Wednesday, September 27, 2017

Petition: Post Concussion Syndrome / Concussion And Traumatic Brain Injury (TBI)

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Saturday, September 16th 2017


New Mexico State Department of Health
Medical Cannabis Advisory Board
Medical Cannabis Program
PO Box 26110
Santa Fe, NM, 87502-6110


Petition: Requesting The Inclusion Of A New Medical Condition: Post Concussion Syndrome / Concussion And Traumatic Brain Injury (TBI)

Table of Contents
Pg.  1 Cover Page
Pg.  2 Petition Introduction
Pg.  3 Petition Purpose and Background
Pg.  27 Relief Requested In Petition
Pg.  27 References
Pg.  28 - 30 Appendix A

 



Petition: Requesting The Inclusion Of A New Medical Condition: Post Concussion Syndrome / Concussion And Traumatic Brain Injury (TBI)

New Mexico’s medical cannabis history started in 1978, after public hearings the legislature enacted H.B. 329, the nation’s first law recognizing the medical value of cannabis. The New Mexico’s medical cannabis program (MCP)  is the only program in the U.S. that places sole responsibility for regulation on the state’s Department of Health. Doctors must comply with state requirements for patients to be considered for applying to the medical cannabis program.

In the Lynn and Erin Compassionate Use Act, (2007) the law states; The Secretary of Health shall establish an advisory board consisting of eight practitioners representing the fields of neurology, pain management, medical oncology, psychiatry, infectious disease, family medicine and gynecology. The practitioners shall be nationally board-certified in their area of specialty and knowledgeable about the medical use of cannabis. The members shall be chosen for appointment by the Secretary from a list proposed by the New Mexico Medical Society. A quorum of the advisory board shall consist of three members. The advisory board shall:
A. review and recommend to the department for approval additional debilitating medical conditions that would benefit from the medical use of cannabis;
B. accept and review petitions to add medical conditions, medical treatments or diseases to the list of debilitating medical conditions that qualify for the medical use of cannabis;
C. convene at least twice per year to conduct public hearings and to evaluate petitions, which shall be maintained as confidential personal health information, to add medical conditions, medical treatments or diseases to the list of debilitating medical conditions that qualify for the medical use of cannabis;
D. issue recommendations concerning rules to be promulgated for the issuance of the registry identification cards; and
E. recommend quantities of cannabis that are necessary to constitute an adequate supply for qualified patients and primary caregivers.

First, do no harm.  As an important step in becoming a doctor, medical students must take the Hippocratic Oath. And one of the promises within that oath is “first, do no harm”.  

We have a sound law in the Lynn and Erin Compassionate Use Act, as Section 2 reads; PURPOSE OF ACT.--The purpose of the Lynn and Erin Compassionate Use Act is to allow the beneficial use of medical cannabis in a regulated system for alleviating symptoms caused by debilitating medical conditions and their medical treatments.
“ARTICLE 2B. LYNN AND ERIN COMPASSIONATE USE ACT
N.M. Stat. Ann. § 26-2B-2 (2009)
    § 26-2B-2. Purpose of act
The purpose of the Lynn and Erin Compassionate Use Act [26-2B-1 NMSA 1978] is to allow the beneficial use of medical cannabis in a regulated system for alleviating symptoms caused by debilitating medical conditions and their medical treatments.
HISTORY: Laws 2007, ch. 210, § 2.
EFFECTIVE DATES. --Laws 2007, ch. 210, § 12 makes the act effective July 1, 2007.”

Mosby’s Medical Dictionary states that “medical treatment” means; the management and care of a patient to combat disease or disorder. Medical treatment includes: Using prescription medications, or use of a non-prescription drug at prescription strength; and or treatment of disease by hygienic and pharmacologic remedies, as distinguished from invasive surgical procedures. Treatment may be pharmacologic, using drugs; surgical, involving operative procedures; or supportive, building the patient's strength. It may be specific for the disorder, or symptomatic to relieve symptoms without effecting a cure.(Mosby's Medical Dictionary, 9th edition.)

What is a chronic medical condition?
A chronic disease is one lasting 3 months or more, by the definition of the U.S. National Center for Health Statistics. Chronic diseases generally cannot be prevented by vaccines or cured by medication, nor do they just disappear. Harvard Medical Dictionary defines chronic as: Any condition that lasts a long time or recurs over time; chronic pain as: Pain that persists after an injury has healed or a disease is over; and chronic pain syndrome as : Long-term, severe pain that doesn't spring from an injury or illness, that interferes with daily life, and is often accompanied by other problems, such as depression, irritability, and anxiety.
What is the meaning of debilitating?
Something that's debilitating seriously affects someone or something's strength or ability to carry on with regular activities, like a debilitating illness. Debilitating comes from the Latin word debilis, meaning "weak." That's why you'll often see the adjective used to describe illness, despite the negative reference.
Petition Purpose and Background

The purpose of this Petition: Requesting The Inclusion Of A New Medical Condition: Post Concussion Syndrome / Concussion And Traumatic Brain Injury (TBI).

This Petition: Requesting The Inclusion Of A New Medical Condition: Post Concussion Syndrome / Concussion And Traumatic Brain Injury (TBI), is being provided to the state Department of Health Medical Cannabis Program so the advisory board can review and recommend to the department for approval additional debilitating medical conditions that would benefit from the medical use of cannabis with the Lynn and Erin Compassionate Use Act.

Who Should Qualify for Medical Cannabis Use?
According to Americans For Safe Access Policy Studies & Research:
Background: The most fundamental aspect of medical cannabis laws is the relationship between a patient and their physician. It is often only the physician and the patient that possess information about a patient’s health condition. However, many public officials and others who oppose medical cannabis laws often make assumptions about people’s health. The media have even fomented such inappropriate assumptions by naming a category of patients “Young Able Bodied Males,” condemning certain patients by visual assessment alone.

Findings: The health care information discussed between a patient and physician is considered private and protected under federal HIPAA laws. It is typically the purview of state medical boards to assess whether a physician has inappropriately recommended cannabis to someone who should not be qualified. Studies have shown in some medical cannabis states that the majority of patients suffer from chronic pain, an ailment that is not obviously detectable by another person. Nevertheless, police will often harass and arrest patients based on the assumption that someone is faking their illness.

Position: Medical professionals should have an unrestricted ability to recommend cannabis therapeutics and that should not be impacted by law enforcement’s perceptions.

Americans For Safe Access policy further states:
“Qualifying medical condition” shall mean any condition for which treatment with medical cannabis would be beneficial, as determined by a patient's qualified medical professional, including but not limited to cancer, glaucoma, positive status for human immunodeficiency virus, acquired immune deficiency syndrome (AIDS), hepatitis C, amyotrophic lateral sclerosis (ALS), Crohn’s disease, Parkinson’s disease, post-traumatic stress disorder, arthritis, chronic pain, neuropathic and other intractable chronic pain, and multiple sclerosis.
“Qualifying patient” shall mean a person who has a written recommendation from a qualified medical professional for the medical use of cannabis.

Post Concussion Syndrome / Concussion And Traumatic Brain Injury (TBI)
(New Research Material Added Starts Here)
Post-concussion syndrome is symptoms that can linger following a concussion. Studies have shown cannabis reduces damage caused from brain injuries and can help patients manage the symptoms of the syndrome.

OVERVIEW OF POST-CONCUSSION SYNDROME

Post-concussion syndrome (PCS) is a variety of symptoms, including headaches and dizziness, that continue for weeks and sometimes months following a concussion. A concussion is a mild traumatic brain injury that typically occurs after a direct blow to the head. Not all concussions lead to post-concussion syndrome, which doesn’t seem to be correlated to the severity of the initial blow. What causes post-concussion symptoms to develop following certain concussions is yet to be identified. According to Mayo Clinic, some experts believe the symptoms come from structural damage to the brain or the disruption of neurotransmitter systems. Others believe that psychological factors may contribute. In addition to headaches and dizziness, post-concussion syndrome commonly causes fatigue, irritability, anxiety, insomnia, loss of concentration and memory, and noise and light sensitivity. Typically, symptoms associated with PCS develop within the first seven to 10 days after a concussion and eventually alleviate within a three-month period. In some cases, however, the symptoms can persist for a year or longer. Treatment for post-concussion syndrome depends on individual symptoms. Headaches are commonly treated with medications. Time, however, is often the best therapy for treating memory and thinking problems.

