1. Yrd.Doç.Dr. Rasim Yılmazer
VERTIGO AND TINNITUS
Yrd.Doç.Dr. Rasim Yılmazer

2. Learning goal and objectives of the lesson
Learning goal of the lesson: Learning goal of the lesson: The learner should know the main clinical features and investigation of the tinnitus
Learning objectives of the lesson the learner will be able to:
describe the tınnıtus, type of tinnitus
explain the evaluation methods for tinnitus
explain the rehabilitation methods for tinnitus

3. Learning goal and objectives of the lesson
Learning goal of the lesson: The learner should know the main clinical features and investigation of the vertigo
Learning objectives of the lesson the learner will be able to:
take a directed history from patient with vertigo
list the evaluation methods for peripheral vestibular system
describe the peripheral causes of vertigo
Skill objectives the learner will be able to
evaluate the patient’s nystagmus during acute attack of peripheral vertigo.
learn how to approach the patient with cochleovestibular pathology

4. Vertigo

5. Steps 1.History Taking 2.Clear definition
(Vertiginous or Nonvertiginous dizziness)
3.Peripheral or Central Vertigo
4.Psychogenic Vertigo

6. Differential diagnosis
1.Dizziness
2.Presyncope
3.Disequilibrium:Unsteady gait
4.Light-headedness
dizziness the term most commonly used by outpatients to describe vertigo; Presyncope usually assoicated with CVD, described as a feeling of impending faint or loss of consciousness but no true syncope (Bp-orthostatic, HR, EKG); Disequilibrium: usually seen in elderly patients, hallmark of this disorder is an unsteady gait (pt with cataracts, neuromuscular CVA, Parkinson’s dx). Light-headedness associated with underlying psychiatric disorders, hyperventilation syndrome.

7. Symptoms Unconscious Pallor Sweating Nausea/Vomiting
Auditory Symptoms :Hearing loss, Tinnitus, aural (ear) fullness
Vertigo associated with high sounds or pressure
Neurologic Symptoms: numbness, weakness, difficulty with swallowing or speech

8. Definition a subjective sensation of movement
May feel either that him involving in space or that objects in the environment are moving around him.

9. History Taking
Description of the sensation (including associated symptoms)
Onset (acute, gradual)
Duration (date sensation was first noted, length of time it lasts)
Intensity (how troubling is it?)
Exacerbations (activities, positions, circumstances that worsen situation)

10. Remissions (activities, positions circumstances that make sensation better)
Medications (prescription, herbal, over the counter)
Other medical problems (diabetes, hypertension, heart disease, etc)
Psychosocial (any stressors?)

11. Physical Examinations
Mental conditions
Vital Signs: Bp,HR
Otoscopy
Ascultation of the neck for bruits
Rinne Test
Weber’s Test

12. Rinne Test

13. Weber’s Test

14. Weber and Rinne Test

15. Dix-Hallpike Maneuver
Neurologic exams
Nystagmus
Romberg’s
Gait
Dix-Hallpike Maneuver

16. Dix-Hallpike Maneuver

17. Peripheral Vertigo vs Central Vertigo
Features
Peripheral Vertigo
Central Vertigo
Conscious
Unconscious
Nystagmus
Horizontal/rotary
Vertical
Related to position changing
Yes No
Symptoms
Auditory symptoms (aural fullness,tinnitus ,hearing loss)
Neurologic symptoms (disequilibrium,gait)

18. Comparison of Common Diseases
Features
BPPV
Meniere (Labyrinthitis)
Psychogenic
Central Vertigo
Type of Vertigo
Positional
Spontaneous
Variable
Duration of Vertigo
1-2min
30min-2hrs
Several years
Several days-months
Symptoms
Auditory symptoms (aural fullness,tinnitus ,hearing loss)
Palpitations,hyperventilation
Neurologic symptoms (Disequilibrium, unconscious)
Nystagmus
Horizontal/rotary
Horizontal
Vertical
Dix-hallpike maneuver +
-/+ -
Neurologic exam (Romberg’s sign)
Treatment
Repositioning Maneuver
1.Salt-restricted diets
2.Diuretics
3.Vestibular suppressants (Meclizine)
4.Surgical;Gentamycin or steroid infusion into the middle ear, sac surgery, vestibular neurectomy
Anti-anxiety or Anti –depression drugs
Further examinations(MRI,CT)

19. Peripheral Vertigo
Benign paroxysmal positional vertigo: most common in adults
Acute Labyrinthitis
Chronic Labyrinthitis (Meniere’s Syndrome)
Toxic Labyrinthitis
Vestibular Neuronitis
Acoustic Nerve Lesions
Labyrinthine Ischemia
Superior semicircular canal dehiscence
Otosclerosis
Trauma
Sudden onset, self-limit, N/V, may caused by otitis media, otoscopy may discover perforation of the suppurative ear dx aggravated by changing positions, horizontal nystagmus, normal neurologic exams; Meniere’s disease associated with tinnitus, hearing loss,n/v; drugs such as Gentamycin, aspirin, ethacrynic acid.

