Pain In The Central Nervous System Essay

which in turn inhibits the second order neurons that transmit the nociceptive signals to the

Acting in accordance with National Institute of Diabetes and Digestive and Kidney Diseases (NIDDK), diabetic neuropathies are family of nerve syndromes affected by diabetes (2009). People with diabetes can be asymptomatic overtime and some can have notable signs with radicular symptoms in the upper and lower extremities (NIDDK, 2009), Moreover, can affect even the digestive, cardiac, and reproductive system in serious conditions (NIDDK, 2009). In fact, based on academic literatures, about two thirds of patients with diabetes have medical or subclinical pathology of nerve (Bansal, Kalita, & Mistra, 2006). The occurrence of neuropathy amplified from approximately 7 percent to 50 percent on admittance at 25 years in consequence (Bansal, Kalita, & Mistra, 2006).

There are many mechanisms for the sensitisation of nociceptors. A common scenario for this occurrence is when peripheral tissue is subjected to exogenous injury, whether it be mechanical, chemical, or toxic. Injury results in localised increase in inflammatory mediators, leading to the sensitisation of nociceptors. Upregulation and increased expression of various membrane receptors is the most common mechanism. Ionotropic receptors, Gq protein-coupled metabotropic receptors, Gs protein-coupled metabotropic receptors, and mitogen-activated protein kinase have been shown to be upregulated in nociceptors in response to the presence of inflammatory mediators (Sessle ed 2008). The resultant effect is increased conductance, lowered threshold for the initiation of action potentials, spontaneous depolarisation, and increased after-discharges to supra-threshold stimuli (Sessle ed 2008). Sprouting, or the growth of neuronal axons into the damaged tissue, also contributes to pathological pain. Increased number of nociceptive axons increases the opportunity for spatial and temporal summation and activation of nociceptors, which under normal conditions would not be activated. Sufficient concentration of inflammatory mediators can also lead to the activation of nociceptors which do not participate in the detection of noxious stimulus (Sessle ed 2008). With an increased number of nociceptors feeding back to the CNS, the sensation of pain is

Chronic pain relief has now emerged with new and great techniques and treatments. The researchers and surgeons are now enhanced with effective drugs to implant and electrical stimulation. The birth of chronic pain can be due to various reasons like from an accident affecting much too sensitive veins and muscles, back injuries, an injury caused while playing sport, and chronic pain can also be occur from health conditions like migraines, diabetes, arthritis, shingles, and cancer. It is not important that a person will be suffering from chronic pain only; he may suffer from acute pain too. The acute pain causes are

Sean Mackey is a M.D, Ph.D, the current Chief of the Division of Pain Medicine, as well as a Redlich professor in several pain and brain related sciences at Stanford. Doctor Mackey leads the research at the Stanford Systems Neuroscience and Pain Laboratory focusing on the dissecting chronic pain and how it effects the nervous system. The SNAPL has also attempted to map out the brain and regions in the spinal cord that understand pain in order to treat these occurrences of chronic pain on a personal level (Stanford Medicine Bio). In order to solve these problems he is mainly explores the effects of different injected drugs, such as Lidocaine, Ondansetron, and Botulinum Toxin, for ameliorating effects or help in linking how different responders

Globally, The number of patients with diabetes is increasing rapidly. By the year 2035, the number of people with diabetes worldwide is expected to rise to 592 million (IDF ATLAS 20131). Diabetic peripheral neuropathy (DPN) is a common microvascular complication of diabetes and a leading cause to amputations in hospitals (Boulton 20052). The prevalence of DPN is estimated to be 50-60% (Sandireddy R 20143). The pain associated with DPN can affect the patient quality of life (QOL). It affects their sleep, lifestyle, work and even can cause or be associated with depression (Jensen MP 20074). It is not well understood whether the mechanism behind peripheral neuropathy with diabetes is hyperglycemia or other insulting pathophysiological mechanism like proinflamatory immune mediators (Herder C 20135, Goh S-Y 20086). One of the possible mechanisms is the demyelination of the small C fiber, this is the leading cause behind the pain sensation with

Serotonin (5-HT) and norepinephrine are primary neurotransmitters of the monoamine pathway and have been implicated in chronic pain (Bardin, 2011). These monoamines, particularly in areas such as the PAG, form a depression-pain interface. The PAG takes information sent from the amygdala, neocortex, and hypothalamus, processes the information, and then sends the modified signals to the brainstem, particularly the RVM (Millan, 2002). Approximately 20% of the neurons within the RVM are serotoninergic. Depending on the receptor, dose, and chronology, 5-HT within the CNS can be either pro- or antinociceptive (Bannister et al., 2009). As such 5-HT's influence on pain modulation can be quite complex.

