The flocculus and paraflocculus (more usually called the cerebellar tonsil) together with the caudal portions of the cerebellar vermis (nodulus and uvula) are part of the oldest portion of the cerebellum or the archicerebellum, also called the vestibulocerebellum1.
The term vestibulocerebellum arose from the fact that it receives both direct and indirect vestibular afferent projections. The vestibular nuclei may be viewed as displaced deep cerebellar nuclei.

Figure 1. Anterior view of brainstem, demonstrating the tonsil and flocculus. 


Figure 2. Anterior surface of the cerebellum, brainstem having been removed. The paraflocculus is more commonly called the tonsil.

The flocculus and adjacent structures are important for gaze holding and stabilisation of visual images upon the retina, smooth pursuit eye movements, and suppression of the vestibular ocular reflexes, for example, during tracking of a visual target with eyes and head.
In particular, the flocculus modulates the brainstem neural integrator network for stabilisation of images on the retina: the nucleus prepositus hypoglossi and medial vestibular nucleus are anatomically linked to the flocculus to make up the neural integrator.

Taken together, two principal components of saccadic innervation are controlled by the cerebellum: pulse size and pulse step

Note that unilateral lesions produce ipsilateral deficits in pursuit and gaze holding2.


Findings seen with floccular lesions3:

  1. Saccadic (low gain) pursuit (eye velocity/target velocity) and loss of VOR cancellation. Saccades are typically spared.
  2. Impaired gaze-holding, with horizontal gaze-evoked nystagmus (characterised by a decaying slow phase velocity waveform)
  3. Primary position downbeat nystagmus
  4. Rebound nystagmus
  5. Postsaccadic drift (glissades), may be observed due to a pulse-step mismatch2

Additional Functions


1. Pursuit and VOR cancellation

Lesions of the flocculus/paraflocculus impair smooth tracking of a moving target, either when the head is still (smooth pursuit) or passively moving (VOR cancellation). Active eye-head tracking is spared. (The dorsal vermis is also involved in pursuit, as are the nodulus and uvula).

The ventral paraflocculus is the primary structure involved in pursuit and VOR cancellation. Unilateral lesions of the ventral paraflocculus cause mild deficits in horizontal and vertical pursuit (both directions) and VOR cancellation, whereas bilateral lesions of the flocculus and ventral paraflocculus cause severe deficits in horizontal and vertical pursuit (both directions) and VOR cancellation. 


Video 1. Abnormal smooth pursuit due to lesion of the flocculus. 



From: Struppp M. Clinical Examination of the Ocular Motor and Cerebellar Ocular Motor System. From:


Video 2. Abnormal pursuit due to a lesion of the flocculus. 


From: Struppp M. Clinical Examination of the Ocular Motor and Cerebellar Ocular Motor System. From:

Similarly to impaired smooth pursuit, abnormal visual fixation suppression of the VOR is a test of the smooth pursuit system (since it uses the same signal as does pursuit, namely, retinal slip). If abnormal, it is indicative of a flocculus/paraflocculus lesion.

Video 3. Abnormal VOR suppression due to lesion of left flocculus.


From: Struppp M. Clinical Examination of the Ocular Motor and Cerebellar Ocular Motor System. From:

2. Gaze Holding and Gaze Evoked Nystagmus (GEN)

Lesions of the flocculus/paraflocculus impair gaze holding, reflecting the role played by the flocculus in the modulation of the brainstem neural integrator network for retinal stabilisation, and the effects of a leaky integrator on gaze holding function.

A lesion of the flocculus is a classical cause of GEN in all directions of gaze.

3. Downbeat Nystagmus

The majority of Purkinje cells of the flocculus are active during downward as opposed to upward pursuit. This up-down asymmetry results in a slow upward drift when the the flocculus is damaged. (The flocculus, like the remainder of the cerebellum, has inhibitory output. One of its primary tasks is to inhibit the superior vestibular nucleus. Therefore, if the flocculus is lesioned, there will tend to be an upward slow drift of the eyes, resulting in downbeat nystagmus.)

