Superior oblique myokymia

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Research on Microvascular Decompression for SOM
Information prepared by ZestyChicken2

I found a follow-up article on one of the MVD procedures done. Unfortunately, the patient suffered reoccurence of his symptoms. This occurs is about 15% of MVDs for Trigeminal Neuralgia, so is not unheard of. They can actually reperform the procedure with usually a high success rate (70-80%). Of course, alot of people aren't up for a second round. There are no documented cases of "redos" of MVDs for SOM. The article mentioned two other individuals who had been given MVDs for trigeminal neuralgia (5the nerve compression) and also had 4th nerve (trochlear) exploration for SOM. Both of them had resolution of SOM symptoms. The authots were not completely convinced they both had SOM, though. One of them seemed to have the opposite symptoms of what we have. He could see down fine but up not so well. Still, the surgery helped him.

I thought I would summarize the results of the MVD procedures performed to date. Keep in mind that vacular compression may be a very rare cause of SOM and that MVD is not for everyone. Many doctors would not recommend it at all. It is very effective for trigeminal neuralgia and facial hemispasm.

Date	Pt Age	Location	Doctors	Result	Post-Op Nerve Palsy	Follow-up	Comments	Reference
1988	50	Hannover, Germany	Samii, Rosahl	Neg	slight for 5 months	22 months	Symptoms reoccured after 2 years resolution	J Neurosurgery Volume 89, Dec 1998, 349-351, 1020-1024
1987	55	Gunzberg. Germany	Rath, Klein	Pos	gone after 6 months	15 months	Patient also had trigeminal neuralgia, SOM symptoms different	J Neurosurgery Volume 91, Aug 1999, 349-351
1990	69	Gunzberg. Germany	Rath, Klein	Pos	none noted	8 years	Patient also had trigeminal neuralgia	J Neurosurgery Volume 91, Aug 1999, 349-351
2000	50	Hannover, Germany	Rosahl, Kaufmann	Neg	Nerve paralysis	1 year	Patient found nerve paralysis to be preferable to SOM	Ophthalmologica 2000; 214:426-428
2004	49	Sapparo, Japan	Hashimoto, Ohtsuka	Pos	slight for 3 months	1 year		J Neuro-Ophthamol, Vol. 24, No. 3, 2004, 237-239
2004	67	Sapparo, Japan	Mikami, Minamida	Pos	none	18 months		Acta Neurochir (Wien) (2005) 147: 1005�?006 DOI 10.1007/s00701-005-0582-7

There is one thing I need to add about the whole vascular compression theory that is fairly interesting. Compression alone is not enough to cause trigeminal neuraglia (5th cranial nerve), facial hemispasm (7th), or SOM (4th). There are people walking around with compression that have no problems. The theory is that something predisposes you to it. A viral infection that perhaps causes damage to the nerve or its nucleus is one theory.

I had a bad viral infection as a teenager where I was sick for 3-4 weeks. I remember having some slight neurolgical problems at the time - just diziness really. Of course, this may or may not have been it. Who hasn't had some sort of bad viral infection at some point?

Anyway, many nerves, including the cranial ones we are talking about, are surrounded by an insulating layer of cells called myelin. There are two types of myelin, one central (in the brain) and one peripheral (surrounding nerves). There is a transition zone at the root exit of these nerves from the brain stem. At this point of transition, the theory goes that the nerve is vulnerable to compression. The pulsatile pressure of the artery causes irritation of the nerve and intermittent firing of the nerve. In cases of the 5th nerve which is mostly sensory, this creates intractible pain. In the case of the 7th nerve which provides motor innervation to the muscles of facial expression, this creates facial spasm. and in the case of the 4th nerve, can create depression and intortion of the eye resulting in diplopia, or double-vision.

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