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Tinnitus
Tinnitus JULIUS WINSTON, M.D., F.A.C.S. *
TINNITUS is a sensation of noise in the ear or in the head which originates autogenously. It is the most difficult symptom with which the otologist has to cope. Tinnitus is almost invariably accompanied by deafness, but deafness may not necessarily be accompanied by tinnitus. Clinically it is seen more frequently in people past middle age. Children rarely complain of it. Tinnitus has been variously compared to the sound of escaping steam, a hum, a roar, a buzzing or a ringing sound. It may be continuous or pulsating in character. Many patients who suffer from chronic tinnitus believe that the intensity of the tinnitus is very loud, although Fowler1 has found the loudness of the tinnitus in these patients to be about 5 decibels and rarely more than 15 decibels. Tinnitus may be classified as (1) vibratory, (2) nonvibratory and (;~) cerebral. VIBRATORY TINNITUS
Vibratory tinnitus is mechanical in origin and is caused by vibrations either in the ear or outside of the ear, which are transmitted to the organ of Corti either directly or indirectly through the solid, liquid or gaseous media of the body. These vibrations are produced by: (1) The blood flow in vessels in or near the ear and may be due to disturbances of the local or general circulation, or to abnormalities in the size, shape and position of the blood vessels. (2) The rhythmic contraction of muscles, e.g., the pharyngeal muscles. This occurs more frequently in neurotic individuals. (3) The opening and closing of the eustachian tubes. (4) The temporomandibular joints. Movements of the mandible may cause clicking sounds, especially when there is a chronic subluxation of the temporomandibular joints. From the Departments of Otolaryngology, School of Medicine and Graduate School of Medicine, University of Pennsylvania, and Graduate Hospital, Philadelphia.
* Associate Professor of Otolaryngology, School of Medicine, University of Pennsylvania; Assistant Professor of Otolaryngology, Graduate School of Medicine, University of Pennsylvania; Associate Otolaryngologist, University of Pennsylvania Hospital; AS8istant Otolaryngologist, Graduate Hospital. 1781
1782
J ulius W inston
Panse advanced the theory that the sound conduction apparatus, which consists of the auricle, the external auditory canal, the tympanic membrane, the maleus, incus, stapes, and the fluid of the labyrinth, not only conducts sound waves, which originate exogenously, centrally to the organ of Corti, but it also transmits autogenous body sounds which have been conducted to the ear by the bones, muscles, liquid and gaseous media of the body in a direction away from the organ of Corti thus preventing these sounds from reaching the organ of Corti. It is, therefore, due to the latter function of the sound conduction apparatus that the normally prevalent sonorous vibrations do not reach the organ of Corti. In acute tubal catarrh and acute otitis media, deafness and tinnitus of a pulsating type are prominent symptoms. Under these conditions, there is impairment in the function of the sound conduction apparatus. With resolution of these inflammatory conditions, the function of the sound conduction mechanism returns to normal and the tinnitus and deafness disappear. The internal carotid artery and the bulb of the internal jugular vein are in close relationship to the middle ear cavity. The internal carotid artery is separated from the anterior middle ear cavity by a thin plate of bone. The bulb of the internal jugular vein is similarly separated from the floor of the tympanic cavity by a thin plate of bone. There may be a congenital dehiscence of the bony plate separating either the internal carotid artery or the bulb of the internal jugular vein from the middle ear cavity. These dehiscences may also be acquired from chronic middle ear infections resulting in bone necrosis. Under these circumstances, tinnitus may result. The resultant tinnitus is low or medium pitched and is pulsating in character when it originates from the artery and is continuous or nonpulsating when it is of venous origin. It can frequently be heard by the examiner if he applies his ear to the patient's ear, either directly or indirectly by means of a Toynbee diagnostic tube. The presence of the highly vascular tumor, the glomus jugularis, in the middle ear may also give rise to tinnitus. The diagnosis may be made by careful otologic and x-ray examination. Remote from the temporal bone, aneurysms within the skull (the basilar and internal auditory arteries being the most frequently involved) may be the cause of a loud tinnitus or bruit localized in the head. Brain tumors compressing an artery or a vein within the skull, the presence of a vascular meningioma, atherosclerotic plaques, murmurs transmitted from the neck vessels in hypertension, cardiac valvular disease, and vascular thyroid glands may also cause loud cranial bruits. These cranial bruits are always synchronous with the pulse. They can frequently be heard through the stethoscope. Stethoscopy should be carried out, according to Poppen,3 with the patient in the sitting, prone and decubitus positions. The bruit can best be heard with the patient's head resting on the stethoscope. These bruits may be harsh, soft, whistling, rumbling,
Tinnitus
1783
