippocampus, as compared to the post-manipulation evaluation. A reduction in the amygdala and hypothalamus (bilaterally) and in the right hippocampus also appeared after manipulation.
Current neuroscience concepts postulate that psychogenic symptoms, including conversion ones, can arise from brain networks involved in processing emotions. Chronic uncontrollable stress is associated with a profound alteration of neural responses in the amygdala and prefrontal cortex. Research on post-traumatic stress disorder (PTSD) indicates that pathological disruptions in this circuit could be a common denominator in the damaging effects of stress on brain functioning.
Burke et al.11 carried out a study on 10 patients with sensory conversion disorder using fMRI, to better define the functional neuroanatomical correlates of the conversion disorder. They observed activation of the paralimbic cortices, of the temporoparietal junction (TPJ) and the suppression of cortical sensory function. The authors also commented on TPJ activation, arguing that this area has a role in multiple high-level cognitive functions such as self-management, theory of mind, sensory integration, and attention. They concluded that the somatosensory system seemed to be suppressed by the emotional centres. Ejareh and Kanaan summarized functional neuroimaging research on conversion disorder, including fMRI, Single Photon Computed Tomography (SPECT), and Positron Emission Tomography (PET)11. They concluded that all studies showed the presence of abnormalities in the neural regions, namely those relevant to the processing of emotions and emotional motor processes, together with the presence of abnormal emotional-motor connectivity and lack of habituation. They identified mechanisms that differed from those operating in feigned MTD and healthy controls. Their studies also imagined the differences in the processing of traumatic life events. Recalling events believed to be of aetiological significance (for conversion) was associated with a type of brain activation similar to that participating in the process of memory suppression. Furthermore, it was associated with brain activation in the supplementary motor area (SMA) and in temporoparietal junction (TPJ), both plausible sites of symptom production. As cited by Broeckle et al., Perez and colleagues provided a systematic overview of conversion disorder imaging studies in order to investigate the neuroanatomical regions involved in motor conversion disorders11.
They concluded that areas relevant to motor planning, motor selection, or autonomic response were particularly important. They proposed several explanatory models of brain function: “disrupted inhibitory capacity with dysfunction of the motor and primary somatosensory cortexes; modifications of the voluntary-intentional abilities with dysfunctions in the prefrontal areas; impaired attention based on dysfunction of the anterior cingulate gyrus, parietal associative cortex, striatum and thalamus”. Broeckle summarised all the analyses and argued that the brain’s emotional, motor planning, and inhibitory processing regions show function abnormalities in motor conversion disorders. Additionally, the review corroborated the similarities found in patients diagnosed with PTSD and dissociative experiences.
Spengler examined two fMRIs performed on female patients before and after voice therapy for conversion dysphonia. Both patients experienced complete symptom resolution after circumlaryngeal massage. During symptoms, both patients showed increased activity in the medial prefrontal regions and reduced emotional reactivity in the amygdala combined with greater connectivity between regions. Spengler hypothesized that these patients may have initially gained control over their negative emotional state via frontally pre-mediated top-down control, which successfully reduced negative emotions and the associated amygdala activity. However, in the long run, such exaggerated control may have disrupted the integrity of the amygdala-prefrontal cortex circuit leading to loss of function, namely of the voice. In 2019, Dietrich et al. studied vocally healthy individuals through fMRI during a stress-induced public speaking protocol11. Subjects also completed a personality questionnaire; they were assigned a negative emotional status rating scale and were requested to provide salivary cortisol samples. There were individual differences in stress- induced brain activations measured by cortisol activity. Higher cortisol levels were associated with lower laryngeal motor cortex activity and lower scores on extroversion scales. Indeed, the key areas associated with exposure to voice control stressors occurred in areas secondary to speech control. The authors reported inactivation of the anterior cingulate cortex (ACC), middle cingulate cortex (MCC), insula, putamen, and thalamus. The authors considered the results critical for interpreting the disordered processes underlying central voice control and psychobiological measurements (cortisol, fear, personality).
From a pragmatic point of view, it is very simple to use a symptomatic rehabilitation tendency in dysphonias with psychogenic aetiology, because the mechanisms triggered to transfer pain can be easily decompensated. The laryngeal manipulation consisting of the manual lowering of the glottic plane makes falsetto impossible, vocalizations mimicking a sobbing voice and the exercises for the retraction of the false vocal folds reduce hypertonia right above the supraglottic plane and therefore it is very simple to teach the patient a new adductive compensation mechanism that does not entail rigidity of the vocal folds’ mucosa. However, the problem with this type of approach is that the reduction of the symptom or its containment does is not tantamount to healing from what triggered it and does not entail the acquisition of any awareness of the function and meaning that such a symptom expression had for the patient11.
