Board recommends 8 new conditions for medical-marijuana use

Sue Vorenberg |

4/13/2009 - 4/14/09
The Department of Health's Medical Advisory Board wants to let more people with chronic conditions into the approved group of patients that can use marijuana for medical purposes.

The board will ask Health Secretary Alfredo Vigil to add eight new conditions to 14 that have so far been included in the state Medical Cannabis Program.

The program provides protection from state prosecution for approved users of medical marijuana. Patients must apply to the state to be eligible.

The proposed new conditions are: chronic muscle inflammation accompanied by muscle weakness; severe osteoarthritis; rheumatoid arthritis; reactive arthritis; post-polio syndrome; Parkinson's disease; Alzheimer's; and severe chronic pain.

Each condition must meet specific requirements to be eligible, and the board is planning to provide data to back up the suggestions in its final proposal, said Deborah Busemeyer, a spokeswoman for the department.

"The secretary will be looking for scientific evidence that the conditions meet legal requirements," Busemeyer said. "That is, that they are chronic, debilitating conditions where the patient can find no relief elsewhere."

Once the board finishes the proposal, Vigil will have 10 days to decide if he will approve some or all of the list.

"It depends on what's in the recommendations," Busemeyer said. "Last time, though, he approved the majority of them, but not all of them."

So far, the approved conditions are: cancer; glaucoma; multiple sclerosis; epilepsy; spinal-cord damage with intractable spasticity; HIV/AIDS; painful peripheral neuropathy; intractable nausea/vomiting; severe anorexia/cachexia; hepatitis-C infection currently receiving antiviral treatment; Crohn's disease; post-traumatic stress disorder; and Lou Gehrig's disease. Hospice patients are also eligible.

There are 284 patients in the program so far.

The state also recently approved a license for the first nonprofit group to produce and distribute marijuana to patients in the program. The group hasn't yet started distribution.

Mirapex, Other Parkinson’s Disease Drugs Linked to Compulsive Gambling, Hypersexuality
Date Published: Tuesday, April 14th, 2009

Mirapex and other dopamine agonists used to treat Parkinson’s Disease have been linked to the development of extreme behaviors by yet another study. According to researchers at the Mayo Clinic, one in five patients taking such drugs in a recent study developed behavior disorders, such as compulsive gambling or hypersexuality.

Dopamine agonists like Mirapex have long been suspected of causing compulsive behavior. The suspicion was bolstered last June, when researchers investigating the link between dopamine agonists and compulsive behavior presented their findings at International Congress of Parkinson’s Disease and Movement Disorders conference in Chicago. The study, which looked at more than 3,000 patients from 46 medical centers in the United States and Canada, found that Parkinson’s patients on dopamine agonists are nearly three times more likely to have at least one impulse-control disorder - including gambling addiction - compared with patients receiving other treatments.

Parkinson’s Disease occurs because of a lack of the neurotransmitter dopamine in certain areas of the brain. A dopamine agonist works by mimicking the effects of this chemical. However, dopamine is also known to produce a “rush” in the brain of people who are anticipating a reward or excitement. Many experts believe that such a biochemical reaction is behind the reports of compulsive behavior linked to dopamine agonists like Mirapex.

The Mayo Clinic study involved 267 patients treated between 2004 and 2006 in a seven-county area around the Mayo clinic. Sixty-six were taking a dopamine agonist at a therapeutic level, but only 38 were using doses in the therapeutic range, 178 were taking carbidopa/levodopa without a dopamine agonist, and 23 were untreated.

Six of the patients taking dopamine agonists developed a behavioral disorder (an occurrence rate of 18.4 percent for this group). Five developed a gambling addiction and five became hypersexual (both disorders developed in three of the patients). Other compulsive behaviors were noted as well. Though in some cases the behaviors continued for years, the Mayo Clinic researchers found that they abated when the patients stopped dopamine agonist therapy.

None of these behaviors were seen in untreated patients, those taking less than a therapeutic dose of a dopamine agonist, or patients receiving treatment with carbidopa/levodopa alone, the researchers said.

The researchers advised that the severity of the problems seen indicated that patients and doctors needed to be more aware of the behavioral side effects associated with dopamine agonists. In at least 2 cases, patients were subjected to intense psychiatric treatment before dopamine agonists were recognized as a likely cause of their disorder.

“Physicians treating Parkinson’s Disease with dopamine agonists should obviously warn the patients, spouses, and families of such risks because they may not recognize the relationship to the drug until disastrous consequences have occurred,” the study authors said.

