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Changing Medicine Together
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~ Epilepsy ~
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Preferred Methods to medicate:
Raw Kief/Greens
Ideally one should be eating Raw Kief/Greens for the A molecule THCA, CBDA etc, Over and above the preferred method of medicating, each cannabinoid & Terpenes plays a roll in healing.
Medicating
Ideally one should be eating Raw Kief/Greens for the A molecule THCA, CBDA etc, Over and above the preferred method of medicating, each cannabinoid & Terpenes plays a roll in healing.
Medicating
- Drops/Oil Dropped under tongue for faster absorption (Soft membrane tissue).
- Sprays, if for internal best applied through nasal sprays for soft tissue. (If Issue is eye's or ear's, apply to correlation)
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CNN
Toddler's seizures treated with Cannabis bad day we give him 1 more Drops under the tongue |
ABC News
Charlottes Web CBD rich Cannabis Charlotte was at rock bottom a few drops a day changed everything. |
Cannabis for Kids, Part 1
Meeting her for the first time Lily's Story Part 1& 2 linked at the end. |
CTV, Canada AM
Zero Seizures, walking & Talking When something works this well, how can they keep ignoring it. |
Epilepsy, Overview:
The medical definition of a seizure is a clinical expression of abnormal, excessive, synchronous discharge of neurons residing primarily in the brain’s cerebral cortex. Alternatively, the term epilepsy encompasses a broad range clinical syndromes characterized by repeated seizures over time unprovoked by an acute systemic or neurological insult. Individuals with epilepsy can manifest any of the seizure types listed below as part of their clinical condition. In fact, the International League Against Epilepsy recognizes over twenty epilepsy syndromes, each defined by a distinct set of signs and symptoms. many epilepsy syndromes have a strong genetic component, including benign familial infantile epilepsy, severe myoclonic epilepsy of infancy (Dravet syndrome), and Landau-Kleffner syndrome. Perhaps the most notable and devastating of these syndromes, Dravet Syndrome, is a severe and intractable epilepsy condition. It presents in the first year of life as a series of prolonged generalized clonic seizures in the setting of otherwise normal cognitive and motor development.
Patients with this syndrome have a high propensity to enter into a life threatening state of status epilepticus, where the brain is in a persistent state of seizure. Unfortunately, children with this syndrome develop persistent gait ataxia – the inability to coordinate walking – in addition to cognitive and behavioral impairments.
Patients with this syndrome have a high propensity to enter into a life threatening state of status epilepticus, where the brain is in a persistent state of seizure. Unfortunately, children with this syndrome develop persistent gait ataxia – the inability to coordinate walking – in addition to cognitive and behavioral impairments.
Epilepsy is a group of neurological disorders characterized by epileptic seizures.[10][11] Epileptic seizures are episodes that can vary from brief and nearly undetectable periods to long periods of vigorous shaking.[1] These episodes can result in physical injuries, including occasionally broken bones.[1] In epilepsy, seizures tend to recur and, as a rule, have no immediate underlying cause.[10] Isolated seizures that are provoked by a specific cause such as poisoning are not deemed to represent epilepsy.[12] People with epilepsy in some areas of the world experience varying degrees of social stigma due to their condition.[1]
The cause of most cases of epilepsy is unknown.[1] Some cases occur as the result of brain injury, stroke, brain tumors, infections of the brain and birth defects, through a process known as epileptogenesis.[1][2][3] Known genetic mutations are directly linked to a small proportion of cases.[4][13] Epileptic seizures are the result of excessive and abnormal neuronal activity in the cortex of the brain.[12] The diagnosis involves ruling out other conditions that might cause similar symptoms, such as fainting, and determining if another cause of seizures is present, such as alcohol withdrawal or electrolyte problems.[4] This may be partly done by imaging the brain and performing blood tests.[4] Epilepsy can often be confirmed with an electroencephalogram (EEG), but a normal test does not rule out the condition.[4]
Epilepsy that occurs as a result of other issues may be preventable.[1] Seizures are controllable with medication in about 70% of cases.[7] Inexpensive options are often available.[1] In those whose seizures do not respond to medication, surgery, neurostimulation or dietary changes may then be considered.[5][6] Not all cases of epilepsy are lifelong, and many people improve to the point that treatment is no longer needed.[1]
