Jason Barker - Medical Cannabis Patient & Organizer with LECUA Patient’s Coalition Of New Mexico 
LECUAPatientsCoalitionNM@gmail.com
dukecitywellness.blogspot.com
Tuesday, February 28th 2017
New Mexico State Department of Health
Medical Cannabis Advisory Board
Medical Cannabis Program
PO Box 26110
Santa Fe, NM, 87502-6110
Medical Cannabis Program
PO Box 26110
Santa Fe, NM, 87502-6110
Petition: Requesting The Inclusion Of A New Medical Condition: Dystonia
Table of Contents
Pg. 1 Cover Page
Pg. 2 Petition Introduction
Pg. 3 Petition Purpose and Background
Pg. 12 Relief Requested In Petition
Pg. 12 - 16 References
Printing Provided By:
Petition Introduction: Requesting The Inclusion Of A New Medical Condition: Dystonia
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”.
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.
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.
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.
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 Medical Treatment petition is; Requesting The Inclusion Of A New Medical Condition: Dystonia.
This petition for the Medical Treatment that pertains to: Requesting The Inclusion Of A New Medical Condition: Dystonia 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.
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.
“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.
Dystonia
Dystonia is a neurological movement disorder in which the sufferer’s muscles contract abnormally and involuntarily; when sustained it can be painful. It can affect one muscle, an entire muscle group, and even the entire body. Symptoms of Dystonia can be very mild to very severe, and they include: cramping, a dragging leg, involuntary pulling of the neck, uncontrollable blinking, and speech difficulties.
Dystonia appears to be related to problems in the basal ganglia (a central part of the brain) and the disorder may be hereditary, or caused by other factors such as birth related complications, physical trauma, infection, or even poisoning. There is no known cure for Dystonia, and treatment has been experimental and limited.
Using Cannabis to Treat Dystonia
Cannabis is a complex medicinal plant that may actually be used to treat a variety of debilitating symptoms caused by a surprisingly large number of ailments. It’s usefulness as a non-lethal medicine (you cannot die from an overdose of cannabis) cannot be overstated and it’s versatility in terms of how it can be consumed and as to how it can be useful for so many illnesses is something to be excited about. However, it is important to remember that consulting with your primary care physician should be your first priority when considering incorporating cannabis into one’s medical regiment and that cannabis is to be used as an adjunct therapy and not a replacement. It is also your responsibility to communicate with your doctor as to how your use of cannabis has affected your health and of your progress with utilizing medical cannabis.
With that said, it may be helpful for individuals looking to treat Dystonia with medical cannabis to know that there are several small case studies and investigations throughout the last decade that suggest cannabinoids may be a viable option to help reduce the symptoms and pain caused by the disorder.
Exciting studies have shown that cannabis may be quite useful for treating individuals suffering from Dystonia for the following reasons: to reduce muscle tension and involuntary, painful muscle contractions; reducing possible nausea; reducing possible anxiety and or depression; and to significantly reduce the pain caused by the contractions.
CANNABIS AND MOVEMENT DISORDERS
Movement disorders and neurodegenerative diseases, which are sometimes interlinked, are among the many conditions that cannabis and cannabinoids may be particularly well suited to treat.
The therapeutic use of cannabis for treating muscle problems and movement disorders has been known to western medicine for nearly two centuries. In reference to the plant's muscle relaxant and anti-convulsant properties, in 1839 Dr. William B. O'Shaughnessy wrote that doctors had "gained an anti-convulsive remedy of the greatest value."27 In 1890 Dr. J. Russell Reynolds, physician to Queen Victoria, noted in an article in The Lancet that for "organic disease of a gross character in the nervous centers . . . India hemp (cannabis) is the most useful agent with which I am acquainted."28
Muscular spasticity is a common condition, affecting millions of people in the United States. It afflicts individuals who have suffered strokes, as well as those with multiple sclerosis, cerebral palsy, paraplegia, quadriplegia, and spinal cord injuries. Conventional medical therapy offers little to address spasticity problems. Phenobarbital and diazepam (Valium) are commonly prescribed, but they rarely provide complete relief, and many patients develop a tolerance, become addicted, or complain of heavy sedation. These drugs also cause weakness, drowsiness, and other side effects that patients often find intolerable.
Extensive modern studies in both animals and humans have shown that cannabis can treat many movement disorders affecting older patients, such as tremors and spasticity, because cannabinoids have antispasticity, analgesic, antitremor, and antiataxia properties.29-40
In the federal court brief filed in support of physicians' right to recommend cannabis, the American Public Health Association states that "marijuana is effective in treating muscle spasticity." They point out that the government's own Institutes of Medicine report on medical use of cannabis found that "current treatments for painful muscle spasms . . . have only limited effectiveness and their use is complicated by various adverse side effects."
They go on to note that "a survey of British and American MS patients reports that after ingesting marijuana a significant majority experienced substantial improvements in controlling muscle spasticity and pain. An extensive neurological study found that herbal cannabis provided relief from both muscle spasms and ataxia (loss of coordination), a multiple benefit not achieved by any currently available medications" (amicus brief in Conant v. McCaffrey, 2001 filing).
Cannabis also has enormous potential for protecting the brain and central nervous system from the damage that leads to various movement disorders. Researchers have also found that cannabinoids can alleviate the damage caused by strokes, as well as brain trauma, spinal cord injury, and multiple sclerosis. More than 100 research articles have been published on how cannabinoids act as neuroprotective agents to slow the progression of such neurodegenerative diseases as Huntington's, Alzheimer's and particularly Parkinson's, which affects more than 52% of people over the age of 85.
An understanding of the actions of cannabis was spurred by the discovery of an endogenous cannabinoid system in the human body. This system appears to be intricately involved in normal physiology, specifically in the control of movement.41-45 Central cannabinoid receptors are densely located in the basal ganglia, the area of the brain that regulates body movement.
Endogenous cannabinoids (which are those cannabinoids produced by our bodies) also appear to play a role in the manipulation of other transmitter systems within the basal ganglia - increasing transmission of certain chemicals, inhibiting the release of others, and affecting how others are absorbed. Research suggests that endogenous cannabinoids play a part in the body's control of movements.46-50
Endocannabinoids have paradoxical effects on the mammalian nervous system: sometimes they block neuronal excitability and other times they augment it. As scientists are developing a better understanding of the physiological role of the endocannabinoids, it is becoming clear that these chemicals may be involved in the pathology of several neurological diseases. Researchers are identifying an array of potential therapeutic targets within the human nervous system.
