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Anton–Babinski syndrome, case report
Ceguera de Anton–Babinski, a propósito de un caso
A. Martín Juan
Corresponding author
albert_mj89@hotmail.com

Corresponding author.
, R. Madrigal, J. Porta Etessam, F. Sáenz-Francés San Baldomero, E. Santos Bueso
Servicio de Oftalmología, Instituto de Investigación Sanitaria del Hospital Clínico San Carlos (IdISSC), Madrid, Spain
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who exhibited a CRA episode&#46; After recovery&#44; she began to refer blurred vision&#46;</p><p id="par0015" class="elsevierStylePara elsevierViewall">Ophthalmological examination produced a visual acuity &#40;VA&#41; of &#8220;finger counting&#8221; in both eyes &#40;BE&#41; about which the patient was apparently not aware &#40;she referred watching TV normally and recognizing persons&#41;&#46; The ophthalmological examination also revealed biomicroscopy within normal ranges&#44; intraocular pressure of 16<span class="elsevierStyleHsp" style=""></span>mmHg in BE&#44; extrinsic ocular motility and eye fundus normal&#44; with intrinsic ocular motility showing pupils in mean midriasis reactive to light in BE and optical coherence tomography &#40;OCT&#44; Heidelberg Engineering Inc&#44; Heidelberg&#44; Germany&#41; normal both in retinal and macular nerve fiber layers &#40;Fig&#46; 1&#41;&#46;</p><elsevierMultimedia ident="fig0005"></elsevierMultimedia><p id="par0020" class="elsevierStylePara elsevierViewall">Neurological examination determined anosognosia&#44; left-side hemiasomatognosia and visual agnosia&#44; together with left hemiparesis and hemi-hypoesthesia&#46; Cerebral magnetic resonance showed cortical hyper-intensity in both occipital lobes in T2 sequence&#44; in precentral right turn and <span class="elsevierStyleItalic">corpus callosus</span> splenius&#44; compatible with subacute ischemia in said areas &#40;Fig&#46; 2&#41;&#46; Accordingly&#44; anoxic encephalopathy after CRA was diagnosed with associated visual impairment&#44; compatible with Anton&#8211;Babinski blindness&#46;</p><elsevierMultimedia ident="fig0010"></elsevierMultimedia><p id="par0025" class="elsevierStylePara elsevierViewall">Since then&#44; the patient was regularly followed up by Neuro-Ophthalmology&#44; exhibiting VA improvement &#40;at present 0&#46;6 monocular in BE&#41;&#44; without ophthalmological alterations and chronic changes in cerebral magnetic resonance&#44; including persistent hyper-intensity in the areas described above as well as parietal lobe atrophy&#46;</p></span><span id="sec0015" class="elsevierStyleSection elsevierViewall"><span class="elsevierStyleSectionTitle" id="sect0055">Discussion</span><p id="par0030" class="elsevierStylePara elsevierViewall">Anton&#8211;Babinski blindness or syndrome is caused by bilateral lesions in associative visual brain areas &#40;Brodman areas 18 and 19 or secondary visual cortex&#41;&#44; giving rise to visual anosognosia involving patient inability to identify said vision impairment&#46;<a class="elsevierStyleCrossRefs" href="#bib0045"><span class="elsevierStyleSup">1&#8211;3</span></a></p><p id="par0035" class="elsevierStylePara elsevierViewall">The most frequent etiology is ischemia or parenchyma hemorrhage as well as other less frequently described causes of such as radiation leukoencephalopathy and adrenoleukodystrophy&#46;<a class="elsevierStyleCrossRefs" href="#bib0045"><span class="elsevierStyleSup">1&#44;3&#8211;5</span></a></p><p id="par0040" class="elsevierStylePara elsevierViewall">Clinical expressions comprise objective poor vision &#40;usually &#8220;perception of light&#8221; or &#8220;bulk movement&#8221; VA&#41; involving visual confabulation of the patient who refers normal vision and attends to describe the environment and to move about without help although with continuous errors&#46;<a class="elsevierStyleCrossRef" href="#bib0070"><span class="elsevierStyleSup">6</span></a> Examination of these patients identifies associated neurologic sensitive-motor impairment &#40;but&#44; by definition&#44; without dementia or memory disorders&#41; and without ophthalmological findings&#46; Neuroimaging tests produce evidence of lesions in both occipital lobes&#46;<a class="elsevierStyleCrossRefs" href="#bib0070"><span class="elsevierStyleSup">6&#44;7</span></a> Additional tests and examinations are required for the etiological diagnostic&#46;</p><p id="par0045" class="elsevierStylePara elsevierViewall">Said clinic is infrequent but must be suspected in patients with strange or inconsistent vision impairment&#46; Evidence of occipital encephalic damage in neuroimaging tests is necessary&#44; excluding any alteration in the proximal visual pathways&#46;<a class="elsevierStyleCrossRefs" href="#bib0070"><span class="elsevierStyleSup">6&#44;7</span></a> Prognostic is variable and several rehabilitation treatments has been described consisting in improving mobility and daily life activities and regularly reminding the patient about said impairment&#46;<a class="elsevierStyleCrossRef" href="#bib0080"><span class="elsevierStyleSup">8</span></a> In the present case&#44; vision gradually improved during hospital stay probably due to the partial functional recovery of ischemic areas&#46;</p><p id="par0050" class="elsevierStylePara elsevierViewall">By way of conclusion&#44; Anton&#8211;Babinski blindness must be considered in patients with CRA or hypoxia where ophthalmological examination is not consistent with the VA referred by the patient&#46;</p></span><span id="sec0020" class="elsevierStyleSection elsevierViewall"><span class="elsevierStyleSectionTitle" id="sect0060">Conflict of Interest</span><p id="par0055" class="elsevierStylePara elsevierViewall">No conflict of interests was declared by the authors&#46;</p></span></span>"
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