churning, or of machinery quality. The character of the bruit may be altered by respiration, or by digital compression of the carotid artery. If the bruit is louder on one side of the skull, digital compression of the carotid artery on the same side may alter the pitch or obliterate the bruit. If only the pitch is changed, the vertebral system is involved. If the contralateral carotid artery is compressed, the bruit usually becomes louder. If the source of the bruit is midline, the bruit can be heard equally well bilaterally. Aneurysms may produce a murmur which may be made louder by increasing the pulse pressure and blood flow, by exercise or stimulants. The diagnosis can also be made by arteriograms. If the basilar artery or one of its branches, e.g., the internal auditory artery, is the site of an aneurysm, a vertebral arteriogram will often disclose the diagnosis and the exact location of the aneurysm. A carotid arteriogram may often demonstrate an aneurysm of the internal carotid artery or any of its intracranial branches. Calcareous arterial plaques involving the aorta or the great vessels of the neck can often be demonstrated on flat x-ray films. The treatment of cranial bruits is the treatment of the underlying cause. When bruits are caused by an intracranial aneurysm, the neurosurgeon can often tie off the aneurysm. The collateral circulation must, however, be good. NONVIBRATORY TINNITUS
N onvibratory tinnitus results from pathologic changes in the auditory neural mechanism. It is almost invariably accompanied by deafness of a nerve or perceptive type. It is usually constant rather than pulsating in character and is comparable to the sound of escaping steam. The pathologic changes of the auditory neural mechanism may be irritative or destructive in nature. These pathologic changes may result from two factors; 1. A toxicity secondary to (a) acute infectious diseases, such as mumps. (b) Drugs; e.g., quinine, salicylates and the streptomycin group of drugs. The latter have been shown to damage the ventral cochlear nuclei in the brain stem4 , 5,6 as well as the peripheral neural mechanism. 7 (c) Metabolic diseases, e.g., diabetes, nephritis and gout. 2. An imbalance of the autonomic nervous system, including"the parasympathetic nervous system. In a large group of patients complaining of tinnitus and nerve deafness, in whom the etiological factors outlined in the first group can be readily ruled out, and who are otherwise in a state of excellent general health, Fowler and FowlerS have found, from observations of the conjunctival blood vessels of patients, evidence which suggests an imbalance in the autonomic nervous system as the cause. Emotional disturbances and sexual maladjustments, frustrations and obsessions, as well as menstruation and natural or artificial meno-
J ulius W ins ton
1784
pause, may be important factors in bringing about such an imbalance in the autonomic nervous system. As a result of this imbalance there are changes in the terminal arterioles, observable in the conjunctiva under high magnification, which lead to dumping of the blood corpuscles forming "blood sludge" whic:h chokes off the arterioles. There is also a transudation of the liquid elements of the blood into the surrounding tissue. The authors reason that this may occur in any organ of the body. In the internal ear, the blood circulation is terminal, i.e., there is no collateral circulation, so that blood sludge forming within the terminal arterioles of the internal ear results in a degeneration of the neural elements which the blocked arterioles supply. This may be the mechanism that causes Meniere's disease (hydrops of the labyrinth), which is characterized by recurrent paroxysmal attacks of vertigo, tinnitus and deafness. The treatment of llonvibratory tinnitus has been most discouraging. Phenobarbital 16 mg. Oi grain) three or four times daily has been widely employed. Its effect in many patients suffering from chronic tinnitus is palliative rather than curative. Vitamin B, either El or B complex, is of value in the treatment of non vibratory tinnitus in only about 10 per cent of cases. Fowler's9 treatment is psychosomatic. It in eludes (a) a careful history; (b) a complete otological examination including audiometry with matching and measurement of the intensity of the tinnitus, and an examination to determine whether exereise, stooping or pressure on the jugular veins or the carotid arteries alters the tinnitus in any way; (c) showing and convincing the patient that his tinnitus is not as loud as he thinks; (d) fitting of the patient with a hearing aid to improve his hearing, and by so doing render the tinnitus subaudible. CEREBRAL TINNITUS
Tinnitus of cerebral origin may be caused by a lesion of the auditory center in the temporal lobe (Broca's area). A tumor or hemorrhage, spontaneous or traumatic, involving this area may also produce an auditory aphasia. The patient can hear pure tones on the audiometer well, but is unable to "hear" speech. Language spoken in his own tongue sounds foreign. The tinnitus which epileptics experience as an aura must be regarded as central or cerebral in origin. The auditory hallucinations of those suffering from a psychosis must be regarded as tinnitus and it is of a complex type. The tinnitus here assumes the sounds of words. The treatment of cerebral tinnitus obviously is the treatment of the cause. SUMMARY
Tinnitus may be defined as a sensation of noise in the ear or in the head, which originates autogenously.
