Nearly 60 years after its first description by Leao, we remain uncertain of the biological role of a phenomenon that seems to be at times beneficial and a normal response of the brain, and at other times, in the case of PIDs, harmful, principally under conditions of ischaemia.
As one speculation, perhaps the apparent paradox can be explained if we see CSD as reflecting the operation of well-conserved intercellular communications in the brain - serving to protect the brain against inflammation and infection. We do well to bear in mind that our relative mastery of infection in the central nervous system - incomplete and perhaps temporary - is only very recent on the time scale on which evolution operates, and there has probably been more survival value for our own and other vertebrate species in effective responses to CNS infection before and during reproductive life than in avoidance of the cost of aberrant, deleterious operation of the same mechanism in the ageing or irretrievably injured brain.
A quite different speculative view of CSD emerges from the recent rapid growth in our knowledge of the physiological role of astrocytes in modulating synaptic function, to the extent that the synapse is now seen as a tripartite entity - pre- and post-synapse, and astrocyte . Perhaps the probability of CSD (variable depending on glia: neuron ratio and other factors) is an inevitable consequence of this arrangement and of the intimate communication between astrocytes through their gap junctions.
We may also speculate that the depolarisation events that we are able to observe propagating across the cortex with current methods and stimuli may occur much more frequently than we can presently detect, but restricted to microfoci of grey matter, not propagating widely, and below the limits of the available resolution and sensitivity. Results of imaging work with glial and organotypic cultures seem to support this possibility.
As the methods of molecular biology expand, so does the range of gene responses to CSD that have been documented, and it is by no means yet certain which are the most significant. However, it does seem likely that we shall learn as much about the biological significance of CSD from greater knowledge of the expression cascades that it initiates as from the longer-established neurophysiological approaches to CSD.
For neurosurgeons studying and caring for acute brain injury, the only certainties are that PIDs, when identified, should be controlled, and that there is more to be learned about the effects of CSD on the human brain before we can reach a view on whether to attempt to control it.
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