Movement disorders can be chronic disorders which arise from the loss or destruction of neurons and other structures in the brain. Interestingly, the activation of cannabinoid receptors was shown to trigger neuronal growth, suggesting that a role in neuronal regeneration.36 Various cannabinoids found in the cannabis plant can modulate the synthesis, uptake or metabolism of the endocannabinoids that are involved in the progression of Huntington's disease, Parkinson's disease, multiple sclerosis, and Alzheimer's disease.51-53
Parkinson's disease has been linked to dysfunction in the body's dopamine system, specifically the production of too much of the neurotransmitter glutamate and oxidative damage to dopaminergic neurons. Studies have found a tight association between cannabinoids and dopamine, and recent research has produced anatomical, biochemical and pharmacological evidence supporting a role for the endogenous cannabinoid system in the modulation of dopaminergic transmission. Furthermore, the CB1 receptor appears to be deregulated in the basal ganglia of mice with this disease. Specifically, the down regulation of the CB1 receptor may be an early event in the beginning of Parkinson's disease.54-456 A profound up regulation of the CB1 receptor may occur after Parkinson's symptoms appear.
Oxidative stress in the brain is a major hallmark of motor and neurological diseases such as Parkinson's and Alzheimer's disease. Cannabinoids are able to protect neurons from oxidative damage.57 The neuroprotective action of cannabinoids appears to result from their ability to inhibit reactive oxygen species, glutamate, and tumour necrosis factor. THC, CBD, and synthetic AM404 all contain phenolic groups in their chemical structure and are thus able to reduce radical oxygen species. Notably CBD has extraordinary antioxidant properties and can effect Calcium homeostasis, both of which lead to positive effects against a wide range of neurodegenerative diseases.58
Few clinical trials have looked at Cannabinoids and Parkinson's disease. However, research has shown that 25% of Parkinson's patients smoke cannabis and 46% of these patients report improvement resulting from side effects of long term levodopa treatment.44 A randomized placebo controlled study using extracts of cannabis produced significant improvements in patients' cognition. The authors note that they did not see improvements in pain or sleep disorders. They speculate that the oral route (versus inhaled) of cannabis ingestion leads to too much variability of cannabinoids in blood.59
Plant cannabinoids, such as CBD have been effective in experimental models of Alzheimer's, Parkinson's, and Huntington's disease. Hence, cannabinods represent an emerging therapeutic option that could be available in the near future. However, cannabinoids are still in an early phase of development but research suggest that they can be useful drugs for the treatment of many disease processes of the brain and central nervous system.
Spasticity and Movement Disorder Medications
Benzodiazepines, levedopa, baclofen, dantrolene sodium, and tizanidine are the most widely used agents for reduction of spasticity. At high dosages, oral medications can cause unwanted side effects that include sedation, as well as changes in mood and cognition.
Benzodiazepines, which include Diazepam (Valium) and Clonazepam (Klonopin, Rivotril), are centrally acting agents that increase the affinity of GABA to its receptor. Diazepam is the oldest and most frequently used oral agent for managing spasticity. Benzodiazepine side effects include sedation, weakness, hypotension, GI symptoms, memory impairment, incoordination, confusion, depression, and ataxia are possible side effects of. Tolerance and dependency may occur and withdrawal on cessation. Tolerance may also lead to unacceptable dosage escalation.
Levedopa is common long-term treatment option for Parkinson's disease. Long-term use can result in diskynesia and is often a reason for not taking the drug. Diskynesia can lead to less control of voluntary movements and can result in tics or chorea. Dikynesia can result in excessive tongue rolling and after years of use it can manifest as "jerky" movements of the head and arms.
Baclofen (Lioresal) has been widely used for spasticity since 1967. It is a GABA agonist. Tolerance to the medication may develop. Baclofen must be slowly weaned to prevent withdrawal effects such as seizures, hallucinations and increased spasticity. It must be used with care in patients with renal insufficiency as its clearance is primarily renal. Side effects are predominantly from central depressant properties including sedation, ataxia, weakness and fatigue. May cause depression when combined with tizanidine or benzodiazepines.
Dantrolene Sodium (Dantrium) acts peripherally at the level of the muscle fiber and works best for cerebral palsy and traumatic brain injury. Because the action of dantrolene sodium is not selective for spastic muscles, it may cause generalized weakness, including weakness of the respiratory muscles. Side effects include drowsiness, dizziness, weakness, fatigue and diarrhea. In addition, hepatotoxicity (liver damage) occurs in < 1% of patients who take dantrolene sodium.
Tizanidine (Zanaflex) facilitates short-term vibratory inhibition of the H-reflex. Tizanidine in conjunction with baclofen or benzodiazepines has potential additive effects, including sedation and the possibility of liver toxicity. Dry mouth, somnolence, asthenia and dizziness are the most common side effects. Liver function problems and hallucinations may also occur.
How Cannabis Compares
By comparison, the side effects associated with cannabis are typically mild and are classified as "low risk." Euphoric mood changes are among the most frequent side effects. Cannabinoids can exacerbate schizophrenic psychosis in predisposed persons. Cannabinoids impede cognitive and psychomotor performance, resulting in temporary impairment. Chronic use can lead to the development of tolerance. Tachycardia and hypotension are frequently documented as adverse events in the cardiovascular system. A few cases of myocardial ischemia have been reported in young and previously healthy patients. Inhaling the smoke of cannabis cigarettes induces side effects on the respiratory system. Cannabinoids are contraindicated for patients with a history of cardiac ischemias. In summary, a low risk profile is evident from the literature available. Serious complications are very rare and are not usually reported during the use of cannabinoids for medical indications.
Is cannabis safe to recommend?
"The smoking of cannabis, even long term, is not harmful to health...." So began a 1995 editorial statement of Great Britain's leading medical journal, The Lancet. The long history of human use of cannabis also attests to its safety - nearly 5,000 years of documented use without a single death. In the same year as the Lancet editorial, Dr. Lester Grinspoon, a professor emeritus at Harvard Medical School who has published many influential books and articles on medical use of cannabis, had this to say in an article in the Journal of the American Medical Association (1995):
One of marijuana’s greatest advantages as a medicine is its remarkable safety. It has little effect on major physiological functions. There is no known case of a lethal overdose; on the basis of animal models, the ratio of lethal to effective dose is estimated as 40,000 to 1. By comparison, the ratio is between 3 and 50 to 1 for secobarbital and between 4 and 10 to 1 for ethanol. Marihuana is also far less addictive and far less subject to abuse than many drugs now used as muscle relaxants, hypnotics, and analgesics. The chief legitimate concern is the effect of smoking on the lungs. Cannabis smoke carries even more tars and other particulate matter than tobacco smoke. But the amount smoked is much less, especially in medical use, and once marihuana is an openly recognized medicine, solutions may be found; ultimately a technology for the inhalation of cannabinoid vapors could be developed.
