1.1.1. Background: Definition, Etiology, and Pathogenesis
A consensus definition of neuropathic pain is ‘pain resulting from a lesion of the somatosensory system, which results in faulty pain signaling’ [1]. The somatosensory system includes the peripheral nerves, spinal cord, and the cerebral cortex. Neuropathic pain is associated with many conditions including spinal cord compression, HIV, amputation, fibromyalgia, multiple sclerosis, postherpetic neuralgia, and diabetic neuropathy, and its pathogenesis in each of these states depends on the associated disease process. In the case of diabetic neuropathy, for example, longstanding hyperglycemia induces many metabolic processes including generation of free radicals and deposition of advanced glycation end-products in the microvasculature supplying peripheral nerves. These degradative processes result in direct toxicity and decreased blood flow, leading to nerve fiber degeneration and hyperexcitability of the primary afferent nociceptors [2].
Pain transmission through nociceptive nerve fibers involves many signaling molecules and ion channels, the most well studied of which are briefly mentioned below. Voltage gated sodium channels are involved in neuronal depolarization, and blockage of these channels is the mechanism of action of many first line pain medications. Transient potential receptor channels are expressed on nociceptive nerve fibers, such as C-fibers, and are involved in the development and maintenance of chronic pain. Blockage of voltage gated calcium channels, an alternative conduit involved in neuronal excitability, is the mechanism of action of gabapentin. Glutamate is the main excitatory neurotransmitter released by nociceptive afferent neurons and binds to the N-methyl-D-aspartic acid receptor, which is involved in central sensitization of spinal nociceptive neurons. Conversely, G-Amino Butyric Acid (GABA) is the main inhibitory neurotransmitter, and activation of GABA receptors causes inhibition of signal transmission. Substance P and Calcitonin Gene Related Peptide (CGRP) are neuropeptides released by nociceptive C-fibers and play a role in pain perception as well as signaling in the hypothalamus and amygdala. Finally, opioid receptors are widely distributed through the CNS and periphery. Presynaptically, opioids inhibit neurotransmitter release by reducing Ca2+ influx. Postsynaptically, opioids cause K+ efflux, which hyperpolarizes the cell and decreases the synaptic transmission [3].
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Patients experiencing neuropathic pain often have comorbid mood disorders, including depression and anxiety. A 2008 epidemiological study by Gustorff et al. suggests that about 34% of neuropathic pain patients experience feelings of depression, 25% report feelings of anxiety, and 60% report strong or predominant sleep disturbances [4]. Animal models have been used to demonstrate an association between neuropathic pain and depressive behavior with associated changes in the amygdala. Gonclaves et al. found increased signs of depressive-like behavior in rats who had undergone spared nerve injury (SNI), a procedure often used to induce neuropathic pain in animal models. They also noted increase amygdala volume in the SNI rats compared to controls [5]. The amygdala is involved in processing emotional states, and thus may be responsible for the connection between chronic pain and negative emotional states like depression and anxiety. Finally, chronic neuropathic pain causes sleep disruption, but sleep disruption also enhances pain perception and reduces pain tolerance [6].
Taken together, the etiology of neuropathic pain is ultimately multifactorial, as there are well established connections between neuropathic pain, depression, anxiety, and sleep problems.
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