1. Introduction
It is estimated that 20% of the European population suffer from chronic pain.1 The understanding of pain in research has considerably developed from the simplistic pain-gate theory.2,3 It is now understood that stimulation of peripheral nociceptors at high threshold triggers central pathways that travel via the lateral spinothalamic tract to the medulla and brainstem.4 Nociceptive information also arrives via spinoreticular and spinomesencephalic tracts; controlling autonomic, arousal and homeostatic responses.56 Sensory firing is just one influence to central pain processing. Cortical areas associated with emotional valence, memory, autonomic and motor control are all seen to activate during a pain experience supporting
…show more content…
Large, fast-conducting fibres (α and β fibres) inhibit small, multi-synaptic, slow-conducting fibres (C-fibre) at the dorsal horn.13 Gaps were missing within this research due to available research resources; Noordenbos13 was unable to investigate past the spinal cord. This statement was unexplained yet it was a development in pain research. Melzack and Wall2 developed the pain-gate theory based from the research by Noordenbos13. The theory explained what Noordenbos13 was unable to prove; impulses are projected to the brain via the dorsal column, where central processes influence the activity of the gate-control system.2
Melzack3 critiqued his own research. The pain-gate was too simplistic and only explained pain as a sensory dimension.3 Rather that, pain is an output of multi-dimensional information being received and processed by a complex neural network within the brain, termed the ‘neuromatrix’.3,14,15 This guided away from the concept that pain was a sensation always produced by injury, inflammation or pathology to pain being a complex experience by multiple influences. The new explanation was also a suggestion to the nature behind some chronic pain conditions.3 Influences affecting such central processing extend from existing synaptic architecture imprinted within memory to neuro-endocrine and immunological influences.3 Despite the resources of such knowledge being
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
To most people, pain is a nuisance, but to others pain controls their life. The feeling discomforts us in ways that can sometimes seem almost imaginable. These feelings can lead to many different side effects if not dealt with or diagnosed. These effects can include depression, anxiety, and incredible amount of stress. The truth about pain is that it is vital to our existence. Without the nervous system responding to pain, we would have no idea if we were touching a hot stove, being stuck by a porcupine’s needles, or something else that could leave a lasting effect upon our bodies without us even knowing anything about it.
Pain perception can be less than might be expected from the extent of a physical injury. This was proven by a scientist called Susana Bantick, Oxford University, and colleagues who carried out a study on the influence of attention distracting pain processing (Bantick et al, 2002). During the experiment, brain processing was measured by measuring brain activity using fMRI. Participants rated pain from 1-10 when noxious heat stimulus was applied to their hand in the scanner. She then followed the same process but gave them a task which required cognitive processing; reducing the amount of focused attention on pain. Bantick, therefore, showed attention distraction can reduce the amount of pain perceived by the individual, also pain processing to the brain was reduced. This provides vital evidence that pain perception does not just depend on the injury alone.
Pain’s inability to remember its own origins strongly suggests an extreme span of time since its beginning – pain has lasted a long time
Many people suffer from chronic widespread pain within their body. Physical pain can be described as unpleasant sensory experiences provoked by real or perceived tissue damage. The perception of pain and nociception can be induced at pressures and temperatures that are tremendous enough to cause some sort of injury or damage. Pain can also be portrayed as a variety of sensations such as lancinating, stabbing, pricking, burning, throbbing, cramping, and aching. Noxious stimuli are detected by specialized neurons called nociceptors. After repeated incidence of injury, nociceptors can be sensitized leading to allodynia and/or hyperalgesia. Allodynia is the perception of pain from normally harmless stimuli. Hyperalgesia is an increase
Mackey (2015) has argued that pain is subjective symptom and is derivative of several biochemical, psychological, and socioeconomic factors, and different cultural groups experience and expresses pain differentially. Jibb et el (2015) have noted that causes of pain are numerus and they have potential affect pain management differently. Pain can be a symptom of a disease, or it can result from invasive treatment and diagnostic procedures. The prefrontal cortex has neurophysiological pathways that responds to pain signals, thereby regulating emotions, cognitions, memory, and attention (Barrett & Chang, 2016).