Interestingly, slow phase velocity may vary, depending on whether primarily the integrator is leaky (decreasing slow phase), or if unstable (increasing slow phase). Thus, in some patients the nystagmus becomes more intense when the patient changes eye position to look in the direction of the slow phase, the opposite of the common pattern in which the nystagmus becomes more intense when the patient looks in the direction of the quick phase (Alexander’s law).

4. Rebound Nystagmus

Video 4. Rebound Nystagmus. 


From: Struppp M. Clinical Examination of the Ocular Motor and Cerebellar Ocular Motor System. From:

Prolonged eccentric gaze (at least for 60 seconds) is often followed by short-lived rebound nystagmus when the eyes return to the primary position; slow phases are directed towards the prior position of eccentric gaze4. Rebound nystagmus usually coexists with other cerebellar signs, and indicates a lesion of the flocculus/paraflocculus or cerebellar pathways5

Normally, a sustained tonic eye position signal must be generated to oppose the elastic restoring forces of orbital tissues that would passively pull the eye back to its initial position. During sustained eccentric gaze the brain attempts to shift its null position towards the new eccentric position in the orbit in which the eyes are now spending most of their time. This reduces the demands on central circuits that must provide the commands to maintain the high level of sustained activity required to keep the eye steady in a far eccentric position. On return to the original, straight-ahead position, a rebound nystagmus occurs, with the eyes drifting toward the eccentric position from which they had just returned. The rebound nystagmus slowly dissipates as the adaptive response decays and brings the neutral or ‘null position’ back to the original straightahead position6.

Note that rebound is also present in normal subjects, if fixation is removed when the eyes are returned to the straight-ahead position after sustained eccentric gaze. This phenomenon presumably reflects the action of a normal adaptive mechanism (which is also intact or even becomes excessive in cerebellar syndromes) that changes the set point or null position of the gaze-holding network toward the eye position that is most frequently used during fixation3
In some patients the mechanism producing rebound nystagmus becomes unstable leading to a centripetal-beating nystagmus on eccentric gaze in which case slow phases are directed outwards3.

Figure 2. Example of rebound nystagmus. A healthy subject looks at a flashing target, first at center (i.e., straight ahead), then eccentrically at 40 degrees to the right for 30 s, and then back to the center.
During eccentric fixation at 40 degrees there is a gaze-evoked nystagmus with the slow phase drifting toward the center, which gradually decreases in intensity. During the rebound period, the slow phase drifts toward the previously-held, eccentric position6.

From: Otero-millan J, Colpak AI, Kheradmand A, Zee DS. Rebound nystagmus, a window into the oculomotor integrator. Prog Brain Res. 2019;249:197-209


Figure 3. An example of the rebound phenomenon shown by an individual with spinocerebellar ataxia type 6:


  1. On looking towards a visual target located on the far left, gaze-evoked nystagmus begins, with inwardly directed, centripetal drifts of the eyes towards the central position and outwardly directed, centrifugal corrective quick phases.
  2. After 35 s of this sustained effort at maintaining eccentric gaze, the slow-phase drift velocity is reduced.
  3. When the eyes are returned to the central position, the nystagmus reverses direction (rebound nystagmus) and slowly dissipates reflecting the adaptation after-effect6

From: Zee DS, Jareonsettasin P, Leigh RJ. Ocular stability and set-point adaptation. Philos Trans R Soc Lond, B, Biol Sci. 2017;372(1718)



5. Postsaccadic Drift

This refers to the brief drift of the eyes lasting several hundred milliseconds following each saccade. This drift reflects a mismatch between the pulse (phasic) and the step (tonic) components of innervation that drive saccades and is due to the abnormal amplitude of the step output of the neural integrator relative to its velocity input, which is the pulse. Normally these two premotor signals are matched precisely, so the eye abruptly stops at the end of the saccade. In monkeys with lesions of the flocculus/paraflocculus, the direction of the postsaccadic drift, onward, or backward, is variable, which suggests that the role of the cerebellum is largely modulatory upon the functions of the premotor brain stem circuits generating these eye movements3.

Modulation of the VOR

Noting that the VOR is a very rapid three neuron arc contained within the brainstem, without direct visual input, it is of importance to point out that VOR function can and must be modulated.  The vestibulocerebellum, chiefly the floccular-nodular lobes, is important for modifying the gain of the VOR, and is perfectly located for this purpose since it receives a direct projection from the canals and projects in turn, via Purkinje cells, onto the vestibular nucleus8. In fact, part of the VOR runs through the vestibulocerebellum as a parallel branch. 

