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Effect of Suboccipital Release on Pain Perception and Autonomic Reflex Responses to Ischemic and Cold Pain Public Deposited

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MLA citation style

Krause, B, et al. Effect of Suboccipital Release On Pain Perception and Autonomic Reflex Responses to Ischemic and Cold Pain. . 1122. https://mushare.marian.edu/concern/generic_works/84d0a353-6f37-4dbd-a080-6c90a941371b?locale=en

APA citation style

Krause, B, Vrable, Abby, Wilson, Thad, Rodimel, Benjamin, Schmale, Trenton, Metzler-Wilson, Kristen, & Schaub, Andrew. (1122). Effect of Suboccipital Release on Pain Perception and Autonomic Reflex Responses to Ischemic and Cold Pain. https://mushare.marian.edu/concern/generic_works/84d0a353-6f37-4dbd-a080-6c90a941371b?locale=en

Chicago citation style

Krause, B., Vrable, Abby, Wilson, Thad, Rodimel, Benjamin, Schmale, Trenton, Metzler-Wilson, Kristen, and Schaub, Andrew. Effect of Suboccipital Release On Pain Perception and Autonomic Reflex Responses to Ischemic and Cold Pain. 1122. https://mushare.marian.edu/concern/generic_works/84d0a353-6f37-4dbd-a080-6c90a941371b?locale=en

Note: These citations are programmatically generated and may be incomplete.

Introduction: In 2012, approximately 19 million adults in the U.S. used some form of manipulative treatment as part of their overall healthcare. Suboccipital release (SOR) is a commonly used manual medicine technique of the head and neck. SOR and related techniques are also used to treat pain from tension-type and migraine headaches. The clinical effects of SOR are purported to be mediated via the autonomic nervous system, but similar to many manual techniques, the neurophysiological data in this area are sparse. Thus, the effects and mechanisms of SOR are unclear and not well understood. Objective: This study aimed to determine the effects of SOR on the cardiovascular system during cold pain and ischemic pain. Methods: 16 healthy subjects (8 women, 8 men) experienced ischemic (forearm post-exercise muscle ischemia; PEMI) and cold (hand cold pressor test; CPT) pain. Beat-to-beat heart rate (HR; ECG), mean arterial blood pressure (MAP; finger photoplethysmography), baroreflex sensitivity (transfer function analysis), and pain perception were measured. SOR or a sham (modified yaw; 30 cycles/min) was performed in the final minute of pain. To probe potential mechanisms and interactions between manual treatment and a prototypic analgesic, oral aspirin (967 mg) was given 60 min prior to testing to reduce prostaglandin synthesis. Results: PEMI increased MAP by 23±2 and 20±2 mmHg; no differences occurred with the addition of SOR or yaw. PEMI modestly elevated HR during ischemia, followed by a significant reduction from baseline with SOR (-3±2 bpm) and yaw (-4±2 bpm); no differences were observed between treatment and sham. CPT increased MAP (SOR=11±1, yaw=9±2 mmHg) and HR (SOR=10±2, yaw=8±3 bpm) prior to SOR and yaw. Neither treatment nor sham blunted MAP increased (SOR=25±2, yaw=22±2 mmHg) with CPT; both decreased HR (SOR=-3±2, yaw=-2±2 bpm) from baseline. PEMI and CPT caused increased pain without treatment modulation. SOR decreased baroreflex sensitivity in the 0.05-0.15 Hz range and increased it in the 0.15-0.35 Hz range compared to yaw. Aspirin slightly attenuated pain but did not alter cardiovascular changes to PEMI and did not interact with SOR or yaw. These data indicate that “hands-on” interventions during acute pain and SOR post-pain have the capacity to modulate certain pain-induced autonomic effects. Conclusion: The primary findings of this study are that acute hypertensive conditions caused by experimental pain were not modulated by SOR, but HR responses were decreased during both SOR and a “hands-on” sham technique. The changes in BP and blood flow due to pain were not altered by the SOR treatment. However, baroreflex sensitivity was altered in both the low and high frequency ranges during the recovery period after experimentally induced pain, regardless of the type of pain. These data indicate that “hands-on” interventions during acute pain and SOR post-pain have the capacity to modulate certain pain-induced autonomic effects.

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