Optimization of Nutrition after Brain Injury: Mechanistic and Therapeutic Considerations

Abstract

Emerging science continues to establish the detrimental effects of malnutrition in acute neurological diseases such as traumatic brain injury, stroke, status epilepticus and anoxic brain injury. The primary pathological pathways responsible for secondary brain injury include neuroinflammation, catabolism, immune suppression and metabolic failure, and these are exacerbated by malnutrition. Given this, there is growing interest in novel nutritional interventions to promote neurological recovery after acute brain injury. In this review, we will describe how malnutrition impacts the biomolecular mechanisms of secondary brain injury in acute neurological disorders, and how nutritional status can be optimized in both pediatric and adult populations. We will further highlight emerging therapeutic approaches, including specialized diets that aim to resolve neuroinflammation, immunodeficiency and metabolic crisis, by providing pre-clinical and clinical evidence that their use promotes neurologic recovery. Using nutrition as a targeted treatment is appealing for several reasons that will be discussed. Given the high mortality and both short- and long-term morbidity associated with acute brain injuries, novel translational and clinical approaches are needed.

Keywords: anoxic brain injury; malnutrition; neuroinflammation; nutrition; status epilepticus; stroke; traumatic brain injury.

Figure 1

Conceptual schematic of the influence of nutritional status on mechanisms of secondary brain injury and recovery after acute brain injury.

Figure 2

Interconnected mechanisms through which ketogenic diet confers broad neuroprotective effects in models of brain injury.

Figure 3

Generation and Sites of Activity of Eicosanoid Lipids. PL: phospholipid transporter, PLA2: phospholipase A2, MRP: multidrug resistance protein transporter, CNS: central nervous system.