Editor’s Note: In April’s “Focus on Refraction” column, authors Marc B. Taub, OD, and Paul Harris, OD, reviewed the case of a pilot experiencing diplopia. They recommended a reevaluation of the prescription and vision therapy. You can read this case at www.reviewofoptometry.com.
Drs. Harris and Taub surely missed the forest for the oak in their article, “As Flexible as an Oak.”
This poorly presented case is clearly one of traumatic fourth cranial nerve palsy compounding an already existing congenital fourth cranial nerve palsy and may well be a double traumatic fourth nerve palsy. Their case is poorly presented because no adequate history of the diplopia is reported. No description of the patient’s current head position (i.e., tilt, rotation or chin up or down) is given. Such a poor presentation indicates the authors’ little or no knowledge of fourth cranial nerve palsy.
The deviations apparently have not been measured or reported in both right and left gaze. This cannot be done behind a phoropter (which only supplies the amount of deviation in the primary position), but can be done with a handheld rotary prism or prism cover test with the patient in right and then left gaze. These results would also have pointed to and helped confirm the correct diagnosis. I should point out the measurement of “break and recovery” in a patient who is already diplopic and who has a damaged cranial nerve with an atrophied superior oblique muscle is absurd and has no meaning.
What we can “tweeze” from their presentation is that the patient had the first complaint of diplopia two years before a concussion. The most probable cause is a congenital fourth nerve palsy finally breaking fusion. We, and they, could have made this diagnosis had an adequate description of the diplopia (as above) been acquired.
The report of a concussion (with subsequent diplopia) seals the diagnosis. The history of a second head trauma (or the first one) may have produced a second fourth nerve palsy, on the opposite side of the midbrain from the first, producing a “double traumatic fourth nerve palsy.”
Congenital or acquired fourth nerve palsy is as common as dirt. I see one or two of these per month and have for 40 years.
The real problem with them is that the subsequent vertical deviation will differ when the patient is right or left gaze from that in the primary position as well as from distance to near. A “compromise” amount of prism can be determined from these measurements and a trial frame with a separate pair of glasses for distance and near. These will not eliminate diplopia in all positions of gaze, but can minimize its effect.
Finally, you cannot repair a damaged cranial nerve with all of the “training,” exercise, electrical stimulation, vitamin C, steroids or any other “hocus pocus” treatment in the world.
—Mark R. Flora, OD, General Eye Medicine, Disease & Injury, Atlantic Eye Associates
Drs. Taub and Harris respond:
We assure Dr. Flora that much of the data that he wanted to see was indeed collected, but only the relevant parts were included in the article.
The suggestion that this was clearly a combination of fourth nerve issues of multiple kinds was not supported by the concomitant nature of the angle of deviation. It is standard practice at Southern College of Optometry to measure the angle(s) of deviation in different directions of gaze. In this instance, the variations were small enough that non-concomitancy was ruled out. We did report that, in different directions of gaze, his ability to keep it single broke, which might suggest non-concomitancy, but the measurements don’t back this up. We viewed the breaking into double as a measure of how fragile his binocular condition was. We all expend more effort when looking eccentrically. In his case, this extra demand was simply the straw that broke the camel’s back. The actual angle of deviation in these eccentric gazes was the same within a standard measuring error.
In terms of the postural observation, this patient had no face turn, head tilt or chin up or down posture. The article, “Visual Conditions of Symphony Musicians” (JAOA, Vol 59, No 12 1988) demonstrates the subtlety of how postural asymmetries over time lead to the development of astigmatism.
Lastly, we are not claiming to repair a damaged nerve. We are simply helping a patient improve his visual abilities using the standard tools of optometric practice. In this instance, we chose to use vision therapy, which is helping our patient increase the volume of space through which he sees single and to do so with less effort and more ease. As he progresses, we look forward to sharing this with our readers.