Gary A. Knutson, DC
Gary A. Knutson, DC,
840 W. 17th Street, Suite 5,
Bloomington, IN 47404.
OBJECTIVE: To determine whether a vectored adjustment of the atlas in patients identified as demonstrating signs of upper cervical joint dysfunction would cause lowering of blood pressure in comparison with resting controls.
DESIGN: Test 1: controlled clinical trial with a treatment (adjustment) group and a control (resting) group. Test 2: controlled clinical trial with subjects serving as their own controls.
SETTING: Private chiropractic practice.
PARTICIPANTS: Test 1: Forty established patients demonstrating signs of upper cervical subluxation/joint dysfunction and 40 established patients without such signs. Test 2: Thirty established patients demonstrating signs of upper cervical subluxation/joint dysfunction. INTERVENTION: Specific, vectored upper cervical (atlas) adjustment or similarly positioned resting.
MAIN OUTCOME MEASURES: Prerest, postrest, and postadjustment systolic, diastolic, and pulse rates as recorded through use of a digital oscillometric sphygmomanometer.
RESULTS: In test 1, subjects receiving adjustment had a significant (P <.001) decrease in systolic blood pressure whereas resting subjects did not. Intergroup comparison of the treatment (adjustment) and control (resting) groups demonstrated a significant difference (P <.001). A greater pre/post drop in systolic pressure was associated with greater age and higher initial systolic pressure. In test 2, the pre/postrest change in systolic blood pressure was not significant. The systolic blood pressure changed significantly (P <.001) from postrest readings to postadjustment readings.
CONCLUSION: The results indicate that palpation and vectored atlas adjustment causes a significant decrease in systolic blood pressure in patients with putative upper cervical subluxation/joint dysfunction in comparison with resting controls. Similar results were also demonstrated when subjects acted as their own controls. The lack of randomization, blinding, and a manipulated control group are factors that weaken these findings. The sudden drop in systolic pressure is proposed to be due to stimulation of the cervicosympathetic reflex or moderation of muscle tone and elimination of the effects of the pressor reflex.
From the FULL TEXT Article
Test 1 of this study revealed a statistically significant decrease in systolic BP between a treatment (palpation and vectored upper cervical adjustment, the necessity being determined by postural checks) group and a nontreatment (resting) group. Test 2, in which the subjects acted as their own controls, also showed a statistically significant decrease in systolic BP from the Postrest reading to the Postadjustment reading.
Within the nonblinded parameters of this study, it can be said that palpation and vectored atlas adjustment of suspect joint dysfunction in the upper cervical spine has an effect that significantly lowers systolic BP in comparison with what is seen in rested controls. The test 1 study also showed that those patients who, in the judgment of the examiner, demonstrated postural distortion (pelvic torsion/unleveling, “short leg,” foot rotations) had significantly higher systolic BP readings than those examined and judged to be free of such distortion.
The lack of blinding of the subjects leaves open the possibility that the decrease in systolic BP was due to a placebo effect. A sham adjustment, perhaps one made through use of an Activator instrument (Activator Methods, Inc) set for no excursion, might help to blind this sort of test. However, neither of the other measurements–diastolic pressure and pulse rate–showed any significant difference between the adjustment and resting groups, which raises the question of why any putative placebo effect would have influenced only the systolic pressure.
Using an adjustive style thrust in a (presumably) noninvolved area of the spine and then checking those results would have helped to control for nonspecific reflex responses. Similarly, having a control group in which each subject was positioned and the atlas transverse palpated would have helped to determine whether the active factor was the thrust of the adjustment or the stimulation of some palpatory reflex. This kind of control is problematic, however, inasmuch as palpation, depending on how forceful it is, might act as an adjustment.
Underinflation of the cuff as a reason for throwing out data could have led to biasing for lowered, not raised, BP after adjustment. However, underinflation happened only rarely, because the sphygmomanometer had a built-in sensor that indicated any need for more cuff pressure while the cuff was being inflated. In addition, although data for some patients were thrown out, the same patients were often examined later and their readings taken without error.
There was a concern in test 1 that inasmuch as the adjustment group’s systolic BP Pre reading was significantly higher than the control group’s, merely being “hypertensive” might result in a greater decrease in systolic pressure after resting and changing positions from supine to sitting. To check for this possibility, the data for the control group were analyzed to isolate those subjects whose prerest systolic BP values were within the confidence level of the mean or above that of the adjusted group (=133 mm Hg). There were 11 of these control group subjects, and they registered essentially no change (+0.1 mm Hg) in Pre reading-to-Post reading systolic pressure. In other words, resting of these “hypertensive” control subjects did not cause a significant lowering of their systolic pressure.
