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Cambria anyone? (Read 3053 times)
Gail
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Raleigh, NC
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Cambria anyone?
Jun 11th, 2011 at 12:30am
 
My headaches were coming 6-7 times a day. Went to the neuro yesterday and as one was starting to hit, she gave me flova (sumatriptan) and Cambria. It is a powder that mixes in water. The stuff actually worked. Since yesterday, I've only had 2 headaches and should be between 12-14 by now. I was using imitrex shots (I use only half at a time so I get 4 shots outof one packet) but the headaches would continue to hit.  Doctor said continuous constricting and dilating was causing inflamation. Cambria calms that down. I am happy to say it worked for me. Anyone going to a neuro/doctor soon might want to ask if you are having multiples a day. I thoguht they were rebounds. Apparently I was wrong. Hopefully verapamil kicks in this weekend and I'll be set for awhile. Won't count my chickens before they are hatched. We all know that's a bad thing to do when your a cluster sufferer. Wishing everyone the best.  Faith and prayers will get you through Smiley One day it will be over and you will be headache free!!
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Bob Johnson
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Re: Cambria anyone?
Reply #1 - Jun 11th, 2011 at 3:52am
 
I can't find a med by that name. Confirm spelling, please.
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Bob Johnson
 
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Dystopia
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Re: Cambria anyone?
Reply #2 - Jun 11th, 2011 at 4:53am
 
Do you mean Cambia?

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« Last Edit: Jun 11th, 2011 at 4:54am by Dystopia »  
 
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Bob Johnson
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Posts: 5965
Kennett Square, PA (USA)
Gender: male
Re: Cambria anyone?
Reply #3 - Jun 11th, 2011 at 7:36am
 
Please read the warnings contained in the link to the drug info site (msg #2 above).

If you getting relief the probability is 90+% that it's from the Imitrex. Pain meds just don't have a place in the treatment of Cluster for headache specialists.

The theory that blood vessels are central to Cluster has been displaced by Peter Goadsby's work which show that a portion of our brain, the hypothalamus, is the central trigger.

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Headache:lessons learned from functional imaging
British Medical Bulletin 2003; 65: 223-234

Arne May
Department of Neurology, University of Regensburg, Regensburg, Germany

Using PET in a larger patient series, significant activations ascribable to the acute cluster headache were observed in the ipsilateral hypothalamic grey matter when compared to the headache-free state44. This highly significant activation was not seen in cluster headache patients out of the bout when compared to the patients experiencing an acute cluster headache attack45. In contrast to migraine25, no brainstem activation was found during the acute attack compared to the resting state. This is remarkable, as migraine and cluster headache are often discussed as related disorders and identical specific compounds, such as ergotamine and sumatriptan, are currently used in the acute treatment of both types of headache46. These data suggest that while primary headaches such as migraine and cluster headache may share a common pain pathway, the trigeminovascular innervation, the underlying pathogenesis differs significantly as might be inferred from the different patterns of presentation and responses to preventative agents46.
Just as it is striking that no brainstem activation occurs in contrast to acute migraine, no hypothalamic activation was seen in experimental pain induced by capsaicin injection into the forehead47. This is important because injection of the forehead would activate first (ophthalmic) division afferents which are the trigeminal division predominantly responsible for pain activation in cluster headache. Thus two other types of first division of trigeminal nerve pain, while sharing neuro-anatomical pathways with cluster headache, do not give rise to


VASCULAR HEADACHE: ARE BLOOD VESSELS INVOLVED?

Taking these observations on acute cluster headache together with what has been observed in experimental head-pain and migraine, the data establish that migraine and CLUSTER HEADACHE, FAR FROM BEING PRIMARILY VASCULAR DISORDERS, ARE CONDITIONS WHOSE GENESIS IS TO BE FOUND IN THE CENTRAL NERVOUS SYSTEM IN PACEMAKER OR CIRCADIAN REGIONS SPECIFIC TO THE SYNDROME. If further studies confirm these findings, a better understanding will be gained of where and how acute and preventative therapy can be targeted.

And,

Interesting to note that he is saying that the primary mode of action is NOT as a vasoconstrictor but on its effect on the central nervous system. Doesn't change our appreciation of this class of meds but suggests we need to change how we think about the nature of CH.
==============================
Handb Exp Pharmacol. 2007;(177):129-43.   


Serotonin receptor ligands: treatments of acute migraine and cluster headache.

Goadsby PJ.

Institute of Neurology, Queen Square, London WC1N 3BG, UK. peterg@ion.ucl.ac.uk

Fuelled by the development of the serotonin 5-HT(1B/1D) receptor agonists, the triptans, the last 15 years has seen an explosion of interest in the treatment of acute migraine and cluster headache. Sumatriptan was the first of these agonists, and it launched a wave of therapeutic advances. These medicines are effective and safe. Triptans were developed as cranial vasoconstrictors to mimic the desirable effects of serotonin, while avoiding its side-effects. IT HAS SUBSEQUENTLY BEEN SHOWN THAT THE TRIPTANS' MAJOR ACTION IS NEURONAL, WITH BOTH PERIPHERAL AND CENTRAL TRIGEMINAL INHIBITORY EFFECTS, AS WELL AS ACTIONS IN THE THALAMUS AND AT CENTRAL MODULATORY SITES, SUCH AS THE PERIAQUEDUCTAL GREY MATTER. Further refinements may be possible as the 5-HT(1D) and 5-HT(1F) receptor agonists are explored. Serotonin receptor pharmacology has contributed much to the better management of patients with primary headache disorders.

PMID: 17087122 [PubMed]
=================================================================
J Clin Neurosci. 2010 Mar 11.

What has functional neuroimaging done for primary headache ... and for the clinical neurologist?
Sprenger T, Goadsby PJ.

UCSF Headache Centre, Department of Neurology, University of California, 1701 Divisadero St, Suite 480, San Francisco, CA 94115, USA.

Our understanding of mechanisms involved in primary headache syndromes has been substantially advanced using functional neuroimaging.

THE DATA HAVE HELPED ESTABLISH THE NOW-PREVAILING VIEW OF PRIMARY HEADACHE SYNDROMES, SUCH AS MIGRAINE AND CLUSTER HEADACHE, AS BRAIN DISORDERS WITH NEUROVASCULAR MANIFESTATIONS, NOT AS DISORDERS OF BLOOD VESSELS.

PMID: 20227279 [PubMed]

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« Last Edit: Jun 11th, 2011 at 7:37am by Bob Johnson »  

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