Stereotactic Stimulation of Posterior Hypothalamic Gray Matter in a Patient with Intractable Cluster Headache

Leone, Massimo; Franzini, Angelo; Bussone, Gennaro

doi:10.1056/nejm200111083451915

Cited by 380 publications

(298 citation statements)

References 5 publications

Supporting

Mentioning

283

Contrasting

Unclassified

Order By: Relevance

“…16 New therapeutic approaches were needed, given that 15-20% of cluster headache patients experience chronic cluster headache, and some of these do not respond to drugs. 17,18 Such patients are a major clinical problem because of the severity and frequency (several times a day) of their headache attacks.…”

Section: Rationale For Hypothalamic Stimulation In Headachementioning

confidence: 99%

“…The first patients to undergo posterior hypothalamic implant had experienced severe attacks occurring many times daily without relief for periods of years. 16 In subsequent studies using another experimental procedure (occipital nerve stimulation, which is less invasive), the criteria were not so strict, 23 and some selected patients had only a few attacks per month. One result of the lack of standardized selection criteria is that patients from different series are not comparable in terms of illness severity.…”

Section: Definition Of Chronicity For Surgical Purposesmentioning

confidence: 99%

“…16 The same group subsequently reported on 16 drug-resistant chronic cluster headache patients who received hypothalamic implants after a mean follow-up of more than 4 years ( Table 1). 38 After the first 2 years, pain abolition or major pain reduction was obtained in 13 of the 16 patients (and in 15 of 18 implants, or 83%).…”

Section: Chronic Painmentioning

confidence: 99%

“…Stimulation to disparate parts of the hypothalamus can cause profound changes in heart rate, cardiac output, vasomotor tone, peripheral resistance, differential blood flow in organs and limbs, frequency and depth of respiration, alimentary tract motility and secretion, and erection and ejaculation. 49 With the development of hypothalamic stimulation, the human hypothalamus has for the first time received long-term stimulation, 16 providing an opportunity to study this brain area. Cortelli et al 52 investigated aspects of autonomic nervous system function in eight patients with chronic drug-resistant cluster headache, before and after implantation of an electrode for unipolar stimulation of the posterior hypothalamus.…”

Section: The Autonomic Nervous System During Hypothalamic Stimulationmentioning

confidence: 99%

“…This area does not correspond to a specific anatomical entity, and there is no consensus as to whether it is part of the posterior hypothalamus or anterior periventricular gray matter. 56 Two sets of stereotactic coordinates have been used to identify this target, those published by Leone et al 16 in 2001 (x ϭ 2 mm lateral to the midline, y ϭ 6 mm behind the midcommissural point, z ϭ 8 below the commissural plane) and the revised coordinates published by Franzini et al 34 in 2003 (x ϭ 2 mm lateral, y ϭ 3 mm posterior, and 5 mm inferior to the midcommissural point).…”

Section: Microrecordingsmentioning

confidence: 99%

See 4 more Smart Citations

Deep Brain Stimulation in Trigeminal Autonomic Cephalalgias

et al. 2010

Self Cite

View full text Add to dashboard Cite

Summary:Cluster headache (CH), paroxysmal hemicrania (PH), and short-lasting unilateral neuralgiform headache attacks with conjunctival injection and tearing (SUNCT syndrome) are primary headaches grouped together as trigeminal autonomic cephalalgias (TACs). All are characterized by short-lived unilateral head pain attacks associated with oculofacial autonomic phenomena. Neuroimaging studies have demonstrated that the posterior hypothalamus is activated during attacks, implicating hypothalamic hyperactivity in TAC pathophysiology and suggesting stimulation of the ipsilateral posterior hypothalamus as a means of preventing intractable CH. After almost 10 years of experience, hypothalamic stimulation has proved successful in preventing pain attacks in approximately 60% of the 58 documented chronic drug-resistant CH patients implanted at various centers. Positive results have also been reported in drug-resistant SUNCT and PH. Microrecording studies on hypothalamic neurons are increasingly being performed and promise to make it possible to more precisely identify the target site. The implantation procedure has generally proved safe, although it carries a small risk of brain hemorrhage. Long-term stimulation is proving to be safe: studies on patients under continuous hypothalamic stimulation have identified nonsymptomatic impairment of orthostatic adaptation as the only noteworthy change. Studies on pain threshold in chronically stimulated patients show increased threshold for cold pain in the distribution of the first trigeminal branch ipsilateral to stimulation. When the stimulator is switched off, changes in sensory and pain thresholds do not occur immediately, indicating that long-term hypothalamic stimulation is necessary to produce sensory and nociceptive changes, as also indicated by clinical experience that CH attacks are brought under control only after weeks of stimulation. Infection, transient loss of consciousness, and micturition syncope have been reported, but treatment interruption usually is not required.