The cause of most cases of epilepsy is unknown.[1] Some cases occur as the result of brain injury, stroke, brain tumors, infections of the brain and birth defects, through a process known as epileptogenesis.[1][2][3] Known genetic mutations are directly linked to a small proportion of cases.[4][13] Epileptic seizures are the result of excessive and abnormal neuronal activity in the cortex of the brain.[12] The diagnosis involves ruling out other conditions that might cause similar symptoms, such as fainting, and determining if another cause of seizures is present, such as alcohol withdrawal or electrolyte problems.[4] This may be partly done by imaging the brain and performing blood tests.[4] Epilepsy can often be confirmed with an electroencephalogram (EEG), but a normal test does not rule out the condition.[4]
Epilepsy that occurs as a result of other issues may be preventable.[1] Seizures are controllable with medication in about 70% of cases.[7] Inexpensive options are often available.[1] In those whose seizures do not respond to medication, surgery, neurostimulation or dietary changes may then be considered.[5][6] Not all cases of epilepsy are lifelong, and many people improve to the point that treatment is no longer needed.[1]
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Traditional Treatment Options
Treatment of epilepsy syndromes is a complex process involving a combination of drug therapy, diet, and even surgical intervention for some intractable cases. Antiepileptic drugs (AED) are administered according to the seizure type which is being treated. Additional factors such as side effect profile, cost, and method of administration are also highly considered, especially in the case of children. While undergoing AED therapy, children will have to have their blood levels closely monitored in order to ensure that drug levels remain in the appropriate range – toxic levels of some AEDs may initiate seizure activity themselves. Patients and caregivers are very familiar with having to slowly increase the dosage of their medication to reach a maintenance dose which will provide optimal seizure control. 
In 20-40% of children with epilepsy syndromes, lack of efficacy and side effects lead to the addition of a second AED to the therapeutic regimen. This further complicates treatment therapy however, as drug interactions and adverse interactions (ex. the induction of new seizure types) become a greater possibility once a second AED is introduced.
Additional options for those who have intractable seizures include consuming a ketogenic diet, which is a diet high in fat and protein and low in carbohydrates. The theoretical basis for this diet stems from the physiological principle that the brain has two sources of fuel: glucose and ketone bodies. By significantly reducing the amount of carbohydrates in the diet, the brain will use ketone bodies as its primary fuel source which lowers the seizure threshold in patients. A meta-analysis of the efficacy of the ketogenic diet showed that after 6 months on the diet, approximately 60% of children had a greater than 50% seizure reduction, with 30% of children having greater than 90% seizure reduction. 
Types of Seizures:
Epileptic seizureThe most common type (60%) of seizures are convulsive.[24] Of these, one-third begin as generalized seizures from the start, affecting both hemispheres of the brain.[24] Two-thirds begin as focal seizures (which affect one hemisphere of the brain) which may then progress to generalized seizures.[24] The remaining 40% of seizures are non-convulsive. An example of this type is the absence seizure, which presents as a decreased level of consciousness and usually lasts about 10 seconds.[2][25] Focal seizures are often preceded by certain experiences, known as auras.[26] They include sensory (visual, hearing, or smell), psychic, autonomic, and motor phenomena.[2] Jerking activity may start in a specific muscle group and spread to surrounding muscle groups in which case it is known as a Jacksonian march.[27] Automatisms may occur, which are non-consciously-generated activities and mostly simple repetitive movements like smacking of the lips or more complex activities such as attempts to pick up something.[27] There are six main types of generalized seizures: tonic-clonic, tonic, clonic, myoclonic, absence and atonic seizures.[28] They all involve loss of consciousness and typically happen without warning. Tonic-clonic seizures
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20 sec response
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occur with a contraction of the limbs followed by their extension along with arching of the back which lasts 10–30 seconds (the tonic phase). A cry may be heard due to contraction of the chest muscles, followed by a shaking of the limbs in unison (clonic phase).
