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RecruitingNCT05477459LICITUpdated Apr 15, 2025

LSD to Improve Cluster Headache Impact Trial

A Phase 2 interventional study of LSD tartrate and Placebo in Chronic Cluster Headache, sponsored by Radboud University Medical Center. Recruiting at 2 sites in Netherlands. Open to participants aged 16 Years to 75 Years. Per ClinicalTrials.gov, last updated 2025-04-15.

Sponsored by Radboud University Medical Center · Phase 2, Interventional, and Treatment

Phase
Phase 2
Study type
Interventional
Enrollment
65
Allocation
Randomized
Ages
16 Years to 75 Years
Sex
All
01

Study summary

This study aims to investigate the efficacy and safety of LSD 25μg every 3 days for 3 weeks versus placebo in the treatment of chronic cluster headache (cCH).

It is a 3-week double-blind placebo-controlled intervention study, preceded by a 4-week baseline observation period and followed by a 5-week post-treatment observation period.

Primary objective: to evaluate the efficacy of LSD 25μg every 3 days for 3 weeks in cCH.

Additional objectives:

  • To evaluate the safety of LSD 25μg every 3 days for 3 weeks in cCH.
  • To explore the exposure-response relationship of 25μg LSD in cCH.
  • To explore cost-effectiveness of treatment with LSD in cCH.
  • To evaluate the efficacy of LSD on health-related quality of life.
Read the detailed description

Treatment of cluster headache consists of acute remedies for attacks (mainly 100% O2, sumatriptan), transitional treatment for temporary frequency reduction (subcutaneous steroid injection at the greater occipital nerve (GON block), oral steroids or frovatriptan) and prolonged prophylaxis (e.g. verapamil, lithium, topiramate). Although the latter compounds have shown some efficacy in reducing the attack frequency, the evidence for their effect is weak. All current prophylactics are prescribed off-label and are limited in their utility due to associated side effects. Despite treatment, many (notably chronic) cluster headache patients continue suffering headache attacks.

Invasive, expensive treatments like hypothalamic deep brain stimulation, occipital nerve stimulation and sphenopalatine ganglion stimulation are last resort options. Recently, a monoclonal antibody targeting calcitonin gene related peptide (CGRP) received FDA approval for episodic cluster headache, but was shown to be ineffective in cCH. Thus, there is a considerable unmet need for effective treatments that are better tolerated, safe and affordable.

In this study, the investigators will assess the efficacy of prophylactic treatment with LSD in cCH. The evidence for the efficacy of LSD is limited, with the majority of data originating from case reports or uncontrolled and retrospective (internet) surveys. Nevertheless, these studies do provide indications that LSD may hold potential as a cluster headache prophylaxis.

The primary objective of this randomized double-blind placebo-controlled trial is to compare the efficacy of LSD 25μg every 3 days for 3 weeks versus placebo in cCH. The investigators aim to show that, at the end of treatment, verum is more efficacious than placebo with comparable tolerability in an ambulatory setting. To explore the sustainability of benefit the investigators will also assess the (sustained) response at 5 weeks post-treatment (8 weeks postrandomization).

If the study findings are positive, LSD should be further studied before use in routine clinical practice. Non-hallucinogenic low-dosed LSD may provide an alternative or adjunctive option for patients who do not respond to or cannot tolerate currently available treatments.

02

Conditions studied

  • Chronic Cluster Headache

Keywords

  • Chronic cluster headache
  • Lysergic acid diethylamide
03

Who can participate

Ages eligible
16 Years to 75 Years
Sexes eligible
All
Accepts healthy volunteers
No

Inclusion criteria

  • CCH according to the International Classification of Headache Disorders version 3 (ICHD-3)
  • At screening: stable weekly attack frequency in the 4 weeks prior to screening (assessed retrospectively), averaging at least 8 per week and each week within a 40% window around the average
  • At randomization: average of at least 8 attacks per week and no absence of attacks on more than two consecutive days during baseline

Exclusion criteria

Exclusion Criteria:

  • Use of excluded concomitant treatment at screening (lithium; other prophylactics if not on a stable dose for less than one month; steroids/GON block within 2 months before screening; sphenopalatinum block, neurostimulation (changed setting within 3 months before screening) or botulinum toxin within 3 months before screening) and during the double-blind phase
  • Use of LSD(-derivatives) (other than investigational drug), psilocybin, ketamine or cannabis within 3 months prior to screening and throughout the study
  • Lifetime and/or family history (first degree relatives) of psychotic or bipolar disorder, suicidal intention or attempt
  • A score of 6 or more on the 'Ervaringenlijst' (PQ-16) to exclude subclinical susceptibility to psychosis
  • Actual abuse of alcohol and/or recreational drugs
  • Lifetime history of cardiac valvular disease
  • History or evidence of cognitive disorder at screening
  • Positive urine drug screen at screening
  • Females: Pregnancy, lactation, no acceptable contraceptive use
04

