Regional cerebral blood flow as predictor of response to occipital nerve block in cluster headache.
Arterial spin Labelling
Cluster headache
Greater occipital nerve block
Regional cerebral blood flow
Trigeminal cephalgia
Journal
The journal of headache and pain
ISSN: 1129-2377
Titre abrégé: J Headache Pain
Pays: England
ID NLM: 100940562
Informations de publication
Date de publication:
12 Aug 2021
12 Aug 2021
Historique:
received:
19
05
2021
accepted:
30
07
2021
entrez:
13
8
2021
pubmed:
14
8
2021
medline:
17
8
2021
Statut:
epublish
Résumé
Cluster headache is an excruciating disorder with no cure. Greater occipital nerve blockades can transiently suppress attacks in approximately 50% of patients, however, its mechanism of action remains uncertain, and there are no reliable predictors of treatment response. To address this, we investigated the effect of occipital nerve blockade on regional cerebral blood flow (rCBF), an index of brain activity, and differences between treatment responders and non-responders. Finally, we compared baseline perfusion maps from patients to a matched group of healthy controls. 21 male, treatment-naive patients were recruited while in a cluster headache bout. During a pain-free phase between headaches, patients underwent pseudo-continuous arterial spin labelled MRI assessments to provide quantitative indices of rCBF. MRIs were performed prior to and 7-to-21 days following treatment. Patients also recorded the frequency of their headache attacks in a daily paper diary. Neuropsychological assessment including anxiety, depression and quality of life measures was performed in a first, scanning free session for each patient. Following treatment, patients demonstrated relative rCBF reductions in posterior temporal gyrus, cerebellum and caudate, and rCBF increases in occipital cortex. Responders demonstrated relative rCBF increases, compared to non-responders, in medial prefrontal cortex and lateral occipital cortex at baseline, but relative reductions in cingulate and middle temporal cortices. rCBF was increased in patients compared to healthy controls in cerebellum and hippocampus, but reduced in orbitofrontal cortex, insula and middle temporal gyrus. We provide new mechanistic insights regarding the aetiology of cluster headache, the mechanisms of action of occipital nerve blockades and potential predictors of treatment response. Future investigation should determine whether observed effects are reproducible and extend to other headache disorders.
Sections du résumé
BACKGROUND
BACKGROUND
Cluster headache is an excruciating disorder with no cure. Greater occipital nerve blockades can transiently suppress attacks in approximately 50% of patients, however, its mechanism of action remains uncertain, and there are no reliable predictors of treatment response. To address this, we investigated the effect of occipital nerve blockade on regional cerebral blood flow (rCBF), an index of brain activity, and differences between treatment responders and non-responders. Finally, we compared baseline perfusion maps from patients to a matched group of healthy controls.
METHODS
METHODS
21 male, treatment-naive patients were recruited while in a cluster headache bout. During a pain-free phase between headaches, patients underwent pseudo-continuous arterial spin labelled MRI assessments to provide quantitative indices of rCBF. MRIs were performed prior to and 7-to-21 days following treatment. Patients also recorded the frequency of their headache attacks in a daily paper diary. Neuropsychological assessment including anxiety, depression and quality of life measures was performed in a first, scanning free session for each patient.
RESULTS
RESULTS
Following treatment, patients demonstrated relative rCBF reductions in posterior temporal gyrus, cerebellum and caudate, and rCBF increases in occipital cortex. Responders demonstrated relative rCBF increases, compared to non-responders, in medial prefrontal cortex and lateral occipital cortex at baseline, but relative reductions in cingulate and middle temporal cortices. rCBF was increased in patients compared to healthy controls in cerebellum and hippocampus, but reduced in orbitofrontal cortex, insula and middle temporal gyrus.
CONCLUSIONS
CONCLUSIONS
We provide new mechanistic insights regarding the aetiology of cluster headache, the mechanisms of action of occipital nerve blockades and potential predictors of treatment response. Future investigation should determine whether observed effects are reproducible and extend to other headache disorders.
Identifiants
pubmed: 34384347
doi: 10.1186/s10194-021-01304-9
pii: 10.1186/s10194-021-01304-9
pmc: PMC8359299
doi:
Substances chimiques
Spin Labels
0
Types de publication
Journal Article
Langues
eng
Sous-ensembles de citation
IM
Pagination
91Subventions
Organisme : Medical Research Council
ID : MR/N026969/1
Pays : United Kingdom
Informations de copyright
© 2021. The Author(s).
