THE ROLE OF MANUAL LARYNGEAL TENSION REDUCTION IN DIAGNOSIS AND MANAGEMENT NELSON Roy, MCLSC CHARLES N. FORD, MD DIANE M. BLESS, PHD MADISON, WISCONSIN
Excessive activity of the extralaryngeal muscles affects laryngeal function and contributes to a spectrum of interrelated symptoms and syndromes including muscle tension dysphonia and spasmodic dysphoriia. Recognition of the role of extralaryngeal tension is helpful in ensuring proper diagnosis and selection of appropriate treatment. This report demonstrates the application of manual laryngeal musculoskeletal tension reduction techniques in the diagnosis and management of laryngeal hyperfunction syndromes. The manual technique consists of focal palpation to determine 1) extent of laryngeal elevation, 2) focal tenderness, 3) voice effect of applying downward pressure over the superior border of the thyroid Ian-dna, and 4) extent of sustained voice improvement following circumlaryngeal massage. The clinical utility of this innovative approach is discussed. KEY WORDS - circumlaryngeal massage, musculoskeletal tension dysphonia, spasmodic dysphonia.
INTRODUCTION
Excessive or "imbalanced" activity of the intrinsic and extrinsic laryngeal muscles affects phonatory function and is considered an important etiologic factor contributing to a spectrum of interrelated symdtoms and syndromes including muscle tension dysphonia (MTD) and spasmodicdysphonia(SD). 1,2 Recognitioii of the contribution of laryngeal and paralaryngeal hypertonicity is critical to proper diagnosis and selection of suitable treatments, regardless of the presumed cause of the voice disorder.
What, precisely, constitutes MTD is unclear. Certain sources have described it as a constellation of vocal symptoms combined with specific glottic and supraglottic contraction pattems.3-6 This description is contrasted with that of others, who suggest at whereas certain laryngoscopic patterns may bexuggestive ot excess muscle tension, no particular" voice quality or glottic configuration should be uniquely identified with musculoskeletal tension voice dis'orders.1 Although confusion surrounds how the disorder should be conceptualized, a recurrent feature in all descriptions is the presence of laryngeal and/or extralaryngeal hyperfunction.7
This excessive muscle activity has been attributed to many sources, including 1) psychological and/or personality factors that tend to induce tension, 2) technical misuses of the vocal mechanism in the context of extraordinary voice demands, 3) learned adaptations following an upper respiratory tract infection, and 4) compensation for underlying disease. Clinically, patients with vocal fold mucosal disease or paralysis or paresis often demonstrate coexisting muscle tension symptoms or patterns. In cases of paralysis, coexisting tension appears to be compensatory, with the patient recruiting extrinsic laryngeal muscles to assist in glottic closure. However, in cases of benign disorders, it is unclear whether the muscle tension pattern temporally preceded the development of the mucosal disease or whether the pattern represents adjustments to compensate for glottic insufficiency. Thus, it is difficult to ascertain whether such muscle tension patterns deserve causal, concomitant, or outcome status. Regardless of the origin, patients with musculoskeletal tension voice disorders usually complain of neck and shoulder tightness, excess vocal effort, and fatigue, with symptoms intensifying with extended voice use. Voice quality symptoms can vary in severity and type, ranging from severely pressed to extreme breathiness with myriad combinations.
Spasmodic dysphonia has come to be regarded as a focal laryngeal dystonia. Others have described it as a syrnptom complex with multiple causes, both neurological and psychological. Despite efforts to improve assessment techniques, the diagnosis continues to be based on auditory-perceptual assessment of vocal symptoms, and to be corroborated by voice therapy failure. As with most dysphonias, SD represents a composite of many elements. Excessive extralaryngeal tension superimposed on the underlying dystonic symptoms can complicate the clinical presentation. This diagnostic predicamentis further compounded by the capacity of musculoskeletal tension voice disorders to masquerade as SD. Therefore, accurate diagnosis and optimal management of these disorders can be accomplished only be defining the contribution of generalized hyperfunction to the dysphonia. Removing the effects of excessive tension or muscle imbalance affords the clinician a more precise representation of the voice disorder.
