Abstract
Monocular elevation deficit can result from either inferior rectus restriction, superior rectus palsy or from supranuclear causes. We report a case of monocular elevation deficit after scleral perforation repair which was managed by surgery on contra lateral eye. This improved elevation of the affected eye with no diplopia in the postoperative period.
Keywords: Monocular elevation deficit, Scleral perforation repair
Background
Monocular elevation deficit (MED) is the limitation of elevation in abduction as well as in adduction, it can be congenital or acquired. A large number of causes like, sarcoidosis, midbrain tumours, acoustic neuroma and pineocytoma have been attributed to cause MED. There are various schools stating the pathophysiology of MED, it is believed that as superior rectus is the main elevator both in abduction and adduction, therefore, MED can be a result of a superior rectus palsy alone.1
But in the presence of a normal superior rectus, inferior rectus (IR) restriction can also cause MED, as in cases of entrapment of IR in cases of orbital floor fracture or infiltration of muscle in cases of sarcoidosis.
Supranuclear lesion in the pretectal area can also lead to MED.2
We came across an interesting case of MED after scleral perforation repair. The patient was managed by weakening the contra lateral elevator.
Case presentation
A 36-year-old man presented to the squint clinic of a tertiary eye care hospital with diplopia in upgaze. He had a history of right eye scleral perforation repair done 2 years ago following trauma with iron rod. The repair was done within hours of presentation at another centre. No records were available of the original injury and repair. It was from the first postoperative day that the patient started having diplopia in upgaze.
There was no history of loss of consciousness following trauma, and the patient had no other systemic illness.
On examination, the patient had a visual acuity of 6/6 in both eye, on slit lamp examination, the patient had right eye superotemporal conjunctival scarring and no abnormality was detected on fundus examination, extraocular movements showed limitation of movements in upgaze (−3) in right eye, limitation of elevation in abduction was more than limitation of elevation in adduction (figure 1). Ductions were tested monocularly, the limitation of elevation in right eye improved to −2 with left eye occluded.
Figure 1.
Preoperative picture showing elevation deficit in right eye, with more limitation noticed during elevation in abduction.
There were no ptosis, lid retraction, compensatory head posture and enophthalmos.
There was no improvement or worsening of symptoms over the course of time and the patient did not receive any management for diplopia previously.
Investigations
Primary and secondary deviations were measured by modified Krimsky’s in all nine gazes. Primary deviations were measured with left eye fixing and secondary deviations were measured with right eye fixing. There were no horizontal deviation and 4 prism dioptre of right hypotropia in primary position and downgaze, hypotropia further increased to 20 prism dioptres in upgaze, and increased to 14 prism dioptre on elevation in abduction. Vertical deviation was eight prism dioptre on elevation in adduction. Bell’s phenomenon was fair. Diplopia charting further revealed diplopia in upgaze, with maximum distance between the red and green stripes being in upgaze. A normal cross response was obtained on Bagolini striated glass test and the stereopsis for near in downgaze was 30 s of arc in Randot stereoacuity test.
Forced duction test done under topical anaesthesia revealed free IR, ruling out IR restriction. Active force generation test for superior rectus had a weak force generation response suggestive of paresis.
Differential diagnosis
Orbital floor fracture and IR entrapment were ruled out, as orbital X-ray was normal and forced duction test was found to be free. A free forced duction test also ruled out all the causes of IR restriction leading to elevation deficit.
MRI was normal, thus excluding supranuclear causes for elevation deficit.
Treatment
The patient was planned for left eye inferior oblique (IO) total anterior positioning to correct the elevation deficit of right eye. The anterior end of IO in this technique is placed at lateral end of IR insertion with posterior end being further down, this results in 10 mm recession.
Outcome and follow-up
In the postoperative period, no limitation of extra ocular movements was noted in the right eye. Vertical deviation was reduced to two prism dioptre which was concomitant.
The patient did not have any anomalous head posture in the postoperative period and was asymptomatic (figure 2).
Figure 2.
Postoperative 1-week showing improvement in elevation deficit.
Discussion
Repaired scleral perforation presenting as elevation deficit in right eye as in our case could be explained by the paresis of superior rectus due to surgery and trauma. Repeated surgeries in the right eye could lead to scarring and fibrosis,3 4 further causing restriction and diplopia in downgaze. Squint surgery was, therefore, planned in the left eye. Total anterior positioning of IO was planned rather than recessing superior rectus so as to protect the anterior segment blood supply and to prevent lid retraction. IO was sutured just anterior to the insertion of the IR muscle as described by Eliot and Nankin,5 thus weakening the elevation effect of IO without affecting the extorsion effect. Contralateral IO weakening procedures are usually reserved for the resurgeries. A weakening procedure done in the contralateral eye increases the innervational distribution to IO and other elevators of that eye,6 and following Hering’s law, this also increases the innervations going to yoke muscle, which are IO and superior rectus of the affected eye, hence improving elevation.
To the best of our knowledge, this is the first case report of elevation deficit after scleral perforation repair which was managed by contra lateral IO total anterior positioning as the primary procedure.
Learning points.
Monocular elevation deficit can result after scleral perforation repair.
Superior rectus paresis can result after trauma and surgery due to partial disinsertion of the muscle.
Weakening of contralateral inferior oblique can be done in post-traumatic cases to prevent diplopia in downgaze.
Footnotes
Contributors: GS worked up the case and reached the diagnosis. AB and GS together wrote the manuscript.
Funding: The authors have not declared a specific grant for this research from any funding agency in the public, commercial or not-for-profit sectors.
Competing interests: None declared.
Provenance and peer review: Not commissioned; externally peer reviewed.
Patient consent for publication: Obtained.
References
- 1. Von Noorden GK. Binocular vision and ocular motility. 6th edn ST Louis: Mosby, 2002. [Google Scholar]
- 2. White JW. Paralysis of the superior rectus and the inferior oblique muscle of the same eye. Arch Ophthal 1942;27:366–71. 10.1001/archopht.1942.00880020152015 [DOI] [Google Scholar]
- 3. Parks MM. Causes of the adhesive syndrome : Helveston EM, Symposium on strabismus, transactions of the new orleans academy of ophthalmology. St Louis, MO: CV Mosby Co, 1978:269–79. [Google Scholar]
- 4. Roizen A, Ela-Dalman N, Velez FG, et al. Surgical treatment of strabismus secondary to glaucoma drainage device. Arch Ophthalmol 2008;126:480–6. 10.1001/archopht.126.4.480 [DOI] [PubMed] [Google Scholar]
- 5. Elliott RL, Nankin SJ. Anterior transposition of the inferior oblique. J Pediatr Ophthalmol Strabismus 1981;18:35–8. [DOI] [PubMed] [Google Scholar]
- 6. O’Donnell FE, Del Monte M, Guyton DL. Simultaneous correction of blepharoptosis and exotropia in aberrant regeneration of the oculomotor nerve by strabismus surgery: a new, simplified ptosis correction for selected cases. Ophthalmic Surg 1980;11:695–7. [PubMed] [Google Scholar]