Références
Cephalalgia. 2011 Apr;31(5):550-61
pubmed: 21216874
BMC Neurol. 2011 Feb 24;11:25
pubmed: 21349186
J Neurosci. 2001 Dec 15;21(24):9896-903
pubmed: 11739597
J Cereb Blood Flow Metab. 2012 Oct;32(10):1909-18
pubmed: 22739621
J Neurol Neurosurg Psychiatry. 2015 Apr;86(4):437-45
pubmed: 24983632
Psychol Methods. 2014 Mar;19(1):92-112
pubmed: 24079923
Curr Neuropharmacol. 2015;13(4):458-65
pubmed: 26412065
Neuroimage. 2016 Jul 1;134:386-395
pubmed: 27015710
Headache. 1986 Feb;26(2):70-3
pubmed: 3957656
Pain. 2013 Jun;154(6):801-7
pubmed: 23582154
J Headache Pain. 2010 Jun;11(3):247-53
pubmed: 20383733
Cephalalgia. 2012 Jan;32(2):109-15
pubmed: 22174349
Neuroimage. 2013 Dec;83:135-47
pubmed: 23769703
Acta Neurol Scand. 1976 Oct;54(4):371-4
pubmed: 973557
J Neurosci. 2006 Mar 29;26(13):3589-93
pubmed: 16571767
Curr Pain Headache Rep. 2010 Apr;14(2):151-9
pubmed: 20425205
Eur J Neurol. 2014 Feb;21(2):338-43
pubmed: 24313966
Cephalalgia. 2016 May;36(6):534-46
pubmed: 26391457
PLoS One. 2013;8(2):e57896
pubmed: 23460913
Neuron. 2007 Jul 5;55(1):157-67
pubmed: 17610824
Cephalalgia. 2007 Nov;27(11):1206-14
pubmed: 17850348
Curr Pain Headache Rep. 2007 Jun;11(3):231-5
pubmed: 17504651
Cell Mol Neurobiol. 2012 Jan;32(1):1-12
pubmed: 21789630
Neuropsychopharmacology. 2016 Jul;41(8):1983-90
pubmed: 26708107
Neurology. 2015 Apr 7;84(14):1402-8
pubmed: 25746559
Neurosci Lett. 2004 May 6;361(1-3):245-9
pubmed: 15135939
J Psychosom Res. 2002 Feb;52(2):69-77
pubmed: 11832252
Ann Indian Acad Neurol. 2018 Apr;21(Suppl 1):S9-S15
pubmed: 29720813
Lancet. 1998 Jul 25;352(9124):275-8
pubmed: 9690407
Pain Rep. 2019 May 15;4(4):
pubmed: 31406952
Arthritis Rheum. 2012 Dec;64(12):3936-46
pubmed: 22933378
Headache. 2016 Sep;56(8):1317-32
pubmed: 27593728
Neurosurgery. 1996 Aug;39(2):426-30; discussion 430-1
pubmed: 8832691
Cephalalgia. 2007 Sep;27(9):1033-42
pubmed: 17666083
J Neurosci. 2009 May 13;29(19):6167-75
pubmed: 19439594
Neuroimage Clin. 2014 Oct 18;6:415-23
pubmed: 25379455
Pain. 2011 Jul;152(7):1469-1477
pubmed: 21339052
J Pain Res. 2019 Jan 04;12:269-281
pubmed: 30655693
Headache. 2012 Feb;52(2):274-82
pubmed: 22082475
Cephalalgia. 2010 Nov;30(11):1383-91
pubmed: 20959433
Cephalalgia. 2013 Apr;33(6):416-20
pubmed: 23359873
N Engl J Med. 2013 Apr 11;368(15):1388-97
pubmed: 23574118
J Neuroendocrinol. 2001 Dec;13(12):1009-23
pubmed: 11722697
Cephalalgia. 2018 Apr;38(4):662-673
pubmed: 28425325
Biol Psychiatry. 2005 Dec 15;58(12):963-8
pubmed: 16005439
Hum Brain Mapp. 2010 Feb;31(2):326-38
pubmed: 19790170
Eur J Pain. 2015 Nov;19(10):1389-405
pubmed: 25899177
Cephalalgia. 2013 Jul;33(9):629-808
pubmed: 23771276
PLoS One. 2018 Aug 1;13(8):e0200535
pubmed: 30067781
Neuroimage. 2006 Aug 1;32(1):256-65
pubmed: 16679031
J Headache Pain. 2014 Oct 02;15:66
pubmed: 25277954
Trends Neurosci. 2015 Feb;38(2):86-95
pubmed: 25541287