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Cannabinoids May Reduce Stroke Damage

Christine Kielhorn PHD
Hemmorhage on MRI scan

CB2 receptors are activated following brain hemorrhage, and this is where cannabinoids will help stop further damage.

When the brain suffers a stroke or a traumatic injury, damage to the brain continues as the brain hemorrhage leads to a snowball effect of inflammation, oxidative stress, and excitotoxicity, or cell death by over-stimulation, usually by the neurotransmitter glutamate.

There aren’t many medications that can be given immediately following brain injury or hemorrhage to mitigate these effects, but because the endocannabinoid system (ECS) regulates all of these mechanisms, cannabinoids could be the perfect treatment.

Stroke Patient in Emergency, brain hemorrhage

Studies Show Endocannabinoids Working to Prevent Further Damage

The activity of the ECS has been studied extensively in animal models of stroke and traumatic brain injury (TBI). These studies have found that the expression of endocannabinoids and cannabinoid receptors in the brain is upregulated following stroke or TBI. For example, levels of the endocannabinoid 2-arachidonoylglycerol (2-AG) spiked following an injury and remained elevated for more than 24 hours. This indicates that the ECS could be working to protect the brain in response to injury. In fact, 2-AG acts as a vasorelaxer, so it improves blood flow in the brain after injury.

Many animal studies looked at the role of cannabinoid receptor CB2 in protecting the brain from damage following TBI or stroke. When cannabinoids that activate the CB2 receptor (also called receptor agonists) were administered prior to the simulation of a stroke, the infarct (or damaged and dead tissue) volume was much smaller than in animals that did not receive the treatment. Doctors found further confirmation of the role of CB2 after administering a cannabinoid that reduces or blocks the activity of the CB2 receptor. When they do so, the infarct size increases.

Brain Hemorrhage Leads to CB2 Receptor Activation And Reduced Inflammation

Activating the CB2 receptor seems to primarily work through the suppression of the inflammatory response. CB­2 receptor agonists reduce the ability of white blood cells to accumulate in the injury site. They do so by limiting their ability to stick to the injured tissue. The reduced expression of intracellular adhesion molecules (ICAM-1) at the injury site as a result of CB2 activation is likely the mechanism causing this. When scientists delete the CB­­2 gene in mice, then ICAM-1 expression increases. So too does pro-inflammatory cytokine tumor necrosis factor alpha (TNF-α). Inhibiting the release of cytokines like TNF-α is one of the known anti-inflammatory mechanisms of CB2 activation. Reducing white blood cell recruitment at the injury site also protects the blood-brain barrier. This shields the injury site from worsening inflammation.

The CB2 receptors also highly express on microglial cells. These are a kind of brain cell that actually relate to macrophages and migrats to the injury site. Microglia contribute to the inflammation response that can cause death of neurons in the area. However, activating the CB2 receptors seems to reduce the effect these cells have, preventing their release of toxic compounds and pro-inflammatory cytokines.

Golden Hour For Stroke Design, brain hemorrhage

CB1 Receptors Stop Glutamate Release, A Molecule That Leads to Brain Cell Death

The CB1 receptor may also play an important role in protecting the brain from excitotoxicity. The neurotransmitter glutamate releases in large amounts following brain injury, causing cell death. However, CB1 activation inhibits various pathways involved in glutamate signaling, preventing glutamate release. The CB1 receptor may also regulate antioxidant pathways. This is because 2-AG reduces the release of reactive oxygen species (ROS) after injury. Cannabinoids themselves are effective antioxidants. This means they may work through other pathways to reduce the effect of ROS release at the injury site.

The large number of studies here are very encouraging. Especially those on the role of cannabinoids and the ECS in mitigating stroke or TBI effects. However, there are no human clinical trials yet. With luck we’ll soon see some demonstrating the efficacy of cannabinoids in reducing brain damage following TBI or stroke.

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Christine Kielhorn
7 Comments
  • Avatar
    Michael J Palframan

    Christine Kielborn, Thanks for Sharing the above information.
    I am Not going to share my experience with the use of Cannibis Oil that I have Learnt Works not on Animal’s but on My Beloved Wife Roselyn.
    The Reason for not Sharing is that I don’t want to to waste you Time nor Mine if no one wants to accept that CANNABIS OIL REPAIRS AS WELL AS HEALS THE BRAIN I KNOW.
    Kindest Regards,
    Michael Palframan.

    November 25, 2017 at 9:12 am Reply
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    mara

    Hi Michael,

    We would love to share your story on our website and our facebook site if you are willing.

    November 30, 2017 at 2:35 am Reply
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    Lauren

    Great post however , I was wanting to know if you
    could write a litte more on this subject? I’d be very grateful if you could elaborate a little bit further.
    Kudos!

    February 11, 2018 at 9:08 pm Reply
    • Avatar
      RxLeaf

      We can definitely look into writing more on the subject of stroke. Was there something in particular that you were wondering about?

      February 12, 2018 at 3:03 am Reply
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    Rubin Thomas

    I’m a brain cancer survivor, I had several heavy rounds of radiation to the back of my head where the tumor was. Had a stroke in 2009 and then another in January 2019, the doctors say that I have these because the radiation has thinned out the blood vessels in my brain, can cbd help this?

    September 17, 2019 at 4:01 pm Reply

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