Symptoms And Treatment Of Neuropathic Pain

Chronic pain has four mechanisms. Nociception is a neural signal of threatened or damaged tissue, and is the classical pain pathway. Central pain states are thought to be caused by abnormal activity in neurons in the afferent pathway. The mechanism for this is not completely understood, and a person may perceive pain where there is no tissue damage. Behavioral pain is communicated by a

Neuropathic pain is described as burning, shooting, and tingling. Nociceptive pain originating from visceral sites is described as aching if localized and cramping if poorly localized; from somatic sites, it is described as throbbing/aching.

Pain is one of the most influential symptoms that leads individuals to reach out to health care professionals to seek relief. Pain is subjective and unique to each person. Some individuals may have a higher pain tolerance than others. According to Frandsen (2014), “Pain is an unpleasant, sensory, emotional sensation associated with actual or potential tissue injury” (p. 889). Pain may be caused by a variety of elements, such as tissue or nerve damage and surgery. There are three main categories that pain is classified by, which are origin, duration, and cause. The main focus of this paper is on acute pain, chronic pain, and phantom pain. It is crucial to know how to assess each type of pain, as well as how to enhance it, or decrease the pain.

In order to better understand parkinsonian CNP and determine what part of the circuitry has been disrupted, it is important to understand normal pain physiology. Acute pain is activated in the presence of a noxious stimulus (such as high heat, pressure, or chemicals), to signal potential or actual tissue damage. Noxious stimuli invoke a response from specialized terminals of peripheral nociceptors, whose cell bodies originate in the peripheral dorsal root ganglia located along the spinal column [261]. These terminals contain transient receptor potential channels, tetrodotoxin channels and ion channels that transduce energy from noxious stimuli into action potentials. The speed of the action potential is directly related to the diameter

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.

The causes and the manner of the development is not fully understood yet. The over view of fibromyalgia is a dysfunction of the central or autonomic nervous system. It is possible that hormones, weak immune system, stressors and a few other influences may cause this disease. Central sensitization is the main make up of this disease. Central sensitization is a result of random nerve activity, enlarged receptive fields, and augmented stimulus responses. Fibromyalgia includes a well-known restraint that blocks pain pathways that control spinal cord responses to painful stimuli. This barrier is weakened in patients with fibromyalgia which helps to worsen the central

Pain can be defined as having two components, sensory and emotional. Nociception is solely the sensory component of pain. Nociceptive pain is usually acute and can produce hyperalgesia, which is an increased sensitivity to the injury site [1, 2]. Chronic pain is defined as pain that outlasts the healing time of an injury, usually lasting about 3 months or more [3], whereas acute pain is a normal sensation that alerts the body of possible injury [2]. Neuropathic pain is chronic, abnormal pain that is spontaneously caused by peripheral or central nerve damage [1-4]. It is usually associated with stimuli that is not normally painful, known as allodynia. This pathological pain may be continuous or episodic and can resemble a stabbing, sharp, or

The syndrome can range from manageable to disabling and difficult. About one-third of patients tend to get better over time. About one-third can be managed with treatment, and about one-third continue to struggle with pain that affects their quality of life. There is some evidence that chronic pain and sensory abnormalities do decrease over time. Unfortunately, there are very few studies looking at the natural history of pain duration of individual neuropathic pain syndromes. Most are retrospective studies using data combined from all sources of pain following surgery. The key takeaway for primary care providers is that PMPS is a real and common problem for many women after mastectomy. This is a neuropathic pain syndrome. It does not indicate

