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LETTER TO EDITOR
Year : 2016  |  Volume : 64  |  Issue : 2  |  Page : 325--327

Spinal cord atrophy: A rare complication of post- electrocution myelopathy

Sanjeev Kumar, Rakesh Shukla 
 Department of Neurology, King George's Medical University, Lucknow, Uttar Pradesh, India

Correspondence Address:
Rakesh Shukla
Department of Neurology, King George's Medical University, Lucknow, Uttar Pradesh
India




How to cite this article:
Kumar S, Shukla R. Spinal cord atrophy: A rare complication of post- electrocution myelopathy.Neurol India 2016;64:325-327


How to cite this URL:
Kumar S, Shukla R. Spinal cord atrophy: A rare complication of post- electrocution myelopathy. Neurol India [serial online] 2016 [cited 2020 Aug 9 ];64:325-327
Available from: http://www.neurologyindia.com/text.asp?2016/64/2/325/177612


Full Text

Sir,

Electrical injury to the nervous system is common because the electric current takes the pathway of least resistance in our body. Delayed neurological complications are reported, but spinal cord atrophy has rarely been documented in literature. We are reporting a case with delayed neurological complications of low-voltage electric injury-induced cervical cord atrophy.

Complications from electrical injury can affect almost every organ system in the body. Electric current is divided into low- (<1000 volt) and high-voltage (>1000 volt) injury. The neurological involvement includes cerebral, spinal cord, and peripheral nerve lesions.[1]

A 19-year-old young man presented with weakness of both upper limbs and atrophy of the left upper limb of a 2-year duration. He had history of sustaining electric injury while repairing a television set at home. His left hand (middle finger) had come in contact with the electric current. He was thrown to the ground and developed loss of consciousness for approximately half an hour. After 1 month of this incident, he noticed heaviness and clumsiness in his left hand during fine motor activities. The weakness was gradually progressive over a 1½-year duration, and from the last 6 months, it had remained static. At the time of admission, he was not able to carry out fine work with his left hand. He also had weakness in lifting heavy objects above his shoulder and atrophy of his left upper limb for the past 1 year. He had no history of fasciculation. He had no complaints of weakness in the lower extremities. There was no history of sensory deficits or of bowel and bladder involvement. He had a scar over his left middle finger. His neurological evaluation revealed that higher mental functions and cranial nerve examination were normal. He had atrophy in the left scapular, periscapular, arm, and forearm muscles [Figure 1]. Motor examination revealed a spasticity of grade 2 (modified Ashworth Scale). The power in the left upper limb was 4/5 at the proximal and 4−/5 in the distal joints, with a weak handgrip; and in the right upper limb, it was 4+/5 both proximally as well as distally. In both lower limbs, power was 4+/5. He had generalized hyper-reflexia in both upper and lower limbs that included exaggerated pectoral and deltoid reflexes. His plantar reflexes were bilaterally extensor. His sensory and cerebellar examination were normal.{Figure 1}

His hematological and biochemical parameters were normal. Serum VDRL (venereal disease research laboratory test) and ELISA (enzyme-linked immunosorbent assay) for HIV (human immunodeficiency virus) were negative. X-ray of the cervical spine was normal. Motor and sensory nerve conduction study was also normal. Concentric needle electromyography done in the left deltoid, supraspinatus, infraspinatus, and biceps muscles showed no spontaneous activity along with a reduced interference pattern suggestive of neurogenic atrophy. Magnetic resonance imaging (MRI) of the cervical spine revealed spinal cord atrophy at C2–C3 level with hyperintense signals in the region of anterior horn cells on T2-weighted image [Figure 2]. A diagnosis of cervical myelopathy was considered in this patient. On the background history of electrical injury, an electrocution-induced myelopathy was considered as the etiological diagnosis. The differential diagnoses included amyotrophic lateral sclerosis and multifocal motor neuropathy with conduction block but these lesions were excluded based on the significant history of electrocution. Physiotherapy and low-dose medication to combat hypertonia were started, but unfortunately, there was no significant improvement in his neurological deficits. There was also no worsening of his symptoms at a follow-up of 6 months.{Figure 2}