20. Peripheral vertigo

22. Central vertigo Brainstem Lesions
Intravascular: Vertebrobasilar insufficiency
Tumors
Intracranial infection
Demyelinating diseases: Multiple Sclerosis, Syringobulbia

23. Conclusions 1.History Taking 2.Physical Examinations
3.Psychogenic Vertigo must be consider
4.Labs for necessary

24. Tinnitus

25. Tinnitus Definition Classification Objective tinnitus
Subjective tinnitus
Theories
Evaluation
Treatment

26. Introduction
Tinnitus -“The perception of sound in the absence of external stimuli.”
Tinnire – means “ringing” in Latin
Includes buzzing, hissing, roaring, clicking, pulsatile sounds
For some, an unbearable sound that drives them to contemplate suicide.

27. Tinnitus May be perceived as unilateral or bilateral
Originating in the ears or around the head
First or only symptom of a disease process or auditory/psychological annoyance

28. Tinnitus 40 million affected in the United States
10 million severely affected
Most common in year-olds
Roughly equal prevalence in men and women

29. Classification
Objective tinnitus – sound produced by paraauditory structures which may be heard by an examiner, often pulsatile
Subjective tinnitus – sound is only perceived by the patient (most common)

30. Tinnitus Pulsatile tinnitus – matches pulse or a rushing sound
Possible vascular etiology
Objective or subjective
Increased or turbulent blood flow through paraauditory structures

31. Objective tinnitus Vascular (pulsatile) Neuromuscular
A/V malformations
Vascular tumors
Venous hum (cardiac murmurs, anemia, BIH, thyrotoxicosis, pregnancy, dehiscent jugular bulb)
Atherosclerosis
Ectopic carotid artery
Persistent stapedial artery
Vascular loops
Neuromuscular
(asynchronous w/ pulse)
Palatomyclonus
Stapedial and tensor tympani muscle spasm
Patulous eustachian tube (nonpulsatile)

32. Arteriovenous Malformations
Congenital lesions
Occipital artery and transverse sinus, internal carotid and vertebral arteries, middle meningeal and greater superficial petrosal arteries
Mandible
Brain parenchyma
Dura

33. Arteriovenous Malformations
Pulsatile tinnitus
Headache
Papilledema
Discoloration of skin or mucosa

34. Vascular tumors Glomus tympanicum Paraganglioma of middle ear
Loud pulsatile tinnitus which may decrease with ipsilateral carotid artery compression
Reddish mass behind tympanic membrane which blanches with positive pressure
Conductive hearing loss

35. Vascular tumors Glomus jugulare Paraganglioma of jugular fossa
Loud pulsatile tinnitus
Conductive hearing loss if into middle ear
Cranial neuropathies

36. Venous hum Benign intracranial hypertension Dehiscent jugular bulb
Transverse sinus partial obstruction
Increased cardiac output from
Pregnancy
Thyrotoxicosis
Anemia

37. Benign Intracranial Hypertension
Also called pseudotumor cerebri
Young, obese, female patients
Hearing loss
Aural fullness
Dizziness
Headaches
Visual disturbance
Papilledema, pressure >200mm H20 on LP

38. Benign Intracranial Hypertension
Sismanis and Smoker 1994
100 patients with pulsatile tinnitus
42 found to have BIH syndrome
16 glomus tumors
15 atherosclerotic carotid artery disease

39. Benign Intracranial Hypertension
Treatment
Weight loss
Diuretics
Subarachnoid-peritoneal shunt
Gastric bypass for weight reduction

40. Neuromuscular Causes Palatal myoclonus Clicking sound
Rapid ( beats/min), intermittent
Contracture of tensor palantini, levator palatini, levator veli palatini, tensor tympani, salpingopharyngeal, superior constrictors
Muscle spasm seen orally or transnasally
Rhythmic compliance change on tympanogram

41. Myoclonus Palatal myoclonus associations:
Multiple Sclerosis and other degenerative neurological disorders
Small vessel disease
Brain stem tumors
Treatments: muscle relaxants, botulinum toxin injection

42. Stapedius Muscle Spasm
Idiopathic stapedial muscle spasm
Rough, rumbling, crackling sound
Exacerbated by outside sounds
Brief and intermittent
May be able to see tympanic membrane movement
Treatments: avoidance of stimulants, muscle relaxants, sometimes surgical division of tensor tympani and stapedius muscles

