Ann Otol 85: 1976
SPASTIC DYSPHONIA FRIEDRICH
S.
BRODNITZ
NEW YORK, NEW YORK
SUMMARY - 130 cases of spastic dysphonia are reviewed with special emphasis on the etiology of the disorder. An analysis of the circumstances surrounding the onset of the disease points strongly to a psychogenic origin of the disease in, at least, the vast majority of the cases.
Of all the disorders of the human voice spastic dysphonia is still the most mysterious, the most poorly understood and the most resistant to successful therapy. Because of the relative rarity of the disorder, laryngologists are frequently not familiar with the syndrome of spastic dysphonia and often do not diagnose it properly when they encounter it. Because of the low incidence of the disorder most reports deal only with a small number of cases. This report includes case histories of 130 patients. Special emphasis will be given to the histories obtained which may throw light on the still disputed etiology of the disease. The first description of spastic dysphonia was given by Traube in 1871. The term is a poor one because "spasticity" is a term used to define a specific neurological disorder that does not quite fit the symptomatology and etiology of this form of dysphonia. Aronson- has suggested the term spasmodic dysphonia, but the original terminology has been used universally in the literature. It will be employed in this review. The two most exhaustive discussions of spastic dysphonia were presented in 1965 in reports to the 13th Congress of the International Association of Logopedics and Phoniatrics: by Kiml" on experimental investigation, and by Bloch" on the neuropsychiatric aspects of spastic dysphonia. The voluminous refer-
ences included over 400 items. Of special interest are the papers by Berendes," Arnold," Heaver," Luchsinger," and more recently, by Aronson.' SYMPTOMATOLOGY
One of the problems in writing about phoniatric problems is the difficulty in describing acoustic phenomena in print. It is much easier to make the proper diagnosis if one has previously had experience with even one case of fullblown spastic dysphonia. Even the busy laryngologist may never have encountered such a case before it first appears in his practice. A good recording of the voice of spastic dysphonia can be obtained from any major Speech and Hearing Center and would be helpful in alerting the laryngologist to the symptoms of spastic dysphonia. Teaching tapes of voice disorders containing representative examples of the different forms of vocal pathology are available." This author has previously described it as follows: "Spastic dysphonia stands at the opposite end of the dynamic scale of functional voice disorders. The aphonic patient has given up communication by the use of phonation, but in spastic dysphonia communication is interfered with by violent contractions of the vocal cords. The patient speaks with great effort in a constricted, highpitched voice.T'? Vowels are interrupted in the middle of the sound. A good de-
---From the Department of Otolaryngology Mount Sinai Medical Center, New York, N.Y. and the Institute of Health Sciences, Hunter College, The City University of New York. 210
Downloaded from aor.sagepub.com at Purdue University Libraries on June 23, 2015
211
SPASTIC DYSPHONIA
scription of spastic dysphonia was given by Berendes: "A disorder of phonation which is characterized by a strained, creaking and choked vocal attack, a tense and squeezed voice sound that is accompanied by extreme tension of the entire phonatory system,"! Many authors have noted the similarity between the glottal symptoms of spastic dysphonia and the oral ones of the stutterer and have called it "laryngeal stuttering." In both conditions, the severity of symptoms may vary greatly with the change of moods and the degree of nervous tension. It varies considerably from case to case, from patients with only mild symptoms to cases where the choking phonation makes communication almost impossible. In many instances the patient is able to produce quite normal phonatory sounds that do not have the character of direct communication. Almost all patients are able to laugh in a perfectly normal way and quite a few of them can sing without vocal cord constriction. INCIDENCE
Spastic dysphonia is usually described as a rare disease. The incidence of the disease may not be as low as reported. It seems quite likely that many cases, especially the milder ones. are never properly labeled. Practically all 130 cases seen by this author in over twentyfive years of phoniatric practice were referred for voice therapy by fellow Iaryngologists. Until the last few years, since laryngologists have become more sophisticated about functional voice problems, almost all patients came with incorrect diagnoses such as ventricular dysphonia. In any case, spastic dysphonia is not a common disorder. Of 2640 patients with all forms of functional voice disorders, the 130 patients with spastic dysphonia constitute only 4.0%. Men and women are equally affected, with women having a slight edge over men in most statistics. Of the 130 patients, 69 were women and 61 men.