- Tonic seizures produce constant contractions of the muscles. A person often turns blue as breathing is stopped.
- clonic seizures there is shaking of the limbs in unison. After the shaking has stopped it may take 10–30 minutes for the person to return to normal; this period is called the "postictal state" or "postictal phase." Loss of bowel or bladder control may occur during a seizure.[29] The tongue may be bitten at either the tip or on the sides during a seizure.[30] In tonic-clonic seizure, bites to the sides are more common.[30] Tongue bites are also relatively common in psychogenic non-epileptic seizures.[30]
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Myoclonic Seizures
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involve spasms of muscles in either a few areas or all over.[31] Absence seizures can be subtle with only a slight turn of the head or eye blinking.[2] The person does not fall over and returns to normal right after it ends.[2] Atonic seizures involve the loss of muscle activity for greater than one second.[27] This typically occurs on both sides of the body.[27]
About 6% of those with epilepsy have seizures that are often triggered by specific events and are known as reflex seizures.[32] Those with reflex epilepsy have seizures that are only triggered by specific stimuli.[33] Common triggers include flashing lights and sudden noises.[32] In certain types of epilepsy, seizures happen more often during sleep,[34] and in other types they occur almost only when sleeping.[35]
About 6% of those with epilepsy have seizures that are often triggered by specific events and are known as reflex seizures.[32] Those with reflex epilepsy have seizures that are only triggered by specific stimuli.[33] Common triggers include flashing lights and sudden noises.[32] In certain types of epilepsy, seizures happen more often during sleep,[34] and in other types they occur almost only when sleeping.[35]
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Post-ictal
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After the active portion of a seizure (the ictal state) there is typically a period of recovery during which there is confusion, referred to as the postictal period before a normal level of consciousness returns.[26] It usually lasts 3 to 15 minutes[36] but may last for hours.[37] Other common symptoms include feeling tired, headache, difficulty speaking, and abnormal behavior.[37] Psychosis after a seizure is relatively common, occurring in 6–10% of people.[38] Often people do not remember what happened during this time.[37] Localized weakness, known as Todd's paralysis, may also occur after a focal seizure. When it occurs it typically lasts for seconds to minutes but may rarely last for a day or two.[39]
Epilepsy can have adverse effects on social and psychological well-being.[24] These effects may include social isolation, stigmatization, or disability.[24] They may result in lower educational achievement and worse employment outcomes.[24] Learning disabilities are common in those with the condition, and especially among children with epilepsy.[24] The stigma of epilepsy can also affect the families of those with the disorder.[29]
Certain disorders occur more often in people with epilepsy, depending partly on the epilepsy syndrome present. These include depression, anxiety, obsessive–compulsive disorder (OCD),[40] and migraine.[41] Attention deficit hyperactivity disorder affects three to five times more children with epilepsy than children without the condition.[42] ADHD and epilepsy have significant consequences on a child's behavioral, learning, and social development.[43] Epilepsy is also more common in children with autism.[4
Certain disorders occur more often in people with epilepsy, depending partly on the epilepsy syndrome present. These include depression, anxiety, obsessive–compulsive disorder (OCD),[40] and migraine.[41] Attention deficit hyperactivity disorder affects three to five times more children with epilepsy than children without the condition.[42] ADHD and epilepsy have significant consequences on a child's behavioral, learning, and social development.[43] Epilepsy is also more common in children with autism.[4
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Ted Tallk
Neurophysiology & Cannabis Neuro-disorders 101 Jokubas Ziburkus, There is something you should know about epilepsy and cannabis |
Charlottes Web
Children on there death bed Epilepsy have Dozens of seizures a day NOW... 0 Seizures or next to it. Bring a tear to your eye! |
Russell Saneto, D.O., Ph.D.
