Tympanotomy and sealing of the round window membrane is effective in the treatment of severe to profound SSNHL. There is evidence that early surgery performed within 5 days is more effective than later surgery. The existence of a detectable lesion of the round window membrane has no significant influence on recovery.
Analysis of 101 patients with severe to profound sudden unilateral hearing loss treated with explorative tympanotomy and sealing of the round window membrane
How dificult is to differentiate these two disorders? You can find some observation which may help you in practice:
Accompanying Symptoms Overlap during Attacks in Menière’s Disease and Vestibular Migraine
Few days ago I saw the pt (45yr wom) with few attacks (three) of strong vertigo accompanied with nausea, vomiting, and pulsating headache. Attacks lasted 48hours and she felt dizzy next 5 days. She hasn’t have any auditory symptoms. She has migraine since she was 20. Exam during last two attacks relieved left-beating Ny.
- Calorics show no labyrinth function at the right side
- VHIT reduced bilaterally
- cVEMP: absent at right side
- oVEMP: absent at both sides
- tonal audiometry: normal hearing
The first attack was 6yr ago and other two this year. Regarding history and her vestibular testing results, one would assume recurrent neuritis at right sides. But pulsating headache, the same one which she has during migraine attacks would favor vestiblar migraine as diagnosis. I doubt Meniere’s disease whenever the attack of vertigo lasts more than 24hour and also, she didn’t have any audiological symptoms jet. The explanation for right vestibular deficit would be ischemic insult as result of vasospasm during the migraneous attacks.
We interpret positive HIT to be due to peripheral vestibular deficit. But it can be seen in patients with cerebellar ataxia also.
False-Positive Head-Impulse Test in Cerebellar Ataxia
Abnormal Head Impulse Test in a Unilateral Cerebellar Lesion
It’s explained by deficit in floccular function.
Isolated floccular infarction: impaired vestibular responses to horizontal head impulse
Here’s a femail patient 59yr; her instability had started 2yr ago very progressively so she can’t walk, even sit unsupported; appendicular ataxia and dysarthria are also obvious signs of cerebellar dysfunction. MRI document marked cerebellar atrophy.
- gaze evoked Ny
- smooth pursuit: saccadic
- very reduced OKN
- bilaterally positive HIT
- positive VVOR test
Very reduced VOR gain
BUT caloric test is normal
Obviously, peripheral vestibular function is preserved. SPV is not elevated, meaning that nodular control of vestibular nuclei is preserved. Markedly reduced VOR gain could be explained by floccular dysfunction.
That means that in a regard of peripheral vestibular assessment in patients with cerebellar ataxia isn’t enough to perform just vhit, but also a caloric test.
Positive VVOR test was explained by three non-functioning compensatory mechanisams: smooth pursuit, OKR, VOR (first two as a sign of central vestibular dysfunction and third as peripheral vestibular dysfunction) and was considered as pathognomonic sign of CANVAS.
Patient with left-sided Meniere’s disease. He’s attack of aural fullness lasts more than 2 months.
Masking was adequate.