Dexanabinol in Severe Traumatic Brain Injury
Summary
Each year a large number of patients are hospitalized at Shock Trauma Centers with severe head injuries. Bleeding into and swelling of these patients' brains may cause compression of vital structures, disability and death. Sometimes surgery is needed. Unfortunately, the investigators have no medication to treat the bad effects of head trauma. Part of the brain damage is due to toxic chemicals (including one called glutamate) that are released by the damaged nerves. Dexanabinol may prevent some of the bad effects of glutamate on the brain and may protect the brain against uncontrollable swelling and death.
Description
Dexanabinol is a synthetic, non-psychotropic cannabinoid derivative that because of its dextro-configuration is compatible with activation of cannabinoid receptors in the brain. It combines the ability to block NMDA receptors and neuroinflammatory cascades in the same molecule. Dexanabinol scavenges free radicals, protects neurons from toxicity of free radical generators and inhibits lipopolysaccharide-induced production of prostaglandin E2, NO and TNF-a by macrophages in culture.
Study Design
Allocation: Randomized, Control: Placebo Control, Endpoint Classification: Safety/Efficacy Study, Intervention Model: Parallel Assignment, Masking: Double-Blind, Primary Purpose: Treatment
Conditions
Traumatic Brain Injury
Intervention
Dexanabinol
Status
Completed
Source
Pharmos
Results (where available)
Links
- Source: http://clinicaltrials.gov/show/NCT00129857
- Information obtained from ClinicalTrials.gov on July 15, 2010
Medical and Biotech [MESH] Definitions
Coma, Post-head Injury
Prolonged unconsciousness from which the individual cannot be aroused, associated with traumatic injuries to the BRAIN. This may be defined as unconsciousness persisting for 6 hours or longer. Coma results from injury to both cerebral hemispheres or the RETICULAR FORMATION of the BRAIN STEM. Contributing mechanisms include DIFFUSE AXONAL INJURY and BRAIN EDEMA. (From J Neurotrauma 1997 Oct;14(10):699-713)
Brain Injuries
Acute and chronic (see also BRAIN INJURIES, CHRONIC) injuries to the brain, including the cerebral hemispheres, CEREBELLUM, and BRAIN STEM. Clinical manifestations depend on the nature of injury. Diffuse trauma to the brain is frequently associated with DIFFUSE AXONAL INJURY or COMA, POST-TRAUMATIC. Localized injuries may be associated with NEUROBEHAVIORAL MANIFESTATIONS; HEMIPARESIS, or other focal neurologic deficits.
Head Injuries, Closed
Traumatic injuries to the cranium where the integrity of the skull is not compromised and no bone fragments or other objects penetrate the skull and dura mater. This frequently results in mechanical injury being transmitted to intracranial structures which may produce traumatic brain injuries, hemorrhage, or cranial nerve injury. (From Rowland, Merritt's Textbook of Neurology, 9th ed, p417)
Brain Hemorrhage, Traumatic
Bleeding within the brain as a result of penetrating and nonpenetrating CRANIOCEREBRAL TRAUMA. Traumatically induced hemorrhages may occur in any area of the brain, including the CEREBRUM; BRAIN STEM (see BRAIN STEM HEMORRHAGE, TRAUMATIC); and CEREBELLUM.
Brain Stem Hemorrhage, Traumatic
Bleeding into structures of BRAIN STEM, including the MIDBRAIN; PONS; or MEDULLA OBLONGATA, as the result of CRANIOCEREBRAL TRAUMA. DIFFUSE AXONAL INJURY is commonly associated. Clinical manifestations may include OCULAR MOTILITY DISORDERS; ATAXIA; PARALYSIS; PERSISTENT VEGETATIVE STATE; and COMA.
Clinical Trials
Multimodal Neurodiagnostic Imaging of Traumatic Brain Injury and Post-Traumatic Stress Disorder
The purpose of this study is to determine whether the brains of persons with and without traumatic brain injury differ in a meaningful way when advanced technology images of the brain are...
Amantadine and Temporal Discrimination in Patients With Traumatic Brain Injury (TBI)
The study will explore the neurocognitive effect of four weeks of treatment with amantadine versus placebo in patients with traumatic brain injury using the Interval Bisection Timing Task....
Preventing Epilepsy After Traumatic Brain Injury With Topiramate
Our hypothesis is that topiramate will reduce acute seizures after traumatic brain injury and will help prevent the development of epilepsy after traumatic brain injury.
Progesterone for the Treatment of Traumatic Brain Injury
The ProTECT study will determine if intravenous (IV) progesterone (started within 4 hours of injury and given for a total of 96 hours), is more effective than placebo for treating victims...
Study of Citicoline for the Treatment of Traumatic Brain Injury (COBRIT)
The Citicoline Brain Injury Treatment (COBRIT) is a randomized, double-blind, placebo controlled, multi-center trial of the effects of 90 days of citicoline on functional outcome in patien...
PubMed Articles
Experimental traumatic brain injury.
ABSTRACT: Traumatic brain injury, a leading cause of death and disability, is a result of an outside force causing mechanical disruption of brain tissue and delayed pathogenic events which collectivel...
Traumatic brain injury can cause numerous behavioral abnormalities including aggression, violence, impulsivity, and apathy, factors that can be associated with criminal behavior and incarceration. To...
Sander AM, Maestas KL, Pappadis MR, Sherer M, Hammond FM, Hanks R, and the NIDRR Traumatic Brain Injury Model Systems Module Project on Sexuality After TBI. Sexual functioning 1 year after traumatic b...
Nutritional therapy in traumatic brain injury : Update 2012.
Severe traumatic brain injury ranks among the most common causes of death in young adults in western countries. Severe traumatic brain injury is typically followed by a pronounced pathophysiological c...
Traumatic brain injury: Intracranial pressure monitoring in traumatic brain injury.
