Military traumatic brain injury: a challenge straddling neurology and psychiatry

Abstract

Military psychiatry, a new subcategory of psychiatry, has become an invaluable, intangible effect of the war. In this review, we begin by examining related military research, summarizing the related epidemiological data, neuropathology, and the research achievements of diagnosis and treatment technology, and discussing its comorbidity and sequelae. To date, advances in neuroimaging and molecular biology have greatly boosted the studies on military traumatic brain injury (TBI). In particular, in terms of pathophysiological mechanisms, several preclinical studies have identified abnormal protein accumulation, blood-brain barrier damage, and brain metabolism abnormalities involved in the development of TBI. As an important concept in the field of psychiatry, TBI is based on organic injury, which is largely different from many other mental disorders. Therefore, military TBI is both neuropathic and psychopathic, and is an emerging challenge at the intersection of neurology and psychiatry.

Keywords: Comorbidity; Diagnosis; Military; Shellshock; Traumatic brain injury; Treatment.

Fig. 1

Relationship between concussion, blast injury, post-traumatic brain sequelae and chronic traumatic encephalopathy (CTE). The broad definition of military TBI can be divided into concussion, blast injury and traumatic sequelae. Among them, concussion can directly or indirectly cause damage of neuronal axon, congestion, haemorrhage, cell oedema and hyperphosphorylation of Tau protein. The blast injury mainly resulted in congestion, haemorrhage and cell oedema. Blast injuries can be the cause of concussion and traumatic sequelae. Concussions can also cause traumatic sequelae. The main cause of CTE is traumatic sequelae. Blast injury can also lead to CTE to a certain extent, while concussion has little relationship with CTE. The pathological manifestations of CTE are mainly congestion, haemorrhage, cell oedema, and hyperphosphorylation of Tau protein. Macroscopically, both military and civilian TBI can be the cause of CTE. Solid black and red arrows indicate associations of pathological mechanisms or clinical manifestations, dashed black arrows indicate relationships among subtypes, and dashed red arrows indicate possible aetiology of CTE. mTBI mild traumatic brain injury

Fig. 2

Neuroinflammatory process after the occurrence of TBI and its long-term consequences. After TBI occurs, it can lead to a range of primary (e.g., damage to blood vessels and cell membranes) or secondary (e.g., ion imbalance, calcium overload, and mitochondrial dysfunction) injuries. These injuries together lead to mitochondrial stress cytotoxicity and secondary damage to the vascular system. Subsequently, astrocytes and microglia are activated, and immune cells in the blood vessels are recruited. Microglia can differentiate into M1 and M2 phenotypes, which can produce pro-inflammatory or anti-inflammatory cytokines in response to cytokines such as interferon-γ (IFN-γ), interleukin-4 (IL-4) and IL-13. Microglia itself also divide and play a role in phagocytosis. These neuroinflammatory mechanisms can promote the formation of new synapses, which is conducive to the self-repair of the nervous system. Long-term chronic inflammation can also lead to neurodegeneration, resulting in a series of irreversible pathological changes (such as Tau protein hyperphosphorylation, Aβ plaque formation, TDP-43 and α -synuclein deposition, etc.). Over the years, neurodegeneration can eventually lead to dementia. Solid black and red arrows indicate associations of pathological mechanisms or clinical manifestations, dashed black arrows indicate relationships among subtypes, and dashed red arrows indicate possible aetiology of CTE. TBI traumatic brain injury, CNS central nervous system, Aβ amyloid-β, TDP-43 trans-reaction DNA-binding protein 43 kD