FINDINGS: EFFECTS OF CANNABIS ON POST-CONCUSSION SYNDROME

While research on cannabis’ direct effect on post-concussion syndrome is lacking, preclinical findings have shown that cannabis offers therapeutic benefits following brain injuries. Studies have shown that the cannabinoids found in cannabis, most specifically cannabidiol (CBD), activate the body’s cannabinoid receptors (CB1 and CB2), though evidence also suggests that the neuroprotective effects from CBD come from the cannabinoid’s activation of the 5-hydroxytriptamine1A (5-HT1A) receptor (Mishima, et al., 2005). When these receptors are activated, they provide protection against neural damage following acute and chronic brain damage (Lopez-Rodriguez, et al., 2013). For example, in one study, the administration of cannabinoids following a traumatic brain injury decreased brain swelling and inflammation and was shown to improve recovery (Shohami, et al., 2011). Another showed that CBD alone provided neuroprotection and limited brain cell death in newborn mice following a hypoxic-ischemic event (Castillo, et al., 2010). Others have showed that cannabinoids, through the activation of the endocannabinoid system, prevent glutamate excitotoxicity, intracellular calcium accumulation, activation of cell death pathways, microglia activation, neurovascular reactivity and circulating leukocytes following a brain injury. Researchers concluded that modulating the endocannabinoid system is an effective way to provide neuroprotection and prevent and reduce brain injury (Fernandez-Lopez, Lizasoain, Moro & Orgado, 2013). Addition research has shown that cannabis’ cannabinoids provide brain and neuroprotection caused by disorders. One found that CBD reduces the oxidative stress and Alzheimer’s hallmark protein (β-amyloid), thus limiting nerve damage caused by the disorder and improving cell viability (Harvey, et al., 2012). An animal study showed that CBD and tetrahydrocannabinol (THC) treatments were effective at delaying and limiting neural damage caused by Huntington’s disease (Sagredo, et al., 2011). Another found that CBD, in addition to providing neuroprotective effects and reducing long-term brain injury, also helped restore neurobehavioral function following a hypoxia-ischemia event (Pazos, et al., 2012). Studies have also shown that cannabis can help post-concussion syndrome patients manage the symptoms associated with the disorder. CBD can lower stress, help combat depression, improve sleep and reduce pain (Abush & Akirav, 2013) (Campos, et al., 2012) (Chagas, et al., 2013) (Russo, Guy & Robson, 2007) (Baron, 2015).

STATES THAT HAVE APPROVED MEDICAL MARIJUANA FOR POST-CONCUSSION SYNDROME

Currently, only the state of Illinois has approved medical marijuana for the treatment of post-concussion syndrome. However, in Washington D.C., any condition can be approved for medical marijuana as long as a DC-licensed physician recommends the treatment. In addition, a number of other states will consider allowing medical marijuana to be used for the treatment of post-concussion syndrome 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”). Also, fourteen states have approved medical marijuana specifically to treat “chronic pain,” which can develop from post-concussion syndrome. These states include: Alaska, Arizona, California, Colorado, Delaware, Hawaii, Maine, Maryland, Michigan, Montana, New Mexico, Ohio, Oregon, Pennsylvania, Rhode Island, Vermont and West Virginia. The states of Nevada, New Hampshire, North Dakota, Ohio and Vermont allow medical marijuana to treat “severe pain.” The states of Arkansas, Minnesota, Ohio, Pennsylvania, Washington and West Virginia have approved cannabis for the treatment of “intractable pain.”

RECENT STUDIES ON CANNABIS’ EFFECT ON POST-CONCUSSION SYNDROME

References: Abush, H., & Akirav, I. (2013). Cannabinoids Ameliorate Impairments Induced by Chronic Stress to Synaptic Plasticity and Short-Term Memory. Neuropsychopharmacology, 38(8), 1521–1534. Retrieved from https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3682147/. Arain, M., Khan, M., Craig, L., and Nakanishi, S.T. (2015, March). Cannabinoid agonist rescues learning and memory after a traumatic brain injury. Annals of Clinical and Translational Neurology, 2(3), 289-94. Retrieved from https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4369278/. Baron, E.P. (2015, June). Comprehensive Review of Medicinal Marijuana, Cannabinoids, and Therapeutic Implications in Medicine and Headache: What a Long Strange Trip It’s Been… Headache, 55(6), 885-916. Retrieved from http://onlinelibrary.wiley.com/wol1/doi/10.1111/head.12570/full. Campos, A. C., Moreira, F. A., Gomes, F. V., Del Bel, E. A., & Guimarães, F. S. (2012). Multiple mechanisms involved in the large-spectrum therapeutic potential of cannabidiol in psychiatric disorders. Philosophical Transactions of the Royal Society B: Biological Sciences, 367(1607), 3364–3378. Retrieved from https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3481531/. Castillo, A., Tolon, M.R., Fernandez-Ruiz, J., Romero, J., and Martinez-Orgado, J. (2010). The neuroprotective effect of cannabidiol in an in vitro model of newborn hypoxic-ischemic brain damage in mice is mediated by CB2 and adenosine receptors. Neurobiology of Disease, 37, 434-440. Retrieved from http://www.sciencedirect.com/science/article/pii/S096999610900309X. Chagas, M.H., Crippa, J.A., Zuardi, A.W., Hallak, J.E., Machado-de-Sousa, J.P., Hirotsu, C., Maia, L., Tufik, S., and Anderson, M.L. (2013, March). Effects of acute systemic administration of cannabidiol on sleep-wake cycle in rats. Journal of Psychopharmacology, 27(3), 312-6. Retrieved from http://journals.sagepub.com/doi/pdf/10.1177/0269881112474524. Donat, C.K., Fischer, F., Walter, B., Deuther-Conrado, W., Brodhun, M., Bauer, R.., and Brust, P. (2014). Early increase of cannabinoid receptor density after experimental traumatic brain injury in the newborn piglet. Acta Neurobiologiae Experimentalis, 74,197-210. Retrieved from http://www.ane.pl/linkout.php?pii=7419. Fernández-López, D., Lizasoain, I., Moro, M. Á., & Martínez-Orgado, J. (2013). Cannabinoids: Well-Suited Candidates for the Treatment of Perinatal Brain Injury. Brain Sciences, 3(3), 1043–1059. Retrieved from https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4061885/. Harvey, B.S., Ohlsson, K.S., Mååg, J.L.V., Musgrave, I.F., and Smid, S.D. (2012, January). Contrasting protective effects of cannabinoids against oxidative stress and amyloid-β evoked neurotoxicity in vitro. NeuroToxicology, 33(1), 138-146. Retrieved from http://www.sciencedirect.com/science/article/pii/S0161813X11002245. Mishima, K., Hayakawa, K., Abe, K., Ikeda, T., Egashira, N., Iwasaki, K., and Fujiwara, M. (2005). Cannabidiol Prevents Cerebral Infarction Via a Serotonergic 5-Hydroxytryptamine1A Receptor–Dependent Mechanism. Stroke, 36, 1071-1076. Retrieved from http://stroke.ahajournals.org/content/36/5/1071.long. López Rodríguez, A.B., Mateos Vicente, B., Romero-Zerbo, S.Y., Rodriguez-Rodriguez, N., Bellini, M.J., Rodriguez de Fonseca, F., Bermudez-Silva, F.J., Azcoitia, I., Garcia-Segura, L.M., and Viveros, M.P. (2011, September). Estradiol decreases cortical reactive astrogliosis after brain injury by a mechanism involving cannabinoid receptors. Cerebral Cortex, 21(9), 2046-55. Retrieved from https://academic.oup.com/cercor/article-lookup/doi/10.1093/cercor/bhq277. Lopez-Rodriguez, A.B., Siopi, E., Finn, D.P., Marchand-Leroux, C., Garcia-Segura, L.M., Jafarian-Tehrani, M.H., and Viveros, M.P. (2013). CB1 and CB2 cannabinoid receptor antagonists prevent minocycline-induced neuroprotection following traumatic brain injury in mice. Cerebral Cortex. Retrieved from https://academic.oup.com/cercor/article-lookup/doi/10.1093/cercor/bht202. Nguyen, B.M., Kim, D., Bricker, S., Bongard, F., Neville, A., Putnam, B., Smith J., and Plurad, D. (2014, October). Effect of marijuana use on outcomes in traumatic brain injury. The American Surgeon, 80(10), 979-83. Retrieved from http://www.ingentaconnect.com/content/sesc/tas/2014/00000080/00000010/art00015.   Panikashvili, D., Shein, N.A., Mechoulam, R., Trembovler, V., Kohen, R., Alexandrovich, A., and Shohami, E. (2006, May). The endocannabinoid 2-AG protects the blood-brain barrier after closed head injury and inhibits mRNA expression of proinflammatory cytokines. Neurobiology of Disease,22(2), 257-74. Retrieved from http://www.sciencedirect.com/science/article/pii/S0969996105003074. Panikashvili, D., Simeonidou, C., Ben-Shabat, S., Hanus, L., Breuer, A., Mechoulam, R., Shohami, E. (2001, October). An endogenous cannabinoid (2-AG) is neuroprotective after brain injury. Nature, 413(6855), 527-31. Retrieved from http://www.nature.com/nature/journal/v413/n6855/full/413527a0.html. Pazos, M.R., Cinquina, V., Gomez, A., Layunta, R., Santos, M., Fernandez-Ruiz, J., and 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), 776-783. Retrieved from http://www.sciencedirect.com/science/article/pii/S0028390812002328.   Post-concussion syndrome. (2014, August 19). Mayo Clinic. Retrieved from http://www.mayoclinic.org/diseases-conditions/post-concussion-syndrome/basics/definition/con-20032705. Russo, E.B., Guy, G.W., and Robson, P.J. (2007, August). Cannabis, pain, and sleep: lessons from therapeutic clinical trials of Sativex, a cannabis-based medicine. Chemistry & Biodiversity, 4(8), 1729-43. Retrieved from http://onlinelibrary.wiley.com/doi/10.1002/cbdv.200790150/pdf. Sagredo, O., Pazos, M.R., Satta, V., Ramos, J.A., Pertwee, R.G., and Fernandez-Ruiz, J. (2011, September). Neuroprotective effects of phytocannabinoid-based medicines in experimental models of Huntington’s disease. Journal of Neuroscience Research, 89(9), 1509-18. Retrieved from http://onlinelibrary.wiley.com/wol1/doi/10.1002/jnr.22682/full. Schurman, L. D., and Lichtman, A. H. (2017). Endocannabinoids: A Promising Impact for Traumatic Brain Injury. Frontiers in Pharmacology, 8, 69. Retrieved from https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5314139/. Shohami, E., Cohen-Yeshurun, A., Magid, L., Algali, M., & Mechoulam, R. (2011). Endocannabinoids and traumatic brain injury. British Journal of Pharmacology, 163(7), 1402–1410. Retrieved from https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3165950/. Xu, Z., Lv, X.A., Dai, Q., Ge, Y.Q., and Xu, J. (2016). Acute upregulation of neuronal mitochondrial type-1 cannabinoid receptor and it’s role in metabolic defects and neuronal apoptosis after TBI. Molecular Brain, 9, 75. Retrieved from https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4971620/.]]>


