Microvascular compression syndrome

Timothy C. Hain, MD   • Page last modified: February 19, 2022

See also: vestibular paroxysmia

loop
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.

History of MVC and the controversy

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

ABR normal

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).

 

Surgical treatment of microvascular compression

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.

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