Timothy C. Hain, MD • Page last modified: February 19, 2022
See also: vestibular paroxysmia
|Microvacular compression due to left intra-IAC loop with vestibular paroxysmia (image due to Dr. Dario Yacovino).|
In microvascular compression syndrome (MVC), vertigo and motion intolerance is attributed to irritation of the vestibular portion of the 8th cranial nerve by a blood vessel. It is a controversial syndrome at present, but in the author's opinion, there is some validity to it. The characteristic symptom of nerve irritation is quite common in clinical practice, and it does usually respond to medication. The controversial part is the origin. If one accepts that these symptoms are always due to blood vessels, than a surgical approach is worth considering. On the other hand, if these symptoms are generally due to other processes, then medical management should be preferred. It is the opinion of the author of this page, that the latter is the case.
The existence of MVC was inferred by analogy to the syndrome of hemifacial spasm, in which it is well accepted that the usual cause is a aberrant blood vessel. Dr. Peter Jannetta, a neurosurgeon in Pittsburgh Pennsylvania, together with Drs Aage Moller and Margarita Moller, pioneered the diagnosis and treatment of this condition. Although hemifacial spasm is now presently well accepted to be related to vascular compression, the numerous other syndromes proposed by Janetta and associates to be related to vascular compression (e.g. trigeminal neuralgia, glossopharyngeal neuralgia, and even essential hypertension) are not as well accepted as being a consequence of vascular compression.
In 1984, Janetta, MB Moller and AR Moller described "Disabling positional vertigo", characterized by a history of vertigo, a small midfrequency notch on audiometry, acoustic reflex abnormalities, and an increased I-III latency with brainstem audio-evoked responses using a "tone burst" stimulus. The "positional vertigo" designation appears to be a misnomer as subsequent authors have not emphasized this finding. Some have indicated that motion intolerance may include repositioning. Jannetta and associates proposed treatment by placing an absorbable sponge between the nerve and the blood vessel. While this treatment is intended to buffer the nerve from the blood vessel, later writers have questioned whether this procedure actually simply damages the 8th nerve, or that it is actually a sham procedure (Schalber and Hall, 1992). Others have suggested that the appropriate treatment is vestibular nerve section (McCabe and Harker, 1983).
|Authors||Subjects||Vertigo or disequilibrium||Hearing loss||Motion Intolerance||Other Symptoms/tests|
|Brookler and Hoffman, 1979||5||5||5||Caloric weakness in 4/5|
|Applebaum and Valvasori,1984 and 1985||10||No caloric weakness, spontaneous nystagmus|
|McCabe and Harker, 1983||8||Brief spells of vertigo 2-3 min||Main symptom||Spontaneous nystagmus|
|Wiet, 1989||6||Yes||Yes||Yes||Air contrast CT|
|McCabe and Gantz, 1989||34||Brief spells||Yes||
Failure of medical management
Air contrast CT
|Ter Bruggen, et al, 1987||10||spells||ABR abnormalities|
|Meyerhoff and Mickey, 1998||2||Yes||Tinnitus, normal MRI|
|Moller, 1990||41||Yes||ABR, I-III latency|
|Ryu et al, 1988||27||Seconds to minutes||20/27||
Tinnitus, decreased calorics
Air contrast CT, ABR not helpful
|Kanzaki and Koyama, 1986||2||Yes||Yes||
Air contrast CT helpful
|Brackmann et al, 2001||20||Triggered by supine->sitting||5%||Yes||Positive air-contrast CT or MRI, ABR not helpful|
|Huffner et al, 2008||32||Brief attacks||50%||At rest||ENG, HV induced nystagmus, CISS MRI 95%|
In spite of numerous papers being published on this condition, the very existence of MVC continues to be questioned. The symptoms of MVC are all nonspecific ones, that could easily be found in other conditions such as Meniere's disease, Migraine or simply a constitutional motion intolerance. No specific convincing test abnormality has yet been demonstrated. The ABR findings reported by Moller to be characteristic of MVC would not be considered abnormal by most clinicians (Schwaber and Hall, 1992). No findings related to blood vessels (e.g. air CT, MRA, etc.) will ever be diagnostic as blood vessels cross the 8th nerve of at least a third of normal individuals (Parnes, 1990).
We advise extreme caution. Logically, only treatments that affect the nerve proximal to the site of irritation seem likely to work. In other words, transtympanic gentamicin treatment and a simple labyrinthectomy seem unlikely to be effective. Vestibular nerve section seems overly aggressive in as much as the diagnosis is so difficult and the disability of nerve section is relatively high.
Sporadic reports continue to be published concerning good results of decompression surgery, (e.g. Bernard-Demanze et al , 2015; Borghei-Razavi et al, 2014; Zhang et al, 2012). These in our opinion carry little weight due to the bias that exists for publishing good results. Yap et al (2008), after reviewing all published studies on MVC, noted that "No standardised outcome measures were used and all studies rely on patient subjective assessment of surgical outcome."
The decompression surgery (e.g. Brackmann et al, 2001 as well as multiple authors in the table above) is risky as it involves a neurosurgical approach to the brainstem area. Because the diagnostic criteria at the moment require response to medication, surgery seems reasonable only as a last resort in individuals who develop medication intolerance, and in whom all other reasonable alternatives have been excluded.