Fluid Biomarkers of Neuro-Glial Injury in Human Status Epilepticus: A Systematic Review

Giovannini, Giada; Meletti, Stefano

doi:10.3390/ijms241512519

Cited by 7 publications

(2 citation statements)

References 105 publications

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“…Comparison of six serum biomarkers (S100B, NSE, GFAP, UCH-L1, NFL, and t-tau) within 24 h of TBI found that GFAP had the highest discrimination for predicting CT abnormalities with a 99% likelihood of better discrimination. However, in mild TBI, the discrimination increased from 0.84 to 0.89; although this was statistically significant, it is only a small increase, with unknown clinical significance [49].…”

Section: Monitoringmentioning

confidence: 79%

Clinical Management in Traumatic Brain Injury

Yan,

Torpey,

Morrisroe

et al. 2024

Biomedicines

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Traumatic brain injury is one of the leading causes of morbidity and mortality worldwide and is one of the major public healthcare burdens in the US, with millions of patients suffering from the traumatic brain injury itself (approximately 1.6 million/year) or its repercussions (2–6 million patients with disabilities). The severity of traumatic brain injury can range from mild transient neurological dysfunction or impairment to severe profound disability that leaves patients completely non-functional. Indications for treatment differ based on the injury’s severity, but one of the goals of early treatment is to prevent secondary brain injury. Hemodynamic stability, monitoring and treatment of intracranial pressure, maintenance of cerebral perfusion pressure, support of adequate oxygenation and ventilation, administration of hyperosmolar agents and/or sedatives, nutritional support, and seizure prophylaxis are the mainstays of medical treatment for severe traumatic brain injury. Surgical management options include decompressive craniectomy or cerebrospinal fluid drainage via the insertion of an external ventricular drain. Several emerging treatment modalities are being investigated, such as anti-excitotoxic agents, anti-ischemic and cerebral dysregulation agents, S100B protein, erythropoietin, endogenous neuroprotectors, anti-inflammatory agents, and stem cell and neuronal restoration agents, among others.

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Section: Monitoringmentioning

confidence: 79%

Clinical Management in Traumatic Brain Injury

Yan,

Torpey,

Morrisroe

et al. 2024

Biomedicines

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“…Some shortcomings need to be acknowledged, however. Clinical variables associated with the risk of seizure occurrence after SE, such as the time to first‐line treatment initiation, 21 peri‐ictal MRI abnormalities, 30 and fluid biomarkers of neurodegeneration and neuroinflammation, 31 were not available for all subjects and were not included. One major flaw was that it was not possible to explore in depth the potential impact of the treatment with ASMs, thereby limiting the generalizability of the results.…”

Section: Discussionmentioning

confidence: 99%

The risk of unprovoked seizure occurrence after status epilepticus in adults

Lattanzi,

Orlandi,

Giovannini

et al. 2024

Epilepsia

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ObjectiveStatus epilepticus (SE) may lead to long‐term consequences. This study evaluated the risk and predictors of seizure occurrence after SE, with a focus on SE due to acute symptomatic etiologies.MethodsProspectively collected data about adults surviving a first non‐hypoxic SE were reviewed. The outcome was the occurrence of unprovoked seizures during the follow‐up. Kaplan–Meier survival curve analysis and log‐rank test were used to analyze the time to seizure occurrence and determine the statistical significance between etiological groups. Three subcategories within acute etiology were considered according to the presence of the following: (1) structural lesion (acute‐primary); (2) brain involvement during systemic disorders (acute‐secondary); and (3) drug or alcohol intoxication/withdrawal (acute‐toxic). Cox proportional hazards model was adopted to estimate hazard ratios (HRs) with the 95% confidence intervals (CIs).ResultsTwo hundreds fifty‐seven individuals were included. Fifty‐four subjects (21.0%) developed seizures after a median of 9.9 (interquartile range 4.3–21.7) months after SE. The estimated 1‐, 2‐, and 5‐year rates of seizure occurrence according to acute SE etiologies were 19.4%, 23.4%, and 30.1%, respectively, for acute‐primary central nervous system (CNS) pathology; 2.2%, 2.2%, and 8.7%, respectively, for acute‐secondary CNS pathology; and 0%, 9.1%, and 9.1%, respectively, for acute‐toxic causes. Five‐year rates of seizure occurrence for non‐acute SE causes were 33.9% for remote, 65.7% for progressive, and 25.9% for unknown etiologies. In multivariate Cox regression model, progressive etiology (adjusted HR [adjHR] 2.27, 95% CI 1.12–4.58), SE with prominent motor phenomena evolving in non‐convulsive SE (adjHR 3.17, 95% CI 1.38–7.25), and non‐convulsive SE (adjHR 2.38, 95% CI 1.16–4.90) were independently associated with higher hazards of unprovoked seizures. Older people (adjHR .98, 95% CI .96–.99) and people with SE due to acute‐secondary CNS pathology (adjHR .18, 95% CI .04–.82) were at decreased risk of seizure occurrence.SignificanceSE carries a risk of subsequent seizures. Both the underlying cause and epileptogenic effects of SE are likely to contribute.

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