We have recently been looking after a complicated trauma patient with brain and chest injuries. The possibility was raised that some of the abnormal brain physiology we saw was due to spreading depolarisation. This has recently been discussed in Nature Reviews Neurology, and by coincidence it is in the same issue as a review by our neurosurgical colleagues on chronic subdural haematoma management.

Spreading depolarisation is an entirely different process to epilepsy and the two studies referred to in the Nature editorial should give us pause for thought about whether we should consider this diagnosis more frequently. The picture above is from a review in Nature Medicine which is well worth reading.

Spreading depolarisation describes abrupt sustained depolarization of neurons which, via multiple cortical depolarisations, lead to local depletion of brain glucose and cortical ischemia. Clear electrophysiological evidence demonstrates that spreading depolarisations occur frequently in patients with subarachnoid hemorrhage, ischemic stroke, intracerebral hemorrhage and traumatic brain injury.

Diagnosis and treatment algorithms have yet to be established. Detection remains difficult – continuous EEG (ESICM guidelines) may help but we are not yet clear how to use it to detect spreading depolarisations. One of the papers reviewed in the NRN piece suggests it may be feasible, however.

Ketamine has been shown to be effective in one study (editorial, correspondence) of 58 patients. This showed that spreading depolarisation is frequent and is independently associated with worse outcome. Interestingly this study demonstrated that around 50% of severe TBI patients exhibited evidence of spreading depolarisations, diagnosed by electrocorticography (placing electrodes directly onto the surface of the brain) in patients following decompressive craniectomy, a diagnostic approach which is not available to the majority of our severe TBI patients.

While awaiting further characterisation of the pathological process we need to be mindful for the potential for this process to occur in our comatose patients with acute brain syndromes. Empirical treatment is a tricker discussion but a trial of ketamine in the face of dire physiology fitting with spreading depolarisation deserves consideration.


Co-operative Study on Brain Injury Depolsarisations (http://www.cosbid.org/)


Review in Journal of Cerebral Blood Flow and Metabolism.

Review in Future Neurology focussing on migraine and stroke.