Clinical detection, evaluation, and management of voice tremor require an ... language pathology evaluation and management of individuals with vocal tremor.
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Julie Barkmeier-Kraemer 1 University of Utah, Salt Lake City, Utah, VSA
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Clinical detection, evaluation, and management of voice tremor require an understanding of the underlying pathophysiology. The purpose of this chapter is to contribute clinically relevant background and information to guide the speechlanguage pathology evaluation and management of individuals with vocal tremor.
Tremor is indicated by the observation of involuntary rhythmic oscillation of structures (Crawford & Zimmerman, 2011; Elble, 2016; Louis, 2016). Pathologic tremor is diagnosed and characterized by the rate and amplitude of the tremor as well as patterns of onset and progression and associated neuropathology (e.g., Parkinson disease, essential tremor, dystonia) (Hallett, 2014; Weiss, 2016). An important tremor classification trait is determining whether tremor activation is a resting- versus actioninduced tremor. For example, individuals diagnosed with Parkinson disease (PD) most typically exhibit a resting tremor. That is, tremor onset occurs once musculature is not voluntarily activated, such as when a hand is supported against gravity while resting on a surface, or in the person’s lap. In contrast, an individual diagnosed with essential tremor (ET) is characterized by an action tremor. That is, the tremor is activated during voluntary muscle contraction associated with posturing or moving limbs.
Vocal tremor is a neurological voice disorder that occurs in isolation, or associated with other neurological disorders such as ET, PD, dystonia, cerebellar degeneration and stroke (Sulica & Louis, 2010; Wolraich et al., 2010). Vocal tremor was described in 1949 (Critchley, 1949) as a “quavering type of speech” due to tremor affecting muscles of speech structures (e.g., lips, tongue, larynx, and diaphragm). Several studies have documented the association of vocal tremor with oscillatory movements of the tongue (Bove et al., 2006; Gamboa et al., 1998; Jiang et al., 2000; Lester et al., 2013; Sulica & Neurolaryngologie
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Louis, 2010), larynx (Ackermann & Ziegler, 1991; Bove et al., 2006; Finnegan et al., 2003; Gamboa et al., 1998; Koda & Ludlow, 1992; Sulica & Louis, 2010; Tomoda et al., 1987), pharyngeal constrictors (Bove et al., 2006; Lester et al., 2013; Sulica & Louis, 2010), soft palate (Bove et al., 2006; Gillivan-Murphy et al., 2016; Panda et al., 2013; Sulica & Louis, 2010), and respiratory musculature (Hachinski et al., 1975; Tomoda et al., 1987). Despite the association between oscillating speech structures and vocal tremor, measures of rate and amplitude of speech structure oscillations corresponding to vocal tremor have not been systematically evaluated. A physiologic conceptual model of vocal tremor was proposed regarding the hypothesized contributions of the respiratory, phonatory, and articulatory structures of the speech mechanism (BarkmeierKraemer, 2010) (see Table 1). The overarching premise of this model is that tremor affecting specific structures of the speech mechanism results in predictable modulation patterns of the acoustic output perceived as vocal tremor. For example, oscillation of the respiratory musculature would cause rhythmic expansion and compression of the chest wall and lungs resulting in modulation of lung pressure during phonation. Modulation of lung pressure is hypothesized to cause sound pressure level (SPL) modulation. Similarly, oscillation internal to the phonatory system is hypothesized to contribute to vocal tremor in two ways. (1) Intrinsic laryngeal muscles contributing to lengthwise oscillation of the vocal folds during phonation (i.e., shortening and lengthening) are hypothesized to cause fundamental frequency (fo) modulation. (2) Intrinsic laryngeal muscles contributing to abduction-adduction oscillation of the vocal folds (i.e., opening and closing) are hypothesized to cause SPL modulation. Finally, oscillation of speech articulators will modify the length (e.g., lips, vertical oscillation of the larynx) and the diameter (i.e., dilation and constriction) of the vocal tract. Such oscillations are hypothesized to associate with modulation of formants 1 (F1) and 2 (F2) resulting in modulation of SPL. A series of studies have been completed to test the physiologic conceptual model of vocal tremor with evidence thus far supporting hypothesized contributions of the respiratory (LeBaron, 2016) and articulatory structures (Ji et al., 2014; Lester et al., 2013).
