When subarachnoid haemorrhage (SAH) occurs, intracranial pressure (ICP) rises which heralds a series of symptoms termed acute ischaemic neurological deficits (AINDs). At the same time, free radicals are generated, and because of deficient scavenging mechanisms in the cerebrospinal fluid (CSF), these free radicals cause lipid peroxidation. Products of lipid peroxidation effect the cerebral arterial wall from the very early stage, probably infiltrating the wall through channels of the wall opening to the CSF space to exhibit inflammatory changes such as subintimal cell proliferation, myonecrosis etc. Lipid peroxidation also leads to degradation of membrane phospholipids, such as phosphatidylcholine (PC) and phosphatidylethanolamine (PE) and to rise in the intracellular level of diacylglycerol (DAG), an intrinsic protein kinase C (PKC) activator. Subsequent release of free arachidonic acid from PC (and/or PE) stimulates the arachidonate cascade which generates various eicosanoids and free radicals contributing to inflammatory changes in the arterial wall. As the intracellular level of DAG is increased, the PKC system is more and more activated, resulting in the development of sustained smooth muscle contraction. This, together with inflammatory changes in the arterial wall, forms the full-fledged picture of delayed cerebral vasospasm, leading to delayed ischaemic neurological deficits (DINDs).