Dr.Hiranmoyee Das, D16233
Abstract
Aim – To study the etiology, clinical features and effectiveness of treatment in postictal blindness.
Methods- A 4-year retrospective review of patients presented with postictal blindness but normal ocular & optic nerve finding was conducted.
Results- 16 cases of postictal blindness studied(10 generalized seizure, 4 focal motor discharge while 2 children had the constellation of migraine headaches). 11 were children. The causes of seizure were idiopathoic, febrile convulsion, ecclampsia & occipital lobe lesion like (trauma & tumour). The duration of postictal blindness was mostly 48- 72hours (1hour and11 months). EEG revealed Occipital discharges were more common in the younger age group, whereas with maturity, tend to be seen more rostrally in the temporal areas.
Conclusion- An EEG should be considered in any patient presenting with sudden onset of unexplained visual loss. Postictal blindness is associated with a favorable outcome when promptly diagnosed and treated appropriately.
Key words: Seizure, blindness, postictal
Introduction
Acute blindness is a rare presentation of epileptic seizures, referring to loss of sight without loss of consciousness associated with electroencephalographic (EEG) epileptic discharges. In 1903 Ashby and Stephenson’ summarized the clinical features of this entity in 11 children and infants (five in their own series).
We report a series of 16 children with documented epileptic blindness, describing the accompanying fits and thereafter the response to therapy to resolve the blindness and control associated seizures.
Methods & materials
This study was done in a 420 bedded multispecialty mission hospital (Nazareth Hospital, Shillong) a tertiary health center, from Jan 2014 to December 2017.
A 4-years retrospective review of patients presented with postictal blindness but normal ocular & optic nerve finding was conducted.
Cortical blindness was associated with normal pupillary reactions and absence of abnormal findings on fundoscopic examination.
Results
16 cases of post ictal blindness studied. 11 were children.
10 cases had generalized seizure and 4 had focal motor discharge. 2 children had the constellation of migraine headaches, focal motor seizures and complete blindness along with occipital EEG discharges
The causes of seizure were idiopathoic, febrile convulsion, eclampia, occipital lobe lesion like trauma & tumour .There does not seem to be a clinical difference between patients with and those without occipital lesions. Some had encephalitis or cerebral malaria.
The duration of postictal blindness was mostly 48- 72hours (1hour and11 months). Blindness was bilateral and continued for days, weeks or months and only exceptionally for hours, sometimes being accompanied by other neurological deficits such as weakness, deafness, aphasia or dementia.
Ten patients with accompanying generalized seizures were treated with valproic acid. They regained full vision and eight became seizure free. 4 children had accompanying focal motor seizures and two additional cases with isolated blindness and focal discharges were treated with carbamazepine, regained full vision and all became asymptomatic within a period of 1-4 years.
EEG revealed Occipital discharges were more common in the younger age group, whereas with maturity, tend to be seen more rostrally in the temporal areas.
Discussion
Our data for patients with epileptic blindness was similar to previous reports regarding the reported duration of blindness and associated seizures, as well as the overall response to therapy and outcome.
Walsh and Hoy2 compared the blindness to postictal (Todd’s) paralysis, the cause of which was thought to be exhaustion of neurons by hyperactivity;
The hypothesis that postictal paralysis is caused by an active inhibitory mechanism was first suggested by Gowers,3 who objected to the “exhaustion theory” that had been proposed by Todd.”4
Kosnik et al.5 described that a hyperpolarisation mechanism developing during the epileptic activity was responsible for ictal or postictal inhibition. In their cases, vision loss for several hours was associated with focal seizures and epileptic discharges involving the occipital lobe.
Brain anoxia could well account for the bilateralism of the blindness and its relatively long duration since the occipital lobes are especially sensitive to anoxia, being located in the cerebral blood supply border zone. In the last two decades with the wide use of cardio-pulmonary resuscitation, many severe hypoxaemic episodes and hypotensive events have occurred. Not uncommonly they have been complicated with cortical blindness.6 Thus, anoxia has been recently considered to be one of the most frequent immediate causes of bilateral cortical blindness.7
Conclusion
Analysis of the literature, in addition to our overall experience, indicates that postictal blindness is associated with a favorable outcome when promptly diagnosed and treated appropriately, resulting in complete resolution of blindness in all and satisfactory control of seizures in most of them.
An EEG should be considered in any patient presenting with sudden onset of unexplained visual loss, even in the absence of other epileptic phenomena.
References
- Ashby H, Stephenson S. Acute amaurosis following infantile convulsions. Lancet 1903;1:1294-6.
- Walsh FB, Hoyt WF. Clinical Neuro-opthalmology. Baltimore: The Williams & Wilkins Co., 1969:127-29.
- Gowers WR. Epilepsy and other chronic convulsive diseases: their causes, symptoms and treatment. London: Old Hickory Bookshop, 1901.
- Todd RB. Clinical lectures on paralysis, disease of the brain and other affections of the nervous system. London, 1856
- .Kosnik E, Paulson GW, Laguna JF. Postictal blindness. Neurology (Minneap) 1976;26:248-50.
- Brierly JB. Cerebral hypoxia (Chap 2). In: Blackwood W, Corsellis JAN, eds. Greenfield’s Neuropathology, London: Edward Arnold, 1976:43-85.
- Sabah AH. Blindness after cardiac arrest. Postgrad Med J 1968;44:513-6.
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