The disease hits almost exclusively in middle age. Very few cases have been reported that occurred in childhood or adolescence. In the cases presented here the average mean age of the onset of the disorder was 50.2 years with the following distribution: 20-30 years, 13 cases; 31-40 years, 21 cases; 41-50 years, 35 cases: 51-60 years, 38 cases; over 60 years, 23 cases. The youngest patient was 27 years old, the oldest 76. ETIOLOGY
When spastic dysphonia was first described as a well defined disorder of the voice it was assumed that it should be considered a psychogenic disease, a form of conversion hysteria. Most of the subsequent authors have accepted a concept of looking at spastic dysphonia as one of two extreme forms of the continuum of functional voice disorders; functional aphonia being the extreme of vocal hypofunction; and spastic dysphonia representing the extreme of hyperfunction. Both disorders were interpreted as the physical manifestations of a deep-rooted emotional conflict. A different interpretation was first attempted in 1960 by Robe and Associates.!' who claimed that they found abnormal brain waves in the EEG of 90% of their patients with spastic dysphonia. This organic concept of the disease has been advocated more recently by Aronson and his associates.' On the strength of extensive investigation of 34 patients, they have come to the conclusion that at least some cases of spastic dysphonia are based on a neurological disorder, most likely in the extrapyramidal tracts. They add that further psychiatric and neurological studies are greatly needed. Subsequent EEG studies have yielded rather inconclusive results. Aronson! obtained normal EEG readings in 17 of 22 patients, only mild dysrhythmic activity in four others, and independent spike foci in one patient. Luchsinger" found only one abnormal registration in six patients.
Downloaded from aor.sagepub.com at Purdue University Libraries on June 23, 2015
212
FRIEDRICH S. BRODNITZ
The most extensive investigation was attempted by Kiml" who studied patients with spastic dysphonia with a wide range of laboratory methods: sonogram, tomogram, pneumography, spirometry, electromyography, measurement of subglottic air-pressure and EEG. All measurements, except the last one, exhibit considerable deviations from the norm; but these elucidate only symptoms of the disease, and they do not contribute anything to the uncovering of the etiology. The EEGs revealed only slight changes in four out of ten cases. At the end of the study Kiml remarks: "One can register everything but one has to know what purpose it really serves," and he quotes Norbert Wiener of cybernetics fame who warned that «we are the slaves of technological discoveries."
Bloch" pleaded the case for the psychogenic character of the disorder and he. too, remarked "that researchers from EEG to hematochemical analysis, from neuro-vegetative to endocrine factors will always find in many cases modifications. But there is the danger that we may not see the forest for the trees". The essential question that should be addressed is: What is cause and what is only a symptom in the complicated interplay of body functions? The stutterer exhibits in his speech a marked deviation from neuromuscular patterns, and the aphonic patient may present a bizarre picture of paradoxic vocal cord action. Still, both conditions are widely accepted as psychogenic in origin. None of the reported abnormal findings in spastic dysphonia are pronounced enough to interpret them as caused by neurological pathology. Years ago the author tried, in six cases' the use of the intravenous injection ~f Amytal®O ( narco-analysis) in the hope that it could be used as therapy. While under the influence of the drug, the patients spoke in a quite normal pattern with only rare traces of
spasmodic speech; but, as soon as the effect of the drug wore off they reverted to disturbed vocal function. Another observation that speaks for the psychogenic etiology is that many patients with spastic dysphonia are able to sing in a normal voice with free H~w of tone and being on target for the different frequencies. This requires greater sharpness of neuromuscular control than does speech, but it does constitute personal communication to as great a degree. This phenomenon runs counter to what one would expect in a patient with neurological pathology but it makes sense if one interprets it as the elimination of a powerful psychological element. The same observation has been made quite often in stutterers. A large number of patients pinpoint with great accuracy the onset of the dysphonia after e~osure to se.vere emotional trauma. FIfty-three patients volunteered under the cautious probing of the intake interview, what they considered to be the event that triggered the development of the disease. A few such incidents are: the death of a near relative (13 cases, five of them from laryngeal cancer); severe automobile accidents leaving them physically unharmed (8 cases); climactic marital crisis \ 8 cases, one of them starting suddenly m divorce court under rough treatment by the opposing lawyer); laryngeal surgery for removal of benign lesions (5 cases). One woman became dysphonic when her husband threatened to kill her; another, after her husband was murdered; a third, after her brother was shot to death in a holdup; a fourth, after witnessing the first epileptic attack of her child. A minister developed spastic dysphonia when he lost his pulpit in the South when he d~monstra~e? with Dr. Martin Luther Kmg for civil liberties. Two cases stand out in significance for the psychogenic etiology: 1. A young psychiatrist was told that his training analysis was com-
