Aerodynamic Measures and Biofeedback as Management in Persistent Paradoxical Vocal Fold Motion and Reverse Phonation Linda M. Carroll and Melin Tan, Bronx, New York Summary: Objectives. Paradoxical vocal fold motion (PVFM) and reverse phonation are characterized by aberrant vocal fold adduction. To date, there have been no studies examining the aerodynamic events during reverse phonation. We present an unusual case of persistent reverse phonation secondary to respiratory distress associated with PVFM. Study Design. Case report. Methods. We present the case of a 42-year-old female with sudden onset of respiratory distress associated with PVFM and persistent reverse phonation. She underwent baseline aerodynamic measurements followed by trial therapy. Through the use of instrumental and tactile aerodynamic biofeedback, the patient was able to coordinate exhalatory breath pressure flow during phonation, which resulted in immediately improved voice quality from highly dysphonic to nearly normal voice quality. Conclusions. Patients with reverse phonation seldom undergo aerodynamic testing as part of the initial diagnostic and management program. Our case study demonstrates the effectiveness of aerodynamic technology to enable a patient with aberrant glottic function to recognize inspiratory phonation events and to reestablish consistent expiratory flow/ pressure egress in speech tasks. Instrumental and tactile biofeedback is effective for reinforcement of normal flow patterns during speech tasks. Key Words: Reverse phonation–Paradoxical vocal fold motion–PVFM–Laryngospasm.
INTRODUCTION Paradoxical vocal fold motion (PVFM) is an uncommon disease characterized by vocal fold adduction during inspiration and/or expiration and functional airway obstruction due to the aberrant active adduction of the vocal folds during inspiration.1,2 Adductive laryngospasms may be triggered by an excessive response to external and internal airway stimuli.2 Prolonged vocal fold adduction during inhalation in an effort to achieve phonation, also known as reverse phonation, is also uncommon as a dominant mode of phonation. To date, there have been no studies examining the aerodynamic events during reverse phonation. We present an unusual case of persistent reverse phonation secondary to respiratory distress associated with PVFM. Presence of reverse phonation was documented during aerodynamic and stroboscopic examination. Case A 42-year-old female executive with report of a previously strong voice and normal articulation presented with a 1 month history of persistent hoarseness, dyspnea, and difficulty coordinating breath during speech. Patient presented following recent hospitalization at an outside hospital 1 month prior, for a first-time onset of respiratory distress and apparent PVFM and a diagnosis of an acute upper respiratory infection. She experienced a distinct sensation of swelling in the nose and throat, difficulty breathing, notable stridor, and change in voice. She was admitted for 4-day Accepted for publication July 29, 2014. From the Department of Otorhinolaryngology – Head and Neck Surgery, Montefiore Medical Center, Bronx, New York. Address correspondence and reprint requests to Melin Tan, Montefiore Medical Center, 3400 Bainbridge Avenue, 3rd Floor, Bronx, NY 10467. E-mail: [email protected] Journal of Voice, Vol. 29, No. 2, pp. 218-222 0892-1997/$36.00 Ó 2015 The Voice Foundation http://dx.doi.org/10.1016/j.jvoice.2014.07.018
intensive care unit admission for close observation without intubation. Bedside fiberoptic laryngoscopy by an otolaryngologist during her hospital stay revealed physical findings consistent with severe acid reflux for which she was already being medically treated. Her past medical history is significant for systemic lupus erythematosus and gastroparesis with frequent vomiting. She had experienced an episode of reflux and regurgitation within 2 days of onset of symptoms. She is married, has two small children (aged 2 and 7 years), and admits to high-stress job. Physical examination findings were significant for a grade-3, P roughness-3, breathiness-0, aesthenia-0, and strain-3 ( ¼ 9) with reverse phonation present during initial laryngeal examination (day one). Laryngeal videostroboscopy was significant for obvious PVFM, with phonation present during inspiration and expiration and otherwise normal laryngeal anatomy (Supplementary Video 1). Despite voicing, no mucosal wave was generated during stroboscopy. Mean speaking fundamental frequency (SF0) during stroboscopy was 454 Hz. Chronic cough was not observed, but high mucosal sensitivity was present. The patient was referred for baseline aerodynamic measures and trial speech/voice/breathing therapy the following day. Aerodynamic measures were obtained using KayPentax Phonatory Aerodynamic System (KayPentax, Montvale, NJ), with repeated /pa/ syllable trains. Patient reported her speech and voice quality on that day to be representative of typical speech. Reverse phonation of her was dominant speech pattern, with voice quality rough, coarse, and dry. Patient was observed to have initial pressure peak for [p] in /pa/ syllable trains, but then minimal (0.54 cm H2O) or no measurable pressure peak during subsequent [p] production during the remainder of task (Figure 1A and B). Although initially attributed to be due to possible saliva in the intraoral tube, later [p] productions in the same syllable train did have