In order to monitor the VOR, there needs to be visual feedback, in the form of the degree of retinal slip, an indication of image stability.  The sites of motor learning or VOR adaptation needs to be at points of convergence of visual and vestibular inputs, where visual-vestibular mismatch (as retinal image slip), can act as a stimulus to recalibrate the VOR9. These visual inputs are crucial for long-term adaptions which allow the brain to monitor and correct the VOR. This adaptive capability can change the gain, the direction, or the phase (temporal relationship between input and output) of the VOR, each of which reduces image motion during head turns.

This visuo-vestibular convergence occurs in :
-The flocculus and ventral paraflocculus:  these areas receive vestibular input from the vestibular nuclei via mossy fibers and visual input from the inferior olivary nucleus via climbing fibers.These are a major input to the Purkinje cells, and In keeping with their general function as cells involved in motor learning, it is appropriate that VOR adaptation takes place at the Purkinje cell.
-The vestibular nucleus: a subset of cells found in the vestibular nucleus, the  flocculus target neurons, is found in the medial vestibular nucleus, and receives input from the flocculus and paraflocculus.

After removal of the flocculus, the gain of the VOR may be slightly increased or decreased, but when challenged, adaptation of the VOR is abolished10. Presumably related to its substantial connections with the vestibular nuclei, isolated lesions of the flocculus may give rise to an abnormal head-impulse test10.


Figure 4. The cerebellar loop for modifying the VOR11.

Note that, in addition to visual input via the inferior olive, there is vestibular nerve input via mossy fibres, which synapse onto the parallel fibres of granule cells. Purkinje cells compare the discrepancy between the visual and vestibular signals and make appropriate changes that are then sent to vestibular nucleus cells that drive the VOR11.

Redrawn from: Klier EM, Angelaki DE. Gaze Stabilization and the VOR. Encycl Behav Neurosci 2010; : 569–75.


Modulation of the tVOR

In patients with cerebellar disease the t-VOR can be profoundly impaired even when the rotational VOR (r-VOR) is intact, and these patients also have defects in adjusting the gain of the r-VOR for the distance of the target of interest, a feature of translatory movements.
These are necessary requirements for adequate gaze stabilization during head rotation, since virtually all head rotations are accompanied by some translation of the head; the flocculus/paraflocculus has neurons that discharge in relation to vergence and this information may be used to adjust the VOR for target distance3.



  1. Kheradmand A, Colpak AI, Zee DS. Eye movements in vestibular disorders. Handb Clin Neurol. 2016;137:103-17.
  2. Jung I, Kim JS. Abnormal Eye Movements in Parkinsonism and Movement Disorders. J Mov Disord. 2019;12(1):1-13.
  3. Kheradmand A, Zee DS. Cerebellum and ocular motor control. Front Neurol. 2011;2:53.
  4. Frohman EM, Solomon D, Zee DS. Vestibular Dysfunction and Nystagmus in Multiple Sclerosis. Int MSJ 1995 3(3):87-99.
  5. 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
  6. Zee DS, Jareonsettasin P, Leigh RJ. Ocular stability and set-point adaptation. Philos Trans R Soc Lond, B, Biol Sci. 2017;372(1718)
  7. Otero-millan J, Colpak AI, Kheradmand A, Zee DS. Rebound nystagmus, a window into the oculomotor integrator. Prog Brain Res. 2019;249:197-209.
  8. Robinson D. How the oculomotor system repairs itself. Investigative Ophthalmology 1975; 14(6):413-16
  9. Wong, A. M. (2008). Eye movement disorders. Oxford: Oxford University Press.
  10. Park HK, Kim JS, Strupp M, Zee DS. Isolated floccular infarction: impaired vestibular responses to horizontal head impulse. J Neurol. 2013;260(6):1576-1582. doi:10.1007/s00415-013-6837-y
  11. Klier EM, Angelaki DE. Gaze Stabilization and the VOR. Encycl Behav Neurosci 2010; : 569–75.