The technology Dr. Grinspoon imagined in 1995 now exists in the form of "vaporizers," (which are widely available through stores and by mail-order) and recent research attests to their efficacy and safety.[44] Additionally, pharmaceutical companies have developed sublingual sprays and tablet forms of the drug. Patients and doctors have found other ways to avoid the potential problems associated with smoking, though long-term studies of even the heaviest users in Jamaica, Turkey and the U.S. have not found increased incidence of lung disease or other respiratory problems. A decade-long study of 65,000 Kaiser-Permanente patients comparing cancer rates among non-smokers, tobacco smokers, and cannabis smokers found that those who used only cannabis had a slightly lower risk of lung and other cancers as compared to non-smokers.[45] Similarly, a study comparing 1,200 patients with lung, head and neck cancers to a matched group with no cancer found that even those cannabis smokers who had consumed in excess of 20,000 joints had no increased risk of cancer.[46]
As Dr. Grinspoon notes, "the greatest danger in medical use of marihuana is its illegality, which imposes much anxiety and expense on suffering people, forces them to bargain with illicit drug dealers, and exposes them to the threat of criminal prosecution." This was the conclusion reached by the House of Lords, which recommended rescheduling and decriminalization.
In January 2013, the American Herbal Products Association (AHPA), which has a 30-year history of developing standards for the herbal products industry, issued recommendations for effectively regulating all aspects of cannabis distribution for patients. The regulatory recommendations, developed over two years by the AHPA Cannabis Committee address guidelines for cultivation, quality-assurance, analytics, cannabis product manufacture and labeling, storefront and delivery services, and personnel training.
In December 2013, the American Herbal Pharmacopeia released a monograph identifying cannabis as a botanical medicine. Written and reviewed by the world’s leading experts on cannabis, the monograph provides a full scientific understanding of the plant, its constituent components, and its biologic effects. It also establishes comprehensive standards for the plant's identity, purity, quality, and botanical properties.
Following the release of the monograph, ASA launched Patient Focused Certification, the first non-profit, third-party certification program based on the AHPA regulatory recommendations and the AHP standards. Patient Focused Certification (PFC) audits cultivators, distributors, manufacturers and laboratories to verify compliance with best-practice standards. PFC includes employee training, compliance inspections, ongoing monitoring, and an independent complaint process for customers, as well as comprehensive reviews of formulations and materials, independent testing, and facility inspections. ( See References II )
Movement disorders and neurodegenerative diseases, which are sometimes interlinked, are among the many conditions that cannabis and cannabinoids may be particularly well suited to treat.
The therapeutic use of cannabis for treating muscle problems and movement disorders has been known to western medicine for nearly two centuries. In reference to the plant's muscle relaxant and anti-convulsant properties, in 1839 Dr. William B. O'Shaughnessy wrote that doctors had "gained an anti-convulsive remedy of the greatest value."27 In 1890 Dr. J. Russell Reynolds, physician to Queen Victoria, noted in an article in The Lancet that for "organic disease of a gross character in the nervous centers . . . India hemp (cannabis) is the most useful agent with which I am acquainted."28
Muscular spasticity is a common condition, affecting millions of people in the United States. It afflicts individuals who have suffered strokes, as well as those with multiple sclerosis, cerebral palsy, paraplegia, quadriplegia, and spinal cord injuries. Conventional medical therapy offers little to address spasticity problems. Phenobarbital and diazepam (Valium) are commonly prescribed, but they rarely provide complete relief, and many patients develop a tolerance, become addicted, or complain of heavy sedation. These drugs also cause weakness, drowsiness, and other side effects that patients often find intolerable.
Extensive modern studies in both animals and humans have shown that cannabis can treat many movement disorders affecting older patients, such as tremors and spasticity, because cannabinoids have antispasticity, analgesic, antitremor, and antiataxia properties.29-40
In the federal court brief filed in support of physicians' right to recommend cannabis, the American Public Health Association states that "marijuana is effective in treating muscle spasticity." They point out that the government's own Institutes of Medicine report on medical use of cannabis found that "current treatments for painful muscle spasms . . . have only limited effectiveness and their use is complicated by various adverse side effects."
They go on to note that "a survey of British and American MS patients reports that after ingesting marijuana a significant majority experienced substantial improvements in controlling muscle spasticity and pain. An extensive neurological study found that herbal cannabis provided relief from both muscle spasms and ataxia (loss of coordination), a multiple benefit not achieved by any currently available medications" (amicus brief in Conant v. McCaffrey, 2001 filing).
Cannabis also has enormous potential for protecting the brain and central nervous system from the damage that leads to various movement disorders. Researchers have also found that cannabinoids can alleviate the damage caused by strokes, as well as brain trauma, spinal cord injury, and multiple sclerosis. More than 100 research articles have been published on how cannabinoids act as neuroprotective agents to slow the progression of such neurodegenerative diseases as Huntington's, Alzheimer's and particularly Parkinson's, which affects more than 52% of people over the age of 85.
An understanding of the actions of cannabis was spurred by the discovery of an endogenous cannabinoid system in the human body. This system appears to be intricately involved in normal physiology, specifically in the control of movement.41-45 Central cannabinoid receptors are densely located in the basal ganglia, the area of the brain that regulates body movement.
Endogenous cannabinoids (which are those cannabinoids produced by our bodies) also appear to play a role in the manipulation of other transmitter systems within the basal ganglia - increasing transmission of certain chemicals, inhibiting the release of others, and affecting how others are absorbed. Research suggests that endogenous cannabinoids play a part in the body's control of movements.46-50
Endocannabinoids have paradoxical effects on the mammalian nervous system: sometimes they block neuronal excitability and other times they augment it. As scientists are developing a better understanding of the physiological role of the endocannabinoids, it is becoming clear that these chemicals may be involved in the pathology of several neurological diseases. Researchers are identifying an array of potential therapeutic targets within the human nervous system.