Linda M. Carroll and Melin Tan
Aerodynamic Measures and Biofeedback in PVFM and Reverse Phonation
219
FIGURE 1. (A) Subject phonation of /papapapapa/ showing erratic air flow and air pressure tracings despite voicing at 230 Hz. (B) Repeated /papapapapa/ with improved use of positive pressure egress but with variable control of normal versus inhalation phonation 230–250 Hz. positive pressure peaks. Clearance of potential saliva through repeated [p] did not change the variable positive-flat-positive pressure tracings during the repeated /pa/ syllable trains. Careful monitoring of adequate labial seal during flattened pressure tracings and evidence of positive pressure peaks within
the same repeated /pa/ task confirmed inspiratory phonation during the syllable train. Air flow, loudness, and pitch were measurable for these events, confirming that patient was using inhalation phonation (negative pressure during /p/, positive flow during /a/).
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FIGURE 2. Posttrial therapy with subject phonation of /papapapapa/ in short pulses and continuous syllable train, showing improved stability and consistency of air flow and air pressure tracings (mean SF0 215 Hz).
Throughout the baseline aerodynamic measurement, air flow, loudness, and voice quality remained stable, as well as level of dysphonia. The patient was unable to execute a maximum phonation task before trial therapy. Trial therapy Through the use of aerodynamic feedback (real-time display of pressure and flow changes), the patient was able to establish positive pressure egress during [p] and [pa] productions (Figure 2). Phonation was extended to multiple /pa/ repetitions with circumferential mask in place and with mask removed. Biofeedback was then transferred to Tadoma technique (speaking against the back of the hand to sense pressure and flow changes),3 adapting speech tasks to functional phrases ‘‘please pass the pepper.’’ Voice quality was immediately improved with the use of positive pressure/flow egress, changing to mild dysphonia: grade-0, roughness-0, breathiness-0, aesthenia-0, and strainP 1 ( ¼ 2). The patient was able to execute maximum phonation task (6.4 seconds maximum phonation) at the end of trial therapy session (20 minutes). She was able to transfer to functional speech tasks, but speech rate remained slowed, and fluidity/ease of speech remained reduced. Projection of voice was markedly easier, but control of volume remained difficult with the patient using louder phonation than needed for the
communication setting. Resistance inhalation techniques were practiced to slow the airflow inhalation rates and maintain an open glottic posture during inhalation. Use of [p] pulsing was implemented to reassure patient of correct airflow egress. The patient was able to sense when airflow egress was reversed (reverse phonation) and hear the immediate deterioration of voice quality. Fluidity of speech remained halted between words as the patient attempted to track positive pressure/airflow movement. Through the use of aerodynamic biofeedback (objective aerodynamic feedback and Tadoma technique), the patient was able to coordinate exhalatory breath pressure flow during phonation, which resulted in immediately improved voice quality from highly dysphonic to nearly normal voice quality. Changes of aerodynamic values pre-post trial therapy are shown in Table 1. Repeat of stroboscopy after airflow/pressure probes revealed normal vocal fold movement and symmetry of mucosal wave propagation (online Supplementary Video 2). SF0 during stroboscopy averaged 299 Hz, indicating a lowering of 7.2 semitones with cessation of reverse phonation from day 1 to day 2. The patient was referred to voice/speech therapy to establish normal breath pacing and directionality, re-establish normal
Linda M. Carroll and Melin Tan
Aerodynamic Measures and Biofeedback in PVFM and Reverse Phonation
221
TABLE 1. Significant Change in Mean Subglottal Pressure Pre-Post Trial Therapy to Address Inhalation Phonation, With no Significant Change (1.4 Semitones) of Fundamental Frequency dB SPL F0 (Hz) Flow (L/s) Psub (cm H2O) Resistance Ohms 96.57 91.80
234.51 215.80
0.185 0.177
0.540 10.38
27.78 58.31
