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percentage of the essential oils in some chemical varieties of cannabis (Russo 2016b).
THE EXPECTED TRAUMA ASSOCIATED WITH DYING AND THE POSSIBILITY OF MINIMIZING PATHWAYS OF SECONDARY DAMAGE WITH THE NEUROPROTECTIVE EFFECTS (ANTI-GLUTAMATERGIC AND ANTI-INFLAMMATORY) OF THE ENDOCANNABINOID SYSTEM
Within the dying process, trauma and tissue-injury are expected and have a distinct etiology. EOL clinicians often describe the dying process as a gradual “shutting down.” However, the fluctuations of heart-rate, respiratory rate, and temperature commonly seen in dying patients exhibit oscillation versus a smooth decline. A dying individual’s presentation resembles, in some ways, the presentation of individuals experiencing medical events such as stroke. Trauma resulting from head-injury and trauma resulting from stroke share a similar pathway of secondary damage (Leker and Shohami 2002). The pathway begins with calcium influx, and is followed by vasoconstriction, caspase activation, oxidative stress, inflammation, and glutamatergic excitotoxicity (Parker 2017; Leker & Shohami 2002). Prevention of secondary pathways of damage with a cannabinoid neuroprotective agent has been shown to minimize the sequalae of head trauma (Mechoulam, Panikashvili & Shohami 2002). In the context of dying, this strategy might potentially reduce symptomatic events associated with the “difficult road.” Although there are many pathways of secondary damage, this article will focus on the anti-glutamatergic and anti-inflammatory neuroprotective activities of the ECS.
Glutamate has been established as a central player in symptomatic events related to CNS-excitement such as seizure activity. Santosh & Sravya (2017:1) write:
Excitability in the human CNS is predominantly mediated by glutamate and recent compelling evidence points to the role of glutamate in excitotoxic damage resulting in seizures as well as maintenance and invasion of malignant glioma.
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