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CVA – Research with cannabinoids

A stroke – mistakenly called a “stroke” – happens when the blood flow to the brain becomes limited or interrupted, which can cause permanent neural damage. Studies have shown that cannabis, when administered shortly after a stroke, limits brain damage and improves recovery.

Stroke Overview

A stroke happens when blood flow to the brain is interrupted or becomes very limited. The brain tissue ends up being deprived of oxygen and nutrients, which can cause the death of neuronal cells in a matter of minutes. Strokes are caused by blockage of arteries – known as ischemic stroke – which accounts for around 85% of all stroke cases; or by a leaking blood vessel, which can lead to a hemorrhagic stroke. A transient ischemic attack (TIA) – also called a mini-stroke – happens when there is a temporary interruption of blood flow to the brain.

Medical care immediately after a stroke helps minimize damage to the brain. Unfortunately, strokes may not present any symptoms, and it is common for a person to not be aware that they have had a stroke. The most common signs include slurred speech, confusion, numbness or paralysis of the face, arm or leg, suddenly blurred or darkened vision, headache accompanied by nausea and difficulty walking.

Strokes can cause temporary or permanent disability, depending on how long blood flow was interrupted and which part of the brain was affected. Seizures, paralysis, difficulty speaking or swallowing, memory loss, pain and emotional problems are complications that can occur after a stroke. If the stroke has affected the right side of the brain, movements and sensations on the left side of the body may be affected. Damage to the left side of the brain can also cause speech or language problems.

A number of risk factors can increase the chances of having a stroke, including: obesity, excessive alcohol consumption, use of cocaine and methamphetamines, tobacco consumption and a sedentary lifestyle. People who have high blood pressure, diabetes, cardiovascular disease, high cholesterol or sleep apnea are also at greater risk of having a stroke. Furthermore, it has been discovered that stroke is more common in men than women and individuals over 55 years of age.

Soon after an ischemic stroke, doctors and nurses work to restore blood flow to the brain as quickly as possible through a variety of procedures, such as administering aspirin or tissue plasminogen activator (TPA). In some cases, it may be necessary to use a catheter to break up or remove the clot that is obstructing blood flow. After a hemorrhagic stroke, attempts are made to control the bleeding with anticoagulant medications or through surgical repair of the damaged blood vessel. It is very common for individuals who survive strokes to have to undergo rehabilitation programs to recover physical abilities and speech.

Effects of cannabis on strokes

Cannabis has proven to be effective in containing damage to cells and offering neuroprotective effects after ischemic events such as strokes. These benefits are due to the presence of one of the main cannabinoids found in cannabis, cannabidiol or CBD. Administering CBD soon after a stroke protects neurons and astrocytes, leading to functional, histological, biochemical and neurobehavioral recovery 10.

Most of the research demonstrating the neuroprotective benefits of CBD comes from animal studies. Piglets given CBD shortly after an ischemic attack were able to recover their brain electrical activity to 46.4% above baseline and only 4 out of 8 experienced seizures, compared to those not given CBD, which only recovered 20.5% of their electrical activity – and all experienced seizures. CBD reduced both effects by more than 50% 1. In studies with mice and rats, CBD has been shown to reduce the volume of infarcts and acute and apoptotic brain damage when administered shortly after an ischemic brain event 3, 11, 7, 8, 15. One study found that administering CBD before and after a stroke yielded potent and long-lasting neuroprotective effects 9.

Brain damage that occurs after stroke is associated with an increase in excitotoxicity, oxidative stress, and inflammation. However, the administration of CBD soon after a stroke has been shown to be effective in preventing these three types of changes 12, 13.

These neuroprotective properties have also been observed in humans. Cannabinoids administered shortly after a stroke caused a reduction in infarct volume and caused significant improvements in short- and long-term brain activity tests, thus demonstrating that they improve functional outcome after strokes 4.

