American Journal of Emergency Medicine xxx (2015) xxx–xxx

Contents lists available at ScienceDirect

American Journal of Emergency Medicine
journal homepage: www.elsevier.com/locate/ajem

Case Report

Acute vertebrobasilar ischemic stroke due to electric injury☆,☆☆,★,★★
Abstract
Electrical injuries are most commonly due to household accidents.
Various factors determine the severity of electric injury, including type
of current, amperage, voltage, tissue resistance, pathway of current,
and duration of contact with the body. Various types of neurologic damage due to electrical injury have been described in literature. It may manifest as peripheral nerve injury, spinal cord damage, seizures, cerebellar
ataxia, hypoxic encephalopathy, and intracerebral hemorrhage. Acute ischemic stroke is an infrequent complication of electrical injury. Herein,
we report a case of middle-aged man, who accidentally sustained highvoltage electrical injury followed by acute vertebrobasilar ischemic
stroke. Magnetic resonance imaging of the brain showed acute infarct
in bilateral cerebellar and medial occipital regions. Computed tomographic angiogram of the brain and neck vessels was normal. Possibly,
in our patient, the mechanism could be related to direct vascular injury
due to electric current.
Most electric injuries are seen in household accidents due to lowvoltage alternating current, although injuries due to high-voltage current
have also been reported [1,2]. The parts of the body, usually prone to injury are skin, muscles, heart, kidneys, blood vessels, and nerves.
Various types of neurologic damage due to electrical injury have
been described in literature including peripheral nerve injury, spinal
cord damage, movement disorders, amyotrophic lateral sclerosis, neuropsychological symptoms, cerebellar ataxia, seizures, hypoxic encephalopathy, and intracerebral hemorrhage [3-5]. We report a case of acute
vertebrobasilar stroke due to electrical injury because of the infrequency of this neurologic complication.
A 40-year-old man while working accidentally touched an overhead
high-tension wire carrying 11000 V and sustained electric injury. The patient became unconscious but regained consciousness on the way to the
hospital. In an emergency, quick initial resuscitation and assessment of
the patient were done with special attention to the airway, breathing,
and circulation. There was no previous history of transient ischemic attack, stroke, hypertension, or diabetes mellitus. The patient was then
transferred to the burn unit. He had 18% burn injury composing of full
and partial thickness burns on the right arm and axilla (entrance or source
points), right thigh, and groin area (exit or ground points) (Fig. 1A-C).
There were no signs of cardiovascular, respiratory, or abdominal involvement. His pulse and blood pressure were normal. The patient was alert,
conscious, and oriented to place, time, and person. His speech was slurred.
Fundi were normal. Visual field examination showed right homonymous
☆ Source(s) of support: Nil.
☆☆ Conflicts of interest: Nil.
★ Acknowledgment: None.
★★ Presentation at meeting: None.

