In addition to balance control problems, a labyrinthitis patient may encounter hearing loss and tinnitus. Labyrinthitis is caused by a virus, but it can also arise from bacterial infection, head injury, an allergy or as a reaction to a particular medicine. Both bacterial and viral labyrinthitis can cause permanent hearing loss, although this is rare.
Labyrinthitis often follows an upper respiratory tract infection (URI).
A prominent and debilitating symptom of labyrinthitis is chronic dizziness. The vestibular system is a set of sensory inputs consisting of three semicircular canals, sensing changes in rotational motion, and the otoliths, sensing changes in linear motion. The brain combines visual cues with sensory input from the vestibular system to determine adjustments required to retain balance. When working properly, the vestibular system also relays information on head movement to the eye muscle, forming the vestibulo-ocular reflex, in order to retain continuous visual focus during motion. When the vestibular system is affected by labyrinthitis, rapid, undesired eye motion (nystagmus), often results from the improper indictations of rotational motion. Nausea, anxiety, and a general ill feeling are common due to the distorted balance signals that the brain receives from the inner ear.
Recovery from a permanently damaged inner ear typically follows three phases:
Chronic anxiety is a common side effect of labyrinthitis which can produce tremors, heart palpitations, panic attacks and depression. Often a panic attack is one of the first symptoms to occur as labyrinthitis begins. While dizziness can occur from extreme anxiety, labyrinthitis itself can precipitate a panic disorder. Three models have been proposed to explain the relationship between vestibular dysfunction and panic disorder:
Prochlorperazine is commonly prescribed to help alleviate the symptoms of vertigo and nausea.
Because anxiety interferes with the balance compensation process, it is important to treat an anxiety disorder and/or depression as soon as possible to allow the brain to compensate for any vestibular damage. Acute anxiety can be treated in the short term with benzodiazepines such as diazepam (Valium); however, long-term use is not recommended because of the addictive nature of benzodiazepines and the interference they may cause with vestibular compensation and adaptive plasticity .
Evidence suggests that selective serotonin-reuptake inhibitors may be more effective in treating labyrinthitis. They act by relieving anxiety symptoms and may stimulate new neural growth within the inner ear, allowing more rapid vestibular compensation to occur. Trials have shown that SSRIs do in fact affect the vestibular system in a direct manner and can increase dizziness.
Some evidence suggests that viral labyrinthitis should be treated in its early stages with corticosteroids such as prednisone, and possibly antiviral medication such as Valtrex and that this treatment should be undertaken as soon as possible to prevent permanent damage to the inner ear.
Vestibular rehabilitation therapy (VRT) is a highly effective way to substantially reduce or eliminate residual dizziness from labyrinthitis. VRT works by causing the brain to use already existing neural mechanisms for adaptation, plasticity, and compensation. The direction, duration, frequency, and magnitude of the directed exercises are closely correlated with adaptation and recovery. Symmetry is more rapidly restored when VRT exercises are specifically tailored for the patient.
One study found that patients who believed their illness was out of their control showed the slowest progression to full recovery, long after the initial vestibular injury had healed. The study revealed that the patient who compensated well was one who, at the psychological level, was not afraid of the symptoms and had some positive control over them. Notably, a reduction in negative beliefs over time was greater in those patients treated with rehabilitation than in those untreated. "Of utmost importance, baseline beliefs were the only significant predictor of change in handicap at 6 months followup."