Research suggests that taking CBD as soon as possible after a stroke has a significant impact on the ability to limit damage and improve recovery. An animal study found that chronic administration of CBD, between 1 and 3 days after a stroke, led to functional improvement and increased survival rates in rats. However, when CBD was administered 5 days after a stroke, it did not inhibit ischemic damage 6.

Recent studies on cannabis in Strokes

  • Administration of CBD shortly after an ischemic event generated an increase of approximately 50% in the recovery of electrical activity in the brain and a 50% reduction in seizures. Neuroprotective effects of the non-psychoactive cannabinoid Cannabidiol in newborn pigs with hypoxic-ischemic encephalopathy. (http://www.nature.com/pr/journal/v64/n6/full/pr2008260a.html)
  • CBD reduced acute and apoptotic brain damage when administered shortly after an ischemic event in mice. In an in vitro mouse model of hypoxic-ischemic brain damage, the neuroprotective effects of cannabidiol were mediated by CB2 and adenosine receptors. (http://www.sciencedirect.com/science/article/pii/S096999610900309X)
  • Cannabinoids administered to humans shortly after a stroke reduced infarct volume and improved the functional response of the brain. Cannabinoids in experimental stroke: a systematic review and meta-analysis. (https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4348386/)

Reference:

  1. Alvarez, F.J., Lafuente, H., Rey-Santano, M.C., Mielgo, V.E., Gastiasoro, E., Rueda, M., Pertwee, R.G., Castillo, A.I., Romero, J., and Martinez-Orgado, J. (2008, December). Neuroprotective effects of the nonpsychoactive cannabinoid cannabidiol in hypoxic-ischemic newborn piglets. Pediatric Research, 64(6), 653-8. Retrieved from
    http://www.nature.com/pr/journal/v64/n6/full/pr2008260a.html.
  2. Capettini, L.S.A., Savergnini, S.Q., da Silva, R.F., Stergiopulos, N., Santos, R.A.S., Mach, F., and Montecucco, F. (2012). Update on the Role of Cannabinoid Receptors after Ischemic Stroke. Mediators of Inflammation, Volume 2012, Article ID 824093, 8 pages. Retrieved from
    https://www.hindawi.com/journals/mi/2012/824093/.
  3. Castillo, A., Tolon, M.R., Fernandez-Ruiz, J., Romero, J., and Martinez-Orgado, J. (2010, February). The neuroprotective effect of cannabidiol in an in vitro model of newborn hypoxic-ischemic brain damage in mice is mediated by CB(2) and adenosine receptors. Neurobiology of Diseases, 37(2), 434-40. Retrieved from
    http://www.sciencedirect.com/science/article/pii/S096999610900309X.
  4. England, T.J., Hind, W.H., Rasid, N.A., O’Sullivan, S.E. (2015, March). Cannabinoids in experimental stroke: a systematic review and meta-analysis. Journal of Cerebral Blood Flow and Metabolism, 35(3), 348-58. Retrieved from
    https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4348386/.
  5. Fernández-Ruiz, J., Moro, M. A., & Martínez-Orgado, J. (2015). Cannabinoids in Neurodegenerative Disorders and Stroke/Brain Trauma: From Preclinical Models to Clinical Applications. Neurotherapeutics12(4), 793–806. Retrieved from
    https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4604192/.
  6. Hayakawa, K., Irie, K., Sano, K., Watanabe, T., Higuchi, S., Enoki, M., Nakano, T., Harada, K., Ishikane, S., Ikeda, T., Fujioka, M., Orito, K., Iwasaki, K., Mishima, K., and Fujiwara, M. (2009, September). Therapeutic time window of cannabidiol treatment on delayed ischemic damage via high-mobility group box1-inhibiting mechanism. Biological & Pharmaceutical Bulletin, 32(9), 1538-44. Retrieved from
