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Labyrinthitis, also known as otitis interna, vestibular neuronitis and vestibular neuritis, is a problem of the inner ear. It results in vertigo and also possible hearing loss or ringing in the ears. It can occur as a single attack, a series of attacks, or a persistent condition that diminishes over three to six weeks. It may be associated with nausea, vomiting. Vestibular neuronitis may also be associated with eye nystagmus.
The cause is often not clear. It may be due to a virus, but it can also arise from bacterial infection, head injury, extreme stress, an allergy, or as a reaction to medication. 30% of affected people had a common cold prior to developing the disease. Both bacterial and viral labyrinthitis can cause permanent hearing loss in rare cases. It appears to be caused by an imbalance of neuronal input between the left and right inner ears.
Vestibular neuritis affects approximately 3.5 per 100,000 people per year. The typical age of onset is between 30 and 60 years, and the age distribution plateau is between 40 and 50 years. There is no significant gender difference. It derives its name from the labyrinths that house the vestibular system, which senses changes in head position.
Signs and symptoms
The main symptom of labyrinthitis is severe vertigo. Rapid and undesired eye motion (nystagmus) often results from the improper indication 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.
Chronic anxiety is a common side effect of labyrinthitis which can produce tremors, heart palpitations, panic attacks, derealization, and depression. Often a panic attack is one of the first symptoms of labyrinthitis. While dizziness can occur from extreme anxiety, labyrinthitis can precipitate a panic disorder. Three models have been proposed to explain the relationship between vestibular dysfunction and panic disorder:
- Psychosomatic model: vestibular dysfunction that occurs as a result of anxiety.
- Somatopsychic model: panic disorder triggered by misinterpreted internal stimuli (e.g., stimuli from vestibular dysfunction), that are interpreted as signifying imminent physical danger. Heightened sensitivity to vestibular sensations leads to increased anxiety and, through conditioning, drives the development of panic disorder.
- Network alarm theory: panic that involves noradrenergic, serotonergic, and other connected neuronal systems. According to this theory, panic can be triggered by stimuli that set off a false alarm via afferents to the locus ceruleus, which then triggers the neuronal network. This network is thought to mediate anxiety and includes limbic, midbrain, and prefrontal areas. Vestibular dysfunction in the setting of increased locus ceruleus sensitivity may be a potential trigger.
Some people will report having an upper respiratory infection (common cold) or a flu prior to the onset of the symptoms of vestibular neuronitis, others will have no viral symptoms prior to the vertigo attack.
Some cases of vestibular neuronitis are thought to be caused by an infection of the vestibular ganglion by the Herpes Simplex type 1 virus. However, the cause of this condition is not fully understood, and in fact many different viruses may be capable of infecting the vestibular nerve.
Acute localized ischemia of these structures also may be an important cause. Especially in children, vestibular neuritis may be preceded by symptoms of a common cold. However, the causative mechanism remains uncertain.
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. The vestibular system also relays information on head movement to the eye muscle, forming the vestibulo-ocular reflex to retain continuous visual focus during motion.
The treatment for vestibular neuronitis depends on the cause. However, symptoms of vertigo can be treated in the same way as other vestibular dysfunctions with vestibular rehabilitation.
Typical treatments include combinations of head and eye movements, postural changes, and walking exercises. Specifically, exercises that may be prescribed include keeping eyes fixated on a specific target while moving the head, moving the head right to left at two targets at a significant distance apart, walking while keeping eyes fixated on a specific target, and walking while keeping eyes fixated on a specific target while also turning the head in different directions. The main function behind repeating a combination of head and eye movements, postural changes and walking is that through this repetition, compensatory changes for the dysfunctions arising from peripheral vestibular structures may be promoted in the central vestibular system (brainstem and cerebellum).
Vestibular rehabilitation therapy 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, neuroplasticity, and compensation.
Rehabilitation strategies most commonly used are:
- Gaze stability exercises - moving the head from side to side while fixated on a stationary object (aimed to restore the Vestibulo-ocular reflex) An advanced progression of this exercise would be walking in a straight line while looking side to side by turning the head.
- Habituation exercises - movements designed to provoke symptoms and subsequently reduce the negative vestibular response upon repetition. Examples of these include Brandt-Daroff exercises.
- Functional retraining - including postural control, relaxation, and balance training.
These exercises function by challenging the vestibular system. Progression occurs by increasing the amplitude of the head or focal point movements, increasing the speed of movement, and combining movements such as walking and head turning.
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."
Vestibular neuronitis is generally a self-limiting disease. Treatment with drugs is neither necessary nor possible. The effect of glucocorticoids has been studied, but they have not been found to significantly affect long-term outcome.
Symptomatic treatment with antihistaminics such as cinnarizine, however, can be used to suppress the symptoms of vestibular neuronitis while it spontaneously regresses. Prochlorperazine is another commonly prescribed medication to help alleviate the symptoms of vertigo and nausea.
Studies have shown that older adults with dementia who take antipsychotics (medications for mental illness) such as prochlorperazine have an increased chance of death during treatment.
Because anxiety interferes with the balance compensation process, it is important to treat an anxiety disorder and/or depression. Acute anxiety can be treated in the short term with benzodiazepines such as diazepam; 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.
In most cases, the condition tends to be self-limiting. In 95% or greater, vestibular neuritis is a one-time experience with most people fully recovering.
Recovery from acute labyrinthine inflammation generally takes from one to six weeks, but it is not uncommon for residual symptoms (dysequilibrium and/or dizziness) to last for many months or even years.
Recovery from a permanently damaged inner ear typically follows two phases:
- An acute period, which may include severe vertigo and vomiting
- approximately two weeks of sub-acute symptoms and rapid recovery
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