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.

Subclinical Ocular Torticollis: A Tilt in Perspective

The subclinical stage of any entity is considered to be a presentation that escapes the more commonly applied clinical tests. Of course this is accentuated when not looking for something, as the famous clinical dictum reminds us: we miss more by not looking than by not seeing. A brief piece in the Australian Journal of General Practitioners last year suggested that a tilt in perspective is sometimes needed when looking at the significance of ocular torticollis.

The article cites a case of long-standing superior oblique palsy in a 95 year-old patient, and reviews application of the Parks-Bielschowsky Three Step Method to isolate paretic muscles, yet notes this this test only has a sensitivity of 70%. This lack of sensitivity, owing to the spread of comitance over time, makes the detection of subtle ocular postural skews more challenging. As the article notes, the treatment of choice in some of these instances may be “refractory prisms”. We blogged about this a few years ago regarding a more sensitive sensory variant of the Three Step Test, and more recently reviewed the art of prescribing prism, particularly for subtle imbalances with vertical vectors.

Whenever you see a child with a subtle head tilt in a consistent direction, it is prudent to assume that there is a vertical or cyclovertical imbalance until proven otherwise. The easiest way to confirm that in free space is to use a red maddox rod/Risley prism together with a fixation light.

With the zero line perfectly perpendicular to the nose, when the head is positioned to eliminate the habitual heat tilt, the patient will observe that the line is slanted. The degrees of torque that you need to angle the Maddox rod before the slant is neutralized gives you a feel for the amount of cyclophoria. While this can be done a trial frame with a loose Maddox rod from your trial set so that the exact number of degrees can be measured, I prefer to do it this way in free space for several reasons. One is that the trial frame is clunky and makes controlling head position more difficult, particularly with younger children. Another is that it makes it easier to measure the amount of residual vertical phoria in conjunction when the cyclorotation is neutralized, and vice-versa. Whenever there is a subtle, but clinically significant vertical or cyclovertical imbalance, go back into the history and ask about the parent’s recollection of torticollis being present in infancy. Due to the spotlight that OTs and PTs place on this in early intervention, parents often recollect this. While that won’t likely influence what you prescribe, it can provide a clue about underlying etiology.

The clinical report that I cited above from the Australian Journal of General Practice provided reference to an interesting review on torticollis from the Journal of Child Neurology. It notes that torticollis can be seen at all ages, from newborns to adults, and can be congenital or postnatally acquired. Congenital primary torticollis usually occurs when there is breech presentation, or trauma during birth, impacting the sternocleidomastoid muscle. Acquired torticollis usually occurs as a result of trauma. This is an entity to bear in mind when there is a history of mTBI, and added to the list of subtle but clinically significant conditions that might otherwise escape detection.

The review in the Journal of Child Neurology by Tomczak and Rosman offers a new classification of torticollis based on dynamic qualities and pathogenesis. Torticollis can be classified as either nonparoxysmal (nondynamic) or paroxysmal (dynamic). Ocular torticollis, in which the head tilt and chin or face turn is due primarily to EOM or visual imbalance, and secondarily to adaptive sternocleidomastoid contracture, is classified as nonparoxysmal. An example of paroxysmal would be primary cervical misalignment contributing secondarily to ocular adaptations involving a vertical or cyclovertical vector. The term paroxysmal may be familiar to you from the condition of BPPV, or Benign Paroxysmal Postional Vertigo. Particularly fascinating is that included in Tomczak and Rosman’s classification of paroxysmal torticollis is an etiology of conversion disorder.

