Investigating Fryette's mechanics in computed tomography scans: an analysis of vertebrae spinal physiology using open-sourced datasets and three-dimensional vertebral orientation.

CONTEXT: Fryette's mechanics is taught as a simplistic model of coupled vertebral movement, fundamental in osteopathic practice. This study seeks to better understand the likelihood of Fryette's model by calculating vertebral orientation in computed tomography (CT) scans. Given previous findings of low angular coupled movements during overall spinal motion, static calculations provide a unique perspective on the likelihood of Fryette's mechanics. OBJECTIVES: This analysis aims to evaluate the efficacy of Fryette's principles in predicting vertebral positioning in CT scans by comparing their 3-dimensional (3D) orientation to movements described by Fryette. METHODS: 3D models of 953 thoracic and lumbar vertebrae were obtained from 82 CT scans within the VerSe`20 open-source dataset. A stepwise algorithm generated three unique symmetry planes for each vertebra, offering 3D angular orientation with respect to the vertebral level below. A total of 422 vertebrae were omitted from the analysis due to the presence of pathologies significant enough to affect their motion, inaccurate symmetry plane calculations, or absence of vertebral level below. The remaining 531 vertebra were analyzed to compare quantitative coupled positioning against expected coupled spinal movements in line with Fryette's mechanics. One-sample proportional z-scoring was implemented for all vertebral levels with an ∝=0.05 and a null hypothesis of Fryette's primed positioning occurring by chance of 50 %. Further analysis was performed with individual z-scoring for each individual level to see which levels were statistically significant. RESULTS: Data from the VerSe`20 dataset revealed that 56.9 % of successfully analyzed vertebrae demonstrated positions compatible with Fryette's mechanics (p=0.0014, power=89 %). The 302 vertebral levels that did display coupled positioning consisted of Type I (166 vertebrae) and Type II (136 vertebrae) compatible with Fryette's mechanics. Levels that demonstrated statistical significance consisted of T5 (p=0, power=99 %), T6 (p=0.0023, power=77 %), T7 (p=0.041, power=46 %), and T10 (p=0.017, power=60 %). CONCLUSIONS: Our analysis suggests that the static positions of vertebrae in CT scans may align with Fryette's descriptions, although not very often. Notably, vertebral levels T5-T7 and T10 exhibit strong evidence of their static positions aligning with expected movements, warranting further investigation into the Fryette phenomenon at these levels. Future studies should explore the dynamic implications of these findings to enhance our understanding of spinal biomechanics.

Activation of the cholinergic antiinflammatory reflex by occipitoatlantal decompression and transcutaneous auricular vagus nerve stimulation.

CONTEXT: The parasympathetic-mediated inflammatory reflex inhibits excessive proinflammatory cytokine production. Noninvasive techniques, including occipitoatlantal decompression (OA-D) and transcutaneous auricular vagus nerve stimulation (taVNS), have been demonstrated to increase parasympathetic tone. OBJECTIVES: To test the hypothesis that OA-D and taVNS increase parasympathetic nervous system activity and inhibit proinflammatory cytokine mobilization and/or production. METHODS: Healthy adult participants were randomized to receive OA-D (5 min of OA-D followed by 10 min of rest; n=8), taVNS (15 min; n=9), or no intervention (15 min, time control; n=10) on three consecutive days. Before and after these interventions, saliva samples were collected for determination of the cytokines interleukin-1ß (IL-1ß), interleukin-6 (IL-6), interleukin-8 (IL-8), and tumor necrosis factor α (TNF-α). Arterial blood pressure and the electrocardiogram were recorded for a 30-min baseline, throughout the intervention, and during a 30-min recovery period to derive heart rate and blood pressure variability markers as indices of vagal and sympathetic control. RESULTS: OA-D and taVNS increased root mean square of successive RR interval differences (RMSSD) and high frequency heart rate variability, which are established markers for parasympathetic modulation of cardiac function. In all three groups, the experimental protocol was associated with a significant increase in salivary cytokine concentrations. However, the increase in IL-1ß was significantly less in the taVNS group (+66 ± 13 pg/mL; p<0.05) than in the time control group (+142 ± 24 pg/mL). A similar trend was observed in the taVNS group for TNF-α (+1.7 ± 0.3 pg/mL vs. 4.1 ± 1.3 pg/mL; p<0.10). In the OA-D group baseline IL-6, IL-8, and TNF-α levels on the third study day were significantly lower than on the first study day (IL-6: 2.3 ± 0.4 vs. 3.2 ± 0.6 pg/mL, p<0.05; IL-8: 190 ± 61 vs. 483 ± 125 pg/mL, p <0.05; TNF-α: 1.2 ± 0.3 vs. 2.3 ± 0.4 pg/mL, p<0.05). OA-D decreased mean blood pressure from the first (100 ± 8 mmHg) to the second (92 ± 6 mmHg; p<0.05) and third (93 ± 8 mmHg; p<0.05) study days and reduced low frequency spectral power of systolic blood pressure variability (19 ± 3 mmHg2 after OA-D vs. 28 ± 5 mmHg2 before OA-D; p<0.05), a marker of sympathetic modulation of vascular tone. OA-D also increased baroreceptor-heart rate reflex sensitivity from the first (13.7 ± 3.0 ms/mmHg) to the second (18.4 ± 4.3 ms/mmHg; p<0.05) and third (16.9 ± 4.2 ms/mmHg; p<0.05) study days. CONCLUSIONS: Both OA-D and taVNS elicited antiinflammatory responses that were associated with increases in heart rate variability-derived markers for parasympathetic function. These findings suggest that OA-D and taVNS activate the parasympathetic antiinflammatory reflex. Furthermore, an antihypertensive effect was observed with OA-D that may be mediated by reduced sympathetic modulation of vascular tone and/or increased baroreceptor reflex sensitivity.

