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Questions and Answers
What is the primary function of pause cells in the brain?
What is the effect of dysfunctional pause cells?
What type of cells inhibit the antagonist muscles of the intended eye movement?
What is the relationship between the discharge rates of excitatory burst cells and inhibitory burst cells?
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What type of cells discharge in relation to eye position?
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Which structure sends information to the contralateral pons for horizontal saccadic control?
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What nerve is responsible for activating the ipsilateral medial rectus during horizontal saccadic control?
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Which structure is involved in vertical saccadic control?
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Which system can move the eyes without interaction from the FEF?
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A patient with a problem in higher cortical areas of control would likely have difficulty with what type of saccade?
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What is characteristic of patients with Huntington's disease?
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What is the term for saccades that are too large or too small?
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What is the term for slow saccades of restricted amplitude?
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What is the term for saccades that are followed by a slow drift back to the original position?
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What is the term for saccades that are too fast or too slow?
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What is the term for corrective saccades that are made to compensate for an initial saccade that undershot the target?
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What happens to the innervation of the paretic lateral rectus after patching the normal eye for a few days?
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What region is responsible for receiving sensory information from the parieto-occipital temporal region?
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Lesions of the frontal eye fields result in which of the following?
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What is the function of the frontal eye fields in generating saccades?
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What is the role of the cerebellum in saccadic control?
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What is the neural map of visual space found in?
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What do efferent projections from the frontal eye fields go to?
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What is the purpose of the frontal eye fields in determining the occurrence of a future saccade?
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What is the purpose of checking if a patient can perform saccades in the absence of a visual task?
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What is the velocity above which catch-up saccades are needed during pursuit?
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What is the primary function of smooth pursuits?
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What is the role of smooth pursuit during combined eye-head tracking?
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What is the latency of smooth pursuit?
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What determines the accuracy of smooth pursuit?
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What is the maximum target velocity that can be tracked by smooth pursuit?
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What type of eye movement is smooth pursuit?
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Patients with lesions in the frontal eye fields (FEF) exhibit difficulty with which type of pursuit?
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Which structure is responsible for a deficit in horizontal pursuit toward the side of the lesion?
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What is the effect of extensive lesions in the cerebellum on pursuit?
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What is a characteristic of abnormal pursuits in patients with multiple sclerosis and cerebellar ataxia?
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What is the term used to describe abnormal pursuits characterized by a jerky or ratchety motion?
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What is the effect of a cerebellar infarction on the right side on pursuit?
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What is a common classification of abnormal pursuits?
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What type of lesions are frequent causes of smooth-pursuit dysfunction?
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Study Notes
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
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Description
Learn about the role of pause cells in regulating saccades during fixation, and their impact on burst neurons and opsoclonus.