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Chiropractic Journal of Australia : CJA March 2012
28 Chiropractic Journal of Australia Volume 42 Number 1 March 2012 neurotransmitters (leading to blood vessel dilatation) have been considered, but have not been found to be essential for the vasodepressor response.22 In addition, a combination of peripheral refex (affecting peripheral vascular tone), and a central refex (affecting cerebral autoregulation) has been investigated.29,30 Other central mechanisms leading to the sympathetically induced blood vessel dilation relate to changes in autonomic outfow originating in the brain stem22 or cortico-hypothalamic centres.24 Dietz states, in relation to syncope, “The nucleus tractus solitarius (NTS) is the site where afferent fbers arising from arterial baroreceptors, cardiopulmonary receptors, and other visceral afferents make the frst synapse and is of key importance in integrating the autonomic control of the cardiovascular system.” 22 In summary, the cause of neurogenic syncope is currently unknown, but is believed to involve relative increases in parasympathetic activity and/or decrease in sympathetic nerve activity. Research and debate continues. Spinal dysfunction and autonomic nerves. A comprehensive discussion on the relationship between the spine and the autonomic nervous system function (ANS) is beyond the scope of this case report. There is a growing body of evidence linking function of the body and the ANS.31 In particular, Sato, and his team of researchers have been investigating since the 1960’s the links between somatic structures (skin, joints, muscles, deep tissues), and the ANS, and Sato’s 300 plus page review is recommended for those interested.32 Some points of relevance from Sato’s work include: (i) Control of organ function occurs through activity of the CNS or through refexes from the peripheral sensory receptors (visceral, somatic and specifc cranial refexes); (ii) Sympathetic nervous system response is mediated at segmental levels in the spinal cord, and at supraspinal levels. Larger sympathetic discharge was induced by stimulation of somatic afferents at adjacent levels in the spinal cord; (iii) The contribution of supraspinal control and segmental spinal refex control varies depending on the organ system involved – in the cardiovascular system there appears to be a dominance of supraspinal refex infuences; (iv) Somatic afferents are mediated by the neurons in the rostral ventrolateral medulla (RVLM).32 Budgell in 2000, reviewed the current literature regarding the effects of somatic stimulation on ANS activity, concluding that there is a “neurophysiological rationale for the concept that aberrant stimulation of spinal or paraspinal structures may lead to segmentally organized refex responses of the autonomic nervous system, which in turn may alter visceral function.” 33 More recent research continues to elucidate the mechanisms involved in somato-autonomic function and its clinical extrapolation.34-37 In addition to these studies, some have looked at specifc effect of upper cervical function on blood pressure or heart rate. Fujimoto et al studied the effect of innocuous mechanical stimuli to the neck, and found “small and sometimes statistically signifcant decreases in heart rate, systolic pressure and diastolic pressure.” 38 A study in 2001 found decreased blood pressure after upper cervical (atlas) adjustments in adult patients.39 In 2002, Koch et al, studied the heart rate responses to mechanical stimuli to the upper cervical region in 695 infants aged 1-12 months, and found that 40.1% of infants had a short term heart rate decrease by 15-83%.40 Another case study, in an infant who died of SIDS, looked at heart rate variability and postural hypotension as a measure of autonomic function.41 There is growing evidence that somatic structures can infuence autonomic nervous system function. Managing the Paediatric Patient with Syncope Some cases of paediatric syncope will be due to pathological causes, requiring referral for medical evaluation. The chiropractor must be able to evaluate the child and make management decisions regarding referral for further tests or a trial of care. The following suggestions may infuence decision making. Determine if the condition is actually syncope. Dizziness, vertigo and drop attacks do not result in loss of consciousness.4 2 Seizures may be more diffcult to differentiate. Distinguishing features include prodomal (e.g. aura) or post-ictal symptoms (e.g. disorientation), and rhythmic movements throughout the event (tonic, clonic or myclonic movements).42 Next, consider the common differential diagnosis options for a child with episodes of loss of consciousness. A thorough history and examination should follow. Cardiac pathology causing syncope, whilst not common, is a potentially fatal condition. The history should seek to establish any cardiovascular signs/symptoms, such as cyanosis, tachypnea, dyspnea/shortness of breath, chest retractions, nasal faring, and wheezing (“heart failure”), sweating, and irritability. Syncope during exercise fags a potentially fatal condition.4 A family history of cardiac disease or congenital heart disease (CHD) should be sought. Examination of the cardiovascular system should include blood pressure, heart rate, auscultation (for murmurs), palpation for ventricular hypertrophy, palpation for bounding pulses and weak lower extremity pulses, palpation for hepatomegaly and peripheral edema, and observation of the skin for cyanosis. Red fags in the paediatric patient with syncope are listed in the Table 2. PAEDIATRIC SYNCOPE MANAGEMENT STEWART Table 2 RED FLAGS IN THE PAEDIATRIC PATIENT WITH SYNCOPE 3,6 exertional onset - chest pain - dyspnea - low back pain - palpitations, - severe headache - focal neurologic defcits - diplopia, ataxia, or dysarthria prior to the syncopal event. - family history of deafness - family history of unexpected death
CJA June 2012