Traumatic brain injuries are brain dysfunctions that are caused by an outside blow to the head. Studies have shown marijuana helps limit brain damage and improves recovery when administered shortly after the traumatic blow.

OVERVIEW OF TRAUMATIC BRAIN INJURIES

A traumatic brain injury (TBI) is a disruption of the normal function of the brain caused by a bump or blow to the head. A mild brain injury, or concussion, can cause temporary brain cell dysfunction, while a more serious injury can cause the brain tissue to bruise, tear or bleed and result in long-term complications or death.
In a TBI, the blow to the head causes damage to the brain cells. The damage can be isolated to the point of impact or can be more widespread if the impact causes the brain to moves back and forth within the skull. In addition, bleeding in the brain, or swelling, can cause greater damage to brain cells.
According to Mayo Clinic, additional complications can arise from TBI’s, including altered consciousness (coma, vegetative state, locked-in syndrome, brain death, etc…), seizures, fluid buildup, blood vessel damage, nerve damage, and intellectual, communication, sensory and behavioral problems.
The physical and psychological symptoms of a TBI can vary significantly and can arise immediately after the traumatic blow or even weeks later. Physical symptoms include a loss of consciousness or being dazed, headache, nausea or vomiting, fatigue, sleeping difficulties, sleeping more than usual and dizziness. It’s not uncommon for sensory problems, like blurred vision or ear ringing to occur. Also, memory and concentration problems, mood changes and a feeling of depression are cognitive symptoms of a TBI.
For mild brain injuries, rest and over-the-counter pain relievers for headaches are often adequate for recovery. More severe brain injuries require emergency care procedures to ensure oxygen, blood levels and blood pressure remain at adequate levels. Medications may be used to help limit secondary damage caused by fluid buildup. In some cases, surgery is required to repair skull fractures or to relief pressure by draining fluid.

FINDINGS: EFFECTS OF CANNABIS ON TRAUMATIC BRAIN INJURIES

Following the blow that leads to TBI’s, the body releases harmful mediators that lead to excitotoxicity, oxidative stress and inflammation and causes secondary, delayed neuronal death (Biegon, 2004). Cannabis, however, has been shown to offer protection to the neural system, thus reducing the amount of brain damage (Mechoulam, Spatz & Shohami, 2002) (Mechoulam & Shohami, 2007) (Mechoulam, Panikashvili & Shohami, 2002) (Biegon, 2004).
It’s cannabis’ two major cannabinoids, tetrahydrocannabinol (THC) and cannabidiol (CBD) that are responsible for these beneficial effects following TBI’s. Cannabinoids have been shown to act on the CB1 and CB2 receptors of the endocannibinoid system, which in turn prevents the release of proinflammatory cytokines that are released after brain drama and cause damage (Panikashvili, et al., 2006). Activating of the CB1 and CB2 receptors also has been shown to stimulate the release of minocycline, which reduces brain swelling and neurological impairment, and diffuses further injuries to the brain’s axons (Lopez-Rodriguez, et al., 2015) (Biegon, 2004).
In one study, cannabinoid administered to mice with brain injuries caused a significant reduction of brain swelling, as well as better clinical recovery, reduced infarct volume, and reduced brain cell death compared to the control group (Panikashvili, et al., 2001). In another, CBD was found to reduce acute and apoptic brain damage (Castillo, et al., 2010). Piglets with brain injuries given CBD experienced less excitotoxicity, oxidative stress and inflammation (Pazos, et al., 2013). Mice that had suffered an impact brain injury showed marked recovery in object recognition and in performing a specific task after CB1 receptors were activated (Arain, Khan, Craig & Nakanishi, 2015). Cannabinoids have even shown to be effective at offering neuroprotection in newborn babies that have experienced a brain injury (Fernandez-Lopez, Lizasoain, Moro & Martinez-Orgado, 2013).
One study found that patients that had detectable levels of THC in their bodies were less likely to die as a result of a traumatic brain injury than those who didn’t (Nguyen, et al., 2014). Just recently, researchers from the University of Arizona found that trauma patients who tested positive for cannabis upon hospital admission were less likely to die during hospitalization (Singer, et al., 2017).

STATES THAT HAVE APPROVED MEDICAL MARIJUANA FOR TRAUMATIC BRAIN INJURIES

Currently, just Illinois, New Hampshire, Washington have approved medical marijuana specifically for the treatment of traumatic brain injuries.
A number of other states will consider allowing medical marijuana to be used for the treatment of traumatic brain injuries 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), and Rhode Island (other conditions subject to approval).
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 TRAUMATIC BRAIN INJURIES