hemianopia. He had mild weakness in right upper and lower limbs
(Medical Research Council grade 4/5). Nystagmus with the fast component toward left side was present. Cerebellar signs were present in form
of limb ataxia, finger-nose incoordination, and dysdiadochokinesia on
both sides (left more than right side). On the right side, deep tendon reflexes were exaggerated, and the Babinski sign was positive.
Complete hemogram, serum electrolytes, renal and liver function
tests, and lipid profile were normal. Serum creatinine phosphokinase
level was raised. Urine biochemical and microscopic analysis was
normal. Urine examination for myoglobin was negative. Electrocardiogram, x-rays of chest, and cervical spine were normal. Computed
tomographic scans of brain showed hypodensity in bilateral cerebellar and left posterior occipital regions (Fig. 2A-C). Magnetic resonance brain diffusion weighted imaging showed acute infarct in
bilateral cerebellar hemisphere (left more than right), vermis, and
left medial occipital areas (Figs. 3A-H and 4A-F). Computed tomographic angiography of the neck and brain vessels was normal
(Fig. 5A-F). Two-dimensional echocardiography was normal. Coagulation profile, including proteins C and S; anticardiolipin antibody;
and homocysteine level were normal.
Electric injury was self-evident from history. Radiographs of the
chest and cervical spine and ultrasound abdomen were done to look
for any associated injury, especially for spinal injury and blunt trauma.
The patient came to us after window period; therefore, thrombolytic
therapy could not be given. He received tetanus toxoid injection. Intravenous antibiotics were given to prevent secondary infection, and burn
wounds were covered with antibiotic dressings (mafenide acetate/
sulfadiazine silver). He was started on antiplatelet (aspirin) therapy
and other supportive treatment along with rehabilitation services.
After 15 days, he underwent cutaneous graft surgery. He gradually improved and was able to walk with support within a month.
The patient was discharged after 1 month. Rehabilitation services,
including physical, occupational, and speech therapy, were continued;
and at 6 months' follow-up, the patient was ambulatory without support. Neurologic examination still showed evidence of cerebellar signs
including dysarthria, finger-nose incoordination, and gait ataxia.
Electric injuries are most commonly due to household accidents.
Acute vertebrobasilar ischemic stroke is an infrequent neurologic complication of electric injury. Most effects due to electric injuries are immediate and transient; however, delayed and permanent manifestations
are also known. Various factors determine the severity of electric injury
including type of current, voltage, amperage, tissue resistance, pathway
of current through the body, and duration of contact [6].
Although few case reports have been described in literature, there
has been little advancement in the understanding of neurologic complication of electric injury [7]. As electric current passes through the body,
thermal burn due to electric injury causes coagulation necrosis [8,9].

http://dx.doi.org/10.1016/j.ajem.2014.12.068
0735-6757/© 2014 Elsevier Inc. All rights reserved.

Please cite this article as: Singh Jain R, et al, Acute vertebrobasilar ischemic stroke due to electric injury, Am J Emerg Med (2015), http://dx.doi.org/
10.1016/j.ajem.2014.12.068

2

R. Singh Jain et al. / American Journal of Emergency Medicine xxx (2015) xxx–xxx

Fig. 1. Photographs of patient showing distribution of burn injury (18%). Right lateral view (a), right arm and axilla (b), and right side of groin and lower abdominal area (c).

Ischemic stroke due to electric injury may occur from various mechanisms. One of the reason may be mechanical injury due to prolonged
muscle contraction. Electric injury causes intense muscle spasms and
sympathetic hyperactivity, which may lead to vasospasm and thrombus
formation or embolism. Another mechanism may be direct underlying
cerebral damage due to thermal burns. Heat dissipated in intracranial
vessels can cause protein conformation changes, cellular dysfunction,
and tunica intima damage resulting in thrombosis with subsequent
thrombosis or rupture [10,11]. Hemodynamic alterations and cardiac
arrest leading to cranial hypoperfusion and watershed infarction can

be alternate mechanism. In our patient, acute vertebrobasilar infarct
may possibly be related to direct vascular injury due to electric current.
All patients who sustain a high-voltage electric injury should undergo hemogram, biochemical tests, cardiac isoenzyme level, urine analysis
for myoglobin, electrocardiogram, and radiographic studies to look for
associated injuries [12]. To conclude, acute vertebrobasilar ischemia
due to electric injury is an uncommon neurologic manifestation. Hospital stay and morbidity in our case were increased due to acute ischemic
event. The exact mechanism of the damage still remains in doubt and
therefore needs further research.

Fig. 2. Computed tomography of brain showing hypodensity in bilateral cerebellar left (a) more than right (b) and left medial occipital areas (c).

Please cite this article as: Singh Jain R, et al, Acute vertebrobasilar ischemic stroke due to electric injury, Am J Emerg Med (2015), http://dx.doi.org/
10.1016/j.ajem.2014.12.068

R. Singh Jain et al. / American Journal of Emergency Medicine xxx (2015) xxx–xxx

3

Fig. 3. a and b, Magnetic resonance imaging brain showing hypointensity in bilateral cerebellar and left medial occipital area on T1-weighted images. Hyperintensity seen in bilateral cerebellum (left more than right), vermis, and left medial occipital areas on fluid attenuation inversion recovery (c and d) and T2-weighted images (e-h).