speech rate, improve fluid transfer to speech, and establishment of flow phonation as sole pattern of phonation. She was recommended to continued practice of [p] pulsing to establish normal exhalatory pressure-flow. DISCUSSION PVFM, also known as laryngospasm, is an uncommon disease characterized by vocal fold adduction during inspiration and/ or expiration and functional airway obstruction due to the active adduction of the vocal folds during inspiration.1,2 Adductor spasms of the larynx may be triggered by an excessive response to external and internal airway stimuli.2 Jackson4 first described sudden laryngeal spasm which could be triggered by to local irritation, with a ‘‘tight closure of the glottic chink by the inspiratory blast.’’ Gallivan et al reported attenuation of inspiratory flow rate and the more commonly described flattened flow-volume loop during pulmonary function testing in laryngospasm patients.5–7 Prior studies by O’Hollaren8 suggested severe subjective dyspnea in patients with laryngospasm. Laryngospasm triggers include asthma, underlying psychological condition, gastroesophageal acid reflux disease, respiratory irritants exposure, central neurologic diseases, viral upper airway infections, and postsurgical procedures.1 Similar to laryngospasm, reverse phonation requires aberrant vocal fold adduction during inspiration; however, it is a prolonged adduction as one phonates. The phonation during inhalation may be considered normal in select languages for isolated words but is uncommon as the dominant mode of phonation.9 Reverse phonation is commonly used during laryngeal examination to visualize mucosal movement of the lower lip of the vocal fold.10 However, under normal circumstances, it requires instruction, as it is not typical for production of vocal sound. Prolonged use of reverse phonation may be found in patients, who lack adequate glottic valving due to arytenoidectomy or significant laryngeal trauma, or may be a response to laryngeal sensitivity or altered neurologic status. A common trait in these patients is a significantly reduced maximum phonation time. Our patient was unable to sustain phonation. Despite voicing, no mucosal wave was generated during stroboscopy. Mean speaking fundamental frequency (SF0) during stroboscopy was 454 Hz. Finger et al9 have reported other laryngospasm features of ventricular distention and ventricular folds separation, but this was not observed in our subject. Recognition and accurate diagnosis of PVFM improve treatment and subsequent normal function in these
28.33 59.47
Maximum Phonation Mean Values (Average of 3 /pa/ Time (s) Syllable Trains — 6.4
Baseline (inhalation phonation) Following trial therapy
challenging patients. Aberrant laryngeal adduction disorders include PVFM and muscle tension dysphonia. Although MTD patients are recognized to have a higher prevalence of glottal constriction during inspiration and a higher prevalence of abnormal glottic closure,11 aerodynamic features of MTD and PVFM differ. Common aerodynamic features of MTD include low airflow and some reduction in intraoral pressure, and prolonged maximum phonation. Reverse phonation, a phonatory behavior found in conjunction with PVFM, has aerodynamic features of normal transglottal flow, minimal subglottal pressure (after initial /pa/ in a /pa/ syllable train), and difficulty executing maximum phonation tasks. Higher SF0 is a common feature of normal reverse phonation but was only observed during stroboscopy examination for our patient.9,11 During aerodynamic testing, our subject was found to have no significant change of SF0 during reverse phonation compared with normal positive airflow phonation. During stroboscopy, a higher SF0 was present (454 Hz) during reverse phonation, which lowered by 11 semitones (299 Hz) after trial therapy. Elevation of SF0 by 5.6 semitones between trial therapy and stroboscopy (5 -minute elapsed time) may indicate higher SF0 due to the stress of laryngeal examination compared with less compromising capture of aerodynamic measures. To date, there have been no studies examining the aerodynamic events during reverse phonation. Wattremez et al12 reported on a patient using continuous reverse phonation but measures were limited to frequency and laryngeal appearance. In our patient, not only were aerodynamic events refolded but also airflow tracings were used for biofeedback therapy with marked immediate response. CONCLUSIONS Patients with reverse phonation seldom undergo aerodynamic testing as part of the initial diagnostic and management program. Our case study demonstrates the effectiveness of aerodynamic technology to enable a patient with aberrant glottic function to recognize inspiratory phonation events and to reestablish consistent expiratory flow/pressure egress in speech tasks. Instrumental and tactile biofeedback is effective for reinforcement of normal flow patterns during speech tasks. Supplementary data Supplementary data related to this article can be found at http:// dx.doi.org/10.1016/j.jvoice.2014.07.018.
