In a small number of surviving patients, after an asymptomatic interval of days to months, there has been an apoplectic onset of hemiplegia with or without aphasia or a striatal or brainstem syndrome, presumably because of thrombotic occlusion of cerebral vessels with infarction of tissue, but this condition has not been well studied.
The separate issue of the relationship of electrical shock exposure and the later development of typical ALS is quite controversial. Most series are hampered by retrospective acquisition of data about the shock. Although we have encountered a few remarkable instances of this association, including two who developed severe amyotrophy of the limb that was in contact with the electrical source many years before, a relationship to typical motor neuron disease has been considered coincidental.
The factors involved in injuries from lightning are less well defined than those from electric currents, but the effects are much the same. Direct strikes are often fatal; nearby strikes produce neurologic damage as described below. Topographic prominences such as trees, hills, and towers are struck preferentially, so these should be avoided; a person caught in the open should curl up on the ground, lying on one side with legs close together.
Arborescent red lines or burns on the skin indicate the point of contact of the energy generated by direct or nearby lightning. The path through the body can be approximately deduced from the clinical sequelae. Death is a result of ventricular fibrillation or of the effects of intense desiccating heat on the brain. Lightning that strikes the head is particularly dangerous, proving fatal in 30 percent of cases. Most persons struck by lightning are initially unconscious, irrespective of where they are struck. In those who survive, consciousness is usually regained rapidly and completely. Rarely, unconsciousness or an agitated-confusional state may persist for a week or two. Persistent seizures are surprisingly rare.
There is usually a disturbance of sensorimotor function of a limb or all the limbs, which may be pale and cold or cyanotic. As a rule, these signs are also evanescent, but in some instances they persist, or an atrophic paralysis of a limb or part of a limb makes its appearance after a symptom-free interval of several months as in the case of electrical injury.
A severe, predominantly motor polyneuropathy has been reported to appear after a variable interval and, while it bears similarities to the motor neuron disorder ostensibly associated with electrical injury discussed in the section above, there is a more persuasive relationship to the less common event of lightning. There are also a few cases on record of recovery from generalized polyneuropathy after lightning injury, but our experience with one case was of profound generalized axonal damage with little recovery (see Chap. 43).
This subject is introduced here with the other forms of spinal cord injury for want of a better way to categorize it. A transient and often asymmetric paraparesis is known to occur following prolonged spinal anesthesia but this is probably the result of a temporary effect of the injected agents on the cauda equina roots (see Chap. 43). A more serious and permanent injury has been caused by inadvertent injection of anesthetic directly into the conus medullaris (see Hamandi et al; Wilkinson et al). The patient reports leg weakness and numbness on one side immediately with the injection or upon awakening if sedation has been used. The MRI reveals an eccentrically placed traumatic lesion within the caudal spinal cord. Although this complication is rare, it has occurred even when experienced anesthesiologists perform the procedure; misidentification of the L3-L4 spinal interspace has been cited as the problem. Flat-tipped needles are as likely to cause injury to the conus as are ones with sharp beveled tips. Arachnoiditis from irritative agents, no longer used to any great extent, in the past caused a myelopathy (see Chap. 10).