This section describes the cause and impact of the problem addressed by the invention described in the subsequent section.
PROBLEM CAUSALITY CHAIN
Deeply innervated within the tissues, where pain is present, are nociceptive C-fibers. These fibers, which are sensitive to mechanical noxious stimulus, are subjected to high tensile loads within a less that optimal postural position.
This mechanical noxious stimulus causes stretching and depolarization of the unmyelinated C-fiber.
Once depolarized, mechanically gated ion channels are activated.
Once activated, an action potential is generated via neurotransmission and neuromodulation of pronociceptive irritants such as neuropeptide substance P or glutamate.
This action potential, and the action potentials of all corresponding tissues crosses the peripheral system to innervate with the central nervous system.
Upon reaching the central nervous system, the action potential depolarizes the presynaptic terminals I and II of the slow, thin C-fibers.
Once depolarized, the pronociceptive irritants are released into the synaptic cleft.
These substances then all activate their corresponding post-synaptic receptors.
Activation of these post-synaptic receptors results in an influx of ions.
These ions then depolarize second order neurons.
Once second order neurons are depolarized, an action potential takes the ascending pathway through the anterolateral tract to the thalamus.
When the thalamus receives the neurotransmission of pain, various automatic responses occur. One is the activation of the substance P and glutamate neuroreceptors in the hypothalamus, amygdala, and periaqueductal grey that allow for pain regulation. The nucleus raphes magnus projects serotonin to the substantia gelatinosa to regulate input from the spinothalamic tract.
PROBLEM IMPACT SUMMARY
As poor posture becomes a chronic behavior, the noxious stimulus of mechanical tension will eventually fatigue the body's natural analgesic response and weaken. The lack of serotonin as an active transmitter will result in dull, aching, and diffuse pain.
This pain, caused by the neurotransmission and neuromodulation of the pronociceptive irritants, is experienced throughout all corresponding nociceptors, silent nociceptors, and interneurons, as long as they are held within this noxious mechanical tension.
Nociceptors innervate skin, periosteum, muscle, tendon, and ligament. It is when these tissues are held in this hypotonic posture, all nociceptors within them will continue with neurotransmission of nonspecific, diffused pain that is difficult to pinpoint.
PROOF OF INVENTION
This section describes the reasoning for and mechanisms by which the invention addresses the aforementioned problem.
INVENTION MECHANISM OVERVIEW
Integrated Biomechanic Technique relieves noxious stimulus via scientifically justified orthopedic massage protocols and stimulates the body's own healing responses, through scientifically justified muscular contraction via corrective exercises.
Noxious stimulus is relieved by releasing tension in the antagonistic tissues. This is achieved by performance of designated orthopedic massage protocols by a certified practitioner.
Upon relief of noxious stimulus there is new proprioceptive feedback. This new information transmits through the muscle spindle sensory organs of all of the corresponding tissue that were released. This provides new neurotransmission through larger, faster sensory fibers of Ia muscle spindle or Ib golgi tendon organs. This new position also halts transmission of pronociceptive irritants via of noxious mechanical tension because their tension is relieved.
Once the noxious stimulus is relieved, corrective exercises are introduced to initiate muscle contraction.
Depolarization occurs with transmission at the neuromuscular junction. An action potential is sent from the motor neuron utilizing saltatory conduction down to the myelinated axon to the terminal bouton.
Once reaching the terminal bouton, this action potential causes a calcium ion influx into the synaptic terminal.
This calcium ion influx causes the synaptic vesicles containing the neurotransmitter acetylcholine to fuse with the plasma membrane.
Exocytosis mechanisms release acetylcholine into the synaptic cleft between the motor neuron terminal and neuromuscular junction of the skeletal muscle fiber.
Acetylcholine diffuses across the synapse, then binds to and activates nicotine acetylcholine receptors at the neuromuscular junction.
Activation of the nicotine receptors opens the intrinsic sodium/potassium channel and activates the end plate potential.
These voltage gated channels experience a wave of ion movement that creates the action potential that spreads from the motor end plate in all directions, initiating muscle contraction. At this point, the nervous system is experiencing stimulation of the large, very fast motor neuron fibers thus gaiting the dull aching pain from the C-fibers at the second order neurons with acetylcholine, instead of substance P or glutamate.
Although mechanisms for defining exactly what happens during all phases of muscle contraction are theoretical, we do know for certain that, by exposing muscular tissue to increased load and increasing amounts of tension will temporarily damage the myofibrils at a microscopic level.
Microtears in the tissue will automatically initiate the body's natural inflammatory healing response, to repair and strengthen the "damaged" tissue. This will increase resting muscular tonus in previously aching, hypotonic muscles and provide a stronger ability to hold ideal posture.
During the initial phases of the IBT program, clients may present with what is known as delayed onset muscle soreness, due to the new stimulus. This is a temporary soreness that is relieved by using specified techniques for soreness indicated within the present invention.
INVENTION OUTCOME SUMMARY
By conservatively and progressively implementing the present invention, we are able to restore optimal muscular tonus and neural transmission.