Innovations In Clinical Neuroscience

MAY-JUN 2017

A peer-reviewed, evidence-based journal for clinicians in the field of neuroscience

Issue link:

Contents of this Issue


Page 18 of 35

Innovations in CLINICAL NEUROSCIENCE [ V O L U M E 1 4 , N U M B E R 5 – 6 , M A Y – J U N E 2 0 1 7 ] 19 pleasurability might augment activity in m otor-related regions, irrespective of whether the skin was itchy or not. 36 Thus, while each of the above disorders present with different primary symptoms, they all share HSA. Imaging s tudies in each of the disorders have found functional abnormalities in overlapping and unique brain areas associated with sensory-related processing. 34–36 TREATMENT IMPLICATIONS A full review of the treatment for these chronic sensations is beyond the scope of this review; however, while each of the aforementioned sensations has sensory specific treatments, two classes of neuromodulatory medications have been shown to effectively treat the central processing aberrations that might occur in chronic pain, nausea, and pruritus symptoms: anticonvulsants and antidepressants. More specifically, those anticonvulsants selectively bind to the α2–δ subunit of neuronal voltage-gated calcium channels (i.e., gabapentin and pregabalin), resulting in inhibition of calcium currents, thus decreasing the excitatory transmitter release and spinal sensitization. 37 Additionally, those antidepressants that interfere in the neuronal reuptake of neurotransmitters such as serotonin and norepinephrine (i.e., tricyclic antidepressants, mirtazapine, duloxetine) result in recruitment of noradrenergic-descending pathways as well as the peripheral recruitment of noradrenaline from sympathetic fibers sprouting into dorsal root ganglia. There is evidence of definitive treatment successes in all three of these chronic sensory sensations with these classes of medications. 37–40 REFERENCES 1. Schrepf A, Harper DE, Williams DA, et al. Somatic awareness and tender points in a community sample. J Pain. 2016;0(0):170–176. doi:10.1016/j.jpain.2016.08.009. 2. Brown RJ, Skehan D, Chapman A, et al. Physical symptom reporting is associated with a tendency to experience somatosensory distortion. Psychosom Med. 2012;74(6):648–655. doi:10.1097/PSY.0b013e3182595358. 3. Oh H-M, Chung M. Botulinum toxin for neuropathic pain: a review of the literature. Toxins (Basel). 2015;7(8):3127–3154. doi:10.3390/toxins7083127. 4. Borsook D. Neurological diseases and pain. Brain. 2012;135(Pt 2):320–344. doi:10.1093/brain/awr271. 5. Vardeh D, Mannion RJ, Woolf CJ, et al. Toward a mechanism-based approach to pain diagnosis. J Pain. 2016;17(9 Suppl):T50–69. doi:10.1016/j.jpain.2016.03.001. 6. Bardoni R. Role of presynaptic glutamate receptors in pain transmission at the spinal cord level. Curr Neuropharmacol. 2013;11(5):477–483. doi:10.2174/1570159X11311050002. 7. Fong A, Schug SA. Pathophysiology of pain. Plast Reconstr Surg. 2014;134:8S–14S. doi:10.1097/PRS.0000000000000682. 8. Scioli-Salter ER, Forman DE, Otis JD, et al. The shared neuroanatomy and neurobiology of comorbid chronic pain and PTSD. Clin J Pain. 2015;31(4):363–374. doi:10.1097/AJP.0000000000000115. 9. Ikoma A, Cevikbas F, Kempkes C, Steinhoff M. Anatomy and neurophysiology of pruritus. Semin Cutan Med Surg. 2011;30(2):64–70. doi:10.1016/j.sder.2011.04.001. 10. Mochizuki H, Kakigi R, Adam R, et al. Central mechanisms of itch. Clin Neurophysiol. 2015;126(9):1650–1660. doi:10.1016/j.clinph.2014.11.019. 11. Wallengren J. Neuroanatomy and neurophysiology of itch. Dermatol Ther. 2005;18(4):292–303. doi:10.1111/j.1529-8019.2005.00041.x. 12. Jovanovic M. Current concepts of pathophysiology, epidemiology and classification of pruritus. Srp Arh Celok Lek. 2014;142(1–2):106–112. doi:10.2298/SARH1402106J. 13. Dhand A, Aminoff MJ. The neurology of itch. Brain. 2014;137(2):313–322. 14. Metz M, Ständer S. Chronic pruritus— pathogenesis, clinical aspects and treatment. J Eur Acad Dermatology Venereol. 2010;24(11):1249–1260. doi:10.1111/j.1468-3083.2010.03850.x. 15. Potenzieri C, Undem BJ. Basic mechanisms of itch. Clin Exp Allergy. 2012;42(1):8–19. doi:10.1111/j.1365- 2222.2011.03791.x. 16. Han L, Dong X. Itch mechanisms and circuits. Annu Rev Biophys. 2014;43:331–355. doi:10.1146/annurev-biophys-051013- 022826. 17. Patel A, Sayuk GS, Kushnir VM, Gyawali CP. Sensory neuromodulators in functional nausea and vomiting: predictors of response. Postgrad Med J. 2013;89(1049):131–136. doi:10.1136/postgradmedj-2012- 131284. 18. Singh P, Yoon SS, Kuo B. Nausea: a review of pathophysiology and therapeutics. Therap Adv Gastroenterol. 2016;9(1):98–112. doi:10.1177/1756283X15618131. 19. Törnblom H, Abrahamsson H. Chronic nausea and vomiting: insights into underlying mechanisms. Neurogastroenterol Motil. 2016;28(5):613–619. doi:10.1111/nmo.12837. 20. Borsook D, Sava S, Becerra L. The pain imaging revolution: advancing pain into the 21st century. Neuroscientist. 2010;16(2):171–185. doi:10.1177/1073858409349902. 21. Stacey BR. Management of peripheral neuropathic pain. Am J Phys Med Rehabil. 2005;84(3 Suppl):S4–16. 22. Tracey I, Mantyh PW. The cerebral signature for pain perception and its modulation. Neuron. 2007;55(3):377–391. doi:10.1016/j.neuron.2007.07.012. 23. Jensen KB, Loitoile R, Kosek E, et al. Patients with fibromyalgia display less functional connectivity in the brain's pain inhibitory network. Mol Pain. 2012;8:32. doi:10.1186/1744-8069-8- 32. 24. Kringelbach M. The functional neuroanatomy of the human orbitofrontal cortex: evidence from neuroimaging and neuropsychology. Prog Neurobiol. 2004;72:341–372. 25. Peyron R, Laurent B, García-Larrea L. Functional imaging of brain responses to pain: a review and meta-analysis (2000). Neurophysiol Clin Neurophysiol. 2000;30(5):263–288. doi:10.1016/S0987-7053(00)00227-6. 26. Karshikoff B, Jensen KB, Kosek E, et al. Why sickness hurts: a central mechanism for pain induced by

Articles in this issue

Archives of this issue

view archives of Innovations In Clinical Neuroscience - MAY-JUN 2017