Neuroanatomy, Vestibulo-ocular Reflex

Article Author:
Swathi Somisetty
Article Editor:
Joe M Das
Updated:
8/8/2019 5:34:14 PM
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Neuroanatomy, Vestibulo-ocular Reflex

Introduction

To maintain a stable perception of the world around us while we engage in normal movements throughout our day, such as walking, we have something known as the vestibulo-ocular reflex (VOR). This reflex keeps us steady and balanced even though our eyes and head are continuously moving when we perform most actions. When we make a head movement, our eye muscles are triggered instantly to create an eye movement opposite to that of our head movement at the exact same speed to readjust the visual world, which, in turn, stabilizes our retinal image by keeping the eye still in space and focused on an object, despite the head motion.[1] 

Structure and Function

The vestibulo-ocular reflex involves three parts[1]:

  1. A peripheral sensory apparatus (which consists of a set of motion sensors: the semicircular canals and the otolith organs (saccule and utricle)
  2. A central processing mechanism
  3. A motor output (which are the eye muscles)

Otolith organs are sensitive to linear acceleration and therefore detect the position of the head relative to gravity and head translation. Semicircular canals, however, are responsible for detecting head rotation since these are sensitive to angular acceleration. These organize in a push-pull structure consisting of one coplanar canal on the left side and another coplanar canal on the right side, which work by coordinating with each other. Humans have a total of six canals arranged in three main planes (anterior, posterior, horizontal) on both sides; each plane has a pair of canals. A canal will get stimulated by head motion towards that canal.[2] When a canal on one side is activated, there is inhibition of the other one during angular head movements. When there are head movements and rotation, the velocity of the movements dictates the difference in firing rate between the two semicircular canals. Hair cells are embedded in a fluid and gelatinous structure called the ampulla in each canal. When our heads rotate, the canal will move relative to the fluid inside of it, which will create a force against the ampulla, causing hair cells to bend. When the head is at rest, vestibular afferents have tonic discharge; this results in a balance between the semicircular canal pairs. Cases of nystagmus and ocular misalignment may be interpreted by understanding the organization and structure of the semicircular canals and otolith organs within the head.[1] Information regarding linear acceleration, angular velocity, and orientation of the head relative to gravity are all collected by these peripheral motion sensors. These sensors relay this information to the central nervous system. Here, information from somatosensors (carrying other sensory information) is combined with motion sensory information to calculate head orientation.

The central nervous system (CNS) is the central processing mechanism, which sends its outputs to the spinal cord and ocular muscles to generate the VOR. Each SSC has excitatory projections to a pair of extraocular muscles in each eye and inhibitory projections to an antagonistic pair of muscles.[2] In addition to the VOR, we also have a vestibulospinal reflex (VSR), which prevents falls by maintaining head and postural stability. It does this by creating compensatory body movements.[1] To attain an even better orientation, this information also goes to cortical structures (posterior insular vestibular cortex (PIVC)) for further integration with tactile, auditory, and proprioceptive inputs. Actions of the VOR and VSR becomes controlled and continuously adjusted as needed by the CNS.[1]

Embryology

Research done on mice and rats shows that vestibular afferents and central neurons have some functionality very early in life. This research suggests that neural network connections between vestibular afferents, central neurons, oculomotor neurons, and extraocular eye muscles are initiated and set up to some extent by birth. Much of this maturation process was shown to be dependent on the growth of the animal and its vestibular organs. Although the development and maturation of the VOR did not seem to be influenced by the presence or absence of visual inputs initially, this was noted to be crucial for the fine-tuning and enhancement of the VOR.[3] The reflex becomes impaired in individuals who are blind.[4]

Blood Supply and Lymphatics

The primary blood supply for the peripheral vestibular system is the labyrinthine artery, which comes from the anterior inferior cerebellar artery. The utricle, small part of the saccule, and superior and horizontal semicircular canals receive supply by the superior vestibular artery, which bifurcates with the anterior inferior cerebellar artery. The cochlea, rest of the saccule, and most of the posterior semicircular canal get supplied by bifurcation of the common cochlear artery. The superior vein drains the horizontal and superior semicircular canal and utricle. The inferior vein is responsible for draining the posterior semicircular canals and saccule.[5]

