A. Endolymphatic Hydrops (Ménière Syndrome)
The cause of Ménière syndrome is unknown. Distention of the endolymphatic compartment of the inner ear is thought to be part of the pathogenesis of the disorder. Although a precise cause of hydrops cannot be established in most cases, two known causes are syphilis and head trauma. The classic syndrome consists of episodic vertigo, with discrete vertigo spells lasting 20 minutes to several hours in association with fluctuating low-frequency sensorineural hearing loss, tinnitus (usually low-tone and “blowing” in quality), and a sensation of unilateral aural pressure (Table 8–3). These symptoms in the absence of hearing fluctuations suggest migraine-associated dizziness. Symptoms wax and wane as the endolymphatic pressure rises and falls. Caloric testing commonly reveals loss or impairment of thermally induced nystagmus on the involved side. Primary treatment involves a low-salt diet and diuretics (eg, acetazolamide). For symptomatic relief of acute vertigo attacks, oral meclizine (25 mg) or diazepam (2–5 mg) can be used. In refractory cases, patients may undergo intratympanic corticosteroid injections, endolymphatic sac decompression, or vestibular ablation, either through transtympanic gentamicin, vestibular nerve section, or surgical labyrinthectomy.
Patients with labyrinthitis suffer from acute onset of continuous, usually severe vertigo lasting several days to a week, accompanied by hearing loss and tinnitus. During a recovery period that lasts for several weeks, the vertigo gradually improves. Hearing may return to normal or remain permanently impaired in the involved ear. The cause of labyrinthitis is unknown. Treatment consists of antibiotics, if the patient is febrile or has symptoms of a bacterial infection, and supportive care. Vestibular suppressants are useful during the acute phase of the attack (eg, diazepam or meclizine) but should be discontinued as soon as feasible to avoid long-term dysequilibrium from inadequate compensation.
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C. Benign Paroxysmal Positioning Vertigo
Patients suffering from recurrent spells of vertigo, lasting a few minutes per spell, associated with changes in head position (often provoked by rolling over in bed), usually have benign paroxysmal positioning vertigo (BPPV). The term “positioning vertigo” is more accurate than “positional vertigo” because it is provoked by changes in head position rather than by the maintenance of a particular posture.
The typical symptoms of BPPV occur in clusters that persist for several days. There is a brief (10–15 sec) latency period following a head movement before symptoms develop, and the acute vertigo subsides within 10–60 seconds, though the patient may remain imbalanced for several hours. Constant repetition of the positional change leads to habituation. Since some CNS disorders can mimic BPPV (eg, vertebrobasilar insufficiency), recurrent cases warrant head MRI/MRA. In central lesions, there is no latent period, fatigability, or habituation of the symptoms and signs. Treatment of BPPV involves physical therapy protocols (eg, the Epley maneuver or Brandt-Daroff exercises), based on the theory that it results from cupulolithiasis (free-floating statoconia, also known as otoconia) within a semicircular canal.
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et al. Benign paroxysmal positional vertigo. Adv Otorhinolaryngol. 2019;82:67–76.
In vestibular neuronitis, a paroxysmal, usually single attack of vertigo occurs without accompanying impairment of auditory function and will persist for several days to a week before gradually abating. During the acute phase, examination reveals nystagmus and absent responses to caloric stimulation on one or both sides. The cause of the disorder is unclear though presumed to be viral. Treatment consists of supportive care, including oral diazepam, 2–5 mg every 6–12 hours, or meclizine, 25–100 mg divided two to three times daily, during the acute phases of the vertigo only, followed by vestibular therapy if the patient does not completely compensate.
et al. Long-term clinical outcome in vestibular neuritis. Curr Opin Neurol. 2019 Feb;32(1):174–80.
et al. Clinical characteristics of benign recurrent vestibulopathy: clearly distinctive from vestibular migraine and Menière’s disease? Otol Neurotol. 2017 Oct;38(9):e357–63.
Labyrinthine concussion is the most common cause of vertigo following head injury. Symptoms generally diminish within several days but may linger for a month or more. Basilar skull fractures that traverse the inner ear usually result in severe vertigo lasting several days to a week and deafness in the involved ear. Chronic posttraumatic vertigo may result from cupulolithiasis. This occurs when traumatically detached statoconia (otoconia) settle on the ampulla of the posterior semicircular canal and cause an excessive degree of cupular deflection in response to head motion. Clinically, this presents as episodic positioning vertigo. Treatment consists of supportive care and vestibular suppressant medication (diazepam or meclizine) during the acute phase of the attack, and vestibular therapy.
et al. Vestibular dysfunction in acute traumatic brain injury. J Neurol. 2019 Oct;266(10):2430–3.
Leakage of perilymphatic fluid from the inner ear into the tympanic cavity via the round or oval window is a rare cause of vertigo and sensory hearing loss. Most cases result from either physical injury (eg, blunt head trauma, hand slap to ear); extreme barotrauma during airflight, scuba diving, etc; or vigorous Valsalva maneuvers (eg, during weight lifting). Treatment may require middle ear exploration and window sealing with a tissue graft; however, this is seldom indicated without a clear-cut history of a precipitating traumatic event.
et al. Diagnosis and treatment of perilymphatic fistula. Adv Otorhinolaryngol. 2018;81:133–45.
Position receptors located in the facets of the cervical spine are important physiologically in the coordination of head and eye movements. Cervical proprioceptive dysfunction is a common cause of vertigo triggered by neck movements. This disturbance often commences after neck injury, particularly hyperextension; it is also associated with degenerative cervical spine disease. Although symptoms vary, vertigo may be triggered by assuming a particular head position as opposed to moving to a new head position (the latter typical of labyrinthine dysfunction). Cervical vertigo may often be confused with migraine-associated vertigo, which is also associated with head movement. Management consists of neck movement exercises to the extent permitted by orthopedic considerations.
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Episodic vertigo is frequently associated with migraine headache. Head trauma may also be a precipitating feature. The vertigo may be temporally related to the headache and last up to several hours, or it may also occur in the absence of any headache. Migrainous vertigo may resemble Ménière disease but without associated hearing loss or tinnitus. Accompanying symptoms may include head pressure; visual, motion, or auditory sensitivity; and photosensitivity. Symptoms typically worsen with lack of sleep and anxiety or stress. Food triggers include caffeine, chocolate, and alcohol, among others. There is often a history of motion intolerance (easily carsick as a child). Migrainous vertigo may be familial. Treatment includes dietary and lifestyle changes (improved sleep pattern, avoidance of stress) and antimigraine prophylactic medication.
et al. Migraine associated vertigo. Adv Otorhinolaryngol. 2019;82:119–26.
I. Superior Semicircular Canal Dehiscence
Deficiency in the bony covering of the superior semicircular canal may be associated with vertigo triggered by loud noise exposure, straining, and an apparent conductive hearing loss. Autophony is also a common feature. Diagnosis is with coronal high-resolution CT scan and VEMPs. Surgically resurfacing or plugging the dehiscent canal can improve symptoms.
et al. Systematic review of round window operations for the treatment of superior semicircular canal dehiscence. J Int Adv Otol. 2019 Aug;15(2):209–14.
et al. Aggregating the symptoms of superior semicircular canal dehiscence syndrome. Laryngoscope. 2018 Aug;128(8):1932–8.