In this regard, numerous voice-facilitating techniques are designed to relieve tension in the laryngeal region. Unfortunately, little objective evidence exists to support the superiority of one technique over another, making it difficult tojudge the cause of voice therapy failure. Failure may be due, at least in part, to techniques that do not yield sufficient laryngeal tension reduction. Recognizing this, Aronson described and advocated the manual laryngeal musculoskeletal tension reduction technique (also known as circumlaryngeal massage) as a direct method to assess and treat laryngeal hyperfunction syndromes. He suggested that chronic posturing of the larynx in an elevated position leads to cramping and stiffness of the hyoid-laryngeal musculature, which contributes to the cause of many dysphonias. He submitted that indirect tension reduction techniques often fail because of the stubborn nature of excess laryngeal musculoskeletal tension. Manual repositioning (lowering) of the larynx by kneading the circumlaryngeal area was offered as the primary approach to reduce tension. Our clinical and research experienced with this and related manual techniques has confirmed their clinical utility as valuable diagnostic and treatment tools. This paper describes the use of manual laryngeal techniques in the identification and management of laryngeal hyperfunction syndromes. METHODS
Techniques for Diagnosis and Prognosis. When using manual circumlaryngeal assessment and treatment techniques, the patient should be educated regarding the untoward effects of excessive musculoskeletal tension on voice, and the possibility that such tensions may underlie some or all of the patient's dysphonia. The sensitivity of the larynx to stress, emotion, and other sources of tension should also be addressed. If, during the inter-view, additional insights regardingcausation areuncovered, amore complete discussion of the voice-anxiety-tension relationship is appropriate. The patient should appreciate that voice disorders are an aggregate of multiple factors, including potential psychological influences. This understanding is important to maintaining normal voice following successful management. Adjunctive psychological counseling and support may also be indicated.
In most cases in which excess laryngeal musculoskeletal tension has persisted for some time, the larynx is suspended high in the neck and the hyoidlaryngeal sling is extremely stiff. Patients commonly report excess effort expended to produce phonation, as well as a dull to severe ache and tightness of the laryngeal region and anterior neck. Clinicians can assess the contribution of excess tension by evaluating the consequences of tension reduction and laryngeal repositioning on voice quality. The degree of voice improvement appears related to the amount of tension reduction. Reduced pain, reduced focal tendemess or modularity, increased thyrohyoid space, and improvement in voice confirms the contribution of poorly regulated muscle tension to voice function.
Musculoskeletal tension can be appraised manually by palpation of the circumlaryngeal area to assess the degree, nature, and location of focal tendemess or modularity (tension) and/or pain in the laryngeal region. Pressure is directed 1) over the major homs of the hyoid bone, 2) over the superior cornu of the thyroid cartilage, and 3) along the anterior border of the stemocleidomastoid muscle and into the suprahyoid musculature, including the posterior belly of the digastric muscle. Focal sites of tension evoke discomfort or pain when pressure is applied. Patients may wince or withdraw (the "jump" sign) when trigger points are identified. This exquisite tenderness in response to pressure in the laryngeal region is considered abnormal. The discomfort is more often unilateral than bilateral, and may radiate to one or both ears. The mobility of the larynx is also tested by attempting to maneuver it side-to-side along the horizontal plane. Resistance of movement is indicative! of generalized extralaryngeal hypertonicity. Excessive tension can also be detected in the suprahyoid region (ie, mylohyoid, geniohyoid, and anterior digastric), especially during upward pitch gliding (see Figure, A).
The extent of laryngeal elevation is assayed by palpating within the thyrohyoid space from the posterior border of the hyoid bone to the thyroid notch. A narrowed or absent thyrohyoid space is highly suggestive of excess muscle tension whereby the larynx is suspended high in the neck. In some patients asked to sustain a vowel at a comfortable pitch and loudness, further laryngeal elevation may occur in synchrony with voice initiation, signalling recruitment of extrinsic muscles. This type of laryngeal "bobbing" is a frequent concomitant of adductor SD.
Manual laryngeal tension reduction. A) Medial suprahyoid musculature is palpated at rest and during upward pitch glide maneuvers. Focal sites of tenderness and tautbands signal excessive muscle activity. B) Signs of excess laryngeal tension are assayed by 1) evaluating presence of focal sites of pain or modularity, 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 (circuralaryngeal 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.