43. Patulous Eustachian Tube
Eustachian tube remains open abnormally
Ocean roar sound
Changes with respiration
Lying down or head in dependent position provides relief
Tympanogram will show changes in compliance with respiration
Associated with significant weight loss, radiation to the nasopharynx

44. Subjective Tinnitus Metabolic Otologic Psych Infectious
Thyroid disorders
Hyperlipidemia
B12 def
Psych
Depression/anxiety
Infectious
Syphilis
Meningitis
Otologic
Hearing loss (presbycusis, noise exposure, otosclerosis, middle ear effusion)
Meniere’s disease
Acoustic neuroma
Ototoxic drugs or substances
Neurologic MS
Head trauma
Much more common, nonpulsatile

45. Conductive hearing loss
Conductive hearing loss decreases level of background noise
Normal paraauditory sounds seem amplified
Cerumen impaction, otosclerosis, middle ear effusion, otosclerosis, perforated TM, EAC swelling are examples
Treating the cause of conductive hearing loss may alleviate the tinnitus

46. Sensorineural hearing loss
Indicates abnormality of the inner ear or cochlear portion of the 8th CN
NIHL(noise induced) and presbycusis most common

47. Other subjective tinnitus
Poorly understood mechanisms of tinnitus production
Abnormal conditions in the cochlea, cochlear nerve, ascending auditory pathways, auditory cortex
Hyperactive hair cells
Chemical imbalance

48. CNS Mechanisms
Reorganization of central pathways with hearing loss (similar to phantom limb pain)
Disinhibition of dorsal cochlear nucleus with increase in spontaneous activity of central auditory system

49. Neurophysiologic Model
Proposed by Jastreboff
Result of interaction of subsystems in the nervous system
Auditory pathways playing a role in development and appearance of tinnitus
Limbic system responsible for tinnitus annoyance
Negative reinforcement enhances perception of tinnitus and increases time it is perceived

50. Role of Depression
Depression is more prevalent in patients with chronic tinnitus than in those without tinnitus
Folmer et al (1999) reported patients with depression rated the severity of their tinnitus higher although loudness scores were the same
Which comes first, depression or tinnitus?

51. Ototoxic Drugs Analgesic ASA, NSAIDs Antibiotics Aminoglycosides
Erthyromycin
Vancomycin
Chloramphenicol
Tetracycline
Loop diuretics
Chemotherapeutic agents
Cisplatin
Vincristine
Methotrexate
Bleomycin
Others
Chloroquine
Heavy metals
Quinine
Heterocyclic antidepressants

52. Evaluation - History Careful history Quality Pitch Loudness
Unilateral vs Bilateral
Constant/intermittent
Onset
Alleviating/aggravating factors

53. Evaluation - History Infection Trauma Noise exposure Medication usage
Medical history
Hearing loss
Vertigo
Pain
Family history
Impact on patient

54. Evaluation – Physical Exam
Complete head & neck exam
General physical exam
Otoscopy (glomus tympanicum, dehiscent jugular bulb)
Search for audible bruit in pulsatile tinnitus
Auscultate over orbit, mastoid process, skull, neck, heart using bell and diaphragm of stethoscope
Toynbee tube to auscultate EAC

55. Evaluation – Physical Exam
Light exercise to increase pulsatile tinnitus
Light pressure on the neck (decreases venous hum)
Valsalva maneuver (decrease venous hum)
Turning the head (decrease venous hum)

56. Evaluation - Audiometry
Pure tone air, bone and speech descrimination scores, tympanometry, acoustic reflexes
Weber and Rinne tests
Pitch matching
Loudness matching
Masking level

57. Evaluation - Audiometry
Vascular or palatomyoclonus induced tinnitus – graph of compliance vs. time
Patulous Eustachian tube – changes in compliance with respiration
Asymmetric sensorineural hearing loss or speech discrimination, unilateral tinnitus suggests possible acoustic neuroma - MRI

58. Laboratory studies As indicated by history and physical exam
Possibilities include:
Hematocrit
FTA-ABS
Blood chemistries
Thyroid studies
Lipid panel
B12, zinc ?