Epilepsy Foundation Northwest Cannabis impacts on Epilepsy A informative breakdown of cannabis and Epilepsy. |
~ How Cannabis Aids ~
studies revealed a potential mechanism for this effect, showing that CBD raised the threshold requirement after one action potential, making it more difficult for subsequent action potentials to fire and propagate seizure activity. The effects of cannabidiol (CBD) on electrically evoked kindled seizures, decreased the (electrical) after discharge (AD), duration and amplitude. Electrophysiologically, the antiseizure effects of CBD were a combination of those of PHT and ESM. The combination of effects may account for the observation that CBD was the most efficacious of the drugs tested against limbic ADs and convulsions. Other properties of CBD were also noted: For example, compared with delta 9-THC, although THC is a Anti-convulsive it is a much more selective anticonvulsant vis-à-vis motor toxicity. CBD also lacks the CNS excitatory effects produced by delta 9-THC, and especially other comparative standard seizure drugs. These characteristics, combined with its apparently unique set of electrophysiological properties, support the suggestion that CBD has therapeutic potential as an antiepileptic/anti-seizure.
Cannabis and Δ(9) -THC are anticonvulsant in most animal models but THC can be proconvulsant in some healthy models(Ones that did not need therapy). The psychotropic effects of Δ(9) -THC limit tolerability. CBD is anticonvulsant in many acute animal models, but there are limited data in chronic models. The antiepileptic mechanisms of CBD are not known, but may include effects on the equilibrative nucleoside transporter; the orphan G-protein-coupled receptor GPR55; the transient receptor potential of vanilloid type-1 channel; the 5-HT1a receptor; and the α3 and α1 glycine receptors. CBD has neuroprotective and antiinflammatory effects, and it appears to be well tolerated in humans,
Regulatory proteins ( eg. Anandamide, 2-AG, THC, CBD, CBC, THCA, THCV, etc ) play a role in controlling cannabinoid signaling via CB1 & 2 receptors which plays a role/regulates most Systems and organs(reviewed in Ref. [37]). The cannabinoid receptor-interacting proteins 1a and 1b (CRIP1a and CRIP1b) are only known to interact with CB1 receptors. Both CRIP1a and CRIP1b directly interact with the C-terminus of the CB1 receptor but not CB2. More clinical studies are needed on the regulation and function of these interacting proteins. Evidence suggests that CRIP1a attenuates CB1 receptor-induced inhibition of Ca2+efflux.37,38 CRIP1a, like CB1, is widely expressed in the brain at high levels.38 It has been suggested that these regulatory proteins play a critical role in modulating CB1 receptor function in the pathogenesis or neuroadaptive response to epilepsy, And other Autoimmune, & neuropsychiatric disorders. There are a number of other regulatory proteins that interact with CB1 to affect signal transduction. Some of these are nonspecific G-protein receptors regulators such as G-protein-coupled receptor kinase-3 (GRK3) and β-arrestin2. These proteins facilitate desensitization and intracellular trafficking of CB1 receptors.39,40 Other regulatory proteins including AP3 and G protein receptor associated sorting protein-1 (GASP1) associate with CB1 and limited number of other G-coupled receptors. These proteins are less promiscuous and associate with only a limited subset of G-coupled receptors. They direct CB1 targeting to lysosomes,41,42 a mechanism of downregulation of response.
Due to the violent nature of epileptic seizures ( Including those with absence seizures (seizure's not physically visible))largely due to inflammation when speaking of internally, the damage is often substantial creating a cascade of potential other problems. The function of the endocannabinoid system in the nervous system is more than just homeostatic prevention of too much excitation or too much inhibition ( regulating up or down ). There is a significant protective and regenerative (repair)function facilitated through cannabinoids ( Cannabis ) and the Endocannabiniod system (ECS) , as well the endocannabinoid system is heavily involved in neuroplasticity.