Further information regarding inappropriate laryngeal posturing and muscle
misuse can be derived by assessing the voice effects of three manipulations: 1)
physically impeding elevation of the larynx by applying downward traction over
the superior border of the thyroid lamina (see Figure, B); 2) compressing the
larynx by exerting anterior-to-posterior (A-P) pressure over the inferior border
of the hyoid bone to reduce excess tension and therefore stiffness of the vocal
folds (see Figure, C); and 3) applying combined medial compression and downward
traction over the superior cornu of the thyroid cartilage.
Laryngeal reposturing or repositioning through brief displacement or by resisting laryngeal elevation provides valuable information regarding potential for improved voice function as well as possible causal mechanisms. By manually stabilizing the larynx, the clinician may stimulate improved voice and briefly interrupt patterns of muscle misuse. These brief moments are immediately identified for the patient and are reinforced. They can be shaped by using digital cueing combined with tension-reduction techniques, to be discussed in the next section. Digital cues can then be faded and the patient taught to rely on sensory feedback (auditory, kinesthetic, and proprioceptive) to maintain improved laryngeal posturing and muscle balance. Manually moving the larynx to a neutral position stimulates easier phonation.
Techniques for Treatment. The manual tension reduction procedure can be undertaken according to the technique of Aronson. The hyoid bone is encircled with the thumb and index finger, which are then worked posteriorly into the tips of the major horns of the hyoid bone. Pressure is applied in a circular motion over the tips of the hyoid bone. The procedure is repeated within the thyrohyoid space, beginning from the thyroid notch and working posteriorly. The posterior borders of the thyroid cartilage medial to the stemocleidomastoid muscles are located and the procedure is repeated there (see Figure, B,D). With the fingers over the superior border of the thyroid cartilage, the larynx is pulled downward and, at times, moved laterally. Sites of focal tenderness, modularity, or tautness are given more attention. Gentle kneadin or sustained pressure may be focused over these sites and then released. In general, the procedure is begun superficially, and the depth of massage is increased according to the degree of tension encountered and the tolerance of the patient. It may be necessary to extend the technique into the medial and lateral suprahyoid musculature. During the above procedures, the patient is asked to sustain vowels or to hum while the cliniciar, notes changes in vocal quality. Improvement in voice and reductions in pain and laryngeal height suggest a relief of tension. The improved voice is shaped from vowels to words, phrases, sentences, and paragraph recitations, and then to conversation. Progress can plateau at any point in the treatment, but recovery takes on its own momentum. Improvements with these techniques often proceed in a nonlinear fashion. Once sufficient tension has been released and the patient assumes a more normal laryngeal posture, progress can be swift, with complete amelioration of the dysphonia. Signs of improvement should be observed within the first session. Some patients may require an extended, intensive treatment session or several sessions, depending on patient tolerance and rate of progress. Generally, if changes do not occur within two sessions, it is unlikely that extralaryngeal muscle tension is the primary or sole explanation for the observed dysphonia. Patients with SD, rather than MTD, may derive short-term benefit from manual techniques; recovery, however, is incomplete and difficult to sustain. The residual dysphonia more accurately reflects the true laryngeal dystonia.
From our series of over 150 cases, the following examples illustrate the use of manual techniques in the assessment and treatment of laryngeal hyperfunction syndromes.
Case 1: Musculoskeletal Tension Dysphonia. A 45-year-old elementary school teacher presented with a year-long history of dysphonia that had begun gradually following upper respiratory tract infection symptoms. Her dysphonia progressively worsened over this period, with no episodes of improved voice. She failed to respond to a 4-week period of voice therapy at a local hospital prior to her referral to our facility. Upon indirect laryngoscopy and videolaryngostroboscopic examination, her larynx was found to be structurally normal, with no evidence of mucosal disease. Noticeable stiffness of both vocal folds was observed, with moderate supraglottic constriction in both the A-P and medial-lateral directions. During a psychosocial interview, the patient denied acute situational conflicts or an increase in life stress preceding the onset of the dysphonia. The patient's vocal quality was described as severely strained-strangled, with frequent voice arrests characteristic of SD. Palpation of the laryngeal region identified focal sites of intense pain over the major homs of the hyoid bone. Although pain was reported bilaterally, it was perceived to be greater on the left side and to refer to the left ear. The larynx was not only sensitive to light pressure, but was also excessively rigid, resisting manual lateral movements. The thyrohyoid space was noticeably narrowed, suggesting laryngeal elevation. Circumlaryngeal massage over the sites of tension and pain was under-taken, and normal voicing was reestablished over a single extended treatment session. The patient reported a relief of tightness and pain concurrent with voice improvements. She was reassessed approximately 1 month later with no evidence of recurrence.
