Epileptogenesis in Posttraumatic Epilepsy

Ngadimon, Irma Wati; Zulazmi, Nurul Atiqah; Shaikh, Mohd Farooq

doi:10.1007/978-981-19-3949-5_20-1

Cited by 1 publication

(1 citation statement)

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“…HMGB1 is typically expressed in cell nuclei but can be passively released by necrotic cells or actively secreted by in ammatory cells in response to injury [4]. Extracellular HMGB1 then behaves as a damage-associated molecular pattern (DAMP), triggering further in ammatory signaling through receptors like toll-like receptor 4 (TLR4) and receptors for advanced glycation end products (RAGE) expressed on neurons and glia [5].…”

Section: Introductionmentioning

confidence: 99%

Role of HMGB1 in posttraumatic epilepsy and cognitive decline among traumatic brain injury patients: A prospective longitudinal study in Kuala Lumpur

Ngadimon,

Mohan,

Shaikh

et al. 2024

Preprint

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Background Posttraumatic epilepsy (PTE) and cognitive impairment are severe complications following traumatic brain injury (TBI). Neuroinflammation likely contributes, but the role of specific inflammatory mediators requires clarification. High mobility group box 1 (HMGB1) is an inflammatory cytokine released after brain injury that may be involved. This prospective longitudinal study investigated whether serum HMGB1 levels are associated with PTE development and cognitive decline over 12 months post-TBI.Methods Serum samples were collected from 41 TBI patients at baseline, 6, and 12 months following TBI. HMGB1 was quantified by ELISA alongside interleukin-1β (IL-1β) and tumour necrosis factor-α (TNF-α). Cognitive assessment using validated neuropsychological assessments were performed at 6 and 12 months. The occurrence of PTE was also tracked.Results HMGB1 remained elevated at 12 months post-TBI only in the subgroup (n = 6) that developed PTE (p = 0.026). Higher HMGB1 levels at 12 months correlated with a greater decline in Addenbrooke's Cognitive Examination scores (p < 0.05). Reductions in HMGB1 (p < 0.05), IL-1β (p < 0.05) and TNF-α (p < 0.001) levels from 6 to 12 months correlated with improvements in cognitive scores. Multivariate regression analysis confirmed that HMGB1 level changes was independently associated with cognitive trajectory post-TBI (p = 0.003).Conclusions Persistently elevated HMGB1 post-TBI associates specifically with epileptogenesis and exacerbates cognitive dysfunction. HMGB1 links acute neuroinflammatory responses to chronic neurological outcomes. Longitudinal tracking supports HMGB1-directed interventions as a strategy for improving prognosis after TBI. Additional multicenter studies can clarify HMGB1's utility as a prognostic biomarker.

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Section: Introductionmentioning

confidence: 99%