Pain is a type of distressing feeling that is caused as a result of a stimuli, which is highly damaging or intense. According to the International Association for the Study of Pain, pain is defined as “An unpleasant sensory and emotional experience associated with actual or potential tissue damage, or described in terms of such damage” (“International Association for the Study of Pain (IASP)”, 2017). Pain is highly critical for the survival of living organisms. The central features of chronic pain are usually caused as a result of sensory abnormalities. Pain generally resolves once the associated stimulus is removed but sometimes pain arises in the absence of any damage or detectable stimulus. The International Association for the Study of Pain (IASP) classifies pain based on certain characteristics. These characteristics include duration and intensity of pain, the cause of the pain, system dysfunction responsible for the pain and regions of the body that is subjected to the pain (Treede et al., 2015).
Clifford J. Woolf of Harvard Medical School classified pain into 3 categories. These include the nociceptive pain, inflammatory pain and pathological pain (Vardeh, Mannion & Woolf, 2016). Apart from the characterization of pain based on its pathophysiology, peripheral source, location, intensity, distribution and nociceptive quality, pain can further be characterized based on its acute or chronic nature and neuropathic or nociceptive dichotomization. These characterizations are regulated by various factors like genes, gender, motivational or emotional circumstance, cognitive interpretations, neuropsychopathology, endorphin concentration as well as social, cultural or religious setting plays an important role. Both the brain and the spinal cord are considered the dynamic pain connectome (Elman & Borsook, 2016).
This report critically evaluates the statement “Pain is all in the Brain”. This report at first gives a brief concept about pain and its association with the brain. Next, it carries out a critical evaluation of journal articles related to this topic, describes the mechanisms of action of pain killers, defines the placebo effect and defines some of the new technologies that are used for management of pain.
Concepts of pain
Acute pain is caused due to tissue damage. It is termed as nociceptive pain or pain that occurs as a result of actual or potential damage to non neural tissues and results in activation of the nociceptors (Mailhot et al., 2012). The pain signals are transmitted from the damaged peripheral tissues via the neurons of the dorsal horn involved in pain transmission to the brain regions that in turn receives the pain inputs. The damages are caused either by the presence of a disease or a lesion. Chronic pain on the other hand lasts longer than acute pain as long as 3 months. Chronic pain is a combination of emotional and sensory experiences. However, it varies between individuals depending on the psychological state of an individual or the meaning and context associated with the pain. Perception of pain is generally influenced by both emotional and cognitive factors and this in turn is associated with the regions of the brain involved in pain perception, control of emotions, expectations and attention. Research have revealed the presence of brain alterations in regions involved in emotional and cognitive regulation of pain (Crofford, 2015).
Nociceptive pain is a type of chronic pain caused that is characterized by a throbbing, aching or sharp sensation resulting from damage to tissues of the body. Nociceptive pain is caused as a result of tumours or cancerous cells spreading to other parts of the body, thereby resulting in blockage to either blood vessels or organs of the body (Lozano-Ondoua, Symons-Liguori & Vanderah, 2013). Neuropathic pain is usually caused as a result of damage to the somatosensory nervous system. Nerves helps the brain to carry out communications with various parts of the body and also acts as a connection that links the spinal cord to the whole body. Various factors can give rise to neuropathic pain like toxins, alcohol, lack of proper nutrition, auto-immunity and infection. These factors damage the nerves that bring about connections between the brain, spinal cord and the rest of the body. Damage to the nerves is characterized by numbness and a burning sensation (Cohen & Mao, 2014). Psychogenic pain is caused as a result of mental, behavioral and emotional factors (Chhabria, 2015). Another form of pain is the breakthrough pain, which is characterized by its sudden nature and the inability of regular pain management systems to alleviate it (Mercadante, 2012).