Tinnitus
1785
There are three types of tinnitus: (1) vibratory, (2) nonvibratoryand (3) cerebral. Vibratory tinnitus results from the transmission of normal body sounds to the organs of Corti by a functionally impaired conduction apparatus, or the transmission of abnormally loud body sounds to the organ of Corti by a normally functioning sound conduction mechanism. Many of the causes, the diagnosis and the treatment of vibratory tinnitus are presented. N onvibratory tinnitus results from an irritation or a degeneration of the auditory neural mechanism and is nearly always accompanied by a perceptive type of deafness of varying degree. Many of the causes, including Fowler's theory of an imbalance of the autonomic nervous system, the diagnosis and treatment are discussed. Cerebral tinnitus results from irritation or damage to the cerebral auditory center (Broca's area) from (a) hemorrhage, spontaneous or traumatic; (b) brain tumors; (c) epilepsy when tinnitus constitutes its aura; (d) psychoses which have auditory hallucinations as one of their symptoms. The treatment of cerebral tinnitus constitutes the treatment of the underlying cause. CONCLUSIONS
Tinnitus is a symptom of many different diseases within or remote from the temporal bone. The treatment is essentially the treatment of the underlying cause. It is therefore obvious that a careful history and a thorough otological and general physical examination are essential if we are to succeed in treating those who present themselves with this symptom. It is also obvious that there is no one satisfactory means of treating tinnitus. REFERENCES
1. Fowler, E. P.: Tinnitus Aurium in the Light of Recent Research. Ann. OtoI., Rhin. & Laryn. 50: 1391 (March) 1941. 2. Kerrison, P. D.: Diseases of the Ear. 4th Ed. Philadelphia, J. B. Lippincott Co., 1930, p. 137. 3. Poppen, J. L.: Cranial Bruit-Its Significance. S. CIin. North America 35: 881886 (June) 1955. 4. Winston, J., Lewey, F. H., Parenteau, A., Marden, P. and Cramer, F. B.: An Experimental Study of the Toxic Effects of Streptomycin on the Vestibular Apparatus of the Cat. Ann. OtoI., Rhin. & Laryng. 57: 738 (Sept.) 1948. 5. Winston, J., Lewey, F. H., Parenteau, A., Marden, P. and Cramer, F. B.: Further Experimental Studies of the Toxic Effects of Streptomycin on the Central Vestibular Apparatus of the Cat. Ann. Otol., Rhin. & Laryng. 58: 988 (Dec.) 1949. 6. Winston, J., Lewey, F. H., Parenteau, A., Spitz, E. B. and Marden, P.: Toxic Effects of Dihydrostreptomycin upon the Central Vestibular Mechanism of the Cat. Ann. OtoI., Rhin. & Laryng. 62: 121 (March) 1953. 7. Hawkins, J. E., Jr. and Lurie, M. H.: The Ototoxicity of Streptomycin. Ann. Otol., Rhin. & Laryng. 61: 789 (Sept.) 1952.
