Traumatic brain injury (TBI) is one of the leading causes of death worldwide in individuals under the age of 45. Triggered by concussions from car accidents, falls, violent contact sports, explosives or by gunshot and stab wounds, TBI affects 1.7 million Americans annually. It is the most commonly identified cause of epilepsy among adults.
The social and economic costs of TBI are considerable given that many who survive severe head injuries suffer permanent behavioral and neurological impairment that adversely impacts learning and memory and often requires long term rehabilitation. An estimated 4 million to 6 million Americans are on disability because of TBI. Even so-called mild cases of TBI can result in post-traumatic seizures, refractory cognitive deficits, and lower life expectancy.
Treatment modalities for TBI are limited with few satisfactory pharmaceutical options available. Surgical intervention, which entails the removal of parts of the skull to reduce intracranial pressure, is an emergency, life-saving measure, and the aftermath can be gruesome.
But hope is on the horizon, thanks in part to U.S. government-sponsored scientific research – and to extensive anecdotal accounts from medical marijuana patients – which highlight the potential of cannabinoid-based therapies for TBI.
In 1998, the Proceedings of the National Academy of Sciences published a groundbreaking report on the neuroprotective properties of cannabidiol (CBD) and tetrahydrocannabinol (THC), two major components of marijuana. Co-authored by a team of researchers (AJ Hampson, M Grimaldi, D Wink and Nobel laureate J Axelrod) at the National Institutes of Mental Health, this preclinical study on rats would form the basis of a U.S. government-held patent on “Cannabinoids as antioxidants and neuroprotectants.”
The patent indicates that CBD and THC were found “to have particular application as neuroprotectants … in limiting neurological damage following ischemic insults, such as stroke or trauma.” These plant cannabinoids were also deemed useful for treating other neurodegenerative conditions, “such as Alzheimer’s disease, Parkinson’s disease and HIV dementia.”
Whereas TBI results from an external blow to the skull, a stroke is caused internally by an arterial blockage or rupture. But TBI and stroke share many of the same pathological features and aberrant molecular mechanisms.
Example of a stroke MRI
TBI and stroke are both acute and potentially lethal injuries, involving a primary ischemic insult that interrupts cerebral blood flow and destroys brain tissue. This is followed by a secondary injury cascade that, if unchecked, can ricochet for several weeks or months, resulting in more brain damage, motor impairment and other adverse “downstream” effects, such as poor concentration, irritability, and sleep problems.
Whether the cause is an occluded blood vessel or blunt external force, the initial trauma triggers a complex sequence of molecular events characterized by the massive release of glutamate (an excitatory neurotransmitter) and the overproduction of reactive oxygen species (free radicals) and other inflammatory compounds. Excessive glutamate and oxidative stress, in turn, lead to microvascular injury, blood-brain barrier breakdown, swollen brain tissue, mitochondrial dysfunction, calcium ion imbalance, neurotoxicity and cell death. The secondary injury cascade is associated with the development of many of the neurological deficits observed after a TBI or a stroke.
Cannabinoids to the rescue
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