To finish on a lighter note, not all head tilts signify primary or secondary ocular torticollis. In some cases a head tilt is adopted consciously or subconsciously without a functional adaptive purpose. But don’t take my word for it. Readers of Best Life Online learn that tilting the head comes in at #22 on the list of 23 subtle ways to make yourself more attractive. And #23 on the list? …. Smile more 🙂

What To Do About Sagging 70-something Year-Olds



Joseph L. Demer is a strabismologist at Jules Stein Eye Institute who originally did his Fellowship in Texas under the guidance of Gunter K. von Noorden in the late 1980s.  In the early 1970s he was a broadcast engineer at KVOA-TV in Tucson while working his way through a degree in electrical engineering at the University of Arizona.  Turning his attention toward humans, he entered a joint M.D., Ph.D. program at Johns Hopkins, earning his degree in biomedical engineering in 1981.  Since that time he has been occupied with the biomechanics of extraocular muscles, and his early work on the involvement of EOM pulley systems in strabismus is reviewed in his chapter in Duane’s Clinical Ophthalmology.

In February 2008, Demer wrote an op-ed published in JAAPOS that advised his fellow surgeons to have more respect for the role of connective tissue in strabismus.  In it, he noted that muscle orbital layers were recognized to insert in pulley connective tissues, and that degeneration of these connective tissues occurs with aging and can be correlated to limitation in vertical duction and sagging of horizontal rectus pulleys.  In the following year Demer co-authored a paper on “Heavy Eye” Syndrome, an acquired strabismus of aging.  To differentiate this from acquired strabismus due to biomechanical forces in high myopia, in which the angle of divergence insufficiency esotropia was larger, Demer referred to this entity as “Sagging Eye” Syndrome.

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The case of a sagging 77 year-old female, representative of this newly identified clinical entity, was presented in the University of Iowa Health Care Eye Rounds a few years ago and is instructive.  It begins: “A 77-year-old female presented with a complaint of intermittent, binocular, horizontal diplopia that had been present for the last six months. The diplopia was only present at distance and she denied double vision with near tasks.”  The patient had a 4 prism diopter esotropia in primary gaze that increased on both left and right gazes, and a very small left hypertropia measuring less than 2 prism diopters in all gaze directions.  She was given a trial of Fresnel prism for symptomatic control of the diplopia.  Follow up at 4 and 10 months showed stable strabismus measurements and no complaints of diplopia. A prescription for ground-in prism was given and she was scheduled for annual follow-up.

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Sagging Eye Syndrome (SES) is nicely summarized by the American Academy of Ophthalmology’s EyeWiki, and differentiated into Age Related Distance Esotropia (ARDE) in which there is distance esotropia with no vertical versus Cyclovertical Strabismus (CVS) in which there is cylovertical diplopia, although the conditions may co-occur.

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The AAO EyeWiki page makes it clear that prism therapy is the treatment of choice for SES, particularly when the angle is small (as it usually is) and the patient is not going to be independent of spectacles anyway.  It also notes that because the patient typically has good fusional reserves, even though the prism is required only for distance, it is accepted well by the patient at all distances.  Parenthetically, this has been my experience in prescribing small amounts of prism for patients with convergence insufficiency or uncompensated vertical drift – even though the prism may be require primarily at one distance or angle, it is often accepted well at all distances and angles of gaze.  There are also select cases where vision therapy can complement the acceptance of prism and stabilize the binocular profile.

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In a new article on the subject in the American Journal of Ophthalmology, Demer and colleagues report on the Prevalence of Sagging Eye Syndrome in Adults with Binocular Diplopia.  The medical records of 945 patients over 40 years of age presenting with acquired diplopia were reviewed.  The most common cause of diplopia in this population was SES (31.4%).  They report that 35% of their patients (104) with SES had ARDE, and 65% (193) had CVS, with combined hyper/eso in 28.2% and hyper alone in 36.7%. The average age of patients with SES was 71.2 years, with a preponderance of females.  Female sex hormones such as progesterone and esotrogen are known to be important in maintaining collagen content by preventing the collagen degradation in women. Since levels of those hormones decrease after menopause and the orbital pulley system is composed of collagen, elastin, and smooth muscle, it would not be surprising for involutional changes in orbital connective tissues to be more common in females than males.