Neuroplasticity involves the sprouting and pruning of synapses, changes in dendritic spine density, and changes in neurotransmitter pathways. It gives rise to all types of adaptive learning, including recovering from a stroke, the conscious act of gaining a new skill, and the unconscious acquisition of a new emotional response. It is also involved in pathological processes such as central sensitization to pain. There are multiple mechanisms by which cannabinoids modulate neural plasticity, including neurogenesis (the formation of new neurons), aiding in long-term potentiation and long-term depression. Research in humans has shown that the administration of exogenous cannabinoids can cause neuroplastic changes. Anandamide and 2-AG are also endogenous neuroprotective agents, produced by the nervous system in response to both chemical and mechanical trauma. Both phytocannabinoids ( Cannabis) and synthetic (GMO) cannabinoids have been shown to decrease glutamate excitotoxicity in a situation of a seizure or a stroke. (Although nature is always best. No side affects) When neurons become injured or ill, they tend to release their contents. Excitatory neurons release levels of glutamate that become toxic to the surrounding cells, and we see a domino effect of excitotoxicity. Cannabinoids have been shown to halt that process. The United States Department of Health and Human Services actually owns a patent on the use of cannabinoids as anti-oxidants and neuroprotectants. The authors of this patent discuss the potential benefit of using cannabinoids in neurodegenerative conditions such as Epilepsy, multiple sclerosis, Alzheimer’s, Parkinson’s, Huntington’s, and more. Cannabinoids also affect autonomic tone. In the sympathetic nervous system, CB1 receptor stimulation will inhibit noroepinephrine release. It will dampen sympathetically mediated pain and modulate the hypothalamic- pituitary-adrenal axis and the hypothalamic locus coerulius-norepinephrine axis.
Cannabis and Δ(9) -THC are anticonvulsant in most animal models but THC can be proconvulsant in some healthy models(Ones that did not need therapy). The psychotropic effects of Δ(9) -THC limit tolerability. CBD is anticonvulsant in many acute animal models, but there are limited data in chronic models. The antiepileptic mechanisms of CBD are not known, but may include effects on the equilibrative nucleoside transporter; the orphan G-protein-coupled receptor GPR55; the transient receptor potential of vanilloid type-1 channel; the 5-HT1a receptor; and the α3 and α1 glycine receptors. CBD has neuroprotective and antiinflammatory effects, and it appears to be well tolerated in humans,
Regulatory proteins ( eg. Anandamide, 2-AG, THC, CBD, CBC, THCA, THCV, etc ) play a role in controlling cannabinoid signaling via CB1 & 2 receptors which plays a role/regulates most Systems and organs(reviewed in Ref. [37]). The cannabinoid receptor-interacting proteins 1a and 1b (CRIP1a and CRIP1b) are only known to interact with CB1 receptors. Both CRIP1a and CRIP1b directly interact with the C-terminus of the CB1 receptor but not CB2. More clinical studies are needed on the regulation and function of these interacting proteins. Evidence suggests that CRIP1a attenuates CB1 receptor-induced inhibition of Ca2+efflux.37,38 CRIP1a, like CB1, is widely expressed in the brain at high levels.38 It has been suggested that these regulatory proteins play a critical role in modulating CB1 receptor function in the pathogenesis or neuroadaptive response to epilepsy, And other Autoimmune, & neuropsychiatric disorders. There are a number of other regulatory proteins that interact with CB1 to affect signal transduction. Some of these are nonspecific G-protein receptors regulators such as G-protein-coupled receptor kinase-3 (GRK3) and β-arrestin2. These proteins facilitate desensitization and intracellular trafficking of CB1 receptors.39,40 Other regulatory proteins including AP3 and G protein receptor associated sorting protein-1 (GASP1) associate with CB1 and limited number of other G-coupled receptors. These proteins are less promiscuous and associate with only a limited subset of G-coupled receptors. They direct CB1 targeting to lysosomes,41,42 a mechanism of downregulation of response.