In this type of therapy, it is important to evaluate all the psychosocial aspects following a functionalist perspective. An example of this could be an oncological patient who starts a dysphonic mechanism with a psychogenic aetiology to express their psychic pain. Such a reactive symptom is indicative of the patient’s inner world. Manipulative therapy may help restore the communicative function between the patient and the environment; it can be used both during cognitive-behavioural psychotherapy and in a more pragmatic perspective during Gestalt therapy, in which experience is the starting point to produce a change. Unfortunately, the vocal disorder is often the only symptom that the patient shows to the outer world. Just as the diagnosis must include both organic and psychic aspects, the therapy must approach the patient holistically. How and when a patient should experience their euphonic voice and be encouraged to preserve it, is a process requiring a multidisciplinary team including an otolaryngologist or speech therapist, a psychiatrist, and a psychotherapist. Furthermore, the appropriate therapy should be chosen depending on the severity degree of the disorder: in the case of conversion dysphonia, the symptom is always exhibited in response to a traumatic or painful event; the therapeutic recall of such an event, if necessary, must be conducted with the most appropriate psychotherapeutic tools.
Voice is a functional voluntary medium through which the patient expresses informative content and verbal messages, as well as the image of themselves, their identity, and their bodily self. If the patient explicitly requests to have their voice restored, symptomatic therapy can be conducted: the doctor must make a correct diagnosis, excluding organic and biochemical causes; the speech therapist must assist the patient in both mechanical and proprioceptive rehabilitation; the psychiatrist and psychotherapist must guide them towards the awareness and resolution of the aetiology. “Curing” the symptoms can resolve the dysfunction; however, the risk is that the disorder finds another way of manifesting itself. Insofar as this risk is concerned, the majority of authors agree that resolved conversion disorders do not convert into another symptom. There are two rehabilitative orientations: the first is based on a symptomatic view that implies the resumption of normal euphony through manipulation; the second is based on psychotherapeutic treatment. However, from a psychological point of view, it is not clear which of the two orientations is the most effective and provides the best outcome for the patient. On one hand, the fact that the voice has been ‘found’ but the cause has not been cured, may open new therapeutic possibilities for the patient and within the framework of a brief strategic/cognitive-behavioural therapy, the new experience may change the patient’s perception of their inner discomfort and resolve it. On the other hand, there is the psychoanalytical approach that aims to get to the root of the inner conflict and can dissolve the patient’s need to trigger the symptomatology conversion mechanism. According to the psycho-dynamic perspective, once the primary causes are resolved, dysphonia disappears. However, this is not always true because when the conversion symptom becomes an integral part of the patient’s vocal habitus, the neuro-motor deviation may persist. That is when speech therapy is required. The therapeutic choice must be evaluated on an ad hoc basis: American schools of thought prefer a symptomatic approach, whilst their Italian counterparts prefer to begin with a psychotherapeutic intervention.
Psychogenic dysphonia comprises a large group of voice disorders that express mental illness through the soma. Despite numerous improvements in its classification, diagnosis and therapy, the literature about this disease shows enormous confusion; in turn, clinical application devotes little attention to it. Within this nosological category, numerous aetiologies are classified by available manuals as a factitious disorder, illness anxiety disorder, somatic symptom disorder, body dimorphism disorder and conversion disorder.
In the treatment of this pathology, the role of laryngologists, ENTs, neurologists and psychiatrists may overlap. After all, the organic and functional symptoms (even the non-apparent ones) that may alter the functioning of the Central Nervous System and the Peripheral Nervous System have been detected, each specialist must decide whose prerogative the treatment of such symptoms must be. Signs and symptoms can be difficult to assess, and they may not be unanimously objective because one symptom may be the external expression of several underlying disorders.
The clinician may find himself disoriented in the search for cause-and-effect relationships between the psyche and soma. This causes high rates of diagnostic errors and a tendency to disregard the problem. In addition, psycho-cognitive disorders may also overlap with one another, which makes the identification of causes and solution strategies a difficult process. Furthermore, psychogenic dysphonia forms related to one’s individual development (adaptive voice mutation and paradoxical voice mutation) and gender, thus creating clinical pictures that can be easily confused with other pathologies (e.g., asthma) and multifactorial syndromes related to the musculoskeletal system (muscle-tension dysphonia).