Our patient presented with weakness of both upper limbs and atrophy of the left upper limb of a 2-year duration that started developing 1 month after he sustained the electric shock. The symptoms were initially progressive for 1½ years and then became static. There was generalized hyper-reflexia, including a bilateral extensor plantar response. The sensory system was normal. The electrophysiological study revealed normal motor and sensory nerve conduction, with evidence of neurogenic pattern on electromyography. The MRI showed cervical spinal cord atrophy along with hyperintense signals in the region of anterior horn cells at the C2–C3 level. This clinical picture is consistent with motor neuron disease secondary to electrical injury. The patient had both immediate (loss of consciousness) and delayed (quadriparesis and atrophy) complications. His scar mark on the left middle finger marked the entry point of the current. The traversing of the current via the peripheral nerves and the cervical cord to the brain led to an immediate loss of consciousness. The patient's left upper limb suffered from significantly increased atrophy and weakness compared with other extremities. His cervical cord damage manifested as a delayed complication in the form of atrophy and gliosis of anterior horn cells. There was no sign of recovery due to the sustained atrophy and gliosis of the spinal cord.

The manifestations of electrical injury depend on the entry and exit points of the current as well as several other factors like amperage, voltage strength, resistance, type of the current, pathway of the current, and duration of the contact. Electrical injuries affect human body by four possible mechanisms: 1. Direct injury; 2. Mechanical injury - it is secondary to either sustaining a fall, or being thrown off as a consequence of force of the current; 3. Thermal burns–it occurs owing to generation of heat in the pathway of significant resistance, such as the skin; and, 4. Electroporation–when the electric current passes through the lipid bilayers of the cell membrane, it forms pores within the membrane. Electroporation results in free passage of ions and fluids, causing loss of ionic gradient within the cells.[2],[3]

Neurological complications of electrical injuries are classified into immediate and transient, immediate and prolonged or permanent, or delayed and progressive.[4] Intracranial hemorrhage, brain edema, cerebral arterial or venous thrombosis, myelopathy, and peripheral nerve disorders are various manifestations of electrical injuries. The pattern of neurological manifestations in patients without obvious spinal injury may be immediate or delayed. The immediate damage develops within minutes-to-hours in the form of weakness and paresthesias. Lower limbs are more affected than the upper limbs, with a subsequently good prognosis. Delayed neurological manifestations occur from days-to-years and manifest as ascending paralysis, amyotrophic lateral sclerosis, or transverse myelitis, with a poor recovery.[5] Electrical injury leading to amyotrophy has rarely been reported in the literature. An history of electric shock as an antecedent event was seen in 1/124 cases of ALS seen over a period of 10 years by Gourie-Devi, et al.[6] Kurtzke considered that physical trauma, whether mechanical, electrical, or operative, is the most potent and the most consistent risk factor involved in the development of ALS.[7] In a systematic review of 31 studies published between 1906 and 2002, 96 individuals who developed neurological syndromes after electrical injury were identified. Of these, 44 had ALS; 1, a progressive upper motor neuron syndrome; 7, a progressive lower motor neuron syndrome; and 44, a non-progressive syndrome. The median interval between electrical injury and the onset of neurological disease was 2.25 years for all progressive syndromes, and within a week for the nonprogressive syndromes. A nonprogressive motor syndrome is also associated with a more severe electrical injury.[8]

Declaration of patient consent

The authors certify that they have obtained all appropriate patient consent forms. In the form the patient(s) has/have given his/her/their consent for his/her/their images and other clinical information to be reported in the journal. The patients understand that their names and initials will not be published and due efforts will be made to conceal their identity, but anonymity cannot be guaranteed.

Financial support and sponsorship

Nil.

Conflicts of interest

There are no conflicts of interest.

References

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6Gourie-Devi M, Suresh TG, Shankar SK. Pattern of motor neuron disease in South India and monomelic amyotrophy (a benign atypical form). In: Gourie-Devi M, editor. Motor Neuron Disease: Global Clinical Pattern and International Research. New Delhi: Oxford 1BH Publishing Co Pvt Ltd; 1987. p. 171-90.
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