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The inflammatory response after TBI involves both the resident microglia and infiltrating inflammatory cells, primarily phagocytic, CD68+/CD163- macrophages apparently stimulated by large quantities of damaged myelin and markedly elevated inflammatory cytokines including IL1, IL-6, IFN and chemokines with degradation of tight junctions (TJs), cytoskeletal rearrangements and protein promoted by adhesion molecules [14]
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The diagnostic process typically involves: Clinical history taking, focusing on symptoms (fatigue, neurological changes, dietary habits) Physical examination for signs of anaemia or neurological impairment Blood tests including full blood count, serum B12, and often folate levels Additional investigations such as intrinsic factor antibodies or parietal cell antibodies if pernicious anaemia is suspected For borderline results, additional tests like holotranscobalamin (active B12) may be considered NICE guidance recommends that treatment should commence based on clinical presentation if neurological symptoms are present, without waiting for laboratory confirmation, as delays can result in irreversible nerve damage
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