DESIREE CARUSO AND DR. ROMI FUNG, ND 2022-05-18 06:21:27
Pain and its impact on cognition
Pain and pain-related diagnoses leads the globe as the most common cause of disability and disease burden, with an estimated 1 in 6 adults suffering from pain and 1 in 10 chronic pain diagnoses in adults per year.1 Pain significantly affects the quality of life of billions of individuals worldwide, and in addition to psychological and social influences of pain, functional domains can also be impacted.2 In fact, the prevalence and epidemiology of pain is continuing to intensify.3 Health care systems have seen a rise in the prevalence of diagnoses such as chronic pain, fibromyalgia, and chronic regional pain syndrome.
A recent revision of the definition of pain was made in 2018, where the task force of the International Association for the Study of Pain (IASP) now currently defines pain as, “[a]n unpleasant sensory and emotional experience associated with, or resembling that associated with, actual or potential tissue damage.”4 Pain can have psychological impacts, and can affect our cognition through neuronal damage. This article aims to introduce the idea of pain as not primarily a physical characteristic, but also can impact our mental and cognitive health.
The correlation between pain and cognitive capacity is highly relevant. Research in the past two decades has provided tremendous insights into the bi-directional relationship that exists between pain and cognition, demonstrating the modulation of these domains on one another.2 Pain is composed of sensory components, afferent components, and cognitive components - an example of the cognitive aspect of pain is illustrated in one’s anticipation of future harm.5 Nociceptors, also known as sensory receptors that monitor damaged tissue and chemical signals indicating damage, become activated by noxious stimuli and thereby stimulate the insula and anterior cingulate cortex in the brain. Activation of these brain regions is connected with the subjective experience of pain.5 At the most elementary level, the pain pathway consists of transduction, transmission, modulation, and perception, respectively.2 One of the proposed pathways of pain and cognition highlights the modulation of the parasympathetic nervous system via baroreceptors.6 Baroreceptors serve as the gatekeepers to noxious stimuli at the level of brainstem nuclei, cortical and subcortical brain regions. Baroreceptors modulate neural activity that reaches these areas of the brain and therefore influences the diverse dimensions of pain perception at the anterior insula.6 Literature examining functional MRI studies in humans demonstrates that the anterior insula is responsible for integrating pain intensity and expectation of painful circumstances. Researchers concluded that the influence of baroreceptors on the anterior insula as a gatekeeper affects pain perception on cognition.6 Additionally, pain can exert its effects on cognition via stimulation of nerve fibers. Two players in the transduction of pain are A and C fibers, responsible for touch and pain, respectively. 2 These sensory fibers project information to the dorsal root ganglion, which are then directed to the central nervous system. With patients experiencing chronic pain, persistent noxious stimuli upregulate A fibers to compensate for an increase in pain information, in addition to C fibers; as a result, leading to hyperalgesia and central sensitization.2
Research in the last decade illustrates that patient-reported attention deficits have risen with the incidence of chronic pain
In clinical parameters, cognition is defined by domains such as attention, perception, memory, motor skills, executive functioning, and verbal and language skills.2 There is current evidence that pain has a direct effect on neuroplasticity, the brain’s ability to change neuronal connections in response to newer information. Chronic pain and hypersensitivity, or hyperalgesia, can influence these neuronal connections and thereby influence long-term memory. More specifically, when an individual experiences chronic pain, they may develop alternate responses to pain at the biochemical level; it is in this context that neuroplasticity may be exerting changes to one’s pain cycle.2 Research in the last decade illustrates that patient-reported attention deficits have risen with the incidence of chronic pain.2 Majority of the clinical studies examining cognition includes participants with chronic pain conditions such as fibromyalgia, migraine, chronic back pain, rheumatoid arthritis, diabetic neuropathy, osteoarthritis, CRPS, peripheral neuropathic pain syndromes, and multiple sclerosis. 2 With respect to neuroplasticity resulting from chronic pain, human studies highlight there is a decreased hippocampal volume, a brain region responsible for behaviour regulation, stress modulation, learning consolidation and short-term memory.2 Congruent with this evidence are findings in which the majority of patients with chronic pain report poor memory, recall, and concentration in their daily activities.2
Confirming that pain can affect cognition and cognitive domains, when pain is reversed, it has been found that cognition can be retrained. A study by Noorani et al. (2022) observed 61 patients with trigeminal neuralgia. What was common amongst the pain resolution group after surgical treatment was the recovery and normalization of the hippocampal volume as opposed to those who did not find significant pain resolution post-surgery.7 Although the study was small, this finding suggests that chronic pain can contribute to hippocampal burden and atrophy, and resolution of pain can contribute to the neuroplasticity of the hippocampus. Thus, treatment and investigation of pain should not be overlooked when working with patients exhibiting cognitive decline.
