For the third time in about eight years, I have the symptoms of what was previously diagnosed as labyrinthitis. This does make sense as I recently was treated for an upper respiratory infection (though it does confirm my disenchantment with antibiotics). Does anyone know if it is common to get recurrences of this? Is one more susceptible after getting it once?

Hi

I had what was diagnosed as Labyrinthitis 3 years ago. It tok six weeks to clear up and my doc said it was highly unlikely that I woud ever get it again.

I did get it again last October and have only recently felt 90% free of the symptons.

I'm not sure if it was labyrithitis this time but it was the exact same symptons...just went on for months.

It came on after a flu like bug and just kinda came and went over the months.

It was the worst thing I have ever had and I pray I do not get it again.......but I am not optimistic as I think I will always suffer with my ears and sinuses and thus be susceptable to it.

Take care
Tuppence

Phil,

I did read somewhere that you are more likely to get it again once you have had it once. I had an attack lasting a few months when I was in my late teens - I am now 28 and am having another attack (getting better now after 5 months).

I hope that this will be the last, but I am not so sure - the only consolation I suppose if any is that from experience I know it will go away eventually.

Strangely enough, my sister and father have both experienced labyrinthitis before - maybe there is something in my makeup that makes me more suseptible?

Hi:

One of my family members has had labyrinthitis a few times. The best strategy we've come with is annual flu shots and avoiding people with strep, etc. The best article I've found to date on this topic is from the emedicine site. Here's a cut & paste on causes, imaging [dx] and treatment. The reason for these specific sections is that in our experience, an accurate diagnosis has been a hit & miss proposition, and too often the antibiotic initially prescribed did not do the job with the result that the pain and damage just continued.

Hope this helps someone.

Good luck,
Jay

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Causes:

The most common cause of LO is bacterial infection of the inner ear that results in suppurative labyrinthitis. Bacterial invasion of the labyrinth can occur via 3 routes: hematogenic spread through the cochlear vasculature, a sequela to otitis media that passes through the round window membrane, or meningogenic spread from the subarachnoid space in meningitis (see Picture 6).

Based on data from 1995, the 3 most common organisms responsible for bacterial meningitis in the United States are H influenzae (0.2 cases per 100,000 population), S pneumoniae (1.1 cases per 100,000 population), and Neisseria meningitidis (0.6 cases per 100,000 population). With the success of conjugate vaccines in preventing invasive H influenzae type b (Hib) disease, S pneumoniae has become the leading cause of bacterial meningitis in the United States. Children younger than 1 year have the highest incidence of pneumococcal meningitis (approximately 10 cases per 100,000 population).

S pneumoniae has the highest incidence of associated LO. The immunogenicity of the S pneumoniae cell wall has been implicated in the propensity to develop LO. In the acute stage, components of the bacterial cell wall trigger local host defenses, which produce a vigorous inflammatory response. In addition, S pneumoniae–induced meningitis generally is treated with bacteriocidal antibiotics that induce hydrolysis of the cell wall and resultant amplification of the inflammatory response. These subcomponents of cell wall teichoic acids are potent activators of the alternative complement pathway. The cells and mechanisms responsible for ossification in LO are unknown; however, several hypotheses have been proposed.

In 1967, Paparella and Sugiura hypothesized that bone-lining cells of the cochlea are pluripotent mesenchymal stem cells that remain uncommitted until stimulated to differentiate into osteoblasts.

In 1985, Kotzias and Linthicum hypothesized that this type of bone originates from osteoblasts within the otic capsule. They suggested that ectopic bone forms on the endosteal layer after inflammatory insult, but the bone is not incorporated beyond the surface.

Additionally, pericytes associated with blood vessels that supply the modiolus and spiral ligament fibroblasts have been hypothesized as cells of origin.

In an antemortem analysis of LO in a human case report, metaplastic bone was reported to have formed within serofibrinous exudate; however, the cell of origin for the osteoneogenesis has not been identified. Because the new bone deposition occurs in continuity with endosteal bone, postmortem studies are not able to differentiate metaplastic bone from osteoplastic bone within the cochlea. The cells and mechanisms responsible for ossification in LO remain undefined.

WORKUP Section 4 of 8

Imaging Studies:

Until recently, LO was diagnosed histologically; however, radiography currently is a tool that can be used to help diagnose LO. Radiographic documentation of osteoneogenesis within the cochlea is possible with a high-resolution computed tomography (HRCT) scan of the temporal bone (see Picture 4 and Picture 5).

In 1 study, some degree of abnormality of the inner ear was noted in 71% of 31 CT scans performed in cochlear implant candidates. Five scans were interpreted as showing ossification within the cochlea. Of these scans, 4 were confirmed at surgery with 1 false-positive result and 1 false-negative result among the 26 scans interpreted as not ossified (4%).

Other authors note a high incidence (63-73%) of CT scan evidence of postmeningitic patients with deafness. They point out that ossification may not always be evident radiographically, with false-negative rates as high as 46%. The high rate of false-negative results may be related to the inability of HRCT scans to detect early histological features of fibrosis and osteoid deposition, which are consistent with the early stages of LO prior to calcification. Despite the exquisite bone detail, HRCT scans may not detect early ossification and soft tissue abnormalities in up to 57% of patients.