Movement disorders can be chronic disorders which arise from the loss or destruction of neurons and other structures in the brain. Interestingly, the activation of cannabinoid receptors was shown to trigger neuronal growth, suggesting that a role in neuronal regeneration.36 Various cannabinoids found in the cannabis plant can modulate the synthesis, uptake or metabolism of the endocannabinoids that are involved in the progression of Huntington's disease, Parkinson's disease, multiple sclerosis, and Alzheimer's disease.51-53
Parkinson's disease has been linked to dysfunction in the body's dopamine system, specifically the production of too much of the neurotransmitter glutamate and oxidative damage to dopaminergic neurons. Studies have found a tight association between cannabinoids and dopamine, and recent research has produced anatomical, biochemical and pharmacological evidence supporting a role for the endogenous cannabinoid system in the modulation of dopaminergic transmission. Furthermore, the CB1 receptor appears to be deregulated in the basal ganglia of mice with this disease. Specifically, the down regulation of the CB1 receptor may be an early event in the beginning of Parkinson's disease.54-456 A profound up regulation of the CB1 receptor may occur after Parkinson's symptoms appear.
Oxidative stress in the brain is a major hallmark of motor and neurological diseases such as Parkinson's and Alzheimer's disease. Cannabinoids are able to protect neurons from oxidative damage.57 The neuroprotective action of cannabinoids appears to result from their ability to inhibit reactive oxygen species, glutamate, and tumour necrosis factor. THC, CBD, and synthetic AM404 all contain phenolic groups in their chemical structure and are thus able to reduce radical oxygen species. Notably CBD has extraordinary antioxidant properties and can effect Calcium homeostasis, both of which lead to positive effects against a wide range of neurodegenerative diseases.58
Few clinical trials have looked at Cannabinoids and Parkinson's disease. However, research has shown that 25% of Parkinson's patients smoke cannabis and 46% of these patients report improvement resulting from side effects of long term levodopa treatment.44 A randomized placebo controlled study using extracts of cannabis produced significant improvements in patients' cognition. The authors note that they did not see improvements in pain or sleep disorders. They speculate that the oral route (versus inhaled) of cannabis ingestion leads to too much variability of cannabinoids in blood.59
Plant cannabinoids, such as CBD have been effective in experimental models of Alzheimer's, Parkinson's, and Huntington's disease. Hence, cannabinods represent an emerging therapeutic option that could be available in the near future. However, cannabinoids are still in an early phase of development but research suggest that they can be useful drugs for the treatment of many disease processes of the brain and central nervous system.
Spasticity and Movement Disorder Medications
Benzodiazepines, levedopa, baclofen, dantrolene sodium, and tizanidine are the most widely used agents for reduction of spasticity. At high dosages, oral medications can cause unwanted side effects that include sedation, as well as changes in mood and cognition.
Benzodiazepines, which include Diazepam (Valium) and Clonazepam (Klonopin, Rivotril), are centrally acting agents that increase the affinity of GABA to its receptor. Diazepam is the oldest and most frequently used oral agent for managing spasticity. Benzodiazepine side effects include sedation, weakness, hypotension, GI symptoms, memory impairment, incoordination, confusion, depression, and ataxia are possible side effects of. Tolerance and dependency may occur and withdrawal on cessation. Tolerance may also lead to unacceptable dosage escalation.
Levedopa is common long-term treatment option for Parkinson's disease. Long-term use can result in diskynesia and is often a reason for not taking the drug. Diskynesia can lead to less control of voluntary movements and can result in tics or chorea. Dikynesia can result in excessive tongue rolling and after years of use it can manifest as "jerky" movements of the head and arms.
Baclofen (Lioresal) has been widely used for spasticity since 1967. It is a GABA agonist. Tolerance to the medication may develop. Baclofen must be slowly weaned to prevent withdrawal effects such as seizures, hallucinations and increased spasticity. It must be used with care in patients with renal insufficiency as its clearance is primarily renal. Side effects are predominantly from central depressant properties including sedation, ataxia, weakness and fatigue. May cause depression when combined with tizanidine or benzodiazepines.
Dantrolene Sodium (Dantrium) acts peripherally at the level of the muscle fiber and works best for cerebral palsy and traumatic brain injury. Because the action of dantrolene sodium is not selective for spastic muscles, it may cause generalized weakness, including weakness of the respiratory muscles. Side effects include drowsiness, dizziness, weakness, fatigue and diarrhea. In addition, hepatotoxicity (liver damage) occurs in < 1% of patients who take dantrolene sodium.
Tizanidine (Zanaflex) facilitates short-term vibratory inhibition of the H-reflex. Tizanidine in conjunction with baclofen or benzodiazepines has potential additive effects, including sedation and the possibility of liver toxicity. Dry mouth, somnolence, asthenia and dizziness are the most common side effects. Liver function problems and hallucinations may also occur.
How Cannabis Compares
By comparison, the side effects associated with cannabis are typically mild and are classified as "low risk." Euphoric mood changes are among the most frequent side effects. Cannabinoids can exacerbate schizophrenic psychosis in predisposed persons. Cannabinoids impede cognitive and psychomotor performance, resulting in temporary impairment. Chronic use can lead to the development of tolerance. Tachycardia and hypotension are frequently documented as adverse events in the cardiovascular system. A few cases of myocardial ischemia have been reported in young and previously healthy patients. Inhaling the smoke of cannabis cigarettes induces side effects on the respiratory system. Cannabinoids are contraindicated for patients with a history of cardiac ischemias. In summary, a low risk profile is evident from the literature available. Serious complications are very rare and are not usually reported during the use of cannabinoids for medical indications.
Is cannabis safe to recommend?
"The smoking of cannabis, even long term, is not harmful to health...." So began a 1995 editorial statement of Great Britain's leading medical journal, The Lancet. The long history of human use of cannabis also attests to its safety - nearly 5,000 years of documented use without a single death. In the same year as the Lancet editorial, Dr. Lester Grinspoon, a professor emeritus at Harvard Medical School who has published many influential books and articles on medical use of cannabis, had this to say in an article in the Journal of the American Medical Association (1995):
One of marijuana’s greatest advantages as a medicine is its remarkable safety. It has little effect on major physiological functions. There is no known case of a lethal overdose; on the basis of animal models, the ratio of lethal to effective dose is estimated as 40,000 to 1. By comparison, the ratio is between 3 and 50 to 1 for secobarbital and between 4 and 10 to 1 for ethanol. Marihuana is also far less addictive and far less subject to abuse than many drugs now used as muscle relaxants, hypnotics, and analgesics. The chief legitimate concern is the effect of smoking on the lungs. Cannabis smoke carries even more tars and other particulate matter than tobacco smoke. But the amount smoked is much less, especially in medical use, and once marihuana is an openly recognized medicine, solutions may be found; ultimately a technology for the inhalation of cannabinoid vapors could be developed.
