• neuroophthalmology
• multiple sclerosis
• ophthalmology
• clinical neurology
• stroke

Martin Lubow (1931–2015)1 is credited with coining the term ‘wall-eyed bilateral internuclear ophthalmoplegia’ (WEBINO).2 Most readers will be familiar with internuclear ophthalmoplegia (INO) and the fact that it can occur bilaterally. So why is WEBINO, as in the case presented by Chen3 in this issue of Practical Neurology, special?

INO is caused by damage to the medial longitudinal fasciculus (MLF). This interrupts the nerve fibres connecting the sixth and third nerve nuclei, which facilitate conjugate horizontal eye movement. A unilateral INO causes slowing, or absence, of adduction of the ipsilateral eye and, usually, gaze-evoked nystagmus of the abducting, contralateral eye during attempted contralateral gaze. Interestingly, adduction is not infrequently preserved in the context of convergence.4 Because these are not the only fibres that travel in the MLF, there may be additional abnormalities due to interruption of the vestibular/otolithic pathways, such as skew deviation or vertical nystagmus. If the INO is bilateral, vertical nystagmus is very common and the vertical vestibulo-ocular reflex is demonstrably impaired.5 INO can result from many different underlying pathologies,5 6 though demyelinating disease is the most common cause of bilateral INO and stroke is the most common cause of unilateral INO.6

In spite of the impaired adduction, many patients with an INO are orthophoric in primary position, that is, their eyes point straight ahead. Some exotropia occurs in up to 60% of cases of unilateral INO4 but diplopia is often absent or surprisingly mild.7 A few patients are esotropic (convergent), particularly early on, possibly due to excessive convergence tone. The number of patients who are markedly exotropic (divergent) is surprisingly small, but many of these demonstrate large, wide-angle, exotropia. Bilateral INOs that show this divergence are labelled WEBINO. Of note, …