References:
Arain, M., Khan, M., Craig, L., and Nakanishi, S.T. (2015, March). Cannabinoid agonist rescues learning and memory after a traumatic brain injury. Annals of Clinical and Translational Neurology, 2(3), 289-94. Retrieved from https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4369278/.
Biegon, A. (2004). Cannabinoids as neuroprotective agents in traumatic brain injury. Current Pharmaceutical Design, 10(18), 2177-83. Retrieved from http://www.eurekaselect.com/62903/article.
Castillo, A., Tolon, M.R., Fernandez-Ruiz, J., Romero, J., 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 Disease, 37(2), 434-40. Retrieved from http://www.sciencedirect.com/science/article/pii/S096999610900309X.
Donat, C.K., Fischer, F., Walter, B., Deuther-Conrado, W., Brodhun, M., Bauer, R.., and Brust, P. (2014). Early increase of cannabinoid receptor density after experimental traumatic brain injury in the newborn piglet. Acta Neurobiologiae Experimentalis, 74,197-210. Retrieved from http://www.ane.pl/linkout.php?pii=7419.
Fernandez-Lopez, D., Lizasoain, I., Moro, M.A., and Martinez-Orgado, J. (2013). Cannabinoids: Well-suited candidates for the treatment of perinatal brain injury. Brain Sciences, 3, 1043-1059. Retrieved from https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4061885/.
Injury Prevention and Control: Traumatic Brain Injury. (2015, February 24). Centers for Disease Control and Prevention. Retrieved from http://www.cdc.gov/traumaticbraininjury/get_the_facts.html.
López Rodríguez, A.B., Mateos Vicente, B., Romero-Zerbo, S.Y., Rodriguez-Rodriguez, N., Bellini, M.J., Rodriguez de Fonseca, F., Bermudez-Silva, F.J., Azcoitia, I., Garcia-Segura, L.M., and Viveros, M.P. (2011, September). Estradiol decreases cortical reactive astrogliosis after brain injury by a mechanism involving cannabinoid receptors. Cerebral Cortex, 21(9), 2046-55. Retrieved from https://academic.oup.com/cercor/article-lookup/doi/10.1093/cercor/bhq277.
Lopez-Rodriguez, A.B., Siopi, E., Finn, D.P., Marchand-Leroux, C., Garcia-Segura, L.M., Jafarian-Tehrani, M., and Viveros, M.P. (2015, January). CB1 and CB2 cannabinoid receptor antagonists prevent minocycline-induced neuroprotection following traumatic brain injury in mice. Cerebral Cortex, 25(1), 35-45. Retrieved from https://academic.oup.com/cercor/article-lookup/doi/10.1093/cercor/bht202.
Mechoulam, R., and Shohami, E. (2007, August). Endocannabinoids and traumatic brain injury. Molecular Neurobiology, 36(1), 68-74. Retrieved from http://link.springer.com/article/10.1007/s12035-007-8008-6.
Mechoulam, R., Spatz, M., and Shohami, E. (2002, April 23). Endocannabinoids and neuroprotection. Science’s STKE, 2002(129). Retrieved from http://stke.sciencemag.org/content/2002/129/re5.full.
Mechoulam, R., Panikashvili, D., and Shohami, E. (2002, February). Cannabinoids and brain injury: therapeutic implications. Trends in Molecular Medicine, 8(2), 58-61. Retrieved from http://www.cell.com/trends/molecular-medicine/fulltext/S1471-4914(02)02276-1.
Nguyen, B.M., Kim, D., Bricker, S., Bongard, F., Neville, A., Putnam, B., Smith J., and Plurad, D. (2014, October). Effect of marijuana use on outcomes in traumatic brain injury. The American Surgeon, 80(10), 979-83. Retrieved from http://www.ingentaconnect.com/content/sesc/tas/2014/00000080/00000010/art00015.
Panikashvili, D., Shein, N.A., Mechoulam, R., Trembovler, V., Kohen, R., Alexandrovich, A., and Shohami, E. (2006, May). The endocannabinoid 2-AG protects the blood-brain barrier after closed head injury and inhibits mRNA expression of proinflammatory cytokines. Neurobiology of Disease,22(2), 257-74. Retrieved from http://www.sciencedirect.com/science/article/pii/S0028390813001238.
Panikashvili, D., Simeonidou, C., Ben-Shabat, S., Hanus, L., Breuer, A., Mechoulam, R., Shohami, E. (2001, October). An endogenous cannabinoid (2-AG) is neuroprotective after brain injury. Nature, 413(6855), 527-31. Retrieved from https://goo.gl/FNFJPH.
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., Martinez-Orgado, J. (2013, August). Mechanisms of cannabidiol neuroprotection in hyopoxic-ischemic newborn pigs: role of 5HT(1A) and CB2 receptors. Neuropharmacology, 71, 282-91. Retrieved from http://www.sciencedirect.com/science/article/pii/S0028390813001238.
Presley, C., Abidi, A., Suryawanshi, S., Mustafa, S., Meibohm, B., and Moore, B.M. (2015). Preclinical evaluation of SMM-189, a cannabinoid receptor 2-specific inverse agonist. Pharmacology Research & Perspectives, 3(4), e00159. Retrieved from https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4506688/.
Schurman, L. D., and Lichtman, A. H. (2017). Endocannabinoids: A Promising Impact for Traumatic Brain Injury. Frontiers in Pharmacology, 8, 69. Retrieved from https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5314139/.
Shohami, E., Cohen-Yeshurun, A., Magid, L., Algali, M., and Mechoulam, R. (2011). Endocannabinoids and traumatic brain injury. British Journal of Pharmacology, 163(7), 1402–1410. Retrieved from https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3165950/.
Singer, M., Azim, A., O’Keefe, T., Khan, M., Jain, A., Kulvatunyou, N., Gries, L., Jehan, F., Tang, A., and Joseph, B. (2017, August 5). How Does Marijuana Effect Outcomes After Trauma in ICU Patients? A Propensity Matched Analysis. The Journal of Trauma and Acute Care Surgery, doi: 10.1097/TA.0000000000001672. [Epub ahead of print]. Retrieved from http://journals.lww.com/jtrauma/Abstract/publishahead/How_Does_Marijuana_Effect_Outcomes_After_Trauma_in.98956.aspx.
Traumatic brain injury. (2014, May 15). Mayo Clinic. Retrieved from http://www.mayoclinic.org/diseases-conditions/traumatic-brain-injury/basics/definition/con-20029302.
Xu, Z., Lv, X.Q., Dai, Q. Ge, Y.Q. and Xu, J. Acute upregulation of neuronal mitochondrial type-1 cannabinoid receptor and it’s role in metabolic defects and neuronal apoptosis after TBI. Molecular Brain, 9,75. Retrieved from https://molecularbrain.biomedcentral.com/articles/10.1186/s13041-016-0257-8.

Beneficial Cannabinoids and Terpenoids Useful for Treating Post Concussion Syndrome And TBI
The cannabis plant offers a plethora of therapeutic benefits and contains cannabinoids and terpenoid compounds that are useful for managing symptoms with Post Concussion Syndrome And TBI. Although much of the scientific research surrounding cannabis has been focused on both Tetrahydrocannabinol (THC) and Cannabidiol (CBD) for their ability to be potent Analgesics and Anti-Nausea (Anti-Emetic) medicines, the following list denotes which cannabinoids and terpenoids also work synergistically with each other for possible therapeutic benefit:
References
Understanding medical cannabis.Elemental Wellness Center, 2014 Jul.
(End of New Research Material Presented)
Currently, there is no effective drug for the treatment of traumatic brain injury and concussions. In the U.S., there are nearly 52,000 deaths and roughly 80,000 cases of severe disability related to traumatic brain injury every year. There are more than 5.3 million people in the U.S. living with disabilities related to traumatic brain injury — numbers far greater than those for multiple sclerosis, Parkinson's disease and Alzheimer's disease.

What is the most common sport causing head injury?
Football accounted for 47,000 of those head injuries, and baseball played a role in 38,394. Cycling was also the leading cause of sports-related head injuries in children under 14, causing 40,272 injuries, roughly double the number related to football (21,878).  

Concussions are also sometimes referred to as mTBI (Mild Traumatic Brain Injury). Concussions are injuries to the head which cause a temporary lapse in the normal operation of brain function. Concussions have many symptoms which could be displayed in a physical, psychological or emotional manner.

In recent years, the clear link between playing football and traumatic brain injuries has been prevalent in the sporting world news.  After a  2013 NFL settlement of $765 million for concussion-related injuries, and new lawsuits springing up as more research comes out, it is more clear than ever that action needs to be taken against such brain injuries.

In 2015, concussion-related injuries were in the spotlight, primarily as a result of the major motion picture – “Concussion”. The movie, based on a true story, highlights the findings of Nigerian-born forensic neuropathologist, Dr. Bennet Omalu, who researched the connection between concussions and what is now known as chronic traumatic encephalopathy (CTE).  His research created an onslaught of scrutiny toward the NFL and has been the catalyst for a class-action lawsuit between the National Football League and thousands of former players.

CTE is a progressive degenerative disease caused by repetitive trauma to the brain. Symptoms include memory loss, migraine headache, confusion, impaired judgment, paranoia, impulse control problems, aggression, depression, and progressive dementia. The brain degenerates even after the trauma has ended and can appear months or years after the trauma has ended. Because of the feelings of depression that are linked to CTE, those afflicted may experience thoughts of suicide.

In recent years, too many professional athletes have already been lost to this, who have committed suicide and were suffering from CTE.  In 2013, former NFL star and Pro Football Hall of Fame Inductee, Junior Seau, took his own life with a self-inflicted gunshot wound to the chest. It was later discovered that he suffered from CTE. Football players are not the only athletes that experience thoughts of suicide due to traumatic brain injuries. BMX pro — the world’s most well known cyclist and X Games Superstar, Dave Mirra, also ended his life by suicide. Those close to him were shocked by his actions and it was found that CTE played a role, as reported by ESPN earlier this year.

