Neuroscience: The Function of Pause Cells

Saccadic Eye Movement

• Pause cells tonically inhibit burst cells to prevent unwanted saccades during fixation
• They inhibit burst neurons within the same paramedian pontine reticular formation
• They help synchronize the activity of premotor burst neurons
• Dysfunctional pause cells result in opsoclonus
• Inhibitory burst cells inhibit antagonist muscles of the intended eye movement
• Their discharge rates are inversely proportional to those of excitatory burst cells
• Tonic cells discharge in relation to eye position, increasing proportionately with eccentric gaze position

Saccadic Control: Horizontal

• Frontal eye field sends information to the contralateral pons (where CN VI and the paramedian pontine reticular formation are)
• CN VI sends the signal to ipsilateral lateral rectus to contract and communicates with the contralateral CN III through the medial longitudinal fasciculus
• CN III activates the ipsilateral medial rectus

Saccadic Control: Vertical

• Frontal eye field sends information to the midbrain (where CN III and CN IV are)
• CN III and CN IV together control the vertical recti and the obliques
• They activate the corresponding muscles

Saccadic System Adaptation

• Patching the normal eye for a few days results in central adaptation within the saccadic system, increasing innervation to the paretic lateral rectus
• The cerebellum is important for saccade adaptation

Saccadic Control: Supranuclear

• Frontal Eye Fields (FEF) are the most important for generating vertical and horizontal saccades
• Efferent projections from frontal eye fields go to the contralateral pons
• They receive sensory information from the parieto-occipital temporal region (POT) and determine the occurrence of a future saccade
• Lesions of the frontal eye fields result in increased saccadic latencies, slowed saccades, and impaired predictive tracking
• The vestibular system can also move the eyes without interaction from the FEF

Anomalies with Saccade Initiation

• Delayed initiation: abnormally long latency (>250 msec)
• Focal lesions, especially of the FEF, can cause abnormal voluntary saccade initiation
• Patients with Huntington's disease have normal amplitude of random saccade and frequency of nystagmus but characteristically abnormal voluntary saccade initiation

Anomalies with Saccade Size

• Dysmetric saccades with associated corrective saccades
• Static overshoot: a high gain saccade seen in cerebellar disease, not frequent in normals
• Hypermetric saccades are made also by patients with VF defects (hemianopia)

Anomalies with Saccade Velocity

• Slowed dynamics: peak velocity 2-std below mean value, increased saccadic duration
• Slowed saccades of restricted amplitude reflect abnormalities of the ocular motor periphery
• They are a sign possibly pointing to: introrbital tumors and contusions, Graves syndrome, hyperthyroidism, Myasthenia gravis

Pursuits Eye Movement

• Allow the eyes to closely follow a moving object
• Pursuit is modified by ongoing visual feedback
• Pursuing a target needs catch-up saccades if moving target velocity is greater than 30 degrees/sec

Functions of Smooth Pursuits

• Stabilizes the image of a small moving target on the fovea
• Cancels the VOR during combined eye-head tracking
• Cancels optokinetic nystagmus during tracking of a small, moving target against a detailed stationary background

Smooth-Pursuit Tracking

• Generated in response to retinal image motion
• Match eye velocity to target velocity; target velocities can be up to 90 deg/sec
• Latency is about 130 msec (compare this to VOR and saccades)
• Accuracy of SP is determined by its gain; smooth pursuit gain -> eye velocity/target velocity
• Smooth pursuit is not a reflexive eye movement

Abnormal Pursuits Classification

• Defects found in: initiation, latency, initial 100 msec open loop response, maximum eye acceleration, gain, and saccadic overlay

Examples of Lesions that Affect Smooth Pursuit

• A cerebellar infarction on the right side causes asymmetric impairment of pursuit
• Multiple sclerosis and cerebellar ataxia cause jerky pursuits in both horizontal directions
• Cerebellar and pontine lesions are frequent causes of smooth-pursuit dysfunction