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Cannibus Oil anyone ? on Dateline last night


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I don't know if anyone caught the Dateline last night about the cannibus oil stopping epileptic seizures .. Has anyone here tried it for CH ?? any better worse ??  im not talking about POT (thc) ..but the cannibus oil (other chemical in it) for seizures ??


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I took an excerpt off the site linked to above ,, note here something I have brought up before ...  low blood serum prolactin ,, just thought I  would point that out if anyone is interested in getting tested for yet another deficiency


A 19-year-old right-handed university student presented to the Montefiore Headache Center for evaluation and management of his cluster headaches. Over the past 2 years, he had a cyclical pattern of stereotyped attacks occurring predictably every 1 to 2 months, lasting approximately 2 weeks. During these 2-week cluster periods, he experienced 1 attack every other day. Each cluster period was typically followed by a remission phase lasting 1 to 2 months. However, over the past 3 months, the frequency gradually increased to 1 to 2 attacks daily. The majority of attacks would abruptly awaken him from sleep at 12:30 am or 4:30 am with excruciating right temporal and peri-orbital pain. Each episode lasted 3 to 4 h untreated, with the pain reaching maximal intensity within 10 min and declining within 10 min at its conclusion. Associated symptoms included ipsilateral tearing and ptosis as well as photophobia and phonophobia. With 60% of attacks, he experienced a visual aura of a colored zigzag arc in the superior hemifield of his vision in the 10 min before pain onset. During the attacks, he experienced restlessness, feeling the need to move about, or if driving a car he would accelerate to a faster speed. He did not drink alcohol, but noted that marijuana use at the onset of his headaches consistently brought complete relief within 5 min of inhalation for each attack. The patientÂ’s mother suffered from migraine and cluster headaches. General physical and neurological examinations were normal. Routine blood tests including serum prolactin, follicle stimulating hormone (FSH), luteinizing hormone (LH), and total and free testosterone levels were normal; urine drug screen was positive for cannabinoids.Brain magnetic resonance imaging and computerized tomography angiography examinations were unremarkable.

Transitional treatment with a tapering course of prednisone over 3 weeks and a greater occipital nerve block performed with 40 mg of methylprednisolone acetate in 1 mL and 3 mL of 0.5% bupivicaine were without benefit.

Numerous prophylactic medications were tried in combination with either minimal success or intolerable adverse effects, including verapamil, lithium, sodium valproate, melatonin, topirimate, nifedipine, indomethacin, zonisamide, venlafaxine, ergotamine tartrate, and clonazepam.

Because of its lack of availability in the United States and the patientÂ’s concern about potential adverse effects, methysergide was not tried for prevention. Treatment with sumatriptan tablets, zolmitriptan nasal spray, ergotamine/caffeine, oxycodone, aspirin/butalbital/caffeine, acetominophen/dichlorphenazon/isometheptene, and indomethacin was ineffective. The patient refused to use subcutaneous sumatriptan because of a strong aversion to needles. Given the lack of responsiveness to multiple

agents, dronabinol 5 mg was substituted for marijuana for acute treatment of his cluster headaches; dronabinol consistently provided dramatic relief within 5 to 15 min of ingestion.

The patient was hospitalized for intractable cluster headache, with complete resolution of his pain after several courses of intravenous dihydroergotamine (DHE), metoclopramide, and diphenhydramine. He was discharged with tapering doses of DHE nasal spray and a regimen of topirimate, sodium valproate, and melatonin for prophylaxis. Following discharge from the hospital, the patientÂ’s headaches became less intense and less frequent, with an attack occurring every other day. Acute attacks remained consistently responsive only to dronabinol 5 mg.


Cannabis and cannabinoid compounds have been used to treat pain and possibly headache for centuries.2There are 2 types of cannabinoid receptors in humans (CB1 and CB2), and only CB1 is expressed in the central nervous system.3 These receptors are located presynaptically, and are thought to modulate neurotransmitter release. CB1 receptors are widely but not universally distributed in the central nervous system, and are particularly concentrated in the hypothalamus.A recent study in mice found CB1 receptors in axons innervating the majority of hypothalamic nuclei, with the exception of the suprachiasmatic and lateral mammilary nuclei.4 Neuroimaging studies of different modalities have consistently highlighted the ipsilateral posterior hypothalamus as a site of pathology and activation in patients with cluster headache.

5 Dronabinol, a synthetic delta-9-tetrahydrocannabinoid, is currently Food and Drug Administration approved for the treatment of nausea and appetite stimulation.

1 Our patientÂ’s rapid improvement of pain within 15 min of use is faster than the reported onset of action of 30 to 60 min.6 This early response could represent a placebo effect. However, the multitude of treatment-responsive attacks, as well as the failure of other acute therapies, are evidence against that phenomenon.

Data on cannabis use among patients with cluster headache are limited. In a recent French study of 113 patients with chronic cluster headache, 29 patients (26%) were regular cannabis consumers.7 However, no mention is made regarding the use of cannabis specifically for acute treatment of cluster attacks. It may be of future interest to ascertain if pain relief can be achieved when recreational marijuana or dronabinol are used in a cluster attack. We would not recommend routine use of recreational or pharmacological preparations of cannabis for treatment of cluster headaches because of the risk of long-term dependence and other potential adverse effects.

However, if our observation can be expanded to other sufferers of this disorder, the use of pharmaceutical cannabinoid compounds could play a role in the treatment of cluster attacks refractory to conventional acute agents. In addition, this observation may provide further insights into the underlying pathophysiology of cluster headache, including modulation of neurotransmitter release in the hypothalamus of cluster sufferers.

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I'd love to ask my doctor for dronabinol just to see what he says...

Sativex is what we have in the UK. And it's licensed only for use with MS patients. Pretty sure its tightly controlled and restricted, and unlikely to be available for anything else...

But we'll see. I might ask just for fun. :). Or ask my neuro (who specialises in MS) next time I see him.

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