Study design

Phase
Phase 2
Primary purpose
Treatment
Allocation
Randomized
Intervention model
Parallel assignment
Masking
Quadruple (Participant, Care provider, Investigator, Outcomes assessor)
Enrollment
65 participants (estimated)

Study arms

  • Experimental
    Verum

    Lysergic diethylamide tartrate (equivalent to 25 microgram LSD base), one dose every 3 days for 3 weeks (totalling 7 vials)

    Drug: LSD tartrate

  • Placebo comparator
    Placebo

    Placebo vial looking like verum vial, one vial every 3 days for 3 weeks (totalling 7 vials)

    Drug: Placebo

Interventions

  • DrugLSD tartrate

    LSD tartrate equivalent to 25 microgram LSD base

    Also known as: Lysergic acid diethylamide

  • DrugPlacebo

    Placebo with equal appearance

05

What researchers measure

Primary outcomes

  1. Mean change in weekly attack frequency, across treatments groups.

    In week 3 post-randomization, compared to the 4-week baseline average per week

    Time frame: week 3 of treatment

Secondary outcomes

  1. Mean change in weekly attack frequency across weeks 4-8 compared to the 4-week baseline and for each week separately.

    Time frame: week 8 post-randomization

  2. 100% reduction (remission rate) in number of weekly attacks in the third treatment week, compared to the 4-week baseline, across treatment groups.

    Rate of subjects with 100% reduction in weekly attack frequency compared to baseline

    Time frame: week 3 post-randomization

  3. ≥50% reduction (50% responder rate) in number of weekly attacks in the third treatment week, compared to the 4-week baseline, across treatment groups.

    Rate of subjects with more than 50% reduction in weekly attack frequency compared to baseline

    Time frame: week 3 post-randomization

  4. ≥30% reduction (30% responder rate) in number of weekly attacks in the third treatment week, compared to the 4-week baseline, across treatment groups.

    Rate of subjects with more than 30% reduction in weekly attack frequency compared to baseline

    Time frame: week 3 post-randomization

  5. 100% reduction (remission rate) in number of weekly attacks across weeks 4-8 compared to the 4-week baseline and for each week separately.

    Rate of subjects with 100% reduction in weekly attack frequency compared to baseline

    Time frame: week 8 post-randomization

  6. ≥50% reduction (50% responder rate) in number of weekly attacks across weeks 4-8 compared to the 4-week baseline and for each week separately.

    Rate of subjects with 50% reduction in weekly attack frequency compared to baseline

    Time frame: week 8 post-randomization

  7. ≥30% reduction (30% responder rate) in number of weekly attacks across weeks 4-8 compared to the 4-week baseline and for each week separately.

    Rate of subjects with 30% reduction in weekly attack frequency compared to baseline

    Time frame: week 8 post-randomization

  8. Mean change in weekly attack frequency in the entire 3 week treatment period compared to the 4-week baseline.

    Time frame: week 3 post-randomization

  9. Mean change in mean headache attack duration (minutes) per week, across treatment groups

    In week 3 compared to the weekly average during 4-week baseline

    Time frame: week 3 post-randomization

  10. Mean change in mean headache attack duration (minutes) per week, across treatment groups

    Across weeks 4-8 compared to the 4-week baseline and for each week separately.

    Time frame: week 8 post-randomization

  11. Mean change in mean headache attack severity (VAS 1-10), across treatment groups

    In week 3 compared to the weekly average during 4-week baseline

    Time frame: week 3 post-randomization

  12. Mean change in mean headache attack severity (VAS 1-10), across treatment groups

    Across weeks 4-8 compared to the 4-week baseline and for each week separately.

    Time frame: week 8 post-randomization

  13. Mean change in number of abortive medication use, across treatment groups

    In week 3 compared to the weekly average during 4-week baseline

    Time frame: week 3 post-randomization

  14. Mean change in number of abortive medication use, across treatment groups

    Across weeks 4-8 compared to the 4-week baseline

    Time frame: week 8 post-randomization

  15. Failure of sustained response'

    Time to initiation of additional prophylactic treatment and/or GON-block during weeks 4-8, across treatment groups

    Time frame: Weeks 4-8 post-randomization

  16. Patient Global Impression of Change (PGIC)

    Patient Global Impression of Change at week 3 post-randomization; scale 0-7, higher scores representing better improvement

    Time frame: Day 21 post-randomization

  17. Patient Global Impression of Change (PGIC)

    Patient Global Impression of Change at week 8 post-randomization; scale 0-7, higher scores representing better improvement

    Time frame: weeks 3 and 8

  18. Health-related quality of life

    Change from baseline in EQ-5D-5L Visual Analogue Scale (VAS) at weeks 3 and 8.

    Time frame: weeks 3 and 8

  19. Hospital Anxiety and Depression Score (HADS)

    Change from baseline in Hospital Anxiety and Depression Scale (HADS) at weeks 3 and 8.

    Time frame: weeks 3 and 8.