The technology Dr. Grinspoon imagined in 1995 now exists in the form of "vaporizers," (which are widely available through stores and by mail-order) and recent research attests to their efficacy and safety.[44] Additionally, pharmaceutical companies have developed sublingual sprays and tablet forms of the drug. Patients and doctors have found other ways to avoid the potential problems associated with smoking, though long-term studies of even the heaviest users in Jamaica, Turkey and the U.S. have not found increased incidence of lung disease or other respiratory problems. A decade-long study of 65,000 Kaiser-Permanente patients comparing cancer rates among non-smokers, tobacco smokers, and cannabis smokers found that those who used only cannabis had a slightly lower risk of lung and other cancers as compared to non-smokers.[45] Similarly, a study comparing 1,200 patients with lung, head and neck cancers to a matched group with no cancer found that even those cannabis smokers who had consumed in excess of 20,000 joints had no increased risk of cancer.[46]
As Dr. Grinspoon notes, "the greatest danger in medical use of marihuana is its illegality, which imposes much anxiety and expense on suffering people, forces them to bargain with illicit drug dealers, and exposes them to the threat of criminal prosecution." This was the conclusion reached by the House of Lords, which recommended rescheduling and decriminalization.
In January 2013, the American Herbal Products Association (AHPA), which has a 30-year history of developing standards for the herbal products industry, issued recommendations for effectively regulating all aspects of cannabis distribution for patients. The regulatory recommendations, developed over two years by the AHPA Cannabis Committee address guidelines for cultivation, quality-assurance, analytics, cannabis product manufacture and labeling, storefront and delivery services, and personnel training.
In December 2013, the American Herbal Pharmacopeia released a monograph identifying cannabis as a botanical medicine. Written and reviewed by the world’s leading experts on cannabis, the monograph provides a full scientific understanding of the plant, its constituent components, and its biologic effects. It also establishes comprehensive standards for the plant's identity, purity, quality, and botanical properties.
Following the release of the monograph, ASA launched Patient Focused Certification, the first non-profit, third-party certification program based on the AHPA regulatory recommendations and the AHP standards. Patient Focused Certification (PFC) audits cultivators, distributors, manufacturers and laboratories to verify compliance with best-practice standards. PFC includes employee training, compliance inspections, ongoing monitoring, and an independent complaint process for customers, as well as comprehensive reviews of formulations and materials, independent testing, and facility inspections. ( See References II )
Beneficial Cannabinoids and Terpenoids Useful for Treating Dystonia
The cannabis plant offers a plethora of therapeutic benefits and contains cannabinoids and terpenoid compounds that are useful for treating a number of ailments and disorders, and recent case studies have shown that both Tetrahydrocannabinol (THC) and Cannabidiol (CBD) may be beneficial for improving motor control and reducing the pain caused by the spasms.
With that said, the following chart also denotes which cannabinoids and terpenoids work synergistically with each other for possible therapeutic benefit. It may be beneficial to seek out strains that contain these cannabinoids and terpenoids.
Rules, Regulations, & Policy Solution For Requesting The Inclusion Of A New Medical Condition: Dystonia
The approval of this petition: Requesting The Inclusion Of A New Medical Condition: Dystonia, 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 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
Understanding medical cannabis.Elemental Wellness Center, 2014 Jul.
Current status of cannabis treatment of multiple sclerosis with an illustrative case presentation of a patient with MS, complex vocal tics, paroxysmal dystonia, and marijuana dependence treated with Dronabinol.Deutsch, Stephen I, et al.
CNS Spectrums: The International Journal of Neuropsychiatric Medicine, 2008 May, 13(5): 393-403.
Cannabis sativa and dystonia secondary to Wilson’s disease.Roca, Urive, et al.
Movement Disorder Society, 2004 Jan, 20(1): 113-115.
Effects of pharmacological manipulations of cannabinoid receptors on severity of dystonia in a genetic model of paroxysmal dyskinesia.Richter, A, et al.
European Journal of Pharmacology, 2002 Nov 15, 454(2-3): 145-151.
A dramatic response to inhaled cannabis in a woman with central thalamic pain and dystonia.Chatteree, Avijit, et al.
Journal of Pain and Symptom Management, 2002 Aug, 24(1): 4-6.
Movement Disorders: Official Journal of the Movement Disorder Society, 2002 Jan, 17(1): 145-149.
Cannabis in movement Disorders.Muller-Vahl, K.R., et al.
Forschende Komplementarmedizin (Research in Complementary Medicine), 1999 Oct, 6(3): 23-27.
(+)-WIN 55,212-2, a novel cannabinoid receptor agonist, exerts antidystonic effects in mutant dystonic hamsters.Richter, Angelika, et al.
Open label evaluation of cannabidiol in dystonic movement disorders.Consroe, Paul, et al.
International Journal of Neuroscience, 1986, 30(4): 277-282.
REFERENCES II
Legal Citations
1. See "The Administration's Response to the Passage of California Proposition 215 and Arizona Proposition 200" (Dec. 30, 1996). https://www.ncjrs.gov/txtfiles/215rel.txt
2. See Conant v. McCaffrey, 172 F.R.D. 681 (N.D. Cal. 1997).
3. See id.; Conant v. McCaffrey, 2000 WL 1281174 (N.D. Cal. 2000); Conant v. Walters, 309 F.3d 629 (9th Cir. 2002).
4. 309 F.3d 629 (9th Cir. 2002).
5. Id. at 634-36.
6. Criminal liability for aiding and abetting requires proof that the defendant "in some sort associate[d] himself with the venture, that he participate[d] in it as something that he wishe[d] to bring about, that he [sought] by his action to make it succeed."Conant v. McCaffrey, 172 F.R.D. 681, 700 (N.D. Cal. 1997) (quotation omitted). A conspiracy to obtain cannabis requires an agreement between two or more persons to do this, with both persons knowing this illegal objective and intending to help accomplish it. Id. at 700-01.
7. 309 F.3d at 634 & 636.
8. Conant v. McCaffrey, 2000 WL 1281174, at *16 (N.D. Cal. 2000).
9. 309 F.3d at 634.
10. See id.. at 635; Conant v. McCaffrey, 172 F.R.D. 681, 700-01 (N.D. Cal. 1997).
11. Gonzales v. Raich, 545 U.S. 1 (2005) 352 F.3d 1222.
12. Third Time the Charm? State Laws on Medical Cannabis Distribution and Department of Justice Guidance on Enforcement. Americans for Safe Access. November 25, 2013. http://americansforsafeacess.org/dojwhitepaper.
Research Citations
13. Adler JN, Colbert JA. Medicinal Use of Marijuana — Polling Results. N Engl J Med 2013; 368:e30. May 30, 2013. DOI: 10.1056/NEJMclde1305159
14. Hanus LO. Pharmacological and therapeutic secrets of plant and brain (endo)cannabinoids. Med Res Rev. 2009 Mar;29(2):213-71. doi: 10.1002/med.20135.