---;;Eli Lilly & ce., Indianapolis, Indiana
Downloaded from aor.sagepub.com at Purdue University Libraries on June 23, 2015
SPASTIC DYSPHONIA
plete. A few weeks after this cutting of the analytical umbilical cord he developed spastic dysphonia. He discussed it with his analyst who agreed to take him back for three more months. Immediately his voice became normal only to revert to the dysphonia when the analyst told him, at the end of these three months, that he should now be able to stand on his own feet. 2. The headwaiter of a luxury restaurant came in for treatment. During the course of the first interview he reported that his voice was very bad at home and among friends but that he could speak with a practically normal voice when he put on his tuxedo and started to serve the guests, slipping into the "role" of an elegant maitre d'hotel. Aside from these 53 patients who could pinpoint the onset of the disorder, there were 28 who exhibited many of the characteristics of severe neuroses. Eight of them had already had long periods of psychiatric treatment before they developed spastic dysphonia. This leaves only about one third of the cases reported in this paper where no obvious psychogenic background could be found. This is not an unusual situation in psychosomatic disorders, particularly in manifestations of conversion hysteria. Of course, everybody who has had freauent contact with cases of spastic dysphonia has entertained the suspicion that an organic neurological factor may be the etiological basis of the more severe forms of the disorder. Possibly, future research with more refined methods may demonstrate such a connection in some cases. As of now, overwhelming proof speaks for a psychogenic disorder, a "neuro-physiologic regression" (Heaver"}, resulting in "a form of psychogenic breakdown of corticothalamic integration" (Arnold 5 ) . THERAPY
Authors who have written about spastic dysphonia agree on the poor results of any form of therapy. There are a number of reasons for this unfortunate
213
state of affairs. In this disorder we deal with a very complex syndrome. As in stuttering, the patient develops patterns of behavior that tend to become more and more deep-seated as time goes by. The increasing impairment of communication itself reinforces the psychological trauma. In contrast to the patient with functional aphonia. who is often strangely indifferent to his inability to phonate, the spastic dysphonic suffers severely. His handicap drives him into seclusion and withdrawal, which makes it difficult to motivate him to cooperate fully with any form of therapy. Psychotherapy has not been too helpful. As mentioned before, a number of patients had already been through prolonged periods of intensive psychotherapy when they came for voice therapy. They may have gained better insight into the psychological background of the disorder, but the patterns of faulty phonation persisted. Eight patients accepted advice to see a psychiatrist and were followed up for a number of years. but only one improved significantly. The small number of patients who could be persuaded to undergo psychotherapy concomitant with voice training is due to the fact that most patients with spastic dysphonia are auite resistant to such a suggestion. Quite often. the only result of the advice to seek psychiatric counselling is that one loses the patient. On the other hand voice training alone has proved to be of very limited value. Freauently the patient improves during the first weeks or months, then reaches a plateau. At this point he often drops out of treatment. Later on he may experience a relapse, but he usually does not return to the orizinal therapist. Figures given by Cooner" illustrate this dismal picture: of 42 patients. only 22 entered therany. Onlv six comnleted it, with results described as excellent (1), good (3) and fair (2). Even such figures have to be interpreted with great caution. Too often the patient with spastic dysnhonia is making the rounds in quest of a simple remedy. He may go from therapist to therapist, each time
Downloaded from aor.sagepub.com at Purdue University Libraries on June 23, 2015
FRIEDRICH S. BRODNITZ
214
being listed as improved or even as cured. All this does not mean that one should leave the patient to his torment without trying to help him. The laryngologist to whom the patient will turn first has an important task to fulfill. First of all, he should be able to recognize the disease and make the correct diagnosis. He should not waste valuable time with inept methods of treatment. The sooner the patient is referred for expert therapy
the better are the chances for improvement of the voice. The worst one can do is to prescribe voice rest, as it will only deepen the anxiety and fear of speaking. Until newer research can achieve a more thorough understanding of the etiology of the disease, and thereby provide a rationale for more successful therapy, the combination of voice therapy with psychotherapy still offers the best chances for ameliorating this disorder.
