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| CASE REPORT |
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| Year : 1989 | Volume
: 37
| Issue : 4 | Page : 196 |
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Anton syndrome and cortical blindness due to bilateral occipital infarction
Madhumathi Misra, Sanatan Rath, Amar Bihram Mohanty
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
 Source of Support: None, Conflict of Interest: None  | Check |
PMID: 2638312 
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 |
| Introduction | |  |
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 | | |
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 | | |
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 | | |
| 1. | Meyer A, Arch Neurol Psychiatry, 4,387-400, 1920.  |
| 2. | Oaboen A.G., Radiology, 123, 93-96, 1977. |
| 3. | Sato M, Tanaka S,Kohama A, Neurosugery 3,300-305, 1986. |
| 4. | Khosla V.K.,Kak V.K., Neurology, India, 35-122,1987. |
| 5. | Jawalkar S, Neurology, India, 35-122,1987. |
| 6. | Misra M, Rath S, Neuroloqy India (in Press), 1987. |
| 7. | Moore M.T., Stern K, Brain.61,70-98,1938. |
| 8. | Maltby GL, Surg,Gynecol Obstet, 74,496-498,1942. |
| 9. | Hoyt WF, Arch. Ophthalmol, 64,74-87,1960. |
| 10. | Linswnberg R, Walsh FB, Trans.Am. Acad. Ophthalmo. Otolaryngol, 1964. |
| 11. | Sunderland S., Brit.J.Surg., 45,422-438, 1958. |
[Figure - 1]
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