15. Grant I, Rael Cahn B. Cannabis and endocannabinoid modulators: Therapeutic promises and challenges, Clinical Neuroscience Research, Volume 5, Issues 2-4, November 2005, Pages 185-199.
16. Alexandros Makriyannis, Raphael Mechoulam and Daniele Piomelli, Therapeutic opportunities through modulation of the endocannabinoid system, Neuropharmacology, Volume 48, Issue 8, June 2005, Pages 1068-1071.
17. Cecilia J. Hillard and Abbas Jarrahian, Accumulation of anandamide: Evidence for cellular diversity, Neuropharmacology, Volume 48, Issue 8, June 2005, Pages 1072-1078.
18. Pacher, P., & Kunos, G. (2013). Modulating the endocannabinoid system in human health and disease–successes and failures. FEBS Journal.
19. Aggrawal S et al. 2009. Medicinal use of cannabis in the United States: historical perspectives, current trends, and future directions. J Opioid Manag. May-Jun;5(3):153-68.
20. Grant I, Atkinson JH, Gouaux B, Wilsey B. (2012). Medical Marijuana: Clearing Away the Smoke. The Open Neurology Journal. 2012 May 4, 6:18-25. DOI: 10.2174/1874205X01206010018.
21. Abrams DI et al (2003). Short-Term Effects of Cannabinoids in Patients with HIV-1 Infection: A Randomized, Placebo-Controlled Clinical Trial. Ann Intern Med. Aug 19;139(4):258-66.5.
22 Russo EB, Mathre ML, et al. (2002). Chronic Cannabis Use in the Compassionate Investigational New Drug Program: An Examination of Benefits and Adverse Effects of Legal Clinical Cannabis. Journal of Cannabis Therapeutics 2(1).
23. Russo EB. (2008) Cannabinoids in the management of difficult to treat pain. Therap and Clincial Risk Manag 4(1) 245-259.
24. Barnes MP (2006). Sativex: clinical efficacy and tolerability in the treatment of symptoms of multiple sclerosis and neuropathic pain. Expert Opin Pharmacother, 7:607-15.
25. Perez J (2006) Combined cannabinoid therapy via an oral mucosal spray. Drugs Today (Barc.), 42:495-501.
26. Selvarajah D et al (2010). Randomized placebo-controlled double-blind clinical trial of cannabis-based medicinal product (Sativex) in painful diabetic neuropathy. Diabetes Care. 33(1):128-30.
27. O'Shaughnessy WB (1838). On the preparations of the Indian hemp, or gunjah (Cannabis indica); their effects on the animal system in health, and their utility in the treatment of tetanus and other convulsive diseases. Transactions of the Medical and Physical Society of Bengal. 18; 40: 71-102, 421-61.
28. Ibid.
29. Zajicek J et al (2003). Cannabinoids for treatment of spasticity and other symptoms related to multiple sclerosis (CAMS study): multicentre randomised placebo-controlled trial. Lancet. Nov 8;362(9395):1517-26.
30. Amtmann D et al (2004). Survey of cannabis use in patients with amyotrophic lateral sclerosis. Am J Hosp Palliat Care. Mar-Apr;21(2):95-104.
31. Baker D et al (2000). Cannabinoids control spasticity and tremor in a multiple sclerosis model. Nature. Mar 2;404(6773):84-7.
32. Lorenz R (2004). On the application of cannabis in paediatrics and epileptology. Neuroendocrinol Lett. Feb-Apr;25(1-2):40-4.
33. Malec J et al (1982). Cannabis effect on spasticity in spinal cord injury. Arch Phys Med Rehabil. Mar;63(3):116-8.
34. Borg J et al (1975). Dose Effects of Smoking Marihuana on Human Cognitive and Motor Functions. Psychopharmacologia. 42, 211-218
35. Dunn M, Ross D (1974). The Perceived Effects of Marijuana on Spinal Cord Injured Males. Paraplegia. 12, 175.
36. Hanigan WC et al (1986). The Effects of Delta-9-THC on Human Spasticity. Journal of the American Society of Clinical Pharmacology & Therapeutics. Feb. 198.
37. Manno JE et al (1970). Comparative Effects of Smoking Marihuana or Placebo on Human Motor & Mental Performance. Clinical Pharmacology & Therapeutics, 11:6, 808-815.
38. Meinck HM et al (1989). Effect of Cannabinoids on Spasticity and Ataxia in Multiple Sclerosis. Journal of Neurology, 236:120-22.
39. Petro D, Ellenberger C Jr (1981). Treatment of Human Spasticity with Delta-9-Tetrahydrocannabinol. Journal of Clinical Pharmacology. 21:8&9, 413S-416S
40. Petro D (1980). Marijuana as a Therapeutic Agent for Muscle Spasm or Spasticity. Psychosomatics. 21:1, 81-85.
41. Howlett AC (1995). Pharmacology of cannabinoid receptors. Annu Rev Pharmacol Toxicol.35:607-634.
42. Abood ME, Martin BR (1996). Molecular neurobiology of the cannabinoid receptor. Intl Rev Neurobiol. 39:197-221.
43. Devane WA et al (1992). Isolation and structure of a brain constituent that binds to the cannabinoid receptor. Science. 258:1946-1949.
44. Barg J et al (1995). Cannabinomimetic behavioral effects of and adenylate cyclase inhibition by two new endogenous anandamides. Eur J Pharmacol. 287:145-152.
45. Klein TW et al (1998). Cannabinoid receptors and immunity. Immunol Today. 797:225-233.
46. Pryce G et al (2003) Cannabinoids inhibit neurodegeneration in models of multiple sclerosis. Brain. Oct;126(Pt 10):2191-202. Epub 2003 Jul 22.
47. Lastres-Becker I et al (2003). Effects of cannabinoids in the rat model of Huntington's disease generated by an intrastriatal injection of malonate. Neuroreport. May 6;14(6):813-6.
48. Mechoulam R, Lichtman AH (2003). Endocannabinoids: Stout guards of the central nervous system. Science. Oct 3;302(5642):65-7.
49. Croxford JL (2003). Therapeutic potential of cannabinoids in CNS disease. CNS Drugs. 17(3):179-202.
50. McCarron RM et al (2003). Antioxidant properties of the vasoactive endocannabinoid, 2-arachidonoyl glycerol (2-AG). Acta Neurochir Suppl. 86:271-5.
51. Zorina et al (2009). Cannabinoid 1 Receptor and Interleukin-6 together induce integration of protein kinase and transcription factor signalling in trigger neurite outgrowth. J of Biological Chemistry, Electronic publication ahead of print 10/27/09.
