J Headache Pain. 2008 Dec 16. [Epub ahead of print]Related Articles, Links
Functional magnetic resonance imaging in episodic cluster headache.

Morelli N, Pesaresi I, Cafforio G, Maluccio MR, Gori S, Di Salle F, Murri L.

University Centre for Adaptive Disorders and Headache (UCADH), Institute of Neurology, Department of Neurosciences, University of Pisa, Pisa, Italy, n.morelli@inwind.it.

We have investigated the cerebral activation centre in four patients with episodic cluster headache (CH) with functional magnetic resonance imaging (f-MRI). The patients underwent MRI scans for anatomical and functional data acquisition in the asymptomatic state, during a headache attack and after subcutaneous administration of sumatriptan. Anatomical images were acquired by means of 3D-MPRAGE sequences and f-MRI images were obtained by means of echo-planar imaging. Data was analysed using the BrainVoyager QX version 1.7.81 software package. IN ALL PATIENTS, THE DATA SHOWED SIGNIFICANT HYPOTHALAMIC ACTIVATION OF THE HYPOTHALAMUS IPSILATERAL TO THE PAIN SIDE, ATTRIBUTABLE TO A HEADACHE ATTACK. OVERALL, WE HAVE DEMONSTRATED THE ANATOMICAL LOCATION OF CENTRAL NERVOUS SYSTEM ACTIVATION BY MEANS THE FIRST F-MRI STUDY IN CH PATIENTS. f-MRI offers a good balance of spatial and temporal resolution, and this method of study appears appropriate for investigating the pathogenetic aspects of primary headaches. POSITRON EMISSION TOMOGRAPHY AND F-MRI MAY BE REGARDED AS LITTLE OR NO IMPORTANCE IN A CLINICAL CONTEXT, THEY DO, HOWEVER, OFFER GREAT POTENTIAL FOR THE EXPLORATION OF HEADACHE PHYSIOPATHOLOGY AND THE EFFECTS OF PHARMACOLOGICAL TREATMENT.

PMID: 19083151 [PubMed]

Very cool...I believe I saw another article on recent brain scanning advances (perhaps the same people, can't remember) that said they have concluded that yes, the hypothalamus IS the culprit, and it also said there was excessive growth of gray cells in the hypothalamus of CH patients... it'd be nice if they could use this to verify a diagnosis.

Quote:

Classified as a trigeminal autonomic cephalalgia, cluster headache is characterized by recurrent short-lived excruciating pain attacks, which are concurrent with autonomic signs. These clinical features have led to the assumption that cluster headache's pathophysiology involves central nervous system structures, including the hypothalamus. In the past decade, neuroimaging studies have confirmed such clinically derived theory by uncovering in vivo neuronal changes located in the inferior posterior hypothalamus. Using a variety of neuro-imaging techniques (functional , biochemical , and structural ) in patients with cluster headache, we are making improvements in our understanding of the role of the brain in this disorder. This article summarizes neuroimaging findings in cluster headache patients, describing neuronal changes that occur during attacks and remission, as well as during hypothalamic stimulation.

Curious, but is there anything new here? I thought MRI was defined as the test of choice, and ipsilateral activity has been noted for a while; Sprenger, Goadsby and others.

Don't get me wrong, I'm hyper happy when anyone looks at CH, even if its just 4 cases, but the lack of depth in research last few years is a bit disconcerting.

Quote:

but the lack of depth in research last few years is a bit disconcerting.

It sure is. There are not enough of us to inspire specific study of CH, we are continually piggy backed with migraine study and treatment for that matter. It's always a money issue.There are some neuros advocating our involvment politically to change this. One of our options is to support OUCH and MAPS.
all the best
the bb

Not sure whether it is new, but having someone apply fMRI (functional MRI), to the onset and treatment function of CH, presents something different than the standard MRI, used primarily to eliminate other possible sources for pain in the brain (which is more of snapshot).

My interpretation only on that.

Here's another one. ;)
Quote:

Institute of Neurology, the National Hospital for Neurology and Neurosurgery, Queen Square, London, UK. peterg@ion.ucl.ac.uk Cluster headache is a form of primary neurovascular headache with the following features: severe unilateral, commonly retro-orbital, pain accompanied by restlessness or agitation, and cranial (parasympathetic) autonomic symptoms, such as lacrimation or conjunctival injection. It occurs in attacks typically of less than 3 h in length and in bouts (clusters) of a few months during which the patient has one or two attacks per day. The individual attack involves activation of the trigeminal-autonomic reflex; thus, such headaches can be broadly classified with the other trigeminal-autonomic cephalgias, such as paroxysmal hemicrania and the syndrome of short-lasting unilateral neuralgiform headache attacks with conjunctival injection and tearing. Observations of circadian biological changes and neuroendocrine disturbances have suggested a pivotal role for the hypothalamus in cluster headache. Functional neuroimaging with PET and anatomical imaging with voxel-based morphometry have identified the posterior hypothalamic grey matter as the key area for the basic defect in cluster headache.