Nerves

Vestibular information comes into the brainstem via the cranial nerve VIII. Signals enter the vestibular nuclear complex, located in the medulla and pons. Four main nuclei comprise the vestibular nuclear complex (superior, inferior, medial, and lateral).[6] Using first-order sensory neurons of cranial nerve V, most of the semicircular canal inputs synapse at the superior and medial nuclei. The medial longitudinal fasciculus is used to send second-order sensory neuron signals ipsi- and contra-laterally to oculomotor cranial nerves III, IV, and VI. Lastly, a third motor neuron is responsible for stimulating the extraocular muscles that cause conjugate eye movements.[7] Also, the vestibular system sends information via the inferior cerebellar peduncle to the cerebellum to modulate the VOR. The flocculonodular lobe and fastigial nuclei are responsible for this fine-tuning. Vestibular data is also processed by the cerebellum, which then aids in the regulation of vestibular reflexes, maintaining posture, and coordination.[5] Other connections to the cerebral cortex, thalamus, and reticular formation assist in coordinating efforts between other central networks and the vestibular system, allowing for enhanced spatial awareness.[7]

Muscles

As mentioned earlier, the VOR works by activating our eye muscles to create eye movements in the exact speed but opposite direction of our head movements to stabilize our retinal images.[1] To recognize the effects of this activation, we must understand the direction of pull on the various eye muscles at play. The horizontal recti are easier to understand than the vertical recti and obliques, which are more complex. The lateral rectus is responsible for abducting the eye, while the medial rectus is responsible for adducting the eye (horizontal recti). The effect of pull on the vertical recti and oblique muscles changes depending on whether the eye is abducted or adducted. When the eye is in abduction, contraction of superior rectus will elevate the eye and contraction of the inferior rectus will depress the eye. When the eye moves into adduction, there is more of an intorsional movement caused by the superior rectus and an extorsional movement caused by contraction of the inferior rectus.[8] During eye abduction, contraction of superior oblique causes intorsion of the eye and contraction of inferior oblique causes extorsion., whereas during adduction, contraction of superior oblique causes depression and contraction of inferior oblique causes elevation.[8]

Surgical Considerations

Surgery is not first-line of treatment for VOR malfunction. The ability to restore the VOR function varies. Due to neuroplasticity, it usually improves spontaneously with time, and no intervention is needed. There are a few suggested interventions for those who do not recover with time. One is an adaptation, and another is exercise-based treatment programs (vestibular rehabilitation therapy). However, it is challenging to restore VOR function at high velocities in severe cases of vestibular loss.[9] The goal of vestibular rehabilitation therapy (VRT) is to practice head and eye movements with different activities and postures. They should repeat movements that stimulate vertigo and continue to expose patients to different types of sensory and motor environments.[10] VOR exercises should start with patients in a seated, still position to assess if there is an aggravation of symptoms such as dizziness, nausea, and anxiety. The exercises can slowly increase in velocity. By gradually increasing the intensity, the capacity of the VOR system will not be overwhelmed. Other methods to rehabilitate VOR function are under development. For example, researchers found that artificial restoration of VOR function is possible by electrically stimulating the LAN branch of the vestibular branch in humans.[11]

Clinical Significance

The implications of a disrupted vestibulo-ocular reflex include oscillopsia and abnormal nystagmus.[12] Oscillopsia results in blurred vision when the head is in motion and objects appear to jiggle and bounce since they do not stay fixed at one point in the retina.[13] Patients are often forced to stop and stay still to read signs. Reading a book may also require great effort since small head movements may cause distortion. Since these patients would need more time to comprehend and process words and letters, undiagnosed children are sometimes wrongly thought to have dyslexia or dyscalculia. Abnormal nystagmus may also blur vision since it causes excessive involuntary eye movements (can be in various directions; side to side or up and down).[14][15] Individuals with VOR malfunction are also likely to be clumsy, get motion sick easily, have sensory issues, difficulty maintaining balance and nausea. If the sensory vestibular organs are not fully functional on either side, the brain will receive conflicting signals regarding movement, causing vertigo.[16][17][18]

Other Issues

Assessment of the vestibulo-ocular reflex takes place using the Halmagyi-Curthoys test, also known as the rapid impulse test. To perform this, the physician will rapidly move the patient’s head in one direction (left or right), and the eyes should remain in place focused on a particular object in front of them despite the head movement. If a patient’s VOR has damage on one side when their head turns to that direction with force, their eyes will follow the direction of the head movement before coming back to their focal point; this would imply some issue in the vestibulo-ocular reflex arc.[19] The VOR may also be tested using the caloric reflex test, where cold water or warm water is poured into the patient’s external auditory canal using a syringe to induce nystagmus. When using cold water, the fast phase of nystagmus should be to the opposite side of the ear filled with the water. However, when using warm water, the fast phase of nystagmus should be on the same side as the water-filled ear. If this eye movement is abnormal and not occurring as described in the patient, there is likely vestibular dysfunction in the side being stimulated by water.[20] Brain death is a complete loss of cerebral function.[21] If performing the caloric reflex test and the VOR is absent in the patient, this is a likely a serious indicator of brain death.[22]



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