Varied aetiology of acute acquired comitant esotropia: A case series

Abstract

This is an observational case series of five cases of acute acquired comitant esotropia (AACE) with diplopia, aged between 5 and 12 years. The duration of presenting complaints ranged from 4 days to 2 months. A detailed ophthalmic evaluation and neuroimaging were done on all patients. Three patients were found to have intracranial pathology. Two patients had pontine glioma and one patient had benign intracranial hypertension. One patient was diagnosed as accommodative spasm and one patient was diagnosed as having Type 2 AACE.We would like to conclude that AACE can be of a varied aetiology ranging from convergence spasm to those harboring serious intracranial diseases. We reiterate that AACE has a small but significant association with intracranial disorders. Neuroimaging is a definite need in cases which cannot be proved to be either Type 1 or 2.

Acute acquired comitant esotropia of childhood: a classification based on 48 children

“…Furthermore, a third patient presented with papilledema due to hydrocephalus. Thus, the risk of an underlying intracranial disease was 6% (3/45) which closely resembles the figures of 10% in other studies (Simon & Borchert 1997;Lyons et al 1999), with findings of hydrocephalus, Chiari type 1 malformation, and brain tumours of primarily the cerebellum, and less frequent of the brain steam, sellar, thalamic region and corpus callosum (Harcourt 1968;Williams & Hoyt 1989;Hoyt & Good 1995;Rosenbaum & Santiago 1999;Hentschel et al 2005;Kemmanu et al 2012).…”

“…Interestingly, we found that children with intracranial disease were significantly older at onset than children without intracranial disease with a mean age of 7.5 years versus 3.8 years. This has not been shown before but can be extracted from literature as the mean age of previous reported cases with AACE with intracranial disease was 7.1 years (range 3-13 years) (Anderson & Lubow 1970;Zweifach 1981;Bixeman & Laguna 1987;Hoyt & Good 1995;Legmann & Borchert 1997;Lyons et al 1999;Kemmanu et al 2012).…”

Evaluation and surgical outcome of acquired nonaccommodative esotropia among older children

“…The association between ANAET and intracranial pathology, especially posterior fossa tumour, has been well documented. [13][14][15][16][17][18] In our report, none of the patients had any acute neuroimaging findings, and 1 patient had chronic findings suggestive of a previous ischemic lesion. Despite the apparent low yield, we would still advocate for careful clinical examination for red flags of intracranial lesions, such as sixth nerve palsy and papilledema, and routine neuroimaging with MRI as part of the preoperative work-up and assessment.…”

Atypical presentation of acute acquired comitant esotropia

“…Comitant esotropia typically presents during infancy or early childhood and is usually benign and unrelated to an underlying neurological disorder . Acute acquired comitant esotropia is an infrequent type of strabismus that develops in children usually older than five years, adolescents and young adults with prior normal binocular vision . A recent study reported an earlier onset, the mean age of onset for acute acquired comitant esotropia being 4.7 years .…”

“…Although frequently idiopathic, acute acquired comitant esotropia can be caused by interruption of binocular vision due to prolonged monocular eye lid closure or occlusive treatment for anisometropic amblyopia, decompensation of pre‐existing esophoria or small‐angle esotropia, loss of vision in one eye secondary to injury or disease, mild to moderate uncorrected myopia in adults, accommodative spasm and intracranial pathology . The last may present with additional signs and symptoms, such as abducting nystagmus, papilloedema, headaches, unsteadiness, as well as inability to achieve fusion with corrective prisms or the synoptophore .…”