Neurocircuitry of pain
The neural sensory apparatus comprises the domains of the biological pain, which includes the nociceptors, regions of the thalamus, amygdala and the nucleus accumbens as well as the afferent neurons. The primary and secondary somatosensory cortices analyze nociceptive signals. However, if the nociceptive signals are inhibited, it results in a placebo effect at the dorsal horn, while if amplified, it results in a nocebo effect (Faasse & Petrie, 2013). This modulation is carried out by brain regions like the insular cortex and the cingulate gyrus by way of connections with the brain stem nuclei like the periaqueductal gray matter. Apart from these, the reticular nuclei, parabranchial nucleus, superior colliculus and hypothalamus receive the pain input from the spinothalamic tract through the regions of the brain stem nuclei and the medial thalamic nuclei. The prefrontal cortex of the brain is associated with the conscious appraisal of pain, its enhancement as well as suppression (Elman & Borsook, 2016; Borsook et al., 2013).
Critical evaluation of data
This part of the report describes and critically evaluates the studies depicted in the articles titled: “Evidence of brain glial activation in chronic pain patients”, “Does rejection hurt? An fMRI study of social exclusion and “Neurological diseases and pain”.
The first article deals with the role played by the glial cells in association with chronic pain. Previously various research works have described the roles of microglial cells and astrocytes in the establishment and subsequent maintenance of chronic pain (Beggs, Trang & Salter, 2012). The translocator protein (TSPO) present in the brain acts as a marker indicating glial activation and this study has shown increased expression of the protein observed in patients suffering from chronic pain of the lower back. Tracers were used to determine the production of the protein in the brain and increased amounts of tracers were observed in the thalamus. Nerve injury causes activation of the and subsequent proliferation of the spinal microglia and the upregulation of receptors like the chemokine receptor CX3CR1 and adenosine triphosphate receptor P2RX4. This in turn results in the induction of hyperalgasia. The production of brain derived neurotrophic factor (BDNF) and the proinflammatory cytokines by activated microglial cells results in activation of the nociceptive neurons. Moreover, trigeminal nerve injuries results in astrocytes exhibiting hypertrophy and also shown to express enzymes like nitric oxide synthase as well as cytokines like the IL1B and chemokines like CXCL2. This study revealed that following injuries to the central nervous system, there is upregulation of TSPO along with increased levels of microglial activity. This study also revealed a negative correlation between thalamic TSPO levels and clinical pain together with circulating levels of interleukin 6, which is a pro-inflammatory cytokine. Thus, the study indicates that expression of TSPO exerts an anti-inflammatory or pain protective effect. Thus, the importance of this study is that glia can act as a therapeutic target in case of chronic pain. Therefore, drugs can be designed to decrease glial activation, thereby inhibiting the release of pro-inflammatory cytokines and subsequent activation of neuropathic pain. Moreover, it also suggests that TSPO ligands can be assigned the role of a novel therapeutic target that can help in the treatment of chronic pain. Thus, apart from using TSPO ligands as a therapeutic target, increased expression of TSPO can be used as a marker for imaging the damaging effects of pain on the brain regions (Loggia et al., 2015).
The second article identifies the regions of the brain that are activated as a result of social exclusion. The study reveals that some of the mechanisms that are activated during physical pain are also activated as a result of psychological pain like social exclusion. The regions of the brain that are activated in both physical as well as social pain are the anterior cingulate cortex and the right ventral prefrontal cortex (Lieberman & Eisenberger, 2015; Eisenberger, 2015). The results of the study suggested that the right ventral prefrontal cortex regulates the distress caused as a result of social exclusion by disrupting the activity of the anterior cingulate cortex. To determine this, a functional magnetic resonance imaging or fMRI was carried out. The anterior cingulate cortex is associated with pain resulting from distress and in turn acts as an alarm system. This is the first study that links the anterior cingulate cortex with the social rejection. Right ventral prefrontal cortex on the other hand is involved in inhibition of the pain caused due to distress and this is carried out by regulation of the activities of the anterior cingulate cortex. Explicit social exclusion was found to activate the regions of the right ventral prefrontal cortex. Moreover, the activity of the anterior cingulate cortex was found to be high during implicit social exclusion. Thus, the study indicates that the neurocognitive functions that are activated during physical pain is analogous to the neurocognitive functions activated during social pain, thereby urging the need for restorative measures. It creates new understandings about the mechanisms of physical and social pain and also indicates that social pain is equally damaging when compared with physical pain, thereby indicating the importance of neurochemical interventions and social support in both the cases (Eisenberger, Lieberma & Williams, 2003).