Arriaga and Carrier conducted a study that suggests high-resolution, fast spin-echo, T2-weighted MRI is clinically helpful in cochlear implant candidates. This type of MRI study can identify cochlear soft tissue abnormalities in areas of residual cochlear patency in cases of LO. These are soft tissue abnormalities that may not be detected on HRCT scan. This prospective study of 13 consecutive patients receiving preoperative, high-resolution, fast spin-echo, T2-weighted MRI scans of the temporal bone identified unanticipated cochlear fibrosis in 1 patient, vestibular schwannoma in 1 patient, and patency in the second turn of the cochlear in a patient with LO. The study also disproved cochlear fibrosis suspected on HRCT imaging in 1 patient. These findings suggest that, in addition to HRCT scans, high-resolution, T2-weighted MRI studies of the temporal bone may be useful preoperatively when considering candidates for cochlear implantation. However, the value of MRI in preoperative assessment of candidates for cochlear implantation is not universally accepted.
Histologic Findings: See Pathophysiology.

TREATMENT Section 5 of 8

Medical Care: Ceftazidime is a first-line agent for the prevention of otogenic and meningogenic labyrinthitis because it reaches higher concentrations in the perilymph and CSF than other CSF-penetrating agents (eg, cefuroxime, cefotaxime).

Steroids have been shown to inhibit the synthesis of connective tissues, impair the formation of granulation tissue, and decrease total collagen formation; however, these effects may be indirect sequelae of inflammatory suppression. Several human and animal studies have demonstrated that steroid-induced immunosuppression may reduce hearing loss associated with bacterial meningitis. Lebel et al found that treatment with dexamethasone caused a statistically significant reduction in subsequent hearing loss. This finding applied only to meningitis that was caused by H influenzae. The mechanism of effect of dexamethasone on meningitis is unknown, but it is hypothesized to result from inhibition of internal mediators of inflammation (eg, interleukin-1 [IL-1], cachectin, prostaglandins). "

Originally posted by leefromphila:
For the third time in about eight years, I have the symptoms of what was previously diagnosed as labyrinthitis. This does make sense as I recently was treated for an upper respiratory infection (though it does confirm my disenchantment with antibiotics). Does anyone know if it is common to get recurrences of this? Is one more susceptible after getting it once?Hello...I too have been diagnosed with Labyrinthitis but my situation was pretty bad too. I was in the hospital for 3 days with severe vomiting and dizziness http://www.healthboards.com/ubb/frown.gif and i a still going through the dizzines part. I am currently off work now until July 2/02 and my wedding is coming up 3 weeks later. I have never gone through this before and it was the scariest thing i have ever been through. I don't wish this upon anyone thats for sure!



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Have a great day!

This was printed on a link for dizziness:

"Vestibular neuronitis, we believe, is due to inflammation in the ear's balance organ. Another theory is that it is caused by an interruption of the blood supply to one branch of the vestibular nerve that goes the labyrinth. It is hard to find anything on a laboratory test or x-ray, though there may be definite abnormalities on the ENG test discussed elsewhere. There is nothing to be seen in the ear. Most of the time there is no hearing loss. It can occur after a cold or virus infection and usually goes away and is forgotten about. Some doctors may call it a viral labyrinthitis, indicating some vague inflammation of the nerve or labyrinth. You may feel fine, then the problem appears out of the blue with frightening suddenness. A person with this entity gets so sick so fast that most of the time they end up in the Emergency room. There is severe vertigo with vomiting and unsteadiness. Vertigo always comes on when you change position but at first it may be so bad that even if you are still you will feel you are whirling. Eventually the problem may happen only when you move or turn or only when you are in a certain position. Then it may cause unsteadiness for a while and go away, perhaps even be forgotten. But you can still attack of full blown vertigo years later. What we can do is treat the more serious problem when there is an attack or recurrence. There should not be any sequelae or permanent damage. That's why it's also considered "benign" or not life-threatening or serious. This is not to minimize the discomfort from the problem. Sometimes the vertigo will degenerate into a less explicitly vertiginous more constant imbalance or lack of sure-footedness."

I experienced this twice and blood test showed I had glandular fever which probably caused the infection. As you can see not a lot to be done for these symtoms.

This was posted a while ago but answers my recent questions about reccurrences of L'itis. Hope it helps others too. I think once you've had it, you are just more susceptible unfortunately. Anyone else had a flu jab? This may help and I am considering it.

xxx

Hi Emsybobs.... you wanted to know about where you can go and get vestibular therapy in the UK... check my last post on 'refrain from taking medication' section.
It certainly helps knowing others are going through the same thing, doesn't it? It's interesting that other people have also had recurrences of it like me - at least having had it before, I know it does eventually go away. I'd still like to know why some people are more prone to it than others though.
Hope you're feeling better.

Ruth
xx

By the way, I would do anything to ensure I don't get this again, but how would the flu jab do this? Have only had flu once in my life (3 years ago). Isn't it a completely different virus?