Walsh & Hoyt: Lesions of the Abducens Nucleus

Lesions of the abducens nucleus cause an ipsilateral palsy of horizontal conjugate gaze because the abducens nucleus contains two groups of neurons: abducens motoneurons that innervate the ipsilateral lateral rectus muscle, and abducens internuclear neurons that innervate the contralateral medial rectus motor neurons via the MLF. Vergence movements of the eyes are spared, however, so that adduction is possible with a near stimulus. Such a localized lesion can be produced experimentally, but it occurs rarely in humans except in Mobius syndrome, a congenital brain stem anomaly with horizontal gaze disturbances, often with an associated facial palsy. This condition occurs in at least some cases from aplasia or hypoplasia of both abducens nuclei. More often, however, the abducens nucleus is affected in association with adjacent tegmental structures, particularly the genu of the facial nerve, the MLF, and the PPRF. Lesions restricted to the abducens nucleus can often be distinguished from those in the adjacent caudal PPRF (see also below), because only in the latter may pursuit and vestibular movements be spared, and only in the former may ipsilateral saccades in the contralateral field be spared by virtue of intact inhibition upon the contralateral abducens nucleus. Gaze-evoked nystagmus on contralateral gaze also occurs in patients with presumed abducens nucleus lesions. Possible mechanisms for the gaze-evoked nystagmus include damage to adjacent vestibular or NPH pathways that are involved in neural integration for gaze-holding, or damage to the paramedian cells and tracts that lie in part in the rostral abducens nucleus and have reciprocal connections with the cerebellar flocculus, a structure also involved in gaze-holding.