cbd stroke patient

The Centre for Medical Cannabis, the organisation that represents companies making cannabis-based products in the UK, looked at products sold in the UK. They found only 11/29 (38%) had the amount of CBD close to what was advertised. It also found that some products contained other substances, like heavy metals that can be harmful and THC, the psychoactive part of cannabis.

Common effects of stroke that people can find difficult to cope with include pain, muscle problems and headaches.

The medicines given by the NHS are manufactured with precise amounts of the active ingredients, and they will be different from the products you can buy over the counter.

At the moment, cannabis products are not prescribed for chronic pain or headaches. It is possible that more research will discover the benefits of CBD or other cannabis products for stroke survivors in future, but at the moment not enough is known about it. If you decide to try CBD oil products, be aware that the quality of cannabis-based products you can buy in shops can vary. So before you spend your money, make sure you find out what you are actually buying.

But can they help stroke survivors?

The honest answer is, we don’t know yet.

If people with certain conditions, like MS-related muscle spasticity or severe epilepsy, find other treatments aren’t working for them, cannabis-based products can be given by doctors.

In recent years, legal cannabis-based products containing cannabidiol (CBD), have become more available. These products are legal because they do not contain THC, the part of cannabis that directly affects the brain.

More people are now trying CBD oil, looking for help with a range of health concerns from acne to sleep problems. You can find them in pharmacies and health food shops, as well as online.

Please remember that cannabis-based products can interact with other medications, so check with your pharmacist or GP first.

Cbd stroke patient

Updated on November 15, 2021

Table of Contents

When the neurons are unable to get the oxygen and nutrients they need, they become damaged and may die off, leaving us with lasting neurological damage.

Royal CBD

An ischemic stroke occurs when blood flow is cut off from regions in the brain. It can happen if a blood or cholesterol clot gets lodged in the cerebral arteries feeding the brain. Once the artery is blocked, blood cannot flow to the region it supplies.

Cbd stroke patient

In 1974, an interactive study comparing CBD and THC in healthy volunteers demonstrated for the first time that CBD could act as an anxiolityc drug [31]. Experimentally, the anxiolytic properties of CBD have been demonstrated in different animal models such as the conditioned emotional response, the Vogel conflict test, and the elevated plus-maze [32,33]. Recently, it has been shown that CBD might exert anxiolytic effects by activating post-synaptic 5-HT1A receptors [34]. 5-HT1A receptors have been shown to play critical roles in the pathophysiology of depression, aggression, and anxiety. It appears to have a role in vasodilatation and neuroprotection [35,36,37,38,39,40]. We previously applied a new approach to the investigation of the neuroprotective mechanism of CBD by examining the effects of a CB1 receptor antagonist, a vanilloid-receptor (VR1) antagonist, and a 5-HT1A receptor antagonist in a 4h MCA occlusion model in mice. Interestingly, the neuroprotective effect of CBD was inhibited by the 5-HT1A receptor antagonist, WAY100135. Furthermore, the increased cerebral blood flow induced by CBD was also in part reduced by WAY100135. In contrast, the CB1 receptor antagonist and VR1 did not inhibit the effect of CBD [22]. Russo and co-workers demonstrated that CBD, but not delta 9 -THC, displaced the 5HT1A agonist, [ 3 H]-8-hydroxy-2-di-n-propylaminotetralin ([ 3 H]-8-OH-DPAT) from the cloned human 5HT1A receptor in a dose-dependent manner, and they have concluded that CBD was an agonist of the 5HT1A receptor [41]. More recently, Magen and co-workers supported that CBD (5 mg/kg, i.p.) induced activation of 5-HT1A receptors located in forebrain regions including the hippocampus, and improved cognitive and locomotor function which were impaired by bile-duct ligation [42]. Taken together, these data indicate that CBD may activate the 5-HT1A receptor which leads to the improvement of cognitive and functional impairment after cerebral ischemia.

Accumulating data now suggest that cannabinoid CB1 receptors contribute to neuroprotection through anti-excitotoxicity [14], the phosphatidylinositol-3 kinase/Akt pathway [17], and hypothermia [18]. We have reported that the neuroprotective and hypothermic effects of delta 9 -THC were related to CB1 receptors [89]. CBD has also been described as protective against global and focal ischemic injury [14,18]. Several groups have recently shown that CBD can interact with cannabinoid CB1 and CB2 receptors. Pertwee and Ross showed that CBD can antagonize the CB1 agonists such as WIN55,212 and CP55940 by acting at prejunctional sites that was unlikely to be cannabinoid CB1 or CB2 receptors [19]. Castillo and coworkers recently demonstrated that CBD implicated the neuroprotective effect mediated by CB2 and adenosine receptors in an in vitro model of newborn hypoxic-ischemic brain damage in mice [21]. In addition, Thomas and coworkers noted that CBD displayed unexpected high potency as an antagonist of CB1 and CB2 receptor agonists [20]. Interestingly, the neuroprotective effect of CBD showed a dose dependent bell shaped curve in mice subjected to middle cerebral artery occlusion (MCAO) [22]. Intraperitoneal injection of CBD 1 or 3 mg/kg but not 10 mg/kg during 4 h MCAO prevented cerebral infarction 24 hours after cerebral ischemia. Other groups have demonstrated that 5 mg/kg was the most effective CBD dose, and that there was a dose-dependent bell-shaped curve for CBD’s effects on the electroencephalographic flattening in gerbils subjected to cerebral ischemia [13]. CBD has been also reported to inhibit anandamide amidase [23] and the reuptake of anandamide [24], suggesting CBD may induce an increase of anandamide signaling within the ischemic brain. Anandamide and other CB1 receptor agonists are known to reduce the release of a variety of neurotransmitters including glutamate via CB1 receptor [25,26,27,28,29]. In our previous study, delta 9 -THC significant reduced the release of glutamate during MCAO, but CBD did not affect glutamate release [30], suggesting that CBD might have other mechanism or stimulate other receptors besides the cannabinoid receptors. The mechanism of this biphasic effect of CBD is still unclear, but CBD may induce cerebroprotective effect through modulating endogenous cannabinoid system.

2.3. Potent Anti-Oxidant Mechanism

In this review we will discuss the recent development of “CBD pharmacology” in ischemic stroke, focusing on the therapeutic potential of non-psychoactive cannabinoid CBD highlighting recent pharmacological advances, new mechanisms of action, and the therapeutic time window for its use in ischemic stroke.

2.2. Serotonin 5-HT1A Receptor-Dependent Mechanism

Cannabis contains over 60 different terpeno-phenol compounds that have been identified so far but the role and importance of many of these has yet to be fully understood. Select structures are shown in Figure 1 . Delta 9 -tetrahydrocannabinol (delta 9 -THC) is the most psychoactive component that was isolated in 1964 by Gaoni and Mechoulam at the Weizmann Institute in Rehovot (Israel). It has been demonstrated to produce hypothermia, learning and memory impairment, impairment of the prepulse inhibition of the startle reflex, catalepsy-like immobilisation, aggressive behaviour, analgesia, hypoactivity and enhancement of preference for high fat diet [1,2,3,4,5,6,84,85,86,87,88]. These effects are at least partly caused by binding to cannabinoid receptor type 1 (CB1) within the brain. So far, two types of cannabinoid receptors have been identified: type1 (CB1 receptor) and type2 (CB2 receptor). CB1 receptors are mainly expressed in the central and the peripheral nervous system. CB2 receptors are found in cells of the immune system, such as lymphocytes and neutrophils, as well as in resident inflammatory cells within the CNS [7,8,9].