Clinical Neurology and Neurosurgery 139 (2015) 311–313

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Clinical Neurology and Neurosurgery
journal homepage: www.elsevier.com/locate/clineuro

Case Report

Late onset reversible cortical blindness following electrocution
Bhumir Chauhan ∗ , Vivek J. Philip, Udaya C. Shankar
Narayana Institute of Neurosciences, Narayana Health City, Bangalore, Karnataka, India

a r t i c l e

i n f o

Article history:
Received 4 April 2015
Received in revised form 14 July 2015
Accepted 11 October 2015
Available online 11 November 2015
Keywords:
Cortical blindness
Electrocution
Reversible
Steroids
Delayed onset

a b s t r a c t
An elderly gentleman presented with acute onset of bilateral visual blurring and generalized headache
after 1 week post electrocution injury. Clinically, the symptoms were attributed to cortical lesion. Magnetic resonance imaging (MRI) of brain revealed bilaterally symmetrical diffusion restriction in parietal
and occipital areas. Treatment with intravenous steroids resulted in remarkable improvement in symptoms. Neurological injury secondary to electrocution is a well described entity having a variety of clinical
presentation. We put forward our experience with this unique case presenting as post electrocution
delayed onset of visual symptoms. Discussion and review of literature related to this clinical entity will
also be presented.
© 2015 Elsevier B.V. All rights reserved.

1. Introduction
Electrical injuries are one of the most common occupational
and household hazards. Local injuries as an immediate effect of
electrical current are a well-known phenomenon. The spectrum of
medical disorders secondary to electrical current injury is extensive and complex. Neurological manifestations secondary to such
injuries are well known but literature description of case reports
is limited. Multiple mechanisms have been considered responsible
for the genesis of these symptoms, but none of them have received a
unified approval. The neurological symptomatology following electrical injury involves multiple anatomical substrates and also has
a temporal diversity in relation to the occurrence of electrocution.
We describe a case having delayed onset of visual symptoms with
symmetrical cortical lesions after electrocution, which in our experience has not been reported earlier in literature.
2. Case report
A fifty year old gentleman was working at a factory on a rainy
day, surrounded by electrical appliances. He suffered from an electrocution, probably from one of the loosened wires lying on a wet
floor. He apparently became unconsciousness immediately and suffered from the burns over his right leg and left hand without any
significant head trauma. On regaining his senses after 30 min, he
had generalized body ache and severe pain over his right leg. He

∗ Corresponding author.
E-mail address: bhumirmeetsu@gmail.com (B. Chauhan).
http://dx.doi.org/10.1016/j.clineuro.2015.10.015
0303-8467/© 2015 Elsevier B.V. All rights reserved.

was rushed to the hospital, where he was given primary management and was admitted for observation. He was discharged in a
few days following an uneventful stay at hospital with no residual
symptoms. One week later, he woke up in the morning with sudden
onset of generalized headache and bilateral visual blurring. He did
not have any history of similar headache in the past. The headache
was severe and associated with vomiting. The visual blurring was
similar in both eyes and was more prominent in lower half of his
visual field. Headache and visual blurring progressed over 2–2 h
after the onset, until they became static and continuous. He denied
diplopia, local eye symptoms or drooping of eye lids. It was not
associated with any other neurological symptoms. He did not have
any vascular risk factors and his previous medical history was not
significant.
When evaluated by an ophthalmologist, local ocular examination was normal. He barely had perception of light in both eyes.
Color vision and perimetry were not possible due to poor visual
acuity. Pupillary reflexes were intact bilaterally without relative
afferent pupillary defect. Neurological examination did not reveal
any other abnormal signs, systemic examination was unremarkable. He had healing burn wounds over right leg and left hand. Blood
pressure was within normal range, carotid bruit was absent and all
peripheral pulsations were palpable. Routine blood investigations
and electrocardiogram did not show any abnormality.
Magnetic resonance imaging (MRI) of brain showed presence of
symmetrical diffusion restriction with corresponding low apparent
diffusion coefficient values in parieto-occipital regions. The lesions
were inhomogeneous and irregular, beyond vascular territories
and strictly cortical in location. T2 and Fluid Attenuation Inversion Recovery (FLAIR) sequences showed subtle hyperintensity in