REFERENCES 1. Aronson AE, Brown JR, Litin EM, et al: Spastic dysphonia: neurological and psychiatric aspects. J Speech Hear Disord 33: 203-218, 1968 2. Kiml J: Recherches experimentales de la dysphonic spastique. Folia Phoniatr (Basel) 17:241-301, 1965 3. Bloch P: Neuro-psychiatric aspects of spastic dysphonia. Folia Phoniatr (Basel) 17: 301-364, 1965 4. Berendes J: Zur Entstehung und Behandlung der Dysphonia Spastica, Z Hals-, Nasen- OhrenheiIkd 44:78, 1938 5. Arnold GE: Spastic dysphonia: changing interpretations of a persistent alHiction. Logos 2:3-14,1959 6. Heaver L: Spastic dysphonia: psychiatric considerations. Logos 2:15-24, 1959 REPRINTS:
7. Luchsinger R, Arnold G: Voice-Speech Language. Belmont, Calif., Wadsworth Publishing Co., 1965, p 331 8. Cooper M: Modern Techniques of Vocal Rehabilitation. Springfield, Chas, C Thomas, 1973 9. Brodnitz FS: Voice Disorders. A collection of recordings. Graduate Program in Communication Disorders, University of Southern California, 1974 10. Brodnitz FS: in Vocal Rehabilitation. American Academy of Ophthalmology and Otolaryngology, 4th edit., 1971, p 80 II. Robex E, Brurnlik J, Moore P: A study of spastic dysphonia: neurologic and encephalographic abnormalities. Laryngoscope 70: 219-245, 1960
Friedrich S. Brodnitz, M.D., 667 Madison Avenue, New York, NY 10021
XV INTERNATIONAL CONGRESS OF BRONCHOESOPHAGOLOGY The XV International Congress of Bronchoesophagology will be held in Sao Paulo, Brazil, March 24-26, 1977, following the II World Congress of Otolaryngology in Buenos Aires. For information write: Dr. Plinio de Mattos Barretto, President of the Congress, Rua Cons. Torres Homem, 371, 01432, Sao Paulo, Brazil.
Downloaded from aor.sagepub.com at Purdue University Libraries on June 23, 2015
SPASTIC DYSPHONIA FRIEDRICH
S.
BRODNITZ
NEW YORK, NEW YORK
SUMMARY - 130 cases of spastic dysphonia are reviewed with special emphasis on the etiology of the disorder. An analysis of the circumstances surrounding the onset of the disease points strongly to a psychogenic origin of the disease in, at least, the vast majority of the cases.
Of all the disorders of the human voice spastic dysphonia is still the most mysterious, the most poorly understood and the most resistant to successful therapy. Because of the relative rarity of the disorder, laryngologists are frequently not familiar with the syndrome of spastic dysphonia and often do not diagnose it properly when they encounter it. Because of the low incidence of the disorder most reports deal only with a small number of cases. This report includes case histories of 130 patients. Special emphasis will be given to the histories obtained which may throw light on the still disputed etiology of the disease. The first description of spastic dysphonia was given by Traube in 1871. The term is a poor one because "spasticity" is a term used to define a specific neurological disorder that does not quite fit the symptomatology and etiology of this form of dysphonia. Aronson- has suggested the term spasmodic dysphonia, but the original terminology has been used universally in the literature. It will be employed in this review. The two most exhaustive discussions of spastic dysphonia were presented in 1965 in reports to the 13th Congress of the International Association of Logopedics and Phoniatrics: by Kiml" on experimental investigation, and by Bloch" on the neuropsychiatric aspects of spastic dysphonia. The voluminous refer-
ences included over 400 items. Of special interest are the papers by Berendes," Arnold," Heaver," Luchsinger," and more recently, by Aronson.' SYMPTOMATOLOGY
One of the problems in writing about phoniatric problems is the difficulty in describing acoustic phenomena in print. It is much easier to make the proper diagnosis if one has previously had experience with even one case of fullblown spastic dysphonia. Even the busy laryngologist may never have encountered such a case before it first appears in his practice. A good recording of the voice of spastic dysphonia can be obtained from any major Speech and Hearing Center and would be helpful in alerting the laryngologist to the symptoms of spastic dysphonia. Teaching tapes of voice disorders containing representative examples of the different forms of vocal pathology are available." This author has previously described it as follows: "Spastic dysphonia stands at the opposite end of the dynamic scale of functional voice disorders. The aphonic patient has given up communication by the use of phonation, but in spastic dysphonia communication is interfered with by violent contractions of the vocal cords. The patient speaks with great effort in a constricted, highpitched voice.T'? Vowels are interrupted in the middle of the sound. A good de-
