by clicking the arrows at the side of the page, or by using the toolbar.
by clicking anywhere on the page.
by dragging the page around when zoomed in.
by clicking anywhere on the page when zoomed in.
web sites or send emails by clicking on hyperlinks.
Email this page to a friend
Search this issue
Index - jump to page or section
Archive - view past issues
Chiropractic Journal of Australia : CJA March 2012
27 Chiropractic Journal of Australia Volume 42 Number 1 March 2012 On examination there was decreased left lateral fexion of the upper cervical spine, with normal C2-7 flexion, normal cervical rotation, and normal occipital motion. The scapulohumeral refex was positive on the left, indicating irritation of upper cervical nerves.8 These fndings are consistent with C1 (atlas) subluxation, with the listing AIL. Subluxation listing protocols have been described elsewhere .9-12 Thoracic, lumbar, sacral, pelvic spine and extremity function were all unremarkable. Upper extremity and lower extremity muscle stretch refexes were graded +3 (normal). The eye examination was unremarkable. Further examination was limited due to patient distress. The examination fndings relating to the atlas subluxation as well as the possible neurological and physiological effects and the method of correction were explained to the mother. Verbal consent to proceed with treatment was obtained. A specifc correction (adjustment) to the atlas subluxation, using the listing C1 AIL was performed, in the seated position, on the mother’s lap, consistent with the Gonstead method of application. No cavitation occurred, and the minimum force to obtain a therapeutic outcome was used. No other treatment was performed. MC was reviewed after 4 days, and at this time the child had not had another episode -- this had been the longest time between episodes since the original onset. The atlas subluxation was present and the associated examination fndings were less severe. The atlas was again adjusted with a further review appointment made for three days. At this visit (3rd visit), the examination fndings consistent with an atlas subluxation were no longer present, and there had been no further episodes. At review one week later (visit 4), examination fndings consistent with an atlas subluxation were again absent, and no further episodes had occurred. MC was rescheduled for a review in 3 weeks. At this visit there had been one episode of LOC which lasted less than one minute, with a recovery period of 2-3 minutes. There had been no apparent trigger such as infection or trauma. On re-examination the examination fndings consistent with the atlas subluxation pattern were present, and the atlas was adjusted. At a review in one week there had been no syncopic episodes, and atlas function was normal. During the following three months one more episode was reported, occurring after rough play with a sibling. LOC occurred lasted 30-40 seconds. DISCUSSION This report is the frst case described in the literature describing chiropractic care being associated with signifcant improvement of syncope in a child. Literature review revealed there has been one case study reporting improvements in a 25 year old female with cervalgia, hypotension and syncope after receiving upper cervical adjustments.13 Other studies have focused on syncopic events as a result of upper cervical examination and treatment14 and the presentation of syncopal events related to acute low back pain (LBP) in adults.15 Another study reported on syncope provoked by head movements.16 The frst consideration is whether the syncope cleared due to the intervention or due to natural history. The natural history (i.e. the chances that the episodes will stop on their own over time) of syncope is dependant on the number of previous episodes. The most important predictor of future episodes of syncope is the number of preceding syncope spells.17-20 The data suggests that those with multiple syncopic events are likely to have continued syncopic events. The child in this case report was having 2-8 episodes per day for periods of up to fve days, with a maximum episode free period of 3 days, over 6 months. It could be argued that the decreased frequency of episodes was due to natural history, however this is unlikely, as the episodes ceased abruptly after the frst visit (versus a more gradual reduction in events), and the episodes changed in their pattern from multiple episodes per day for multiple days, to single isolated episodes separated by 41 days, then 42 days. In addition, the one relapse which occurred at day 41 after the frst visit was associated with positive examination fndings for the same atlas subluxation pattern. It is possible that minor trauma was associated with re-occurrence of the atlas subluxation. This type of re-occurrence of spinal dysfunction is felt to be more likely in the early period of corrective care (i.e. the frst 6 weeks), possibly due to reduced articular ligament integrity and increased articular instability. The re-correction at this time led to a further syncope episode free period of approximately 42 days followed by another episode, triggered by mild trauma during play. Possible mechanisms leading to resolution in this case A detailed explanation of the underlying mechanisms possibly responsible for the improvement in this case is beyond the scope of this case report; however some possible mechanisms will be presented. Further research will need to be conducted on a larger group of patients. The concept of a triggering autonomic stress has been postulated as a possible mechanism in syncope.21 One possible explanation is that in some cases of syncope an upper cervical subluxation irritates brain stem structures, particularly the cardiovascular centre, leading to stimulation of vagal-excitatory nerves or sympatho-inhibitory nerves. The mechanisms causing vasovagal syncope are yet to be proven. Initial theories looked at increased vagal activity, but this has been shown to be unlikely as a primary response due to (i) atropine medications, or pacing, whilst blocking vagal activity, does not prevent the hypotension22 and (ii) denervation of vagal afferents does not prevent the syncopic response.23 Other studies have found the parasympathetic nervous system (PNS) to have a role, with the PNS implicated in pre-syncope (leading to bradycardia),24 and simultaneous involvement of both systems (bradycardia and peripheral arteriolar dilatation).25 However, there is a general agreement that the incidence of purely vagal involvement in vaso-vagal syncope is not high, and that sympathetic nervous system withdrawal is most important in the vasodepressor response.23, 24, 26-28 Despite this, the exact neural mechanism involved in the sympathetic nervous system withdrawal remains elusive. Theories regarding the release of nitric oxide and epinephrine PAEDIATRIC SYNCOPE MANAGEMENT STEWART
CJA June 2012