<p>Over a century ago, Charles Sherrington introduced the concept of the brain’s unity, emphasizing the collaboration of different sensory and motor functions. This is exemplified by the vestibulo-ocular reflex, which integrates sensory signals to control eye position. Biomedical engineer David Robinson expanded on this by highlighting neural integration over time, balancing sensory differentiation and integration to maintain consistent actions and perceptions. A classic dysfunction of the ocular motor neural integrator is gaze-evoked nystagmus, where the eye position decays towards a neutral position, and it is dependent upon orientation of gaze in orbit. This dysfunction is not limited to gaze holding. Studies have shown that unilateral brainstem lesions affecting the paramedian pontine reticular formation (PPRF) result in the loss of ipsilateral conjugate eye movements. The neural integrator, located in the medial vestibular nucleus (MVN) and nucleus praepositus hypoglossi (NPH), combines all ocular motor signals in their final common pathway. In macaques, acute, reversible lesions in these areas can lead to (reversible) gaze-evoked nystagmus and loss of other eye movements. If the lesions are ipsilateral, they cause unilateral deficits, which are reversible over time. This phenomenon, however, is not exclusive to animal models and can be seen in human patients with acute (reversible) mechanical compression of the neural integrator regions. Here, we report two cases of such deficits, highlighting that reversible focal unilateral neural integrator dysfunction can cause reversible “hemi” ocular motor deficits, affecting pursuit, saccades, and gaze holding in a unidirectional, opposite fashion.</p>