52. Sandyk R et al (1986). Effects of Cannabinoids in Huntington's Disease. Neurology, 36, 342.
53. Rodriguez De Fonseca F et al (2001). Role of the endogenous cannabinoid system as a modulator of dopamine transmission: implications for Parkinson's disease and schizophrenia. Neurotox Res. Jan;3(1):23-35.
54. Garcia-Arencibia, M. et al (2009) Cannabinoid CB1 receptors are early down-regulated followed by a further up regulation in the basal ganglia of mice with deletion of specific PARK genes. J of Neural Transmission (In Press).
55. Garcia-Arencibia, M. (2009) Cannabinoids and Parkinson's Disease. Current Drug Targets-CNS and Neurological Disorders (In Press)
56. Orgado et al (2009). The Endocannabiod system in neuropathological states. International Review of Psychiatry 21(2): 172-180.
57. Izzo et al (2009) Non-psychotropic plant cannabinoids: new therapeutic opportunities from an ancient herb. Trends in Pharamcological Sciences Vol 30 No 10: 515-527.
58. Venderoza et al (2004). Survey on cannabis use in Parkinson's disease: Subjective improvement of motor symptoms. Movement Disorders, 19: 1102-1106.
59. Carroll et al (2004). Cannabis for dyskinesia in Parkinson's disease: a randomized double blind crossover study. Neurology 63(7):1245-1250.
60. De Lago et al (2007). Cannabinoids and neuroprotection in motor-related disorders. CNS & Neurological Disorders- Drug targets, 6:377-387.
61. Hazekamp A et al (2006). Evaluation of a vaporizing device (Volcano(R)) for the pulmonary administration of tetrahydrocannabinol. J Pharm Sci 95 (6) Apr 24: 1308-1317.
62. Sidney S et al (1997). Marijuana Use and Cancer Incidence. Cancer Causes and Control; 8: 722-728.
63. Tashkin D (2006). Marijuana Use and Lung Cancer: Results of a Case-Control Study. American Thoracic Society International Conference. May 23, 2006.
64. Lancet 1; 1823.
65. United States Assumes Control of Cannabis. JAMA. 1937;109(13):31B-38B. doi:10.1001/jama.1937.02780390177058
Legal Citations
1. See "The Administration's Response to the Passage of California Proposition 215 and Arizona Proposition 200" (Dec. 30, 1996). https://www.ncjrs.gov/txtfiles/215rel.txt
2. See Conant v. McCaffrey, 172 F.R.D. 681 (N.D. Cal. 1997).
3. See id.; Conant v. McCaffrey, 2000 WL 1281174 (N.D. Cal. 2000); Conant v. Walters, 309 F.3d 629 (9th Cir. 2002).
4. 309 F.3d 629 (9th Cir. 2002).
5. Id. at 634-36.
6. Criminal liability for aiding and abetting requires proof that the defendant "in some sort associate[d] himself with the venture, that he participate[d] in it as something that he wishe[d] to bring about, that he [sought] by his action to make it succeed."Conant v. McCaffrey, 172 F.R.D. 681, 700 (N.D. Cal. 1997) (quotation omitted). A conspiracy to obtain cannabis requires an agreement between two or more persons to do this, with both persons knowing this illegal objective and intending to help accomplish it. Id. at 700-01.
7. 309 F.3d at 634 & 636.
8. Conant v. McCaffrey, 2000 WL 1281174, at *16 (N.D. Cal. 2000).
9. 309 F.3d at 634.
10. See id.. at 635; Conant v. McCaffrey, 172 F.R.D. 681, 700-01 (N.D. Cal. 1997).
11. Gonzales v. Raich, 545 U.S. 1 (2005) 352 F.3d 1222.
12. Third Time the Charm? State Laws on Medical Cannabis Distribution and Department of Justice Guidance on Enforcement. Americans for Safe Access. November 25, 2013. http://americansforsafeacess.org/dojwhitepaper.
Research Citations
13. Adler JN, Colbert JA. Medicinal Use of Marijuana — Polling Results. N Engl J Med 2013; 368:e30. May 30, 2013. DOI: 10.1056/NEJMclde1305159
14. Hanus LO. Pharmacological and therapeutic secrets of plant and brain (endo)cannabinoids. Med Res Rev. 2009 Mar;29(2):213-71. doi: 10.1002/med.20135.
15. Grant I, Rael Cahn B. Cannabis and endocannabinoid modulators: Therapeutic promises and challenges, Clinical Neuroscience Research, Volume 5, Issues 2-4, November 2005, Pages 185-199.
16. Alexandros Makriyannis, Raphael Mechoulam and Daniele Piomelli, Therapeutic opportunities through modulation of the endocannabinoid system, Neuropharmacology, Volume 48, Issue 8, June 2005, Pages 1068-1071.
17. Cecilia J. Hillard and Abbas Jarrahian, Accumulation of anandamide: Evidence for cellular diversity, Neuropharmacology, Volume 48, Issue 8, June 2005, Pages 1072-1078.
18. Pacher, P., & Kunos, G. (2013). Modulating the endocannabinoid system in human health and disease–successes and failures. FEBS Journal.
19. Aggrawal S et al. 2009. Medicinal use of cannabis in the United States: historical perspectives, current trends, and future directions. J Opioid Manag. May-Jun;5(3):153-68.
20. Grant I, Atkinson JH, Gouaux B, Wilsey B. (2012). Medical Marijuana: Clearing Away the Smoke. The Open Neurology Journal. 2012 May 4, 6:18-25. DOI: 10.2174/1874205X01206010018.
21. Abrams DI et al (2003). Short-Term Effects of Cannabinoids in Patients with HIV-1 Infection: A Randomized, Placebo-Controlled Clinical Trial. Ann Intern Med. Aug 19;139(4):258-66.5.
22 Russo EB, Mathre ML, et al. (2002). Chronic Cannabis Use in the Compassionate Investigational New Drug Program: An Examination of Benefits and Adverse Effects of Legal Clinical Cannabis. Journal of Cannabis Therapeutics 2(1).
23. Russo EB. (2008) Cannabinoids in the management of difficult to treat pain. Therap and Clincial Risk Manag 4(1) 245-259.
24. Barnes MP (2006). Sativex: clinical efficacy and tolerability in the treatment of symptoms of multiple sclerosis and neuropathic pain. Expert Opin Pharmacother, 7:607-15.
