Related Experiment Video
Updated: Aug 3, 2026
11:02
Vagus Nerve Stimulation as a Tool to Induce Plasticity in Pathways Relevant for Extinction Learning
Published on: August 21, 2015
23.3K
VNS-induced dose-dependent pupillary response in refractory epilepsy
Andrés Torres Sánchez1, Marie Dawant2, Venethia Danthine3
1Institute of Neuroscience (IoNS), Catholic University of Louvain, Brussels, Belgium; Innoviris, Brussels Institute for Research and Innovation, Chaussée de Charleroi 112, 1060, Brussels, Belgium.
Summary
Vagus Nerve Stimulation (VNS) causes a dose-dependent pupillary dilation response (PDR) that differs between epilepsy responders and non-responders, suggesting PDR as a new biomarker for VNS therapy.
Area of Science:
- Neuroscience
- Epilepsy Research
- Biomarker Development
Background:
- The Locus Coeruleus (LC) releases norepinephrine, contributing to Vagus Nerve Stimulation's (VNS) antiepileptic effects.
- LC activity influences pupil dilation, offering a potential link to VNS efficacy.
Purpose of the Study:
- To investigate the dose-dependent relationship between VNS intensity and Pupillary Dilation Response (PDR).
- To explore PDR as an objective biomarker for optimizing VNS therapy and predicting patient response.
Main Methods:
- Retrospective analysis of 14 VNS-implanted patients (9 responders, 5 non-responders).
- VNS intensities were varied from 0.25 mA to 2.25 mA, with concurrent pupil size tracking.
- Individual curve fitting analyzed the VNS intensity-PDR relationship.
Main Results:
- Pupillary Dilation Response (PDR) increased with VNS intensity, especially in responders.
- An inverted U-shaped VNS intensity-PDR relationship was observed in 6 patients.
- A significant interaction between VNS intensity and responder status was identified, independent of subjective perception.
Conclusions:
- VNS elicits a dose-dependent PDR that distinguishes between responders and non-responders.
- The inverted U-shaped dose-response curve in nearly half of patients indicates a maximal VNS effect.
- VNS-induced PDR is proposed as a novel and objective biomarker for VNS treatment response.
Related Concept Videos
01:30Ligand-Gated Ion Channel Receptor: Gating Mechanism
Ligand-gated ion channels are transmembrane proteins that play a vital role in intercellular communication and functions of the nervous system. They allow the influx of ions across the membrane once the neurotransmitter binds, allowing the subsequent transmission of electrical excitation across the neurons. Other ligand-gated ion channels, like the γ-aminobutyric acid (GABA) receptor, permit anions like chloride into the cells on the binding of the GABA molecule. Their entry into the cell...
01:23Drugs Acting on Autonomic Ganglia: Stimulants
Ganglionic stimulants activate NM nicotinic receptors in autonomic ganglia, falling into two categories: nicotine mimetics [e.g., lobeline, dimethylpiperazine, tetramethylammonium] and muscarinic receptor agonists [e.g., muscarine, methacholine]. The first category's action is rapid and blocked by nicotinic receptor antagonists, while the second category's action is delayed and blocked by atropine-like agents. Nicotine, an alkaloid, affects the heart rate by stimulating sympathetic or...
01:12Local Anesthetics: Adverse Effects
While local anesthetics are generally safe and well-tolerated, they can occasionally cause adverse effects that vary in severity. Local anesthetics can induce toxicity at two distinct levels. They can either produce local effects through direct contact with the neural elements or be absorbed into the bloodstream from the injection site, leading to systemic effects.
Once absorbed into the systemic circulation, local anesthetics can affect the organs that depend on the functioning of sodium...
Once absorbed into the systemic circulation, local anesthetics can affect the organs that depend on the functioning of sodium...
01:28Chemotherapy-Induced Nausea and Vomiting: Neurokinin-1 Receptor Antagonists
Neurokinin 1 (NK1) receptors are distributed across the GI tract, vagal afferents, and key CNS regions including the central vomiting center and chemoreceptor trigger zone (CTZ) Chemotherapy agents stimulate enterochromaffin cells in the gastrointestinal (GI) tract to release large amounts of substance P (SP). SP is a neuropeptide released by specific sensory nerves in response to many different stressors, including those in the GI mucosa affected by chemotherapy. SP binds and activates these...
01:24Drug Toxicity: Dose-Dependent Reactions
Drug toxicities can be stratified into pharmacological, pathological, or genotoxic based on their mechanisms. The incidence and severity of these toxicities generally increase with the drug's concentration in the body and exposure time.Pharmacological toxicity is evident when the therapeutic effects of drugs overshoot into adverse reactions in a predictable, dose-dependent manner. Central nervous system (CNS) depression from barbiturates is a classic example, with effects escalating from...
01:30Drug Toxicity: Allergic Reactions
Drug-related allergies are immune-mediated responses triggered by the administration of pharmacological agents. These hypersensitivity reactions are classified based on the immune mechanisms involved. The four primary types—Type I, II, III, and IV—are mediated by different immunological pathways and exhibit distinct clinical manifestations.Type I Hypersensitivity/ IgE-Mediated Reactions: Immunoglobulin E (IgE) immediately mediates Type I hypersensitivity reactions. Upon initial exposure to a...