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Table 1 – Physiologic conceptual model of vocal tremor. Oscillating speech structures
Tremor physiology
Acoustic correlate
Respiratory Chest wall/lungs
Rhythmic expansion and compression of the lungs
Modulation of SPL
Phonatory Vocal fold abduction/adduction Vocal fold length changes
Rhythmic opening and closing of the vocal folds Rhythmic elongation and shortening of the vocal folds
Modulation of SPL Modulation of f0
Articulatory Laryngeal vertical oscillation Pharyngeal and oral tract diameter changes
Rhythmic lengthening and shortening of the vocal tract Rhythmic dilation and constriction of the vocal tract
Modulation of F1 and F2
Brown and Simonson (1963) described vocal tremor in a patient cohort as exhibiting “rhythmic alterations of pitch and, particularly, of loudness of vowels and continuant consonants in each word.” The rhythmic modulation of pitch and loudness associated with vocal tremor can be acoustically characterized and measured as fo and SPL, respectively (see Figure 1). Acoustic evaluation of vocal tremor rate and amplitude has documented acoustic modulation rates from 3 to 12 Hz with modulation amplitudes from 20% to 30% (Barkmeier-Kraemer et al., 2011; Dromey et al., 2002; Gamboa et al., 1998). Interestingly, acoustic measures can identify acoustic modulations indicative of vocal tremor when listeners cannot perceive vocal tremor patterns (unpublished study). Measures of rate and amplitude of fo, SPL, F1 and F2 may also offer indirect inference as to the speech structures affected by vocal tremor (Barkmeier-Kraemer, 2010; Ji et al., 2014; LeBaron, 2016). Finally, acoustic measures enable quantification of pre- and post-treatment vocal tremor characteristics (Barkmeier-Kraemer et al., 2011). Neurolaryngologie
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Figure 1 – Acoustic display of vocal tremor during 1 second of sustained phonation of [a]. The top panel displays the raw acoustic signal and the two bottom signal plots display the relative sound pressure level (SPL) and fundamental frequency (f0).
Brown and Simonson (1963) observed that the tremulous voice quality severity across a cohort of individuals varied by speech context. That is, vocal tremor ranged from being undetectable during speech sounds produced with a short voicing duration (e.g., [s] and [t]) to being more perceptible during production of speech sounds produced with longer voicing durations (e.g., [m] and [a]) (Brown & Simonson, 1963). Although vocal tremor was best detected during sustained phonation, more severe cases exhibited a tremulous voice quality affecting connected speech to the degree that intelligibility was impaired (Brown & Simonson, 1963). A recent study systematically replicated these findings by comparing naïve listener ratings of overall severity of voice aberrance and the severity of “shakiness” of female speakers with vocal tremor during three speech contexts: (a) sustained phonation of the vowel [a], (b) production of a sentence loaded with all-voiced speech sounds (i.e., “We were away a year ago”), and (c) production of a sentence loaded with voiceless speech sounds (i.e., “Pop took his socks off”) (Lederle et al., 2012). On average, five speakers diagnosed with vocal tremor were perceived by listeners to exhibit the greatest levels of voice “shakiness” during sustained phonation than during sentence context (Lederle et al., 2012) (see Figure 2). Interestingly, all five speakers were judged with similar overall severity of “shakiness” during sustained phonation, but varied widely in the degree of “shakiness” perceived during each of the Neurolaryngologie
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sentence contexts (see Figure 3). For example, Speaker 1 showed little difference in average shakiness across all three speech contexts, whereas Speaker 5 showed the greatest perceived shakiness during sustained phonation, the second greatest degree of shakiness during production of the voice-loaded sentence, and the least degree of shakiness during production of the voiceless-loaded sentence. Thus, Speaker 1 appeared to be more severely impacted by vocal tremor given the consistent degree of shakiness perceived across all three speech contexts. In contrast, Speaker 5 showed less vocal tremor severity impact during connected speech contexts with nearly normal voicing during production of the voiceless-loaded sentence. These findings suggest that the severity of vocal tremor detected during sustained phonation may not predict the impact of vocal tremor on connected speaking. Rather, the ability to shorten voicing duration appears to be important. Figure 2 – This figure shows the average rating of overall severity by speech context as judged by naïve listeners for speakers with vocal tremor.
