Table 1.
All neuroimaging findings in cluster headache and other trigeminal-autonomic cephalalgias
| Reference | No. of subjects and diagnosis | Timing of the scan | Neuroimaging techniques | Main results |
|---|---|---|---|---|
| Norris et al. [23] | 1 episodic CH | During the attack | SPECT | No differences in mean CBF |
| Sakai et al. [24] | 9 episodic CH | SPECT | Increased CBF | |
| Henry et al. [25] | 3 episodic CH | Inside a bout during an attack | SPECT | No differences in mean CBF |
| Nelson et al. [26] | 26 episodic CH |
4 during the attack. 7 after nitroglycerine, alcohol, histamine or oxygen |
SPECT | Patients showed a variable pattern of increased or decreased mean CBF |
| Krabbe et al. [27] | 18 episodic CH |
18 outside the attacks 8 during the attack |
SPECT | No differences in mean CBF |
| Di Piero et al. [28] | 7 episodic CH | Outside of a bout | SPECT | CBF lower in contralateral primary sensorimotor and thalamic regions compared to healthy subjects |
| Hsieh et al. [29] | 7 episodic CH |
4 during the bout 3 out of the bout (nitroglycerine-induced attacks) |
PET |
Increased rCBF in the right caudal and rostrocaudal ACC, temporo-polar region, supplementary motor area, bilaterally in the primary motor area, premotor areas, opercular region, insula/putamen, and lateral inferior frontal cortex rCBF lower in the bilateral posterior parietal cortex, occipito-temporal region and prefrontal cortex |
| May et al. [30] | 9 chronic CH | During a bout (nitroglycerine-induced attacks) | PET | Inferior hypothalamic grey matter activation ipsilateral to the headache side. Increased rCBF in the contralateral ventroposterior thalamus, the anterior cingulate cortex, and in the insulae bilaterally |
| Sprenger et al. [31] | 1 chronic CH | During a bout (spontaneous attacks) | PET | Inferior hypothalamic grey matter activation. Increased rCBF in the medial thalamus and contralateral perigenual ACC |
| May et al. [32] | 17 episodic CH |
9 during a bout 8 outside of a bout (nitroglycerine-induced attacks) 1 spontaneous attack |
PET MRA |
Activation ACC bilaterally, ipsilateral posterior thalamus, ipsilateral basal ganglia, ipsilateral inferior posterior hypothalamus, frontal lobes, insulae bilaterally, contralateral inferior frontal cortex. Increased CBF in the internal carotid artery ipsilateral to the headache side, both in CH patients and in experimentally induced pain |
| Sprenger et al. [4] | 11 episodic CH patients | In- and outside of a bout | FDG-PET | Increased metabolism in the perigenual ACC, posterior cingulate cortex, the orbitofrontal cortex including the nucleus accumbens, ventrolateral prefrontal cortex, DLPFC and temporal cortex, cerebellopontine area. Hypometabolism in the perigenual ACC, prefrontal and orbitofrontal cortex |
| Lodi et al. [34] |
18 episodic CH 8 chronic CH |
10 in- and 8 outside of a bout | 1H-MRS | Reduction of NAA in the hypothalamus of all the patient groups |
| Wang et al. [35] | 47 episodic CH | In- and outside of a bout | 1H-MRS | Reduction of NAA and Cho/Cr metabolite ratio in the hypothalamus |
| May et al. [36] | 25 episodic CH | In- and outside of a bout | VBM | Increase in bilateral hypothalamic gray matter volume |
| Sprenger et al. [6] |
6 episodic CH 1 chronic CH |
During the bout, but out of an acute attack | PET with the opioidergic ligand [11C]diprenorphine | Decreased tracer binding in the pineal gland |
| Morelli et al. [39] | 4 episodic CH | Inside the bout during an acute attack | fMRI | Activation of hypothalamus, pre-frontal cortex, anterior cingulate cortex, contralateral thalamus, ipsilateral basal ganglia and the insula and the cerebellar hemispheres bilaterally |
| Matharu et al. [43] | 7 PH | During acute attack-off indomethacin or pain-free-off indomethacin or pain-free due to indomethacin administration | H152O PET |
Activation in the contralateral posterior hypothalamus, contralateral ventral midbrain, ipsilateral lentiform nucleus, anterior and posterior cingulate cortices, bilateral insulae, bilateral frontal cortices, contralateral temporal cortex, contralateral postcentral gyrus, precuneus, and contralateral cerebellum. Indomethacin administration turned off the persistent metabolic activation observed during acute attack-off indomethacin |
| May et al. [45] | 1 SUNCT | During 6 consecutive attacks | fMRI | Activation in the ipsilateral inferior posterior hypothalamic gray matter |
| Cohen et al. [47] | 2 SUNCT | During the attacks | fMRI | Activation in the inferior posterior hypothalamic gray matter bilaterally |
| Sprenger et al. [46] | 1 probable SUNCT | During the attack | fMRI | Activation in the ipsilateral hypothalamic gray matter, cingulate cortex, insula, temporal cortex, and frontal cortex |
| Sprenger et al. [48] | 1 SUNCT | During attacks induced touching the upper with the lower lip | fMRI | Activation in the hypothalamic gray matter bilaterally |