A big issue to be resolved concerns terminology. In different countries and different schools of clinical vocology, pathologies and similar views on them are expressed with different terms, whereas similar words are sometimes used to indicate pathologies with different aetiology. Nowadays, the terminological problem could explain the lack of clinical attention to the issue and the lack of clarity in the scientific literature. In addition, the multitude of symptoms, e.g., aphonia, breathy voice, sudden changes of register, alteration of the fundamental frequency, alterations of the vocal tract attitude, the stable clinical pictures of the disorders and the coexistence of organic pathologies, can induce the clinician to resort to different therapies while forgetting the holistic approach the human being deserves.
Other diagnostic and classification problems concern instrumental accuracy. A low-resolution endoscopy, for example, may not highlight some organic problems (e.g., a small sulcus). These, combined with behavioural traits, may corroborate a psychogenic diagnosis when no organic and distinctive sign appear. Other diagnostic problems relate to the lack of multi-specialist training. Surgeons often limit themselves to analysing only the anatomy, clinicians observe the functioning, leaving out psychic aspects whereas psychiatrists lack the skill to deal with organic evidence. Patients often struggle to express their inner discomfort, so a weary voice due to exhaustion (phonasthenia) can be easily mistaken for psychogenic dysphonia.
Other neurological pathologies, such as paralysis, may ensue from iatrogenic or infectious causes without any apparent evidence. Furthermore, dysphonia forms based on a deficiency (e.g., vitamins essential amino acids, etc.) or on drug use (side effect) are difficult to investigate, since the chemical elements involved cause microscopic and biochemical defects that cannot be detected even by the most accurate diagnostic methods and can therefore be pinpointed only through a thorough anamnesis. The only possible approach to minimize diagnostic errors, guide the patient towards effective treatment and lead them to complete recovery is a narrative approach combined with careful listening to the patient. This approach puts the clinician and the patient on the same level and allows a profound and ergonomic relationship.
Therapy too is prone to different approaches based on different philosophies, from manipulation to pharmacological treatments, from psychotherapy to symptomatic treatments of various kinds.
1. Bergamini G., Fustos R., Casolino D., Inquadramento delle disfonie in “Le disfonie: Fisiopatologia clinica ed aspetti medico-legali”. Relazione ufficiale LXXXIX congresso nazionale S.I.O., 2002, 97-112.
2. Formigoni P, Zecchini B, Spinelli E, A. Caroggio, LXXXIX Congresso Nazionale, San Benedetto del Tronto, Le disfonie: fisiopatologia, clinica ed aspetti medico legali.
3. Forini M., Farabollini B., Pennacchi A., Napoletano A., Vocal Cord Dysfunction, Inquadramento delle disfonie in “Le disfonie: Fisiopatologia clinica ed aspetti medico-legali”. Relazione ufficiale LXXXIX congresso nazionale S.I.O., 2002.
4. Magnani S., Curare la voce, Franco Angeli Editore, 2015, 2a edizione, Milano.
5. Magnani S. Il bambino e la sua voce. 122-139, Franco Angeli, 1999.
6. Magnani S., Le disfonie psicogene, Creative Commons Attribuzione, Settembre 2018.
7. Magnani S., Vivere di voce, Franco Angeli Editore, 2016, Milano.
8. Magnani S., Fussi F., Ascoltare la voce, Franco Angeli Editore, 2008, Milano.
9. Andreasen NC, Bardach J. Dysmorphophobia: symptom or disease? Am J Psychiatry, 1977;134:673-5.
10. Asprella Limonati G, Minnini G. Il disturbo di voce come sintomo di disagio psichico nell’adolescenza. Acta Phon Lat 2000;22:43-60.
11. Linehan, M. Trattamento cognitivo-comportamentale del disturbo borderline. Raffaello Cortina Editore, 2011, Milano.
12. Morrison MD, Rammage LA. Muscle misure voice disorders: description and classification. Acta Otolaryngol 1993;113:428-34.
13. Schindler A, Gilardone M, Spadola Bisetti M, Di Rosa R, Ottavini F. L’esame obiettivo nella sindrome disfonica. Acta Phon Lat 2000;22:355-63.
14. Aronson, AE. Clinical Voice Disorders: An Interdisciplinary Approach (3 ed.). 1985, Mishawaka, IN, U.S.A: Published by Thieme-Stratton Corp.
15. Aronson AE. Disturbi da conversione vocale, in “I disturbi della voce: metodologia clinica ed interdisciplinare”, 141-175, 1985, Masson.
16. Aronson AE. Trattamento dei disordini specifici della voce. In “I disturbi della voce: metodologia clinica ed interdisciplinare”, 224-263, 1985, Masson.
17. Aronson AE., I disturbi della voce. 1985, Masson Italia Editori, Milano.
18. Aronson AE, Peterson HW. Ja., Litin EM. (1966), Psychiatric symptomatology in functional dysphonia and aphonia. J. Speech Hear. Dis., 31: 115-127.
