Neuro-Inflammation Modulation and Post-Traumatic Brain Injury Lesions: From Bench to Bed-Side

Abstract

Head trauma is the most common cause of disability in young adults. Known as a silent epidemic, it can cause a mosaic of symptoms, whether neurological (sensory–motor deficits), psychiatric (depressive and anxiety symptoms), or somatic (vertigo, tinnitus, phosphenes). Furthermore, cranial trauma (CT) in children presents several particularities in terms of epidemiology, mechanism, and physiopathology—notably linked to the attack of an immature organ. As in adults, head trauma in children can have lifelong repercussions and can cause social and family isolation, difficulties at school, and, later, socio-professional adversity. Improving management of the pre-hospital and rehabilitation course of these patients reduces secondary morbidity and mortality, but often not without long-term disability. One hypothesized contributor to this process is chronic neuroinflammation, which could accompany primary lesions and facilitate their development into tertiary lesions. Neuroinflammation is a complex process involving different actors such as glial cells (astrocytes, microglia, oligodendrocytes), the permeability of the blood–brain barrier, excitotoxicity, production of oxygen derivatives, cytokine release, tissue damage, and neuronal death. Several studies have investigated the effect of various treatments on the neuroinflammatory response in traumatic brain injury in vitro and in animal and human models. The aim of this review is to examine the various anti-inflammatory therapies that have been implemented.

Nicotinamide mononucleotides alleviated neurological impairment via anti-neuroinflammation in traumatic brain injury

“…TBI is initially caused by mechanical damage, but its secondary damage is complex and diverse. Substantial evidence suggested that cellular cascade of inflammation participates in secondary brain injury [36][37][38][39]. However, short-term inflammation after TBI is protective, while long-term, intense inflammation can damage the brain [40].…”

Relationship between medical history and multiple sclerosis: A-case-control study

“…Neuronal inflammation is a complex process that involves a variety of factors, including tissue damage, blood-brain barrier permeability, production of reactive oxygen species, and the release of cytokines. [16] Glial cells, such as oligodendrocytes, astrocytes, and microglia, are also involved in this process, which can manifest in both local and systemic forms. Local glial activation can lead to a systemic immune response.…”

The Putative Role of Neuroinflammation in the Interaction between Traumatic Brain Injuries, Sleep, Pain and Other Neuropsychiatric Outcomes: A State-of-the-Art Review

“…Non-pharmacological integrative approaches including mind/body therapies such as yoga, breathing exercises, meditation, all of them being associated with sleep quality improvement as well, have also been demonstrated to reduce pro-inflammatory cytokines and have proved some positive effects on depression, anxiety, cognition, and pain [178]. Moreover, several plant-based interventions (herbs/spices) currently under investigation [179]. While their non-invasiveness and harmless nature make them appealing as supportive therapy, more research is needed before obtaining any firm conclusion regarding their efficacy.…”