One of the most common consequences of spontaneous subarachnoid haemorrhage is delayed cerebral ischemia (DCI), which is caused by cortical spreading depolarizations (CSDs). Waves of neuronal and glial depolarizations in the cortex cause a disruption of neuronal ionic homeostasis, resulting in potassium efflux and sodium and calcium inflow. After aneurysmal subarachnoid haemorrhage, CSDs in the cerebral cortex are involved in the aetiology of both acute and delayed cerebral ischemia (aSAH). CSDs cause microvascular vasoconstriction and, as a result, hypoperfusion and the propagation of ischemia in injured brain areas and brain areas at risk, such as those next to subarachnoid haemorrhage (SAH). A number of research have been conducted in order to reduce secondary damage that develop hours to days following an acute insult. Due to its pharmacodynamic effects at the cellular level, ketamine, which was previously prohibited in the neurosurgical population due to the possibility of producing intracranial hypertension, has re-emerged as a possible neuroprotective medication. Anti-inflammatory processes, as well as controls over microthrombosis and cell apoptosis, as well as modification of brain excitotoxicity and CSDs, are among these effects. Retrospective studies corroborated the benefits of ketamine on CSD control and, as a result, DCI in patients with SAH, but no change in clinical outcome was observed. In prospective randomised studies, the effect of ketamine on the occurrence/development of DCI needs to be established.
Author (S) Details
Leandro Custódio do Amaral
Neurosurgeon, Rede Mater Dei de Saúde, Hospital Metropolitano Odilon Behrens and Fundação Benjamin Guimarães, Hospital da Baleia, Brazil.
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