Rajendra Singh Jain DM1
Sunil Kumar MD ⁎
Desai Tushar Suresh MD2
Rakesh Agarwal MD3
Department of Neurology, Sawai Man Singh Medical College
Jaipur, Rajasthan, India
⁎Corresponding author. Tel.: +919571414284
E-mail addresses: drrsjain@yahoo.com (R. Singh Jain)
doc.kumarsunil@hotmail.com (S. Kumar)
tushar.desai85@gmail.com (D.T. Suresh)
drraggarwalneuro@gmail.com (R. Agarwal)

1

Tel.: +91 9414073579

2

Tel.: +91 8239897150

3

Tel.: +91 9829343263

http://dx.doi.org/10.1016/j.ajem.2014.12.068

References
[1] Christensen JA, Herman RT, Balis GA, Wuamett JD. Delayed neurological injury secondary to high-voltage current, with recovery. J Trauma 1980;20:166–8.
[2] Singerman J, Gomez M, Fish JS. Long-term sequelae of low voltage electrical injury. J
Burn Care Res 2008;29(5):773–7.
[3] Ramati A, Rubin LH, Wicklund A, Pliskin NH, Ammar AN, Fink JW, et al. Psychiatric
morbidity following electrical injury and its effects on cognitive functioning. Gen
Hosp Psychiatry 2009;31(4):360–6.
[4] Morse JS, Morse MS. Diffuse electrical injury-comparison of physical and neuropsychological symptom presentation in males and females. J Psychosom Res 2005;58(1):51–4.
[5] Chudasama S, Goverman J, Donaldson JH, van Aalst J, Cairns BA, Hultman CS. Does
voltage predict return to work and neuropsychiatric sequelae following electrical
burn injury? Ann Plast Surg 2010;64(5):522–5.
[6] Baxter CR. Present concepts in the management of major electrical injury. Surg Clin
North Am 1970;50:1401–18.
[7] Cherington M, Yarnell P, Hallmark D. MRI in lightning encephalopathy. Neurology
1993;43:1437–9.
[8] Childbert M, Maiman D, Sances A, Myklebust J, Prieto TE, Swiontek T, et al. Measure
of tissue resistivity in experimental electric burns. J Trauma 1985;25:209–15.
[9] Puschel K, Brinkman B, Lieske K. Ultrastuctural alteration of skeletal muscles after
electrical shock. Am J Forensic Med Pathol 1985;6:246–51.
[10] Lee RC, Kolodney MS. Electrical injury mechanisms: electrical breakdown of cell
membranes. Plast Reconstr Surg 1987;80(5):672–9.
[11] Lee RC. Injury by electrical forces: pathophysiology, manifestation and therapy. Curr
Probl Surg 1997;34(9):667–765.
[12] Hussmann J, Kucan JO, Russell RC, Bradley T, Zamboni WA. Electrical injuriesmorbidity, outcome and treatment rationale. Burns 1995;21(7):530–5.

Please cite this article as: Singh Jain R, et al, Acute vertebrobasilar ischemic stroke due to electric injury, Am J Emerg Med (2015), http://dx.doi.org/
10.1016/j.ajem.2014.12.068

4

R. Singh Jain et al. / American Journal of Emergency Medicine xxx (2015) xxx–xxx

Fig. 4. a to f, Diffusion restriction seen in bilateral cerebellar (left more than right), vermis, and left medial occipital areas on diffusion weighted imaging brain (upper collum) and corresponding fall in apparent diffusion coefficient value (lower column).

Fig. 5. Computed tomographic angiography of neck vessels including right (a) and left (b) internal carotid and right (c) and left (d) vertebral arteries as well as brain vessels (e and f) were
normal.

Please cite this article as: Singh Jain R, et al, Acute vertebrobasilar ischemic stroke due to electric injury, Am J Emerg Med (2015), http://dx.doi.org/
10.1016/j.ajem.2014.12.068