222 REFERENCES 1. Karaman E, Duman C, Alimoglu Y, Isildak H, Oz F. Paradoxical vocal cord motion–haloperidol usage in acute attack treatment. J Craniofac Surg. 2009;20:1602–1604. 2. Shiba K, Isono S, Nakazawa K. Paradoxical vocal cord motion: a review focused on multiple system atrophy. Auris Nasus Larynx. 2007;34:443–452. 3. Reed CM, Rabinowitz WM, Durlach NI, Braida LD, Conway-Fithian S, Schultz MC. Research on the Tadoma method of speech communication. J Acoust Soc Am. 1985;77:247–257. 4. Jackson CJC. Motor neuroses of the larynx. New York, NY: The MacMillan Company; 1942. 5. Gallivan GJ, Hoffman L, Gallivan KH. Episodic paroxysmal laryngospasm: voice and pulmonary function assessment and management. J Voice. 1996; 10:93–105. 6. Christopher KL, Wood RP 2nd, Eckert RC, Blager FB, Raney RA, Souhrada JF. Vocal-cord dysfunction presenting as asthma. N Engl J Med. 1983;308:1566–1570.
Journal of Voice, Vol. 29, No. 2, 2015 7. Ophir D, Katz Y, Tavori I, Aladjem M. Functional upper airway obstruction in adolescents. Arch Otolaryngol Head Neck Surg. 1990;116: 1208–1209. 8. O’Hollaren MT. Masqueraders in clinical allergy: laryngeal dysfunction causing dyspnea. Ann Allergy. 1990;65:351–356. 9. Finger LS, Cielo CA. Reverse phonation–physiologic and clinical aspects of this speech voice therapy modality. Braz J Otorhinolaryngol. 2007;73: 271–277. 10. Lehmann QH. Reverse phonation: a new maneuver for examining the larynx. Radiology. 1965;84:215–222. 11. Robb MP, Chen Y, Gilbert HR, Lerman JW. Acoustic comparison of vowel articulation in normal and reverse phonation. J Speech Lang Hear Res. 2001;44:118–127. 12. Wattremez A, Delpech C, DeBrugiere C, Chevallier G, Herman P. Reverse phonation: pathological and therapeutic aspects. Study of a clinical case. Rev Laryngol Otol Rhinol (Bord). 2011;123: 51–55.
INTRODUCTION Paradoxical vocal fold motion (PVFM) is an uncommon disease characterized by vocal fold adduction during inspiration and/or expiration and functional airway obstruction due to the aberrant active adduction of the vocal folds during inspiration.1,2 Adductive laryngospasms may be triggered by an excessive response to external and internal airway stimuli.2 Prolonged vocal fold adduction during inhalation in an effort to achieve phonation, also known as reverse phonation, is also uncommon as a dominant mode of phonation. To date, there have been no studies examining the aerodynamic events during reverse phonation. We present an unusual case of persistent reverse phonation secondary to respiratory distress associated with PVFM. Presence of reverse phonation was documented during aerodynamic and stroboscopic examination. Case A 42-year-old female executive with report of a previously strong voice and normal articulation presented with a 1 month history of persistent hoarseness, dyspnea, and difficulty coordinating breath during speech. Patient presented following recent hospitalization at an outside hospital 1 month prior, for a first-time onset of respiratory distress and apparent PVFM and a diagnosis of an acute upper respiratory infection. She experienced a distinct sensation of swelling in the nose and throat, difficulty breathing, notable stridor, and change in voice. She was admitted for 4-day Accepted for publication July 29, 2014. From the Department of Otorhinolaryngology – Head and Neck Surgery, Montefiore Medical Center, Bronx, New York. Address correspondence and reprint requests to Melin Tan, Montefiore Medical Center, 3400 Bainbridge Avenue, 3rd Floor, Bronx, NY 10467. E-mail: [email protected] Journal of Voice, Vol. 29, No. 2, pp. 218-222 0892-1997/$36.00 Ó 2015 The Voice Foundation http://dx.doi.org/10.1016/j.jvoice.2014.07.018
