Extraocular movements

1. Voluntary conjugate movements of the eyes to the opposite side are probably intitiated in area 8 (middle frontal gyrus) of the frontal lobe and work with the superior colliculus to initiate saccadic (a.k.a. high velocity) eye movements; saccadic movements are different from smooth pursuit movements which are generated in the ipsilateral parieto-occipital cortex and the ipsilateral cerebellum; saccadic latency is prolonged in Huntington’s and Parkison’s disease
   1. lesions and corresponding effects:
      1. an infarct of one frontal lobe causes paresis of contralateral gaze and the eyes will involuntarily turn toward the side of the cerebral lesion
         1. however a lesion of the deep cerebrum or thalamus may cause the eyes to deviate away from the side of the lesion
      2. midbrain lesions affecting the pretectum on both sides of the midline and lesions in the region of the posterior commissure interfere with conjugate movements in the vertical plane
         1. upward gaze is affected far more frequently than downward gaze because the fibers subserving upgaze cross rostrally and posteriorly between the rostral interstitial nucleus of the medial longitudinal fasciculus (riMLF) nuclei (near the pineal body) and are subject to interruption before descending to the oculomotor nuclei whereas the pathways for downgaze project directly downward from the riMLF
         2. bilateral infarction of the rostral midbrain just medial and dorsal to the red nuclei may cause a paralysis of downward gaze
      3. lesions of individual extraocular eye movement muscles
         1. CN 3 – ptosis and inability to rotate the eye upward, downward, or inward; eye deviates outward and slightly down; commonly compressed by aneurysms (travels between the PCA and superior cerebellar artery), tumor, or temporal lobe herniation (NOTE: painful opthalmoplegia is most often traced to a tumor or inflammatory or granulomatous process in the anterior portion of the cavernous sinus or superior orbital fissure)
         2. CN 4 – weakness for moving eye down when the eye is aligned medially; eye deviates up and in; commonly seen in head trauma
         3. CN 6 – paralysis of outward movement; eye deviates medially; commonly seen in basilar skull fractures, brainstem tumors, hydrocephalus
      4. Nystagmus
         1. Two types: 1) jerk nystagmus where movements alternate between a slow component and a fast corrective component (the direction is named by the fast component) and 2) pendular nystagmus where the oscillations are roughly equal in rate in both directions
            1. labyrinthine nystagmus is elicited by stimulating the external auditory canal while brainstem and cerebellar nystagmus is brought out by having the patient fixate upon and follow a moving target
            2. most common cause of nystagmus is drug intoxication
         2. unilateral lesions of the parietal region may cause a loss of the optokinetic nystagmus which normally appears when watching a rotating drum; when the drum is rotated toward the side of the lesion there is a normal response but when it is rotated away there is an anormal response or no response (presumably due to a loss of efferent pathways from the parietal cortex to the lower centers for conjugate gaze); frontal lobe lesions allow the eyes to deviate tonically in the direction of the target with no fast phase correction
         3. upbeat vertical nystagmus is observed in patients with demyelinative or vascular disease, tumors and Wernicke’s disease but the exact cause is unknown
         4. downbeat nystagmus is always of central origin and is commonly seen in syringobulbia, Chiari malformation (lesions at the cervicomedullary junction) and Wernicke’s disease
         5. cerebellopontine disease often causes bilateral horizontal nystagmus
         6. convergence nystagmus is often less in lesions of the pineal region or upper midbrain
         7. seesaw nystagmus (one eye up and one eye down) is seen in parasellar masses
         8. oscillopsia (illusory movement of the environment in up and down or side to side direction) may be caused by brainstem lesions involving the vestibular nuclei
         9. spasmus mutans – often seen in infants
         10. ocular bobbing (spontaneous jerk of the eyes in a downward direction) usually seen in comatose patients with large destructive lesion of the pons
         11. opsoclonus (rapid, conjugate oscillations of the eyes in horizontal, rotatory, and vertical directions, a.k.a. dancing eyes) is seen in paraneoplastic syndromes or drug intoxication
   2. the corticofugal pathway for saccadic horizontal gaze travels to the brainstem in two bundles; the first is the dorsal transthalamic bundle which is uncrossed and goes through the anterior limb of the internal capsule to the superior colliculus and periaqueductal gray matter with another branch projecting to the rostral part of oculomotor nucleus and rostral interstitial nucleus of the medial longitudinal fasciculus (riMLF) and interstitial nucleus of Cajal (iC) which are both involved in vertical eye movements; the second path is more ventral and descends through the posterior limb of the internal capsule and terminates on the contralateral paramedian pontine reticular formation (PPRF) which in turn projects to the CN 6 nucleus
   3. ultimately all pathways mediating saccadic and pursuit movements in the horizontal plane as well as vestibular and optokinetic movements converge onto the PPRF; the PPRF and the medial vestibular nuclei function as a neural integrator and relay station for horizontal saccade pathways; the interstitial nucleus of Cajal and the medial vestibular nuclei perform the integrative function for vertical saccade pathways – however, the neural signals that encode smooth pursuit and vestibular and optokinetic movements bypass the PPRF and project independentaly to the abducens nuclei
      1. abducens nucleus contains two groups of neurons which project to the ipsilateral lateral rectus muscle and to the contralateral riMLF and then to the medial rectus neurons of the oculomotor nucleus
         1. a lesion of the MLF results in unilateral internuclear opthalmoplegia (INO) which is an inability to adduct the eye with lateral gaze to the opposite side but a preserved ability to adduct the eye with convergence
            1. bilateral INO disease is virtually diagnostic of MS
   4. vertical gaze is different from horizontal gaze because vertical eye movements are under bilateral control of the cortex and upper brainstem; these pathways converge in the riMLF just rostral to the oculomotor nucleus at the junction of the midbrain and thalamus
      1. medial cells of the riMLF subserve upward gaze and the lateral cells downgaze; Remember: common strength exercise is ‘lat’ pull’downs’
         1. frontal and parietal eye fields project to the riMLF and interstitial nucleus of Cajal
         2. interstitial nucleus of Cajal projects to ipsi and contralateral CN 3 nuclei as well as CN 4 nuclei
         3. riMLF nuclei innervate nuclei of CN 3 and 4; the riMLF are connected through the posterior commissure to account for bilateral vertical movements
      2. vertical gaze center is in the midbrain at the midbrain/thalamus junction (rostral PPRF) while the horizontal gaze center (caudal PPRF) is in the pons
         1. stimulation of the superior colliculus produces conjugate movement of the eyes to the opposite side
2. Vestibular influences are important in stabilizing images on the retina, this is done via the vestibulo-ocular reflex – a movement of the eyes equal and opposite to that of the head
   1. the flocculus and posterior vermis of the cerebellum receive abundant sensory projections from proprioceptors of the cervical musculature, retinas, proprioceptors of the eye, auditory and tactile receptors, superior colliculi and PPRF
   2. cerebellar efferents project to the vestibular nuclei which in turn influence horizontal and vertical gaze centers
   3. lesions of the flocculus and vermis cause defects in smooth pursuit; with one sided lesions of the vestibulocerebellum, the inhibitory discharges of the Purkinje cells onto the ipsilateral medial vestibular nucleus are removed and the eyes deviate away from the lesion – this may also cause overshooting of the eyes (a.k.a. hypermetria)
      1. 1. NOTE: the medial vestibular nuclei sends fibers to the contralateral ocular movement nuclei (directly to contralateral CN 6 as well as contralateral CN 3, 4, interstitial nucleus of Cajal and riMLF through the MLF) accounting for the ‘looking away’ from cerebellar lesions