![]() Īt the state level, various laws have been passed to decriminalize cannabis, allowing for different levels of medical and recreational use in at least 29 states. In addition to its antiemetic properties, cannabis consumption creates appetite stimulation and has been used for cachexia as well as conditions such as AIDS, Parkinson’s, and Alzheimer’s, ALS, inflammatory bowel disease, and migraine/headaches. ![]() Cannabis has also been used to augment treatment for several neurological disorders, including peripheral neuropathy, muscle spasticity from MS, and epilepsy. Cannabis and/or cannabinoid agents have been used to treat chronic non-cancer pain, with a review of 15 of 18 trials demonstrating analgesic effects compared to placebo. However, as a schedule 1 drug, cannabis availability for research and academic purposes is severely limited, making quality evidence-based data difficult to establish. Both of these medications are not schedule 1 drugs and are used primarily to treat chemotherapy-induced nausea and vomiting.Ĭannabis has been used therapeutically for multiple other medical conditions as well. There are, however, two synthesized cannabinoids that the Food and Drug Administration (FDA) has approved as medications in 1985, dronabinol (Marinol) and nabilone (Cesamet). The Controlled Substances Act of 1970 classified cannabis and its cannabinoids as a schedule 1 substance, meaning cannabis has been determined to have a high potential for abuse and having no accepted medical use. Although it was categorized as an illegal substance via the Marijuana Tax Act of 1937, marijuana today is the most used illicit drug according to the 2015 National Survey on Drug Use and Health. Other newer, off-label treatments for CHS have been proposed.Ĭannabis has a long history linking to many cultures its use has been dated back many millennia. The usual treatment for nausea, vomiting, and abdominal pain may not be effective for patients with CHS. SummaryĬHS should be in the differential diagnosis for any patient with nausea, vomiting, and abdominal pain. Theories proposed to explain CHS including chronic stimulation of the CB1 receptor, binding of the CB1 receptor causing decreased gut motility, desensitization of CB1 receptors (these CB1 receptors generally have antiemetic effects), or interaction of the TRVP-1 receptor with the ennocannabinoid system. Two cannabinoid receptors (CB1, CB2) have been identified. ![]() The pathophysiology of CHS may be due to dysregulation of the endocannabinoid system. Alternative treatments have been suggested. Typical treatment for nausea, vomiting, and abdominal pain may not be effective in patients with CHS. ![]() This review describes the clinical presentation and treatment for cannabinoid hyperemesis syndrome (CHS). ![]()
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