intensive care unit admission for close observation without intubation. Bedside fiberoptic laryngoscopy by an otolaryngologist during her hospital stay revealed physical findings consistent with severe acid reflux for which she was already being medically treated. Her past medical history is significant for systemic lupus erythematosus and gastroparesis with frequent vomiting. She had experienced an episode of reflux and regurgitation within 2 days of onset of symptoms. She is married, has two small children (aged 2 and 7 years), and admits to high-stress job. Physical examination findings were significant for a grade-3, P roughness-3, breathiness-0, aesthenia-0, and strain-3 ( ¼ 9) with reverse phonation present during initial laryngeal examination (day one). Laryngeal videostroboscopy was significant for obvious PVFM, with phonation present during inspiration and expiration and otherwise normal laryngeal anatomy (Supplementary Video 1). Despite voicing, no mucosal wave was generated during stroboscopy. Mean speaking fundamental frequency (SF0) during stroboscopy was 454 Hz. Chronic cough was not observed, but high mucosal sensitivity was present. The patient was referred for baseline aerodynamic measures and trial speech/voice/breathing therapy the following day. Aerodynamic measures were obtained using KayPentax Phonatory Aerodynamic System (KayPentax, Montvale, NJ), with repeated /pa/ syllable trains. Patient reported her speech and voice quality on that day to be representative of typical speech. Reverse phonation of her was dominant speech pattern, with voice quality rough, coarse, and dry. Patient was observed to have initial pressure peak for [p] in /pa/ syllable trains, but then minimal (0.54 cm H2O) or no measurable pressure peak during subsequent [p] production during the remainder of task (Figure 1A and B). Although initially attributed to be due to possible saliva in the intraoral tube, later [p] productions in the same syllable train did have
Linda M. Carroll and Melin Tan
Aerodynamic Measures and Biofeedback in PVFM and Reverse Phonation
219
FIGURE 1. (A) Subject phonation of /papapapapa/ showing erratic air flow and air pressure tracings despite voicing at 230 Hz. (B) Repeated /papapapapa/ with improved use of positive pressure egress but with variable control of normal versus inhalation phonation 230–250 Hz. positive pressure peaks. Clearance of potential saliva through repeated [p] did not change the variable positive-flat-positive pressure tracings during the repeated /pa/ syllable trains. Careful monitoring of adequate labial seal during flattened pressure tracings and evidence of positive pressure peaks within
the same repeated /pa/ task confirmed inspiratory phonation during the syllable train. Air flow, loudness, and pitch were measurable for these events, confirming that patient was using inhalation phonation (negative pressure during /p/, positive flow during /a/).
220
Journal of Voice, Vol. 29, No. 2, 2015
FIGURE 2. Posttrial therapy with subject phonation of /papapapapa/ in short pulses and continuous syllable train, showing improved stability and consistency of air flow and air pressure tracings (mean SF0 215 Hz).
