Peripheral nervous system defined

Neuropathic pain is defined as spontaneous pain and hypersensitivity to pain associated with damage to or pathologic changes in the peripheral nervous system as in painful diabetic peripheral neuropathy (DPN), acquired immunodeficiency syndrome (AIDS), polyneuropathy, post-herpetic neuralgia (PHN) or pain originating in the central nervous system (CNS), that which occurs with spinal cord injury, multiple sclerosis, and stroke. Functional pain, a relatively newer concept, is pain sensitivity due to an abnormal processing or function of the central nervous system in response to normal stimuli. Several conditions considered to have this abnormal sensitivity or hyperresponsiveness include fibromyalgia and irritable bowel syndrome. 

At this point, it is important to note that a nerve is defined as a bundle of neuronal axons some are afferent and some are efferent. A nerve does not consist of entire neurons, only their axons. Furthermore, nerves are found only in the peripheral nervous system. Bundles of neurons with similar functions located within the CNS are referred to as tracts. Therefore, technically speaking, no nerves are within the brain or the spinal cord. 

Central nervous system myelin contains some unique proteins 58 Peripheral nervous system myelin also contains unique proteins 63 Some classically defined myelin proteins are common to both peripheral and central myelin 64... 

NGF also has actions within the CNS, although it is not particularly abundant in the CNS. Its synthesis appears to be largely restricted to the hippocampus and neocortex, and even in these regions it is present at relatively low concentrations relative to the other neurotrophins. The most prominent population of NGF-responsive neurons expressing TrkA are the basal forebrain cholinergic neurons. The principal projections of these neurons are to the hippocampus and cortex, which conforms with the concept that NGF acts as a target-derived trophic factor in the CNS, just as it does in the peripheral nervous system (PNS). NGF also acts on a subpopulation of cholinergic neurons within the striatum. These interneurons express the NGF receptor, TrkA, and respond to NGF. However, they do not appear to rely entirely on NGF for their survival, and the specific actions of NGF on this neuronal population have not been clearly defined. NGF may also have autocrine actions in the CNS, as some neuronal populations have been identified that express both TrkA and NGF. 

Lewy body pathology is also the defining feature of several other, rarer diseases, such as Lewy body dysphagia and pure autonomic failure. In these diseases, Lewy bodies and neurites are largely limited to the enteric and peripheral nervous systems. In Parkinson s disease, Lewy body pathology is also present in the enteric and autonomic nervous systems. 

Neurotoxicity can be defined as any adverse effect on the structure or function of the nervous system related to exposure to a chemical substance (US-EPA 1998, OECD 2004c). According to the TGD (EC 2003), neurotoxicity can be defined as the induction by a chemical of adverse effects in the central or peripheral nervous system, or in sense organs and a substance is neurotoxic if it induces a reproducible lesion in the nervous system or a reproducible pattern of neural dysfunction. ... 

The role of neurotrophins in the pathogenesis of allergic disease and asthma has been appreciated only recently. Neurotrophins are a family of growth factors that have common receptors and physiologic effects and are the principal regulators of neuronal activity, differentiation and maintenance. In humans, there are at least four defined neurotrophins also termed NGFs. These polypeptides include NGF, neurotrophin 3 (NT-3), neurotrophin 4/5 (NT-4/5) and brain-derived neurotrophic factor (BDNF). They all act on a common group of tropomyosin-related tyrosine kinase (Trk) receptors. Neurotrophin receptors are expressed in the neurons of both the central and peripheral nervous systems. 

Local application of concentrated sodium channel blockers can provide complete pain relief through nerve conduction block (local anesthetics). This approach to pain relief is limited to a few applications involving short-term treatment of acute pain, since sodium channels are also vital to conduction in the heart, CNS, skeletal muscle, and non-nociceptive sensory neurons. However, some types of chronic pain signaling appear to be sensitive to sodium channel blockers at concentrations that do not cause conduction block. In particular, neuropathic pain, defined as chronic pain resulting from a primary lesion or dysfunction of the peripheral nervous system by the International Association for the Study of Pain (IASP) [58], is thought to originate from aberrant signaling in the nervous system and can be ameliorated by sodium channel blockers. 

Thiamin was the first of the vitamins to be demonstrated to have a clearly defined metabolic function as a coenzyme indeed, the studies of Peters group in the 1920s and 1930s laid the foundations not only of nutritional biochemistry but also of modern metabolic biochemistry and neurochemistry. Despite this, the mechanism by which thiamin deficiency results in central and peripheral nervous system lesions remains unclear in addition to its established coenzyme role, thiamin regulates the activity of a chloride transporter in nerve cells. 

Patients with increasing muscular weakness may offer widely diverse histories, signs and symptoms of their complaint. On examination, the condition may often be related at once to disease of the central or peripheral nervous system or, if clearly defined, to one of the classical myopathies. Doubts may frequently arise, however, and where further... 