1786
J ulius W ins ton
8. Fowler, E. P. and Fowler, E. P. Jr.: An Explanation of Certain Types of Tinnitus and Deafness. Laryngoscope 60: 919 (Sept.) 1950. 9. Fowler, E. P.: The Emotional Factor in Tinnitus Aurium. Laryngoscope 58: 145 (Feb.) 1948. 5839 Chester Avenue Philadelphia 43, Pennsylvania
TINNITUS is a sensation of noise in the ear or in the head which originates autogenously. It is the most difficult symptom with which the otologist has to cope. Tinnitus is almost invariably accompanied by deafness, but deafness may not necessarily be accompanied by tinnitus. Clinically it is seen more frequently in people past middle age. Children rarely complain of it. Tinnitus has been variously compared to the sound of escaping steam, a hum, a roar, a buzzing or a ringing sound. It may be continuous or pulsating in character. Many patients who suffer from chronic tinnitus believe that the intensity of the tinnitus is very loud, although Fowler1 has found the loudness of the tinnitus in these patients to be about 5 decibels and rarely more than 15 decibels. Tinnitus may be classified as (1) vibratory, (2) nonvibratory and (;~) cerebral. VIBRATORY TINNITUS
Vibratory tinnitus is mechanical in origin and is caused by vibrations either in the ear or outside of the ear, which are transmitted to the organ of Corti either directly or indirectly through the solid, liquid or gaseous media of the body. These vibrations are produced by: (1) The blood flow in vessels in or near the ear and may be due to disturbances of the local or general circulation, or to abnormalities in the size, shape and position of the blood vessels. (2) The rhythmic contraction of muscles, e.g., the pharyngeal muscles. This occurs more frequently in neurotic individuals. (3) The opening and closing of the eustachian tubes. (4) The temporomandibular joints. Movements of the mandible may cause clicking sounds, especially when there is a chronic subluxation of the temporomandibular joints. From the Departments of Otolaryngology, School of Medicine and Graduate School of Medicine, University of Pennsylvania, and Graduate Hospital, Philadelphia.
* Associate Professor of Otolaryngology, School of Medicine, University of Pennsylvania; Assistant Professor of Otolaryngology, Graduate School of Medicine, University of Pennsylvania; Associate Otolaryngologist, University of Pennsylvania Hospital; AS8istant Otolaryngologist, Graduate Hospital. 1781
1782
J ulius W inston
Panse advanced the theory that the sound conduction apparatus, which consists of the auricle, the external auditory canal, the tympanic membrane, the maleus, incus, stapes, and the fluid of the labyrinth, not only conducts sound waves, which originate exogenously, centrally to the organ of Corti, but it also transmits autogenous body sounds which have been conducted to the ear by the bones, muscles, liquid and gaseous media of the body in a direction away from the organ of Corti thus preventing these sounds from reaching the organ of Corti. It is, therefore, due to the latter function of the sound conduction apparatus that the normally prevalent sonorous vibrations do not reach the organ of Corti. In acute tubal catarrh and acute otitis media, deafness and tinnitus of a pulsating type are prominent symptoms. Under these conditions, there is impairment in the function of the sound conduction apparatus. With resolution of these inflammatory conditions, the function of the sound conduction mechanism returns to normal and the tinnitus and deafness disappear. The internal carotid artery and the bulb of the internal jugular vein are in close relationship to the middle ear cavity. The internal carotid artery is separated from the anterior middle ear cavity by a thin plate of bone. The bulb of the internal jugular vein is similarly separated from the floor of the tympanic cavity by a thin plate of bone. There may be a congenital dehiscence of the bony plate separating either the internal carotid artery or the bulb of the internal jugular vein from the middle ear cavity. These dehiscences may also be acquired from chronic middle ear infections resulting in bone necrosis. Under these circumstances, tinnitus may result. The resultant tinnitus is low or medium pitched and is pulsating in character when it originates from the artery and is continuous or nonpulsating when it is of venous origin. It can frequently be heard by the examiner if he applies his ear to the patient's ear, either directly or indirectly by means of a Toynbee diagnostic tube. The presence of the highly vascular tumor, the glomus jugularis, in the middle ear may also give rise to tinnitus. The diagnosis may be made by careful otologic and x-ray examination. Remote from the temporal bone, aneurysms within the skull (the basilar and internal auditory arteries being the most frequently involved) may be the cause of a loud tinnitus or bruit localized in the head. Brain tumors compressing an artery or a vein within the skull, the presence of a vascular meningioma, atherosclerotic plaques, murmurs transmitted from the neck vessels in hypertension, cardiac valvular disease, and vascular thyroid glands may also cause loud cranial bruits. These cranial bruits are always synchronous with the pulse. They can frequently be heard through the stethoscope. Stethoscopy should be carried out, according to Poppen,3 with the patient in the sitting, prone and decubitus positions. The bruit can best be heard with the patient's head resting on the stethoscope. These bruits may be harsh, soft, whistling, rumbling,