Throughout the baseline aerodynamic measurement, air flow, loudness, and voice quality remained stable, as well as level of dysphonia. The patient was unable to execute a maximum phonation task before trial therapy. Trial therapy Through the use of aerodynamic feedback (real-time display of pressure and flow changes), the patient was able to establish positive pressure egress during [p] and [pa] productions (Figure 2). Phonation was extended to multiple /pa/ repetitions with circumferential mask in place and with mask removed. Biofeedback was then transferred to Tadoma technique (speaking against the back of the hand to sense pressure and flow changes),3 adapting speech tasks to functional phrases ‘‘please pass the pepper.’’ Voice quality was immediately improved with the use of positive pressure/flow egress, changing to mild dysphonia: grade-0, roughness-0, breathiness-0, aesthenia-0, and strainP 1 ( ¼ 2). The patient was able to execute maximum phonation task (6.4 seconds maximum phonation) at the end of trial therapy session (20 minutes). She was able to transfer to functional speech tasks, but speech rate remained slowed, and fluidity/ease of speech remained reduced. Projection of voice was markedly easier, but control of volume remained difficult with the patient using louder phonation than needed for the
communication setting. Resistance inhalation techniques were practiced to slow the airflow inhalation rates and maintain an open glottic posture during inhalation. Use of [p] pulsing was implemented to reassure patient of correct airflow egress. The patient was able to sense when airflow egress was reversed (reverse phonation) and hear the immediate deterioration of voice quality. Fluidity of speech remained halted between words as the patient attempted to track positive pressure/airflow movement. Through the use of aerodynamic biofeedback (objective aerodynamic feedback and Tadoma technique), the patient was able to coordinate exhalatory breath pressure flow during phonation, which resulted in immediately improved voice quality from highly dysphonic to nearly normal voice quality. Changes of aerodynamic values pre-post trial therapy are shown in Table 1. Repeat of stroboscopy after airflow/pressure probes revealed normal vocal fold movement and symmetry of mucosal wave propagation (online Supplementary Video 2). SF0 during stroboscopy averaged 299 Hz, indicating a lowering of 7.2 semitones with cessation of reverse phonation from day 1 to day 2. The patient was referred to voice/speech therapy to establish normal breath pacing and directionality, re-establish normal
Linda M. Carroll and Melin Tan
Aerodynamic Measures and Biofeedback in PVFM and Reverse Phonation
221
TABLE 1. Significant Change in Mean Subglottal Pressure Pre-Post Trial Therapy to Address Inhalation Phonation, With no Significant Change (1.4 Semitones) of Fundamental Frequency dB SPL F0 (Hz) Flow (L/s) Psub (cm H2O) Resistance Ohms 96.57 91.80
234.51 215.80
0.185 0.177
0.540 10.38
27.78 58.31
speech rate, improve fluid transfer to speech, and establishment of flow phonation as sole pattern of phonation. She was recommended to continued practice of [p] pulsing to establish normal exhalatory pressure-flow. DISCUSSION PVFM, also known as laryngospasm, is an uncommon disease characterized by vocal fold adduction during inspiration and/ or expiration and functional airway obstruction due to the active adduction of the vocal folds during inspiration.1,2 Adductor spasms of the larynx may be triggered by an excessive response to external and internal airway stimuli.2 Jackson4 first described sudden laryngeal spasm which could be triggered by to local irritation, with a ‘‘tight closure of the glottic chink by the inspiratory blast.’’ Gallivan et al reported attenuation of inspiratory flow rate and the more commonly described flattened flow-volume loop during pulmonary function testing in laryngospasm patients.5–7 Prior studies by O’Hollaren8 suggested severe subjective dyspnea in patients with laryngospasm. Laryngospasm triggers include asthma, underlying psychological condition, gastroesophageal acid reflux disease, respiratory irritants exposure, central neurologic diseases, viral upper airway infections, and postsurgical procedures.1 Similar to laryngospasm, reverse phonation requires aberrant vocal fold adduction during inspiration; however, it is a prolonged adduction as one phonates. The phonation during inhalation may be considered normal in select languages for isolated words but is uncommon as the dominant mode of phonation.9 Reverse phonation is commonly used during laryngeal examination to visualize mucosal movement of the lower lip of the vocal fold.10 However, under normal circumstances, it requires instruction, as it is not typical for production of vocal sound. Prolonged use of reverse phonation may be found in patients, who lack adequate glottic valving due to arytenoidectomy or significant laryngeal trauma, or may be a response to laryngeal sensitivity or altered neurologic status. A common trait in these patients is a significantly reduced maximum phonation time. Our patient was unable to sustain phonation. Despite voicing, no mucosal wave was generated during stroboscopy. Mean speaking fundamental frequency (SF0) during stroboscopy was 454 Hz. Finger et al9 have reported other laryngospasm features of ventricular distention and ventricular folds separation, but this was not observed in our subject. Recognition and accurate diagnosis of PVFM improve treatment and subsequent normal function in these