The third article describes the role of chronic pain in the development of various neurological diseases. Neurological disorders are caused due to a variety of reasons like neuroinflammation, neurodegeneration and injuries to the central nervous system. Chronic pain is described as a disease of the brain that causes alterations of neural networks thereby affecting brain chemistry, structure and function. Pain may result as a consequence of disease or can act as a marker for disease. Most of the neurological diseases primarily arise from chronic pain. The pain acts as a course of the neurological disease and is linked with the development of changes in the central nervous system resulting from pain. Pain is an integral part of Parkinson’s disease, which is a neurodegenerative disease. Patients suffering from Parkinson’s disease also exhibit the phenomenon of temporal summation. Parkinson’s disease results in greater sensitization to repeated pain stimuli indicating changes in supraspinal inputs to systems that modulate pain (Ha & Jankovic, 2012). Moreover, processing of pain is altered in neurodegenerative conditions like Alzheimer’s disease. Moreover, pain tolerance also increases with increase in disease severity. Although the thalamic nuclei and the sensory or discriminative cortex remains unaltered in Alzheimer’s disease, however, changes in the hippocampus, prefrontal cortex and limbic structures may be the reason for the loss of cognitive functions and subsequent increase in pain tolerance. Moreover, it can also be due to decrease in pain modulation carried out in regions such s the periaqueductal grey. Thus, instead of responding or interpreting the pain, patients with Alzheimer’s disease show abnormal behaviors like agitation, aggression, among others. Huntington’s disease is another neurodegenerative disease that affects the brain, particularly the regions of the thalamus that is involved in sensory perception. Moreover, the basal ganglia is also affected, which plays an important role in the processing of both chronic and acute pain. This in turn results in alterations in the processing of pain in patients affected by Huntington’s disease. Apart from neurodegenerative diseases, pain has also been associated with neuromuscular diseases such as amyotrophic lateral sclerosis (Carter et al., 2012). Moreover, this study also reflects on the importance of CT scan and MRI in the targeted delivery of drugs to regions of nerves with the objective to carry out pain management. An example is the use of adriamycin, which can be delivered to the dorsal root ganglion in order to prevent pain. Diagnosis and measurement of pain is particularly problematic and challenging in the case of patients with neurodegenerative diseases. These are painDETECT, diffusion tensor imaging, among others. These technologies work on the principle of measurement of grey matter and resting state networks (Borsook, 2012).
Neurotransmitters and pain
Neurotransmitters are chemical messengers that help in the transmission of signals across the chemical synapse like a neuromuscular junction. They are also involved in the transmission of signals from one nerve cell or neuron to another, or to either a muscle cell or a gland cell. Glutamate, gamma aminobutyric acid, dopamine and serotonin are some of the examples of neurotransmitters found in the brain. Neurotransmitters not only play an important role in the behavior or mood of an individual but also is involved in perceptions of pain. High glutamate levels in the brain are associated with chronic pain. Gamma amino butyric acid or GABA is also responsible for the development of many pain states. Increased secretion of endorphins (a neurotransmitter) is associated with high levels of pain and it helps to reduce the pain perceptions by binding to the opiate receptors of the brain. Its mode of action is similar to drugs like codeine and morphine, which are also involved in relieving pain (Pureti? & Demarin, 2012).