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B. Chauhan et al. / Clinical Neurology and Neurosurgery 139 (2015) 311–313

Fig. 1. MRI brain shows symmetrical diffusion restriction in bilateral occipital and parietal areas (A) and corresponding low intensity in ADC image (B). The T2 (C) and FLAIR
(D) sequences show subtle high intensity signals in similar areas. GRE image (E) is negative for any abnormalities.

corresponding areas. Intracranial plus extracranial angiogram and
venogram were normal (Fig. 1). Radiological possibilities of infarction, edema or demyelination were considered.
Investigations to diagnose underlying vascular risk factors were
negative. Blood pressure monitoring did not show any fluctuations.
After 24 h of onset, the headache became more severe with worsening of vision as well. He was initiated on intravenous steroids
at the dose of 1 g methylprednisolone per day, which was continued for a total of 3 days. His symptoms of headache and visual
blurring improved significantly after steroid therapy was started.
He was able to count fingers at 4 m distance. He was discharged
after 6 days of hospital stay with improved vision and no residual
headache. He followed up as an outpatient after 4 weeks with an
improved visual acuity of 6/9 (Snellen’s chart) bilaterally. He was
functionally independent and was able to carry out his social and
occupational responsibilities.
3. Discussion
Electrical current is governed by three parameters: voltage,
resistance and amperage. Severe form of electrical injury has been
described as electrocution. Electrocution accidents are a common
occupational hazard and are also seen in household environment.
The nature of current, alternating current (AC) and direct current
(DC), also influences the severity of injuries sustained in these

accidents. Most of the accidents are secondary to exposure to AC
which is the more destructive as compared to DC. The extent of
injury is also decided by other factors such as voltage, duration
of exposure, resistance offered by body parts, area of contact,
presence of protective devices, etc. Effect of electricity on the body
can be broadly classified as direct and indirect effects. The direct
or local effects are well described and more common in occurrence. However, it is the indirect effect which is more complex
in terms of anatomical involvement and temporal profile after an
electrocution.
Neurologically speaking, electric current can affect almost
any part of the neural axis. The symptoms can be as nonspecific as headache, lethargy, fatigue, exhaustion, spasms, cramps,
joint weakness or physical sensitivity [1]. Specifically diagnosable
syndromes affecting peripheral nerves, muscles, autonomic symptoms, spinal cord, cerebral cortex and psychiatric manifestations
have been recognized. It requires a high index of suspicion and
knowledge regarding the temporal association so as to diagnose
these entities.
Cherington [2] proposed four categories of neurological sequelae that could result from electrical trauma. The categories
are:
1) Immediate and transient: symptoms occur at the time of incident and spontaneous remission occurs over hours to days.

B. Chauhan et al. / Clinical Neurology and Neurosurgery 139 (2015) 311–313
Table 1
Previously reported cases with stroke or stroke like presentation after the electrocution and delay of onset after the incident.
Author

Delay from incident

Deficits

Critchley
Langworthy
Haase and Luhan
Gans and Glaser
Present case

9 months
1 day
3 weeks
4 days
7 days

Right hemiparesis and aphasia
Right hemiplegia
Right hemiplegia
Right homonymous hemianopia
Cortical blindness

