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Labyrinthitis is an ailment of the inner ear[dead link] and a form of unilateral vestibular dysfunction. It derives its name from the labyrinths that house the vestibular system, which senses changes in head position. Labyrinthitis can cause balance disorders, vertigo, hearing loss and tinnitus.
Labyrinthitis is usually caused by a virus, but it can also arise from bacterial infection, head injury, extreme stress, an allergy or as a reaction to medication. Both bacterial and viral labyrinthitis can cause permanent hearing loss.
Labyrinthitis often follows an upper respiratory tract infection (URTI).
Signs and symptoms
A prominent and debilitating symptom of labyrinthitis is severe vertigo. 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. When the vestibular system is affected by labyrinthitis, 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.
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."
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[by whom?] have shown that SSRIs do in fact affect the vestibular system in a direct manner and can decrease dizziness.[verification needed] Studies have shown that older adults with dementia who take antipsychotics (medications for mental illness) such as prochlorperazine (prescribed in the UK for Labyrinthitis) have an increased chance of death during treatment.
Some evidence suggests that viral labyrinthitis should be treated in its early stages with corticosteroids such as prednisone, and possibly antiviral medication such as valacyclovir and that this treatment should be undertaken as soon as possible to prevent permanent damage to the inner ear.
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 if permanent damage occurs.
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
A damaged balance system has little ability to repair itself. The body recovers from the injury by having the part of the brain that controls balance re-calibrate itself to compensate for the unmatched signals being sent from the damaged and well ears. This compensation process occurs naturally in most people, but some patients require vestibular rehabilitation therapy (VRT).
When a sudden injury occurs to one side of the balance system, the patient may feel very sick for hours to a few days with a spinning feeling, unsteadiness, lightheadedness, and often sweating, nausea, and vomiting. This is because the signals being sent from the two balance organs are no longer equal and opposite, and the brain interprets the difference as constant movement. Researchers theorize that after this initial period the brain recognizes that the signals being received from the ears are incorrect and turns the signals off through a process called the cerebellar clamp. When the clamp is in place, the spinning and much of the 'sick' feeling improve. The patient feels unsteady while standing, because the signals normally used to maintain balance have been turned off. The patient may also report dizziness or blurred vision with movements. Vision and proprioception (the sense of pressure at the bottom of the feet) are also used to maintain balance, so the patient can walk but will feel unsteady and may fall in the dark or on soft or bumpy floors such as thick carpet, grass, or gravel.
At this point most patients are well enough to get out of bed and visit a doctor. The doctor sees a person who is not spinning but whose gait is ataxic. If the patient is not given an opportunity to clearly describe what has happened, he or she may be referred to neurology to rule out stroke because of this ataxic gait. If balance testing is performed during the acute (immediate) compensation phase, test results may incorrectly suggest that the patient has damage to both sides of the balance system because the [clarify] reduces the eye movements that are looked for during balance testing. The cerebellar clamp may persist for days to a few weeks after the initial injury.
During the acute compensation phase, the cerebellum slowly releases the clamp, gradually allowing more signals from the balance organs to pass to the balance areas of the brain. As the brain receives these signals, it fine-tunes their interpretation, in order to account for the difference between the ears. The brain must receive signals from the balance organs to be able to modify its interpretation of these signals.
For most patients, movements made during normal daily activities are enough to achieve chronic (long-term) compensation, usually in two to four weeks after the injury has occurred. Once the chronic compensation process is complete, the patient is essentially symptom-free. If unsteadiness and/or motion provoked dizziness persist after that time, compensation is not complete and the physician may prescribe a program of VRT.
VRT is administered by a specially-trained physical therapist. It is designed to provide small, controlled and repeated 'doses' of the movements and activities that provoke dizziness in order to desensitize the balance system to the movements, and enhance the fine-tuning involved in long-term compensation. VRT is most effective when administered by a therapist who has special training and specializes in this unusual form of therapy.
After the symptoms go away the balance system remains injured - the brain has adapted to the injury. For many patients, dizziness will return months or years after compensating for a balance system injury. It is critical for the physician to find out what type of dizziness the patient has. If the patient describes another severe attack of spinning with unsteadiness and nausea lasting hours to days, this suggests decompensation: the brain has 'forgotten' the fine-tuning procedure it developed during the chronic compensation phase described above.
Events that can provoke decompensation include a bad cold or the flu, minor surgery, long vacations, or anything that stops normal daily activity for a few days. Recovery after decompensation is exactly like the recovery that occurs during the chronic compensation phase. Movements and activities are the stimuli the brain needs to fine-tune the system. Sufferers are often recommended to keep their exercise program instructions handy so that they can begin the exercises immediately if symptoms return. Usually recovery after decompensation is quicker than the recovery after the initial injury to the balance system.
Failure to compensate
Two things are required in order to compensate for an injury. First, the brain must receive signals from the balance organs. This means that movements must not be avoided, because movements create the signals the brain needs to compensate for the injury. Secondly, the balance areas of the brain must be capable of change.
During the early stages of dizziness, many physicians counsel their patients to avoid quick movements and reduce their activities. Most patients will be prescribed anti-dizziness medications such as Antivert (meclizine), Valium (diazepam), Xanax, Phenergan, or Compazine. This is fine during the acute stages of a dizziness problem in order to reduce the dizziness symptoms that persist for hours or days even when the patient is not moving. However, once the acute phase is past, inactivity and medications can interfere with the long-term compensation process. Any medication that makes the brain sleepy, including all of the anti-dizziness medications, can slow down or stop the process of compensation, so they are often not appropriate for long-term use. Most patients who fail to compensate are found to either be strictly avoiding certain movements, using anti-dizziness medications daily, or both. Treatment includes VRT, gradual reduction, and eventual elimination of these medications.
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