Finally, in test 1, although the systolic BP Pre reading of the adjustment group was significantly different from the systolic BP Pre reading of the control group (140.7 mm Hg vs 124; P < .001), the postintervention (adjustment or resting) systolic BP values for the two groups were not significantly different (130.4 vs 123.5 mm Hg; P = 0.34). This indicates that although the adjustment group’s systolic pressure Post reading was still higher than that of the control group, the elevation was not statistically significant.
As a check against the possibility that some unknown difference between the adjustment and control groups was responsible for the change in systolic BP, another test was done. In this test, test 2, the subjects served as their own controls. Three BP checks were done: a Prerest reading, a Postrest reading, and a Postadjustment reading. As in test 1, there was a significant decrease in systolic BP from the Postrest check to the Postadjustment check (P < .001). This indicates that the pre/post differences in systolic BP were most likely due to the adjustment and that in test 1 they were not due to some unknown difference between the treatment (adjustment) and control (resting) groups.
Despite the fact that the subjects in test 2 served as their own controls, there are some factors that could have confounded the BP readings, inducing potential error in the tests performed. Studies examining changes in systolic BP from supine to sitting, as opposed to supine to standing (because of concerns about orthostatic hypotension), are few. One study done on hypertensive subjects (110 males aged 16-64 years) found a slight (+3 mm Hg) increase in systolic BP (from 153 to 156 mm Hg) when the position was changed from supine to sitting.31 However, the subjects in that study were rested far longer in the supine position (30 minutes) and after changing their position to sitting (10 minutes) before BP readings were taken than the subjects in the present study. A study of normotensive patients (22 men and 25 women aged 21-59 years) also found a slight (+3 mm Hg) increase in systolic BP in women when they changed position from supine to sitting.32 Again, the resting times were longer–10 minutes each for supine and after changing to sitting–than those used in this study.
Another confounding factor is the finding that repeated checks of BP without adequate time for stabilization between the readings result in a decrease in systolic pressure: an average of -3.2 mm Hg was found in one study33 and -3 to -4 mm Hg was found in another. 
How these confounding factors might have affected the results in the studies is not known. Changing the protocol to allow for longer stabilization times after changing positions and use of a second or third BP check might help to eliminate these variables. However, as far as the present study is concerned, the rise in systolic BP that might have occurred in changing positions from supine to sitting may have offset any decrease associated with from taking a second BP reading without sufficient stabilization time.
A last critical note: these studies did not examine the long-term effects of vectored adjustment of putative upper cervical subluxation/joint dysfunction on BP, so no conclusions can be drawn as to any general positive health effects of lowering BP. Indeed, the BP changes noted may be only a short-term reaction to the stimulus of the adjustment.
Older subjects versus younger subjects
It is known that with age, arteries progressively stiffen [35, 36] and the arterial wall becomes thicker.  These changes have a minimal effect on resting BP, but as pressure levels rise the effect becomes more pronounced.  White and Carrington  found that elderly men had a greater increase in systolic BP to induced pressor reflex and concluded that “the significantly greater rise in systolic BP in these elderly subjects supports the view that this response is exaggerated by increased arterial stiffness in older individuals.”
These age-related changes in arteries are the likely reason for the findings noted in the present study. In test 1, as the age of the patient increased, the drop in systolic BP after adjustment increased (Fig 1). The decrease in systolic BP up to the age of 55 years (n = 22) for the adjustment group was -7.6 mm Hg (± 1.2 mm Hg); however, at 55 years and older (n = 18), the change in systolic BP post adjustment group rose to an average of -13.8 mm Hg (± 3.6 mm Hg)–a significant difference (P = .02). The figures in test 2 were nearly the same; the postadjustment change in systolic BP up to age 55 (n = 17) was -7.8 mm Hg (± 3.0 mm Hg), whereas after age 55 (n = 13) the change was -14.9 mm Hg (± 3.6 mm Hg)-a significant difference (P = .006).
Age and lack of arterial compliance is associated with higher systolic pressure, and this may explain why there was a greater percentage decrease in systolic pressure after adjustment with higher initial pressures (Fig 2).