28.33 59.47
Maximum Phonation Mean Values (Average of 3 /pa/ Time (s) Syllable Trains — 6.4
Baseline (inhalation phonation) Following trial therapy
challenging patients. Aberrant laryngeal adduction disorders include PVFM and muscle tension dysphonia. Although MTD patients are recognized to have a higher prevalence of glottal constriction during inspiration and a higher prevalence of abnormal glottic closure,11 aerodynamic features of MTD and PVFM differ. Common aerodynamic features of MTD include low airflow and some reduction in intraoral pressure, and prolonged maximum phonation. Reverse phonation, a phonatory behavior found in conjunction with PVFM, has aerodynamic features of normal transglottal flow, minimal subglottal pressure (after initial /pa/ in a /pa/ syllable train), and difficulty executing maximum phonation tasks. Higher SF0 is a common feature of normal reverse phonation but was only observed during stroboscopy examination for our patient.9,11 During aerodynamic testing, our subject was found to have no significant change of SF0 during reverse phonation compared with normal positive airflow phonation. During stroboscopy, a higher SF0 was present (454 Hz) during reverse phonation, which lowered by 11 semitones (299 Hz) after trial therapy. Elevation of SF0 by 5.6 semitones between trial therapy and stroboscopy (5 -minute elapsed time) may indicate higher SF0 due to the stress of laryngeal examination compared with less compromising capture of aerodynamic measures. To date, there have been no studies examining the aerodynamic events during reverse phonation. Wattremez et al12 reported on a patient using continuous reverse phonation but measures were limited to frequency and laryngeal appearance. In our patient, not only were aerodynamic events refolded but also airflow tracings were used for biofeedback therapy with marked immediate response. CONCLUSIONS Patients with reverse phonation seldom undergo aerodynamic testing as part of the initial diagnostic and management program. Our case study demonstrates the effectiveness of aerodynamic technology to enable a patient with aberrant glottic function to recognize inspiratory phonation events and to reestablish consistent expiratory flow/pressure egress in speech tasks. Instrumental and tactile biofeedback is effective for reinforcement of normal flow patterns during speech tasks. Supplementary data Supplementary data related to this article can be found at http:// dx.doi.org/10.1016/j.jvoice.2014.07.018.
222 REFERENCES 1. Karaman E, Duman C, Alimoglu Y, Isildak H, Oz F. Paradoxical vocal cord motion–haloperidol usage in acute attack treatment. J Craniofac Surg. 2009;20:1602–1604. 2. Shiba K, Isono S, Nakazawa K. Paradoxical vocal cord motion: a review focused on multiple system atrophy. Auris Nasus Larynx. 2007;34:443–452. 3. Reed CM, Rabinowitz WM, Durlach NI, Braida LD, Conway-Fithian S, Schultz MC. Research on the Tadoma method of speech communication. J Acoust Soc Am. 1985;77:247–257. 4. Jackson CJC. Motor neuroses of the larynx. New York, NY: The MacMillan Company; 1942. 5. Gallivan GJ, Hoffman L, Gallivan KH. Episodic paroxysmal laryngospasm: voice and pulmonary function assessment and management. J Voice. 1996; 10:93–105. 6. Christopher KL, Wood RP 2nd, Eckert RC, Blager FB, Raney RA, Souhrada JF. Vocal-cord dysfunction presenting as asthma. N Engl J Med. 1983;308:1566–1570.
Journal of Voice, Vol. 29, No. 2, 2015 7. Ophir D, Katz Y, Tavori I, Aladjem M. Functional upper airway obstruction in adolescents. Arch Otolaryngol Head Neck Surg. 1990;116: 1208–1209. 8. O’Hollaren MT. Masqueraders in clinical allergy: laryngeal dysfunction causing dyspnea. Ann Allergy. 1990;65:351–356. 9. Finger LS, Cielo CA. Reverse phonation–physiologic and clinical aspects of this speech voice therapy modality. Braz J Otorhinolaryngol. 2007;73: 271–277. 10. Lehmann QH. Reverse phonation: a new maneuver for examining the larynx. Radiology. 1965;84:215–222. 11. Robb MP, Chen Y, Gilbert HR, Lerman JW. Acoustic comparison of vowel articulation in normal and reverse phonation. J Speech Lang Hear Res. 2001;44:118–127. 12. Wattremez A, Delpech C, DeBrugiere C, Chevallier G, Herman P. Reverse phonation: pathological and therapeutic aspects. Study of a clinical case. Rev Laryngol Otol Rhinol (Bord). 2011;123: 51–55.
