Pediatric Balint's Syndrome Variant: A Possible Diagnosis in Children.

Swetha Sara Philip,Gordon N Dutton,Sunithi Elizabeth Mani

doi:10.1155/2016/3806056

Abstract

Balint's syndrome is well described in adults, but not in children. It is caused by bilateral posterior parietal lobe damage and comprises a triad of simultanagnosia (inability to simultaneously see more than a small number of items), optic ataxia (impaired visual guidance of movement of the limbs and body), and apraxia of gaze (inability to volitionally direct gaze despite the requisite motor substrate) often associated with homonymous lower visual field loss. We, here, describe five children (four males, one female; mean age 7.4 years, [range 4−11 years]; birth weight ≤ 2.5 kg; four were born ≤ 36 weeks of gestational age and one at 40 weeks) who presented to the Cerebral Visual Impairment Clinic at a tertiary care center in South India with clinical features remarkably consistent with the above description. In all children neuroimaging showed bilateral parietooccipital gliosis with regional white matter volume loss and focal callosal thinning, consistent with perinatal hypoxic ischemic encephalopathy and possible neonatal hypoglycemia.

Highlights

Balint’s syndrome is well described in adults [1]. It is characterized by a triad of visual spatial difficulties related to simultanagnosia [2], optic ataxia [3], and psychic paralysis of gaze [1, 4]
We have identified 5 children who presented to the Cerebral Visual Impairment (CVI) clinic in a tertiary care center in South India between 2011 and 2012 with visual behaviors consistent with that of Balint’s syndrome
Most children with CVI have other neurological problems, but when it occurs in isolation the diagnosis can be overlooked and go unrecognized

Summary

Case Report

Balint’s syndrome is well described in adults, but not in children. Here, describe five children (four males, one female; mean age 7.4 years, [range 4−11 years]; birth weight ≤ 2.5 kg; four were born ≤ 36 weeks of gestational age and one at 40 weeks) who presented to the Cerebral Visual Impairment Clinic at a tertiary care center in South India with clinical features remarkably consistent with the above description. In all children neuroimaging showed bilateral parietooccipital gliosis with regional white matter volume loss and focal callosal thinning, consistent with perinatal hypoxic ischemic encephalopathy and possible neonatal hypoglycemia

Introduction

Normal Present Present Present

Discussion