Accurate assessment of pain is a major prerequisite for the adequate pain control (positive) to assess the potential effects of the analgesic drug effect. Assessment of pain in patients with dementia is generally a particularly challenging to loss symptomology inherent communication capabilities of the condition to limit the subjective reports of pain is expected to be due to that the healthy adult. Maintenance and inspection of pain causal factors leading to pain, may be a somatic cell or psychological, or to investigate the interaction of the two. The Mechanism of the result of the test is therefore the source or pain, etc. (i. e., Musculoskeletal), internal (i.e., internal), neuropathy (e.g., diabetic neuropathy), functions, or mental (that

Nociceptive pain is the pain experienced when the body is damaged by temperature, chemical, or mechanical means. When damage is caused, afferent neurons respond and the four phases of nociception result. Transduction occurs when the free ends of silent nociceptors convert toxic experience into an electrical current, leading to a nerve impulse. The nerve impulse is then transmitted to the dorsal root ganglion in the spinal cord, then the dorsal horn at the base of the brain and on to the brain, where it is recognised as pain. The perception of pain occurs when the electrical impulse leads to release of neurotransmitters from the nociceptor endings in the brain. It is further processed into a more specific sensation such as sharp, dull, aching

Thus, serotonergic innervation from the DRN greatly affects the modulation of a fear-like behavior. However, the 5-HT pathway from the DRN to the LC was critical only in pain modulation and not in the elaboration of defensive behavioral responses. It Both the non-selective and the selective serotonergic antagonists in the LC were found to impair the increase in the nociceptive threshold caused by the defensive reaction mediated by the DMH. It may be the case that the connective pathway between the DRN and the LC modulates the nociceptive

Diabetes is considered a very ancient disease, with early observations made in Egypt 1500 BC. The disease has always been well known for its severe implications on the lifestyle of patients. Diabetes has a very long-lasting and complex history, which is well documented. There are historical milestones that have been significant for understanding the disease and developing treatments. This paper reviews such historical events, including the discovery of insulin, that have been influential on modern diabetic medicine. Moreover, patient experiences with insulin injections are also discussed. A fascinating component of diabetic history is also the transition from fairly unsophisticated treatment approaches to more medically developed procedures in the Twentieth Century. This review also examines early ideas of the insulin pen injector and describes how the first NovoPen in 1985 was developed. This will contribute to the background information of the research project, which aims to investigate what impact the first NovoPen in 1985 had on the treatment of diabetes. The research project will take clinical, as well as patient experiences of using the first NovoPen into consideration to reach a conclusion about its influence on treating diabetes. Nowadays, new generations of the NovoPen family have been developed, which are very popular among diabetic patients as a treatment option. Due to this remarkable history of the NovoPen in diabetic medicine, it is of interest to investigate

Many serotonergic projections from the raphe nucleus terminate in the superficial laminae of the dorsal horn, an area strongly associated with nociceptive processing (Todd, 2010). These axons can be found throughout the dorsal horn but are most numerous in the superficial laminae.

Reactive hypoglycemia, a rare form of hypoglycemia, increases insulin levels after the consumption of excess carbohydrates, leading to a drop in blood glucose levels. This differs from conventional hypoglycemia where blood glucose drops several hours after a meal, but can easily be returned to normal by the consumption of food. Reactive hypoglycemia can cause fatigue, dizziness, shakiness, and in extreme cases, a coma. Although no effective treatments exist, glucagon, a peptide hormone derived from pancreatic alpha cells, seems to reduce symptoms. In the proposed experiment, the effectiveness of glucagon relative to a regimen of dietary control, exercise, and Acarbose will be tested on Zucker-diabetic-fatty (ZDF) rats (Rattus rattus). Three

Pain is something that connects all of us. From birth to death we can identify with each other the idea and arguably the perception of it. We all know we experience it, but what is more important is how we all perceive it. It is known that there are people out there with a ‘high’ pain tolerance and there are also ones out there with a ‘low’ pain tolerance, but what is different between them? We also know that pain is an objective response to certain stimuli, there are neurons that sense and feel pain and there are nerve impulses that send these “painful” messages to the brain. What we don’t know is where the pain

Nociception is the sensation of pain which is normally a warning signal to brain in respond to a potential hazard. Generally noxious stimulations are detected by specialised high-threshold sensory neurons, which are refer to nociceptors. The signals are then transferred to an electrical potential and conducted to the brain via spinal cord. However sometimes abnormal nociception can lead to a moderate to severe pain although a noxious stimulus is missing. This kind of pain are usually trigger by nerve injury, while the pain sensation remains after the tissue had been healed. Although the prevalence of neuropathic pain is not significant, about 7% to 8% of the European population is affected, and about 5% are suffering severe pain (Torrance et al., 2006; Bouhassira et al., 2008). Normally the neuropathic pain is induced by injury of somatosensory nerves, and the pain remains after the tissue being healed. It can bring abnormal nociception while noxious stimuli are missing, which called dysesthesia. Beside, pain can be triggered by non-painful stimuli, which is called allodynia). Many research has linked the neuropathic pain to neuronal damages where endogenous ATP being released. Therefore purinergic receptors that can respond to ATP are involved. In this essay, after a brief introduction of P2X receptors, the role of microglial P2X4 and P2X7 in neuropathic pain will be discussed.