I know traditional analgesics like paracetomol, codeine etc don't work for cluster headaches but my question is why exactly?

Is it purely because of the time factor and that they take to long to get into the system?

Or is it because CH's are 'wired up' in our brains in such a fashion that the way ordinary painkillers work simply dont touch CH even if the painkiller could be pushed into the body fast enough?

As I understand it there are 2 factors at work. Because of the intense level of pain CH causes, you have to use opiates, other narcotics, OTC's etc., in absolutely obscene doses before you obtain any relief. The negative side effects of any of those medications, at those doses, are bad news.

When we talk about the meds that take too long to absorb, we're generally talking about the oral abortives like cafergot and zomig, that aren't pain killers, but work to stop the actual mechanism of the pain. (The vasoconstrictors Vietvet was mentioning.) Because of the length of time it takes for them to get into the belly, disolve and get to work in the blood stream, most don't have much success with them.

Hope that helps with the question!

Joe

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.
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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]