To summarize, patients with SES typically present with some or all of the following:

*Deep superior sulcus
*High upper lid crease
*Aponeurotic blepharoptosis
*Small angle hypotropia
*Small angle excyclotorsion
*Small angle esotropia (greater for distance than near)
*Mild limitation in supraduction
*Normal horizontal saccadic velocity

Once you know about this condition, you will start to recognize it more often among geriatric patients.  In contrast with acquired divergence insufficiency under the age of 40 which is suspect for tumor, vascular, or neurologic disease, diagnosis of SES can spare the patient expensive and low yield neurological testing and focus on alleviating symptoms and improving quality of life.

A Personal Approach to Prescribing Vertical Prism

In Part 1 we introduced a patient self-diagnosed as having agoraphobia who wrote two paperback memoirs available through Amazon touting the benefit of a small amount of vertical prism in her glasses.  In Part 2 we reviewed the logic of prescribing small amounts of vertical prism.  In those blogs I included a link to a 2017 interview on Gary Gerber’s Power Hour with the wife/husband team of Dr. Debby Feinberg (an optometrist) and Dr. Mark Rosner (an ER physician).  I’d encourage you to listen to that, as well as to their initial interview which was conducted in 2015.  It details the patient types which include those experiencing unresolved headaches, motion sickness, visual-vestibular disintegration, nausea, gait/balance/postural issues, head tilt/neck pain, anxiety, agoraphobia, photophobia, and reading disabilities.  They estimate that VH (Vertical Hetereophoria)/SOP (Superior Oblique Palsy) as a subset of BVD (Binocular Vision Disorder) occurs in up to 10% of the population, and that small amounts of vertical prism that sets both eyes in synchrony results in 80% treatment success.

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Of note, a caller during this interview asked specifically about the measurement device used for Neurolenses (formerly manufactured by Stereo Optical and now bundled as part of eyeBrain Medical which this year formed a collaborative with IDOC).  Dr. Feinberg replied that she tried the device in her office, but found that because at least 60% of her patients had some form of brain injury, they required out-of-instrument testing often through trial framing that didn’t lend itself to testing with the device.  As an aside, Neurolens has a fixed progressive or contoured horizontal prism of 0.375^ base-in for each lens maximal in the reading area added to the distance power (total of 0.75^ BI OU).  My personal approach is to be sensitive to small amounts of either horizontal or vertical prism, sometimes using both, and sometimes utilizing yoked prism effects.  This is due to the significance of subtle cyclovertical asynchrony (at the cortical level)/misalignment (at the motoric level).

Here is the test protocol that I have evolved, done entirely out of the phoropter:

  • Measure dissociated phoria with Red Maddox Rod/Risely Prism measure at distance and near, comparing vertical phoria with measuring prism over right eye vs. left eye.  Near testing is done at the habitual reading or work distance and angle of gaze (typically below eye level).
  • Probe vertical fixation disparity distance and near, taking note of unilateral vs. bilateral slip, and asymmetry.  Again, near testing is below eye level.
  • Present a horizontal line of letters and measure vertical vergence range at distance and near.  Look for asymmetry (for example, a right hyper of 1^ should be confirmed with diplopia occurring on BU^ sooner than BD^, and/or recovery BU^ poorer than BD^.
  • If there is habitual head tilt, do the Worth 4 Dot test looking for diplopia that occurs in the field opposite to the habitual tilt.  See if the tentative vertical prism in primary gaze helps extends the range of single vision.
  • Do Wirt Stereo Circles without prism and then repeat with tentative vertical prism to note any improvement.
  • Have patient look at a paragraph of print and gain a sense of comfort or performance, then repeat with tentative vertical prism to note any improvement.
  • If there is significant horizontal or cyclophoria, repeat with prism in place and see if it lessens considerably.  If not, repeat the vertical phoria measure with horizontal prism as derived through horizontal associated phoria or disparity.
  • With tentative prism in place, take the patient out into an open space and note any change in head posture or gait, and elicit their sense of comfort in space as they look around as well as out into the open as through a window across the street with cars passing by.
  • Based on history and your testing, decide with the patient where the area of greatest concern is, distance or near.  Many times the patient will be able to absorb the same prism in low amounts for all distance.  But that may not be the case.
  • When distance and near differ based on angle of gaze, consider yoked prism.  You can factor the net prism by Rxing different yoked values to preserve the net vertical difference between the two eyes.
  • Consider the influence of vertical prism on accommodative balance, as well as the effect of plus lenses on vertical heterophoria and the indications for asymmetrical plus power at near.  You would expect lateral interactions through the CA/C and AC/A relationships, but don’t assume that vertical prism has no impact on accommodation and vice-versa.  You can probe accommodative balance at near under binocular conditions with Bernell’s  polarized duochrome test slide.

