By Vincent De Bono, DC CSCS
The ability to perform a smooth and coordinated body movement is accomplished through an eloquent feedback loop based through the muscle spindle fibers. Injuries to the musculo-skeletal system, particularly injuries to joints, can distribute this feedback loop leading to dysfunctional movement patterns and muscle weakness through inhibition.
THE aLPHA-GAMMA FEEDBACK LOOP
First, a quick review of the alpha-gamma feedback loop in the function of muscle spindle fibers. There are two main types of fibers within the muscle, extrafusal fibers which are the fibers we commonly think of when we view a cross-section of skeletal muscles. They make up the bulk of the muscle fibers and generate the force and strength during a muscle contraction. The extrafusal fibers are innervated by alpha motor neurons when these neurons fire the muscle contracts.
Running parallel to the extrafusal fibers are the intrafusal fibers, muscle spindles, which are highly specialized and play a primarily sensory role. The intrafusal fibers, muscle spindles, respond primarily to stretch, as the intrafusal fibers are lengthened they will cause a contraction of the extrafusal fibers to shorten the muscle. As an example, picking up a heavy load to perform a bicep curl will initially result in a sudden lengthening as the weight is picked up, the muscle spindle fibers quickly react to overcome this load and contract the extrafusal fibers to shorten the muscle, thereby lifting the weight. However, as the extrafusal fibers shorten the muscle spindle would become slack and any sensory feedback would be lost (remember these fibers respond to stretch). To prevent this the intrafusal fibers (muscle spindles) are contractile and innervated by gamma motor fibers.
It is the co-activation of alpha motor neurons to shorten the extrafusal fibers and gamma motor neurons to shorten the intrafusal fibers (muscle spindles) that allow for sustained feedback throughout the shortening phase of muscle contraction. One other critical component of this loop is that the alpha-motor neuron pool within the muscle also receive direct sensory information from 1a fibers from the muscle spindle and that excitatory input from Ia afferents is necessary to achieve full muscle activation.
HOW DOES THIS EFFECT CLINICAL PRACTICE?
What does this all mean in terms of clinical practice? Essentially, an injury or pathology to a joint may result in weakness and inhibition of the muscles surrounding that joint due to neurological impairment of the 1a fibers. As an example, osteoarthritis of the knee causes an impairment in normal Ia afferent feedback (termed γ-loop dysfunction) that limits quadriceps α-motoneuron firing.
It is thought that γ-loop dysfunction is caused by a loss of sensory output from damaged mechanoreceptors within the arthritic knee joint. This result in neurological inhibition of the quadriceps leading to weakness and eventually atrophy. In physical medicine practices joint injuries and pathologies, such as osteoarthritis, are common presentations and rehabilitation strategies that do not address the neurological inhibition from γ-loop dysfunction may not be effective in attaining a complete and lasting outcome.
rehabilitation strategies
This is where ARP Neuro becomes a critical component in the rehabilitation strategies to arthritic or injured joints. The stimulus delivered by the ARP Neuro Rx-100 is generated through a resistance-capacitance (RC) circuit which creates a smoother wave form due to the capacitance aspect of the circuit having the capability to store energy and slowly discharge this energy between cycles (think of the light on a computer continuing to glow for a few seconds after you shut it off, this represent the capacitors within the computer discharging there stored charge).
Interestingly, neurons act as a biological RC circuit since the neuron has the capability of storing charges and slowly releasing this charge as the stimulus subsides, in other words the transmission of an impulse does not abruptly end, the capacitance aspect of the neuron permits a slow decrease in the transmission (again, think of the glowing light down computer). The resistance aspect of the RC circuit model in a neuron is largely controlled by the amount of ion channels that open during transmission of an impulse, the more ion channels that open the less resistance and in theory the greater conductance of the nerve.
Getting back to the neurological inhibition (γ-loop dysfunction), the dysfunction or inhibition of the 1a fibers may be due to an increased resistance of these fibers due to fewer ion channels opening during impulse transmission. With ARP Neuro sending an impulse in a waveform that is naturally generated by neurons (think RC circuit) but at a much higher rate than can generated by the body, 500 contractions per second, appears to have the effect of reestablishing feedback from the 1a fibers as demonstrated by the increased contraction strength encountered post ARP Neuro therapy.
This perhaps may be a result of the ARP Neuro stimulus causing additional ion channels to open within the 1a neuron thereby decreasing resistance and increasing conductance of these signals to the alpha-motor neuron pool. In short, the ARP Neuro stimulus seems to reverse the γ-loop dysfunction a key factor in overcoming arthrogenic muscle inhibition. Overcoming the arthrogenic muscle inhibition due to joint injury will now permit proper loading and biomechanics of the involved joint leading to better long-term outcomes.
RE-examining neuromuscular electrical stimulation (nems)
The emerging evidence on the profound effect of neuromuscular electrical stimulation (NEMS) combined with active movements on overcoming muscle inhibition from joint injury should drive any physical medicine practitioner to re-examine NEMS and its role in their practice.
As the science has advanced our understanding of the effect of NEMS technology has also advanced and with use NEMS units such as ARP Neuro having the capability if delivering 500 contractions per second with a stimulus like what the body generates naturally but at a much higher rate may lead to dramatic improvements to the long-term outcomes for our patients.
References:
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