Imaging finding
Case 179
【Progress】
Two cases who admitted in our hospital were diagnosed vestibular neuritis. Other two cases were outpatients and diagnosed that their causes were unknown. As time progress, the symptoms improved in each case.
【Discussion】
The inner ear composes of cochlea and semicircular canals and functions hearing and balance. Cochlea is in charge of hearing and semicircular canals and otolith are in charge of balance (1).
There are several common vestibular diseases: benign paroxysmal posture vertigo (BPPV), Meniere’s disease, vestibular neuritis, vestibular labyrinthitis and migraine (2-4).
In BPPV, vertigo and nystagmus occur in the specific posture such as facing upward when you take a thing on a shelf, facing downward when you wash your hair or facing parallel when rising or lying down. The nystagmus of BPPV is rotary, relatively specific with the most common complaint “I feel dizzy when I roll over in bed.” It arises from otolith (debris) floating in the semicircular canals. Repositioning debris is considered to improve vertigo and nystagmus in the treatment of BPPV.
Meniere’s disease causes symptoms of rotary vertigo (which last hours to days), fluctuating hearing loss, tinnitus and a sensation of fulness or pressure in the ear. It arises from hydrops of endolymph in the semicircular canals and cochlear (4). Etiology of Meniere’s is still unknown: spontaneous, virus or allergy, et al., are listed.
Vestibular neuritis and vestibular labyrinthitis indicate internal ear inflammation and are probably caused by virus infection. Symptoms of vestibular neuritis are attributed to vestibule nerve to semicircular canals: sudden onset rotary vertigo, nausea and vomiting. Meanwhile, symptoms of vestibular labyrinthitis are attributed to inflammation of semicircular canals and cochlea: not only rotary vertigo, nausea and vomiting but also hearing loss and tinnitus. In short, the symptoms of vestibular neuritis are limited to be rotary vertigo but those of vestibular labyrinthitis are rotary vertigo plus hearing loss (5-7). As a result, the symptoms of restibular labyrinthitis is similar to those of Meniere’s disease.
Gadlinium-enhanced T1WI MRI is known to show the enhanced swollen vestibular nerve in vestibular neuritis and to show the swollen enhancement of both cochlear and semicircular canals in vestibular labyrinthitis. Meanwhile, fat suppression T2WI might be useful to detect the hydrops of endolymph in Meniere’s disease (2-7).
Nerve vascular compression indicates that cerebellar branch artery contacts and compresses cranial nerve, which arises specific symptoms. Hemifacial spasm is well accepted to be related to vascular compression, However, trigeminal neuralgia and glossopharyngeal neuralgia are equivocal and the other symptoms proposed by Janetta et al., are not well accepted (9, 10).
In our four cases, although MRI showed anterior inferior cerebellar branch artery contacted and compressed to VIII nerve, it was not clear that they were pathogenic. Two cases were diagnosed vestibular neuritis, one case vestibular labyrinthitis, and vestibular migrane.
【Summary】
In this week, we present four cases suffering from vertigo, nausea, vomiting hearing loss, tinnitus and/or migraine. Two cases were diagnosed vestibular neuritis, vestibular migrane and suspicious vestibular labyrinthitis. MRI with time of flight and heavy T2WI showed vestibular-cochlear nerve compression by AICA branch artery. We should keep in mind; benign paroxysmal posture vertigo (BPPV) arises from otolith (debris) floating in the semicircular canals with vertigo and specific rotary nystagmus; Meniere’s disease arises from hydrops of endolymph in the semicircular canals and cochlear with symptoms of vertigo and hearing loss; vestibular neuritis and vestibular labyrinthitis arises from virus infection, vestibular neuritis causes vertigo and nystagmus, while vestibular labyrinthitis does not only vertigo and nystagmus but also hearing loss and tinnitus.
【References】
1.Yousry I, Camelio S, Schmid UD et al (2000) Visualization of cranial nerves I-XII: value of 3D CISS and T2-weighted FSE sequences. Eur Radiol 2000;10(7):1061–1067
2.Casselman J, et al. MRI of the cranial nerves—more than meets the eye: technical considerations and advanced anatomy. Neuroimaging Clin N Am 2008;18(2):197–231
3.Sheth S, Branstetter BF 4th, Escott EJ (2009) Appearance of normal cranial nerves on steady-state free precession MR images. Radiographics 29(4):1045–1055
4.Saremi F, Helmy M, Farzin S, Zee CS, Go JL (2005) MRI of cranial nerve enhancement. AJR Am J Roentgenol 185(6):1487–1497
5.Bartual-Pastor J. Vestibular neuritis: etiopathogenesis. Rev Laryngol Otol Rhinol (Bord) 2005;126(4):279–281
6.Park KM, et al. A case of acute vestibular neuritis visualized by three-dimensional FLAIR-VISTA magnetic resonance imaging. Neuroophthalmology 2014; 38:60–61
7.Karlberg M, et al. Acute vestibular neuritis visualized by 3-T magnetic resonance imaging with high-dose gadolinium. Arch Otolaryngol Head Neck Surg 2004;130(2):229–232
8.Yamane H, et al. Three-dimensional cone beam computed tomography imaging of the membranous labyrinth in patients with Meniere's disease. Acta Otolaryngol. 2014 Oct;134(10):1016-21
9.Jannetta PJ. Arterial compression of the trigeminal nerve at the pons in patients with trigeminal neuralgia. Journal of Neurosurgery 1967: 26: 159-162.
10.Haller S, et al. Imaging of neurovascular compression syndromes: trigeminal neuralgia, hemifacial spasm, vestibular paroxysmia, and glossopharyngeal neuralgia. AJNR Am J Neuroradiol 2016; 37:1384–1392
2020.1.29