| Paramedian pontine reticular formation | |
| Latin: | formatio reticularis pontis paramediana |
The paramedian pontine reticular formation (PPRF) (also known as paraabducens nucleus) is a subset of neurons of the oral and caudal pontine reticular nuclei mediating horizontal gaze.[1] It is situated in the pons adjacent to the abducens nucleus.[2] It projects to the ipsilateral abducens (cranial nerve VI) nucleus, and contralateral oculomotor (cranial nerve III) nucleus to mediate conjugate horizontal eye movements and saccades.
The PPRF is situated in the pons just ventralmedial to the abducens nucleus. It is located anterior and lateral to the medial longitudinal fasciculus. It is continuous caudally with the nucleus prepositus hypoglossi.[3]
The PPRF (and adjacent regions of the pons) are traversed by fibers projecting to the abducens nucleus that mediate smooth pursuit, vestibular reflexes, and gaze holding.[4]
The PPRF receives afferents from:
The PPRF mediates horizontal conjugate gaze (i.e. simultaneous horizontal movement of both eyes) by projecting to both:
The pararaphal nucleus - one of distinct neuron population in the PPRF - projects to the flocculus of the cerebellum.
The PPRF mediates horizontal conjugate eye movements. It is important in mediating saccadic eye movements. It is probably not involved in smooth pursuit.
The PPRF generates excitatory bursts that are delivered to the ipsilateral abduecens nucleus to drive ipsilateral saccades (inhibitory saccadic stimuli are meanwhile delivered to the abducens nucleus from the contralateral medulla oblongata).
Destructive lesions of the PPRF cause ipsilateral horizontal conjugate gaze palsy and mostly impair ipsilateral horizontal saccades, however, other horizontal and vertical eye movements may also be affected as the PPRF contains multiple distinct populations of neurons important in saccade generation, as well as being traversed by nerve fibers involved in eye movements that elsewhere; dysfunction of horizontal saccades will additionally also indirectly disrupt (slow and misdirect) vertical saccades (though slowing of all saccades may also be accounted for by destruction of adjacent omnipause neurons of the interposited raphe nucleus).
In the short-term, unilateral lesions of the PPRF may be characterised clinically by contralateral deviation of the eyes; looking contralaterally induces nystagmus characterised by quick twitches directed contralaterally whereas ipsilateral twitches are slow and do not move beyond the midline. More extensive lesions will also affect inhibition of antagonists, abolishing ipsilateral saccades.
Lesions of the medial pontine regions are relatively common. Due to the small size of the arteries in the area, the most common cause of a local lesion is an infarction due to lipohyalinosis and hypertension. Like other small arteries of the brain, these vessels are vulnerable to microemboli, especially those generated due to turbulence or low-flow states in those with artificial heart valves or arrhythmias, respectively.[6] Unilateral lesions of the PPRF produce characteristic findings: