%0 Journal Article
%T Recurrent Bilateral Occipital Infarct with Cortical Blindness and Anton Syndrome
%A Kiu Kwong Yew
%A Sanihah Abdul halim
%A Ahmad Tajudin Liza-Sharmini
%A John Tharakan
%J Case Reports in Ophthalmological Medicine
%D 2014
%I Hindawi Publishing Corporation
%R 10.1155/2014/795837
%X Bilateral cortical blindness and Anton syndrome, are most commonly caused by ischaemic stroke. In this condition, patients have loss of vision but deny their blindness despite objective evidence of visual loss. We report a case of a patient with multiple cardiovascular risk factors who developed recurrent bilateral occipital lobe infarct with Anton syndrome. A suspicion of this condition should be raised when the patient has denial of blindness in the presence of clinical and radiological evidence of occipital lobe injury. Management of this condition should focus on the underlying cause, in which our patient requires secondary stroke prevention and rehabilitation. 1. Introduction Cortical blindness refers to loss of vision caused by bilateral occipital lobe lesions with presence of intact anterior visual pathway [1, 2]. Anton syndrome (visual anosognosia) is a rare complication of cortical blindness with denial of loss of vision by patient who is unable to see [2, 3]. Such patient may confabulate during visual examinations or offer excuses for their symptoms or may endanger themselves to prove that they are capable of seeing [2]. With damage to the visual association cortex, patients are unable to acknowledge their visual deficit [2, 4]. Ischemic stroke is the most common cause of cortical blindness [1, 4]. We describe one case with Anton syndrome secondary to recurrent bilateral occipital infarct. 2. Case Presentation A 57-year-old man with background history of diabetes mellitus, hypertension, hyperlipidemia, and bilateral occipital lobe infarct 5 years ago presented with sudden bilateral loss of vision for a 3-day duration associated with slurred speech. It was preceded by occipital headache. He had history of bilateral occipital lobe infarcts five years ago with both eyes (OU) vision of only perception to light (PL). There was no neurological deficit apart from slurring of speech. He had no symptoms of denial of visual deficit at that time. CT brain showed multiple infarcts in both parietooccipital regions. One month after being discharged from hospital, his vision still maintained at PL OU and it slowly recovered. He was capable of watching television and reading with glasses 6 months after the stroke. Since then, the vision remained stable until the current events. His vision prior to the first episode of stroke was clear without glasses. He was not compliant to his medication. On arrival in emergency unit during this episode, he was fully conscious with blood pressure of 124/83£¿mmHg. He was orientated to time, place, and person. Apart from
%U http://www.hindawi.com/journals/criopm/2014/795837/