They still haven't fully proven the theory that atlas realignment decompresses the RVLM...the latest study released this year came to the conclusion that "gee, in the next study we should probably enroll patients with actual hypertension/rvlm compression issues." Okay, that was mean. But still!!
Here are some 2007 studies that indicate but don't prove there may be a relationship between realignment and RVLM decompression.http://www.nature.com/jhh/journal/v21/n ... 2133a.html
Minor misalignment of the Atlas vertebra can potentially injure, impair, compress and/or compromise brainstem neural pathways. The relationship between hypertension and presence of circulatory abnormalities in the area around the Atlas vertebra and posterior fossa of the brain has been known for more than 40 years.3, 4, 5 Studies by Jannetta et al.6 note arterial compression of the left lateral medulla oblongata by looping arteries of the base of the brain in 51 of 53 hypertensive patients who underwent left retromastoid craniectomy and microvascular decompression for unrelated cranial nerve dysfunctions. Such compression was not present in normotensive patients. Treatment by vascular decompression of the medulla was performed in 42 of the 53 patients and amelioration of hypertension was noted in 76%.6 Moreover, studies to clarify the mechanism by which decompression of the left rostral ventrolateral medulla relieves neurogenic hypertension are summarized in a review.7 It is clear from these studies that a sub-population of hypertensive patients improved their BP after microvascular decompression.
Changes in the anatomical position of the Atlas vertebra and resultant changes in the circulation of the vertebral artery lend itself to worsening of hypertension. Recent studies by Akimura et al.8 using magnetic resonance (MR) imaging examined hypertensive patients and compared them to controls, evaluating the relationships between the upper ventrolateral medulla and vertebral arteries and branches. They noted compression in 90.6% of 32 hypertensive cases, this was in contrast to controls and those with secondary hypertension who failed to demonstrate a significant incidence of compression. Furthermore, two other studies using MR imaging techniques also demonstrated a significant association between compression of the vertebral artery and changes in the posterior fossa of hypertensive but not normotensive individuals.9, 10 Thus, alterations in Atlas anatomy can generate changes in the vertebral circulation that may be associated with elevated levels of BP.
The findings of this pilot study represent the first demonstration of a sustained BP lowering effect associated with a procedure to correct the alignment of the Atlas vertebra. The improvement in BP following the correction of Atlas misalignment is similar to that seen by giving two different antihypertensive agents simultaneously.11, 12 Moreover, this reduction in BP persisted at 8 weeks and was not associated with pain or pain relief or any other symptom that could be associated with a rise in BP.http://www.nature.com/jhh/journal/v21/n ... 2134a.html
Other studies support the notion that changes in the cerebral circulation that is related to the position of the Atlas vertebra can affect BP. Coffee et al.9 reviewed MR images and demonstrated a significant association between pulsatile arterial compression of the ventrolateral medulla and presence of hypertension. They concluded that subjects with hypertension should have an evaluation of their posterior fossa for evidence of anatomic abnormalities.9 In fact, data linking changes in Atlas anatomy and posterior fossa circulatory changes associated with hypertension date back more than 40 years and are reviewed by Reis.4
The notion that the central nervous system participates at the development, maintenance and progression of the essential hypertensive state dates back to almost a century ago and throughout the years it has received a consistent number of experimental and clinical supports. These include the evidence that central neural factors participate at the short- and long-term blood pressure control and that abnormalities in neurogenic modulation of the cardiovascular function characterize the early as well as the more established forms of the essential hypertensive state.1 A further support to the so-called 'neurogenic hypothesis' of hypertension comes from the evidence of a close link between some hypertensive states and neurovascular compression of the rostral ventrolateral medulla, that is, an area of the central nervous system with an important efferent pathway of the sympathetic nervous system.2, 3, 4, 5 This association is strengthened by the evidence that in different experimental animal models electrical, chemical or mechanical stimulation of the ventricular medulla triggers a transient pressor response.6, 7 It is also strengthened by the finding that in subgroups of patients with severe and/or resistant hypertension microsurgical decompression at the level of the rostral ventrolateral medulla substantially improves blood pressure control, leading to a long-term blood pressure normalization in a not negligible number of patients.3, 8, 9, 10 The favourable haemodynamic outcome of the surgical intervention is likely to be triggered by a sympathetic deactivation, as several indirect and/or direct markers of adrenergic neural drive, such as plasma and urinary noradrenaline, low-frequency/high-frequency spectral power ratio as well as efferent postganglionic sympathetic nerve firing rate, have all shown a consistent and rather homogeneous reduction of adrenergic cardiovascular drive following surgical decompression.10, 11
In the present issue of the Journal of Human Hypertension, Bakris et al.12 add a new piece of information to the above-mentioned findings, by providing evidence on the favourable blood pressure lowering effects of chiropractic procedures capable to correct misalignment of the Atlas vertebra and thus to induce medullary vascular decompression. According to a double-blind, placebo-controlled study design, hypertensive patients with documented evidence of vertebral misalignment were randomized either to a chiropractic vertebral realignment procedure or to a sham intervention. The primary efficacy end point of the study was represented by the effects of the approach on sphygmomanometric systolic and diastolic blood pressure values, which were reduced at the end of the 8-week follow-up period by about 14 and 8 mm Hg, respectively (placebo-corrected values).12
The intriguing findings provided by Bakris et al. in this pilot study arise a number of questions that hopefully will be matter of future investigations. First, how are satisfactorily documented in the present study are the blood pressure lowering effects of the chiropractic procedure? Second, do the consistent short-term blood pressure lowering effects of the intervention persist over the long-term period? Third, does the lack of any effect of the intervention on heart rate really rule out any participation of sympathetic neural mechanisms at the blood pressure reduction? Fourth, is the procedure associated with additional favourable cardiovascular effects, such as end organ damage regression? Finally, do the results of the present study imply that a misalignment of the Atlas vertebra represents a risk factor for development of hypertension and that the chiropractic procedure stands as a new antihypertensive therapeutic approach?
A study limitation is represented by the fact that the assessment of the blood pressure lowering effects of the intervention was based on clinical blood pressure measurements, which in a trial testing the effectiveness of a hypertensive intervention is known to encompass various limitations.13 An important one is the lack of information on the ability of the approach to lower blood pressure in daily-life conditions, that is, during the 24-h period. A further 'intrinsic weakness' of the study refers to the lack of information on the blood pressure lowering effects of the chiropractic intervention in the long-term period (months and years), as it has been carried out for the evaluation of the antihypertensive effects of surgical microvascular decompression.10 As far as heart rate as marker of adrenergic function is concerned, the lack of any change of this variable following the intervention does not necessarily imply that the chiropractic procedure has no sympatholytic effects. This is because heart rate is a poor and insensitive marker of sympathetic function, poorly correlating with more robust humoral or neurophysiological indices of adrenergic cardiovascular drive, such as plasma noradrenaline or muscle sympathetic nerve firing rate.14, 15 Other relationships to adrenergic function, such as age, heredity, concomitant drug therapies and so on, will also need to be considered in any study.16, 17, 18
In conclusion, the study by Bakris et al. provides new interesting information on the favourable blood pressure lowering effects of microvascular decompression caused by chiropractic procedure. Before recommending this therapeutic strategy in the current clinical practice, however, it seems reasonable to wait for the results of large-scale clinical trials aimed at defining the long-term effects of the intention on clinic and ambulatory blood pressure as well as on some surrogate end points, such as cardiac and vascular target organ damage.