I ANATOMY            

II PHYSIOLOGY                 







Smooth-pursuit movements allow clear vision of a moving target by holding the image steady on the fovea.

In addition, the smooth pursuit system cancels the VOR during combined eye-head tracking1.  During smooth tracking of a target that moves in the same direction as the head, smooth pursuit cancels VOR; otherwise, the VOR would move the eyes in the opposite direction of intended gaze.

Smooth pursuit eye movements are most often affected by medication or advancing age.  These can affect the diverse structures responsible for normal smooth pursuit: visual cortex, medial temporal area, medial superior temporal area, frontal eye fields, dorsolateral pontine nuclei, cerebellum (flocculus), and vestibular and ocular motor nuclei

The patient is asked to track visually an object moving slowly in horizontal and vertical directions (10–200/s) while keeping the head stationary2. The speed of smooth pursuit movements is proportional to target speed.
The presence of corrective saccades is established; these indicate the gain of smooth pursuit (ratio of eye movement velocity to target velocity) as being abnormal:

Marked asymmetries of smooth pursuit indicate a structural lesion. For example, if the smooth pursuit is saccadic to the left, this may indicate a left-sided lesion of the flocculus/paraflocculus.

Lesions in different areas of the cerebellum have different effects on smooth pursuit.
The ventral paraflocculus is the primary structure involved in pursuit and VOR cancellation, and bilateral lesions of the flocculus and ventral paraflocculus cause severe deficits in horizontal and vertical pursuit (both directions) and VOR cancellation, as seen in spinocerebellar ataxias.
Lesions of the vermis and fastigial nucleus also lead to deficits in horizontal pursuit.
Lesions involving the rest of the pursuit pathway (ie, starting from the level of medial vestibular nucleus) will also affect the VOR because pursuit and the VOR share similar pathways from this point forward.

Pursuit Pathways
The smooth-pursuit pathways within the brainstem and cerebellum share circuitry with the generation of vestibular movements. For example, the cerebellar output for smooth pursuit relays in part through the medial vestibular nucleus (MVN) and the adjacent nucleus prepositus hypoglossi (NPH), before reaching the ocular motor nuclei2.

Visual information is relayed from the striate cortex to the extrastriate areas (areas V2 and V3), where neurons are specialized for motion, with large receptive fields, strong direction selectivity, and activity that encodes both target and eye motions. From extrastriate cortex, signals are realted to the area MT (middle temporal), and then to the medial superior temporal area (MST), and subsequently to the smooth pursuit regions of the frontal eye field, as well as posterior parietal cortex.
These extrastriate areas have projections directly to the brainstem, to the ipsilateral dorsolateral pontine nuclei (DLPN).  This, in turn, projects to the cerebellum, to the contralateral flocculus/ventral paraflocculus and the dorsal vermis, underscoring the vital importance of the cerebellum for the generation of smooth pursuit. These cerebellar regions project to the medial vestibular nucleus, and then to the abducens nucleus
Vertical pursuit follows the same way, excepting that the projection from MT and MST is to the rostral nucleus reticularis tegmenti pontis of the basal pons. Cerebellar projections are to the y-group (not the MVN).
The nucleus prepsitus hypoglossi-MVN complex and INC perform integration, in the mathematical sense, for conjugate horizontal and vertical pursuit, respectively, by transforming eye velocity signals to eye position signals1.

The pursuit system has a functional architecture similar to that of the saccadic system. Rather than being controlled primarily by areas in extrastriate cortex specialized for processing visual motion, pursuit involves an extended network of cortical areas (eg, frontal eye field) and other subcortical structures (eg, superior colliculus and basal ganglia) that are also important for saccadic eye movements. Thus, although the traditional view is that pursuit and saccades are two distinct systems, it may be more accurate to consider the two movements as different outcomes from a shared cascade of sensorimotor functions1.


Figure 1. Measurement of eye position and velocity during smooth pursuit:

Note that most subjects cannot voluntarily generate pursuit movements in the absence of a moving target: the subject must be able to fixate the target, in order that normal pursuit to be assessed.


Note that using the OKN drum is a useful method to examine pursuit.

Video 1. Examining smooth pursuit I





Video 2. Examining smooth pursuit II





Video 3. Examining smooth pursuit III








  1. Wong, A. M. (2008). Eye movement disorders. Oxford: Oxford University Press.
  2. Strupp M, Kremmyda O, Adamczyk C, et al. Central ocular motor disorders, including gaze palsy and nystagmus. J Neurol. 2014;261 Suppl 2:S542-58
  3. Kheradmand A, Colpak AI, Zee DS. Eye movements in vestibular disorders. Handb Clin Neurol. 2016;137:103-17.