25. Perez J (2006) Combined cannabinoid therapy via an oral mucosal spray. Drugs Today (Barc.), 42:495-501.
26. Selvarajah D et al (2010). Randomized placebo-controlled double-blind clinical trial of cannabis-based medicinal product (Sativex) in painful diabetic neuropathy. Diabetes Care. 33(1):128-30.
27. O'Shaughnessy WB (1838). On the preparations of the Indian hemp, or gunjah (Cannabis indica); their effects on the animal system in health, and their utility in the treatment of tetanus and other convulsive diseases. Transactions of the Medical and Physical Society of Bengal. 18; 40: 71-102, 421-61.
28. Ibid.
29. Zajicek J et al (2003). Cannabinoids for treatment of spasticity and other symptoms related to multiple sclerosis (CAMS study): multicentre randomised placebo-controlled trial. Lancet. Nov 8;362(9395):1517-26.
30. Amtmann D et al (2004). Survey of cannabis use in patients with amyotrophic lateral sclerosis. Am J Hosp Palliat Care. Mar-Apr;21(2):95-104.
31. Baker D et al (2000). Cannabinoids control spasticity and tremor in a multiple sclerosis model. Nature. Mar 2;404(6773):84-7.
32. Lorenz R (2004). On the application of cannabis in paediatrics and epileptology. Neuroendocrinol Lett. Feb-Apr;25(1-2):40-4.
33. Malec J et al (1982). Cannabis effect on spasticity in spinal cord injury. Arch Phys Med Rehabil. Mar;63(3):116-8.
34. Borg J et al (1975). Dose Effects of Smoking Marihuana on Human Cognitive and Motor Functions. Psychopharmacologia. 42, 211-218
35. Dunn M, Ross D (1974). The Perceived Effects of Marijuana on Spinal Cord Injured Males. Paraplegia. 12, 175.
36. Hanigan WC et al (1986). The Effects of Delta-9-THC on Human Spasticity. Journal of the American Society of Clinical Pharmacology & Therapeutics. Feb. 198.
37. Manno JE et al (1970). Comparative Effects of Smoking Marihuana or Placebo on Human Motor & Mental Performance. Clinical Pharmacology & Therapeutics, 11:6, 808-815.
38. Meinck HM et al (1989). Effect of Cannabinoids on Spasticity and Ataxia in Multiple Sclerosis. Journal of Neurology, 236:120-22.
39. Petro D, Ellenberger C Jr (1981). Treatment of Human Spasticity with Delta-9-Tetrahydrocannabinol. Journal of Clinical Pharmacology. 21:8&9, 413S-416S
40. Petro D (1980). Marijuana as a Therapeutic Agent for Muscle Spasm or Spasticity. Psychosomatics. 21:1, 81-85.
41. Howlett AC (1995). Pharmacology of cannabinoid receptors. Annu Rev Pharmacol Toxicol.35:607-634.
42. Abood ME, Martin BR (1996). Molecular neurobiology of the cannabinoid receptor. Intl Rev Neurobiol. 39:197-221.
43. Devane WA et al (1992). Isolation and structure of a brain constituent that binds to the cannabinoid receptor. Science. 258:1946-1949.
44. Barg J et al (1995). Cannabinomimetic behavioral effects of and adenylate cyclase inhibition by two new endogenous anandamides. Eur J Pharmacol. 287:145-152.
45. Klein TW et al (1998). Cannabinoid receptors and immunity. Immunol Today. 797:225-233.
46. Pryce G et al (2003) Cannabinoids inhibit neurodegeneration in models of multiple sclerosis. Brain. Oct;126(Pt 10):2191-202. Epub 2003 Jul 22.
47. Lastres-Becker I et al (2003). Effects of cannabinoids in the rat model of Huntington's disease generated by an intrastriatal injection of malonate. Neuroreport. May 6;14(6):813-6.
48. Mechoulam R, Lichtman AH (2003). Endocannabinoids: Stout guards of the central nervous system. Science. Oct 3;302(5642):65-7.
49. Croxford JL (2003). Therapeutic potential of cannabinoids in CNS disease. CNS Drugs. 17(3):179-202.
50. McCarron RM et al (2003). Antioxidant properties of the vasoactive endocannabinoid, 2-arachidonoyl glycerol (2-AG). Acta Neurochir Suppl. 86:271-5.
51. Zorina et al (2009). Cannabinoid 1 Receptor and Interleukin-6 together induce integration of protein kinase and transcription factor signalling in trigger neurite outgrowth. J of Biological Chemistry, Electronic publication ahead of print 10/27/09.
52. Sandyk R et al (1986). Effects of Cannabinoids in Huntington's Disease. Neurology, 36, 342.
53. Rodriguez De Fonseca F et al (2001). Role of the endogenous cannabinoid system as a modulator of dopamine transmission: implications for Parkinson's disease and schizophrenia. Neurotox Res. Jan;3(1):23-35.
54. Garcia-Arencibia, M. et al (2009) Cannabinoid CB1 receptors are early down-regulated followed by a further up regulation in the basal ganglia of mice with deletion of specific PARK genes. J of Neural Transmission (In Press).
55. Garcia-Arencibia, M. (2009) Cannabinoids and Parkinson's Disease. Current Drug Targets-CNS and Neurological Disorders (In Press)
56. Orgado et al (2009). The Endocannabiod system in neuropathological states. International Review of Psychiatry 21(2): 172-180.
57. Izzo et al (2009) Non-psychotropic plant cannabinoids: new therapeutic opportunities from an ancient herb. Trends in Pharamcological Sciences Vol 30 No 10: 515-527.
58. Venderoza et al (2004). Survey on cannabis use in Parkinson's disease: Subjective improvement of motor symptoms. Movement Disorders, 19: 1102-1106.
59. Carroll et al (2004). Cannabis for dyskinesia in Parkinson's disease: a randomized double blind crossover study. Neurology 63(7):1245-1250.
60. De Lago et al (2007). Cannabinoids and neuroprotection in motor-related disorders. CNS & Neurological Disorders- Drug targets, 6:377-387.
61. Hazekamp A et al (2006). Evaluation of a vaporizing device (Volcano(R)) for the pulmonary administration of tetrahydrocannabinol. J Pharm Sci 95 (6) Apr 24: 1308-1317.
62. Sidney S et al (1997). Marijuana Use and Cancer Incidence. Cancer Causes and Control; 8: 722-728.
63. Tashkin D (2006). Marijuana Use and Lung Cancer: Results of a Case-Control Study. American Thoracic Society International Conference. May 23, 2006.
64. Lancet 1; 1823.
65. United States Assumes Control of Cannabis. JAMA. 1937;109(13):31B-38B. doi:10.1001/jama.1937.02780390177058
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