It has been long demonstrated that Ca " is essential for neurotransmitter release. The existence of multiple types of Ca " channels and the fact that several of them can coexist in the same cell type has raised questions about which channel (or channels) contribute to the control of the dehvery of the Ca " necessary to trigger a secretory signal in a particular synapse. We will therefore review throughout this section how the different Ca " channel subtypes (defined by co-conotoxin blockade of neurosecretion) control the release of neurotransmitters depending on the synapse, the neurotransmitter, and the animal species. Tables 5.4 through 5.7 summarize how Ca " entry through different Ca " channel subtypes control neurotransmitter release at different sites of the central and peripheral nervous system, motor nerve terminals, and chromaffin cells. 

Diabetic neuropathy was defined at the San Antonio Consensus Conference as a descriptive term meaning a demonstrable nerve disorder, either clinically evident or subclinical, that occurs in the setting of diabetes mellitus without other causes for peripheral neuropathy. The neuropathic disorder includes manifestations in the somatic or autonomic parts of the peripheral nervous system ... 

Diabetic neuropathy is a chronic condition caused by hyperglycaemia, characterized by progressive morphological destruction of the peripheral nervous system, accompanied by loss of peripheral nerve function. Clinically, loss of function is defined by distal loss of sensibility, muscular strength and loss of deep tendon reflexes as well as by autonomic dysfunction of viscera and blood vessels. 

As mentioned earlier in Section 3, serotonin (3) activates a series of well-defined receptors in the central and peripheral nervous systems [81, 82]. The 5-HT3 receptor comprises a... 

In addition to the weU-defined opioid systems in the central nervous system, the three opioid peptides and their precursor mRNA have also been identified in peripheral tissues. ( -Endorphin is most abundant in the pituitary, where it exists in corticotroph cells with ACTH in the anterior lobe and in melanotroph cells with MSH in the intermediate lobe (59). Enkephalin and pre-pro-enkephalin mRNA have been identified in the adrenal medulla (60) and this has been the source of material for many studies of pro-enkephalin synthesis and regulation. Pre-pro-enkephalin mRNA has also been identified in the anterior and posterior lobes of the pituitary (61). mRNA for all three opioid precursors has been identified in the reproductive system (62—64). POMC... 

B, Thiamin Coenzyme in pyruvate and a-ketoglutarate, dehydrogenases, and transketolase poorly defined function in nerve conduction Peripheral nerve damage (beriberi) or central nervous system lesions (Wernicke-Korsakoff syndrome)... 

Association of Pain, neuropathic pain is defined as pain initiated or caused by a primary lesion, dysfunction in the nervous system". Neuropathy can be divided broadly into peripheral and central neuropathic pain, depending on whether the primary lesion or dysfunction is situated in the peripheral or central nervous system. In the periphery, neuropathic pain can result from disease or inflammatory states that affect peripheral nerves (e.g. diabetes mellitus, herpes zoster, HIV) or alternatively due to neuroma formation (amputation, nerve transection), nerve compression (e.g. tumours, entrapment) or other injuries (e.g. nerve crush, trauma). Central pain syndromes, on the other hand, result from alterations in different regions of the brain or the spinal cord. Examples include tumour or trauma affecting particular CNS structures (e.g. brainstem and thalamus) or spinal cord injury. Both the symptoms and origins of neuropathic pain are extremely diverse. Due to this variability, neuropathic pain syndromes are often difficult to treat. Some of the clinical symptoms associated with this condition include spontaneous pain, tactile allodynia (touch-evoked pain), hyperalgesia (enhanced responses to a painful stimulus) and sensory deficits. 

Physiologically, hypertension may be defined as an elevation of blood pressure above the normal limits of variability. There are at least five basic factors involved in the maintenance of blood pressure. Aberrations of any one or a combination of these factors could produce an elevation affecting principally systolic or diastolic pressure, or influencing both more or less equally. These factors include peripheral resistance, elasticity of the arteries, cardiac output (heart rate and stroke volume), blood volume, and viscosity of the blood. The central nervous system, the endocrine glands, and the kidney must exert their influence on blood pressure through the above factors. 

Application of in vitro test methods have become advantageous in specific cases, such as structurally defined compounds and delayed neuropathy, since target cell data and biochemical processes associated in delayed neuropathy are known. Microscopic studies reveal that cases of OPIDN have degeneration of axons followed by demyelination of the nervous system.25,26 Epidemiologic studies have indicated mild impairment of the brainstem, spinal cord, and peripheral nerve functions in Gulf War veterans.27 Such studies are consistent with the spectrum of OPIDN syndrome. The main nerve agents have been shown to inhibit NTE in vitro as well as in vivo. Sarin has been shown to produce delayed neurotoxicity when administered at higher doses in protected hens.25-27... 

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