Dr. Dustin Sulak, DO, says, “Cannabis could potentially be beneficial to all sports, but especially those with high risk for head injury, because it can likely protect participants from the long term consequences of concussion and brain trauma.”

THC and other naturally occurring cannabinoids act on brain injury as a general neuroprotective agents with antioxidant properties, which can have crucial roles in treatment of Concussions, CTE and Traumatic Brain Injury.  Post-concussion syndrome is symptoms that can linger following a concussion. Studies have shown cannabis reduces damage caused from brain injuries and can help athletes manage the symptoms of the syndrome.
In a study conducted with mice afflicted with brain injuries at the Hebrew University in Israel, researchers found that the subjects had an increased level of a cannabinoid called 2-Arachodonoyl (2-AG). The researchers theorized that this compound was increased in order to protect the brain from trauma. Working on this theory, the researchers administered more 2-AG to the subjects and discovered that the compound did indeed protect the brain. Though it has only been tested on animals, Dr. Shahomi, a researcher on the project, says she doesn’t “see any problems with using a drug from this family to treat patients.”
Research from the study at the Hebrew University conclude that 2-AG works in three ways.
“First, it reduces the levels of glutamate, a toxic molecule, released after injury. Second, it decreases the amount of free radicals and TNF (a chemical that induces inflammation) after injury. Third, it increases the blood supply to the brain. All three mechanisms are essential for limiting the damage done after the primary injury.”
By definition, neuroprotection is an effect that may result in salvage, recovery or regeneration of the nervous system, its cells, structure and function. It is thought that there are many neurochemical modulators of nervous system damage. An antioxidant is a molecule that inhibits the oxidation of other molecules. Oxidation is a chemical reaction that can produce free radicals, leading to chain reactions that may damage cells. Antioxidants such as thiols or ascorbic acid (vitamin C) terminate these chain reactions. That’s right, just like vitamin C - THC and CBD all do the body good.
Cannabis has shown a wealth of potential in traumatic brain injury. Unique properties of the herb may help the brain repair itself after trauma, including trauma from a concussion. Overall, there are three main characteristics that make cannabis a promising treatment for concussions and other forms of head trauma. These include,

1. Reduced brain inflammation

The cannabis plant contains neuroprotective antioxidants. These neuroprotectants have many functions, including preventing stress-related damage and reducing inflammation in the brain. One major impact of a concussion or any sort of head trauma is increased neural inflammation.
A 2014 study from Tel Aviv University found that microdoses of psychoactive THC reduced brain swelling in rodent models. The researchers write,
Our results suggest that an ultralow dose of THC that lacks any psychotrophic activity protects the brain from neuroinflammation-induced cognitive damage and might be used as an effective drug for the treatment of neuroinflammatory conditions, including neurodegenerative diseases.

2. Neuroprotection

These same anti-inflammatory effects may prove very useful in treating a concussion. Surprisingly, the US government also thinks that cannabis is a promising treatment for head injury. The Feds currently hold a patent on nonpsychoactive CBD as a neuroprotective agent.
In the patent application, they write,
The cannabinoids [in cannabis] are found to have particular application as neuroprotectants, for example in limiting neurological damage following ischemic insults, such as stroke and trauma, or in the treatment of neurodegenerative diseases, such as Alzheimer’s disease, Parkinson’s disease and HIV dementia.
So, even the US government admits that compounds in the cannabis plant may decrease the damage from head and brain trauma, as well as from strokes, oxygen deprivation, and neurodegenerative diseases.
Further, research from 2013 found that the endocannabinoid system (ECS) plays a crucial role in the brain’s ability to repair itself.  The ECS is the pathway in which cannabis engages with the body. The study articulates that therapeutic cannabinoids may provide protection against nerve cell damage after acute injury.

3. Pre-treatment with cannabis prevents damage

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There is evidence that pre-treatment with cannabis can help protect against possible concussions associated with certain occupations. These include professional athletics, horseback riding, and other lifestyle activities that make a person more susceptible to concussions.
This doesn’t necessarily mean go out and smoke some herb every day. Rather, this may be a case where having a little CBD oil on hand or using it as a dietary supplement may be beneficial.
In an interview with Fox News, Dean Petkanas, CEO of KannaLife Sciences, explains,
“You have a repository of chemicals in the plant. But, more prominantly we’ve found in some preclinical research that cannabidiol (CBD) acts as a neuroprotectant. So, in the parlence of pharmaceutical science, we could be using that as a prophilaxis against repetative concussive injury.”
Simply stated, pharmaceutical companies are hoping to make drugs that would prevent brain damage from concussions before they happen.
While much of the research has focused on CBD, preclinical research shows that psychoactive THC may be helpful as well. A 2014 study found that patients with traumatic brain injury who had detectable levels of THC in their systems at the time of an accident were less likely to die from brain trauma.

Cannabis and post-concussion syndrome

Post-concussion syndrome (PCS) is a complex condition that sometimes follows a concussion. The symptoms of PCS can last for months after the initial brain injury.
According to the Mayo Clinic, some of the symptoms include,
  • Headaches
  • Dizziness
  • Fatigue
  • Irritability
  • Anxiety
  • Insomnia
  • Loss of concentration and memory
  • Noise and light sensitivity
Unfortunately, PCS is also blamed for many persisting psychiatric problems after a concussion. Risks for depression and suicide increase after head trauma. Recent research has found that even one concussion may triple the long-term risk of suicide.
Cannabis therapies may be able to improve PCS symptoms. One 2012 rodent study suggested that cannabinoid treatments may help improve memory and cognitive performance after stress-related neuropsychiatric conditions.
Additional rodent studies have found that CBD is an extremely fast-acting antidepressant. Many conventional pharmaceutical options take up to 6 weeks to kick in. In this study, rodents under stress that were treated with CBD showed improvements just minutes after their first dose. CBD continued to work over time.

Medical Cannabis and the NFL

National Football League (NFL) players wear helmets for a reason. Though, as recent lawsuits show, a little padding is not enough to protect against the potentially life-long damage caused concussive and sub-concussive head trauma. Over the past few years, some experts have hypothesized that external protection is not enough.
Legendary psychiatrist Dr. Lester Grinspoon, Professor emeritus at Harvard University, thinks that the NFL should study medical cannabis.
After publishing an open letter explaining his position, he told Fusion,
“The NFL should pay attention to the fact that we are now pretty confident that cannabis, marijuana, has as a medicine, some qualities about which make it clear that it is neuroprotective.”
In a way, compounds in cannabis are like internal shock absorbers, checking back the damage sustained with a concussion and other forms of head trauma.
We’re talking about a particular formulation of the cannabinoids. That is, a formulation which is largely made of CBD, or cannabidiol, and to a much lesser exent, tetrahydrocannabinol. And of course, along with it, the kinds of other phytochemicals like terpeneoids.
Grinspoon goes on to state that this cannabis formulation is completely nonpsychoactive. NFL players and anyone else suffering a concussion can reap the benefits of cannabis without any added haziness from a psychoactive high. Instead, the high-CBD formulation is much more like a high-quality hemp extract.
More research on cannabis and concussion and PCS are sorely needed. But, as Grinspoon suggests, many medical scientists have confidence that the herb has some serious brain-healing potential.
Now, cannabis hopefuls just need governments around the world to permit access to the plant.
These cannabinoids as antioxidants and neuroprotectants are also why the U.S. Patent Office issued patent #6630507 to the U.S. Health and Human Services Department. The patent lists the use of certain cannabinoids found within the cannabis plant as useful in additional neurodegenerative diseases such as Alzheimer's, Parkinson's, and HIV dementia.

Since cannabis contains compounds recognized and endorsed by an agency of the U.S. government- Why is it that cannabis remains on the Federal Schedule One list of drugs?
As this patent is a direct contradiction of the government’s own definition for the classification of a Schedule I drug and it should provide the professional sports world reason enough to allow for the use of cannabis.

The non-psychoactive part of cannabis known, as CBD, also has the potential to treat and even prevent concussions. The NFL should set an example by investing in cannabis research to see how it can help improve the health of its players. The new studies have found that certain properties in cannabis can help shield the brain from injury. Like all cannabinoids, CBD helps the body by imitating the endocannabinoids produced in the body as part of the endocannabinoid system, and has also been found to have the potential to reduce inflammation in the brain when brain trauma occurs.
When the brain is injured, three main processes lead to spreading brain damage that becomes permanent, said Dustin Sulak, medical director for Integr8 Health in Maine. Those are the swelling of the brain, the damaging of neurons and the damaging of molecules. CBD limits all three of these damaging processes “unlike most pharmaceuticals” which target just one specific problem, Sulak said. “THC also has profound neuroprotective effects that in many cases are more powerful than those of CBD, but the best results are achieved by using the combination,” Sulak continued.

