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Possible causative mechanisms of CNS inflammation and neuroglial reactivity include direct effects through injury or infection of the brain, reactivation of endogenous microbial reservoirs in CNS cells, autoimmune reactivity with specific neural, glial, or immune system targets, repetitive mechanical strain, cerebrovascular hypertension, cerebral hypoperfusion and/or ischemia, recognition of danger-associated molecular patterns (DAMP), vagal dysfunction, norepinephrine or angiotensin II overload, or, generally, exposure to chronic stress (VanElzakker, 2013
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Early and accurate diagnosis is important because prompt treatment can improve the prognosis of HCU and prevent irreversible complications (16,17)
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