Thursday, 8 May 2014

Why is Manual Osteopathy So Effective?



How Does Manual Osteopathy Help Patients?   

Osteopathic research has shown that there are a few known mechanisms affecting individuals who receive osteopathic manual treatment. Here we explain eight known mechanisms.

First mechanism: OMT increases joint mobility by producing a barrage of impulses in muscle spindle afferents and smaller-diameter afferents ultimately silencing facilitated γ (gamma) motoneurons as proposed by Korr. This theory is supported by several recent studies by the Pickar lab and by findings that low back pain patients have altered proprioceptive input from muscle spindles. Recent work has also shown that that OMT modifies the discharge of Group I and II afferents. This has been accomplished by recording single-unit activity in muscle spindle and Golgi tendon organ afferents in an animal model during manipulation.

A second mechanism is that OMT, by mechanically opening the intravertebral foramina (IVF), decreases pressure on the dorsal roots. Substantial evidence shows that the dorsal nerve roots and dorsal root ganglia are susceptible to the effects of mechanical compression. Compressive loads as low as 10 mg applied to dorsal roots increase the discharge of Group I, II, III and IV afferents. This compression can also alter non--impulse-based mechanisms (eg, axoplasmic transport) and cause edema and hemorrhage in the dorsal root. OMT mechanically decreases the pressure in the IVF by gapping the facet joints and opening the IVF. For instance, the synovial space of the lumbar facet joints increases by about 0.7 mm in individuals receiving OMT. This doesn't seem like much, but as with any therapy there is usually a course of care involved. Even in moderate stenosis patients treated by manual osteopaths typically see significant pain reduction following a period of 1-2 weeks of treatment.

A third mechanism is based on findings that persistent alterations in normal sensory input resulting from an injury can increases the excitability of neuronal circuits in the spinal cord. Osteopathic OMT works by applying non-noxious mechanical inputs to these circuits. This involves mechanisms similar to the pain-gate theory proposed by Melzack and Wall wherein activation of A-α and A-β fibers can reduce chronic pain and increase pain threshold levels. This is supported by studies where OMT of the lumbar region decreases central pain processing as measured via pin-prick tests. Additional studies have shown a reduction in central pain sensitivity after OMT using graded pressure and noxious cutaneous electrical stimulation.

A fourth mechanism involves β-endorphin mechanisms. Studies have shown increases in beta-endorphin levels after OMT but not after control interventions.

Fifth mechanism: Substantial evidence also shows that OMT activates paraspinal muscle reflexes and alters motoneuron excitability. These effects are still being studied and appear to differ depending on whether performed on patients in pain or pain-free subjects.

A sixth mechanism involves inhibition of somatosomatic reflexes by alterations in muscle spindle input produced by OMT. It is thought that OMT may normalize spindle biomechanics and improve muscle spindle discharge.

In humans, osteopathic manual treatment can decrease heart rate and blood pressure while increasing vagal afferent activity as measured by heart-rate variability. OMT in rats have been shown to produce an inhibitory effect on the cardiovascular excitatory response and reduce both blood pressure and heart rate. 

Osteopathic soft tissue therapy have been shown to impact behavioral manifestations associated with chronic activation of the HPA axis such as anxiety and depression, while decreasing plasma, urinary, and salivary cortisol and urinary corticotropin releasing factor-like immunoreactivity (CRF-LI). 

Manual stimulation in rats has been shown to significantly increase glucocorticoid receptor gene expression which enhanced negative feedback inhibition of HPA activity and reduced post-stress secretion of ACTH and glucocorticoid.

 




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