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   Table of Contents      
CASE REPORT
Year : 1989  |  Volume : 37  |  Issue : 4  |  Page : 196

Anton syndrome and cortical blindness due to bilateral occipital infarction


The Neuro-ophthalmic Section, P.G. Dept. of Neurosurgery, SCB Medical College & Hospital, Cuttack - 753 007, India

Correspondence Address:
Madhumathi Misra
The Neuro-ophthalmic Section, P.G. Dept. of Neurosurgery, SCB Medical College & Hospital, Cuttack - 753 007
India
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Source of Support: None, Conflict of Interest: None


PMID: 2638312

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How to cite this article:
Misra M, Rath S, Mohanty AB. Anton syndrome and cortical blindness due to bilateral occipital infarction. Indian J Ophthalmol 1989;37:196

How to cite this URL:
Misra M, Rath S, Mohanty AB. Anton syndrome and cortical blindness due to bilateral occipital infarction. Indian J Ophthalmol [serial online] 1989 [cited 2021 Feb 24];37:196. Available from: https://www.ijo.in/text.asp?1989/37/4/196/26047


  Introduction Top


Sudden bilateral cortical blindness with preserved pupil­lary reaction was first postulated by Meyen [1] in 1920 to be due to occipital lobe involvement. Denial of visual loss in such patients with cortical blindness constitutes Anton's syndrome. Since the introduction of computerised to­mographic (CT) scan, occipital lobe infarct causing cor­tical blindness is being increasingly recognised [2],[6]. This report will describe a case of Anton syndrome and cortical blindness due to occipital lobe infarction diag­nosed by CT scan.


  Case report Top


With a background of pre eclamptic toxaemia, a 25 year old female presented with mild right hemiparesis after unconsciousness for 5 days due to hypertensive encepha­lopathy. After recovery, she was alert, co-operative and communicable but was unable to move about and per­form routine work. She frequently dashed against ob­jects and met with minor accidents at home, but never admitted to blindness on enquiry. On physical examina­tion, there was no light perception in either eye and optokinetic nystagmus could not be elicited. Both pupils were equally reactive to light and accomodation, ocular movements were full and opticfundi appeared normal on ophthalomoscopy.

Routine blood tests, CSF analysis and skull radiographs were normal. CT Scan demonstrated bilateral occipital lobe infarction.[Figure - 1].


  Discussion Top


In 1920 Meyer [1] first reported occipital lobe infarction and postulated compression of branches of the posterior cerebral artery (PCA) as the causal factor. Homonymus hemianopia due to unilateral occipital infarct was re­ported by Moore and Stern [7] in 1938,Maltby [8] in 1942, and Hyot in 1960. CT finding of the occipital lobe infarct was first shown by Nosborn [2] in 1977. Since then, elevated in­tracranial pressure leading to tentorial herniation with compression of PCA at the free margin of the tentorial aperture and subsequent occipital infarct has been documented by CT scan by various authors [3],[6]. Various CT reports on occipital infarct show variability in the territory of the occipital area involved [3]. The variability is thought to be caused by the anatomical variation of the tentorium and PCA. The point where the PCA is com­pressed against the free edge of the tentorium will vary from case to case, a narrow tentorial aperture is liable to compress the PCVA in the more proximal part, resulting in a wide area of infarction over the occipital lobe [3],[4],[9],[10],[11].

Others believe that infarction is of venous origin with compression of the calcarine vein as it runs towards the great vein of Galen but this hypothesis is less accepted than the arterial compression hypothesis [3],[10],[11]

The patient reported here recovered from hypertensive encephalopathy with sequelae of slight hemiparesis in the right side and cortical blindness/Anton syndrome due to bilateral occipital infacts shown by CT scan. It is only rarely, that the causal lesion and its clinical mani­festations are so convincingly correlated.

 
  References Top

1.
Meyer A, Arch Neurol Psychiatry, 4,387-400, 1920.  Back to cited text no. 1
    
2.
Oaboen A.G., Radiology, 123, 93-96, 1977.  Back to cited text no. 2
    
3.
Sato M, Tanaka S,Kohama A, Neurosugery 3,300-305, 1986.   Back to cited text no. 3
    
4.
Khosla V.K.,Kak V.K., Neurology, India, 35-122,1987.   Back to cited text no. 4
    
5.
Jawalkar S, Neurology, India, 35-122,1987.   Back to cited text no. 5
    
6.
Misra M, Rath S, Neuroloqy India (in Press), 1987.   Back to cited text no. 6
    
7.
Moore M.T., Stern K, Brain.61,70-98,1938.   Back to cited text no. 7
    
8.
Maltby GL, Surg,Gynecol Obstet, 74,496-498,1942.   Back to cited text no. 8
    
9.
Hoyt WF, Arch. Ophthalmol, 64,74-87,1960.  Back to cited text no. 9
    
10.
Linswnberg R, Walsh FB, Trans.Am. Acad. Ophthalmo. Otolaryngol, 1964.  Back to cited text no. 10
    
11.
Sunderland S., Brit.J.Surg., 45,422-438, 1958.  Back to cited text no. 11
    


    Figures

  [Figure - 1]


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