Migraine secondary to superior oblique myokymia.

Superior oblique myokymia (SOM) is characterized by intermittent, small-amplitude, monocular, paroxysmal, high-frequency oscillations. These oscillations are mainly torsional in the primary gaze position and in abduction and evoke oscillopsia during paroxysms (1). The term SOM was first used by Hoyt and Keane in 1970 (2), but the first case recognizable as SOM was described by Duane in 1906 (3). The pathophysiology of this condition is not clear. Often the patients are otherwise healthy, but sometimes vascular compression of cranial nerve IV may be responsible (4, 5), and rarely it is associated with other neurological diseases, such as adrenoleukodystrophy (6), retinitis pigmentosa, astrocytoma, multiple sclerosis and cerebellar tumour (7). The disorder may have spontaneous remissions, which can last for days or up to years, and relapses (1). There have been several reports that anticonvulsants, especially carbamazepine, have a therapeutic effect (8, 9). In recent years, gabapentin has also been reported to be effective (10, 11). When medication is unsuccessful, surgery, involving tenotomy or a tenectomy of the superior oblique muscle, combined with inferior oblique myectomy may be performed (1). Recently, surgical decompression of cranial nerve IV has been found to be beneficial when vascular compression is con- firmed on magnetic resonance imaging (MRI), but there is the danger of superior oblique palsy (4). The choice of treatment is related to the intensity and duration of the visual symptoms and to the degree of disability the disorder may have caused. Pareja et al. (12), in a recent and exhaustive review of primary trochlear headache and other trochlear painful disorders, have considered the possible causes of headache secondary to involvement of the trochlear region, including superior oblique muscle myofascial pain, but migraine secondary to SOM was not reported.