Measureable changes in the neuro-endocrinal mechanism following spinal manipulation
Introduction
Spinal manipulation (SM) is a specific ‘hands-on’ clinical approach used by a variety of health practitioners such as the physiotherapists, chiropractors and osteopaths to treat musculo-skeletal pain [1]. Initial theories to explain the physiological effects of SM centred on the biomechanical paradigm [2] together with the gate control theory [3]. However an increasing number of studies show that the effects of SM are beyond biomechanical changes only [4]. This has led to the proposal of various neurophysiological theories to explain the effects of SM [5], [6], [7]. According to the neurophysiological theory, SM has the potential to initiate a cascade of neurophysiological responses in the peripheral and central nervous system [5].
Inflammation is a normal response to disturbed homeostasis caused by infection, injury or trauma and is associated with the production of numerous pro-inflammatory and immune-regulatory cytokines and neurotransmitters [8]. The production of such mediators has been shown to increase in patients with lower back pain [9]. Pain in turn triggers the activation of various protective body reactions, mediated by the central nervous system (CNS). The control of inflammation and thereby the immune system by the CNS implies that the CNS can assist tissue healing or trigger the opposite [10].
There is a functional cross-talk or reciprocal communication between the CNS and the immune system [11]. The afferent communication occurs via primary afferent nociceptive neurons and by cytokines secreted by immune cells in the inflamed tissues. The efferent communication occurs via the peripheral ANS (mainly sympathetic nervous system (SNS)) and neuroendocrine system (example: hypothalamic–pituitary–adrenal (HPA) axis) [11]. Adrenal glucocorticoids, the end product of the HPA axis have long been known for their anti-inflammatory and immunosuppressive effects [12]. Evidence also indicates that catecholamine’s, the end products of the SNS, modulate several immune parameters [11], [12]. In summary, both acute and chronic inflammation is modulated by the SNS and the HPA axis.
The modulatory effect of inflammation by the SNS may be of special interest for manual therapists. This is because at least part of the effects observed following SM may be due to change in the activity of the SNS. Pioneering works of Irvin M Korr have not only demonstrated the role of SNS as a mediator between somatic and supportive process, but also how sustained sympathetic tone plays a significant role in disease. Through various experiments, Korr further showed changes in cutaneous patterns of sympathetic activity in clinical abnormalities of the musculoskeletal system [13], [14], [15], [16], [17], [18]. Therefore SNS changes following SM may have important implications. However, depending on the segment manipulated these effects could vary. Specifically, cervical manipulation elicits a parasympathetic response and a thoracic/lumbar SM elicits a sympathetic response [19].
SM may also have an effect on the HPA axis [20]. Early works of Andrew Taylor Still (founder of osteopathic medicine) and Daniel Palmer (founder of chiropractic) have debated the potential role of SM on endocrinal mechanisms and thereby various immune disorders [21], [22]. Although the influence of SM on the transmission and transduction of pain stimulus has been well understood [5], [23]; the mechanism through which SM influences tissue healing through reduction of inflammatory response is still unclear. Therefore a hypothesis is proposed that takes into account the autonomic effects following SM and the sequential effect it may have on tissue healing via co-activation of endocrine systems.
Section snippets
The hypothesis
Null hypothesis: A thoracic SM will not result in measureable changes in the neuro-endocrinal system response.
Alternate hypothesis: A thoracic SM will result in measureable changes in the neuro-endocrinal system response.
Evaluation of the hypothesis
The hypothesis is proposed based on the following. Anatomically the ganglion of the sympathetic nervous system lies just anterior to the costovertebral joint of the thoracic spine. Thoracic SM may therefore result in direct or indirect excitation of preganglionic sympathetic cells in the thoracolumbar spine. Further, the transduction of mechanical input (SM) excites various mechanoreceptors. The volley of innocuous stimuli then travels up from the dorsal horn to several regions of the brain
Discussion
We proposed that a SM of the thoracic spine in humans will be associated with a neuro-endocrinal response. Substantial evidence has demonstrated the neurophysiological effects of SM [7], [34], [55], [56], with a prominent role given to the SNS [5], [28]. Recent systematic reviews further confirm the short-term sympatheto-excitatory effects associated with SM [29], [57]. These SNS changes following SM may also be associated with changes in supraspinal mechanisms that control pain. Supraspinal
Future implications and conclusion
The ANS and the HPA axis are commonly involved in various chronic pain syndromes. These clinical disorders include chronic fatigue syndrome [61], fibromyalgia, auto-immune diseases [62]; diabetes [63], gastro-intestinal disorders [64]; cardiovascular problems [65]; and asthma [66]. An important strategy in managing these syndromes is to identify effective treatments that target multiple key mechanisms involved in pain [67]. Therefore the neuro-endocrinal mechanisms could be such targets of
Conflict of interest
None.
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