Age should be taken into consideration when postmanipulation changes in BP are being investigated; a population of students in their 20s and 30s may not demonstrate a statistically significant effect. Such may have been the case in a study of normotensive chiropractic students that found a small but statistically significant drop in both systolic and diastolic BP after adjustment in comparison with what was found in motion-palpated control subjects. 
I propose here that the decrease in systolic BP was likely due to stimulation or normalization of upper cervical muscle spindle/GTO output. Bolton et al11 found considerable evidence that in the cat the vestibular system influences the sympathetic and respiratory nerves.  The vestibulosympathetic reflexes have been hypothesized to offset orthostatic hypotension in positional changes by raising BP. As a counter to the vestibulosympathetic reflexes, cervicosympathetic reflexes, whose origin seems to be in upper cervical muscle spindles and/or GTOs, act in opposition by decreasing BP.  These reflex pathways are complicated, and examination of them, performed in studies of cats, is only recent. However, this explanation is anatomically and physiologically sound and fits what was seen in these 2 studies–a sudden drop in systolic BP after adjustment of putative upper cervical subluxation.
In a similar study of the upper cervical spine, Purdy et al  found that touching, massage, or manipulation of the suboccipital muscles lead to “sympathetic dampening,” measured by a decrease in the pulse amplitude and height of the dicrotic notch. The effect was greatest with suboccipital manipulation. Again, this may be an effect of the cervicosympathetic reflex. Regardless of mechanism, the Purdy et al  study did show decreases in peripheral sympathetic tone with stimulation of the upper cervical spine.
A long-term (2-month) drop in BP (-27 mm Hg systolic, -13 mm Hg diastolic) after specific upper cervical adjustment of hypertensive patients deemed to be atlas-subluxated has been reported.  It is proposed here that such long-term BP changes may be due to a postadjustment moderating effect on global muscle tone. The upper cervical spine is associated with postural control, [16-18] and upper cervical adjustment had been noted to cause immediate reductions in postural distortion. [24-27] Muscle contraction causes increased need for blood flow, yet the pressure of contraction can completely close the intrinsic arteries. The intramuscular arteries become completely closed above a 30% maximal voluntary contraction  in back extensor muscles, this occurs above a 40% maximal voluntary contraction.  To supply the contracting or hypertonic muscle, BP must increase, which is the function of the pressor reflex. Manipulation that causes a decrease in muscle tone could reduce the pressor reflex and BP.
The pressor reflex involves neural receptors inside the muscle that respond to contraction and are responsible for a series of physiologic effects that act to increase BP, forcing blood through the contracted muscle. According to Rowell et al,  the idea that cardiovascular-respiratory responses to exercise originated from chemoreceptors in skeletal muscle originated in 1886. The term ergoreceptors was initially used to describe the intrinsic muscle afferents that are sensitive to mechanical and metabolic changes related to muscle work.  These muscle afferents include (1) mechanoreceptors that are sensitive to pressure and tension and send signals via myelinated group III fibers and (2) metaboreceptors that are sensitive to chemical substances, the signals transmitted by group IV nonmyelinated fibers. 
A high proportion of afferent fibers in the group III and IV range are now known to respond to chemical and mechanical stimuli, which suggests that free nerve endings may be able to provide information about nonnoxious events.  As Mitchell et al  remark, “These two categories [group III and IV mechanoreceptors and metaboreceptors and group III and IV pain signaling nociceptors] are likely to represent two poles of a continuum, with most of the group III and IV afferents lying somewhere in between.”
Muscle contraction (and stretch) immediately stimulates the intrinsic mechanoreceptors, causing an instant increase in cardiac sympathetic nerve activity and resulting in rapid increases in heart rate, left ventricular contractility, and cardiac output.  However, the mechanoreceptive group III muscle afferents have a rapid adapting property, and their discharges return to almost control level within seconds after the onset of contraction. [43, 44] As the metabolic products of contraction build up, the chemically stimulated group IV metaboreceptors become responsible for the sympathetically mediated physiologic changes.