Case 2: Spasmodic Dysphonia. A 35-year-old receptionist reported a 10-month history of gradually deteriorating voice. She complained of increased effort to produce voice, with significant vocal fatigue. She reported feelings of depression, which she attributed to her communication difficulties. Her dysphonia was characterized as pressed-strained, with an abrupt, staccato-like quality consistent with adductor SD. Palpation of the circumlaryngeal area revealed a large thyrohyoid space, with mild tenderness over the superior comu of the thyroid cartilage. Downward traction on the larynx produced no observable improvement in voice quality. The larynx was mobile laterally. These findings were considered minimal in terms of extralaryngeal tension. A trial of manual laryngeal tension reduction administered over three consecutive sessions was successful in alleviating the tenderness in the laryngeal region. Although modest, transient improvements in voice were detected, they could not be stabilized or generalized. A diagnosis of neurological adductor SD with mild reactive tension was offered. The patient was referred forbotulinum toxin injection and responded well. She continues to receive periodic injections with impressive results. She attends a voice disorders support group.
Case 3: Spasmodic Dysphonia With Muscle Tension Dysphonia. A 50-year-old woman had a 4-year history of botulinum injections for SD, with variable but generally favorable results. However, the patient developed an unremitting severe dysphonia (bordering on aphonia) that persisted for 6 months and did not respond to three successive botulinum treatments. A videolaryngostroboscopic examination confirmed the recurrence of hyperkeratotic mucosal changes of the right vocal fold and evidence of posterior laryngitis consistent with laryngopharyngeal reflux. Both vocal folds were extremely stiff and phonation was accompanied by noticeable supraglottic valving. Upon palpation of the paralaryngeal area, the patient complained of significant tightness and pain. Focal sites of modularity were identified. The thyrohyoid space was minimal. The entire hyoidlaryngeal sling was extremely tense and fixed. Downward traction over the superior comu of the thyroid cartilage resulted in immediate improvement in voice production. The mucosal changes were judoed to be insufficient to explain the severity of the patient's voice disturbance. The patient was considered to have a severe musculoskeletal tension component contributing to her dysphonia. She was submitted to a week-long period of twice-daily therapy sessions, combining multiple voice therapy techniques administered by several clinicians. The voice disorder remained resistant to all indirect tension-reduction techniques. Following intense circumlaryngeal massage, the patient achieved an approximation of normal voicing despite persistent laryngeal mucosal abnormalities. She encountered difficulty in stabilizing these improvements beyond the therapy room. She has been instructed in the self-administration of these manual techniques.
It was speculated that the cause of her extreme laryngeal and extralaryngeal hypertonicity was related to attempts to compensate for both mucosal changes and her underlying dystonic symptoms. These difficulties, combined with concurrent stressful life events and a tendency in this individual for anxiety to manifest in the musculoskeletal system, were sufficient to generate MTD superimposed on mild SD symptoms. In this case, when the deleterious effects of excess muscle tension were stripped from the dysphonia, the clinician was better able to appreciate the consequences of both the vocal fold mucosal changes and the underlying dystonia. DISCUSSION
Manual techniques, including circumlaryngeal massage, augment the voice practitioner's diagnostic and treatment armamentarium. Given the potential for musculoskeletal tension disorders to coexist with and mimic neurological SD, it is exceedingly important for diagnosticians to appreciate the effects of poorly regulated laryngeal and paralaryngeal tension. Such recognition can avoid unnecessary medical or surgical intervention. These manual techniques can assist in identifying and recognizing the role of laryngeal and extralaryngeal hyper-tonicity in the perceived voice disturbance. During palpation, the presence of laryngeal pain and tenderness, stiffness, and elevation should raise the index of suspicion for the existence of excessive musculoskeletal tension. The inf luence of abnormal muscular tensions (ie, nondystonic) can be verified by the patient's positive response to diagnostic therapy using laryngeal reposturing techniques such as circumlaryngeal massage. By identifying neurological SD patients who also present with generalized laryngeal hypertonicity, clinicians can also interpret suboptimal responses to botulinum treatments and prospectively advise a therapy regimen combining manual laryngeal tension reduction (or some other behavioral approach to reduce tension) with botulinum injections.