A recent systematic review of Kingston et al. (2014) concluded that spinal JM largely leads to sympatho-excitation as the dominant paradigm of neurophysiological mechanisms underlying pain relief. Kingston el al. (2014) cited only 1 study that utilized the PA
The etiology of chronic pain is complex and may be due to a number of different factors. Current therapeutics often fail to produce adequate analgesia for moderate-to-severe pain
Proposed by Ronald Melzack and Patrick Wall in 1965, the Gate Theory of Pain accounts for both "top-down" brain influences on pain perception as well as the effects of other tactile stimuli (e.g. rubbing a banged knee) in appearing to reduce pain. It proposed that there is a "gate" or control system in the dorsal horn of the spinal cord through which all information regarding pain must pass before reaching the brain. The Substantia Gelatinosa (SG) in the dorsal horn controls whether the gate is open or closed. An "open gate" means that the transmission cells (i.e., t-cells) can carry signals to the brain where pain is perceived; a "closed gate" stops the t-cells from firing and no pain signal is sent to
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
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
Pain is not only defined as a sensation or a physical awareness, but also entails perception. Moreover, pain is an unpleasant and an uncomfortable emotion that is transferred to the brain by sensory neurons. There are various kinds of pain and how one perceives them is varied as well. Certain parts of the brain also play a key role in how one feels pain such as the parietal lobe, which is involved in interpreting pain while the hypothalamus is responsible for the response to pain one has. Although some believe pain is just a physical awareness and is in the body, pain is all in one’s mind because the perception of pain and the emotion that controls its intensity differs in individuals and when pain itself is administered to the body, the brain determines the emotions one attaches to each painful experience.
Neuropathic pain is a widespread health[1]. It is a complex disorder that leads to chronic illness. Although considerable progress has been made, the mechanisms of neuropathic pain have not been fully elucidated[2]. Accumulating evidence indicates that neuroinflammatory may play a critical role in the initiation and maintenance of neuropathic pain, which is now considered to be a neuroimmune disorder[3-6]. Researches showed that activation of glial cells (microglia and astrocytes) contributes to central nervous system neuroinflammation and promotes central sensitization, as well as subsequent development and maintenance of neuropathic pain[7-9]. In addition, several studies have shown that inhibiting microglial and astrocytic activation have analgesic effects in neuropathy[10-12]. Whereas, currently available drugs are either insufficiently effective, or produce undesirable side effects[6].
Pain is a personalized individual experience that is subjective and complex. It is, by definition, the result of unpleasant stimuli transmitted by the nervous system to the brain in an effort to alert one that something is wrong within the body (Ignatavicius, 2013). This stimuli can result anywhere from that of a pin-prick of a needle to that of an extensive burn as the result of a house fire. Moreover, pain can be emotional and mental as with that of difficult heartbreak or loss of loved one. All in all, the nature of pain is mystery to many health care professionals as it acts as a protective mechanism towards the body but varies from patient to patient. It is because of this that pain as a whole is “whatever the experiencing person says it is, existing wherever he or she says it does” (Ignatavicius, 2013). Even with its universality, this description of pain rests on the belief that the only person with the authority to describe the pain is the one experiencing it. It is with this belief and the lack of objective testing that all accounts of pain be taken seriously and managed in matter that is both efficient and ethical.
The most vital functions of the nervous system is to provide information about the occurrence or threat of injury. One of the ways this is done is in form of pain. However, sometimes, established pain can go beyond its protective role, thus becoming a disease in itself than just being a symptom. This condition is called chronic pain. The injury or the precipitating event can be physical (like in case of phantom limb pain or post-surgical pain), infection (as with post-herpetic neuralgia), systemic disease (like with diabetic neuropathy), drug (chemotherapy induced peripheral neuropathy) or can sometimes be unknown (trigeminal neuralgia, migraine, cluster headache, etc.) Even today, the pathological processes involved in genesis, establishment and continuation of such diseases are poorly understood. Eventually, such painful conditions usually remain refractory to available treatments.