  20. Pharmacokinetic (PK)-pharmacodynamic (PD) modelling

    Plasma LSD concentrations on day 18 post-randomization frequency

    Time frame: Day 18 post-randomization

  21. Cost-effectiveness analysis (CEA) from a societal perspective comparing the LSD intervention with usual care.

    Healthcare use and productivity losses will be measured by patient questionnaires (iMCQ, and iPCQ)

    Time frame: Week 1, 3 and 8

  22. Efficacy of treatment masking

    measured as perceived treatment assignment on a 5-point scale (likely verum/possibly verum/don't know/possibly placebo/likely placebo).

    Time frame: Week 1 and 3 post-randomization

Other outcomes

  1. Alcohol consumption

    Units of alcohol consumed during baseline, treatment and follow-up

    Time frame: during the entire 12-week duration of the study

  2. PK-PD modelling

    Correlation between individual pharmacokinetics of LSD and relative change of weekly attack frequency

    Time frame: Week 1 and 3

06

Study locations

2 of 2 sites recruiting
  • Leiden University Medical Center (LUMC)
    Leiden, Netherlands
    • Martien van Liefland · Contact · LICIT@LUMC.nl · 071 526 21 11
    • Rolf Fronczek, MD, PhD · Principal investigator
    • Martien van Liefland, MD · Sub investigator
    Recruiting
  • Canisius-Wilhelmina Ziekenhuis (CWZ)
    Nijmegen, Netherlands
    • Julia Jansen · Contact · LICIT@cwz.nl · 024 365 82 10
    • Willemijn Leen, MD, PhD · Principal investigator
    • Julia Jansen, MD · Sub investigator
    Recruiting
07

References and documents

Publications

  • Hoffmann J, May A. Diagnosis, pathophysiology, and management of cluster headache. Lancet Neurol. 2018 Jan;17(1):75-83. doi: 10.1016/S1474-4422(17)30405-2. Epub 2017 Nov 23. PubMed 29174963 ↗
  • Rozen TD, Fishman RS. Cluster headache in the United States of America: demographics, clinical characteristics, triggers, suicidality, and personal burden. Headache. 2012 Jan;52(1):99-113. doi: 10.1111/j.1526-4610.2011.02028.x. Epub 2011 Nov 11. PubMed 22077141 ↗
  • Tepper SJ, Stillman MJ. Cluster headache: potential options for medically refractory patients (when all else fails). Headache. 2013 Jul-Aug;53(7):1183-90. doi: 10.1111/head.12148. Epub 2013 Jun 28. PubMed 23808603 ↗
  • McGeeney BE. Cannabinoids and hallucinogens for headache. Headache. 2013 Mar;53(3):447-58. doi: 10.1111/head.12025. Epub 2012 Dec 20. PubMed 23278122 ↗
  • Andersson M, Persson M, Kjellgren A. Psychoactive substances as a last resort-a qualitative study of self-treatment of migraine and cluster headaches. Harm Reduct J. 2017 Sep 5;14(1):60. doi: 10.1186/s12954-017-0186-6. PubMed 28870224 ↗
  • Sewell RA, Halpern JH, Pope HG Jr. Response of cluster headache to psilocybin and LSD. Neurology. 2006 Jun 27;66(12):1920-2. doi: 10.1212/01.wnl.0000219761.05466.43. PubMed 16801660 ↗
  • Schindler EA, Gottschalk CH, Weil MJ, Shapiro RE, Wright DA, Sewell RA. Indoleamine Hallucinogens in Cluster Headache: Results of the Clusterbusters Medication Use Survey. J Psychoactive Drugs. 2015 Nov-Dec;47(5):372-81. doi: 10.1080/02791072.2015.1107664. Epub 2015 Nov 23. PubMed 26595349 ↗
  • de Coo IF, Naber WC, Wilbrink LA, Haan J, Ferrari MD, Fronczek R. Increased use of illicit drugs in a Dutch cluster headache population. Cephalalgia. 2019 Apr;39(5):626-634. doi: 10.1177/0333102418804160. Epub 2018 Oct 5. PubMed 30290701 ↗

Individual participant data

Plan to share: Yes — Individual patient data underlying publication, after deidentification, will be shared upon request to the corresponding author

Supporting information: Study protocol

08

Registry details

Key details

Study ID
NCT05477459
Lead sponsor
Radboud University Medical Center
Collaborators
ZonMw: The Netherlands Organisation for Health Research and Development, Canisius-Wilhelmina Hospital, Leiden University Medical Center
Responsible party
Sponsor
First posted
Jul 28, 2022
Start date
Apr 16, 2025 (estimated)
Primary completion
Apr 2027 (estimated)
Completion
Apr 2027 (estimated)
Last update
Apr 15, 2025

Study contacts

Julia Jansen, MD
Contact
julia.jansen@cwz.nl
+31 24 3658765
Kees Kramers, Prof.
principal investigator · Radboud University Medical Center

Oversight

Data monitoring committee
Yes
FDA-regulated drug
No
FDA-regulated device
No
View the source record on ClinicalTrials.gov ↗

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