Search This Site Timothy C. Hain, MD. Last updated: 5/7/99. Please read our disclaimer.
Otoneurology Index
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In microvascular compression syndrome (MCS), 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.
The existence of MCS is 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. They 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 |
| 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 |
In spite of numerous papers being published on this condition, its very existence continues to be questioned. The symptoms of MCS are all nonspecific ones, that could easily be found in other conditions such as Meniere's disease or Migraine. No specific convincing test abnormality has yet been demonstrated. The ABR findings reported by Moller to be characteristic of MCS 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).
At the present writing, microvascular compression syndrome is felt to be rare. Characteristically it is a syndrome of vestibular or auditory symptoms that respond to treatment with medications for neuralgia (e.g. carbamazepine), and in which other reasonable causes (i.e. Meniere's disease, Migraine, labyrinthitis, fistula) have been excluded. "Quick spins" and acquired motion intolerance may be characteristic clinical symptoms, although at the present writing, studies looking subpopulations with those particular index symptoms for response to decompression surgery have not been made (and probably they will never be done). Air contrast CT or MRI/MRA are not diagnostic if a blood vessel is seen, it need not be viewed with concern, but MRI/MRA may help in excluding alternative causes. ABR, if abnormal on the side of auditory symptoms supports the diagnosis, but a normal ABR does not exclude it. In essence, this syndrome cannot be definitively diagnosed until a surgical exploration has been done and the patient is cured on follow-up.
The author suggests the following set of tests for an individual in whom the diagnosis of microvascular compression is contemplated:
It is the author's view that a trial of treatment with carbamazepine (an anticonvulsant that is a sodium channel blocker) seems worthwhile for both the index symptom of "quick spins", and severe motion intolerance. Recently a drug called "trileptal", a relative of carbamazepine, has been made available. Addition of Baclofen may be reasonable if there is a partial response. Other treatments of neuralgia, such as other anticonvulsants may also be considered.
We advise 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. The decompression surgery 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 are medication intolerant, and in whom all other reasonable alternatives have been excluded.
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