Tinnitus
1783
churning, or of machinery quality. The character of the bruit may be altered by respiration, or by digital compression of the carotid artery. If the bruit is louder on one side of the skull, digital compression of the carotid artery on the same side may alter the pitch or obliterate the bruit. If only the pitch is changed, the vertebral system is involved. If the contralateral carotid artery is compressed, the bruit usually becomes louder. If the source of the bruit is midline, the bruit can be heard equally well bilaterally. Aneurysms may produce a murmur which may be made louder by increasing the pulse pressure and blood flow, by exercise or stimulants. The diagnosis can also be made by arteriograms. If the basilar artery or one of its branches, e.g., the internal auditory artery, is the site of an aneurysm, a vertebral arteriogram will often disclose the diagnosis and the exact location of the aneurysm. A carotid arteriogram may often demonstrate an aneurysm of the internal carotid artery or any of its intracranial branches. Calcareous arterial plaques involving the aorta or the great vessels of the neck can often be demonstrated on flat x-ray films. The treatment of cranial bruits is the treatment of the underlying cause. When bruits are caused by an intracranial aneurysm, the neurosurgeon can often tie off the aneurysm. The collateral circulation must, however, be good. NONVIBRATORY TINNITUS
N onvibratory tinnitus results from pathologic changes in the auditory neural mechanism. It is almost invariably accompanied by deafness of a nerve or perceptive type. It is usually constant rather than pulsating in character and is comparable to the sound of escaping steam. The pathologic changes of the auditory neural mechanism may be irritative or destructive in nature. These pathologic changes may result from two factors; 1. A toxicity secondary to (a) acute infectious diseases, such as mumps. (b) Drugs; e.g., quinine, salicylates and the streptomycin group of drugs. The latter have been shown to damage the ventral cochlear nuclei in the brain stem4 , 5,6 as well as the peripheral neural mechanism. 7 (c) Metabolic diseases, e.g., diabetes, nephritis and gout. 2. An imbalance of the autonomic nervous system, including"the parasympathetic nervous system. In a large group of patients complaining of tinnitus and nerve deafness, in whom the etiological factors outlined in the first group can be readily ruled out, and who are otherwise in a state of excellent general health, Fowler and FowlerS have found, from observations of the conjunctival blood vessels of patients, evidence which suggests an imbalance in the autonomic nervous system as the cause. Emotional disturbances and sexual maladjustments, frustrations and obsessions, as well as menstruation and natural or artificial meno-
J ulius W ins ton
1784
pause, may be important factors in bringing about such an imbalance in the autonomic nervous system. As a result of this imbalance there are changes in the terminal arterioles, observable in the conjunctiva under high magnification, which lead to dumping of the blood corpuscles forming "blood sludge" whic:h chokes off the arterioles. There is also a transudation of the liquid elements of the blood into the surrounding tissue. The authors reason that this may occur in any organ of the body. In the internal ear, the blood circulation is terminal, i.e., there is no collateral circulation, so that blood sludge forming within the terminal arterioles of the internal ear results in a degeneration of the neural elements which the blocked arterioles supply. This may be the mechanism that causes Meniere's disease (hydrops of the labyrinth), which is characterized by recurrent paroxysmal attacks of vertigo, tinnitus and deafness. The treatment of llonvibratory tinnitus has been most discouraging. Phenobarbital 16 mg. Oi grain) three or four times daily has been widely employed. Its effect in many patients suffering from chronic tinnitus is palliative rather than curative. Vitamin B, either El or B complex, is of value in the treatment of non vibratory tinnitus in only about 10 per cent of cases. Fowler's9 treatment is psychosomatic. It in eludes (a) a careful history; (b) a complete otological examination including audiometry with matching and measurement of the intensity of the tinnitus, and an examination to determine whether exereise, stooping or pressure on the jugular veins or the carotid arteries alters the tinnitus in any way; (c) showing and convincing the patient that his tinnitus is not as loud as he thinks; (d) fitting of the patient with a hearing aid to improve his hearing, and by so doing render the tinnitus subaudible. CEREBRAL TINNITUS
Tinnitus of cerebral origin may be caused by a lesion of the auditory center in the temporal lobe (Broca's area). A tumor or hemorrhage, spontaneous or traumatic, involving this area may also produce an auditory aphasia. The patient can hear pure tones on the audiometer well, but is unable to "hear" speech. Language spoken in his own tongue sounds foreign. The tinnitus which epileptics experience as an aura must be regarded as central or cerebral in origin. The auditory hallucinations of those suffering from a psychosis must be regarded as tinnitus and it is of a complex type. The tinnitus here assumes the sounds of words. The treatment of cerebral tinnitus obviously is the treatment of the cause. SUMMARY
Tinnitus may be defined as a sensation of noise in the ear or in the head, which originates autogenously.
