Abstract
Dear Editor,
I read with interest the paper by Ping-Kun Chen and Shuu-Jiun Wang, “Ophthalmoplegic migraine: Migraine variant or cranial neuralgia?” (1).
The hypothesis supporting demyelination and remyelination, as it happens in chronic inflammatory demyelinating polyneuropathy, to explain the pathogenesis of ophthalmoplegic migraine (OM) seems highly unlikely in light of what we previously emphasized (2).
In chronic inflammatory demyelinating polyneuropathy, the nerve enlarges at every episode and the contrast enhancement lasts also in the remission period. In OM the nerve enlarges and enhances at the attack, but enlargement and enhancement reduce or disappear during the remission period.
The hypothesis that headache with ophthalmoplegia is related to irritation of the sensory fibers of the ophthalmic division of the trigeminal nerve would not explain attacks of OM with IV and VI cranial nerves deficit, as reported by Lal et al. (3).
In 2009 Lal et al. (3) proposed the pathogenetic theory of ischemic breakdown of the blood-neural barrier, and in 2010 we correlated the reversible failure of the barrier to magnetic resonance imaging (MRI) findings and suggested that enlargement and enhancement of the nerve is well correlated to vasogenic edema of the nerve at the root entry zone where, especially in children, the barrier is deficient (2).
It is possible that a little amount of demyelination and remyelination occurs in OM because of ischemia and not inflammation, but this fact alone does not explain the MRI findings in the disease.
The case quoted in Chen and Wang’s paper (1) of a neurinoma of the III cranial nerve mimicking OM seems fantastic.
In fact the pathogenesis suggested by the authors that the tumor “might release a chemical substance(s) intermittently, which stimulates trigeminal nerve receptors, explaining the paroxistic occurrence of headaches,” and “the relieving ophthalmoplegia might be explained by edema of the surrounding areas, also due to the putative substance(s)” is not realistic.
The reported pathological specimen strongly resembles normal myelin, and ultimately the child continued his ophthalmoplegic migraine attacks after surgery.
According to Lal et al. (3), we are convinced that the pathogenesis of OM is the reversible failure of the blood-neural barrier due to ischemia secondary to migraine attack, and that in the future the disease should be classified under migraine and not under cranial neuralgia.