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(Dr. Curt Baxstrom alluded to this in his comments at the end of the previous blog, writing: “Skeffington suggests in some of his writings that the earliest finding of an accommodative issue is a vertical finding. Thus these patients should probably have accommodation tested regarding amplitudes, flexibility and sustainability.”)

A general tip.  I much prefer to use high quality large diameter round prisms for probing and trial.  I use the set available through Optomat in Spain.  In many instances I’m able to do the steps above using loose prism over one eye or the other.  Because of the lightness and large diameter of the lenses, they are very easy to maneuver even without the accompanying trial frame.  And in the low powers that we use, the etched prism amount and base direction is very helpful.

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For reference, here are some additional useful links discussing the application of prism to binocular vision disorders:

Facial Asymmetry, Head-to-Toe Cyclorotation, and Craniosacral Therapy

One of the first steps in examination is to be an astute observer of the patient.  In some instances this involves observing a patient’s gait as they walk down the hallway or enter an exam room.  When the doctor’s staff conducts diagnostic testing before she or he greets the patient, this may involve the doctor’s initial visual impressions of the patient in the chair.  But in some instances you either don’t pick up on subtle cues the first time around, or the patient may present differently the second or third time you see her than the first time.  In Malky’s case, I suspect I simply wasn’t as astute an observer on her prior visit to our office as I was yesterday.

Here, with her mother’s consent, is a picture of Malky as she sat in my exam chair yesterday.  What do you notice?


Just by my priming you, I’m guessing that you’ll detect the subtle asymmetry.  Malky has what I’ll call a cyclorotation of her right orbit (slanting downward to the right) and a corresponding slant of her right shoulder downward.  You’ll also note that her right earring is slightly lower than her left earring, indicating the subtle slope of the cranium downward to the right.  She also has a subtle face turn toward the right.  In case all this is difficult to see, here are linear reference points.


I mentioned in a blog a couple of years ago that Adelbert Ames Jr., a pre-eminent experimental psychologist last century responsible for the Ames Illusion and the design of the leaf room, had significant facial asymmetry and resultant cyclophoria.  His happens to match Malky’s.  You can see Ames’ right orbit sloped downward, his right shoulder lower, and his right ear lower than his corresponding left head-neck-shoulder anatomical landmarks.


Once you begin to notice craniofacial asymmetries, you’ll increase your own visual abilities in being a more sensitive observer.  You might say that you’ll up the sensitivity of your JNDs as if you had an internal protractor to gauge the degrees of tilt.


I eyeballed Malky’s asymmetries to be in the neighborhood of 10 degrees.  In addition to the objective slants, slopes, tilts, and turns, we clinically see these skews translated into measurement asymmetries thorough cyclorotation on the Van Orden Binocular Behavior Pattern, Cheiroscopic Tracings, or Maddox Rod in free space.  Most often the patient will have compensatory postural skews that allow them to report good subjective alignment and ranges in their head/body posture, but exhibit significant vertical or cyclovertical imbalance when you insists that they sit up straight and hold their head in a straight position.  They invariably reveal fusion anomalies in the field opposite to their habitual skew.  A personal favorite quick probe in free space is the Press Three Step in which the patient reports normal fusion in habitual posture, but diplopia or unstable fusion when tilting their head or body 180 degrees opposite to the habitual angle.