According to a study from the Los Angeles Biomedical Research Institute, patients with traumatic brain injury who also tested positive for THC had a significantly lower mortality rate.
The study included 446 patients who suffered traumatic brain injuries and underwent a urine test for the presence of THC in their system, which 82 patients tested positive for. Of those 82 patients who tested positive for THC, only 2.4 percent died, whereas 11.5 percent of the patients without THC in their systems died.

When CBD is administered with THC, it reduces its psychoactive effects. Therefore a person could take the combination of the two chemicals, protecting the brain without any impairment or euphoria.
According to Sulak, in the case of football players, the cannabinoids would be best consumed prior to the injury, however it would still be effective post injury.
“If CBD were present in the brain at the time of the injury, instead of administered 15-30 minutes later, the beneficial effects would likely be even more profound,” Sulak said.

“Since CBD has other beneficial properties desired by professional athletes, such as pain and anxiety relief, and enhanced healing of injured muscle and bone, it would certainly make sense to take CBD for prevention before an injury.”

Former Super Bowl champions Marvin Washington, Scott Fujita and Brendon Ayanbadejo helped start a conversation two years ago,  calling on the NFL to incorporate medical cannabis in their strategy for treating and preventing concussions. Eugene Monroe continued the debate earlier this year when he became the first current player to call on the NFL to look at the benefits of medical cannabis. He has since been joined by Derrick Morgan.  

Currently, only the state of Illinois has approved medical cannabis for the treatment of post-concussion syndrome. However, in Washington D.C., any condition can be approved for medical cannabis as long as a DC-licensed physician recommends the treatment. In addition, a number of other states will consider allowing medical cannabis to be used for the treatment of post-concussion syndrome with the recommendation from a physician. These states include: California (any debilitating illness where the medical use of cannabis 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”).

Also many states have approved medical cannabis specifically to treat “chronic pain,” which can develop from post-concussion syndrome. These states include: Alaska, Arizona, California, Colorado, Delaware, Hawaii, Maine, Maryland, Michigan, Montana, New Mexico, Ohio, Oregon, Pennsylvania, Rhode Island and Vermont. The states of Nevada, New Hampshire, North Dakota, Ohio and Vermont allow medical cannabis to treat “severe pain.” The states of Arkansas, Minnesota, Ohio, Pennsylvania and Washington have approved cannabis for the treatment of “intractable pain.”

Athletes and professional sports leagues in general have a large influence on our culture, as of 2012 Americans spent $25.4 billion directly on professional sports.  And if these leagues change their policies on cannabis, they can make a major league impact to help change the way people think about cannabis, how it is used and the people who use it.  If the NFL were to finance this research into cannabis for Concussions, CTE and Traumatic Brain Injury -the potential impact reaching into future generations is tremendous. Not only would the league attempt to cure a major medical question that plagues modern sports, but it could potentially set a precedent in professional sports world,  pushing cannabis research forward to fully discover the whole plant’s potential.

The looseness of the NFL’s current cannabis policy, as well as Commissioner Goodell’s recent statement that the league is willing to support research into cannabis for medical uses specific to football injuries, suggest that this possibility is becoming a viable future option.

We need to continue developing our understanding of cannabinoid neurobiology in order to most effectively utilize the numerous therapeutic properties of cannabis. We can then unleash the full spectrum of benefits cannabinoids, the therapeutic effects and synergistic terpenoids are able to provide and discover innovative new treatments that could quite possibly help the millions of people who continue to suffer from Concussions, CTE, and Traumatic Brain Injury.

While smoking is unlikely the optimal delivery method for cannabis in athletes, the use of cannabis can have performance-enhancing effects by reducing anxiety, thus promoting optimal performance under stressful conditions like competition, improving mood, and supporting post-exercise relaxation and sleep.1
Other studies have described improved oxygenation to tissues, improved vision, ability to forget previous traumatic experiences related to the activity, reduction in muscle spams, and pain relief.2  Recent animal research demonstrates decreased damage and improved healing after skeletal muscle injury,3 and protection of the brain in head injury.4  Many of my patients have also reported improved focus, increased optimism, and an easier time, “being in the flow.” Cannabis could potentially be beneficial to all sports, but especially those with high risk for head injury, because it can likely protect participants from the long-term consequences of concussion and brain trauma. (See References Below)
What is Traumatic Brain Injury

A traumatic brain injury, also known as TBI or intracranial injury, is generally the result of a sudden, violent blow or jolt to the head. The brain is launched into a collision course with the inside of the skull, resulting in possible bruising of the brain, tearing of nerve fibers and bleeding.
Study: Cannabis-Based Medicines As Potential Treatments For Traumatic Brain Injuries
A recent study published in The American Surgeon was titled “Effect of Marijuana Use on Outcomes in Traumatic Brain Injury.” In this study, researchers concluded that patients who had detectable levels of THC in their bodies were less likely than those who did not to die as a result of traumatic brain injury (TBI). The retrospective study examined the data of 446 cases of traumatic brain injuries over a three year period, involving patients who had been treated at Harbor-UCLA Medical Center in Torrance, CA.

THC Helps Prevent Death From Traumatic Brain Injury

Overall, 18.4% of patients traumatic brain injury in the sample had toxicology reports positive for the presence of THC, and the death rate for all cases examined was 9.9%. After adjusting for differences that may confound results (such as age, gender, and classification of injury), the death rate for TBI patients with THC-negative toxicology reports (i.e. without detectable levels of THC in their body) was 11.5%, but for traumatic brain injury patients with THC-positive reports was only 2.4%. Therefore, the survival of THC-positive TBI patients was approximately 80 times more than the survival of THC-negative TBI patients.
Interpretation Of The Study’s Results
The fact that this was a retrospective analysis, as opposed to a double-blind, placebo-controlled, randomized trial, limits the ability to determine a cause-effect relationship from the study (i.e. it cannot be determined from this study alone that THC is the direct cause of the decreased rate of death from TBI). Additionally, the frequency of cannabis use of the THC-positive patients and the method of delivery used by the traumatic brain injury patients (e.g. smoking, vaporizing, ingesting) was unknown.
“…therefore, the survival of THC-positive TBI patients was approximately 80 times more than the survival of THC-negative TBI patients.”
According to a Reuters article on the study, “One concern with the study, according to [Dr. David] Plurad (one of the study’s authors), is that the test for THC could not distinguish between occasional and regular users. A person could test positive after having used marijuana days or even weeks before.” This is largely due to the fact that THC is fat-soluble, and can therefore accumulate in your fat cells instead of being immediately excreted by the body, like water-soluble compounds.
Plurad also states that while similar studies conducted in the past found that alcohol was protective from TBI death, the presence/absence of THC in these studies was not controlled for. Therefore, the potential exists (“potential” being the key word) that the patients who had detectable levels of alcohol in their body in these studies also had THC in their system, which is what actually led to the neuroprotective results. Because of this, the validity of these past studies’ results may be limited. Additionally, the researchers in the currently reviewed study also examined the effect of alcohol on traumatic brain injury death rate, and found that “[alcohol] didn’t turn out to be as protective as the presence of the marijuana”.
More Evidence for Utility of Cannabinoid-Based Medicines
While the results of this study do not definitively prove that the use of cannabis (at levels resulting in physiologically detectable levels of THC) will help to prevent death in the case of a traumatic brain injury, they do lend to a growing body of evidence that endogenous cannabinoids (i.e. those occurring naturally in our bodies, such as 2-AG) and exogenous cannabinoids (e.g. those found in the cannabis plant, or synthetic forms) may prevent or halt brain injury, even in infants.
For instance, a 2013 study published in Neuropharmacology found that when administered to piglets who had sustained hypoxic-ischemic brain injury (i.e. caused by low oxygen), CBD (cannabidiol), one of the most frequently occurring compounds in cannabis, “exerts robust neuroprotective effects… modulating excitotoxicity, oxidative stress and inflammation.”
A 2001 study published in Nature found that administration of 2-AG to mice that had sustained closed head injury prevented “secondary injury” that follows the primary closed head injury (e.g. it reduced the occurrence of brain edema, decreased size of the area of damage and death of cells in the hippocampus [an area of the brain involved in memory]) and improved recovery. According to an abcNEWS article on the study, “The cannabinoid, 2-AG, is believed to work in three ways. First, it reduces the levels of glutamate, a toxic molecule, released after injury. Second, it decreases the amount of free radicals and TNF (a chemical that induces inflammation) after injury. Third, it increases the blood supply to the brain. All three mechanisms are essential for limiting the damage done after the primary injury.”
In a 2006 study published in found that dexanabinol, a synthetic cannabinoid derivative, while found to be safe, was not effective in treating TBI (dexanabinol does not produce the intoxication caused by cannabis strains with psychoactive levels of THC because instead of binding to CB1 and CB2 receptors, it functions by blocking NMDA/glutamate receptors and neutralizing free radicals which can damage the body).
All of these findings signify the validity of research into the effects of THC and other naturally occurring cannabinoids on brain injury and as general neuroprotective agents, which may have roles in treatment of neurodegenerative diseases like ALS, Alzheimer’s, Concussion, CTE,  Parkinson’s, Huntington’s, TBI and others. ( Source )
Endocannabinoid Degradation Inhibition Improves Neurobehavioral Function, Blood-Brain Barrier Integrity, and Neuroinflammation following Mild Traumatic Brain Injury [https://www.ncbi.nlm.nih.gov/pubmed/25166905]
J Neurotrauma. 2015 Mar 1;32(5):297-306. doi: 10.1089/neu.2014.3508. Epub 2014 Dec 19.