Study identifies gene that contributes to Parkinson's disease
April 4, 3:01 PM ·

MJFF has funded over $142 million in research to date

A new study helps to explain why people who carry mutations in a gene known as Nurr1 develop a rare, inherited form of Parkinson's disease (PD), the most prevalent movement disorder in people over the age of 65. A research team from the University of California, San Diego School of Medicine and the Salk Institute for Biological Studies in La Jolla has identified a protein in the brain of mice that protects neurons from excessive inflammation, which can lead to neurodegenerative disorders such as Parkinson's disease.

Their study, which identifies the protective function of a protein called Nurr1 and defines the pathway by which it works, was published in the April 3rd edition of the medical journal Cell.

Parkinson's disease belongs to a group of conditions called motor system disorders, which are the result of the loss of dopamine-producing brain cells. The four primary symptoms of PD are trembling in hands, arms, legs, jaw, and face; rigidity, or stiffness of the limbs and trunk; slowness of movement; and impaired balance and coordination. As these symptoms become more pronounced, patients may have difficulty walking, talking, or completing other simple tasks.

Contact: Cathleen Genova

A new study in the April 3rd issue of the journal Cell, a Cell Press publication, helps to explain why people who carry mutations in a gene known as Nurr1 develop a rare, inherited form of Parkinson's disease, the most prevalent movement disorder in people over the age of 65.

They have found evidence that the gene normally acts to suppress an inflammatory response and, in turn, the production of neurotoxins in the brain. Those neurotoxins can otherwise spawn the damage to dopaminergic neurons that is characteristic of Parkinson's disease. The findings not only offer new insight into the causes of the disease, but also may point to new avenues for therapy, according to the researchers.

In its normal form, "the gene protects against Parkinson's," said Christopher Glass of the University of California, San Diego. "This system functions in the brain, and probably in other parts of the body, to protect from the deleterious effects of excessive inflammation." When the Nurr1 gene is disabled, as it is in those with the rare familial form of Parkinson's disease, it leads to a pattern of inflammation that is exaggerated in both magnitude and duration, he added.

The causes of most common forms of Parkinson's remain poorly understood, but the disease is generally associated with an inflammatory component involving cells known as microglia, the researchers explained. Those microglia act as sentinel cells, keeping a lookout for potential infection or tissue injury in the central nervous system.

As for Nurr1, studies had found it plays an important role in dopaminergic neurons and that people with a rare mutant form of the gene produce too little of the protein it encodes, leading them to develop Parkinson's disease late in life. Earlier reports also showed that Nurr1 operates in cells other than neurons, where its activity is increased by inflammatory factors.

Glass and his colleague Kaoru Saijo, also of UCSD, suspected that Nurr1's roles outside of neurons might also be involved in Parkinson's disease. Indeed, they've now shown that Nurr1 limits the activity of pro-inflammatory neurotoxic mediators in microglia and in cells known as astrocytes, which serve as support cells to neurons. When Nurr1's activity is reduced, microglia launch an exaggerated inflammatory response that is amplified further by astrocytes. It is this overreaction that leads to the production of factors that ultimately kill dopaminergic neurons.

The findings suggest that inflammation may be an important general contributor to Parkinson's disease, which in the vast majority of cases has not been traced to any genetic cause, Saijo said. The researchers noted that while experts have grown to appreciate that Parkinson's disease has an inflammatory component, questions still remain about its role as a cause or consequence of the disease.

"We think if inflammation is not an initiating event, it is definitely a part of the process that could amplify the disease," Glass said. That's a key point moving forward, he said, because it suggests there should be further efforts to evaluate and test anti-inflammatory therapies in the treatment of Parkinson's. Treatments designed to interrupt the signals between microglia and astrocytes might hold additional promise for fighting the disease.

The new results may also have implications for the ultimate success or failure of stem cell therapies, Glass said. If the progression of Parkinson's disease is significantly influenced by inflammation as the researchers suggest, then any cell-based therapies designed to replace the dopaminergic neurons that are lost with new ones will also "have to deal with this process."

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The researchers include Kaoru Saijo, University of California, San Diego, La Jolla, California, CA; Beate Winner, The Salk Institute for Biological Studies, La Jolla, CA; Christian T. Carson, The Salk Institute for Biological Studies, La Jolla, CA; Jana G. Collier, University of California, San Diego, La Jolla, California, CA; Leah Boyer, University of California, San Diego, La Jolla, California, CA, The Salk Institute for Biological Studies, La Jolla, CA; Michael G. Rosenfeld, University of California, San Diego, La Jolla, California, CA, Howard Hughes Medical Institute; Fred H. Gage, The Salk Institute for Biological Studies, La Jolla, CA; and Christopher K. Glass, University of California, San Diego, La Jolla, California, CA.