Occipitoatlantal decompression and noninvasive vagus nerve stimulation slow conduction velocity through the atrioventricular node in healthy participants.

CONTEXT: Management of atrial fibrillation includes either rhythm control that aims at establishing a sinus rhythm or rate control that aims at lowering the ventricular rate, usually with atrioventricular nodal blocking agents. Another potential strategy for ventricular rate control is to induce a negative dromotropic effect by augmenting cardiac vagal activity, which might be possible through noninvasive and nonpharmacologic techniques. Thus, the hypothesis of this study was that occipitoatlantal decompression (OA-D) and transcutaneous auricular vagus nerve stimulation (taVNS) not only increase cardiac parasympathetic tone as assessed by heart rate variability (HRV), but also slow atrioventricular conduction, assessed by the PQ-interval of the electrocardiogram (EKG) in generally healthy study participants without atrial fibrillation. OBJECTIVES: To test whether OA-D and/or transcutaneous taVNS, which have been demonstrated to increase cardiac parasympathetic nervous system activity, would also elicit a negative dromotropic effect and prolong atrioventricular conduction. METHODS: EKGs were recorded in 28 healthy volunteers on three consecutive days during a 30 min baseline recording, a 15 min intervention, and a 30 min recovery period. Participants were randomly assigned to one of three experimental groups that differed in the 15 min intervention. The first group received OA-D for 5 min, followed by 10 min of rest. The second group received 15 min of taVNS. The intervention in the third group that served as a time control group (CTR) consisted of 15 min of rest. The RR- and PQ-intervals were extracted from the EKGs and then used to assess HRV and AV-conduction, respectively. RESULTS: The OA-D group had nine participants (32.1%), the taVNS group had 10 participants (35.7%), and the CTR group had nine participants (32.1%). The root mean square of successive differences between normal heartbeats (RMSSD), an HRV measure of cardiac parasympathetic modulation, tended to be higher during the recovery period than during the baseline recording in the OA-D group (mean ± standard error of the mean [SEM], 54.6 ± 15.5 vs. 49.8 ± 15.8 ms; p<0.10) and increased significantly in the taVNS group (mean ± SEM, 28.8 ± 5.7 vs. 24.7 ± 4.8 ms; p<0.05), but not in the control group (mean ± SEM, 31.4 ± 4.2 vs. 28.5 ± 3.8 ms; p=0.31). This increase in RMSSD was accompanied by a lengthening of the PQ-interval in the OA-D (mean ± SEM, 170.5 ± 9.6 vs. 166.8 ± 9.7 ms; p<0.05) and taVNS (mean ± SEM, 166.6 ± 6.0 vs. 162.1 ± 5.6 ms; p<0.05) groups, but not in the control group (mean ± SEM, 164.3 ± 9.2 vs. 163.1 ± 9.1 ms; p=0.31). The PQ-intervals during the baseline recordings did not differ on the three study days in any of the three groups, suggesting that the negative dromotropic effect of OA-D and taVNS did not last into the following day. CONCLUSIONS: The lengthening of the PQ-interval in the OA-D and taVNS groups was accompanied by an increase in RMSSD. This implies that the negative dromotropic effects of OA-D and taVNS are mediated through an increase in cardiac parasympathetic tone. Whether these findings suggest their utility in controlling ventricular rates during persistent atrial fibrillation remains to be determined.