The physiologic changes induced by the muscle mechanoreceptor and metaboreceptor afferents include all of the following: increased ventilation [40, 41]; increased heart rate [40, 41, 45]; increased sympathetic tone to the blood vessels serving the kidney [42, 46] and adrenal glands ; changes in vasomotor signal to noncontracting muscles and skin [41, 45, 47]; increases in glucose production, plasma concentration of glucose, adrenocorticotropic hormone, Met-enkephalin, and B-endorphin; and decreases in plasma insulin.  All of these effects act to increase BP [40, 49, 50] and increase the blood and nutrient flow though contracted muscle(s). The effect of the pressor reflex can be dramatic. An experiment in which the metabolic products of contraction were trapped in the relatively small flexor muscles of the little finger caused an overall increase in systolic BP of 70 mm Hg.  Outside the special conditions generated in the laboratory, however, the effects of the pressor reflex may be larger with the involvement of larger muscle groups [40, 43, 51] and fast-twitch muscle fibers. [36, 42]
Long-term/chronic increases in BP may come from renal sympathetic artery stimulation and vasoconstriction. Decreased blood flow to the kidneys causes the body to retain fluid; blood volume increases, cardiac output increases, and BP rises, forcing more blood through the kidney and the contracted muscle(s). The decrease in serum aldosterone noted in one study of manipulation and hypertension may be related to this mechanism.9
Changes in skin flow patterns have been noted as an effect of the pressor reflex. [41, 45, 52-54] The sympathetic stimulation associated with the pressor reflex involves complex interactions to control BP and skin blood flow through use of sudomotor and vasomotor stimulation and inhibition. Although the metaboreflex affects peripheral vasculature and may induce vasoconstriction and a rise in BP,  this vasoconstriction may not be manifest in skin blood flow. 
Skin blood flow pattern changes in response to muscle contraction in normothermia have been found to be under what is called central command–ie, the sympathetic centers in the brain [52, 53] or the muscle mechanoreceptor afferents.  In hyperthermic conditions, muscle metaboreceptor output seems to inhibit the active skin vasodilator system. 
If joint dysfunction causes a pressor reflex significant enough to involve changes in central command, abnormal skin thermal patterns may present because of sympathetic vasomotor activity. Such abnormal skin thermal patterns may be noted by means of thermography and other heat-sensing instrumentation. Although such altered cutaneous heat patterns could be indicative of joint dysfunction, they would not likely be segmentally related. Central command could alter sympathetic tone in the skin of the upper thoracic spine as a result of a pressor reflex from muscle contraction and joint dysfunction in the lumbopelvic spine.
Peer-reviewed literature on the use of thermography as an aid in determining chiropractic subluxation is limited [55-57]; discussion of theoretic physiologic models relating subluxation to thermographic changes even more so.  Some models postulate thermographic changes segmentally related to chiropractic subluxation ; other models postulate thermographic patterns that are not necessarily related to any segmental dysfunction, according to a written communication from members of the Chiropractic Institute of Thermography and Diplomats of the International Chiropractors Association College of Thermography. An explanation for the nonsegmental thermographic patterns associated with subluxation may be skin vascular blood flow changes due to pressor reflex.
Alterations of visceral physiology with manipulation
Nansel and Szlazak58 argued persuasively that sustained somatic sympathetic discharge to segmentally related viscera in putative joint dysfunction is not likely to occur, let alone cause frank visceral pathosis. On the other hand, the pressor reflex response to muscle contraction has been shown to involve sympathetic stimulation to the heart, [40, 41, 45] lungs, [40, 41] kidneys, [42, 46] adrenal glands,  muscles and skin, [41, 45, 47] and glucoregulatory system.  Elimination of putative joint dysfunction and moderating abnormal muscle contraction(s) may have positive effects, normalizing the physiology of these organs and hormonal regulatory systems. Although this line of thought is a logical extension of the argument for the involvement of a pressor reflex in joint dysfunction, it is speculative and needs study.
Palpation and vectored adjustment of subjects (n = 40) with putative upper cervical joint dysfunction diagnosed by postural distortions significantly lowered systolic BP both from pretreatment to posttreatment (P < .001) and in comparison with a similar resting control group (n = 40; P < .001). Another test in which subjects (n = 30) were used as their own controls also showed a significant decrease in systolic BP from resting to postadjustment values (P < .001). I propose that the sudden decrease in systolic BP noted in both of these tests was due to stimulation of cervicosympathetic reflexes or possibly to moderation of muscle tone and elimination of the effects of the pressor reflex. This study also found a greater decrease in systolic BP after adjustment in subject patients with increasing age. Associations between the effects of the pressor reflex and thermographic findings and the potential for alterations of visceral physiology in joint dysfunction have been discussed. Further studies involving (1) blinding, (2) testing for direct connections between joint dysfunction, muscle hypertonicity, and the pressor reflex, and (3) the possibility of long-term reduction in systolic BP, are recommended.