We read with interest the article titled “Lateral Rectus Superior Compartment Palsy” by Clark and Demer and would like to make certain observations on this intriguing subject of great clinical importance.

Superior and inferior halves of horizontal recti are known to develop from superior and inferior mesodermal complexes, respectively. If the nerve supply was to be strictly tiered, then inappropriate axonal targeting likely will translate into a congenital cranial dysinnervation disorder phenotype akin to Duane retraction syndrome sans co-contraction. Precise neuronal compartmentalization in an acquired setting would be hard to replicate. The authors refrain from conjecturing as to why the superior compartment is inordinately susceptible to damage by diverse nonspecific etiologies, or why the inferior compartment is notoriously immune to such insults. Etiologies are diverse, mostly compressive lesions in the subarachnoid space; it is difficult to conceptualize as to how generic compression translates into highly selective injury to the axons of the superior compartment.

Surgically cranial/caudal tenotomies of up to 80% tendon width are known to engender A/V pattern strabismus rather than present as palsy/paresis. Superior tenotomy of lateral rectus would generate a V pattern or treat A pattern; the authors did not comment on any pattern strabismus in their series.

From a purely mechanistic point of view, superior compartment palsy likely would engender intorsion rather than extorsion, as happens with inferior transposition of the lateral rectus. The authors’ finding of extorsion exceeding 10 degrees in many sans intorsion in any patient merits explanation. Any such torsional change would in any case be minuscule, as full-width horizontal muscle transpositions are able to bring about only about 7 degrees of torsional change at most. Extorsion in excess of 10 degrees is typically generated by cyclovertical muscle involvement like bilateral fourth nerve palsies; unilateral superior compartment lateral rectus palsy is highly unlikely to be the culprit and other avenues have to be explored. Such patients will likely also complain of torsional diplopia, a symptom not encountered in isolated acquired lateral rectus palsies including the present series. Patients at serial numbers 3, 5, 6, 10, 11, and 13 have nonisolated lateral rectus palsy with a cyclovertical component riding piggyback. This would make correlation with vertical deviation and torsion inconsistent, congealing results and inferences. Also, torsion is assessed bilaterally; since we do not know about torsion in the other eye, many conditions like ocular tilt reaction may be missed and skew inferences further.

It is not known how many subjects had concurrent tight ipsilateral medial recti, a common sequela to lateral rectus palsies of long standing that has enormous bearing on clinical picture and management. Also, deviation in primary position as well as degree of abduction deficit for complete vs incomplete palsies are overlapping. Correlation between atrophy and amount of paresis may not have an algorithmic relationship. The fellow eye of patients could have served as a better control than volunteers from the population.

Thus, in our humble opinion, this study raises certain issues of clinical importance in diagnosis and management of lateral rectus palsy that need further clarification and rationalization.