Both similarities and differences exist between Bielschowsky type AACE (described originally by Bielschowsky and later modified by Hoyt and Good), and the patients described in our case series [3, 4]. Comitant esodeviation without evidence of paralysis of the extraocular muscles, similar deviation at distance and near fixation, as well as various degrees of myopia, are consistent with the definition suggested by Bielschowsky, Hoyt and Good. Further, we assumed that dynamic preponderance of the medial rectus muscles after sustained near work played a pivotal role in the development of esotropia in our patients. However, unlike Bielschowsky’s postulation in which uncorrected myopia was the key etiology of this form of strabismus, eight of 12 patients with myopic refractive error in our study wore glasses, and none of these patients was reluctant to wear glasses before or after presentation to our clinic. In addition, the corrected visual acuity of the eight patients with myopia was 20/20 in both eyes, and the uncorrected visual acuity was 20/20 in both eyes in the other four patients with hyperopia,
The Bagolini striated glasses test was performed in all patients at initial presentation, and the results showed unsuppressed esotropia in all cases [15]. We repeated the Bagolini striated glasses test in patients who underwent strabismus surgery at 3 months after the operation, and the results revealed normal binocular single vision in all three patients. And all patients who received strabismus surgery regained normal stereopsis proved by Titmus test. Moreover, mere smartphone restriction for 1 month led to a significant decrease in esodeviation in all patients, which would not occur in decompensated monofixation syndrome. Based on these observations, we believe that monofixation syndrome can be excluded in our patients [16].
Myasthenia gravis may present with acute comitant strabismus. However, our patients did not show any sign of ptosis, change in strabismus pattern, or other signs of muscle weakness throughout the follow-up period; further, the angle of deviation did not vary on repeated testing from day to day throughout the follow-up period. Although spasm of near reflex or accommodation is a possible differential diagnosis, this can be excluded based on the absence of episodic miosis, psychogenic or organic causes, consistency of eye deviation and refractive error in our patients after cycloplegia [17, 18]. Refractive esotropia is also a possible differential diagnosis, but all patients in our study were myopic or mildly hyperopic, and refractive correction did not show any change in the degree of esodeviation in patients with hyperopia. Bilateral sixth nerve paresis might evolve into comitant esodeviation without motility limitations in the future. However, the absence of trauma history, brain lesions, or vascular disorder, the similarity in esodeviation at near and far fixation, and the reduction in esodeviation after smartphone restriction could be discriminating factors between bilateral sixth nerve paresis and comitant esodeviation in our patients.
As proposed in previous articles, many authors have emphasized that a high index of clinical suspicion should be maintained for intracranial lesions as a cause of AACE, because AACE can be the sole sign of intracranial disease [19–21]. However, all patients in our case series had undergone neurologic examination, including neuroimaging, and no abnormalities were detected.
Burian-Franceschetti type AACE can also be a possible diagnosis. Comitant convergent strabismus without a definitive underlying cause, the presence of diplopia, the moderate degree of the angle of deviation, and good functional outcome after strabismus surgery meets the diagnostic criteria. However, most of our patients were myopic and none of our patients had experienced recent physical or psychological stress due to exhaustion that might have caused acute onset of eyeball deviation in the aforementioned type of esotropia.
The type of esotropia observed in our case series most closely resembles “acute concomitant esotropia of adulthood” described by Spierer [22]. They share common characteristics, such as the development of comitant esotropia with normal corrected visual acuity in both eyes, regaining of normal stereopsis after surgical correction of esotropia, as well as similar angle of deviation at distance and near fixation, absence of neurologic disease, and mainly myopic refraction error. The mechanism by which patients with myopia and good stereopsis develop comitant esotropia is still not clear.
Video display terminal (VDT) work itself was shown to induce abnormalities in accommodation and vergence compared with ordinary hard copy work (non-VDT work) [23, 24]. Thus, it is conceivable that excessive smartphone use at a close reading distance and the resultant abnormalities in accommodation and vergence in adolescents with low fusional divergence capacity or previous latent esophoria (inherently susceptible to the development of esotropia) can lead to dynamic preponderance of the medial rectus muscles, resulting in the development of manifest esotropia; the mechanism of which was initially proposed by Bielschowsky [3, 4, 25].
The absence of diplopia in some patients and the presence of only intermittent diplopia at distance fixation in others might indicate that dynamic hypertonus of the medial rectus muscles and the resultant development of esotropia progress slowly [26]. Refraining from smartphone use caused a decrease in the degree of esodeviation, which partially supports this mechanism. However, evidence is insufficient to supportthis proposal. The exact mechanism by which comitant esotropia develops in myopic or slightly hyperopic patients without previous manifest deviation remains unclear and has yet to be determined.
The orthophoric position and normal fusional capacity were re-established postoperatively in three patients who received bilateral medial rectus recession. As Spierer [22] proposed, normally developed binocular vision is disrupted after the onset of strabismus; therefore, the binocular capacity is potentially preserved and is later regained after the strabismus is surgically corrected.
The limitations of this case series include small sample size and the fact that we studied only patients with AACE who used smartphones excessively. AACE is a disease entity with undefined prevalence, but it is certainly considered rare. Therefore, although medical chart review was performed for patients who had visited the tertiary pediatric ophthalmology and strabismus service during a period of several years, the sample size was small [14]. In addition, we could not perform a comparative analysis between AACE patients with and without history of excessive smartphone use because of the paucity of AACE patients.
A distinct causal relationship between AACE and excessive smartphone use was not proven in our patients. However, other types of AACE, such as Bielschowsky type, Burian-Franceschetti type, AACE caused by intracranial tumor, and other causes of esotropia in adolescences, can be excluded in our case series. Further, extensive and comprehensive questioning and history taking revealed that only excessive smartphone use (more than 4 h per day) for a long period of time was common in all patients with AACE who were not diagnosed with Bielschowsky type, Burian-Franceschetti type, and AACE related to neurologic disease. In addition, smartphone restriction led to a significant decrease in esodeviation in all patients. Therefore, we speculate that excessive smartphone use could lead to the development of AACE.
Further, it is unclear whether other confounding factors (e.g., other forms of near work such as reading or sewing) may have influenced the clinical results. However, according to questioning and history taking, a gross difference did not exist in hours spent studying, reading, or other possible near-visual activities in AACE patients with a history of excessive smartphone use, when compared with AACE patients due to other causes. Further case-controlled studies with larger study populations are warranted. Moreover, we did not obtain an accommodation measurement by using dynamic retinoscopy or other devices that would give a more objective measure of accommodative power.