Neurol Sci. 2013 May;34 Suppl 1:71-3.
Cluster headache: what has changed since 1999?
Leone M, Cecchini AP, Tullo V, Curone M, Di Fiore P, Bussone G.
SourceDepartment of Neurology, Headache Centre and Pain Neuromodulation Unit, C. Besta Neurological Institute and Foundation, Milan, Italy, leone.m@istituto-besta.it.

Abstract
The peripheral and central origin of pain in cluster headache (CH) and trigeminal autonomic cephalgias (TACs) has been matter of debate. In the last decade, a number of information came from both animal and human studies. This paper briefly highlights main data from these studies. Taken together, THERE IS NOW SUFFICIENT BODY OF EVIDENCE INDICATING THAT CH and TACs can be regarded as a unique headache spectrum-syndrome, DUE TO INVOLVEMENT OF SPECIFIC BRAIN AREAS.

PMID:23695050[PubMed]

Take the full information re. source to your local library and they can get copy for you.

But also,

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]
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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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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.

Yes.  Thank you!