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08-03-2012, 11:06 AM
<strong>Endocannabinoids potently protect the newborn brain against AMPA-kainate receptor-mediated excitotoxic damage.</strong>
Abstract
Brain lesions induced in newborn mice or rats by the glutamatergic agonists ibotenate (acting on NMDA and metabotropic receptors) or S-bromowillardiine (acting on AMPA-kainate receptors) mimic some aspects of white matter cysts and transcortical necrosis observed in human perinatal brain damage associated with cerebral palsy. Exogenous and endogenous cannabinoids have received increasing attention as potential neuroprotective agents in a number of neurodegenerative disorders of the adult. One recent study showed neuroprotection by the cannabinoid agonist WIN-55212 in a newborn rat model of acute severe asphyxia. The present study was designed to assess the neuroprotective effects of the endogenous cannabinoid anandamide using a well-defined rodent model of neonatal excitotoxic brain lesions. In this model, anandamide provided dose-dependent and long-lasting protection of developing white matter and cortical plate reducing the size of lesions induced by S-bromowillardiine. Anandamide had only marginal neuroprotective effect against ibotenate-induced cortical grey matter lesions. Anandamide-induced neuroprotection against AMPA-kainate receptor-mediated brain lesions were blocked by a CB1 antagonist but not by a CB2 antagonist. Furthermore, anandamide effects were mimicked by a CB1 agonist but not by a CB2 agonist. Real-time PCR confirmed the exp<b></b>ression of CB1 receptors, but not CB2 receptors, in the untreated newborn neocortex. Finally, neuroprotective effects of anandamide in white matter involved increased survival of preoligodendrocytes and better preservation of myelination. The present study provides experimental support for the role of endocannabinoids as a candidate therapy for excitotoxic perinatal brain lesions.
Statement Before City Council Re: Medical Marijuana
Morgan, MD, John P. "Statement Before City Council Re: Medical Marijuana." Feb. 23, 2004.
A comparison of cannabis sativa to papaver somniferum, the opium poppy, is apt. Humans found products of both plants useful and pleasurable under certain circumstances, and began to cultivate them. Products of both were used to relieve symptoms (and for other effects), although the use of both also produced fear and attempts to control their production and use. Thirty to forty years ago the appeal of the poppy to humans was elucidated elegantly. The principal constituent of opium, morphine, was found to produce its effects in animals by interacting with a pre-existing structural and functional component of the brain. Morphine binds to a receptor tissue and that binding, changes the function of cells. Further, the receptors were not waiting for morphine, but were ordinarily activated by compounds produced by the brain which provoked effects which we must assume were useful and part of normal brain function. Understanding of this system has lead to pharmacological exploitation of it. We now produce many versions of morphine which bind to the receptor, may be given by various routes and produce variations in effect. We even produce drugs which block the receptor and are useful under certain circumstances.
The marijuana (perhaps cannabis is a better term) story is similar and in many ways identical. The effects of cannabis are largely due to the presence of a chemical (delta-9-tetrahydrocannabinol, THC) which binds to pre-existing receptors in human calls and that binding alters cellular function. The receptors are part of a structural and functional system. We produce chemicals which bind to the cannabinoid receptors and it is clear that the system is useful and part of normal brain function. There is now active research producing compounds related to THC and products to deliver THC in various ways. There are even cannabinoid receptor blockers which are chiefly used in research to promote understanding of this built-in cannabinoid system in our brains.
Activation of the cannabinoid system by delivering THC to receptor sites provokes a variety of effects. Many of those effects, not all, reduce cellular response to stimuli. There is adequate evidence that THC is therapeutic in diminishing pain perception, diminishing nausea and vomiting in response to many stimuli, and reducing muscle tone and spasm secondary to multiple sclerosis, cerebral palsy and spinal cord injury. Interestingly, THC is one of the very few compounds that humans consistently respond to with increased appetite.