19. Downing EJ, Braman SS, Fox MJ, Corrao W. Factitious asthma, physiological approach to diagnosis. J Am Med Assoc 1982;248:2878-81.
20. Watson BC, McIntire D, Roark RM, Schaefer SD. Statistical analyses of electromyographic activity in spasmodic dysphonia and normal control subjects. J Voice 1995;9:3-15.
21. Canals Ruiz P, Villoslada Prieto C, Marco Peiro A, Lopez Catala F, Peris Beaufils JL. Electromyographic study of psychogenic dysphonias. Acta Otorrinolaringol Esp 1998;49:400-3.
22. Lacy TJ, McManis SE. Psychogenic stridor. Gentile Hosp Psychiatry 1994;16:213-23.
23. Luchsinger R., Arnold G.E. Voice Speech Language, Wadsworth Publishing Company, inc, 1965, Belmont, California.
24. Brugman SM, Neuman SK. Vocal cord dysfuction. Medical/Scientific Update 1993;11:1-6.
25. Gallivan GJ, Hoffman L, Gallivan KH. Episodic paroxismal laryngospasm: voice and pulmonary function assessment and management. J Voice 1996;10:93-105.
26. Hayes JP, Nolan MJ, Brennan N, Fitzgerald MX. Three case of paradoxical vocal cord adduction followed up over a 10 year period. Chest 1993;104:678-80.
27. American Psychiatric Association. Diagnostic and Statistical Manual of Mental Disorders. 3th Ed. Revised. DSM-III-R. Washington DC: APA 1987.
28. Boone, D., McFarlane, S. The Voice and Voice Therapy. (4 th ed.). 1988, New Jersey (NJ), USA: Prentice Hall, Englewood Clis.
29. Boone, D., McFarlane, S., Berg, SL. The Voice and Voice Therapy. (7 th ed.). 2005, Boston USA: Allyn and Bacon.
30. Stemple, J., Glaze, L., Klaben., BG. Clinical voice pathology: theory and management. 2000, 3rd Singular Publishing Group, San Diego, USA.
31. Andersson K, Schalen L. Etiology and treatment of psychogenic voice disorder: results of a follow-up study of thirty patients. J Voice, 1998;12:96-106.
32. Baker J. Psychogenic dysphonia: peeling back the layers. J Voice 1998;12:527-35.
33. Le Hulche F, Allali A. La voix. Tome 2. Paris: Masson 1990.
34. Butcher P. Psychological processes in psychogenic voice disorder. Eur J Disord Commun 1995; 30:467-74.
35. Millar A, Deary IJ, Wilson JA, MacKenzie K. Is an organic/functional distinction psychologically meaningful in patients with dysphonia? J Psychosom Res 1999;46:497-505.
36. Ricci Maccarini A, Bergamaschi M. La riabilitazione con psicoterapia. In: Galletti G “La riabilitazione delle insufficienze glottiche e neoglottiche”. Acta Otorhinolaryngol Ita 1990; 10:254-7.
37. Koufman, J.A., Blalock, P.D. Vocal fatigue and dysphonia in the professional voice user: Bogart-Bacall syndrome. Laryngoscope 1998,98:493–499.
38. Lieberman, J. Principles and techniques of manual therapy: application in the management of dysphonia. 1998. In T. Harris, S. Harris, J. S. Rubin, D. M. Howard (Eds.), “The voice clinical handbook” (pp. 91–138). London: Whurr Publishers.
39. Roy, N., Bless, DM. Manual circumlaryngeal techniques in the assessment and treatment of voice disorders. Curr Opin in Otol Head Neck Surg 1998,6:151– 155.
40. Roy, N., Bless, D. M., Heisey, D., Ford, C. N. Manual circumlaryngeal therapy for functional dysphonia: An evaluation of short and long-term treatment outcomes. Journal of Voice 1997,11:321–331.
41. Roy, N., Ford, CN., Bless, DM. Muscle tension dysphonia and spasmodic dysphonia: The role of manual laryngeal tension reduction in diagnosis and treatment. Annals of Otol, Rhino, and Laryng 1996,105:851–856.
42. Roy, N., Leeper, HA. Effects of the manual laryngeal musculoskeletal tension reduction technique as a treatment for functional voice disorders: Perceptual and acoustic measures. Journal of Voice 1993,7:242–249.
43. Tasko, SM., Roy, N., Harvey, S. Using manual laryngeal tension reduction techniques with benign mucosal disorders. Paper presented at the convention of the American Speech- Language-Hearing Association, 1994, New Orleans, LA.
AUDIOLOGY RECENT POSTS
RECOMMENDED FOR YOU