show abstract

Section: Rationale For Hypothalamic Stimulation In Headachementioning

confidence: 99%

Section: Definition Of Chronicity For Surgical Purposesmentioning

confidence: 99%

Section: Chronic Painmentioning

confidence: 99%

Section: The Autonomic Nervous System During Hypothalamic Stimulationmentioning

confidence: 99%

Section: Microrecordingsmentioning

confidence: 99%

See 3 more Smart Citations

Deep Brain Stimulation in Trigeminal Autonomic Cephalalgias

et al. 2010

Self Cite

View full text Add to dashboard Cite

show abstract

Effect of Infusion of Calcitonin Gene-Related Peptide on Cluster Headache Attacks

et al. 2018

View full text Add to dashboard Cite

IMPORTANCE Signaling molecule calcitonin gene-related peptide (CGRP) induces migraine attacks and anti-CGRP medications abort and prevent migraine attacks. Whether CGRP provokes cluster headache attacks is unknown. OBJECTIVE To determine whether CGRP induces cluster headache attacks in episodic cluster headache in active phase, episodic cluster headache in remission phase, and chronic cluster headache. DESIGN, SETTING, AND PARTICIPANTSA randomized, double-blind, placebo-controlled, 2-way crossover study set at the Danish Headache Center, Rigshospitalet Glostrup, in Denmark. Analyses were intent to treat. Inclusion took place from December 2015 to April 2017. Inclusion criteria were diagnosis of episodic/chronic cluster headache, patients aged 18 to 65 years, and safe contraception in women. Exclusion criteria were a history of other primary headache (except episodic tension-type headache <5 days/mo), individuals who were pregnant or nursing; cardiovascular, cerebrovascular, or psychiatric disease; and drug misuse.INTERVENTIONS Thirty-seven patients with cluster headaches received intravenous infusion of 1.5 μg/min of CGRP or placebo over 20 minutes on 2 study days.MAIN OUTCOMES AND MEASURES Difference in incidence of cluster headache-like attacks, difference in area under the curve (AUC) for headache intensity scores (0 to 90 minutes), and difference in time to peak headache between CGRP and placebo in the 3 groups. RESULTSOf 91 patients assessed for eligibility, 32 patients (35.2%) were included in the analysis. The mean (SD) age was 36 (10.7) years (range, 19-60 years), and the mean weight was 78 kg (range, 53-100 kg). Twenty-seven men (84.4%) completed the study. Calcitonin gene-related peptide induced cluster headache attacks in 8 of 9 patients in the active phase (mean, 89%; 95% CI, 63-100) compared with 1 of 9 in the placebo group (mean, 11%; 95% CI, 0-37) (P = .05). In the remission phase, no patients with episodic cluster headaches reported attacks after CGRP or placebo. Calcitonin gene-related peptide-induced attacks occurred in 7 of 14 patients with chronic cluster headaches (mean, 50%; 95% CI, 20-80) compared with none after placebo (P = .02). In patients with episodic active phase, the mean AUC from 0 to 90 minutes for CGRP was 1.903 (95% CI, 0.842-2.965), and the mean AUC from 0 to 90 minutes for the placebo group was 0.343 (95% CI, 0-0.867) (P = .04). In patients with chronic cluster headache, the mean AUC from 0 to 90 minutes for CGRP was 1.214 (95% CI, 0.395-2.033), and the mean AUC from 0 to 90 minutes for the placebo group was 0.036 (95% CI, 0-0.114) (P = .01). In the remission phase, the mean AUC from 0 to 90 minutes for CGRP was 0.187 (95% CI, 0-0.571), and the mean AUC from 0 to 90 minutes for placebo was 0.019 (95% CI, 0-0.062) (P > .99).CONCLUSIONS AND RELEVANCE Calcitonin gene-related peptide provokes cluster headache attacks in active-phase episodic cluster headache and chronic cluster headache but not in remission-phase episodic cluster headache. These results suggest anti-CGRP drugs ma...

show abstract

TRPV1 Receptors and Migraine

Holland

Goadsby

2010

Vanilloid Receptor TRPV1 in Drug Discovery

View full text Add to dashboard Cite

Stereotactic Stimulation of Posterior Hypothalamic Gray Matter in a Patient with Intractable Cluster Headache

Cited by 380 publications

References 5 publications

Deep Brain Stimulation in Trigeminal Autonomic Cephalalgias

Deep Brain Stimulation in Trigeminal Autonomic Cephalalgias

Effect of Infusion of Calcitonin Gene-Related Peptide on Cluster Headache Attacks

TRPV1 Receptors and Migraine

Contact Info

Product

Resources

About