So, now that we have gone over in detail what happens when we have subluxations, or hypomobile (restricted) vertebral segments, lets review everything at once. Again there are 3 main contributors to subluxations: chemical, physical, and physiological. With all 3 there is abnormal muscular responses which eventually cause altered biomechanics. When the tissues around a segment are hypertonic, or tight, this restricts the motion of the joint itself, forming a subluxations.
There are 5 different types of changes that can happen when we have a hypomobile segment, 4 of which we discussed in detail. These changes are: biomechanical, connective tissue, vascular, neurological, and physiological. Biomechanical and connective tissue changes occur when there is cell degeneration due to hypomobility. Vascualar changes include venous stasis which then irritates the dorsal root ganglion (due to toxins in the venous blood), causing spontaneous discharge into the CNS that results in a pertetuated abnormal motor response. Neurological changes are mainly due to the decrease in mechanoreceptor (the ability to tell the brain where the body is in space) activity leading to an overall increase in nociceptor (noxious stimuli that may or may not be interpretted as pain) activity. Lastly there is physiological changes, which are all different depending on the tissue that is affected (ie. skin, adipose, ligaments, muscle, tendons, bone, and dura mater).
Biomechanical, connective tissue, vascular, and neurological changes all end up sending signals into the spinal cord. From here there are 3 routes that the signal may take. The signal may cross the spinal cord and ascend the spinal cord via the spinothalamic tract. Research has shown that about 90% of nociception is inhibited before it reaches the thalamus (which is where pain is interpreted in the brain). This means that only about 10% of nociception actually reaches the brain and is interpreted as painful.
The signal may also go to the lateral horn (intermediolateral cell column), which then synapses (sends another signal) to the sympathetic chain. There are many different signals that can be sent out from this point. An example is when the sympathetic chain synapses on the splanchnic nerve which then activates the chromaffin cells of the adrenal medualla creating an increase in the epinephrine production.
Lastly the signals coming into the spinal cord may also travel to the anterior horn and synapse, further perpetuatig immobilization and myospasm. Thus leading to more hypomobility, decreased mechanoreceptor activity, and cell damage (continuing the whole cycle over again).
Hopefully this short summary gives you an idea of how everything fits together. I understand that this is an incredibly complex conversation, which is why it can be hard to articulate exactly why it is so important to be adjusted regularly. I like to tell my patients simply that with adjustments I am able make a joint move properly and thus facilitate feeling and functioning better. If you have ever been adjusted you know how amazing if feels, and now after our week long discussions you know why you don't feel so great when you aren't adjusted.
There are 5 different types of changes that can happen when we have a hypomobile segment, 4 of which we discussed in detail. These changes are: biomechanical, connective tissue, vascular, neurological, and physiological. Biomechanical and connective tissue changes occur when there is cell degeneration due to hypomobility. Vascualar changes include venous stasis which then irritates the dorsal root ganglion (due to toxins in the venous blood), causing spontaneous discharge into the CNS that results in a pertetuated abnormal motor response. Neurological changes are mainly due to the decrease in mechanoreceptor (the ability to tell the brain where the body is in space) activity leading to an overall increase in nociceptor (noxious stimuli that may or may not be interpretted as pain) activity. Lastly there is physiological changes, which are all different depending on the tissue that is affected (ie. skin, adipose, ligaments, muscle, tendons, bone, and dura mater).
Biomechanical, connective tissue, vascular, and neurological changes all end up sending signals into the spinal cord. From here there are 3 routes that the signal may take. The signal may cross the spinal cord and ascend the spinal cord via the spinothalamic tract. Research has shown that about 90% of nociception is inhibited before it reaches the thalamus (which is where pain is interpreted in the brain). This means that only about 10% of nociception actually reaches the brain and is interpreted as painful.
The signal may also go to the lateral horn (intermediolateral cell column), which then synapses (sends another signal) to the sympathetic chain. There are many different signals that can be sent out from this point. An example is when the sympathetic chain synapses on the splanchnic nerve which then activates the chromaffin cells of the adrenal medualla creating an increase in the epinephrine production.
Lastly the signals coming into the spinal cord may also travel to the anterior horn and synapse, further perpetuatig immobilization and myospasm. Thus leading to more hypomobility, decreased mechanoreceptor activity, and cell damage (continuing the whole cycle over again).
Hopefully this short summary gives you an idea of how everything fits together. I understand that this is an incredibly complex conversation, which is why it can be hard to articulate exactly why it is so important to be adjusted regularly. I like to tell my patients simply that with adjustments I am able make a joint move properly and thus facilitate feeling and functioning better. If you have ever been adjusted you know how amazing if feels, and now after our week long discussions you know why you don't feel so great when you aren't adjusted.
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