Traumatic brain injury (TBI) is one of the most common and financially devastating health problems in our society. There are an estimated 1.5 million cases of TBI annually in the United States, with at least 235,000 resultant hospitalizations and approximately 50,000 fatalities per year.1 More than 5 million persons in the United States are TBI survivors. Once the acute care period has ended, many TBI patients are left with motor, cognitive, or emotional dysfunction as a result of their injury.2 Although several therapies have shown benefit in preclinical models, there has been a notable failure of clinical translation, with a large number of late phase II and III trials failing to confirm benefit in human subjects. Thus, the treatment of TBI remains largely supportive, directed toward management of cerebral edema and intracranial hypertension via temporizing measures, such as administration of osmotic agents, hyperventilation, and ventricular drainage.3 None of these interventions have been definitively demonstrated to improve long-term functional outcome.4 The failure of preclinical therapies to translate into clinical benefit may derive from the heterogeneity of TBI pathology, which includes diffuse axonal injury, cerebral contusion, intracerebral hemorrhage (ICH), subarachnoid hemorrhage (SAH), and extraparenchymal hemorrhage. These primary insults are exacerbated by a secondary neuroinflammatory cascade of cerebral hypoperfusion and ischemia, oxidative stress, cerebral edema, and intracranial hypertension.
The 3-hydroxy-3-methylglutaryl coenzyme A (HMG CoA) reductase inhibitors, also known as “statins,” are an ideal candidate therapy for acute brain injury. Statins influence multiple mechanisms of acute and secondary neuronal injury; they have endothelial and vasoactive properties, as well as anti-oxidant, anti-inflammatory, anti-excitotoxicity, and anti-thrombotic effects. Statin treatment would be practical to implement in TBI because statins have wide availability, Food and Drug Administration approval, a favorable adverse event profile, and a track record of safety in critically ill populations.Preclinical data supports the benefit of statins in many of these disease processes include brain ischemia ,intracranial hemorrhage, SAH.clinical trials clearly show a benefit of statins in Ischemic stroke, SAH, TBI, alzaimeres pateints.
This study investigated the effects of simvastatin in moderate traumatic brain injury to improve GCS,GOS and protection of formation of delayed brain contusion , delayed ischemic lesions and decrease time of hematoma resorption,mortality complication like DVT,Pneumonia. In this study, patients in the randomized groups are divided into (A&B) ( Simvastatin and placebo), study done constantly and visited patients on days 1, 3 and 10, discharge time, and at months 1, 3 and 6 the information collected. Patients with a factor of between 8-12 GCS and patients GCS less than 8 and greater than 12 are excluded. Simvastatin dose of 80 mg daily for ten days to patient data and weekly with alkaline phosphate for complication myositis check. The primary outcome include GCS on days 1, 3 and 10 and GOS on mount 1,3,6 Q