Following the blow that leads to TBI’s, the body releases harmful mediators that lead to excitotoxicity, oxidative stress and inflammation and causes secondary, delayed neuronal death (Biegon, 2004). Cannabis, however, has been shown to offer protection to the neural system, thus reducing the amount of brain damage (Mechoulam, Spatz & Shohami, 2002) (Mechoulam & Shohami, 2007) (Mechoulam, Panikashvili & Shohami, 2002) (Biegon, 2004).
It’s cannabis’ two major cannabinoids, tetrahydrocannabinol (THC) and cannabidiol (CBD) that are responsible for these beneficial effects following TBI’s. Cannabinoids have been shown to act on the CB1 and CB2 receptors of the endocannibinoid system, which in turn prevents the release of proinflammatory cytokines that are released after brain drama and cause damage (Panikashvili, et al., 2006). Activating of the CB1 and CB2 receptors also has been shown to stimulate the release of minocycline, which reduces brain swelling and neurological impairment, and diffuses further injuries to the brain’s axons (Lopez-Rodriguez, et al., 2015) (Biegon, 2004).
In one study, cannabinoid administered to mice with brain injuries caused a significant reduction of brain swelling, as well as better clinical recovery, reduced infarct volume, and reduced brain cell death compared to the control group (Panikashvili, et al., 2001). In another, CBD was found to reduce acute and apoptic brain damage (Castillo, et al., 2010). Piglets with brain injuries given CBD experienced less excitotoxicity, oxidative stress and inflammation (Pazos, et al., 2013). Mice that had suffered an impact brain injury showed marked recovery in object recognition and in performing a specific task after CB1 receptors were activated (Arain, Khan, Craig & Nakanishi, 2015). Cannabinoids have even shown to be effective at offering neuroprotection in newborn babies that have experienced a brain injury (Fernandez-Lopez, Lizasoain, Moro & Martinez-Orgado, 2013).
One study found that patients that had detectable levels of THC in their bodies were less likely to die as a result of a traumatic brain injury than those who didn’t (Nguyen, et al., 2014).
THE MAJORITY OF A CANNABIS FLOWER’S WEIGHT IS PLANT MATTER, WHICH HAS RELATIVELY NO BENEFIT TO PATIENTS!
THE POPULARITY OF CANNABIS CONCENTRATES, LIKE BHO (SHATTER, WAX, SAP, ETC.), HAS ADDED BIT MROE CONFUSION FOR THE INEXPERIENCED PATIENT. THESE CONCENTRATES ROUTINELY ARE LAB TESTED AT 60%, 70%, AND EVEN 80% THC. OBVIOUSLY, THAT IS A MUCH HIGHER PERCENTAGE THAN YOU WILL SEE IN ANY SAMPLE OF FLOWERS. THAT’S BECAUSE IT IS BASED ON THE OVERALL WEIGHT OF THE SAMPLE, AND PURE CONCENTRATES ARE ONLY CANNABINOIDS AND TERPENES.
1G OF FLOWER AND 1G OF CONCENTRATE WILL HAVE VASTLY DIFFERENT LEVELS OF CANNABINOIDS, EVEN IF THEY COME FROM THE SAME PLANT. AS OF NOW, IT’S LEFT UP TO PATIENTS TO CALCULATE THE CANNABINOID LEVELS OF EACH PRODUCT FOR THEMSELVES; THIS PUTS AN UNNECESSARY BURDEN ON you
SCIENTIFIC STUDIES INVOLVING SMOKED AND VAPORIZED CANNABIS HAVE ALREADY SPECIFY EXACT CANNABINOID DOSAGES IN MILLIGRAMS
CLEARLY LABELING THE AMOUNT OF CANNABINOIDS IN A GIVEN SAMPLE WOULD BE A GREAT TOOL TO HELP REGULATE THE MEDICAL CANNABIS INDUSTRY. 50MG THC IS MUCH MORE MEANINGFUL TO PATIENTS THAN “SINGLE DOSE” WHEN CONSIDERING HOW MUCH THEY NEED.
BLAZE BRAND uses the same process everytime so the results are consistant
Currently there is no effective drug for the treatment of traumatic brain injury. In the U.S., there are nearly 52,000 deaths and roughly 80,000 cases of severe disability related to traumatic brain injury every year. From Service Veterans , Civil service workers, firemen and police officers, amature and Proffesional athleats.
There are more than 5.3 million people in the U.S. living with disabilities related to traumatic brain injury — numbers far greater than those for multiple sclerosis, Parkinson's disease and Alzheimer's disease. "Brain injury is not a one-shot deal. The primary injury occurs from the initial hit. Neurochemical injuries can cause secondary damage," said Dr. Ken Strauss of Temple University. The secondary effects of brain injuries, such as swelling and the release of toxic chemicals, can be more damaging than the initial blow, said Dr. Esther Shohami, lead author of the study.
The cannabinoid, 2-AG, is believed to work in three ways. First, it reduces the levels of glutamate, a toxic molecule, released after injury. Second, it decreases the amount of free radicals and TNF (a chemical that induces inflammation) after injury. Third, it increases the blood supply to the brain. All three mechanisms are essential for limiting the damage done after the primary injury. Dr. Shohami said she didn't "see any problems with using a drug from this family to treat patients." Other cannabinoids have been approved for use in humans with very minimall side effects.
In fact, one pharmaceutical company is trying to develop a similar drug for humans. With the help of researchers at the Hebrew University, Pharmos is set to begin the final stage of clinical trials of Dexanabinol — a drug that is essentially the mirror image of THC, the active ingredient in marijuana. Because it is not exactly like THC, it does not bind to the same part of the brain, and therefore does not have the unwanted side effects.
However, the drug appears to exert effects similar to other cannabinoids on the brain after injury — that is, a decrease in toxic chemicals and swelling. The first two phases of clinical trials were completed in Israel to test for safety. The third and final phase of the trials is set to begin in Europe in January, followed closely by trials in the U.S.
"Helmets are for preventing primary injury, and hopefully this work can protect people from the secondary effects," Dr. Strauss said.