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Labyrinthitis

Labyrinthitis is a balance disorder that usually follows an upper respiratory tract infection (URI). It is, as the name suggests, an inflammatory process affecting the labyrinths that house the vestibular system of the inner ear. more...

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Medicines

Labrynthitis causes vertigo, disequilibrium, and sometimes nystagmus beating away from affected ear. Hearing loss is commonly present in the infected ear. Nausea, anxiety and a general ill feeling are common due to the distorted balance signals that the brain receives from the inner ear. There are also sometimes cochlear symptoms such as tinnitus and hearing loss. It appears labyrinthitis is caused by a virus (the herpes virus has been implicated) but 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. Prochlorperazine is commonly prescribed for all types of the infection, which helps with the nausea and sickness. Recovery from acute labyrinthine inflammation generally takes from one to six weeks, however it is not uncommon for residual symptoms (disequilibrium and/or dizziness) to last for many months or even years (Bronstein, 2002).

Labyrinthitis and Anxiety

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 (Simon et al, 1998):

  • Psychosomatic model: vestibular dysfunction which occurs as a result of anxiety.
  • Somatopsychic model: panic disorder triggered by misinterpreted internal stimuli (eg. 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 which 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.

Treatment

Because anxiety interferes with the 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, 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 (Solomon and Shepard, 2002). Evidence suggests that selective serotonin reuptake inhinbitors (SSRI) 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. 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.

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Otitis media with effusion in a patient who had previously undergone a stapedectomy
From Ear, Nose & Throat Journal, 8/1/05 by Arun K. Gadre

A 55-year-old woman presented with a 6-week history of decreased hearing and a sensation of fullness in her left ear. Her symptoms arose following an upper respiratory tract infection. She also reported otalgia soon alter the onset of a cold 6 weeks earlier. The pain abated following antibiotic therapy, which had been prescribed by her primary care physician. However, the left ear fullness and the diminished hearing persisted. She had no history of vertigo, but she did report intermittent tinnitus. Of note, she said that she had undergone a stapedectomy 25 years earlier, and her postoperative hearing was good.

On examination, the tympanic membrane was retracted and a straw-colored fluid could be seen behind an intact tympanic membrane (figure). The tympanic membrane was in contact with the long process of the incus, and the wire loop of the stapedectomy prosthesis could be seen through it. Bone conduction was greater than air conduction on a tuning fork test, and Weber's test lateralized to the left. An audiogram confirmed these findings. Clinical and audiologic correlates of labyrinthitis were not present.

[FIGURE OMITTED]

Myringotomy and ventilation tube placement reversed the conductive hearing loss, and the patient remained well during follow-up.

From the Division of Otology/Neurotology, the Department of Otolaryngology--Head and Neck Surgery, University of Texas Medical Branch at Galveston.

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