The importance of voicing duration and perception of vocal tremor was directly evaluated in a student thesis completed at the University of Iowa (Twohig, 2008). Eight female adult participants diagnosed with vocal tremor were recorded while producing sentences using legato (elongated) versus staccato (shortened) voicing duration. Neurolaryngologie
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Listeners judged the severity of tremor perceived in audio recordings of the speakers with vocal tremor. No difference was identified between vocal tremor severity ratings and voicing duration conditions. However, a robust correspondence occurred between the measured voicing duration produced by speakers and ratings of tremor severity. Specifically, speakers with a voicing duration of 500 ms or less were judged by listeners as having mild to no vocal tremor. In contrast, those with voicing durations averaging higher than 500 ms were judged with moderate to severe vocal tremor (Twohig, 2008). Thus, the ability to produce voicing durations 500 ms or less is an important determination in those with vocal tremor, particularly relevant to their potential for modifying speaking patterns as a potential treatment. Figure 3 – The figure shows the average rating of the degree of shakiness by speech context and speaker with vocal tremor as judged by naïve listeners.
Finally, speaking rate is important to assess when evaluating an individual with vocal tremor. Those with vocal tremor typically speak at a slower rate (3 syllables/s) than normal speakers (5 syllables/s) (Lundy et al., 2004). The slower speaking pattern in those with vocal tremor may be a speaking strategy adopted to improve their intelligibility to listeners. Alternatively, speaking more slowly may be an adaptation to the anticipated tremor perturbation. Unfortunately, slowed and prolonged voicing Neurolaryngologie
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duration enhances the opportunity for listeners to hear vocal tremor in affected speakers. Overall, clinical judgments of vocal tremor severity need to be compared across sustained phonation and connected speech contexts including the speaker’s ability to volitionally shorten voicing duration. Such information helps determine the individual’s potential to benefit from speech therapy.
The predominant medical approach for treating vocal tremor is pharmaceutical. The most common pharmaceutical treatment for vocal tremor is injection of botulinum toxin (Botox®) into laryngeal or strap musculature (Adler et al., 2004; Bove et al., 2006; Gurey et al., 2013; Kendall & Leonard, 2011; Sulica & Louis, 2010; Warrick et al., 2000). This approach works best for individuals exhibiting predominant laryngeal tremor with less evidence of tremor in other structures of the vocal tract (Bove et al., 2006). Systemic medications may be prescribed to treat vocal tremor with less well documented benefits (Justicz et al., 2016; Nida et al., 2016). The medications used to treat tremor systemically include propranolol (beta blocker), primidone (anti-seizure), clonazepam (anti-anxiety), gabapentin (anticonvulsant), topiramate (anticonvulsant), mirtazapine (antidepressant), and alcohol ingestion (Julius & Longfellow, 2016; Ondo, 2016).
Speech treatment has been of recent interest for treating vocal tremor. One earlier study referenced that an individual with vocal tremor benefited from speech therapy; however the methods used were not described (Massey & Paulson, 1985). Another investigation studied the use of “inspiratory breathing exercises” aimed at lowering laryngeal positioning and strengthening respiratory usage without measurable gains (Hilo, 2012). Another approach reported through online media described the use of “singsong” approaches to cure laryngeal tremor (Fischer, 2010). However, no published findings were found. Finally, a case study was published describing the foundation upon which current speech methods reported in this chapter were derived (BarkmeierKraemer et al., 2011). In the latter case, the key features related to vocal tremor patterns
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of worsening and improving during modification of voicing duration as well as pitch and loudness changes informed current the current speech treatment. Key fundamental concepts regarding successful speech treatment strategies for those with vocal tremor include recognizing that vocal tremor occurs due to: (1) actioninduced tremor patterns, (2) prolonged voicing durations, and (3) tremor affecting specific speech muscles and structures. One of the key features to vocal tremor is that it is associated with volitional muscle contraction, including breathing activities. Thus, vocal tremor is action-induced such that vocal tremor increases in amplitude proportional to muscle contraction. Consequently, identification of affected speech structures and speaking activities that worsen or lessen the amplitude of the vocal tremor informs optimal approaches that will facilitate reduced muscle contraction. Individuals with