A number of case reports remark on temporary improvement in neurologic function after the administration of corticosteroids. This therapy should be tried because in some patients it appears to arrest the process short of complete destruction of all sensory and motor tracts. Claims have also been made of regression of early symptoms in response to the administration of heparin split products and of hyperbaric oxygen, but most have not been confirmed.
Among acute physical injuries to the spinal cord, those caused by electric currents and lightning, despite their rarity, are of great interest because they produce unusual clinical syndromes. Electrical forces can also injure the brain and peripheral nerves. These effects are noted only briefly here, because they are infrequent. It is the spinal cord that is most consistently and severely damaged.
In the United States, inadvertent contact with an electric current causes approximately 1,000 deaths annually and many more nonfatal but serious injuries. About one-third of the fatal accidents result from contact with household currents.
The factor that governs the damage to the nervous system is the amount of current, or amperage, with which the victim has contact, not simply the voltage, as is generally believed. In any particular case, the duration of contact with the current and the resistance offered by the skin to current (greatly reduced if the skin is moist or a body part is immersed in water) are of importance. The physics of electrical injuries is much more complex than these brief remarks indicate (for a full discussion, see the reviews by Panse and by Winkelman).
Any part of the peripheral or central nervous system may be injured by electric currents and lightning. The effects may be immediate, which is understandable, but of greater interest are the instances of neurologic damage that occur after a delay of 1 day to 6 weeks (1 week on average) and a rarer syndrome (the existence of which is disputed) of anterior horn cell damage that arises after many years. The immediate effects are the result of direct heating of nervous tissue, but the pathogenesis of the delayed effects is not understood. They have been attributed to vascular occlusive changes induced by the electric current, a mechanism proposed to underlie the similar delayed effects of radiation therapy (see earlier). However, the latent period is measured in many months or a few years rather than in days and the course is more often progressive than self-limited. Moreover, the few postmortem studies of myelopathy as a consequence of electrical injury have disclosed a widespread demyelination of long tracts, to the point of tissue necrosis in some segments, and relative sparing of the gray matter, but no abnormalities of the blood vessels. There may also be spinal fracture from the vigorous muscle contraction.
The extraordinary syndrome of focal muscular atrophy occurring with a delay of weeks to years after an electric shock has been described by Panse under the title spinal atrophic paralysis. It occurs when the path of the current, usually of low voltage, is from arm to arm (across the cervical cord) or from an arm to leg. When the head is one of the contact points, the patient becomes unconscious or suffers tinnitus, deafness, or headache for a short period following the injury. Pain and paresthesias occur immediately in the involved limb but these symptoms are transient. Mild weakness, also unilateral, is immediate, followed in several weeks or months by muscle wasting, most often taking the form of segmental muscular atrophy. The syndrome simulates a regional form of amyotrophic lateral sclerosis (ALS) or transverse myelopathy (most patients have some degree of weakness and spasticity of the legs). However, we have encountered cases of asymmetric and profound atrophic weakness of the arms that began almost two decades after the shock and progressed over many years without long tract signs, both with a previously presumed diagnosis of amyotrophic lateral sclerosis. In contrast to injuries caused by high current, which affects mainly the spinal white matter (see earlier), it is the gray matter that is injured in cases of spinal atrophic paralysis, at least as judged from the clinical effects.