Hierarchy of oculomotor control
Supranuclear
- Cortical control
- Pursuits
- Parietal lobe
- Saccades
- Frontal eye fields (frontal lobe)
- Basal ganglia
- SC
- Thalamus
- Cerebellum
- Fine tuning all eye movements including
- Modulation
- Adaptation of vestibulo-ocular responses
- Saccades
- Pursuits
- Vergence
- Location within cerebellum performing ocular motor control
- Vestibulocerebellum
- Consist of
- Flocculus
- Paraflocculus
- Nodulus
- Ventral uvula
- Function
- Stabilization of sight during motion
- Dorsal vermis of the posterior lobe and fastigial nuclei
- Function
- Voluntary gaze shifting (saccades, pursuits and vergence)
Nuclear
- Brainstem
- Rostral interstitial nucleus of medial longitudinal fasciculus (riMLF)
- Ocular motor cranial nerve nuclei
Infranuclear
- Ocular motor nerve
- Extra ocular muscles
Differentiating from supranuclear to nuclear disease
- Stimulate vestibular ocular reflexes:
- Vestibular ocular reflex do not require supranuclear (cortical input) everything occurs in the brainstem
- Doll's maneuver
- Can do this for both vertical and horizontal gaze palsies

4 types of eye movements
flowchart LR A["Versions = gaze movements,<br />conjugate eye movements,<br />associated ocular movements"] B["Fast conjugate eye movements (saccades)"] C["Slow conjugate eye movements"] D["Volitional, targeted,<br />spontaneous saccades"] E["Fast phases of optokinetic<br />and vestibular nystagmus"] F["Smooth pursuit and slow phases<br />of optokinetic nystagmus"] G["Vergences = disjugate or<br />disjunctive eye movements"] H["Accommodative vergence"] I["Fusional vergence"] J["Vestibulo-ocular reflex and<br />slow phases of vestibular nystagmus"] %% Connections from main categories A --> B A --> C G --> H G --> I %% Detailed subtypes B --> D B --> E C --> F C --> J
Vestibular-optokinetics
- Function: maintain eye position with respect to changes in head and body position.
- Stimulus: change in head and body posture
- Latency: 10 msec
- Velocity: as high as 300 degrees/sec
- Neural connections
- Vestibulo-ocular reflex
- Input
- Labyrinthine semicircular canals
- Otoliths organs
- Sensitivity to linear acceleration, generate compensatory eye movements during translational movements of the head.
- Vision
- Using smooth muscle pursuits to supplement vestibular-optokinetic
- Somatosensors (muscle spindles and joint receptors)
- Processing
- Vestibular nuclei
- Examination
- Bedside caloric testing
- Can determining the side of a peripheral vestibular lesion.
- Check to ensure tympanic membranes is intact
- Supine + head flexed 30 degrees.
- Flexion of the head places the lateral semi-circular canals in a vertical position.
- Irrigate the external auditory canals on each side with a small amount of ice water
- A normal response can be elicited with as little as 0.2 mL
- Normal: the ear that is irrigated exhibits nystagmus with its quick phase in the opposite direction.
- Abnormal: Failure to elicit this response indicates loss of unilateral vestibular function.
- Disease
- Parietal or temporal lobe lesion: abnormal optokinetic towards the side of lesion
Smooth pursuits
- Function: holds target image steady during linear movement of object or self
- Eg when walking or item moving
- To keep target that is on the fovea to be always on the fovea
- Has similar neural pathway as saccades
- Retinal information on the speed and direction of a moving target is projected on the striate visual cortex of the occipital lobes. → This information is relayed to the ipsilateral middle temporal visual area, the frontal eye fields, and the pontine nuclei in a retinotopic fashion → modification of the visual impulses in the cerebellum and vestibular nuclei → impulse projected to the ocular motor nuclei.
- Smooth pursuit movements are identified with the ipsilateral occipital lobes, in contrast to saccadic movements, which are identified with the contralateral frontal lobes
- Stimulus for smooth pursuit
- Visual stimuli: the target moving across the retina, usually within or near the fovea OR
- Non visual stimuli: proprioceptive information related to the movement of one's own limbs, may be sufficient to generate smooth tracking movements.