Examples under this category are sudden loss of consciousness
and retrograde amnesia.
2) Immediate and prolonged or permanent: symptoms occur at the
time of incident and persist for days to years or indefinitely. Brain
hematoma, infarction, etc. are common examples.
3) Delayed and progressive: symptoms are absent at the time
of incident but present after a delay and are progressive in
nature. The delay is variable, ranging from few days to years
after the incident. This category is exemplified by disorders like
demyelinating diseases, movement disorders, hydrocephalus,
thrombosis, etc.
4) Linked or coupled: the indirect effects of the incident occur. For
example, head injuries following a fall after the electrocution.
The spectrum of neurological manifestations following electrical injury is vivid. Literature describes cases with peripheral
neuropathy, seizures, central nervous system complications
(myelopathy, encephalopathy, venous sinus thrombosis), movement disorders, headache and memory disturbances. Neuropsychological manifestations include insomnia, emotional disturbances, anxiety, phobia to electricity, inability to concentrate,
post-traumatic stress disorder, etc.
As in our case, acute stroke or stroke like presentation has been
described in previous case reports. Gans and Glaser described a
case with acute visual symptoms 4 days after the electrocution
secondary to left occipital cortical infarct (Table 1) [3].
The mechanisms for genesis of delayed neurological symptoms are speculative and variable. One of the earliest description
of brain biopsy specimen after death from electrocution showed
incomplete perivascular necrosis, demyelination, swelling of oligodendroglia with compression of cortical gray ribbon cells. Later, it
was suggested alteration of proteins in the endothelial cells which
may lead to thrombosis and vascular compromise in the affected
areas. Another hypothesis is that over excitation of neuronal cells
through the electric current releases glutamate in excess which is
capable of cell death. Excess glutamate also results in generation
of free radicals through oxidative stress mechanisms and result in
cytotoxicity. It is possible that the effects of oxidative stress are
delayed and cumulative. Theory of extraporation [4] explains that
electric field induces ‘pores’ in the cell membrane, resulting in temporary dysfunction or cell death. This theory explains those cases
which have transient symptoms following the electric injury and
are self-limiting. The end result of above mentioned mechanisms

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possibly leads to edema, dysmyelination, ischemia or infarction,
which in turn manifest as acute or delayed onset symptoms. However, other aspects of pathogenesis such as variability in delay of
onset, involvement of isolated areas of neural axis in an individual,
severity of symptoms and underlying pathological variations still
remains unexplained.
Our speculation of causal relation is based on sudden onset of
symptoms with radiological correlate occurring after latency of
7 days of the incident. Almost all the possibilities leading to our
clinical scenario were ruled out through history, examination and
investigations. The clinical profile along with the radiological picture resembles that of posterior reversible leukoencephalopathy
syndrome, and a possible role of electric injury leading to this syndrome cannot be refuted with certainty in this case. Also, since
the initial event of loss of consciousness was unwitnessed, possibility of delayed clinical presentation of initial anoxia cannot be
denied. However, the temporal aspect of this case, reversibility with
steroids and previous literature description of delayed neurological insults after electrocution cannot be ignored. Our decision to
treat with steroids was based on possibility of edema or demyelination. We reviewed a similar case report of visual symptoms post
electrocution, which improved with steroid therapy [5]. Still, role of
steroids in such cases remains elusive and needs further correlation
with significant number of similar cases.
4. Conclusion
In summary, neurological sequelae following electrocution have
wide diversity in terms of symptoms, neuroanatomical involvement, temporal profile and pathogenesis. Even the involvement of
site remote from contact can be affected. It is important to remember the entity of delayed onset neurological injury post electrical
injury. Radiological lesions may help in understanding the pathology in some cases. To the best of our knowledge, this is the first
description of a reversible blindness of delayed onset after electrocution with radiological evidence. The occurrence of delayed onset
of cortical blindness following electrocution and its reversibility
with steroids marks the salient features and learning points in this
case.
References
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current pathway, IEEE Trans. Biomed. Eng. 51 (August (8)) (2004) 1449–1459.
[2] M. Cherington, Central nervous system complications of lightning and electrical
injuries, Semin. Neurol. 15 (September (3)) (1995) 233–240.
[3] M. Gans, J.S. Glaser, Homonymous hemianopia following electrical injury, J. Clin.
Neuroophthalmol. 6 (December (4)) (1986) 218–223.
[4] C.B. Freeman, M. Goyal, P.R. Bourque, MR imaging findings in delayed reversible
myelopathy from lightning strike, Am. J. Neuroradiol. 25 (May (5)) (2004)
851–853.
[5] I. Pérez-Molina, J.M. Velázquez-Pérez, B. Mondéjar-Marín, S. Navarro-Muñoz, A.
Pedrosa-Guerrero, A. Alvarez-Tejerina, [Neurological sequelae following electrocution. A case report and review of the literature], Rev. Neurol. 43 (November
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