Abstract
We thank Dr. Ambrosetto for showing interest in our editorial (1). He questioned the hypothesis of chronic inflammation in ophthalmoplegic migraine (OM) and, instead, he proposed that ophthalmoplegia is likely caused by reversible hypoxic-ischemic breakdown of the blood-neural barrier, which results from migraine-related vasospasm.
Research has shown that vasospasm is not seen in the reported cases of OM. In fact, a recent magnetic resonance imaging (MRI) study demonstrated dilation of the middle meningeal and middle cerebral arteries during migraine attacks (2). In the acute stage of OM, contrast enhancement of the affected cranial nerves is common but not universal (3). Some of these patients do not recover completely and had residual engorgement of their affected cranial nerves (4). In addition, several secondary lesions of the cranial nerves were also reported in patients with typical presentations of OM. Actually, whether it be primary or secondary OM, the clinical phenomenon is a severe and prolonged migraine-like headache attack followed by ophthalmoplegia. Therefore, migraine is suggested as a trigger of ophthalmoplegia.
We considered that migraine attacks can trigger ophthalmoplegia in susceptible patients with primary OM, whereas the threshold of ophthalmoplegia might be reduced in the affected nerves during migraine attacks in patients with secondary OM. Of note, reversibility is not universal in cases with OM. While we agree with Dr. Ambrosetto that OM is one migraine variant, we feel that his hypothesis of reversible breakdown of the blood-neural barrier needs more evidence.