In summary, our clinical and research experience with this technique leads us to agree with Aronson's contention that all patients with voice disorders, regardless of cause, should be assessed for the presence of excess laryngeal musculoskeletal tension, either as a primary or as a secondary cause of the dysphonia. Manual laryneal techniques serve as important procedures in ensuring proper diagnosis of and selection of appropriate treatments for both MTD and SD.
REFERENCES
1. Aronson AE. Clinical voice disorders:an interdisciplinary approach. 3rd ed. New York, NY: Thieme, 1990.
2. Greene M, Mathieson L. The voice and its disorders. 5th ed. London, England: Whurr, 1989.
3. Morrison MD, Nichol H, Rarnmage LA. Diagnostic criteria in functional dysphonia. Lar-yngoscope 1986;94:1-8.
4. Moriison MD, Rammage LA, Gilles MB, Pullan CB. Harriish N. Muscular tension dysphonia. i Otolarynool 1983; 12:
5. Morrison NM, Rammage L. Muscle misuse voice disorders: description and classification. Acta Otolaryngol (Stockh) 1993;113:428-34.
6. KoufmanJA,BlalockPD.Classification and approach to patients with functional voice disorders. Ann Otol Rhinol Laryngol 1982;91:372-7.
7. Hillman RE, Holmberg EB, Perkell JS, Walsh M, Vaughn C. Objective assessment of vocal hyperfunction: an experimental framework and initial results. J Speech Hear Res 1989;32:37392.
8. Rammage LA, Nichol H, Morrison MD. The psychopathology of voice disorders. Hum Commun Canada l987;11:215.
9. Ludlow C, Hallett M, Sedory S, Fujita M, Naunton R. The pathophysiology of spasmodic dysphonia and its modification by botulinum toxin. In: Berardelli A, Benecke R, Manfredi M, Marsden C, eds. Motor disturbances. 2nd ed. Orlando, Fla: Academic Press, 1990:274-88.
10. Marsden C, Sheehy M. Spastic dysphonia, Meige's disease, and torsion dystonia. Neurology 1982;36:446-70.
11. Schaefer S. Neuropathology of spasmodic dysphonia. Laryngoscope 1983;93:1183-204.
12. Blitzer A, Brin M, Fahn S, Lovelace R. Clinical and laboratory characteristics of laryngeal dystonia: a study of I 10 cases. Laryngoscope 1988;98:636-40.
13. Sapir S. Psychogenic spasmodic dysphonia: a case study with expert opinions. J Voice 1995;9:270-81.
14. Cooper M. Treating spasmodic dysphonia with direct voice rehabilitation. Advance 1993;3:6-7.
15. Boone DR, McFarlane S. The voice and voice therapy. 4th ed. Englewood Cliffs, NJ: Prentice Hall, 1988.
16. Reed CG. Voice therapy: a need for research. J Speech Hear Disord 1980;45:157-69.
17. Roy N, Leeper HA. Effects of the manual laryngeal musculoskeletal tension reduction technique as a treatment for functional voice disorders: perceptual and acoustic measures. J Voice 1993;7:242-9.
INTERAMERICAN ASSOCIATION OF PEDIATRIC OTORHINOLARYNGOLOGY
The biannual meeting of the Interamerican Association of Pediatric Otorhinolaryngology will be held in Sao Paulo, Brazil, September2l-24,1997. For information, contact Office of the Secretary, Tania Sih, MD, PhD, Rua Itapeva, 366, Suite 102,01332-000, Sao Paulo SP, Brazil; telephone 55 11 283-4645 or 283-3396; fax 55 11 826-9652 or 542-6037.
From the Department of tolaryngology-Head and Neck Surgery, UniversiryofWisconsin-Madison,Madison, Wisconsin.Mis workwas supported by the National Center forvoice and Speech through grantP60 00976 from the National Institute on Deafness and Other Communication Disorders.
Presented at the meeting of the American Laryngological Association, Orlando, Florida, May 4-5, 1996.
CORRESPONDENCE - Nelson Roy, MClSc, Dept of Otolaryngology-Head and Neck Surgery, F4/214 Clinical Science Center, 600 ffighland Ave, Madison, WI 53792-2436.