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I ANATOMY                

 

II PHYSIOLOGY OF        EYE MOVEMENTS 

III EXAMINATION: EYE MOVEMENTS & NYSTAGMUS 

IV FIXATION INSTABILITY   

V SUPRANUCLEAR to NUCLEAR  

 VI VESTIBULAR     SYSTEM 

VIII CN PALSIES, VISUAL FIELDS, PUPIL & THE EYE

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Saccadic pulse dysmetria is a hallmark of disease within the cerebellum and cerebellar-pathways.The dorsal vermis and fastigial nucleus are key cerebellar structures concerned with the control of saccadic accuracy and in the calibration of the size of the saccadic pulse.

Lesions of the dorsal "oculomotor" vermis and the fastigial nucleus typically give rise to inaccurate saccades (dysmetria).  These generally take the form of hypermetric or “overshoot saccades” and, on less commonly, hypometric saccades. 
Lesions in this regions can also produce macrosaccadic oscillations. 

   1. The Fastigial Oculomotor Region (FOR) on each side facilitates the generation of saccades toward the opposite side and helps with the termination of saccades toward the same side1.

    2. The dorsal (oculomotor) vermis OMV behaves in a similar but reciprocal way through an inhibitory effect on the FOR. Therefore, the pattern of saccade dysmetria with lesions in the OMV is the opposite to that with lesions in the FOR: saccade hypometria toward the same side and hypermetria toward the opposite side (ie saccade contrapulsion)1.

 

Video 1. Hypermetric Saccades

 

(vv)Hypermetricsaccade.mp4(tt)

 

Other functions of the FOR and OMV

Lesions involving the dorsal vermis also produce deficits of SP, especially at onset. and termination, whereas the vestibulocerebellum is more concerned with pursuit during sustained tracking.  Patients with dorsal vermis lesions show moderate, ipsilateral deficits of sustained pursuit. Similarly, inactivation of one fastigial nucleus impairs the onset of contralateral pursuit but enhances acceleration of ipsilateral pursuit2.
The OMV and its underlying FOR have a similar functional contribution to control of pursuit as for the saccades. Thus, with lesions of the FOR, pursuit away from the side of the lesion is impaired, while with lesions of the OMV, pursuit is impaired toward the same side.

Integration of vestibular and proprioceptive information in the rostral fastigial nucleus of the vestibular cerebellum is vital for  accurate control of posture and balance  self motion perception.

 

 

Figure 1. Control of burst neurons by the fastigial nuclus and the cerebellar vermis3

Cerebellar control of saccades can be understood if one considers the neuroanatomical circuitry: caudal to the excitatory burst neurons (EBN) area of the paramedian pontine reticular formation (PPRF) is an area of the medullary reticular (MRF) formation which contains inhibitory burst neurons (IBN), which project to the contralateral abducens nucleus.

Firing of both EBMs and IBMs on the right side, for instance, would provide an excitatory pulse to the right abducens nucleus and a saccade to the right, as well as concurrent inhibition of the antagonist muscles, the left lateral rectus and the right medial rectus via interneurons in the medial longitudinal fasciculus. 

In addition, both the pontine and medullary reticular formations (PPRF and MRF) receive excitatory projections from the contralateral fastigial nucleus, via the uncinate fasciculus.  This pathway crosses the midline and bends around the superior cerebellar peduncle on the way to the brainstem.

Saccade accuracy and Fastigial Nucleus Lesions

A lesion of the left fastigial nucleus, or the underlying deep cerebellar white matter in the region of the right superior cerebellar peduncle, would result in decreased excitation of EBNs and IBNs on the right.  This could account for the hypometria of rightward saccades. 
Concomitantly, with a right hook bundle lesion, one sees hypermetric saccades to the left, away from the side of the lesion. (Contrapulsion).

Fastigial cells have also been implicated in decelerating ipsilateral saccades.  Similarly to the antagonist burst of an agonist-antagonist muscle activation, cells in the left fastigial nucleus will fire prior to the end of leftward saccades, excite IBNs on the right, and inhibit abducens motor neurons on the left side. A failure to generate this inhibition would result in a prolongation of the pulse applied to the left abducens motor neurons and consequently hypermetric saccades.

Lesions of the Inferior Cerebellar Peduncle (Wallenberg syndrome)
Fastigial neurons receive inhibitory projections from Purkinje cells of the ipsilateral cerebellar vermis.  The Purkinje cells receive climbing fibre input from the contralateral inferior olive via the inferior cerebellar peduncle, as well as mossy fibre input via the middle cerebellar peduncle.  When a climbing fibre excites a Purkinje cell, there is a refractory period with diminished Purkinje cell inhibitory activity on fastigial neurons. 

A lesion of the inferior cerebellar peduncle therefore will cause loss of climbing fibre input, and fewer Purkinje cell refractory periods. This results in a net increase in Purkinje cell inhibition of fastigial neurons.

For example, a lesion of the left inferior cerebellar peduncle causes increased left Purkinje cell activity and increased inhibition of the left fastigial nucleus.  This leads to ipsipulsion with hypermetric saccades to the left and hypometric saccades to the right.

 

References
  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. Frohman EM, Solomon D, Zee DS. Vestibular Dysfunction and Nystagmus in Multiple Sclerosis. Int MSJ 1995 3(3):87-99.