Addressing sources of pain and mitigating inflammatory processes should be a central focus in combination with psycho-social interventions. Interrupting the pain catastrophization cycle and reinterpreting the sensations of pain has been a cornerstone in the literature showing reduced pain severity.5
Based on research conducted by Suarez-Roca et al. (2021), afferent stimulation of the vagus nerve decreases chronic pain scores. Vagus nerve stimulation delivers analgesic effects; some of these analgesic effects are brought by modulation of inflammatory pathways.8 Vagal tone activation can be achieved by mechanical methods such as auricular acupuncture, or electrical stimulation such as transcutaneous electrical nerve stimulation (TENS).6 One study that investigated the impacts of vagal electrostimulation highlighted the reduction of pro-inflammatory cytokines in vitro, and significantly mitigated pain severity in rheumatoid arthritis patients.6 Thus, researchers deduced electrical stimulation of the vagus nerve activates the parasympathetic nervous system and decreases pain via proposed biochemical mechanisms including cytokines. Applying these principles to patients, treatment options that mitigate inflammation may dually impact the pain cycle, and cognition. Curcumin may display anti- inflammatory properties by blocking TNF directly in in vitro and in vivo studies, and in various types of cells.9 In vivo and in vitro studies of Boswellia serrata suggest interception of inflammatory mediators and may slow the progression of inflammatory, and conditions associated with pain, including osteoarthritis.10
Observation and identification of pain in patients is crucial, followed by prevention and treatment of pain in its early stages. Influencing pain patterns and pathways can be achieved in primal stages of chronic pain, prior to neuroplasticity influences on brain regions and the subsequent cognitive domains. Effective pain management requires a holistic approach, encompassing interventions involving symptomatic reduction, structural alignment, modulating inflammation, co-factors and nutrients for repair and structure, rehabilitation, and psychosocial and emotional support.
REFERENCES
1. Goldberg, D. S., & McGee, S. J. (2011). Pain as a global public health priority. BMC public health, 11, 770. https://doi. org/10.1186/1471-2458-11-770
2. Khera, T., & Rangasamy, V. (2021). Cognition and Pain: A Review. Frontiers in psychology, 12, 673962. https://doi. org/10.3389/fpsyg.2021.673962
3. Mills, S., Nicolson, K. P., & Smith, B. H. (2019). Chronic pain: a review of its epidemiology and associated factors in populationbased studies. British journal of anaesthesia, 123(2), e273– e283. https://doi.org/10.1016/j.bja.2019.03.023
4. Raja, S. N., Carr, D. B., Cohen, M., Finnerup, N. B., Flor, H., Gibson, S., Keefe, F. J., Mogil, J. S., Ringkamp, M., Sluka, K. A., Song, X. J., Stevens, B., Sullivan, M. D., Tutelman, P. R., Ushida, T., & Vader, K. (2020). The revised International Association for the Study of Pain definition of pain: concepts, challenges, and compromises. Pain, 161(9), 1976–1982. https://doi. org/10.1097/j.pain.0000000000001939
5. Garland E. L. (2012). Pain processing in the human nervous system: a selective review of nociceptive and biobehavioral pathways. Primary care, 39(3), 561–571. https://doi. org/10.1016/j.pop.2012.06.013
6. Suarez-Roca, H., Mamoun, N., Sigurdson, M. I., & Maixner, W. (2021). Baroreceptor Modulation of the Cardiovascular System, Pain, Consciousness, and Cognition. Comprehensive Physiology, 11(2), 1373–1423. https://doi.org/10.1002/cphy.c190038
7. Noorani, A. Hung, P. SP., Zhang, J. Y., et al. (2022). Pain Relief Reverses Hippocampal Abnormalities in Trigeminal Neuralgia. The Journal of Pain, 23(1); 141-155.
8. Chakravarthy, K., Chaudhry, H., Williams, K., & Christo, P. J. (2015). Review of the Uses of Vagal Nerve Stimulation in Chronic Pain Management. Current pain and headache reports, 19(12), 54. https://doi.org/10.1007/s11916-015-0528-6
9. He, Y., Yue, Y., Zheng, X., Zhang, K., Chen, S., & Du, Z. (2015). Curcumin, inflammation, and chronic diseases: how are they linked?. Molecules (Basel, Switzerland), 20(5), 9183–9213. https://doi.org/10.3390/molecules20059183
10. Bannuru, R. R., Osani, M. C., Al-Eid, F., & Wang, C. (2018). Efficacy of curcumin and Boswellia for knee osteoarthritis: Systematic review and meta-analysis. Seminars in arthritis and rheumatism, 48(3), 416–429. https://doi.org/10.1016/j. semarthrit.2018.03.001
Mathur, V. A., Khan, S. A., Keaser, M. L., Hubbard, C. S., Goyal, M., & Seminowicz, D. A. (2015). Altered cognition-related brain activity and interactions with acute pain in migraine. NeuroImage. Clinical, 7, 347–358. https://doi.org/10.1016/j. nicl.2015.01.003
Polaski, A. M., Phelps, A. L., Kostek, M. C., Szucs, K. A., & Kolber, B. J. (2019). Exercise-induced hypoalgesia: A meta-analysis of exercise dosing for the treatment of chronic pain. PloS one, 14(1), e0210418. https://doi.org/10.1371/journal.pone.0210418
DESIREE CARUSO is a 4th year naturopathic student at CCNM. She has an undergraduate degree in biology during which she played collegiate soccer. Her special interests include concussions, postconcussion syndrome, sports medicine, and pain management.
DR. ROMI FUNG, ND practices in Richmond, BC. A graduate of CCNM, Romi helps patients living with dementia improve their quality of life by taking an integrative and functional approach. On top of his practice, Romi is currently a Ph.D. candidate in Aging and Health at Queen’s University, an Adjunct Clinical Faculty and Academic Faculty teaching Traditional Asian Medicine at the Canadian College of Naturopathic Medicine – Boucher Campus. DrRomiFungND.com
©Annex. View All Articles.