    https://www.jstage.jst.go.jp/article/bpb/32/9/32_9_1538/_pdf.
  7. Hayakawa, K., Mishima, K., Abe, K., Hasebe, N., Takamatsu, F., Yasuda, H., Ikeda, t., Inui, K., Egashira, N., Iwasaki, K., and Fujiwara, M. (2004, October 25). Cannabidiol prevents infarction via the non-CB1 cannabinoid receptor mechanism. Neuroreport, 15(15), 2381-5. Retrieved from
    http://journals.lww.com/neuroreport/pages/articleviewer.aspx?year=2004&issue=10250&article=00016&type=abstract.
  8. Hayakawa, K., Mishima, K., Irie, K., Hazekawa, M., Mishima, S., Fujioka, M., Orito, K., Egashira, N., Katsurabayashi, S., Takasaki, K., Iwasaki, K., and Fujiwara, M. (2008, December). Cannabidiol prevents a post-ischemic injury progressively induced by cerebral ischemia via a high-mobility group box1-inhibiting mechanism. Neuropharmacology, 55(8), 1280-6. Retrieved from
    http://www.sciencedirect.com/science/article/pii/S0028390808001974.
  9. Hayakawa, K., Mishima, K., Nozako, M., Hazekawa, M., Irie, K., Fujioka, M., Orito, K., Abe, K., Hasebe, N., Egashira, N., Iwasaki, K., and Fujiwara, M. (2007, September). Delayed treatment with cannabidiol has a cerebroprotective action via a cannabinoid receptor-independent myeloperoxidase-inhibiting mechanism. Journal of Neurochemistry, 102(5), 1488-96. Retrieved from
    http://onlinelibrary.wiley.com/doi/10.1111/j.1471-4159.2007.04565.x/full.
  10. Lafuente, H., Alvarez, F.J., Pazos, M.R., Alvarez, A., Rey-Santano, M.C., Mielgo, V., Murgia-Esteve, X., Hilario, E., and Martinez-Orgado, J. (2011, September). Cannabidiol reduces brain damage and improves functional recovery after acute hypoxia-ischemia in newborn pigs. Pediatric Research, 70(3), 272-7. Retrieved from
    http://www.nature.com/pr/journal/v70/n3/full/pr2011171a.html.
  11. Mishima, K., Hayakawa, K., Abe, K., Ikeda, T., Egashira, N., Iwasaki, K., and Fujiwara, M. (2005, May). Cannabidiol prevents cerebral infarction via a serotonergic 5-hydroxytryptamine1A receptor-dependent mechanism. Stroke, 36(5), 1077-82. Retrieved from
    http://stroke.ahajournals.org/content/36/5/1071.long.
  12. Pazos, M.R., Cinquina, V., Gomez, A., Layunta, R., Santos, M., Fernandez-Ruiz, J., Martinez-Orgado, J. (2012, October). Cannabidiol administration after hypoxia-ischemia to newborn rats reduces long-term brain injury and restores neurobehavioral function. Neuropharmacology, 63(5), 776-83. Retrieved from
    http://www.sciencedirect.com/science/article/pii/S0028390812002328.
  13. Pazos, M.R., Mohammed, N., Lafuente, H., Santos, M., Martinez-Pinilla, e., Moreno, E., Valdizan, E., Romero, J., Pazos, A., Franco, R., Hillard, C.J., Alvarez, F.J., and Martinez-Orgado, J. (2013, August). Mechanisms of cannabidiol neuroprotection in hypoxic-ischemic newborn pigs: role of 5HT(1A) and CB2 receptors. Neuropharmacology, 71, 282-91. Retrieved from
    http://www.sciencedirect.com/science/article/pii/S0028390813001238.
  14. Stroke. (2015, July 30). Mayo Clinic. Retrieved from
    http://www.mayoclinic.org/diseases-conditions/stroke/home/ovc-20117264.
  15. Walsh, S.K., Hepburn, C.Y., Kane, K.A., Wainwright, C.L. (2010, July). Acute administration of cannabidiol in vivo suppresses ischaemia-induced cardiac arrhythmias and reduces infarct size when given at reperfusion. British Journal of Pharmacology, 160(5), 1234-42. Retrieved from
    https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2936031/.