**1. Introduction**

Aneurysmal subarachnoid hemorrhage (SAH) is a complex condition with an intricate and poorly understood pathophysiology. Increasing evidence strongly suggests that neuroinflammation plays a critical role after SAH, but conventional anti-inflammatory treatments have failed to improve clinical outcome [1]. Clinical research on SAH has mainly focused on delayed cerebral ischemia (DCI); however, DCI does not encompass the entire spectrum of pathological and clinical manifestations of SAH [2–4]. Although cerebral infarction is associated with poor clinical outcome and death after SAH, a significant proportion of SAH patients without cerebral infarction suffer from cognitive deficits and mood disorders and a reduced ability for activities of daily living and working, even in the long term [5, 6]. The absence of a close correlation between DCI and functional recovery indicates an

ongoing pathophysiological process has been overlooked in SAH. The failure of the recent major NEWTON 2 clinical trial, of sustained intraventricular release of nimodipine, is the latest in a series of unsuccessful phase 3 randomized controlled trials (RCTs) to improve clinical outcome after SAH and further reinforces the need to identify novel therapeutic strategies [7, 8].

Nutrition is essential to human health, and appropriate nutritional support is currently considered a standard of care for critically ill patients. Malnutrition including depletion of essential micronutrients—frequently occurs among critically ill patients and is associated with an increased risk of morbimortality [9]. However, the clinical relevance of key nutrient deficiencies in acute neurological illnesses has not been thoroughly investigated. EPA and DHA are essential constituents of endothelial and neuronal membranes, respectively, and also the precursors of key mediators involved in resolution of inflammation and endogenous neuroprotection [10, 11]. Although massive loss of brain DHA in SAH patients was first reported over 15 years ago, the pathological significance of this process and the role of inflammation resolution following SAH have largely been ignored [11, 12]. Therapeutic interventions aimed at stimulating inflammation resolution and recovering the homeostasis of the brain and other vital organs after SAH could improve patients' functional outcome [13].

This chapter provides an overview of the potentially harmful consequences of selective deficiency of omega-3 FAs on brain structure and function in SAH patients. Moreover, given the possible clinical relevance to SAH and the growth and rupture of intracranial aneurysms (IAs), we provide a detailed discussion of recent findings on the role of omega-3 FAs in resolution of inflammation, with a focus on brain homeostasis.
