Modulation Of Cortical Hemodynamic Responses During The Craniocervical Flexion Test In Individuals With Post-traumatic Headache

PURPOSE: Optical neuroimaging provides a portable and relatively low-cost method for assessing physiologic biomarkers that may help inform the diagnosis and treatment of chronic pain conditions. This study aimed to determine if cortical hemodynamic responses are modulated with increasing contraction intensity during a clinical test of deep neck flexor endurance in individuals with persistent post-traumatic headache and neck pain (PTH) following concussion. METHODS: Eighteen participants (age 30 ± 4 years; 85% men) with PTH performed the craniocervical flexion test (CCFT) at 3 contraction intensities (5 x 10-sec isometric holds at 22, 26, and 30 mmHg) using a pressure biofeedback unit placed behind the cervical spine. Changes in oxygenated hemoglobin (∆O2Hb) were measured using functional near-infrared spectroscopy (fNIRS) with 20 optodes positioned on the scalp overlying prefrontal (PFC) and primary motor (M1) cortices. ∆O2Hb was compared across contraction intensities using ANOVA for repeated measures. RESULTS: M1 ∆O2Hb progressively decreased with increases in contraction intensity (mean (SD) 22 mmHg = -4.07 ± 12.00 μM, 26 mmHg = -8.13 ± 22.10 μM, 28 mmHg = -10.49 ± 26.18 μM ; F = 4.253, p = 0.033). PFC ∆O2Hb was small (0.55 ± 2.94 μM) and did not change across contraction intensities (F = 1.96, p = 0.174). CONCLUSIONS: As the intensity of deep neck flexor exercise increases, hemodynamic activity decreases in the primary motor cortex with no corresponding modulation of activity in the prefrontal cortex. These findings are the first to show that fNIRS is sensitive to modulation of hemodynamic activity within the primary motor cortex during deep neck flexor exercise in a clinical population with persistent headache following concussion. Future work will examine mechanisms underlying the suppression of M1 hemodynamic activity during CCFT and will investigate fNIRS as a biomarker of treatment response to therapeutic neck exercise for the clinical management of PTH. Supported by NIH Grant R21NS109852