Defected Peripheral Nervous System Essay

is known about the mechanisms of the CNS. This review focuses on the Peripheral Nerve Injury and

There is strong evidence that administration of VEGF in contused subjects helps recovery of fine motor skills, reduction of lesion tissue loss, prevention of excessive cell death in neurons, and remyelination of oligodendrocytes8. The ability of VEGF to promote neural plasticity is a double edged sword, however. The same mechanisms are implicated in the induction of neuropathic pain following contusive injury9. Administration of VEGF also increases the permeability of the blood-spinal cord barrier following injury, increasing the influx of oxygenated blood to the injury site. While this may be beneficial to some extent, the simultaneous influx of immune cells attenuates the secondary injury

Chronic Neuropathic Pain after Spinal Cord Injury: Spinal cord injury (SCI) affects up to 500,000 people every year around the world (Singh et al., 2014) with devastating physical, psychological and social consequences. SCI not only damages motor systems, it also directly affects sensory systems, causing chronic, debilitating neuropathic pain. The incidence of neuropathic pain after SCI is extremely high, with at least half and up to 90% of SCI individuals experiencing neuropathic pain, described as paroxysmal pain that can be continuous and may be evoked by any sensory stimulus, not necessarily painful. Current pharmacological interventions offer minimal, transient relief to a minority (30%) of sufferers of SCI-induced neuropathic pain (Cousins, 2012). Current treatment strategies utilize conventional drugs for chronic pain, which only address pain symptomatically and cannot provide lasting relief or prevent relapse of symptoms, leading to drug dependency and further reducing quality of life for SCI patients. Due to the myriad events that take place after SCI, delineating the causes of neuropathic pain development is difficult. Neuropathic pain in general, and more so in SCI, has an inherent degeneracy in mechanisms, which is likely why targeted pharmacological treatment approaches often fail to provide significant relief.

This is a picture of brain cells. There is a lot of controversy between the brain healing itself and not. There is some research that the brain tries to heal itself when damaged. Apparently brains can make new nerve cells by a process called neurogenesis. This is picture that shows neurogenesis. First the cells form. Half of the cells formed die off. Some of the cells become support cells. Only a small percent are stem cells that can become nerve cells. There is now research on new nerve-cell growth and how it can be maximized and directed toward the most damaged areas of the brain. There are rehabilitation therapies that stimulate sprouting of existing nerve cells, causing them to make connections to other nerve cells. The brain can recruit surviving parts to take over the functions of the damaged areas.

Describe the four lobes of the brain. Include the following information in your essay. (250 words)

and modication of synaptic strength represent the neurological bases for spinal cord neuroplasticity [3].

Neurotransmitters: chemicals that enable messages (nerve impulses) to pass from one cell to another, if chemicals are not produced in the right amounts, the message pathway becomes confused or blocked

Spinal Cord Injury (SCI) can result in loss or permanent damage of motor, sensory or autonomic function, generally caused by physical trauma to the spinal cord. In humans the most common type of SCI is hemisection or contusion (Nandoe-Tewarie et al. 2009). This incomplete injury, leads to swelling or compression of the spinal cord due to bone displacement, resulting in partial loss of function and/or sensation. Complete severing of the spinal cord fibres can occur, although less often, and results in impairment of all function and sensation below the trauma site (Sobani et al. 2010). Due to the complicated physiology of the spinal cord and central nervous system, and their diminished regenerative properties, currently, there have been no effective forms of treatment of SCI.

Currently, 285,000 US citizens suffer from spinal cord injury (SCI), and 99.6% of these individuals are paralyzed to some extent.1 SCI is the result of a mechanical insult to the spine that damages the spinal cord. This is followed by secondary SCI, which involves a series of biochemical events resulting in further neuronal and glial cell death.2 Astrocytes, the most abundant glial cell of the central nervous system (CNS), provide neurons with structural and neurotrophic support as well as protection from toxins. Following primary injury, damaged glia are unable to provide damaged neurons with the support necessary for axonal regeneration. Individuals that suffer from SCI are limited to two forms of treatment: 1) administration

The above process to neuronal regeneration takes place both in the peripheral and central nervous system however, a number of factors are present in the CNS for example Spinal cord injury causes a rapid stop of regeneration of damaged axons. The site of a spinal cord injury as a result of the phenomena occur eventually to produce a cavity filled with liquid syringomyelic CSF and covered with a layer of glial scar. This scar and cavity form a loss of continuity of long nerve pathways of the spinal cord and prevent the occurrence of neuronal regeneration process. Work on cellular therapies allowed researchers to isolate and implement of clinical transplantation experiments olfactory ensheathing glia (OGC). This is a population of cells with unique properties to stimulate the regeneration of CNS axons - opening the locking the glial scar, screening of regenerating axons and produce around casing. OGC activity may however be very limited in the case of spinal cord tissue defects dividing the axon ends. To solve the problem of syringomyelic cavity and loss of continuity of spinal cord tissue caused further studies of biomaterials. The aim is to create an artificial extracellular matrix that is likely to constitute a bridge for regenerating spinal cord fibers. Such an implant would stimulate neuronal regeneration process by establishing a physical connection between the ends of the spinal cord and could increase the efficiency of the use of OGC.

The nervous system of the human body can be separated into two parts: the Central Nervous System (CNS) and the Peripheral Nervous System (PNS). The brain and the spinal cord make up the Central Nervous System, which is the nervous system’s processing center. The Peripheral Nervous System “consists of nerves that branch from the Central Nervous System and connect it to other body parts” (Shier, Butler, Lewis 2015). The somatic nervous system and autonomic nervous system are the subdivisions of the Peripheral Nervous System. In this essay, I will distinguish between the Central Nervous System and the Peripheral Nervous System.

For decades scientists have been working to try and find a way to remedy the various ailments that spinal cord injuries can bring, but with

There are a number of factors that can alter a person’s heart rate. It can be environmental, physical, mental, or chemically-induced (Hjortskov et al, 2004). One such factor that can induce a change in heart rate is mental activity and stress (Bernardi, et al., 2000). Heart rate, even without any sort of environmental stimulus such as mental activity, is controlled primarily by the Autonomic Nervous System (ANS). This is a division of the Peripheral nervous system that controls the function and regulation of internal organs such as the heart (Kamath, Fallen, and McKelvie, 1991). The ANS can be further divided into two systems: parasympathetic and sympathetic systems.

A major site of injury that puts many essential neurons at risk is the spinal cord, which contains many neurons essential for proper motor functionality. The spinal cord is made up of nervous tissue within spinal vertebrae. The spinal cord receives sensory information from the skin, muscles, joints, tissues, as well as other parts of the body, and then relays information to and from the brain. Injury to the spinal cord can cause dislocation of vertebrae, resulting in various paralyzing disabilities such as quadriplegia (paralysis from the neck down) or paraplegia (paralysis of the lower body). The severity of the disability depends on the location of the injury (Schwab et al. 2002). There are two main phases of spinal cord injury. The first phase is physical tissue destruction, which is followed by tissue loss caused by irregular blood supply to the injury site. Because of this disrupted blood supply,

Further study: the authors suggest that further study about interrogating of potential mechanisms of repair will reveal the roles of ABMCs in mediating spinal cord injury repair. This suggestion indicates that the authors were aware of their study limitations, which prevented them in determining and explaining the physiological roles and mechanisms of AMBMCs in the process of spinal cord injury repair. By correctly pointing out the limitation of the study and suggesting the further study, the authors have decreased the possible impact of the limitation on the validity of the study.