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.
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