In the old days, when kids wore real shoes with heels, the oculo-cranio-facial asymmetry could easily be seen to translate in postural skews down through the shoulders, pelvic region and feet evident in wearing down the heel on one side faster than the other side.  So in Malky’s case, her right heel would wear down considerably faster than the left heel, because her postural skew shifts weight-bearing toward that side.  Naturally we can address the visual sequelae through vectors of prism or expand cylcofusional vergence ranges through vision therapy.  But sometimes the patient is better served by an osteopathic or physical therapy approach that gets more directly at the whole body – specifically craniosacral therapy.  After all, this is a head-to-toe issue of which oculo-visual manifestations are just a component.




The Press Three Step – Part 2

The Parks Three Step was first introduced by Bielschowsky in 1935 to isolate paralytic eye muscles, and is used primarily to localize the responsible muscle in oblique or cyclovertical deviations to pinpoint cranial nerve dysfunction or to plan eye muscle surgery for non-comitant strabismus.  By definition a hypertropia exists on the cover test in primary gaze, and changes as the patient gazes to the left or right, and then tilts left or right.  The first step of the test involves no eye or head movement; the second step involves eye movement; and the third step involves head and neck movement with the eyes counter-rolling in doll’s eye fashion.    It is well-known that the Parks Three Step becomes less accurate in identifying the paretic  muscle over time due to the spread of comitance.  Sensory correlates of the Parks Three Step are usually limited to something like the Hess-Lancaster Screen, most recently computerized by Spectrum Software.

The Hess Test principle is also inherent in the plot of motor fields used in Home Therapy Systems’ Motor Field Test.  The limitation of the Hess Test of course is that eye movements to the nine cardinal positions of gaze are involved but head and neck movements are purposely limited.  It struck me one day that I’d like to combine the motor elements of the Parks Test with the sensory elements of the Hess Test and voila:  Parks + Hess = Press (okay, a little bit of poetic license there) as depicted in Part 1.

The reason I’m placing emphasis on all three planes of neck rotation is that it activates the  COR, or Cervico-Optical Reflex.  The COR is part of the reflex arc providing positional awareness through proprioceptive feedback to the EOM nuclei.


Though the VOR (Vestibulo-Ocular Reflex) tends to get all the headlines (no pun intended), the gain of the COR and the gain of the VOR are mutually interactive in balancing eye, head, and neck movement to maintain fusion through postural interaction with the extraocular muscles.  The two clinical conditions in which patients typically report cervical or neck discomfort are torticollis and whiplash, but there are subclinical version of this where patients have more subtle discomfort, headaches, dizziness, or vertigo associated abnormalities of the COR.

I am therefore proposing that the Press Three Step serves as clinical biomarker for a lag in the plasticity of the gain of the COR as the patient actively rotates his neck through the three principal planes – horizontal, vertical, and oblique.  In practical terms, we’re looking for diplopia or difficulty fusing in a particular plane in contrast to its polar coordinate.  In other words, if as the patient maintains fixation on the target rotating L with eyes to the R the target doubles, then rotating R with eyes L should result in more comfortable fusion.  The patient’s habitual head posture in these cases is a vector representing the coordinates for best fusion.

Why bother?  On to the applications of therapy and prism in Part 3.

The Press Three Step

I know it’s a bit gauche to name a test after oneself, but I’ve grown fond of a sensory/COR version of the Parks Three Step for cyclovertical motor anomalies and what the heck –  Press is also a name with five letters that begins with “P” and ends with “S”, so let’s have a go at it.


