Benjamin Seshadri
- B.Sc. (University of Victoria, 2024)
Topic
Imaging Cerebral Blood Flow Responses to a Transient Trigeminal Nerve Stimulus During Parasympathetic Pharmacological Blockade
School of Exercise Science, Physical and Health Education
Date & location
- Friday, July 3, 2026
- 10:00 A.M.
- McKinnon Building, Room 092
Examining Committee
Supervisory Committee
- Dr. Kurt Smith, School of Exercise Science, Physical and Health Education, University of Victoria (Supervisor)
- Dr. David Kennedy, School of Exercise Science, Physical and Health Education, UVic (Member)
External Examiner
- Dr. Michael Tymko, Department of Human Health Sciences, University of Guelph
Chair of Oral Examination
- Dr. Brian Christie, School of Medical Sciences, UVic
Abstract
The autonomic nervous system plays a critical role in the regulation of cerebral blood flow (CBF), yet the contribution of parasympathetic nervous activity (PNA) towards cerebrovascular control during moments of neurogenic stress (headache) remains poorly understood. The trigeminal nerve (cranial nerve V) is thought to play a central role in the generation of many primary headache disorders through its involvement in pain transmission and regulation of cerebrovascular tone. Brain Freeze Headache (BFH) is a transient headache induced by cold stimulation of the palate, providing a practical and non-invasive model through which we can explore activation of the trigeminal nerve. The objective of this thesis, assessed in two separate studies, was to characterize intracranial and extracranial cerebrovascular responses to BFH, and to determine the influence of pharmacologic parasympathetic blockade on these responses. Study #1 investigated forty-two healthy adults during BFH while middle cerebral artery (MCA) and internal carotid artery (ICA) vascular hemodynamics were assessed using transcranial doppler and vascular duplex ultrasound. The primary findings of study #1 indicated that BFH elicits a significant increase in intracranial and extracranial cerebral perfusion. MCAv increased by 27.3% (p < 0.0001), while ICA blood flow increased by 12.2% (p = 0.0013). Cerebrovascular conductance markedly increased despite only modest elevations in mean arterial pressure, suggesting that BFH induces active neurogenic vasodilation of downstream cerebral microvasculature. Study #2 investigated twenty-three healthy adults during BFH following intravenous infusion of both peripheral parasympathetic blockade with glycopyrrolate and central parasympathetic blockade with atropine. The primary findings of study #2 indicate that the intracranial MCA cerebrovascular response to BFH is attenuated under PNA blockade (p = 0.03) while having no significant effect on ICA flow (p = 0.89). It appears that PNA blockade disrupts downstream vasodilatory signalling of the cerebral vasculature, resulting in a blunted increase in CBF during BFH. Collectively, the findings presented in this thesis suggest that PNA plays a critical role in mediating the cerebrovascular vasodilation that occurs following acute activation of the trigeminal nerve.