Dexanabinol in Severe Traumatic Brain Injury

Last updated: May 4, 2006
Sponsor: Pharmos
Overall Status: Completed

Phase

3

Condition

Traumatic Brain Injury

Memory Loss

Neurologic Disorders

Treatment

N/A

Clinical Study ID

NCT00129857
PH-2000-1
  • Ages 18-65
  • All Genders

Study 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.

Eligibility Criteria

Inclusion

Inclusion Criteria:

  • Traumatic head injury within the last 6 hours

  • Glasgow Coma Motor score of 2 to 5; severity requires intracranial pressure (ICP)monitoring

  • Brain computed tomography (CT) showing intracranial parenchymal abnormality andhemodynamically stable

  • An informed consent

Exclusion

Exclusion Criteria:

  • Penetrating head injury

  • Spinal cord injury

  • Coma due to pure epidural hematoma with initial Glasgow Coma Scale (GCS) of => 12

  • Previous major cerebral damage

  • Concomitant severe conditions

Study Design

Total Participants: 860
Study Start date:
January 01, 2001
Estimated Completion Date:
September 30, 2004

Study 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.