Author information

Abstract

Traumatic brain injury (TBI) is an increasingly frequent and poorly understood condition lacking effective therapeutic strategies. Inflammation and oxidative stress (OS) are critical components of injury, and targeted interventions to reduce their contribution to injury should improve neurobehavioral recovery and outcomes. Recent evidence reveals potential protective, yet short-lived, effects of the endocannabinoids (ECs), 2-arachidonoyl glycerol (2-AG) and N-arachidonoyl-ethanolamine (AEA), on neuroinflammatory and OS processes after TBI. The aim of this study was to determine whether EC degradation inhibition after TBI would improve neurobehavioral recovery by reducing inflammatory and oxidative damage. Adult male Sprague-Dawley rats underwent a 5-mm left lateral craniotomy, and TBI was induced by lateral fluid percussion. TBI produced apnea (17±5 sec) and a delayed righting reflex (479±21 sec). Thirty minutes post-TBI, rats were randomized to receive intraperitoneal injections of vehicle (alcohol, emulphor, and saline; 1:1:18) or a selective inhibitor of 2-AG (JZL184, 16 mg/kg) or AEA (URB597, 0.3 mg/kg) degradation. At 24 h post-TBI, animals showed significant neurological and -behavioral impairment as well as disruption of blood-brain barrier (BBB) integrity. Improved neurological and -behavioral function was observed in JZL184-treated animals. BBB integrity was protected in both JZL184- and URB597-treated animals. No significant differences in ipsilateral cortex messenger RNA expression of interleukin (IL)-1β, IL-6, chemokine (C-C motif) ligand 2, tumor necrosis factor alpha, cyclooxygenase 2 (COX2), or nicotinamide adenine dinucleotide phosphate oxidase (NOX2) and protein expression of COX2 or NOX2 were observed across experimental groups. Astrocyte and microglia activation was significantly increased post-TBI, and treatment with JZL184 or URB597 blocked activation of both cell types. These findings suggest that EC degradation inhibition post-TBI exerts neuroprotective effects. Whether repeated dosing would achieve greater protection remains to be examined.

Endocannabinoids and traumatic brain injury.

Br J Pharmacol. 2011 Aug;163(7):1402-10. doi: 10.1111/j.1476-5381.2011.01343.x.

Author information

Abstract

Traumatic brain injury (TBI) represents the leading cause of death in young individuals. It triggers the accumulation of harmful mediators, leading to secondary damage, yet protective mechanisms are also set in motion. The endocannabinoid (eCB) system consists of ligands, such as anandamide and 2-arachidonoyl-glycerol (2-AG), receptors (e.g. CB1, CB2), transporters and enzymes, which are responsible for the 'on-demand' synthesis and degradation of these lipid mediators. There is a large body of evidence showing that eCB are markedly increased in response to pathogenic events. This fact, as well as numerous studies on experimental models of brain toxicity, neuroinflammation and trauma supports the notion that the eCB are part of the brain's compensatory or repair mechanisms. These are mediated via CB receptors signalling pathways that are linked to neuronal survival and repair. The levels of 2-AG, the most highly abundant eCB, are significantly elevated after TBI and when administered to TBI mice, 2-AG decreases brain oedema, inflammation and infarct volume and improves clinical recovery. The role of CB1 in mediating these effects was demonstrated using selective antagonists or CB1 knockout mice. CB2 were shown in other models of brain insults to reduce white blood cell rolling and adhesion, to reduce infarct size and to improve motor function. This review is focused on the role the eCB system plays as a self-neuroprotective mechanism and its potential as a basis for the development of novel therapeutic modality for the treatment of CNS pathologies with special emphasis on TBI.
© 2011 The Authors. British Journal of Pharmacology © 2011 The British Pharmacological Society.

Endocannabinoids and neuroprotection.[https://www.ncbi.nlm.nih.gov/pubmed/11972360]
Sci STKE. 2002 Apr 23;2002(129):re5.
Abstract
Traumatic brain injury (TBI) releases harmful mediators that lead to secondary damage. On the other hand, neuroprotective mediators are also released, and the balance between these classes of mediators determines the final outcome after injury. Recently, it was shown that the endogenous brain cannabinoids anandamide and 2-Arachidonoyl glycerol (2-AG) are also formed after TBI in rat and mouse respectively, and when administered after TBI, they reduce brain damage. In the case of 2-AG, better results are seen when it is administered together with related fatty acid glycerol esters. Significant reduction of brain edema, better clinical recovery, and reduced infarct volume and hippocampal cell death are noted. This new neuroprotective mechanism may involve inhibition of transmitter release and of inflammatory response. 2-AG is also a potent modulator of vascular tone, and counteracts the endothelin (ET-1)-induced vasoconstriction that aggravates brain damage; it may thus help to restore blood supply to the injured brain.

