Towards solving enigmas in electrical injury

The paper by Park and colleagues in the previous issue of Critical Care highlights vascular changes in electrical injury and finds them to be relatively long-lasting and significant. This finding is consistent with long-lasting disability seen clinically in electrically injured patients. Furthermore, the authors report that the changes seen in the shocked part of the body are accompanied by similar changes that are measurable in other parts of the body but that are not involved with electric current. This latter finding is of significant importance. A psychological syndrome - consistent and predictable - exists following an electrical injury. The causation is enigmatic. Recent psychiatric research indicates the importance of circulating cortisol and brain-derived neurotrophic factor (BDNF), which causes loss of hippocampal volume, in the genesis of depression. This psychiatric research has stimulated a speculative theory of the genesis of the psychological effects of electric shock. The paper by Park and colleagues is circumstantial support for the possibility that such a process is real and available.


Introduction
Th is writer was most interested to see the paper by Park and colleagues [1] in the previous issue of Critical Care. It represents a useful addition to the theory of electrical injury and tends to support speculation that has recently been advanced in regard to causation of the injury.
Consequences of electrical injury have always been enig matic. Whereas the magnitude and pathway of the current can be predicted fairly readily and descriptions of the damage that occurs can be given, the tissue and biochemical changes that underlie much of the symptomatology are very poorly understood. Furthermore, causes of the long-term consequences of the injury have not been elucidated.

Electrical injury
Two groups of fi ndings characterize the injury. Firstly, physical fi ndings of pain, paresthesia, weakness, and easy fatigability are seen in the limbs aff ected by the passage of current. Th e easy fatigability is especially problematic -'I haven't got the stamina I used to; I use the limb for a while, and then pay for it for days' . Typically, patients are referred to neurologists, but gross testing is usually normal. Neurologists most often conclude that there has been no neurological injury and a number, therefore, will say that there has been no injury at all. Th is grossly disadvantages patients, and the present author has wondered whether the site of injury, possibly at the neuromuscular junction or the sensory nerve terminal, is too fi ne to be demon strated by gross testing. Secondly, there is a very commonly and consistently reported syndrome of long-lasting psycho logical disability [2][3][4][5][6][7]. It is this disability that can be the most distressing and the most limiting for a patient [8].

The enigma of causation
Th e enigma, especially for the psychological component, is that there seems to be a production of symptoms, in this case arising from the brain, quite remote from the passage of current. How injury in one part of the body can aff ect -quite organically -another part, including the brain, is an enigma.
Th e Critical Care paper refocuses attention on vascular abnormalities and demonstrates signifi cant and longlasting abnormalities in vascular function. Th e genesis of these, it seems, centers on the vascular endothelium and damage to it. It is not quite clear, though, just what is involved -the endothelium or perhaps the nerva vaso rum or indeed other structures. Th e vascular abnormalities are, in themselves, important as far as the fi rst group of symptoms is concerned. One hopes to see further work in derived areas. Certainly, research on any changes in the results could take into account any change with signifi cant exercise, and this may shed light on the fatigability mentioned above. Also, more identi fi cation of the particular vasoactive mediators of the vascular fi ndings would be important. Th e physiology of the change in reactivity would readily assist and may lead us to a means of relieving it.

Abstract
The paper by Park and colleagues in the previous issue of Critical Care highlights vascular changes in electrical injury and fi nds them to be relatively longlasting and signifi cant. This fi nding is consistent with long-lasting disability seen clinically in electrically injured patients. Furthermore, the authors report that the changes seen in the shocked part of the body are accompanied by similar changes that are measurable in other parts of the body but that are not involved with electric current. This latter fi nding is of signifi cant importance. A psychological syndrome -consistent and predictable -exists following an electrical injury. The causation is enigmatic. Recent psychiatric research indicates the importance of circulating cortisol and brain-derived neurotrophic factor (BDNF), which causes loss of hippocampal volume, in the genesis of depression. This psychiatric research has stimulated a speculative theory of the genesis of the psychological eff ects of electric shock. The paper by Park and colleagues is circumstantial support for the possibility that such a process is real and available.
But further observations made in the paper are interesting. In particular, the observation that the opposite limb was partially aff ected in the same way as the shocked limb is a fascinating fi nding and is perhaps of fundamental importance.

Causation in electrical injury
Th is writer has speculated on the possible causation of remote injuries, especially the infl uence on the brain and cerebral function, with the psychological symptoms in mind. Th e author has speculated on possible causative mechanisms and these may be many. Th e major mechanism might be, for example, a neurohumoral mechanism, in which the injured part or the injury process causes peripheral release of some neuroactive substance, which in turn acts on the brain. Or the major mechanism may be a reverse conduction mechanism. It is known that peripheral activation of pain receptors activates a complex set of interactions at the spinal cord level (turning acute pain into a chronic pain syndrome in which 'pain is the disease' rather than its cause), and reverse conduction superiorly via the cord to the brain may exist. No doubt, there may be several other mechanisms.

Psychiatric fi ndings
Solving this enigma has not been attempted. One thought [9] invoking the release of humoral substance(s) has been advanced, bearing in mind recent psychiatric research indicating the importance of cortisol and brain-derived neurotrophic factor (BDNF) in the genesis of, in particular, traumatic depression [10]. Consequent loss of hippocampal volume is seen in depression [11][12][13][14], and there is some evidence of this fi nding specifi cally in electrical injury [15].
Th e fi nding of vascular reactivity, more general than just within the shocked limb, may add some support to a neurohumoral mechanism. Although the fi nding is mentioned only in passing, the present writer fi nds it to be of signifi cance. One might hope to see further research that extends the present study and searches for the substance concerned and its mechanism of action. In addition, any correlation with hippocampal size in relation to the shock -as well as possibly other cerebral changes -would be of great interest. Th is writer has indeed used the term post-electric shock syndrome to describe the constellation that is seen. Th e incorporation of the syndrome into the Diagnostic and Statistical Manual of Mental Disorders would be satisfying. It may be that we are moving closer to an explanation.

Conclusions
Th e paper by Park and colleagues [1] is to be commended, not only for its fi ndings but also for the pointers it gives to further important research.