---From the Department of Otolaryngology Mount Sinai Medical Center, New York, N.Y. and the Institute of Health Sciences, Hunter College, The City University of New York. 210
Downloaded from aor.sagepub.com at Purdue University Libraries on June 23, 2015
211
SPASTIC DYSPHONIA
scription of spastic dysphonia was given by Berendes: "A disorder of phonation which is characterized by a strained, creaking and choked vocal attack, a tense and squeezed voice sound that is accompanied by extreme tension of the entire phonatory system,"! Many authors have noted the similarity between the glottal symptoms of spastic dysphonia and the oral ones of the stutterer and have called it "laryngeal stuttering." In both conditions, the severity of symptoms may vary greatly with the change of moods and the degree of nervous tension. It varies considerably from case to case, from patients with only mild symptoms to cases where the choking phonation makes communication almost impossible. In many instances the patient is able to produce quite normal phonatory sounds that do not have the character of direct communication. Almost all patients are able to laugh in a perfectly normal way and quite a few of them can sing without vocal cord constriction. INCIDENCE
Spastic dysphonia is usually described as a rare disease. The incidence of the disease may not be as low as reported. It seems quite likely that many cases, especially the milder ones. are never properly labeled. Practically all 130 cases seen by this author in over twentyfive years of phoniatric practice were referred for voice therapy by fellow Iaryngologists. Until the last few years, since laryngologists have become more sophisticated about functional voice problems, almost all patients came with incorrect diagnoses such as ventricular dysphonia. In any case, spastic dysphonia is not a common disorder. Of 2640 patients with all forms of functional voice disorders, the 130 patients with spastic dysphonia constitute only 4.0%. Men and women are equally affected, with women having a slight edge over men in most statistics. Of the 130 patients, 69 were women and 61 men.
The disease hits almost exclusively in middle age. Very few cases have been reported that occurred in childhood or adolescence. In the cases presented here the average mean age of the onset of the disorder was 50.2 years with the following distribution: 20-30 years, 13 cases; 31-40 years, 21 cases; 41-50 years, 35 cases: 51-60 years, 38 cases; over 60 years, 23 cases. The youngest patient was 27 years old, the oldest 76. ETIOLOGY
When spastic dysphonia was first described as a well defined disorder of the voice it was assumed that it should be considered a psychogenic disease, a form of conversion hysteria. Most of the subsequent authors have accepted a concept of looking at spastic dysphonia as one of two extreme forms of the continuum of functional voice disorders; functional aphonia being the extreme of vocal hypofunction; and spastic dysphonia representing the extreme of hyperfunction. Both disorders were interpreted as the physical manifestations of a deep-rooted emotional conflict. A different interpretation was first attempted in 1960 by Robe and Associates.!' who claimed that they found abnormal brain waves in the EEG of 90% of their patients with spastic dysphonia. This organic concept of the disease has been advocated more recently by Aronson and his associates.' On the strength of extensive investigation of 34 patients, they have come to the conclusion that at least some cases of spastic dysphonia are based on a neurological disorder, most likely in the extrapyramidal tracts. They add that further psychiatric and neurological studies are greatly needed. Subsequent EEG studies have yielded rather inconclusive results. Aronson! obtained normal EEG readings in 17 of 22 patients, only mild dysrhythmic activity in four others, and independent spike foci in one patient. Luchsinger" found only one abnormal registration in six patients.
Downloaded from aor.sagepub.com at Purdue University Libraries on June 23, 2015
212
FRIEDRICH S. BRODNITZ
The most extensive investigation was attempted by Kiml" who studied patients with spastic dysphonia with a wide range of laboratory methods: sonogram, tomogram, pneumography, spirometry, electromyography, measurement of subglottic air-pressure and EEG. All measurements, except the last one, exhibit considerable deviations from the norm; but these elucidate only symptoms of the disease, and they do not contribute anything to the uncovering of the etiology. The EEGs revealed only slight changes in four out of ten cases. At the end of the study Kiml remarks: "One can register everything but one has to know what purpose it really serves," and he quotes Norbert Wiener of cybernetics fame who warned that «we are the slaves of technological discoveries."
