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  • Disease Description

    Traumatic brain injury occurs when an external mechanical force causes brain dysfunction.

    Traumatic brain injury usually results from a violent blow or jolt to the head or body. An object penetrating the skull, such as a bullet or shattered piece of skull, also can cause traumatic brain injury.

    Mild traumatic brain injury may cause temporary dysfunction of brain cells. More serious traumatic brain injury can result in bruising, torn tissues, bleeding and other physical damage to the brain that can result in long-term complications or death. -


    In 2010 the US Centers for Disease Control and Prevention calculated the rate of traumatic brain injury emergency visits to be 823.7 per 100,000 visits.

    Current Treatments

    Mild traumatic brain injuries usually require no treatment other than rest and over-the-counter pain relievers to treat a headache. However, a person with a mild traumatic brain injury usually needs to be monitored closely at home for any persistent, worsening or new symptoms. He or she also may have follow-up doctor appointments.

    Emergency care for moderate to severe traumatic brain injuries focuses on making sure the person has an adequate oxygen and blood supply, maintaining blood pressure, and preventing any further injury to the head or neck. This can be accomplished with a variety of medications (diuretics, anti-seizure drugs, coma-inducing drugs) or surgical techniques. -

    Evidence for and Proposed Mechanism of Action of Cannabinoids

    Animal models have shown cannabinoids to be neuroprotective after trauma, demonstrating reduced glutamate excitotoxicity, free radical damage, and inflammatory response.3, 4 Other animal studies have shown decreased vasospasm and inhibition of tumor necrosis factor-a, both of which are associated with neuroprotection.5, 6

    Aditionally a 3-year retrospective review of registry data at a surgical intensive care unit of patients sustaining traumatic brain injury demostrated that a positive THC screen is associated with decreased mortality in these adult patients.

    1. Yoles E, Belkin M, Schwartz M. HU-211, a nonpsychotropic cannabinoid, produces short- and long-term neuroprotection after optic nerve axotomy. J Neurotrauma 1996;13:49–57.

    2. Brewter ME, Pop E, Foltz RL, et al. Clinical pharmacokinetics of escalating IV doses of dexanabinol (HU-211), a neuroprotectant agent, in normal volunteers. Int J Clin Pharmacol Ther 1997;35: 361–5.

    3. Durmaz R, Ozsandik A, Sahintu¨rk V, et al. Dexanabinol prevents development of vasospasm in the rat femoral artery model. Neurosurg Rev 2008;31:215–23.

    4. Brewter ME, Pop E, Foltz RL, et al. Clinical pharmacokinetics of escalating IV doses of dexanabinol (HU-211), a neuroprotectant agent, in normal volunteers. Int J Clin Pharmacol Ther 1997;35: 361–5.

    5. Nguyen et al. Effect of Marijuana Use of Outcomes in TBI. Presented at the 25th Annual Scientific Meeting of the Southern California Chapter of the American College of Surgeons, January 17–19, 2014

  • Category
    Critical Ailments
  • Created
    Thursday, 16 March 2017
  • Group admin

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