NCT03446456

Vasopressin and Pain Perception in the Brain

Active, enrolled Phase 1, PHASE2 Results posted Last updated 20 May 2025

What this trial tests

Phase 1, PHASE2 trial testing Arginine vasopressin in Acute Pain in 40 participants. Participants enrolled and being followed up; not accepting new ones.

Timeline

17 September 2018

Primary endpoint
30 June 2026

31 December 2026

Quick facts

Lead sponsor	University of Maryland, Baltimore
Phase	Phase 1, PHASE2
Status	Active, enrolled
Study type	INTERVENTIONAL
Allocation	randomized
Design	parallel
Masking	double
Primary purpose	basic science
Enrollment	40
Start date	17 September 2018
Primary completion	30 June 2026
Estimated completion	31 December 2026
Sites	1 location across United States

Drugs / interventions tested

• Arginine vasopressin — full drug profile →
• Saline
• Observational learning
• fMRI data aquisition

Conditions studied

• Acute Pain — all drugs for Acute Pain →

Sponsor

University of Maryland, Baltimore

Who can join

Adults 18 to 65, any sex, with Acute Pain. Patients with the condition only — healthy volunteers not accepted.

Results — posted to ClinicalTrials.gov

Per-arm endpoint measurements with 95% confidence intervals where reported. Source: trial results section.

Change in BOLD Singal in Supplementary Motor Area Compared to Whole Brain Average During the Painful Stimulation Primary · Day 2, the average of 24 trials of painful stimulations with each stimulation lasting 20 seconds

Blood oxygenation level dependent (BOLD) responses will allow the identification of relative activation/deactivation in the brain as a result of events (e.g. painful stimulations) that will be given during the experiment. Changes in the Percentage of BOLD signal are calculated as the BOLD signal in the right supplementary motor area during the 20-second heat pain divided by the whole-brain average BOLD signal during that 20-second heat pain.

Group	Value	95% CI
Saline	0.485	± 0.271
Arginine Vasopressin	0.482	± 0.387

Heating Temperature Secondary · Day 1 (calibration)

On Day 1, the heating temperature was calibrated to the individual level. The heating temperature corresponding to 50 out of 100 visual analog scale pain ratings was selected as the testing temperature for day 2 (test).

Group	Value	95% CI
Saline	44.16	± 0.77
Arginine Vasopressin	44.44	± 0.83

Implicit Association Test (IAT) Response Latency Difference Secondary · Day 1

The IAT is a behavioral test that examines racial biases via measuring the strength of associations between concepts (e.g., African-American, Asian, White) and evaluations (good, bad). Participants were asked to press a response key when they saw images (people) or words (good/bad) on the screen. Response latencies (RL) were measured in milliseconds using E-prime as the reaction time to press the response key. An RL difference (D) score was calculated as 1) Compute the standard deviation (SD) of RL from overall trials; 2) M1 is the mean of RL in the condition where "White" and "good" share the

Group	Value	95% CI
Saline	0.03	± 0.37
Arginine Vasopressin	0.07	± 0.32

Pain Ratings Secondary · Day 2 (test)

Participants will provide their pain on a Visual Analogue Scale raging from 0=no pain to 100= maximum unbearable pain. Normal value will be absence of pain.

Group	Value	95% CI
Saline	44.84	± 24.49
Arginine Vasopressin	47.19	± 26.27

Sponsor's own description

The feeling of pain is not just a sensory experience, but is also influenced by emotions, beliefs and expectations, making pain a highly subjective experience. This is evident in clinical practice, where the behavior of the physician and the treatment context can strongly influence the pain experience of patients. Research has shown that patients' expectation that a treatment will reduce pain influences individual perception of pain, even if the treatment has no active ingredient. The expectancy-induced analgesia emerges due to a modulation of the individual pain experience of patients by an engagement of endogenous inhibitory systems in the central nervous system.

The development of expectancy-induced analgesia can be generated in several ways. The investigators have previously demonstrated that social information and observational learning (e.g. the patient observes analgesia in another person receiving a treatment) can lead to expectancy-induced analgesia and pain reduction. However, the neural mechanisms (mechanisms in the brain) of how these expectancies are acquired and the neural mechanisms of analgesia induced by observational learning are unknown.

The investigators recently established a procedure to investigate neural mechanisms of observational learning in placebo analgesia. Here the investigators propose to investigate the influence of vasopressin, a neurotransmitter that is important for social interaction, on observational learning.

The investigators will use functional magnetic resonance imaging (fMRI), a non-invasive method, to investigate neural activity in humans. Participants will either receive vasopressin or saline with a nasal spray. During fMRI scanning, participants will then undergo an observational learning phase, where the study participants will learn the experience of analgesia in another person through a video, and a testing phase, where participants will perceive painful stimulations with the same cues as the observational phase. The comparison of the vasopressin group and the saline group will allow us to investigate how vasopressin influences behavioral effects of observational learning on pain perception as well as its effect on the neural processing of observational learning.

A better understanding of how the human brain processes observationally-induced analgesia would allow us to improve the therapeutic context of pain treatments by increasing the contextual factors which help patients cope with pain.

Publications & conference data

No peer-reviewed publications indexed yet for this trial.