In electrocution injuries, the overall mortality may reach 5%. Electrical injuries have been reported to occur in low-voltage settings, such as with household use, and high-voltage exposures from occupational hazards and lightning strikes . Given the nature of these injuries, most of the literature has been reported as case studies with limited data regarding the evaluation and treatment of neurological complications.
Several pathophysiological mechanisms of injury to the nervous system have been proposed, including thermal injury, electroporation, and vascular damage through direct injury as well as indirect injury.
Electrical current flows from an area of low resistance to high resistance. Low areas of resistance include muscle, nerve and blood vessels. High-resistance tissue includes skin, connective tissue and bone, which suffer greater heat injury, typically at entry and exit sites but damage may be caused in any structure along the path of the current [2–4]. Nervous tissue provides a low-resistance route for electrical current. As the electrical current travels through tissue, neurons with larger surface area are more likely to be damaged by electroporation, in which the increase in cellular permeability and conductivity caused by permanent conformational change to membrane proteins ultimately leads to cell death . The heat loss that occurs as current flows through tissues of increasing resistance causes damage to the intima and adventitia of the vasculature, such as thrombosis, necrosis of the vascular wall, vasospasm and spread into nearby tissue [3, 4]. Most patients survive the initial insult, limiting the pathological work-up, with few postmortem studies available for review . Morbidity of electrocution has been related to electrothermal injury causing direct tissue damage with secondary ischemic changes from vascular insult. An accurate prognosis is challenging given the variations in the duration and extent of injury, the frequency of current, and the anatomic site. There are relatively few reports that correlate the clinical, electrophysiological and imaging changes that occur with electrocution injuries .
Classification of injuries has been divided by onset of symptoms. Silversides  divided the stages into immediate, secondary and late effects. Immediately after an electrical current passes through the human body, thermal injury occurs within nerve cells, manifesting effects such as altered sensorium and/or loss of consciousness, severe pain, hearing and vision changes, motor signs (including paralysis), respiratory compromise, or sensory complaints. Recovery occurs within 24 hours. Secondary effects include temporary paralysis and autonomic disturbances. The late effects are noted to start after five days, manifesting as hemiplegia, movement disorders, brainstem dysfunction and cranial neuropathies [4, 7].
Spinal cord injuries have also been classified into transient and permanent disability. Motor deficits occur more often than sensory disturbances  and are secondary to vascular damage incurred by the anterior spinal artery and its branches [4, 8–12], which supply two thirds of the spinal cord, including the lateral corticospinal tracts, spinothalamic tracts and the anterior horn cells along with the central gray matter of the spinal cord. This hypothesis may be supported by the susceptibility of smaller lumen vessels to injury, with less dissipation of heat to surrounding structures compared with their larger vessel counterparts .
Ko et al. carried out a retrospective study of spinal cord injuries related to electrical burns. They reported that 11 out of 13 patients with entry wounds in the head and neck region were found to have quadriplegia with exit sites located in the upper extremities, and paraplegia with exit sites located in the lower extremities. Most of these patients were noted to have hypotonia acutely in the first two to ten days after injury in an ascending pattern. It was postulated that this pattern of injury was related to ischemic damage to the arterial blood supply and vulnerability in the spinal cord. These findings provided the rationale to administer prostaglandin E1 (10μg/day for three weeks) or steroid therapy to reduce ischemic injury to the spinal cord .
Early discovery of extensive myelopathy of the cervical spine is aided by neuroimaging. Most of the described cases used T2 hyperintensities, correlating to clinical deficits . Initial imaging of our patient did not show any significant changes to explain his quadriparesis. However, repeat imaging performed roughly one week after initial MRI of his brain and cervical spine showed extensive involvement of the pyramidal tracts as well as cord edema, which explained our patient’s clinical findings. It was felt that the bilateral lesions involving the corticospinal tracts particularly contributed to our patient’s paresis. As with our case, serial imaging may prove essential for identifying delayed sequelae associated with electrocution injuries. A differential diagnosis made with radiology may be wide and includes neoplasm, infarction and electrocution injury. Repeat imaging may assist in making the correct diagnosis. Exploring additional neuroimaging modalities may be beneficial, such as magnetic resonance spectroscopy. Electrodiagnostic studies, such as evoked potentials, nerve conduction studies and electromyography may have prognostic value. The latter two modalities can help determine the severity of motor axonal loss, stemming from anterograde anterior horn cell degeneration in the ventral gray matter. Technical aspects limit the value of these studies secondary to the presence of skin injury and accessibility.
No established guidelines are available in the literature regarding the treatment of high-voltage electrical injury. Each case has been treated with supportive care. Early treatment of electrical injury starts with initial fluid resuscitation, respiratory support and prevention of infection. The lack of systematic guidelines makes clinical care for the patient with electrocution injuries challenging. Work-up of the neurological deficit with imaging or electrodiagnostic studies, treatment, and prognosis for recovery is dictated by the personal experience of the physician. There are no randomized double-blinded trials available on electrocution. The majority of the information comes from isolated cases, case series and animal experimental models, with fewer articles available in the radiology and neurological literature.
No consensus exists regarding medication use. High-dose intravenous steroids and prostaglandin E1 were cited in the literature as early treatment modalities. Neurological morbidity has been variable. Some case studies with delayed findings of severe myelopathy due to electrocution injury did not show full recovery  while other case reports showed near complete resolution of motor deficits with aggressive physical therapy . Multidisciplinary management approaches involving the intensivist, neurologist, plastic surgeon, physical and occupational therapists, and psychologist, as well as a nutritionist, is necessary to achieve the best possible outcomes. Long-term neurological follow-up is justified by the rich body of evidence of delayed complications cited in the literature.