Bloch" pleaded the case for the psychogenic character of the disorder and he. too, remarked "that researchers from EEG to hematochemical analysis, from neuro-vegetative to endocrine factors will always find in many cases modifications. But there is the danger that we may not see the forest for the trees". The essential question that should be addressed is: What is cause and what is only a symptom in the complicated interplay of body functions? The stutterer exhibits in his speech a marked deviation from neuromuscular patterns, and the aphonic patient may present a bizarre picture of paradoxic vocal cord action. Still, both conditions are widely accepted as psychogenic in origin. None of the reported abnormal findings in spastic dysphonia are pronounced enough to interpret them as caused by neurological pathology. Years ago the author tried, in six cases' the use of the intravenous injection ~f Amytal®O ( narco-analysis) in the hope that it could be used as therapy. While under the influence of the drug, the patients spoke in a quite normal pattern with only rare traces of
spasmodic speech; but, as soon as the effect of the drug wore off they reverted to disturbed vocal function. Another observation that speaks for the psychogenic etiology is that many patients with spastic dysphonia are able to sing in a normal voice with free H~w of tone and being on target for the different frequencies. This requires greater sharpness of neuromuscular control than does speech, but it does constitute personal communication to as great a degree. This phenomenon runs counter to what one would expect in a patient with neurological pathology but it makes sense if one interprets it as the elimination of a powerful psychological element. The same observation has been made quite often in stutterers. A large number of patients pinpoint with great accuracy the onset of the dysphonia after e~osure to se.vere emotional trauma. FIfty-three patients volunteered under the cautious probing of the intake interview, what they considered to be the event that triggered the development of the disease. A few such incidents are: the death of a near relative (13 cases, five of them from laryngeal cancer); severe automobile accidents leaving them physically unharmed (8 cases); climactic marital crisis \ 8 cases, one of them starting suddenly m divorce court under rough treatment by the opposing lawyer); laryngeal surgery for removal of benign lesions (5 cases). One woman became dysphonic when her husband threatened to kill her; another, after her husband was murdered; a third, after her brother was shot to death in a holdup; a fourth, after witnessing the first epileptic attack of her child. A minister developed spastic dysphonia when he lost his pulpit in the South when he d~monstra~e? with Dr. Martin Luther Kmg for civil liberties. Two cases stand out in significance for the psychogenic etiology: 1. A young psychiatrist was told that his training analysis was com-
---;;Eli Lilly & ce., Indianapolis, Indiana
Downloaded from aor.sagepub.com at Purdue University Libraries on June 23, 2015
SPASTIC DYSPHONIA
plete. A few weeks after this cutting of the analytical umbilical cord he developed spastic dysphonia. He discussed it with his analyst who agreed to take him back for three more months. Immediately his voice became normal only to revert to the dysphonia when the analyst told him, at the end of these three months, that he should now be able to stand on his own feet. 2. The headwaiter of a luxury restaurant came in for treatment. During the course of the first interview he reported that his voice was very bad at home and among friends but that he could speak with a practically normal voice when he put on his tuxedo and started to serve the guests, slipping into the "role" of an elegant maitre d'hotel. Aside from these 53 patients who could pinpoint the onset of the disorder, there were 28 who exhibited many of the characteristics of severe neuroses. Eight of them had already had long periods of psychiatric treatment before they developed spastic dysphonia. This leaves only about one third of the cases reported in this paper where no obvious psychogenic background could be found. This is not an unusual situation in psychosomatic disorders, particularly in manifestations of conversion hysteria. Of course, everybody who has had freauent contact with cases of spastic dysphonia has entertained the suspicion that an organic neurological factor may be the etiological basis of the more severe forms of the disorder. Possibly, future research with more refined methods may demonstrate such a connection in some cases. As of now, overwhelming proof speaks for a psychogenic disorder, a "neuro-physiologic regression" (Heaver"}, resulting in "a form of psychogenic breakdown of corticothalamic integration" (Arnold 5 ) . THERAPY
