But he wasn’t finished. In February of 1980, Dr. Mechoulam teamed up with South American researchers to publish a study regarding cannabis and epilepsy. This study is seen as one of the earliest double-blind studies of CBD on clinical subjects. The study Dr. Mechoulam and his team conducted included 16 people, many of whom were children, who all suffered from severe epilepsy. The results were startling: Every subject who received CBD experienced improvement in their condition with little to no side effects. This anticonvulsant study has since proven to be an integral milestone in the world of clinical marijuana research, but largely went unnoticed at the time. 

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Some users may experience an episode of acute psychosis, which usually abates after six hours, but in rare instances, heavy users may find the symptoms continuing for many days.[52] A reduced quality of life is associated with heavy cannabis use, although the relationship is inconsistent and weaker than for tobacco and other substances.[53] It is unclear, however, if the relationship is cause and effect.[53]

Regarding marijuana use in children, parents should be aware of changes in a child's behavior, although this may be difficult with teenagers. Parents should look for withdrawal, depression, fatigue, carelessness with grooming, hostility, and deteriorating relationships with family members and friends. In addition, changes in academic performance, increased absenteeism or truancy, lost interest in sports or other favorite activities, and changes in eating or sleeping habits could be related to drug use. However, these signs may also indicate problems other than use of drugs.
The endocannabinoid system is tonically active in control of pain, as demonstrated by the ability of SR141716A (rimonabant), a CB1 antagonist, to produce hyperalgesia upon administration to mice (Richardson et al 1997). As mentioned above, the ECS is active throughout the neuraxis, including integrative functions in the periacqueductal gray (Walker et al 1999a; Walker et al 1999b), and in the ventroposterolateral nucleus of the thalamus, in which cannabinoids proved to be 10-fold more potent than morphine in wide dynamic range neurons mediating pain (Martin et al 1996). The ECS also mediates central stress-induced analgesia (Hohmann et al 2005), and is active in nociceptive spinal areas (Hohmann et al 1995; Richardson et al 1998a) including mechanisms of wind-up (Strangman and Walker 1999) and N-methyl-D-aspartate (NMDA) receptors (Richardson et al 1998b). It was recently demonstrated that cannabinoid agonists suppress the maintenance of vincristine-induced allodynia through activation of CB1 and CB2 receptors in the spinal cord (Rahn et al 2007). The ECS is also active peripherally (Richardson et al 1998c) where CB1 stimulation reduces pain, inflammation and hyperalgesia. These mechanisms were also proven to include mediation of contact dermatitis via CB1 and CB2 with benefits of THC noted systemically and locally on inflammation and itch (Karsak et al 2007). Recent experiments in mice have even suggested the paramount importance of peripheral over central CB1 receptors in nociception of pain (Agarwal et al 2007)

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