الفهرس 
Pathophysiology of Brain InjuryOnly 14 pages are availabe for public view
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Abstract
The knowledge of the pathophysiology of traumatic head injury is necessary for adequate and patient-oriented treatment. As the primary insult, which represents the direct mechanical damage, fully treated influenced, target of the treatment is the limitation of the secondary damage. It is influenced by changes in cerebral blood flow, impairment of cerebrovascular autoregulation, cerebral metabolic dysfunction and inadequate cerebral oxygenation. Furthermore, excitotoxic cell damage and inflammation may lead to apoptotic and necrotic cell death. Understanding the multidimensional cascade of secondary brain injury offers differentiated therapeutic options.
Serial clinical examination is not possible in poor-grade patients, so the interest in invasive and non-invasive brain monitoring techniques, including measurements of cerebral perfusion and ICP, venous oximetry (jugular bulb catheters), brain tissue oxygen tension (PbtO2), microdialysis, continuous electroencephalography (EEG), and trans-cranial dopplex (TCD) are used .Results are best interpreted when assessed using multimodality brain monitoring protocols.
Biomarkers would have important applications in diagnosis, prognosis and clinical research of brain injuries. Biochemical markers are considered to be a simple and a rapid diagnostic tool that will immensely facilitate allocation of the major medical resources required to treat brain injuries.
A large number of biomarkers of injury to different cell types and structures within the CNS can be detected in CSF and peripheral blood. S100β protein is predominantly expressed in astrocytes that can be detected in human CSF and serum and is considered as an indicator of astrocytic damage after moderate-to-severe brain injury that reflects blood-brain barrier (BBB) disruption. Neuron Specific Enolase (NSE) is a glycolytic enzyme family (enolases) predominantly located in neurons and neuroectodermal cells and serves as a marker of neuronal damage.
Increases in serum GFAP levels after TBI have been shown to be predictive of elevated intracranial pressure (ICP), reduced mean arterial pressure; low cerebral perfusion pressure, poor Glasgow coma score (GCS), and increased mortality. The myelin basic protein (MBP) is a major protein component of myelin, and is released into the CSF and blood after white matter injury. Tau protein is a microtubule-associated structural protein located within axons. After acute stroke, tau increased in the CSF and serum and serum tau levels correlated to lesion size and severity.
Neuroimaging provides biomarkers of underlying structural and physiological abnormalities in TBI, and these pathological changes occur in regions and within neural systems that give rise to the common types of neurobehavioral and neurocognitive squeals associated with TBI. Neuroimaging methods provide objective biomarkers of injury and damage that need to be incorporated into neuropsychological outcome studies.
Computed tomography (CT) remains the modality of choice for the initial assessment of acute head injury because it is fast, widely available, and highly accurate in the detection of skull fractures and acute intracranial hemorrhage. Magnetic resonance imaging (MRI) is recommended for patients with acute brain injury when the neurological findings are unexplained by computed tomography. Both CT and MRI are highly sensitive for the detection of intracranial hemorrhage, but MRI is much more sensitive than CT in detecting acute ischemic changes and, as such, is more accurate in diagnosing patients presenting with acute focal neurologic deficits.
Conventional MRI sequences (which include T1-and T2-weighted, fluid- attenuated inversion recovery (FLAIR; good for the detection of edema) and gradient recalled echo (GRE; for the detection of blood products) have been clearly shown to be better than CT for the detection of some lesions, particularly traumatic axonal injury, posterior fossa lesions, and brain stem lesions.
Magnetic resonance imaging, including advanced sequences, clearly has much to offer in the detection of injury, the prediction of outcome, and greater understanding of the pathophysiology processes that occur after a brain injury. Diffusion tensor imaging (DTI) is a relatively new MRI modality that capitalizes on the diffusion of water molecules for brain imaging and detects axonal injury and abnormalities in white matter connectivity after mild TBI. A recent MRI development is Susceptibility weighted imaging (SWI), which shows promise for imaging the cerebral vasculature, micro-bleeds, iron deposition, and calcification. Magnetic resonance spectroscopy (MRS) can be used to explore cellular metabolic status and evidence of cellular injury and so may provide important insights in to the complex biochemical and pathophysiological processes after TBI.