- Latency: 125ms
- Feedback substrate is usually continuous and slow; objects that move fast may require a combination of pursuit and saccadic movements.
- Cortical centres
- Middle temporal and medial superior temporal gyrus
- Ipsilateral cortical control
- Examination
- Ask the patient to hold the head still while tracking a small target, such as the tip of a pencil, held 1m away, Move the target at a slow, uniform speed, and observe whether the eye movements match the velocity and direction of the target.
- If smooth pursuit is too slow (gain is low) then catch-up saccades will be noted
- If smooth pursuit is too fast (gain is high) then back-up saccades area noted
- Pursuit movements naturally deteriorate with age.
- Smooth pursuit movements are also particularly sensitive to drugs, which may affect the results of testing. Such drugs include phenytoin, barbiturates, diazepam, chloral hydrate, methadone, alcohol, and marijuana.
- Disease
- Low gain → saccadic pursuit
- Poor initiation → frontal/parietal lobe lesion
- Deficits found usually in both vertical and horizontal plane
Saccades
- Function: rapidly bring object of interest to focus on fovea
- Can be
- Volitional (voluntary refixations) OR
- Neural connection
- Originate:
- Frontal eye fields
- Aka
- Brodmann's area 8
- Posterior middle frontal gyrus
- Initiating saccades in the contralateral direction
- Via: descending pathways to superior colliculi
- Superior colliculi has topographically arranged visual fields
- When the target image arrives to the fovea a negative feedback system is initiated to cause the eye movement to end.
- Involuntary (quick phases of vestibular and optokinetic nystagmus)
- A ballistic process: once started cannot be stopped
- Stimulus
- Visual reflexive: parietal lobe contralateral
- An object in the peripheral vision
- Latency: 200ms
- Memory guided or volitional: frontal lobe contralateral
- Centre
- Horizontal saccades: PPRF → Pons
- Vertical saccades:
- Rostral interstitial nucleus of medial longitudinal fasciculus (riMLF)+Posterior commissure (PC) → midbrain
- riMLF projects to
- Ipsilateral: Motor neurons of depressor muscle
- Bilateral: Motor neurons of elevator muscle
- Interstitial nucleus of Cajal (INC) projects
- Via posterior commissure
- To
- Motor neurons of contralateral nuclei of the 3rd and 4th CN AND
- Contralateral INC
- Definitions in describing saccades
- Latency
- Duration of stimulus to movement
- Disease: Prolonged latency: degenerative disorders
- Accuracy
- Arrival of eyes on target
- Velocity and conjugation
- Degree to which 2 eyes move together
- Disease
- Slow saccades in horizontal plane
- Pons
- Slow saccades in vertical plane
- Midbrain
- Hypometric saccades:
- Saccade that falls short of intended target
- Disease
- PPRF lesion
- Hypermetric saccades: overshoots the target
- Disease
- Cerebellar lesions
Horizontal Eye Movements
Anatomy
- Originate
- The contralateral frontal lobe (for saccades) OR
- The ipsilateral parietal lobe (for smooth pursuits).
- The impulses carrying information about these movements travel through the internal capsule to the paramedian pontine reticular formation (PPRF) in the pons .
- Horizontal gaze centre
- Consist of:
- Paramedian pontine reticular formation (PPRF)
- Abducens nucleus in the pons.
- The left gaze center controls saccades to the left and smooth pursuit to the left.
- The converse is true for the right gaze center.
- These are not similar to the origin of the impulse
- Neural connections
- This image is for saccadic pathway
- Frontal lobe gaze center → PPRF → ipsilateral sixth nerve nucleus. The projection then reaches the contralateral third nerve nucleus via the medial longitudinal fasciculus (MLF).
Disease
Internuclear ophthalmoplegia (INO)
- The side of the INO is named by the side of the adduction deficit, which is ipsilateral to the MLF lesion. Because of the close proximity of the MLF to the midline, bilateral involvement may not be uncommon (BINO).