The development of fuller understanding and exploitation of the effects of cannabis has been delayed by societal and legislative reactions to the widespread use of cannabis by young people in the Western democracies, beginning in the 1960's, for the purpose of having fun. This negative reaction and aversion to cannabis is also fueled by the fact that it is commonly ingested by smoking it using cigarettes and pipes. Many who wish to use cannabis for apparent medical reasons wish to smoke it, and that act remains usually illegal in the United States. In truth, the current federal administration remains committed to continuing and expanding that criminalization of all cannabis use in the USA at incredible costs to taxpayers, patients and truth.
Cannabis smoking is always compared to tobacco smoking in terms of health consequences, and some who might support medical cannabis fear tobacco-like consequences. The current federal administration through its ministry of propaganda (The Office of Drug Control Policy), is actively directing a campaign to frighten Americans into believing that smoking of cannabis might even be worse for human health than the smoking of tobacco. This is not even close to true. Despite dire predictions there is no evidence that the smoking of cannabis alone causes lung cancer. It is with real concern that I tell you that the bronchial cells of cannabis smokers show pre-cancerous changes. This has been known for 20 years. Yet there are no reported cases of cancer in marijuana-only smokers. Further, strong evidence indicates that marijuana smoking even in unusually large doses does not produce the most crippling lung disorder, emphysema. The absence of these toxicities reflects the much lower dose of smoke and its irritants inhaled by users of cannabis. Not only do they smoke fewer cigarettes, but they rarely continue their smoking careers for years in the fixed pattern of tobacco use.
I agree with those who think the future of cannabinoid medication may not involve smoking; even though There is meaningful and positive research in using vaporizing devices to reduce the irritant load in cannabis smoke. However currently, there are really no alternatives to smoking cigarette and pipe-delivered plant material, for patients who find benefit in cannabis. I believe strongly that the harm in permitting this kind of use approaches zero.
Sincerely,
John P. Morgan, M.D.
source: http://www.lindesmit...yc_comments.cfm
![[Image: Medical-marijuana-patient.jpg]](http://www.freetobacco.info/wp-content/uploads/2011/02/Medical-marijuana-patient.jpg)
Treatment of human spasticity with delta 9-tetrahydrocannabinol.
Abstract
Spasticity is a common neurologic condition in patients with multiple sclerosis, stroke, cerebral palsy or an injured spinal cord. Animal studies suggest that THC has an inhibitory effect on polysynaptic reflexes. Some spastic patients claim improvement after inhaling cannabis. We tested muscle tone, reflexes, strength and performed EMGs before and after double-blinded oral administration of either 10 or 5 mg THC or placebo. The blinded examiner correctly identified the trials in which the patients received THC in seven of nine cases. For the group, 10 mg THC significantly reduced spasticity by clinical measurement (P less than 0.01). Quadriceps EMG interference pattern was reduced in those four patients with primarily extensor spasticity. THC was administered to eight other patients with spasticity and other CNS lesions. Responses varied, but benefit was seen in three of three patients with "tonic spasms." No benefit was noted in patients with cerebellar disease.