This is a patient who I evaluated yesterday.  His leftward habitual head tilt is rather obvious, but he has no discernible hyper deviation on primary gaze with cover testing when he holds his head straight.  The sensory test using a three step is conducted using a Worth-4-Dot or similar target in the same way the motor there step is done, but in this instance we’re using diplopia as the key variable rather than hyperdeviation.


The patient fuses in primary gaze, seeing only one circle at the bottom.

Step 1: Compare fusion on head tilt to the left vs. right shoulder



Step 2: Compare fusion on head rotation to the right vs. left



Step 3: Compare fusion on chin-up vs. chin-down position



A negative response is the patient reporting a lustrous single circle in all three planes of rotation, oblique, horizontal, and vertical.  A positive response is diplopia in any plane of head rotation.  Typically the patient’s habitual head tilt or face turn is in the field of action that adaptively improves fusion, so if the patient habitually tilts toward the left shoulder, a forced tilt to the right of equal or greater magnitude will elicit diplopia.

I refer to this as a sensory/COR analog of the Parks Three Step because the Parks only activates head and neck reflexes in its third step.  I’ll elaborate on the significance of the COR (Cervico-Ocular Reflex) in this context in Part 2, which is particularly relevant for patients with a history of torticollis as well as patients with a history of mTBI/whiplash.

The Vestibular System and EOMs

VestibularLike so many of our body’s systems, the vestibular system is something we take for granted until it malfunctions.  Yet the vestibular system is truly a sixth sense, as our colleague Dr. Curt Baxstrom from Federal Way, WA is fond of reminding us.  I stumbled upon a book that organizes recent research and thinking on this sixth sense, and it dovetails nicely with some of the concepts I began to explore with you last year on visual centers of gravity.  I’m going to highlight a few things about the semicircular canals, which play such a crucial role in orienting us to the environment.  There are three coplanar canals functioning as partners in encoding rotary head movements.  Each of these pairs works in a push-pull fashion similar to the three pairs of EOMs to encode the component of angular motion in its plane.

VOR & EOMThe figure above shows how the canals and EOMs are linked so that the push/pull excitation/inhibition of the semicircular canals signals eye movements.  The planes of these three coplanar semicircular canals nearly align with the planes of the extraocular muscles to which they are connected by three-neuron reflex arcs. The figure shows how a specific pattern of excitation/inhibition the left anterior and right posterior canals results in upward movement of the eyes.  As indicated by the coloring, excitation (green) of the left anterior canal and inhibition (red) of the right posterior canal causes contraction (green) of the left superior rectus and right inferior oblique, and relaxation of their antagonists – the left inferior rectus and right superior oblique.

Once you start thinking more about these interrelationships, you will no longer view subtle ocular motor deficits in isolation as “an eye problem”.  Consider for example a subtle head tilt with an induced cyclovertical imbalance that can occur secondary to unilateral loss of function in the utricle.  The utricle is the part of the labyrinth serving the semicircular canals that detects head tilts in the horizontal plane.  The diagram below shows an ocular tllt reaction secondary to a left head due to impairment of the left utricle

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Vestibulopathies and vestibular neuritis are not as uncommon as one would think, and the increasing numbers of patients experiencing ABI due to concussions and other forms brain injury mean that you will be collaborating with ENTs more than ever before.  We recently had a patient who was being managed at Johns Hopkins for superior canal dehiscence, and I have had a number of patients through the years who suffered from BPPV, the most common vestibular disorder.  Any patient with a primary or secondary vestibular disorder may potentially benefit from lenses, prisms, or vision therapy as a complement to pharmacologic, surgical, or VRT considerations.


