Stroke and Cannabidiol

Stroke – Medical Marijuana Research Overview

13 October, 2015

Strokes are when blood flow to the brain is limited or interrupted, potentially causing permanent neural damage. Studies have shown marijuana, when administered shortly after a stroke, effectively limits brain damage and improves recovery.

Overview of Stroke

A stroke is when blood flow to the brain is interrupted or markedly limited. The brain tissue is deprived of oxygen and nutrients, which can cause brain cells to die within minutes. Strokes are caused by blocked arteries, which is referred to as an ischemic stroke and accounts for about 85% of all strokes, or by the leaking of a blood vessel, which is called a hemorrhagic stroke. A transient ischemic attack (TIA) is when there is a temporary disruption of blood flow to the brain.

Prompt medical response to a stroke helps minimize brain damage. Unfortunately, strokes can be asymptomatic and it’s not uncommon for one to be unaware they’ve suffered a stroke. The common signs of a stroke include slurred speech, confusion, numbness or paralysis of the face, arm or leg, sudden blurred or blackened vision, a sudden headache that could be accommodated with nausea, and trouble walking.

Strokes can cause both temporary and a permanent disability, depending on how long blood flow is disrupted and which part of the brain was affected. Seizures, paralysis, difficulty talking or swallowing, memory loss, emotional problems, and pain are complications that can develop following a stroke. If the stroke affected the right side of your brain, movement and sensation on the left side of the body could be impaired. If the stroke damaged the right side of the brain, movement and sensation on the left side could be affected. Damage on the left side of the brain can also cause speech or language problems.

An array of risk factors can increase the risk of a stroke. These include: being overweight or obese, heavy drinking, use of cocaine and methamphetamines, cigarette smoking, and physical inactivity. Those who have high blood pressure, high cholesterol, diabetes, cardiovascular disease or obstructive sleep apnea also have a higher risk of experiencing a stroke. In addition, African-Americans have a higher risk of stroke than people of other races and men have a higher overall risk than women. Being over the age of 55 is also associated with a greater risk of stroke.

Following ischemic strokes, medical professionals work to restore blood flow to the brain as quickly as possible through a variety of treatment procedures, which can include the administration of aspirin or tissue plasminogen activator (TPA). In some cases, a catheter may be needed to maneuver a tiny decide into the brain to physically break up or remove the clot blocking blood flow. Following a hemorrhagic stroke, doctors will attempt to control bleeding with anti-platelet drugs or through the surgical repair of the leaking blood vessel. Stroke survivors will likely have to participate in a rehabilitation program to recover physical and speech abilities.

Findings: Effects of Cannabis on Stroke

Cannabis has proven to be effective at limiting the cell damage and providing neuroprotective effects following ischemic events like strokes. These benefits are due to the presence of one of the major cannabinoids found in cannabis, cannabidiol (CBD). Administering CBD shortly after a stroke protects neurons and astrocytes from damage, and therefore leads to improved functional, histological, biochemical, and neurobehavior recovery (Lafuente, et al., 2011).

Most research demonstrating CBD’s neuroprotective benefits are found in animal trials. Piglets given CBD shortly following an ischemic attack were able to recover their brain’s electrical activity to 46.4% of their baseline and only 4 out of 8 experienced seizures, compared to piglets that did not receive CBD, which recovered 20.5% of their brain’s decreased electrical activity and all experienced seizures. CBD reduced both effects by more than 50% (Alvarez, et al., 2008). In mice and rat trials, CBD has shown to reduce infarct volume and acute and apoptotic brain damage when administered shortly after an ischemic brain event (Castillo, et al., 2010) (Mishima, et al., 2005) (Hayakawa, et al., 2004) (Hayakawa, et al., 2008) (Mishima, et al., 2005) (Walsh, Hepburn, Kane & Wainwright, 2010). One study found that administering CBD both before and after a stroke caused potent and long-lasting neuroprotection (Hayakawa, et al., 2007).

The brain damage that occurs following strokes is associated with increases in excitotoxicity, oxidative stress and inflammation. However, administering CBD shortly after a stroke occurs has shown effective at preventing all three of these alterations (Pazos, et al., 2013) (Pazos, et al., 2012).

These neuroprotective findings have been experienced in human subjects as well. Cannabinoids administered to humans shortly after experiencing a stroke caused a reduction in infarct volume and caused significant improvements in both early and late brain activity scores, thus demonstrating they improve functional outcome following strokes (England, Hind, Rasid & O’Sullivan, 2015).

Research suggests that administering CBD as quickly as possible following a stroke makes a significant impact on its ability to limit damage and improve recovery. An animal study found that repeated treatment with CBD from 1 and 3 days after a stroke caused a functional improvement and increased survival rats. When CBD was given 5 days after a stroke, however, it did not improve ischemic damage (Hayakawa, et al., 2009).

States That Have Approved Medical Marijuana for Stroke

Currently, no states have approved medical marijuana specifically for the treatment of stroke. However, a number of states will consider allowing medical marijuana to be used for the treatment of stroke with the recommendation from a physician. These states include: California (any debilitating illness where the medical use of marijuana has been recommended by a physician), Connecticut (other medical conditions may be approved by the Department of Consumer Protection), Massachusetts (other conditions as determined in writing by a qualifying patient’s physician), Nevada (other conditions subject to approval), Oregon (other conditions subject to approval), Rhode Island (other conditions subject to approval), and Washington (any “terminal or debilitating condition”).

In Washington D.C., any condition can be approved for medical marijuana as long as a DC-licensed physician recommends the treatment.

Recent Studies on Cannabis’ Effect on Stroke


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 cannabinodi cannabidiol in hypoxic-ischemic newborn piglets. Pediatric Research, 64(6), 653-8.

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.

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.

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.

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.

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.

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.

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.

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.

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.

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.

Stroke. (2015, July 30). Mayo Clinic. Retrieved from

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.

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