Utility Of Neuron Specific Enolase in Traumatic Brain Injury in Assessing Severity and Outcome in Neuro-Critical Patients. An Observational Study

Introduction:

Traumatic brain injury (Ischemic stroke) is a major global health issue, ranking as the second leading cause of death and the primary cause of adult disability worldwide. Given the broad range of possible outcomes for patients—which can vary from complete recovery to death—and the availability of various treatment options, identifying prognostic factors that can quickly and accurately predict clinical outcomes is crucial.

NSE protein is in the cytoplasm of neurons and plays a role in energy metabolism. As NSE has significant use in several neurological disorders, such as head injury, intracerebral haemorrhage, cardiac arrest, anoxic encephalopathy, encephalitis, and status epilepticus . Recent studies have investigated its relationship with ischemic stroke and its characteristics, such as infarcted brain volume, the severity of clinical manifestations, and short- and long-term prognosis. Despite these efforts, current research on the effectiveness of NSE as a blood biomarker for acute ischemic stroke has not provided conclusive results, and its impact on the outcomes of these patients remains poorly understood.

Neuron-specific enolase (NSE) is an essential protein most recognized for its enzymatic properties during the late stages of glycolysis. NSE has a myriad of other cellular functions and acts primarily on neuronal and neuroendocrine tissues. Under normal physiological conditions, NSE is not secreted into extracellular space, however, during cellular injury or death, NSE can be both leaked into the extracellular space and upregulated in response to the damaged neuronal tissue. NSE has been used as a biomarker in numerous pathological conditions in humans. For decades, NSE assessment has been notable for its usefulness in patients who have certain neuroendocrine malignancies or those who suffer from hypoxic brain damage due to cardiac arrest or ischemic stroke. Additionally, as scientists and clinicians work to risk stratify and guide prognosis in traumatic brain and spinal cord injuries, NSE assessment has shown promise as a biomarker. Though elevated serum levels of NSE in patients after mild traumatic brain injury (TBI) have been reported in multiple studies, the single use of NSE for risk stratification or outcome prognosis in mild TBI appears to have limitations. In severe TBI, higher NSE concentrations are associated with elevated intracranial pressure, severity of traumatic brain damage, adverse outcomes, and mortality. Albeit promising, there remains a lack of standardization with regards to timing of the blood sampling, cutoff ranges and assays when utilizing NSE as a biomarker for traumatic brain injury.

An ideal blood biomarker for stroke should provide reliable results, enable fast diagnosis, and be readily accessible for practical use. Neuron-specific enolase (NSE), an enzyme released after neuronal damage, has been studied as a marker for brain injury, including cerebral infarction

 Aims & objective:

To assess neuron specific enolase as a biomarker to evaluate severity of brain damage and prediction of outcome in neurocritical patients with traumatic brain damage.

Material and methods:

After institutional ethical clearance, this observational study will include 100 patients with traumatic brain injury in this study. Patients presenting in our icu within 72hours of onset of symptoms will be included in our study. Neuron specific enolase will be done for such patients and will be repeated after 72 hours again.

Following parameters will be studied:

1)     correlation between NSE levels and injury severity, assessed by NIHSS score at icu admission

2)     affected brain volume versus NSE levels : In this method, the infarcts size is calculated as follows: the area (A × B) of the infarct size is measured at the plane with the largest infarct expansion; this area is then multiplied by the number of scan slices on which the infarct is visible multiplied by the slice thickness (C); the resulting volume is then divided by 2

**3)**relationship between functional outcome and NSE levels. 30 days post-discharge outcome with the NSE levels. We will also try to ascertain any cutoff value of the NSE level to predict mortality at 48 h after admission.