A Pair of Eyeballs Walks Into the Office – Part 3

RH1Robert is 65 years old and began seeing double about five years ago.  A pair of eyeballs never walks into the office in isolation and, as a practice becomes more specialized it will attract certain niche patients.  We have met them along the way in these blog posts, and an increasing niche is adult patients with strabismus.  One who we revisited yesterday in Part 2 is Greg, and Robert could just as well be his big brother.  As you give Robert’s face a closer look you’ll notice that has a mild anatomical left hyper.  Not only does his left eye appear to be slightly higher in the orbit, but his left ear appears to be slightly higher than the right as well.  We visited postural adaptations and skews last week in terms of visual centers of gravity and Robert tilts his head slightly to the right.  Before giving you his key optometric findings, I’ll share a little bit more about his background.


Adaptogens_cover-image_v6At age 50 Robert faced some serious health challenges and found himself pursuing holistic pathways to healing.  Many of the principles that he followed are summarized well in a new book on adaptogens by Donald R. Yance.  

At age 60, when he began to experience double vision, it seemed natural for Robert to think of turning toward an optometrist well-versed in nutritional optometry.  He did so, but found himself increasingly frustrated by his double vision that seemed to defy the best nutritional counseling and guidance.  Robert had been using over-the-counter readers with no need for a distance Rx since undergoing cataract surgery in both eyes in his early 50s.  He went to a conventional primary care optometrist who prescribed 1.50^ BD in his left lens, but the improvement in double vision was fleeting.  He was having considerable difficulty reading, and even when driving was now finding himself closing one eye to see clearly.  Robert sensed that he was unravelling quickly, and the optometrist offered him no other recourse than to consult with a strabismus surgeon who advised that strabismus surgery was imperative.

To shorten an already long story, Robert’s cover test in my office showed that with his head held straight he has a constant left hyper-exotropia with diplopia.  Parks 3 step revealed a right superior rectus paresis.  His best field of fusion was when looking down and to the left, so Robert’s habitual head position was now with his chin upward and head tilted to the right where he still retained a high degree of sensory fusion including random dot stereopsis.


What do you think Robert’s VO Star and Cheiroscopic Tracings look like?   The VO Star is very useful to map out vertical imbalances and central suppression zones, but we often find that cheiroscopic tracing maps out cyclovertical imbalances more dramatically.  Such was the case as you can see in Robert’s findings here.
CheiroIt was very revealing, when I sat down with Robert during our post-evaluation conference to learn that as much as he wanted to improve his vision, he was just as intent on understanding what his eyes were doing.




Postural Skews and Stereo Views – Part 2

At the end of Part 1 I suggested an experiment in which you would tilt your head toward one shoulder and see how much offset you could tolerate before losing the stereo view in the picture below.  Then tilt your head in the opposite direction and see if the amount of tilt before you lose it just about the same.


The amount that you should be able to tilt your head to the right or left before losing fusion should be roughly equal — about 12 degrees before you experience double vision or suppression, and about 8 degrees before you recover fusion.  As Dr. Margareten pointed out in his comments following Part 1, that doesn’t leave much wiggle room.  Even if you’re not an optometrist, you can probably visualize how small an angle of torsion or tilt 12 degrees is from your school days protractor (I know, I’m dating myself).



I like a term that David Guyton used regarding the ability to tolerate fusional imbalances of this is nature, which is perturbation.  (You can read Guyton’s article here.)  I’m convinced after many years of practice, after having done routine cheiroscopic tracings and red Maddox rod testing in free space, that the prevalence of patients with binocular instability the includes cyclovertical imbalance is under-recognized.

It is my contention that sustained S3D viewing will unmask these patients because their ability to compensate either while wearing 3D polarized glasses or even in auto-stereoscopic viewing such as you can do with the photo above, will be compromised.  These types of binocular imbalances may be primary or secondary effects of postural skews.  And normally it is a head-to-toe problem that includes every pivot point in the body such as head, neck, shoulders, pelvis, feet — and don’t forget to count the eyes as ball-in-socket pivot points.  As pointed out by Guadalupe Mejia in the Journal of Behavioral Optometry, this ultimately translates into problems with visual-vestibular integration, and induces feelings of dizziness or discomfort.

So what can we do about this?