Pain relieving drugs and their mechanisms
Morphine is a pain relieving drug that binds to opioid receptors and activates them. The 3 classes of receptors are the Mu, kappa and delta receptors. Activation of these receptors results in pain relief. The opioids bring about their pharmacological actions by binding to the receptors present on the neuronal cell membrane. It prevents the release of neurotransmitters that are associated with chronic pain. Codeine is another opioid that like morphine bind to the opioid receptors thereby preventing the transmission of pain sensation and it also increases pain tolerance, causing sedation and depressed breathing (Jones & Brown, 2017).
Placebo Effect
Placebo effect is a response to an intervention that is not actually a treatment but the conditions of the patient improves since the expectations of the patient is that the intervention is beneficial to them. Placebo effects are potent pain relievers. The placebo analgesic response is based on the principles of psychological and neurobiological understandings. Recent research has revealed that placebo effects can act as painkillers by promoting the release of opioids and nonopioids in the human body. Apart from these, observational learning and social support also contributes to the placebo effects. Verbal suggestions play an important role in inducing pain reduction and thereby placebo effect by enabling the patient to recall experiences related to previous analgesia and in turn stimulating their desire to cope with the pain. Expectations related to pain relief can be heightened by use of a pill, which has a direct effect of reducing the painful stimuli and evoking analgesia. Placebo effects are known to affect regions of the brain and is related to the brain structure like the density of the gray matter. Research revealed that grey matter density of the dorsolateral prefrontal cortex, nucleus accumbens and insula are associated with increased placebo analgesics effects. Functional connection between the rostral anterior cingulate cortex and the right frontoparietal network positively affects the analgesic expectations. Placebo effects have been shown to activate regions of the dorsolateral prefrontal cortex, the hypothalamus, periaqueductal gray, amygdale and the anterior cingulated cortex. Pharmacological treatments or interventions that provide pain relief are associated with placebo effects that in turn determines the positive therapeutic outcomes (Medoff & Colloca, 2015).
Due to significant rise of opioid epidemics, researchers try to find out alternatives methods for relieving pain. Some of the recently developed technologies are the HEAT Pain Pro TENS Device, Radiofrequency ablation device, ActiPatch, BURST DR Stimulation and the Virtual reality. The HEAT Pain Pro TENS Device functions by transmitting electrical pulses across the skin and nerves, thereby preventing the pain signals to reach the brain. Moreover, it also results in the release of endorphins that is responsible for providing pain relief. The radiofrequency ablation device uses heat generated from alternating current to denervate tissues that form a part of the peripheral nervous system. The ActiPatch uses electromagnetic activity to reduce the pain perception ability of the brain. The BurstDR stimulation technology provides pain relief by carrying out spinal cord stimulation. The virtual reality technology provides a high level of sensory experience to the patients and reduces pain by its ability to engage the patients in activities that require interaction and a high level of brain attention (Www.clinicalpainadvisor.com, 2017).
Conclusion
Pain is associated with its connections directly with the brain. Studies have reported that chronic pain can have a long term effect on the regions of the brain, thereby having effects on the individual at a psychological level. Cells of the brain and spinal cord of individuals suffering from long lasting chronic pain undergo deterioration and in turn may give rise to symptoms of depression and other neurological diseases. However, with the onset of neurological diseases, changes in the brain chemistry and structure bring about alterations in the pain processing ability of the brain. However, opioids play an important role in providing pain relief and in addition to these modern technologies have also been found to be successful in providing pain relief.
Reference List
Beggs, S., Trang, T., & Salter, M. W. (2012). P2X4R+ microglia drive neuropathic pain. Nature neuroscience, 15(8), 1068-1073.
Borsook, D. (2012). Neurological diseases and pain. Brain, 320-344.
Borsook, D., Edwards, R., Elman, I., Becerra, L., & Levine, J. (2013). Pain and analgesia: the value of salience circuits. Progress in neurobiology, 104, 93-105.
