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LETTER TO EDITOR
Year : 2008  |  Volume : 56  |  Issue : 1  |  Page : 88-89

Cortical blindness with absent visually evoked potential in non-ketotic hyperglycemia


1 Department of Ophthalmology, Jawaharlal Institute of Postgraduate Medical Education and Research, Pondicherry-605 006, India
2 Department of Medicine, Jawaharlal Institute of Postgraduate Medical Education and Research, Pondicherry-605 006, India

Date of Web Publication21-Dec-2007

Correspondence Address:
Arvind Gupta
Department of Ophthalmology, Jawaharlal Institute of Postgraduate Medical Education and Research, Pondicherry-605 006
India
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Source of Support: None, Conflict of Interest: None


DOI: 10.4103/0301-4738.37607

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How to cite this article:
Gupta A, Rao VA, Pandian DG, Das AK. Cortical blindness with absent visually evoked potential in non-ketotic hyperglycemia. Indian J Ophthalmol 2008;56:88-9

How to cite this URL:
Gupta A, Rao VA, Pandian DG, Das AK. Cortical blindness with absent visually evoked potential in non-ketotic hyperglycemia. Indian J Ophthalmol [serial online] 2008 [cited 2020 Feb 26];56:88-9. Available from: http://www.ijo.in/text.asp?2008/56/1/88/37607

Dear Editor,

A 19-year-old boy was referred to us for loss of vision. He had presented to the hospital two days before with the history of one episode of generalized seizure lasting for 20 to 25 sec and was in altered sensorium for two days. His blood glucose and serum osmolarity were more than 600 mg% and 308 meq/L respectively. Blood ketone bodies were normal and urinary ketone bodies were negative. There was no metabolic acidosis. He was diagnosed as having non-ketotic hyperglycemia (NKH). He was not a known case of any seizure disorder or diabetes mellitus. He improved within three days of treatment, with insulin and intravenous fluids.

On recovering, he complained of bilateral loss of vision. Ocular examination revealed vision of hand movements in both eyes. Anterior segment and posterior segment examinations including pupillary reactions and fluorescein angiography were normal. Menace reflex was absent and malingering tests were negative. He was diagnosed to have cortical blindness. Visually evoked potential (VEP) was absent in both eyes. Lumbar puncture showed normal study. Electroencephalogram, computed tomogram and magnetic resonance imaging brain were normal.

His vision improved to 20/80 and 20/60 in the right eye and left eye respectively after two weeks of follow-up. It improved to 20/20 at eight weeks of follow-up and VEP returned to normal.

Transient cortical blindness is used to describe an apparent lack of visual functioning, despite anatomically and structurally intact eyes. Transient visual loss may occur with seizures as an ictal or post-ictal phenomenon and is usually seen with status epilepticus.[1],[2] Its duration varies from less than one minute to days or can be even permanent.[1],[3] In our case, though the patient complained of visual loss after two days of seizure the insult might have occurred at the time of seizure and since the patient was in altered sensorium for two days, he might not have realized.

Hyperglycemia may cause seizures commonly involving the occipital lobe and rarely, the frontal lobe.[4] In NKH glucose metabolism is decreased and energy requirement is met by GABA shunt.[5] By increasing GABA metabolism, which is an important neurotransmitter inhibiting the epileptogenic phenomenon, hyperglycemia reduces the seizure threshold.

Cortical blindness is caused by hypoxia or anoxia involving the occipital lobes caused by either vascular insufficiency or by increased metabolic rate during periods of seizures.[6] Hyperviscosity in NKH may cause dehydration of glial and other supporting tissues with accumulation of free radicals. The resulting cytotoxic edema might restrict diffusion of substances which may cause transient blindness.[7] Non-ketotic hyperglycemia is known to cause homonymous hemianopia without any evidence of any structural lesion evident on scanning[8] but there is no report of cortical blindness in NKH patients.

Some reports suggest that VEP may show a varied result and may not be useful in establishing a diagnosis,[9] other reports suggest prognostic importance of VEP with absent VEP response foretelling poor prognosis for visual recovery.[10] However, in our case, despite absent VEP at presentation, patient regained full vision.

Cortical blindness should be considered in a patient with visual loss following NKH with or without seizure, but radiological investigation should be carried to rule out any foci of seizure. Further, absent VEP may not be indicative of poor prognosis.

 
  References Top

1.
Joseph JM, Louis S. Transient ictal cortical blindness during middle age: A case report and review of the literature. J Neuroophthalmol 1995;15:39-42.  Back to cited text no. 1
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2.
Aldrich MS, Vanderzant CW, Alessi AG, Abou-Khalil B, Sackellares JC. Ictal cortical blindness with permanent visual loss. Epilepsia 1989;30:116-20.  Back to cited text no. 2
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3.
Chung SJ, Lee JH, Lee SA, No YJ, Im JH, Lee MC. Co-occurrence of seizure and chorea in a patient with nonketotic hyperglycemia. Eur Neurol 2005;54:230-2.  Back to cited text no. 3
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4.
Hadjikoutis S, Sawhney IM. Occipital seizures presenting with bilateral visual loss. Neurol India 2003;51:115-6.  Back to cited text no. 4
[PUBMED]  Medknow Journal  
5.
Bodis-Wollner I, Atkin A, Raab E, Wolkstein M. Visual association cortex and vision in man: Pattern-evoked occipital potentials in a blind boy. Science 1977;198:629-31.  Back to cited text no. 5
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6.
Sadeh M, Goldhammer Y, Kuritsky A. Postictal blindness in adults. J Neurol Neurosurg Psychiatry 1983;46:566-9.  Back to cited text no. 6
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7.
Backhouse O, Leitch RJ, Thompson D, Kriss A, Charris D, Clayton P, et al. A case of reversible blindness in maple syrup urine disease. Br J Ophthalmol 1999;83:250-1.  Back to cited text no. 7
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8.
Paiboonpol S. Epilepsia partialis continua as a manifestation of hyperglycemia. J Med Assoc Thai 2005;88:759-62.  Back to cited text no. 8
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9.
Lavin PJ. Hyperglycemic hemianopia: A reversible complication of nonketotic hyperglycemia. Neurology 2005;65:616-9.  Back to cited text no. 9
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Harden CL, Rosenbaum DH, Daras M. Hyperglycemia presenting with occipital seizures. Epilepsia 1991;32:215-20.  Back to cited text no. 10
[PUBMED]    



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