Denervated Muscle Observation Research

6. The reattached nerves would not recover as quickly and completely as the reattached muscles after Jim’s surgery because the body will repair itself by regenerating the muscles. Theses regenerating nerve muscles will automatically grow down the nerve and restore muscle by supplying it with nerves through regrowth. If they connect correctly the motor nerve to muscle and sensory nerve to skin will recover. If they do not connect correctly, they will not completely

The muscular system is an organ system composed of roughly 650 to 850 muscles. The muscular systems consist of skeletal, smooth and cardiac muscles. The muscular system collectively works with other organ systems to permit movement, posture, conduction of heat and the circulation of blood throughout the human body.

Muscle strength and neuromuscular control is compromised. This could develop into long-term muscle weakness and motor planning dysfunction. Transcutaneous electrical nerve stimulation (TENS) could be utilized to help control pain and improve muscle weakness related to arthrogenic muscle inhibition. Evidence shows that TENS is effective in improving maximal voluntary torque and electromyographic signals of muscles (Konishi, McNair, & Rice, 2017). Mr. Versace may benefit from TENS on quadriceps femoris muscle to minimize muscle strength deterioration

The nerve receives stimulation from the central nervous system to contract (shorten) during dorsiflexion. “Muscle contraction is an active process and requires energy (derived from glucose) in the form of adenosine triphosphate (ATP)”. (O’Callaghan M 2013). ATP “is molecular store of chemical energy for chemical reactions” (Waugh & Grant 2014). The muscles relax when stimulation stops therefore returning to original length. In order for muscles to operate at optimum levels there has to be a good blood supply in order to provide oxygen, nutrients, calcium and also to remove waste materials.

(2013), "spinal gray matter, particularly the anterior horns, usually show the most severe involvement." Post-polio syndrome shows similar signs of motor neuron deficits from the original polio virus. When effected by polio, a person will lose muscle strength due to axonal degeneration. Once degeneration has occurred, there will be a reinnervation of the denervated muscle fibers to allow for recovery of the muscle strength (Goodman, Fuller, & O'Shea, 2012). Post-polio syndrome speeds up the progression of denervation twice as fast than regular aging alone

One comes to mind that added insight from today’s lesson was antagonist muscles. When we were as to rotate our bodies to one side while looking the opposite side made it difficult to execute the task of easily rolling a patient over. The neck muscles oppose or reverse the desired movement, by contracting slightly to provide some resistance. reading it in a book is one thing but seeing in action is another, and in my opinion, a better way to retain and learn a topic.

The recovery from illness or injury often requires otherwise healthy humans to undergo a period of muscle disuse (e.g. bed rest or limb immobilization). A major consequence of disuse is skeletal muscle atrophy. The ensuing impairments in muscle function, metabolic rate and insulin sensitivity, and accrual of body fat mass following two or more weeks of muscle disuse have been well documented. Studies investigating muscle disuse atrophy generally employ relatively long experimental periods, ranging from two to as long as 17 weeks of bed rest or limb immobilization. However, over the last decade, efforts have been made within healthcare systems to reduce the duration of bed rest/immobilization that patients endure due to illness or injury. At

As we learned, inside our muscles we have both thin and thick filaments, in which the thick are made of myosin, and the thin are composed of actin. When these proteins pull together, they cause muscle contraction. They remain this way, until ATP attaches to the myosin and forces it to let go of the actin (howstuffworks.com). Basically, muscles need ATP in order to release from a contracted state, because it is used to pump the calcium out of the cells, allowing the fibers to unattached. When a person is alive, their muscle cells utilize energy to transport calcium ions to the outside of the cells, which is when the muscles are released from the contracted state. When a person dies, the membranes of the muscle cells become more absorbent to calcium ions, therefore they are unable to contract and the actin and myosin will remain latched until decomposition begins taking place

Spinal muscular atrophy is a genetic disease that affects a part of the nervous system that controls voluntary muscle movement. Spinal muscular atrophy involves the loss of nerve cells called motor neurons in the spinal cord, which may also be known as motor neuron disease. The motor neurons receive “signals” from the brain to the spinal cord, and then they in turn send signals to our muscles. When these signals do not transmit properly, this is what causes spinal muscular atrophy. It is the number one genetic cause for newborn deaths. There are four types of spinal muscular atrophy, based on age the patient is, and the highest physical milestone achieved by the patient. Type 1 also known as Werdnig Hoffman disease, Type 2 also known

With this new discovery, we can take those nerves and put them to use. Dr. Todd Kuiken of the RIC developed the procedure, which he calls the “targeted muscle reinnervation.” The motor cortex in the brain controls the voluntary muscles. These nerves are rerouted. These nerves are attached to a working muscle and the nerves grow into these muscles. The motor

Reinnervation is also required if myofibre development is to continue. In cases of nerve axon damage (axonotmesis) muscle wasting remains until nerve regeneration is

These alterations in morphologic remodeling in the aged NMJ further results in more dispersed AChR, with greater spatial uncoupling between ACh vesicle clusters and receptor clusters. As studied by Gonzalez, de Cabo, Studenski, & Ferrucci (2014), the morphological changes together with physiological alterations results in a remodeling of the motor unit and in a decline of the number of motor neurons, particularly the type II muscle fiber (fast and glycolytic muscle fibers). These changes lead to excitation–contraction uncoupling, and a loss of communication between the nervous and muscular system, causing a decline in skeletal muscle strength and muscle

It is known that following primary sensory axonal injury there is a slight increase in regeneration of their central axons, meaning that the increase in growth status after injury causes regeneration. Previous studies have looked into conditioning lesion and found that primary sensory neurons can in fact increase their growth capacity and enhance regeneration after injury, activating ciliary neurotrophic factors (CNTF), interleukin-6 (IL-6), and the cAMP signaling pathway among others in conditioning lesion. In the current article the researchers investigated whether ATP injection into peripheral nerves were able to mimic the effects of nerve injury in promoting regeneration of sensory neurons both in vivo and in vitro, so that the growth and

The author states that the experimental group received a dorsiflexion component to the stretch compared to the control group. It is unclear however, whether it is a static stretch or if the researcher is providing an alternating plantarflexion to dorsiflexion movement (similar to nerve gliding). The study by Lai, et al.5 did not look at neurodynamic responses in any other limbs other than the limb that was being tested. Lohkamp and Small7 found that the responses of stretch and pain may not solely be caused by nervous tissue in asymptomatic participants due to the symptoms occurring outside of the area of the median nerve. It is unclear what neurodynamic effect(s) lower extremity nerve gliding techniques would have of the upper limb nerve tension tests. Research into the effects of lower extremity nerve flossing techniques on upper extremity neurodynamics could further develop our understanding of the complex interconnectedness of the nervous system. Clinically, lower extremity neurodynamic mobilization exercises that have an impact on upper extremity nerve tension could be used to decrease neural tension of a limb that is immobilized for any period of time, or if pain is preventing movement in the limb. By giving the nervous system more slack, the patient could have relief of neurodynamic symptoms in the immobilized limb. In the study performed by Gupta8, the effects of sciatic

Injuries to the sciatic nerve can cause complete or incomplete los of motor, sensory and autonomic function due to degeneration (Sun&Zhao). Nerve growth factor (NGF) is essential for the stimulation of peripheral nerve regeneration. More specifically NGF is a neuropeptide that function to regulate growth, maintenance and proliferation of neurons. These factors all led to the to NGF helping with the repair of injured nerves. When NGF is given to patients in a solution the solution is rapidly diffused and not able to be absorbed by the damaged nerves for an adequate amount of time. In order to get NGF to be retained longer in the nerve researchers hope to develop a way