59. Imaging Pulsatile tinnitus Reviewed by Weissman and Hirsch (2000)
Contrast enhanced CT of temporal bones, skull base, brain, calvaria as first-line study
Sismanis and Smoker (1994) recommended CT for retrotympanic mass, MRI/MRA if normal otoscopy

60. Glomus tympanicum – bone algorithm CT scan best shows extent of mass
May not be able to see enhancement of small tumor
Tumor enhances on T1-weighted images with gadolinium or on T2-weighted images

61. Glomus Tympanicum
From: Weissman JL, Hirsch BE. Imaging of tinnitus: a review. Radiology 2000;216:343.

62. Glomus Tympanicum
From: Weissman JL, Hirsch BE. Imaging of tinnitus: a review. Radiology 2000;216:343.

63. Imaging Glomus jugulare Erosion of osseous jugular fossa
Enhance with contrast, may not be able to differentiate jugular vein and tumor
Enhance with T1-weighted MRI with gadolinium and on T2-weighted images
Characteristic “salt and pepper” appearance on MRI

64. Glomus jugulare
From: Weissman JL, Hirsch BE. Imaging of tinnitus: a review. Radiology 2000;216:344.

65. Glomus jugulare “salt and pepper appearance”
From: Weissman JL, Hirsch BE. Imaging of tinnitus: a review. Radiology 2000;216:344.

66. Imaging
Arteriovenous malformations – readily apparent on contrasted CT and MRI
Normal otoscopic exam and pulsatile tinnitus may be dural arteriovenous fistula
Often invisible on contrasted CT and MRI/MRA
Angiography may be only diagnostic test

67. Imaging
Shin et al (2000)
MRI/MRA initially if subjective pulsatile tinnitus
Angiography if objective with audible bruit in order to identify dural arteriovenous fistula

68. Imaging Acoustic Neuroma
Unilateral tinnitus, asymmetric sensorineural hearing loss or speech descrimination scores
T1-weighted MRI with gadolinium enhancement of CP angle is study of choice
Thin section T2-weighted MRI of temporal bones and IACs may be acceptable screening test

69. Acoustic Neuroma
From: Weissman JL, Hirsch BE. Imaging of tinnitus: a review. Radiology 2000;216:348.

70. Acoustic Neuroma
From: Weissman JL, Hirsch BE. Imaging of tinnitus: a review. Radiology 2000;216:348.

71. ENT Referral ENT Referral
Collins RD. Algorithmic diagnosis of symptoms and signs: a cost-effective approach. 2d ed. Philadelphia: Lippincott Williams & Wilkins, 2003:568-9.

72. Treatments Multiple treatments
Avoidance of dietary stimulants: coffee, tea, cola, etc.
Smoking cessation
Avoid medications known to cause tinnitus
Reassurance
White noise from radio or home masking machine

73. Treatments - Medicines
Many medications have been researched for the treatment of tinnitus:
Intravenous lidocaine suppresses tinnitus but is impractical to use clinically
Tocainide is oral analog which is ineffective
Carbamazepine ineffective and may cause bone marrow suppression

74. Treatments - Medicines
Alprazolam (Xanax)
Johnson et al (1993) found 76% of 17 patients had reduction in the loudness of their tinnitus using both a tinnitus synthesizer and VAS (dose 0.5mg-1.5 mg/day)
Dependence problem, long-term use is not recommended

75. Treatments - Medicines
Nortriptyline and amitriptyline
May have some benefit
Dobie et al reported on 92 patients
67% nortriptlyine benefit, 40%placebo
SSRI’s
Ginko biloba
Extract at doses of mg per day
Shown to be effective in some trials and not in others
Needs further study
Niacin

76. Treatments
Hearing aids – amplification of background noise can decrease tinnitus
Maskers – produce sound to mask tinnitus
Tinnitus instrument – combination of hearing aid and masker

77. Treatments Tinnitus Retraining Therapy Based on neurophysiologic model
Combination of masking with low level broadband noise for several hours per day and counseling to achieve habituation of the reaction to tinnitus and perception of the tinnitus itself

78. Treatments Electrical stimulation of the cochlea
Transcutaneous, round window, promontory stimulation have all been tried
Direct current can cause permanent damage
Steenersen and Cronin have used transcutaneous stimulation of the auricle and tragus decreasing tinnitus in 53% of 500 patients

79. Treatments Cochlear implants
Have shown some promise in relief of tinnitus
Ito and Sakakihara (1994) reported that in 26 patients implanted who had tinnitus 77% reported either tinnitus was abolished or suppressed, 8% reported worsening

80. Treatments
Surgery
Used for treatment of arteriovenous malformations, glomus tumors, otosclerosis, acoustic neuroma
Some authors have reported success with cochlear nerve section in patients who have intractable tinnitus and have failed all other treatments, this is not widely accepted

81. Treatments Biofeedback Hypnosis Magnetic stimulation Acupuncture
Conflicting reports of benefit

82. Conclusions
Tinnitus is a common problem with an extensive differential
Need to identify medical process if involved
Pulsatile/Nonpulsatile is important distinction
Unilateral vs Bilateral
Associated hearing loss, vertigo
Thorough head and neck physical exam and audiometry testing is necessary for all patients
In general, tinnitus that is pulsatile, unilateral, and assoc w/ other unilateral otologic symptoms is more worrisome and should warrant ENT referral.