Dean - Neuro-Protection after Traumatic Brain Injury: Novel Strategies

Deans' Stroke Musing

Nothing really new here but it does put the problem into more scientific terms than I can regarding the neuronal cascade of death. Vol 3 Issue 6  Neuro-Protection after Traumatic Brain Injury: Novel Strategies. -- Deans' Stroke Musing

I. Introduction

Traumatic brain injury (TBI), also known as acquired brain injury, head injury, or brain injury, causes substantial disability and mortality. Traumatic Brain Injury is a significant public health problem worldwide and is predicted to surpass many diseases as a major cause of death and disability by the year 20201. The majority of TBI cases (60%) are a result of road traffic injuries (RTI), followed by falls (20-30%), and violence (10%)2. In India it is estimated nearly 1.6 million individuals will sustain TBI and seek hospital care annually3.RTI are the leading cause of TBI in India accounting for 45-60% of TBI, and falls account for 20-30% of TBI, paralleling the findings from the Global Burden of Disease Study4. Traumatic brain injury causes mechanical tissue destruction which can be supposed to be the primary mechanism of brain injury that results in neuronal cell death causing cerebral edema and rise in intracranial tension contributing to impaired cerebral vasoregulation, cerebral ischemia/hypoxia and brain damage. Primary injury itself acts as trigger for secondary mechanism responsible for brain injury i.e. the neuronal cell death associated with cerebral ischemia is due to the lack of oxygen and glucose, and may involve the loss of ATP, excitotoxicity of glutamate, oxidative stress, reduced neurotrophic support, and multiple other metabolic stresses5. One major event taking place at the moment of TBI is the massive ionic in flux referred to as traumatic depolarization. Excitatory amino acids may play a vital role in this depolarization. This represents one of the most important mechanisms of diffuse neuronal cell dysfunction and damage associated with TBI. Cerebral edema and associated increased intracranial pressure are the major immediate consequences of TBI that contribute to most early deaths. There are at least two kinds of delayed and progressive pathobiological changes induced by TBI. One of these is axonal damage, which is not the direct consequence of traumatic tissue tearing. Rather, results from complex axolemmal or cyto-skeletal changes, or both, which lead to cyto-skeletal collapse and impairment of axoplasmic transport. The other change in traumatized brains occurs concomitantly with compromised blood brain barrier (BBB) function. Secondary damage in TBI is influenced by changes in cerebral blood flow (CBF), cerebral metabolic dysfunction and inadequate cerebral oxygenation. Excitotoxic cell damage and inflammation may lead to apoptosis6. Furthermore, it is also becoming clear that these secondary insults are, to a significant degree, are preventable. Since multiple derangements starts simultaneously it is essential to have effective neuroprotective therapy to prevent early brain damage. Management of head injury focuses on preventing, detecting and correcting the secondary brain injury after trauma. Duration and severity of such secondary brain damage influences the possible outcome. Unfortunately, numerousneuroprotective drugs have failed to demonstrate beneficial effects in Phase II/III clinical trials, despite previous encouraging preclinical results7. However, some drugs that have been approved for use in the clinic have neuroprotective effects, and these could be used for the treatment and improvement in functional recovery in patients of traumatic brain injury.

Lots more at the link Vol 3 Issue 6 Neuro-Protection after Traumatic Brain Injury: Novel Strategies.

See the original article Neuro-Protection after Traumatic Brain Injury: Novel Strategies
                                  in Dean's Stroke Musing