Injuries from lightning and electrical injuries involve multiple systems of the body, however neurological symptoms are very widely reported. A disabling neuropsychological syndrome is also noted. This paper presents a comprehensive review of neurological and neuropsychological symptoms. Partial theories of causation for these injuries have been advanced, however, there is no convincing explanation for both delay in onset of symptoms and also the genesis of the neuropsychological syndrome. A theory of causation is proposed which satisfies both these constraints. This theory suggests circulating hormones such as cortisol, together with nitric oxide and oxidant free radicals from glutamatergic hyper-stimulation, act on tissues remote from the injury path including the hippocampus. This theory opens a research path to explore treatment options.

review the Common Factors Model, the Empirically Validated Therapy Model , and the Recovery Model of therapeutic change and effectiveness. In general, psychotherapy appears to be effective and common factors account for more of the variance than do specific techniques. However, in some areas, particularly in the treatment of anxiety disorders, behavioral and cognitive behavioral therapies may be more effective than other treatments. The Recovery Model is an overarching model of change which can incorporate empirically validated therapies and which makes use of common factors. This model is consistent with empirically supported concepts concerning improvement of mental health but needs further research.

In the past, victims of electrical and lightning injuries have been assessed in a manner lacking a systematic formulation, and against ad hoc criteria, particularly in the area of neuropsychological disability. In this manner patients have, for example, only been partially treated, been poorly or incorrectly diagnosed, and have been denied the full benefit of compensation for their injuries. This paper contains a proposal for diagnostic criteria particularly for the neuropsychological aspects of the post injury syndrome. It pays attention to widely published consistent descriptions of the syndrome, and a new cluster analysis of post electrical injury patients. It formulates a proposal which could be incorporated into future editions of the American Psychiatric Association's Diagnostic and Statistical Manual (DSM). The major neuropsychological consequences include neurocognitive dysfunction, and memory subgroup dysfunction, with ongoing consequences, and sometimes including progressive or delayed psychiatric, cognitive, and/or neurological symptoms. The proposed diagnostic criteria insist on a demonstrated context for the injury, both specifying the shock circumstance, and also physical consequences. It allows for a certain delay in onset of symptoms. It recognizes exclusory conditions. The outcome is a proposal for a DSM classification for the post electrical or lightning injury syndrome. This proposal is considered important for grounding patient treatment, and for further treatment trials. Options for treatment in electrical or lightning injury are summarised, and future trials are foreshadowed.

The author reviews literature pertaining to the efficacy and safety of electroconvulsive therapy (ECT), with emphasis on the controversy concerning whether ECT causes brain damage. ECT does appear to be effective in the treatment of severe depression and possibly mania. The types of memory problems caused by ECT are discussed, and evidence suggests that most of these deficits are transitory. Although most evidence points toward modern ECT not causing brain damage, there are still some findings that raise questions about safety. Ethical issues involving this treatment's use, its availability to the public, and informed consent procedures are discussed.

Although all theories discussed are speculative, the formation of hypotheses is always a starting point in the scientific process. In cases where there is delayed neurological damage with a vascular origin, it is possible that free radicals resulting from oxidative stress may gradually damage spinal vascular endothelial cells, cutting off blood supply, and ending in death of spinal neurons. When the delayed condition is demyelination without vascular damage, it is possible that the free radicals from oxidative stress are formed directly from the lipids found in abundance in myelin cells. The electroporation hypothesis, the formation of additional pores in neurons, may best explain immediate or progressive changes in structure and function after lightning or electrical injury.