Korean J Ophthalmol Vol.23, No.3, 2009 Fig. 3. Nine cardinal photographs showing esotropia of 8PD without lateral incomitance at 18 months after bilateral 6-mm recession of the me- dial rectus muscles. sults, such as varying degrees of bilateral sixth nerve paresis. Spread of comitance is another suggested mechanism.15 The presenting clinical symptoms of patients with brain tu- mors are diverse, depending on the tumor’s location and size, and sometimes, the age of the patient. Unlike various symptoms such as headache, vomiting, or more specific focal signs, acute comitant esotropia is a very unusual first sign of a brain tumor. Nevertheless, some authors have noted acute comitant esotropia as the first sign of a brain tumor.16-18 For example, Dikici et al.16 reported a 3-year-old boy presenting with acute comitant esotropia as the first sign of cerebellar astrocytoma, and the patient had no other neurologic signs or symptoms except moderate bilateral papilledema. Our case also presented with acute comitant esotropia as the first sign of cerebellar tumor, except our patient only had very mild bilateral papilledema. Zweifach17 presented the case of a 9-year-old boy with acute comitant esotropia in the absence of any neurologic symptoms or signs when first examined. Twenty eight months later, when he developed signs of posterior fossae dysfunction, he was found to have a cerebellar medulloblastoma. Musazadeh et al.18 also reported a 3-year-old boy with late onset esotropia without any neurologic signs and symptoms on first presen- tation. Eight months after first presentation, a brain MRI was performed to work-up the patient’s intense headache, and ima- ging and biopsy revealed a cerebellar astrocytoma. It is practically impossible to perform a radiologic exami- nation of all children with isolated, acute comitant esotropia. No single clinical sign can reliably reveal the rare patient with acute onset of comitant esotropia secondary to a brain tumor. Lyons et al.19 have emphasized that a high index of clinical suspicion should be maintained, and a neuro-imaging study 230 should be considered in the absence of expected findings asso- ciated with acute comitant esotropia such as hypermetropia, fusion potential, atypical features, or neurologic signs. In conclusion, it is important to remember that acute comitant esotropia in the absence of other neurologic signs and symptoms in infancy or childhood may be the first sign of an underlying brain tumor. References 1. von Noorden GK, Campos EC. Binocular vision and ocular mo- tility: Theory and management of strabismus, 6th ed. St Louis: C.V. Mosby Company, 2002;338. 2. Watson AP, Fielder AR. Sudden-onset squint. Dev Med Child Neurol 1987;29:207-11. 3. Anderson WD, Lubow M. Astrocytoma of the corpus callosum presenting with acute comitant esotropia. Am J Ophthalmol 1970; 69:594-8. 4. Bixenman WW, Laguna JF. Acquired esotropia as initial mani- festation of Arnold-Chiari malformation. J Pediatr Ophthalmol Strabismus 1987;24:83-6. 5. Williams AS, Hoyt CS. Acute comitant esotropia in children with brain tumors. Arch Ophthalmol 1989;107:376-8. 6. Astle WF, Miller SJ. Acute comitant esotropia: a sign of intracranial disease. Can J Ophthalmol 1994;29:151-4. 7. Simon JW, Waldman JB, Couture KC. Cerebellar astrocytoma manifesting as isolated, comitant esotropia in childhood. Am J Ophthalmol 1996;121:584-6. 8. Lewis AR, Kline LB, Sharpe JA. Acquired esotropia due to Arnold- Chiari I malformation. J Neuroophthlmol 1996;16:49-54. 9. Liu GT, Hertle RW, Quinn GE, Schaffer DB. Comitant esodeviation resulting from neurologic insult in children. J AAPOS 1997;1: 143-6. 10. Lennerstrand G. Central motor control in concomitant strabismus. Graefes Arch Clin Exp Ophthalmol 1988;226:172-4.