Lesion of the sixth nerve nucleus or paramedian pontine reticular formation and the adjacent medial longitudinal fasciculus (MLF) forms the classic manifestation of one-and-a-half syndrome, that is, ipsilateral gaze palsy and internuclear ophthalmoplegia (INO). On its basis, an additional involvement of seventh nerve causing peripheral facial palsy was called eight-and-a-half syndrome . Because of the close proximity of these structures, lesions in dorsal pontine tegmentum may lead to several variants of eight-and-a-half syndrome . In our case, the patient showed bilateral eight-and-a-half syndrome (also known as the 16-syndrome [3,4,5]) with radiological evidence of symmetric caudal pontine involvement. Precisely, the lesion of current case was located in bilateral facial colliculus, an elevation on the floor of the fourth ventricle in the dorsal pons housing the abducens nucleus (contains abducens nerve and MLF) and genu of facial nerve. Therefore, in our patient, we speculate that the complete ophthalmoplegia on horizontal gaze was bilateral INO resulting from the abducens nucleus involvement and the facial palsy was from the involvement of both facial nerves at the genu. In our case, the action of lifting goods, similar to the Valsava maneuver, might aggravate right-to-left shunt thus contributing to potential embolism in the distal part of paramedian potine perforating artery with its terminal supplying both sides of dorsal pons.
Impairment of MLF may be responsible for UBN as the structure affects vertical eye velocity in both directions but slightly more for the downward system, resulting in compensating UBN . Moreover, bilateral MLF lesions causing INO was reported to be more frequent in upward gaze-evoked nystagmus but not on primary gaze position [7,8,9], which was consistent with our case. The occurrence of UBN was also related with damage to the ventral tegmental tract (VTT) arising from the superior vestibular nucleus . However, pontine damage involving VTT are mostly large lesions in the ventral tegmentum or the posterior basis pontis at the upper pons level , which was different from the restricted small lesions of dorsal pontine in our patient. Therefore, the gazed-evoked UBN in our case was more likely to result from MLF involvement rather than VTT involvement.
With respect to differential diagnosis, symmetric dorsal pontine tegmentum lesions should raise the awareness of demyelinating disease such as multiple sclerosis  or neuromyelitis optica spectrum disorders. In our case, a rapid onset to the disease peak during Valsava maneuver, negative finding of demyelination evidences in CSF and follow-up MRI, and improvement of symptoms after stroke intervention add support to the diagnosis of a pontine tegmentum infarction.