Archive for dicembre 2011

Cefalea a grappolo meccanismi

Dati e Controversie
Cefalea a Grappolo e ruolo dell’ ipotalamo

L’ipotalamo appare quale struttura di fondamentale rilievo nel meccanismo della cefalea a grappolo. In questo quindi estremamente diversa dalle forme emicraniche che vedono un’attivazione del tronco encefalico (brain-stem). L’accordo su questo livello di meccanismo è di notevole spessore sebbene vi sian da ricercare ulteriori elementi. Queste notazioni circa il meccanismo e la genesi son strettamente correlate alle linee terapeutiche che vengono a derivarne e son connesse ai risultati degli studi di farmacologia clinica attuati con principi atti ad intervenire appunto a livello ipotalamico
Dati e lavori personali degli afferenti alla Fondazione Sicuteri-Nicolodi
Nicolodi M. Cefalea a grappolo come triade sindromica ipotalamica. MilanoMedicina – Corso Cefalee, Milano 25-29 novembre 1991, p 14-19
21.Sicuteri F., Nicolodi M. Quasi epileptic foci as generators of central pain and electrical abnormalities in brainstem of migraine sufferers: An hypothesis. Cephalalgia 7 (6) pp 54-56, 1987
.Sicuteri F, Nicolodi M, Poggioni M. The hypothalamic neuroendocrine connection as a new target for the therapy of cluster headache. Cephalalgia 11(11):246-247, 1991
Nicolodi M, Poggioni M, Sicuteri F. The activity of Gn-RH agonist in severe cluster headache is compatible with a defective supraspinal analgesia. The semantic ford of idiopathic headaches, Catania 10-12 ottobre 1991, p 18
Nicolodi M, Sicuteri F, Poggioni M. Hypothalamic modulation of nociception and reproduction in cluster headache – II- Testosterone-induced increase of sexual activity in males with cluster headache. Cephalalgia 13: 258-60, 1993
Nicolodi M, Sicuteri F, Poggioni M. Hypothalamicl modulation of nociception and reproduction in cluster headache -I- Therapeutic trials of leuprolide. Cephalalgia, 13: 253-7, 1993
Nicolodi M. Cefalea a grappolo come triade sindromica ipotalamica. MilanoMedicina – Corso Cefalee, Milano 25-29 novembre 1991, p 14-19

Dall’ Estero

Volume 357, Issue 9261, 31 March 2001, Pages 1016-1017

Research Letters
Brainstem activation specific to migraine headache
A Bahra MRCPa, c, MS Matharu MRCPa, c, C Buchelb, c, RSJ Frackowiak Profb, c, PJ Goadsby ProfDSca, c, ,

Findings from functional imaging studies have shown activation of the brainstem during migraine without aura (MWOA) and activation of the hypothalamus during cluster headache. We assessed a patient with cluster headache and migraine by positron emission tomography during an active cluster headache after he had taken 1•2 glyceryl trinitate. The patient developed a typical MWOA, during which we saw activation in the dorsal rostral brainstem. There was no activation in the region of the hypothalamus. Our findings provide evidence that migraine involves the brainstem, and show several areas involved in cluster headaches. Our data show the potential for objective distinction between primary headache syndromes with functional imaging, in disorders hitherto distinguished on clinical grounds.

Early Report
Hypothalamic activation in cluster headache attacks
Arne May DrMDa, , , Anish Bahra MRCPa, Christian Büchel MDb, Richard SJ Frackowiak FRCPb, Peter J Goadsby MDa
Cluster headache, one of the most severe pain syndromes in human beings, is usually described as a vascular headache. However, the striking circadian rhythmicity of this strictly half-sided pain syndrome cannot be readily explained by the vascular hypothesis. We aimed to assess changes in regional cerebral blood flow (rCBF) in patients with cluster headache.
We used positron emission tomography (PET) to assess the changes in rCBF, as an index of synaptic activity, during nitroglycerin-induced cluster headache attacks in nine patients who had chronic cluster headache. Eight patients who had cluster headache but were not in the bout acted as a control group.
In the acute pain state, activation was seen in the ipsilateral inferior hypothalamic grey matter, the contralateral ventroposterior thalamus, the anterior cingulate cortex, and bilaterally in the insulae. Activation in the hypothalamus was seen solely in the pain state and was not seen in patients who have cluster headache but were out of the bout.
Our findings establish central nervous system dysfunction in the region of the hypothalamus as the primum movens in the pathophysiology of cluster headache. We suggest that a radical reappraisal of this type of headache is needed and that it should in general terms, be regarded as a neurovascular headache, to give equal weight to the pathological and physiological mechanisms that are at work.