- Lesion at the MLF: if R sided
- Saccades and pursuit
- R sided MLF non-functioning → Rt CN6 cannot communicate with contralateral Lt CN3 →
- Resulting in (during left gaze)
- Right eye unable to adduct
- Left eye able to adduct
- The dissociated horizontal nystagmus in the non-affected abducting eye can be explained by Hering’s law of equal innervation, whereby in this case, the 'weak' medial rectus prompts the cortex to increase innervation to it. This results in additional increased, and therefore excessive, innervation to the contralateral lateral rectus causing horizontal nystagmus during abduction
- Here the weak right medial rectus that is weak prompts the cortex to increase innvervation to it. The left eye Lateral rectus has abducted also receives more innervation to it causing nystagmus to form.
- Pearls & Oy-sters: The medial longitudinal fasciculus in ocular motor physiology - PubMed (nih.gov)
- Wall-eyed bilateral internuclear ophthalmoplegia: review of pathogenesis, diagnosis, prognosis and management - PubMed (nih.gov)
- Failure of adduction on the side of the lesion and nystagmus of the abducting eye.
- Cranial vs caudal INO
- If the eyes are able to converge (vergence is intact): lesion is in pons
- If the eyes are not able to converge (vergence is not intact): lesion is in the midbrain.
- Pretectal area (mesencephalic reticular formation just Dorsal to the CN3) is the vergence centre and is located in the midbrain
- If you cover the Right eye the left eye that was not able to abduct can now abduct
- Bilateral INO
- Both eyes cannot adduct
- Since both MLF is damaged and cannot send signals to the CN3 from CN6 → medial rectus in both eyes cannot adduct
A gaze palsy
- Impairment of the conjugate horizontal gaze to one side or the other.
One and a half syndrome
- Consist of (In right sided lesion)
- A full Horizontal gaze palsy=in both eyes
- Impairment of conjugate horizontal gaze to the side ipsilateral to the lesion AND
- Half a horizontal gaze palsy=in one eye
- INO on gaze to the side contralateral to the lesion.
- Lesion: lesion in pons causing simultaneous involvement of
- PPRF (paramedian pontine reticular formation) AND
- Ipsilateral MLF
- Impairment of right lateral conjugate gaze (due to interruption of the right PPRF) and an INO on left lateral gaze (due to interruption of the right MLF).
Vertical eye movements
Anatomy
- Supra-nuclear (cortical)
- Saccades
- Contralateral frontal lobe's visual field
- Pursuit
- Ipsilateral parietal lobe
- Nuclear
- Vertical gaze centre
- Located in the midbrain's Pretectal area/thalamo-mesencephalic junction
- Consist of
- Rostral interstitial nucleus of medial longitudinal fasciculus
- Interstitial Nucleus of Cajal
- Motor nuclei
- CN3
- At level of superior colliculus
- CN4
- At level of inferior colliculus
- Infra-nuclear:
- CN3 → superior rectus, inferior rectus, inferior oblique
- CN4 → Superior Oblique
- Difference between
- Is bilaterally innervated
- Ipsilateral Parietal lobe (Pursuit) + Contralateral frontal lobe (saccades) send out signal to PPRF
- PPRF activates neurons in the riMLF
- riMLF send fibers caudally to the
- Inferior rectus subnucleus of the ipsilateral CN3 AND
- Contralateral superior oblique nucleus CN4.
- Not shown in this diagram, fibers from the contralateral PPRF carry corresponding signals simultaneously.
- The upgaze fibres crosses at the posterior commissure
- Ipsilateral Parietal lobe (Pursuit) + Contralateral frontal lobe (saccades) send out signal to PPRF
- PPRF activates neurons in the riMLF.
- riMLF → interstitial nuclear of cajal → posterior commissure to the
- Superior rectus subnucleus of the contralateral CN3 AND
- Inferior oblique subnucleus of the ipsilateral CN3.
- Not shown in this diagram, fibers from the contralateral PPRF carry corresponding signals simultaneously.