<strong>Blind Cerebral Palsy Victim Sues City Over Medical Marijuana</strong>
<div><iframe width="459" height="344" src="https://www.youtube.com/embed/YPJASQeG3ZQ?feature=oembed" frameborder="0" allowfullscreen="true"></iframe>
</div>
Abstract
Brain lesions induced in newborn mice or rats by the glutamatergic agonists ibotenate (acting on NMDA and metabotropic receptors) or S-bromowillardiine (acting on AMPA-kainate receptors) mimic some aspects of white matter cysts and transcortical necrosis observed in human perinatal brain damage associated with cerebral palsy. Exogenous and endogenous cannabinoids have received increasing attention as potential neuroprotective agents in a number of neurodegenerative disorders of the adult. One recent study showed neuroprotection by the cannabinoid agonist WIN-55212 in a newborn rat model of acute severe asphyxia. The present study was designed to assess the neuroprotective effects of the endogenous cannabinoid anandamide using a well-defined rodent model of neonatal excitotoxic brain lesions. In this model, anandamide provided dose-dependent and long-lasting protection of developing white matter and cortical plate reducing the size of lesions induced by S-bromowillardiine. Anandamide had only marginal neuroprotective effect against ibotenate-induced cortical grey matter lesions. Anandamide-induced neuroprotection against AMPA-kainate receptor-mediated brain lesions were blocked by a CB1 antagonist but not by a CB2 antagonist. Furthermore, anandamide effects were mimicked by a CB1 agonist but not by a CB2 agonist. Real-time PCR confirmed the exp<b></b>ression of CB1 receptors, but not CB2 receptors, in the untreated newborn neocortex. Finally, neuroprotective effects of anandamide in white matter involved increased survival of preoligodendrocytes and better preservation of myelination. The present study provides experimental support for the role of endocannabinoids as a candidate therapy for excitotoxic perinatal brain lesions.
CEREBRAL PALSY / CANNABIS
Statement Before City Council Re: Medical Marijuana
Morgan, MD, John P. "Statement Before City Council Re: Medical Marijuana." Feb. 23, 2004.
A comparison of cannabis sativa to papaver somniferum, the opium poppy, is apt. Humans found products of both plants useful and pleasurable under certain circumstances, and began to cultivate them. Products of both were used to relieve symptoms (and for other effects), although the use of both also produced fear and attempts to control their production and use. Thirty to forty years ago the appeal of the poppy to humans was elucidated elegantly. The principal constituent of opium, morphine, was found to produce its effects in animals by interacting with a pre-existing structural and functional component of the brain. Morphine binds to a receptor tissue and that binding, changes the function of cells. Further, the receptors were not waiting for morphine, but were ordinarily activated by compounds produced by the brain which provoked effects which we must assume were useful and part of normal brain function. Understanding of this system has lead to pharmacological exploitation of it. We now produce many versions of morphine which bind to the receptor, may be given by various routes and produce variations in effect. We even produce drugs which block the receptor and are useful under certain circumstances.
The marijuana (perhaps cannabis is a better term) story is similar and in many ways identical. The effects of cannabis are largely due to the presence of a chemical (delta-9-tetrahydrocannabinol, THC) which binds to pre-existing receptors in human calls and that binding alters cellular function. The receptors are part of a structural and functional system. We produce chemicals which bind to the cannabinoid receptors and it is clear that the system is useful and part of normal brain function. There is now active research producing compounds related to THC and products to deliver THC in various ways. There are even cannabinoid receptor blockers which are chiefly used in research to promote understanding of this built-in cannabinoid system in our brains.
Activation of the cannabinoid system by delivering THC to receptor sites provokes a variety of effects. Many of those effects, not all, reduce cellular response to stimuli. There is adequate evidence that THC is therapeutic in diminishing pain perception, diminishing nausea and vomiting in response to many stimuli, and reducing muscle tone and spasm secondary to multiple sclerosis, cerebral palsy and spinal cord injury. Interestingly, THC is one of the very few compounds that humans consistently respond to with increased appetite.
The development of fuller understanding and exploitation of the effects of cannabis has been delayed by societal and legislative reactions to the widespread use of cannabis by young people in the Western democracies, beginning in the 1960's, for the purpose of having fun. This negative reaction and aversion to cannabis is also fueled by the fact that it is commonly ingested by smoking it using cigarettes and pipes. Many who wish to use cannabis for apparent medical reasons wish to smoke it, and that act remains usually illegal in the United States. In truth, the current federal administration remains committed to continuing and expanding that criminalization of all cannabis use in the USA at incredible costs to taxpayers, patients and truth.
