All conjugate eye movements are associated with neural commands which have been characterised by velocity and position information.

For saccades, the velocity command referred to as the pulse generates the initial sequence for movements of the eyes.  The position element, or step, is derived from the velocity information by the process of neural integration.  The step function acts to overcome the elastic restoring forces of orbital tissue and thereby is responsible for steady gaze holding.  The neural integrators for horizontal eye movements include the medial vestibular nucleus and the nucleus prepositus hypoglossi.  The interstitial nucleus of Cajal (INC) is an important component of the vertical neural integrator.

Destructive frontal eye fields (FEF) lesions initially produce ipsilateral gaze preference.  However, patients typically recover the ability to gaze voluntarily into the contralateral field.  These lesions are supra-nuclear and can be distinguished from nuclear insults by the preservation of oculocephalic reflexes. 

There are a number of deficits in saccadic movements, some of which may be subtle and easily overlooked.  Dysmetria of rapid gaze shifting, delayed saccadic initiation, and decreased saccadic velocity are common saccadic abnormalities.  

When saccades appear to be slow, but with no limitation in the range of motion, the disturbance is usually in the circuits that specifically generate premotor saccade commands. Selective slowing of horizontal saccades occurs with lesions in the pons (pontine paramedian reticular formation or PPRF) and selective slowing of vertical saccades suggests dysfunction within the upper midbrain (rostral interstitial nucleus of the medial longitudinal fasciculus or riMLF)1.

Midbrain Centres:

Pontine and pontomedullary centers

 

Figure 1. Midbrain and pontine gaze centres.

 

 

References

  1. Kheradmand A, Colpak AI, Zee DS. Eye movements in vestibular disorders. Handb Clin Neurol. 2016;137:103-17.