Authors who have written about spastic dysphonia agree on the poor results of any form of therapy. There are a number of reasons for this unfortunate
213
state of affairs. In this disorder we deal with a very complex syndrome. As in stuttering, the patient develops patterns of behavior that tend to become more and more deep-seated as time goes by. The increasing impairment of communication itself reinforces the psychological trauma. In contrast to the patient with functional aphonia. who is often strangely indifferent to his inability to phonate, the spastic dysphonic suffers severely. His handicap drives him into seclusion and withdrawal, which makes it difficult to motivate him to cooperate fully with any form of therapy. Psychotherapy has not been too helpful. As mentioned before, a number of patients had already been through prolonged periods of intensive psychotherapy when they came for voice therapy. They may have gained better insight into the psychological background of the disorder, but the patterns of faulty phonation persisted. Eight patients accepted advice to see a psychiatrist and were followed up for a number of years. but only one improved significantly. The small number of patients who could be persuaded to undergo psychotherapy concomitant with voice training is due to the fact that most patients with spastic dysphonia are auite resistant to such a suggestion. Quite often. the only result of the advice to seek psychiatric counselling is that one loses the patient. On the other hand voice training alone has proved to be of very limited value. Freauently the patient improves during the first weeks or months, then reaches a plateau. At this point he often drops out of treatment. Later on he may experience a relapse, but he usually does not return to the orizinal therapist. Figures given by Cooner" illustrate this dismal picture: of 42 patients. only 22 entered therany. Onlv six comnleted it, with results described as excellent (1), good (3) and fair (2). Even such figures have to be interpreted with great caution. Too often the patient with spastic dysnhonia is making the rounds in quest of a simple remedy. He may go from therapist to therapist, each time
Downloaded from aor.sagepub.com at Purdue University Libraries on June 23, 2015
FRIEDRICH S. BRODNITZ
214
being listed as improved or even as cured. All this does not mean that one should leave the patient to his torment without trying to help him. The laryngologist to whom the patient will turn first has an important task to fulfill. First of all, he should be able to recognize the disease and make the correct diagnosis. He should not waste valuable time with inept methods of treatment. The sooner the patient is referred for expert therapy
the better are the chances for improvement of the voice. The worst one can do is to prescribe voice rest, as it will only deepen the anxiety and fear of speaking. Until newer research can achieve a more thorough understanding of the etiology of the disease, and thereby provide a rationale for more successful therapy, the combination of voice therapy with psychotherapy still offers the best chances for ameliorating this disorder.
REFERENCES 1. Aronson AE, Brown JR, Litin EM, et al: Spastic dysphonia: neurological and psychiatric aspects. J Speech Hear Disord 33: 203-218, 1968 2. Kiml J: Recherches experimentales de la dysphonic spastique. Folia Phoniatr (Basel) 17:241-301, 1965 3. Bloch P: Neuro-psychiatric aspects of spastic dysphonia. Folia Phoniatr (Basel) 17: 301-364, 1965 4. Berendes J: Zur Entstehung und Behandlung der Dysphonia Spastica, Z Hals-, Nasen- OhrenheiIkd 44:78, 1938 5. Arnold GE: Spastic dysphonia: changing interpretations of a persistent alHiction. Logos 2:3-14,1959 6. Heaver L: Spastic dysphonia: psychiatric considerations. Logos 2:15-24, 1959 REPRINTS:
7. Luchsinger R, Arnold G: Voice-Speech Language. Belmont, Calif., Wadsworth Publishing Co., 1965, p 331 8. Cooper M: Modern Techniques of Vocal Rehabilitation. Springfield, Chas, C Thomas, 1973 9. Brodnitz FS: Voice Disorders. A collection of recordings. Graduate Program in Communication Disorders, University of Southern California, 1974 10. Brodnitz FS: in Vocal Rehabilitation. American Academy of Ophthalmology and Otolaryngology, 4th edit., 1971, p 80 II. Robex E, Brurnlik J, Moore P: A study of spastic dysphonia: neurologic and encephalographic abnormalities. Laryngoscope 70: 219-245, 1960
Friedrich S. Brodnitz, M.D., 667 Madison Avenue, New York, NY 10021
XV INTERNATIONAL CONGRESS OF BRONCHOESOPHAGOLOGY The XV International Congress of Bronchoesophagology will be held in Sao Paulo, Brazil, March 24-26, 1977, following the II World Congress of Otolaryngology in Buenos Aires. For information write: Dr. Plinio de Mattos Barretto, President of the Congress, Rua Cons. Torres Homem, 371, 01432, Sao Paulo, Brazil.
Downloaded from aor.sagepub.com at Purdue University Libraries on June 23, 2015
