Last reviewed 10/2012
- What is Microvascular Compression Syndrome?
- How is Microvascular Compression Syndrome Diagnosed?
- How is Microvascular Compression Syndrome Treated?
- Research on Microvascular Compression
What is Microvascular Compression Syndrome?
In microvascular compression syndrome (MCS), vertigo, tinnitus and motion intolerance is attributed to irritation 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 the usual cause is a similar aberrant blood vessel affecting the 7th cranial nerve. Dr. Peter Jannetta, a neurosurgeon in Pittsburgh Pennsylvania, together with the husband and wife team of Aage Moller and Margarita Moller, pioneered the treatment of this condition. Although hemifacial spasm is now well accepted to be related to vascular compression, the numerous other syndromes proposed by Janetta and associates to be related to vascular compression (for example, trigeminal neuralgia, glossopharyngeal neuralgia, and even essential hypertension) are not as well accepted as being a consequence of vascular compression.
In 1984, Janetta and the Mollers 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). Another small study suggested that treatment with carbamazepine was beneficial for a majority of patients (Kanashiro et al, 2005).
There are many symptoms that have been attributed to MCS including disabling vertigo, severe motion intolerance, tinnnitus, and neuralgic like “quick spins”. As the very existence of MCS continues to be questioned, it is understandable therefore that the symptoms of MCS are ones that could be found in other conditions, such as Meniere’s disease or Migraine.
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 (for example, carbamazepine), and in which other reasonable causes (such as Meniere’s disease, Migraine, labyrinthitis, fistula) have been excluded. “Quick spins” and acquired motion intolerance may be characteristic clinical symptoms; however, at the present writing, studies looking at subpopulations with those particular index symptoms for response to decompression surgery have not been made (and probably they will never be done).
How is Microvascular Compression Syndrome Diagnosed?
No specific convincing test abnormality has yet been demonstrated. The auditory brainstem response (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 (for example, with air computed tomography (CT), magnetic resonance imaging (MRI), etc.) will ever be diagnostic since blood vessels cross the 8th nerve of at least a third of normal individuals (Parnes, 1990).
The author suggests the following set of tests for an individual in whom the diagnosis of microvascular compression is contemplated:
- Magnetic resonance imaging (MRI) with gadolinium
- Electroencephalogram (EEG) (if there are paroxysmal symptoms)
- Electronystagmography (ENG)
- Fluorescent treponemal antigen (FTA),
- Fasting glucose
- Auditory Brainstem Response (ABR)
Some tests that are commonly obtained in this situation may be misleading. Air contrast CT or MRI/MRA are not diagnostic, even if a blood vessel is seen. MRI/MRA are mainly useful in excluding alternative causes. Auditory brainstem response (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.
How is Microvascular Compression Syndrome Treated?
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 and it appears to be safer than carbamazepine. 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. Specific decompression surgery to move the blood vessel off of the nerve is somewhat 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.
A recent review article evaluated all published cases of surgically treated vestibulocochlear microvascular compression (Yap, 2008). The authors found that most studies have been small and of low quality; however, they also reported that the majority of patients reported improvement in symptoms with little or no side effects. A report of 15 patients treated surgically found that 53.3 percent improved and 20 percent were completely cured (Guevara, 2008). Further clinical study is needed before surgery can be recommended.
Research Studies in Microvascular Compression Syndrome
As the very existence of microvascular compression syndrome is presently questioned, at the American Hearing Research Foundation (AHRF), we are presently most interested in diagnostic research. We have funded basic research on similar conditions in the past. Learn more about donating to American Hearing Research Foundation (AHRF).
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- Guevara N et al. Microvascular decompression of cochlear nerve for tinnitus incapacity: pre-surgical sata, surgical analyses and long-term follow-up of 15 patients. European Archives of Oto-Rhino-Laryng; 2008: 265(4):397-401.
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