Overview Of TBI
https://youtu.be/T0WBMM7WKL4

Open Letter to NFL Commissioner Roger Goodell

By Lester Grinspoon, MD on January 04, 2016 Originally published by O'Shaughnessy's (BeyondTHC.com)
I am among the millions of people who enjoy football as a spectator sport. However, I am becoming increasingly uncomfortable with the growing specter that many of these athletes will pay the price of developing Chronic Traumatic Encephalopathy (CTE) to a greater or lesser extent as they grow older. I believe that any change in the rules of the game which would accommodate these concerns would also diminish its popularity. I also believe that attempts to improve protective equipment can only go so far without seriously diminishing the skills and capacities of the player. Football is a violent game and every one involved in it knows that there will certainly be injuries. However, most injuries manifest themselves immediately, are orthopedic, not life-threatening, and with the help of nature and orthopedic medicine, will sooner or later heal. Injury to the brain is another matter.
The skull is nature’s way of protecting this most important organ, the brain. However, strong as this container is, it cannot protect the contents from concussion. And most assuredly it offers no protection against the consequences of repeated concussions which can lead to the development of CTE. And unlike orthopedic injuries, the effects of this syndrome only manifest themselves over the course of years and they are always irreversible and often devastating. The piece of equipment meant to protect the head is the helmet, which is excellent at protecting the container but not the contents. Furthermore, given the limitations imposed by physics, anatomy and neurophysiology, I question whether there is any helmet design which can do much more to limit the frequency or severity of concussions. It is for this reason that I believe it is important to look for internal protection against this kind of devastation.
Over the last two decades interest, knowledge and use of marijuana as a medicine has grown exponentially. People who are knowledgeable about cannabinopathic medicine believe that marijuana is neuroprotective. This understanding has grown from both clinical experience and animal research. It is also well known that it is remarkably free of toxicity. Furthermore, it is been learned relatively recently that one of the constituents of marijuana is a cannabinoid known as cannabidiol (CBD), which has no psychoactive properties; in other words, no amount of it would lead to a “high.” Increasingly, it is being sought as a medicine because it is both an anti-inflammatory and an antioxidant and it is free of psychoactivity. It is a very promising development, but the kind of research that will be necessary to establish this as a general medicine useful preventively in patients who are more likely to develop strokes because they suffer from heart arrhythmias or with patients who are subjected to other kinds of brain trauma will have to await the funding of this research. Funding for this kind of research is usually provided by a pharmaceutical company which wants to develop a new medicine for the market and, in order to do so, has to provide the Food and Drug Administration (FDA) with the research data which establishes both efficacy and safety. It is highly unlikely that a pharmaceutical company will get involved in this expensive research in this instance because a high ratio CBD/THC is now available in those states which have legalized the medicinal use of cannabis. The only other source of funding would be the US government which is not likely to provide it.
I would propose two actions for the NFL which have a good chance of decreasing the devastation of CTE. The NFL pockets are deep enough to support a crash research program to determine that this combination of cannabinoids is effective in preventing the consequences of concussion so that we will know for sure whether or not it will protect against this threat to the players. Secondly, I would also urge the NFL to drop its urine testing marijuana program so that players who believe that a high ratio CBD/THC substance may be useful to them in this regard will be free to use it without objection by the NFL.
Sincerely, Lester Grinspoon M.D.  Emeritus Professor of Psychiatry at Harvard Medical School    Author of Marihuana Reconsidered (Harvard University Press, 1971) and Marijuana, the Forbidden Medicine (Yale University Press, 1993, 1997)
Rules, Regulations, & Policy Solution For Requesting The Inclusion Of A New Medical Condition: Concussions, CTE and Traumatic Brain Injury
The approval of this Petition: Requesting The Inclusion Of A New Medical Condition: Concussions, CTE and Traumatic Brain Injury, that is being provided to the state Department of Health Medical Cannabis Program so the advisory board can review and recommend to the department for approval of additional debilitating medical conditions that would benefit from the medical use of cannabis with the Lynn and Erin Compassionate Use Act. The approval of this petition would bring the Department of Health in compliance with the intent of the law and uphold the spirit of the Lynn and Erin Compassionate Use Act, 2007. Fulfilling both;“ Section 2. PURPOSE OF ACT.--The purpose of the Lynn and Erin Compassionate Use Act is to allow the beneficial use of medical cannabis in a regulated system for alleviating symptoms caused by debilitating medical conditions and their medical treatments” And  Section 6. ADVISORY BOARD CREATED--DUTIES: The advisory board shall: A. review and recommend to the department for approval additional debilitating medical conditions that would benefit from the medical use of cannabis.” New Mexico’s medical cannabis history started in 1978.  After public hearings the legislature enacted H.B. 329, the nation’s first law recognizing the medical value of cannabis...the first law.

References
View the complete pdf of “Cannabinoids and brain injury: therapeutic
Implications”
by Raphael Mechoulam, David Panikashvili and Esther Shohami
1 Saugy, M., et al. “Cannabis and sport.” British journal of sports medicine40.suppl 1 (2006): i13-i15.
2 Huestis, Marilyn A., Irene Mazzoni, and Olivier Rabin. “Cannabis in Sport.”Sports medicine 41.11 (2011): 949-966.
3 Yu, T., et al. “Beneficial effects of cannabinoid receptor type 2 (CB2R) in injured skeletal muscle post-contusion.” Histology and histopathology (2015).
4 Mechoulam, Raphael, David Panikashvili, and Esther Shohami. “Cannabinoids and brain injury: therapeutic implications.” Trends in molecular medicine 8.2 (2002): 58-61.
5 Fishbein, Miriam, et al. “Long-term behavioral and biochemical effects of an ultra-low dose of Δ9-tetrahydrocannabinol (THC): neuroprotection and ERK signaling.” Experimental brain research 221.4 (2012): 437-448.
6 Durst, Ronen, et al. “Cannabidiol, a nonpsychoactive Cannabis constituent, protects against myocardial ischemic reperfusion injury.” American Journal of Physiology-Heart and Circulatory Physiology 293.6 (2007): H3602-H3607.
7 Ribeiro, Alison, et al. “Cannabidiol, a non-psychotropic plant-derived cannabinoid, decreases inflammation in a murine model of acute lung injury: Role for the adenosine A 2A receptor.” European journal of pharmacology678.1 (2012): 78-85.
8 Pazos, M. R., et al. “Cannabidiol administration after hypoxia–ischemia to newborn rats reduces long-term brain injury and restores neurobehavioral function.” Neuropharmacology 63.5 (2012): 776-783.
9 Tetrault, Jeanette M., et al. “Effects of marijuana smoking on pulmonary function and respiratory complications: a systematic review.” Archives of Internal Medicine 167.3 (2007): 221-228.
10 Bolla, Karen I., et al. “Neural substrates of faulty decision-making in abstinent marijuana users.” Neuroimage 26.2 (2005): 480-492.
11 Borg J, Gershon S, Alpert M (1975) Dose effects of smoked marijuana on human cognitive and motor functions. Psy- chopharmacologia 42:211–218
12 Campos, Daniel R., Mauricio Yonamine, and Regina L. de Moraes Moreau. “Marijuana as doping in sports.” Sports medicine 33.6 (2003): 395-399.

Appendix A: An Americans for Safe Access (ASA) national report was released on December 8th, 2016 and calls for an end to contradictions between federal and state guidelines with regard to medical cannabis policies. The Americans for Safe Access briefing book, “Medical Cannabis in America”, showing that not only do opiate related deaths drop an average of 24.8% in states with medical cannabis laws, the report also notes that the Department of Justice has spent an estimated $592 million to date in arrests, investigations, enforcement raids, pretrial services, incarceration, and probation.

Plant Count For Producers Based On Patient Population Growth For Adequate Supply Proposed: Legislators could easily solve this by looking to Americans For Safe Access for this policy.

About Americans for Safe Access.
The mission of Americans for Safe Access (ASA) is to ensure safe and legal access to cannabis for therapeutic use and research.  ASA was founded in 2002, by medical cannabis patient Steph Sherer, as a vehicle for patients to advocate for the acceptance of cannabis as medicine. With over 100,000 active members in all 50 states, ASA is the largest national member-based organization of patients, medical professionals, scientists and concerned citizens promoting safe and legal access to cannabis for therapeutic use and research. ASA works to overcome political, social and legal barriers by creating policies that improve access to medical cannabis for patients and researchers through legislation, education, litigation, research, grassroots empowerment, advocacy and services for patients, government's, medical professionals, and medical cannabis providers.

WHEREAS cannabis (marijuana) has been used as a medicine for at least 5,000 years and can be effective for serious medical conditions for which conventional medications fail to provide relief;

WHEREAS modern medical research has shown that cannabis can slow the progression of such serious diseases as Alzheimer’s and Parkinson’s and stop HIV and cancer cells from spreading; has both anti-inflammatory and pain-relieving properties; can alleviate the symptoms of epilepsy, PTSD and multiple sclerosis; is useful in the treatment of depression, anxiety and other mental disorders; and can help reverse neurological damage from brain injuries and stroke;

WHEREAS the World Health Organization has acknowledged the therapeutic effects of cannabinoids, the primary active compounds found in cannabis, including as an anti-depressant, appetite stimulant, anticonvulsant and anti-spasmodic, and identified cannabinoids as beneficial in the treatment of asthma, glaucoma, and nausea and vomiting related to illnesses such as cancer and AIDS;

WHEREAS the American Medical Association has called for the review of the classification of cannabis as a Schedule I controlled substance to allow for clinical research and the development of cannabinoid-based medicines;

WHEREAS the National Cancer Institute has concluded that cannabis has antiemetic effects and is beneficial for appetite stimulation, pain relief, and improved sleep among cancer patients;

WHEREAS the American Herbal Pharmacopoeia and the American Herbal Products Association have developed qualitative standards for the use of cannabis as a botanical medicine;

WHEREAS the U.S. Supreme Court has long noted that states may operate as “laboratories of democracy” in the development of innovative public policies;

WHEREAS twenty-eight states and the District of Columbia have enacted laws that allow for the medical use of cannabis;

WHEREAS seventeen additional states have enacted laws authorizing the medical use of therapeutic compounds extracted from the cannabis plant;

WHEREAS more than 17 years of state-level experimentation provides a guide for state and federal law and policy related to the medical use of cannabis;

WHEREAS accredited educational curricula concerning the medical use of cannabis have been established that meets Continuing Medical Education requirements for practicing physicians;

WHEREAS Congress has prohibited the federal Department of Justice from using funds to interfere with and prosecute those acting in compliance with their state medical cannabis laws, and the Department of Justice has issued guidance to U.S. Attorneys indicating that enforcement of the Controlled Substances Act is not a priority when individual patients and their care providers are in compliance with state law, and that federal prosecutors should defer to state and local enforcement so long as a viable state regulatory scheme is in place.

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