Neural Science and Vision – Part 7


Smack in the middle of Principles of Neural Science in Section IV on Perception, after the extensive treatment given to vision we reviewed in Parts 1 through 6, we find a chapter dedicated to the Vestibular System. Unless you are Curt Baxstrom, the vestibular system isn’t likely uppermost on your mind. But even if you’re not Curt, the last entry of that chapter, on page 647, should raise your eyebrows. It is titled “Bilateral Vestibular Hypofunction Interferes With Normal Vision”.

We’ll work our way up to that last entry, but first let’s take a look at some intriguing interrelationships between the neuroanatomy of the vestibular and visual systems. Back in 2014 I blogged about the significance of the fact that the planes of the three semicircular canals nearly align with the planes of the extraocular muscles to which they are connected by three-neuron reflex arcs. Once you start thinking more about these interrelationships, you will no longer view subtle ocular motor deficits such as cyclovertical imbalances as isolated eye problems.

Page 634 of Principle of Neural Science explains it this way: “The canal planes are also roughly aligned to the pulling planes of specific eye muscles. The pair of horizontal canals lies in the pulling plane of the lateral and medial rectus muscles. The left anterior and right posterior canal pair lie in the pulling plane of the left superior and and inferior rectus and right superior and inferior oblique muscles. The right anterior and left posterior pair occupies the pulling plane of the left superior and inferior rectus muscles.”

But it is on page 636 that the real fun begins. Here we learn than the vestibular nerve projects ipsilaterally from the vestibular ganglion to four vestibular nuclei in the pons and medulla. These nuclei integrate signals from the vestibular organs with signals from the spinal cord, cerebellum, and visual system. The vestibular nuclei project to oculomotor nuclei and reticular and spinal centers concerned with gaze and postural movement, as well as the thalamus. Through reciprocal connections with the cerebellum, vestibular nuclei help to regulate eye movements, head movements, and posture. (Vestibular nuclei also receive inputs from the accessory optic system, which Brodsky famously called the fugitive visual control system in infantile strabismus.) Most pertinent to our discussion, the superior and medial vestibular nuclei receive fibers from the semicircular canals and otoliths, and send fibers to the oculomotor centers that include nuclei of CN III, IV, and VI, as well as neural integrators for converting head velocity into head position signals for horizontal and vertical eye movements.

A remaining chunk of the chapter is devoted to a subject of VOR, or the vestibulo-ocular reflex, about which we’ve blogged extensively before. The co-authors of this chapter, J. David Dickman and Dora Angelaki, provide a scintillating account of what makes the VOR so special. Consider the following: “The afferent signal from the semicircular canals is proportional to head velocity, while the compensatory eye movement requires eye position changes. To convert velocity to position requires temporal integration (simple calculus) that occurs through neural networks in the brain stem nuclei for most head motion speeds. However at high rotation frequencies, the viscoelastic properties of the eyeball muscles and surrounding tissues provide an additional integration step. Thus, the rotational VOR is thought to consist of two parallel processes.”

[Once again, Larry Macdonald was prescient in stating that the brain writes equations for eye muscles to solve. And even though a pair of eyeballs never walks into your office, the impact of its viscoelastic properties provides renewed appreciation of the motor part of neural integration, and for the eyes as specialized joints adapted for sight.]

There are two types of VOR, rotational (rVOR) and translational (tVOR). As Dickman and Angelaki explain, rVOR is a full-field image stabilization reflex, whereas the goal of tVOR is to selectively stabilize images on the fovea. In general, the two eyes moves disjunctively, consisting of either a pure vergence movement or a combination of vergence and conjugate eye movements. [As an aside, this renders the classic debate among New Yorkers vs. Californians moot as to whether prismatic jumps should be called “jump ductions” or “jump vergence” – it can be either or both!] In practice, although the direction of the evoked eye movement is consistent with geometric predictions, tVOR typically under-compensates for near-target viewing, with gains of only about 0.5. As noted on page 643, one reason why adaptation to PALs can be challenging is that the VOR must use different increases in gain for the differing array of added plus lens powers.

Most people are able to adapt to progressives because the VOR is a highly modifiable reflex, with the brain continuously monitoring its performance by evaluating the clarify of vision during head movements. A wide open field of inquiry is the effect that acquired brain injury has on VOR gain. I have a hunch that plasticity is constrained in TBI, which is why even patients who had been successfully adapted to PALs prior to ABI may have functional difficulties post-trauma. If you really want to geek out on rVOR/tVOR, there’s a nice open access article in Neuro-Otology/Frontiers in Neurology on Vestibulo-Ocular Responses and Dynamic Visual Acuity During Horizontal Rotation and Translation.

Here’s a gem from page 645: In the past decade it has become increasingly clear that the function of the vestibular system is as important for cognitive processes as it is for reflexes. Perceptual functions of the vestibular system include:

  1. Tilt perception – awareness of spatial orientation relative to gravity.
  2. Visual-vertical perception – neural representation of the visual scene is modified by static vestibular and proprioceptive signals that indicate the orientation of the head and body.
  3. Visuospatial constancy – despite the constant change in retinal image due to movement of eyes, head, and body, stability of the percept is critical not only for vision by for sensorimotor transformations that update motor goals for eye and limb movements.

So what about that tease I gave you at the outset regarding “Bilateral Vestibular Hypofunction Interferes With Normal Vision” on page 647? The most common reason for simultaneous loss on bth sides is ototoxicity due to aminoglycoside antibiotics such as gentamicin, streptomycin, or tobramycin. As described on page 648, a physician who lost his vestibular hair cells because of a toxic reaction to streptomycin wrote a dramatic account of this loss. Immediately after the onset of streptomycin toxicity, he could not read without steadying his head to keep it motionless. Even after partial recovery he could not read signs or recognize friends while talking in the street; he had to stop to see clearly!

Now imagine, if you will, how many children and young adults on antibiotics for an extended period have varying degrees of bilateral vestibular hypofunction, and how that may contribute to compromised visual-vestibular interaction and impaired reading.

2 thoughts on “Neural Science and Vision – Part 7

  1. Great stuff, so difficult to isolate visual vs. vestibular inputs and their integration. They are reciprocally interwoven. I hope to digest this further!!!!

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