________________________________________________________________________ Dizziness and Vertigo
The acute onset of sudden sensorineural hearing loss with severe vertigo, nausea, and vomiting can leave patients bed- ridden until the symptoms subside. Upper respiratory tract infection precedes the onset of vestibulo-cochlear symptoms in up to 50%. Vertigo usually resolves after several days to weeks, due to spontaneous partial recovery of vestibular func- tion and central compensation of residual unilateral vestibular deficits. Unsteadiness and positional vertigo can persist for months, and return of hearing usually coincides with return of vestibular function [34; 35]. Herpes zoster oticus (Ramsay-Hunt syndrome) is labyrinthitis due to reactivation of a latent varicella zoster virus infection. Inflammation of the vestibulo-cochlear nerve causes vertigo and symptoms of deep, burning, auricular pain followed by eruption of a vesicular rash in the external auditory canal and concha. Symptoms usually improve after several weeks, but permanent hearing loss is common [15; 19]. Bacterial Labyrinthitis Viral labyrinthitis should be differentiated from the more dan- gerous disorder of bacterial labyrinthitis, which occurs through direct bacterial invasion (suppurative labyrinthitis) or passage of bacterial toxins and other inflammatory mediators into the inner ear (serous labyrinthitis) [35; 36]. The bacteria that cause labyrinthitis are the same bacteria responsible for meningitis and otitis; potential bacterial causes include Streptococcus pneu- moniae, Neisseria meningitidis, Streptococcus species, Staphylococcus species, Escherichia coli , and Mycobacterium tuberculosis [35]. Profound hearing loss, severe vertigo, ataxia, and nausea and vomiting are common symptoms of bacterial labyrinthitis. Suppurative labyrinthitis almost always results in permanent, profound unilateral hearing loss (or bilateral loss with menin- gitis). Serous labyrinthitis results in unilateral, high-frequency hearing loss in the affected ear. Regardless of etiology, bacte- rial labyrinthitis accounts for 35% of all adult-onset cases of hearing loss [35]. MÉNIÈRE DISEASE Ménière disease is a clinical syndrome of cochlear and ves- tibular symptoms with a prevalence of 34 to 190 per 100,000 population, an age of onset ranging from the third to seventh decades of life, and a slight female predominance. The odds of Ménière disease are greater among older subjects, persons of European descent, and severely obese persons. Common comorbid conditions in Ménière disease include arthritis, psoriasis, gastroesophageal reflux disease, irritable bowel syn- drome, and migraine [15; 37]. The clinical features of Ménière disease are characterized by sudden, fluctuating, unilateral low-frequency sensorineural hearing loss with tinnitus and aural fullness and by sponta- neous attacks of vertigo with nausea and vomiting, usually lasting hours [15]. Cochlear symptoms can occur between vertigo episodes. Vertigo is often more frequent in the first years of Ménière disease, but the clinical course is variable, with cochlear and vestibular symptoms taking years to develop
in some patients. Bilateral sudden sensorineural hearing loss, migraine, BPPV, or systemic autoimmune disease develops in a subgroup of patients [37]. Ménière disease is idiopathic but is also associated with endolymphatic hydrops, a process whereby accumulation of excess pressure within the inner ear endolymphatic system causes fluctuating hearing loss, episodic vertigo, tinnitus, and aural fullness (i.e., pressure and uncomfortable fullness in the ears) [38]. An interaction of genetics and environmental factors is thought to determine the onset of Ménière disease. While associated with the accumulation of endolymph in the cochlear duct and vestibular organs, endolymphatic hydrops per se does not fully account for the frequency of vertigo attacks, progression of hearing loss, and other clinical features of Ménière disease [37].
The Bárány Society recommends that familial Ménière disease should be considered if at least one other relative (first- or second-degree) fulfills all the criteria of definite or probable Ménière disease.
(https://content.iospress.com/articles/journal-of- vestibular-research/ves00549. Last accessed September 30, 2024.) Level of Evidence : Expert Opinion/Consensus Statement
BILATERAL VESTIBULOPATHY Bilateral vestibulopathy (also called bilateral vestibular loss) has both central and peripheral processes. The cardinal symptoms of bilateral vestibulopathy reflect the pathophysiology, includ- ing motion-dependent postural vertigo with unsteady gait and stance that worsens in darkness and on uneven ground (vestibulo-spinal impairment), and oscillopsia with blurred vision when walking or moving the head (vestibulo-ocular reflex impairment). Patients with bilateral vestibulopathy are typically symptom-free when sitting or lying [39; 40]. The prevalence of bilateral vestibulopathy in the U.S. adult population is 28 per 100,000. The age distribution ranges from youth to old age, depending on etiology, and the mean age at diagnosis is 50 to 60 years. About 60% of patients develop bilateral vestibulopathy slowly and progressively; depending on etiology, 40% of patients have a clinical course marked by episodes of dizziness leading incrementally to bilateral loss of vestibular function [40; 41]. Bilateral vestibulopathy involves atrophy of the hippocampus, with associated impairments in spatial memory and navigation. It is the most frequent cause of motion-dependent postural vertigo in older patients. The three most frequently identified causes of bilateral vestibulopathy are ototoxic aminoglycosides, bilateral Ménière disease, and meningitis, but most cases are idiopathic [39; 40].
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