Transient receptor potential (TRP) are ligand-gated controlled ion channels that function in the process of nociception where transmission pain signals by nociceptors are carried as impulses from the sensory nerves to the central nervous system through afferent neurons (Dai 2016; Marwaha et al., 2016). Nociceptors, also called noxious stimulus detectors, are pain sensory receptors made up of myelinated and unmyelinated neuron fibers that relay action potentials to the central nervous system (CNS) and peripheral nervous system (PNS), which are interpreted as pain (Woolf et al., 2007). Transient receptor potentials detect chemical or physical stimuli that trigger nociceptor activation that result in pain perception (Marwaha et al., 2016). The TRP channels control physiological perception of temperature, taste, pheromones and painful mechanical sensory inputs, which is accomplished through six different TRPs (TRPV1, TRPV2, TRPV3, TRPV4, TRPM8, and TRPA1) (Dai 2016; Marwaha et al., 2016). Interestingly, all six TRP channels of the three TRP family types are expressed in afferent pain sensing nociceptors (Dai 2016; Marwaha et al., 2016). This suggests that all six of the TRP channels are involved in pain perception. The afferent nociceptors are hyper-activated in diseases including neuropathic pain and peripheral inflammation. Recent findings suggest that TRP channels function in a critical position with the association of these diseases. Researchers are exploring novel

The classification of chronic pain include three wide classes: first one is pain due to tissue disease or damage (nociceptive pain, such as osteoarthritis), second is pain caused by abnormality in somatosensory system (neuropathic pain, such as diabetic neuropathy), and the last one is eistance of both of nociceptive and neuropathic pain (mixed pain, such as chronic radicular back pain) (Baron et al.

PMPS can develop shortly after surgery or may be delayed up to several months and can persist for years if it left untreated. The pain is often described as a neuropathic pain and is usually felt in the region innervated by the affected nerves. The exact mechanism is uncertain, but is thought to be the result of damage to nerve pathways, particularly the intercostobrachial nerve (lateral cutaneous branch of T2), during operative procedures on the breast and/or axilla

According to the European Federation of Neurological Societies (EFNS) guidelines on neuropathic pain assessment and the American Acade-my of Neurology (AAN)-EFNS guidelines on TN management (Cruccu G et al., 2006) the neurophysiological recording of trigeminal reflexes represents the most useful and reliable test for the neurophysiological diagnosis of trigeminal pains. (Figure 1.1). In patients presented with pain in the trigeminal territory, trigeminal reflexes offer the clinician with useful information. Abnormalities are often discovered in divi-sions that appear clinically unaffected. An objective demonstration of dysfunction is provided in all patients with pain secondary to a docu-mented disease, such as symptomatic trigeminal neuralgia,

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

The Idiopathic typical Trigeminal Neuralgia is attributed by five cardinal features: “Paroxysmal, Provocable, unilateral pain, confined to trigeminal territory, without loss of pain” (Devi at al., 2015); A disorder is considered paroxysmal if there are sudden recurrence and intensification of symptoms (Wikipedia, 2015). The pain from Type 1 is often triggered by a light breeze, cold, vibrations, brushing of the teeth, shaving, eating and talking. The Atypical Type, on the other hand, is often bilateral, constant, non-paroxysmal, unprovoked by external stimuli, and less intensified than Type 1 (Devi at al., 2015). Both types of pain may occur in the same patient, and could occasionally be simultaneous. Symptoms of trigeminal neuralgia comprise a sharp, stabbing twinge on one side of the face that commonly begins at the angle of the mandible. During an attack, patients are noted to shield their face to prevent it from being touched by anyone. Sufferers usually experience recurrent pain every few hours. One attribute that differentiates Trigeminal Neuralgia from Migraines, is that TGN only occurs when the patient is awake and not

The International Association for the Study of Pain defines pain as “an unpleasant sensory and emotional experience associated with actual or potential tissue damage, or described in terms of such damage” (1979). Pain is actually the culprit behind warranting a visit to a physician office for many people (Besson, 1999). Notoriously unpleasant, pain could also pose a threat as both a psychological and economic burden (Phillips, 2006). Sometimes pain does happen without any damage of tissue or any likely diseased state. The reasons for such pain are poorly understood and the term used to describe such type of pain is “psychogenic pain”. Also, the loss of productivity and daily activity due to pain is also significant. Pain engulfs a trillion dollars of GDP for lost work time and disability payments (Melnikova, 2010). Untreated pain not only impacts a person suffering from pain but also impacts their whole family. A person’s quality of life is negatively impacted by pain and it diminishes their ability to concentrate, work, exercise, socialize, perform daily routines, and sleep. All of these negative impacts ultimately lead to much more severe behavioral effects such as depression, aggression, mood alterations, isolation, and loss of self-esteem, which pose a great threat to human society.