Cannabis smoking is always compared to tobacco smoking in terms of health consequences, and some who might support medical cannabis fear tobacco-like consequences. The current federal administration through its ministry of propaganda (The Office of Drug Control Policy), is actively directing a campaign to frighten Americans into believing that smoking of cannabis might even be worse for human health than the smoking of tobacco. This is not even close to true. Despite dire predictions there is no evidence that the smoking of cannabis alone causes lung cancer. It is with real concern that I tell you that the bronchial cells of cannabis smokers show pre-cancerous changes. This has been known for 20 years. Yet there are no reported cases of cancer in marijuana-only smokers. Further, strong evidence indicates that marijuana smoking even in unusually large doses does not produce the most crippling lung disorder, emphysema. The absence of these toxicities reflects the much lower dose of smoke and its irritants inhaled by users of cannabis. Not only do they smoke fewer cigarettes, but they rarely continue their smoking careers for years in the fixed pattern of tobacco use.
I agree with those who think the future of cannabinoid medication may not involve smoking; even though There is meaningful and positive research in using vaporizing devices to reduce the irritant load in cannabis smoke. However currently, there are really no alternatives to smoking cigarette and pipe-delivered plant material, for patients who find benefit in cannabis. I believe strongly that the harm in permitting this kind of use approaches zero.
Sincerely,
John P. Morgan, M.D.
source: http://www.lindesmit...yc_comments.cfm
Jaqueline Patterson, Cerebal Palsay video included
Cerebral palsy is a group of disorders that affect a person's ability to move and to maintain balance and posture. The disorders appear in the first few years of life. Usually they do not get worse over time. People with cerebral palsy may have difficulty walking. They may also have trouble with tasks such as writing or using scissors. Some have other medical conditions, including seizure disorders or mental impairment. Cerebral palsy happens when the areas of the brain that control movement and posture do not develop correctly or get damaged.There is no cure for cerebral palsy, but treatment can improve the lives of those who have it. Treatment includes medicines, braces, and physical, occupational and speech therapy.
- National Institute of Neurological Disorders and Stroke
source: http://www.medicalca...documentary.htm
Cerebral palsy is a group of disorders that affect a person's ability to move and to maintain balance and posture. The disorders appear in the first few years of life. Usually they do not get worse over time. People with cerebral palsy may have difficulty walking. They may also have trouble with tasks such as writing or using scissors. Some have other medical conditions, including seizure disorders or mental impairment. Cerebral palsy happens when the areas of the brain that control movement and posture do not develop correctly or get damaged.There is no cure for cerebral palsy, but treatment can improve the lives of those who have it. Treatment includes medicines, braces, and physical, occupational and speech therapy.
- National Institute of Neurological Disorders and Stroke
source: http://www.medicalca...documentary.htm
Treatment of human spasticity with delta 9-tetrahydrocannabinol.
Abstract
Spasticity is a common neurologic condition in patients with multiple sclerosis, stroke, cerebral palsy or an injured spinal cord. Animal studies suggest that THC has an inhibitory effect on polysynaptic reflexes. Some spastic patients claim improvement after inhaling cannabis. We tested muscle tone, reflexes, strength and performed EMGs before and after double-blinded oral administration of either 10 or 5 mg THC or placebo. The blinded examiner correctly identified the trials in which the patients received THC in seven of nine cases. For the group, 10 mg THC significantly reduced spasticity by clinical measurement (P less than 0.01). Quadriceps EMG interference pattern was reduced in those four patients with primarily extensor spasticity. THC was administered to eight other patients with spasticity and other CNS lesions. Responses varied, but benefit was seen in three of three patients with "tonic spasms." No benefit was noted in patients with cerebellar disease.
<strong>Blind Cerebral Palsy Victim Sues City Over Medical Marijuana</strong>
<div><iframe width="459" height="344" src="https://www.youtube.com/embed/YPJASQeG3ZQ?feature=oembed" frameborder="0" allowfullscreen="true"></iframe>
</div>