Tinnitus
1785
There are three types of tinnitus: (1) vibratory, (2) nonvibratoryand (3) cerebral. Vibratory tinnitus results from the transmission of normal body sounds to the organs of Corti by a functionally impaired conduction apparatus, or the transmission of abnormally loud body sounds to the organ of Corti by a normally functioning sound conduction mechanism. Many of the causes, the diagnosis and the treatment of vibratory tinnitus are presented. N onvibratory tinnitus results from an irritation or a degeneration of the auditory neural mechanism and is nearly always accompanied by a perceptive type of deafness of varying degree. Many of the causes, including Fowler's theory of an imbalance of the autonomic nervous system, the diagnosis and treatment are discussed. Cerebral tinnitus results from irritation or damage to the cerebral auditory center (Broca's area) from (a) hemorrhage, spontaneous or traumatic; (b) brain tumors; (c) epilepsy when tinnitus constitutes its aura; (d) psychoses which have auditory hallucinations as one of their symptoms. The treatment of cerebral tinnitus constitutes the treatment of the underlying cause. CONCLUSIONS
Tinnitus is a symptom of many different diseases within or remote from the temporal bone. The treatment is essentially the treatment of the underlying cause. It is therefore obvious that a careful history and a thorough otological and general physical examination are essential if we are to succeed in treating those who present themselves with this symptom. It is also obvious that there is no one satisfactory means of treating tinnitus. REFERENCES
1. Fowler, E. P.: Tinnitus Aurium in the Light of Recent Research. Ann. OtoI., Rhin. & Laryn. 50: 1391 (March) 1941. 2. Kerrison, P. D.: Diseases of the Ear. 4th Ed. Philadelphia, J. B. Lippincott Co., 1930, p. 137. 3. Poppen, J. L.: Cranial Bruit-Its Significance. S. CIin. North America 35: 881886 (June) 1955. 4. Winston, J., Lewey, F. H., Parenteau, A., Marden, P. and Cramer, F. B.: An Experimental Study of the Toxic Effects of Streptomycin on the Vestibular Apparatus of the Cat. Ann. OtoI., Rhin. & Laryng. 57: 738 (Sept.) 1948. 5. Winston, J., Lewey, F. H., Parenteau, A., Marden, P. and Cramer, F. B.: Further Experimental Studies of the Toxic Effects of Streptomycin on the Central Vestibular Apparatus of the Cat. Ann. Otol., Rhin. & Laryng. 58: 988 (Dec.) 1949. 6. Winston, J., Lewey, F. H., Parenteau, A., Spitz, E. B. and Marden, P.: Toxic Effects of Dihydrostreptomycin upon the Central Vestibular Mechanism of the Cat. Ann. OtoI., Rhin. & Laryng. 62: 121 (March) 1953. 7. Hawkins, J. E., Jr. and Lurie, M. H.: The Ototoxicity of Streptomycin. Ann. Otol., Rhin. & Laryng. 61: 789 (Sept.) 1952.
1786
J ulius W ins ton
8. Fowler, E. P. and Fowler, E. P. Jr.: An Explanation of Certain Types of Tinnitus and Deafness. Laryngoscope 60: 919 (Sept.) 1950. 9. Fowler, E. P.: The Emotional Factor in Tinnitus Aurium. Laryngoscope 58: 145 (Feb.) 1948. 5839 Chester Avenue Philadelphia 43, Pennsylvania