Delayed neurodegenerative syndromes following lighting and electrical injury has been known since the early 1930s (Critchley 1934, Silversides 1964). There is little in the literature both because of the low frequency of occurrence and for ethical reasons as one cannot do experiments in this area. However, what is described in case studies is a delayed onset in symptoms and deterioration in cognitive functioning over time, followed by an increase in emotional distress. The delay of symptoms has been observed to be as much as 1 to 5 years after the injury, and the symptoms tend to be more subtle, pervasive, and difficult to diagnose (Wesner and Hickie 2013, Bryan et al 2009).
Imaging studies suggest that electrical injuries have a more significant impact on brain functioning rather than on brain structure. For example, MRI and CT scans are often not indicative of structural impairment while EEGs may show nonspecific impairment in the brain’s electrical activity (Bryan et al 2009). There are cases where cognitive and psychological disorders become manifest even when the pathway of electrical current apparently does not cross the brain, and when structural damage to the brain is not found (Ramati et al., 2013, Pliskin et al 1994). EEG findings are significantly mixed with non-specific patterns of abnormality (specifically slowing), yet are distinct from patterns observed in concussive head injuries (Primeau et al 1995, Ramati et al 2013). SPECT scans have noted patterns by abnormal perfusion and functional MRI scans have revealed compensatory patterns of activation (Bryan et al 2009).
Evidence exists supporting potential mechanisms for immediate and delayed neurological disorders. The delayed theories share an underlying biochemical mechanism: an electrically mediated overstimulation of glutamate receptors in combination with elevated cortisol levels lead to an increase in damaging free radicals that mediate structural and functional damage (Reisner 2014, Pliskin et al 1994). The increase in free radicals may cause an eventual breakdown of the endothelial cells which make up the capillaries, thereby leading to vascular breakdown and starvation of the targets they supply. Alternatively, free radicals may be formed directly in the lipid-rich myelin, or cell membranes of myelin cells. With regard to the electroporation hypothesis (small holes within the brain tissue), it is unclear as to whether electroporation would cause immediate versus delayed neurological damage (Bryan 2009, Lee 1997).
Many who suffer electrical injuries have considerable difficulty returning to work. Depression, anxiety, and post-traumatic stress disorder are common, as are memory impairment, attention issues, pain, and loss of sensory sensitivity (Bryan et al 2009, Primeau et al 1995, Pliskin et al 1994). Acute neurologic symptoms after electrical injury have a better prognosis for recovery than delayed-onset neurologic symptoms do. (Wesner and Hickie 2013). In some cases, structural damage will resolve, while clinical symptoms remain (Bryan et al 2009). However, in general, there is little published on prognosis.
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