Neuroanatomy and Pathophysiology
The location of the lesion determines the type of palsy. Nonselective horizontal gaze palsies are caused by lesions in the Abducens nucleus. This is where the cranial nerve VI leaves on its way to the Lateral rectus muscle, which controls eye movement horizontally away from the midline of the body. The cranial nerve VI also has interneurons connecting to the medial rectus, which controls horizontal eye movement towards from the midline of the body. Since the lateral rectus controls movement away from the center of the body, a lesion in the abducens nucleus disrupts the pathways controlling outward movements, not allowing the right eye to move right and the left eye to move left. Nerve VI has the longest subarachnoid distance to its target tissue, making it susceptible to lesions. Lesions anywhere in the abducens nucleus, cranial nerve VI neurons, or interneurons can affect eye movement towards the side of the lesion. Lesions on both sides of the abducens nucleus can cause a total loss of horizontal eye movement.
One other type of gaze palsy is a horizontal saccadic palsy. Saccades are very quick involuntary eye movements. The paramedian pontine reticular formation(PPRF), also in the pons is responsible for saccadic movement, relaying signals to the abducens nucleus. Lesions in the PPRF cause what would be saccadic horizontal eye movements to be much slower or in the case of very severe lesions, nonexistent. Horizontal gaze palsies are known to be linked to Progressive Scoliosis. This occurs because pathways controlling saccadic movements are disrupted by the lesion and only a slow movements controlled by a different motor pathways are ineffected.
Lesions in the midbrain can interfere with efferent motor signals before they arrive at the pons. This can also cause slowed horizontal saccadic movements and failure for the eye to reach its target location during saccades. This damage normally happens in the oculomotor nucleus of the midbrain As in horizontal saccadic palsy, the saccades are stopped or slowed from the disrupted pathway, only in this case the signal is disrupted before it reaches the PPRF.
One-and-a-half syndrome is associated with damage to the paramedian pontine reticular formation and the medial longitudinal fasciculus. These combined damages cause both a complete gaze impairment on the ipsilateral side and a "half" gaze impairment on the contralateral side. As seen in horizontal saccadic palsy, the impairment of the contralateral side gaze is caused by the disrupted pathways coming from the PPRF, while the "half" impairment is from the signal passing through the medial longitudinal fascicles not being able to reach its target. One-and-a-Half syndrome is normally associated with horizontal gaze.
Although more rare than horizontal, one-and-a-half syndrome from damage to the paramedian pontine reticular formation and the medial longitudinal fasciculus can be shown to affect vertical gaze. This can cause impairment of vertical gaze, allowing only one eye to move vertically.
Read more about this topic: Conjugate Gaze Palsy