Altered hypothalamic functional connectivity in cluster headache: a longitudinal resting-state functional MRI study (original) (raw)
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Abnormal Brain Functional Connectivity of the Hypothalamus in Cluster Headaches
The aim of this study was to detect the abnormality of the brain functional connectivity of the hypothalamus during acute spontaneous cluster headache (CH) attacks ('in attack') and headache-free intervals ('out of attack') using resting-state functional magnetic resonance imaging (RS-fMRI) technique. The RS-fMRI data from twelve male CH patients during 'in attack' and 'out of attack' periods and twelve age-and sex-matched normal controls were analyzed by the region-of-interest-based functional connectivity method using SPM5 software. Abnormal brain functional connectivity of the hypothalamus is present in CH, which is located mainly in the pain system during the spontaneous CH attacks. It extends beyond the pain system during CH attack intervals.
Resting state fMRI in cluster headache: which role?
Neurological Sciences, 2015
The pathophysiology of cluster headache (CH) is not well-known. For several years, the most widely accepted theory was that CH was triggered by hypothalamus with secondary activation of the trigeminal-autonomic reflex. However, it was recently suggested that the posterior hypothalamus might be an actor of the pain modulating network more involved in terminating rather than triggering attacks. To investigate this hypothesis, resting state fMRI could provide valuable information on functional connectivity between brainstem and hypothalamus, as well as other brain structures that could be involved in CH pathophysiology. In this framework, here we review recent studies investigating functional connectivity by means of resting state fMRI. Despite the important findings of these studies, we suggest that important steps in the comprehension of CH pathophysiology will be done when the scientific community will use the new methodological approaches recently suggested to study functional connectivity in the brainstem.
Cephalalgia : an international journal of headache, 2016
Previous imaging studies on the pathogenesis of cluster headache (CH) have implicated the hypothalamus and multiple brain networks. However, very little is known regarding dynamic bout-associated, large-scale resting state functional network changes related to CH. Resting-state functional magnetic resonance imaging data were obtained from CH patients and matched controls. Data were analyzed using independent component analysis for exploratory assessment of the changes in intrinsic brain networks and their relationship between in-bout and out-of-bout periods, as well as correlations with clinical observations. Compared to healthy controls, CH patients had functional connectivity (FC) changes in the temporal, frontal, salience, default mode, somatosensory, dorsal attention, and visual networks, independent of bout period. Compared to out-of-bout scans, in-bout scans showed altered FC in the frontal and dorsal attention networks. Lower frontal network FC correlated with longer duration...
Brain Topography, 2016
Background: The pathomechanism of cluster headache (CH) is not entirely understood, but central and peripheral components were suggested. A recent report showed that transcranial magnetic stimulation measured cortical excitability was increased in the hemisphere ipsilalteral to the pain. In the current study we set out to investigate the amplitude of resting brain fMRI activity to find signatures of the increased excitability. Methods: High resolution T1 weighted and resting state functional MRI images were acquired from seventeen patients with CH in pain free period and from twenty-six healthy volunteers. Patients' data were normalized (e.g. inverted along the midsagittal axis) according to the headache side. Independent component analysis and a modified dual regression approach were used to reveal the differences between the resting state networks. Furthermore, the timecourses were decomposed into five frequency
Functional magnetic resonance imaging in episodic cluster headache
The Journal of Headache and Pain, 2008
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.
Cluster headache: A review of neuroimaging findings
Current Pain and Headache Reports, 2007
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 neuroimaging techniques (functional [eg, functional MRI], biochemical [eg, magnetic resonance spectroscopy], and structural [eg, morphometry]) 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.
Functional anatomy of headache: hypothalamus
Headache Medicine
There is now compelling evidence that the hypothalamus exerts a major role in the mechanism of headache triggering. Pain and concomitant changes in the hormonal secretory pattern occur during an attack of headache when hypothalamic structures are involved. During spontaneous migraine or cluster headache attacks activation of the hypothalamus is shown by positron emission tomography. Over the past 10 years a number of patients with refractory chronic cluster headache have received neurostimulation of the posteroinferior hypothalamus as a form of treatment. The clinical use of deep brain stimulation (DBS) is based on the theory of posterior hypothalamic nucleus dysfunction as the cause of cluster headache attacks. In this article the authors review the functional anatomy of the hypothalamic region and its neighborhood, using silicone-injected cadaveric head and MRI. In conclusion, a better understanding of the functional anatomy of the hypothalamus and its neighborhood is imperative f...
Local field potentials reveal a distinctive neural signature of cluster headache in the hypothalamus
Cephalalgia, 2009
Cluster headache (CH) is a debilitating neurovascular condition characterized by severe unilateral periorbital head pain. Deep brain stimulation of the posterior hypothalamus has shown potential in alleviating CH in its most severe, chronic form. During surgical implantation of stimulating macroelectrodes for cluster head pain, one of our patients suffered a CH attack. During the attack local field potentials displayed a significant increase in power of approximately 20 Hz. To the authors' knowledge, this is the first recorded account of neuronal activity observed during a cluster attack. Our results both support and extend the current literature, which has long implicated hypothalamic activation as key to CH generation, predominantly through indirect haemodynamic neuroimaging techniques. Our findings reveal a potential locus in CH neurogenesis and a potential rationale for efficacious stimulator titration.