Carter, G. T., Miró, J., Abresch, R. T., El-Abassi, R., & Jensen, M. P. (2012). Disease burden in neuromuscular disease: the role of chronic pain. Physical medicine and rehabilitation clinics of North America, 23(3), 719-729.
Chhabria, A. (2015). Psychogenic pain disorder–differential diagnosis and treatment. J. Assoc. Physicians India, 63, 36-40.
Cohen, S. P., & Mao, J. (2014). Neuropathic pain: mechanisms and their clinical implications. Bmj, 348(f7656), 1-12.
Crofford, L. J. (2015). Chronic pain: where the body meets the brain. Transactions of the American Clinical and Climatological Association, 126, 167.
Eisenberger, N. I. (2015). Social pain and the brain: Controversies, questions, and where to go from here. Annual Review of Psychology, 66, 601-629.
Eisenberger, N. I., Lieberman, M. D., & Williams, K. D. (2003). Does rejection hurt? An fMRI study of social exclusion. Science, 302(5643), 290-292.
Elman, I., & Borsook, D. (2016). Common brain mechanisms of chronic pain and addiction. Neuron, 89(1), 11-36.
Faasse, K., & Petrie, K. J. (2013). The nocebo effect: patient expectations and medication side effects. Postgraduate medical journal, postgradmedj-2012.
Ha, A. D., & Jankovic, J. (2012). Pain in Parkinson’s disease. Movement Disorders, 27(4), 485-491.
International Association for the Study of Pain (IASP). (2017). Iasp-pain.org. Retrieved 30 December 2017, from https://www.iasp-pain.org/
Jones, A. K. P., & Brown, C. A. (2017). Predictive mechanisms linking brain opioids to chronic pain vulnerability and resilience. British Journal of Pharmacology.
Lieberman, M. D., & Eisenberger, N. I. (2015). The dorsal anterior cingulate cortex is selective for pain: Results from large-scale reverse inference. Proceedings of the National Academy of Sciences, 112(49), 15250-15255.
Loggia, M. L., Chonde, D. B., Akeju, O., Arabasz, G., Catana, C., Edwards, R. R., … & Riley, M. (2015). Evidence for brain glial activation in chronic pain patients. Brain, 138(3), 604-615.
Lozano-Ondoua, A. N., Symons-Liguori, A. M., & Vanderah, T. W. (2013). Cancer-induced bone pain: Mechanisms and models. Neuroscience letters, 557, 52-59.
Mailhot, J. P., Vachon?Presseau, E., Jackson, P. L., & Rainville, P. (2012). Dispositional empathy modulates vicarious effects of dynamic pain expressions on spinal nociception, facial responses and acute pain. European Journal of Neuroscience, 35(2), 271-278.
Medoff, Z. M., & Colloca, L. (2015). Placebo analgesia: understanding the mechanisms. Pain management, 5(2), 89-96.
Mercadante, S. (2012). Pharmacotherapy for breakthrough cancer pain. Drugs, 72(2), 181-190.
Pureti?, M. B., & Demarin, V. (2012). Neuroplasticity mechanisms in the pathophysiology of chronic pain. Acta Clin Croat, 51(2), 1.
Treede, R. D., Rief, W., Barke, A., Aziz, Q., Bennett, M. I., Benoliel, R., … & Giamberardino, M. A. (2015). A classification of chronic pain for ICD-11. Pain, 156(6), 1003.
Vardeh, D., Mannion, R. J., & Woolf, C. J. (2016). Toward a Mechanism-Based approach to pain diagnosis. The Journal of Pain, 17(9), T50-T69.
Www.clinicalpainadvisor.com, A. (2017). Five New Technologies for Pain Management. Clinical Pain Advisor. Retrieved 30 December 2017, from https://www.clinicalpainadvisor.com/treatments/new-technologies-for-pain-to-know-about/article/561986
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