Due to the violent nature of epileptic seizures ( Including those with absence seizures (seizure's not physically visible))largely due to inflammation when speaking of internally, the damage is often substantial creating a cascade of potential other problems. The function of the endocannabinoid system in the nervous system is more than just homeostatic prevention of too much excitation or too much inhibition ( regulating up or down ). There is a significant protective and regenerative (repair)function facilitated through cannabinoids ( Cannabis ) and the Endocannabiniod system (ECS) , as well the endocannabinoid system is heavily involved in neuroplasticity.
Neuroplasticity involves the sprouting and pruning of synapses, changes in dendritic spine density, and changes in neurotransmitter pathways. It gives rise to all types of adaptive learning, including recovering from a stroke, the conscious act of gaining a new skill, and the unconscious acquisition of a new emotional response. It is also involved in pathological processes such as central sensitization to pain. There are multiple mechanisms by which cannabinoids modulate neural plasticity, including neurogenesis (the formation of new neurons), aiding in long-term potentiation and long-term depression. Research in humans has shown that the administration of exogenous cannabinoids can cause neuroplastic changes. Anandamide and 2-AG are also endogenous neuroprotective agents, produced by the nervous system in response to both chemical and mechanical trauma. Both phytocannabinoids ( Cannabis) and synthetic (GMO) cannabinoids have been shown to decrease glutamate excitotoxicity in a situation of a seizure or a stroke. (Although nature is always best. No side affects) When neurons become injured or ill, they tend to release their contents. Excitatory neurons release levels of glutamate that become toxic to the surrounding cells, and we see a domino effect of excitotoxicity. Cannabinoids have been shown to halt that process. The United States Department of Health and Human Services actually owns a patent on the use of cannabinoids as anti-oxidants and neuroprotectants. The authors of this patent discuss the potential benefit of using cannabinoids in neurodegenerative conditions such as Epilepsy, multiple sclerosis, Alzheimer’s, Parkinson’s, Huntington’s, and more. Cannabinoids also affect autonomic tone. In the sympathetic nervous system, CB1 receptor stimulation will inhibit noroepinephrine release. It will dampen sympathetically mediated pain and modulate the hypothalamic- pituitary-adrenal axis and the hypothalamic locus coerulius-norepinephrine axis.
A Few Related Symptoms
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Appetite -
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Clinical Studies
Study - 1979 - An electrophysiological analysis of the anticonvulsant action of cannabidiol on limbic seizures in conscious rats.
Study - 2003 - Virginia Commonwealth University - Marijuana and its receptor protein in brain control epilepsy
Effects of WIN 55,212-2 (a non-selective cannabinoid CB1 and CB2 receptor agonist) on the protective action of various classical antiepileptic drugs in the mouse 6 Hz psychomotor seizure model
Study - 2003 - Virginia Commonwealth University - Marijuana and its receptor protein in brain control epilepsy
- VCU study is first to test anticonvulsant potential of marijuana and brain recurrent seizures.
Effects of WIN 55,212-2 (a non-selective cannabinoid CB1 and CB2 receptor agonist) on the protective action of various classical antiepileptic drugs in the mouse 6 Hz psychomotor seizure model
Patents
US6630507 Autoimmune Disorders; Cannabiniods as antioxidants & neuroprotectants
US6410588B1 1998-04-14 2002-06-25 anti-inflammatory agents The Mathilda And Terence Kennedy Institute Of Rheumatology Use of cannabinoids as anti-inflammatory agents
US6410588B1 1998-04-14 2002-06-25 anti-inflammatory agents The Mathilda And Terence Kennedy Institute Of Rheumatology Use of cannabinoids as anti-inflammatory agents