vocal tremor commonly impose increased effort levels during voicing to overcome or “control” their vocal tremor at the level of their throat with reduced airflow. Laryngeal and pharyngeal muscles are thus overly activated resulting in increased tremor during speaking. Methods that facilitate respiratory-phonatory coordination can offload increased muscle tension in the upper airway structures resulting in reduced vocal tremor amplitude. Several therapy approaches can achieve this goal including the accent method, confidential voicing, and flow phonation. Successful restoration of respiratory-phonatory coordination is critical to successful reduction of vocal tremor amplitude and therapy skill progression. Vocal tremor is characterized by a slow rate of modulation of the voice (i.e., 3-12 Hz). Thus, reducing voicing duration to disrupt these slow cyclic modulations reduces the ability for listeners to detect vocal tremor during speaking. Based on prior work (Twohig, 2008), the ability to reduce voicing duration to 500 ms or shorter significantly reduces detection of vocal tremor by listeners. Consequently, training those with vocal tremor to shorten voicing duration is one of the most successful methods for reducing the perception of vocal tremor during speaking. This is achieved by progressive training in speaking with reduced voicing duration starting with single syllable production and voiceless speech sounds (e.g., “ha” or “he”). Thereafter, focus is on expansion of reduced Neurolaryngologie
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voicing duration skills to all-voiced words, typically used phrases and sentences, and then paragraph reading and conversation. Identification of the specific structures affected by tremor can be achieved during the oral mechanism examination, laryngeal imaging, or voice function testing. The most informative testing in this regard focuses on the laryngeal musculature during sustained phonation of [i] at varied pitch and loudness levels to determine which muscles are likely “sources” of vocal tremor: (a) higher pitches with lengthwise vocal fold oscillation implicates the cricothyroid muscle, (b) lower pitches with lengthwise vocal fold oscillation implicates the thyroarytenoid muscle, (c) loudness changes associated with arytenoid abduction/adduction oscillation implicates the interarytenoid muscle, and (d) loudness changes associated with arytenoid abduction/adduction oscillation during breathy phonation implicates the posterior cricoarytenoid muscle. Other structures to observe during these tasks include pharyngeal wall, base of tongue, and laryngeal vertical oscillations. Understanding pitch and loudness patterns that worsen the individual’s vocal tremor informs modifications to their typical intonation patterns that may help to further reduce detection of the vocal tremor during conversational speaking. Table 2 summarizes the key features to speech therapy strategies successfully used to treat vocal tremor. Current therapy methods can be completed in 4 to 8 one-hour therapy sessions completed once weekly. Pre- and post-treatment outcomes used to determine clinical gains include acoustic measures, frequency of vocal tremor detection by listeners, and the Voice Handicap Index (VHI). Thus far, those with mild to moderately severe vocal tremor appear to benefit best from this method of treatment.
In summary, evaluation of individuals with vocal tremor requires understanding of the pathophysiology associated with this neurological voice disorder and specific contributions of speech structures to individual vocal tremor patterns. Individuals exhibiting the ability to reduce voicing duration during varied speech contexts, or
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volitional manipulation of voicing may be candidates for learning speech therapy strategies that reduce the presence of vocal tremor during speaking. Table 2 – Summary of key elements to the vocal tremor speech treatment program. Therapy objective Increase respiratoryphonatory coordination
Shorten voicing duration (≤ 500 ms)
Link specific speech structures exhibiting tremor to contexts that worsen and lessen vocal tremor
Methods > Accent method > Flow phonation > Confidential voicing > Easy voice onset > Yawn-sigh > Resonant voicing > Easy voice onset using "h" words and build toward all words typically spoken > Practice volitional shortened voicing duration using phrase context (e.g. voiceless-loaded speech sounds and then voice-loaded speech sounds) > Shape toward sentences, reading paragraphs, conversation > Tweak intonation patterns > Encourage shorter phrase length > Insert pauses for air replenishment > Reduce, or increase speaking rate as deemed beneficial
Outcome Reduce upper airway muscle tension and tremor amplitude
Reduce the frequency of detecting vocal tremor during conversation due to reduced voicing duration < 500 ms
Further modify individual speaking patterns to lessen speaking patterns that increase vocal tremor amplitude
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