Module 15: Chronic and Neuropathic Pain

what is chronic pain?

pain that persists more than 3-6 months. Pain that outlasts the usual time for tissue healing/recovery period. It often considered its own medical condition so treatment strategies for it are going to differ compared to acute pain management

what is the prevalence of chronic pain?

approx 50 million living with chronic pain, and 17 million of these adults live with chronic pain that substantially restricts their ability to participate in daily activities of their lives

what are examples of chronic pain?

chronic neck or back pain, migraines, arthritis or joint pain, neuropathic pain, cancer pain (tho cancer pain is its own category kind of)

what is the general mechanism underlying chronic pain?

there is “re-wiring” of the nervous system to maintain pain signals, which lead to altered pain processing. the painful stimulus amplifies itself so much that even after initial stimulus resolves, the pain remains. known as sensitization

what is peripheral sensitization?

sensitization that occurs at the site of tissue injury- injury to the vascularized tissue initiates the inflammatory process, when cells that flood the area release pro-inflammatory chemicals it the area, and these bind to the nociceptors and cause the ion channels to open, leading to an influx of positive ions, leading to a lowered threshold. this results in nociceptors firing more easily and more frequently

what is the clinical presentation of peripheral sensitization?

see all the cardinal signs of inflammation (redness, heat, edema, pain). because the “volume has been turned up to max volume” at the tissue level, now will experience pain with a normally mildly painful stimuli (hyperalgesia)

what is central sensitization?

sensitization that occurs when the CNS gets stuck in a heightened pain response mode, pain signals are amplified within the spinal cord and brain. With repeated input, the neurons become more excitable and increasingly responsive to the pain signals, so now even the smallest of stimuli can be perceived as painful (allpdynia). over time, the CNS can also become less dependent on peripheral input, this is why pain persists even after tissue healing

What are the components of the biopsychosocial model of chronic pain?

sensory (biological), cognitive (psychological), and affective (emotional/social) factors

what is the characteristic presentation of chronic pain?

pain symptoms can be both physical and emotional. Natural response to pain is to guard, which can lead to muscle stiffness and weakness. Often leads to sensory changes like hyperalgesia, allodynia, sleep disturbances and fatigue, and emotion/mood changes (like loss of interest in activities once enjoyed, feelings of worry/anxiety/depression)

what is the relationship between affective domain and chronic pain?

individuals with chronic pain have higher incidence of psychological factors of depression and anxiety. treating one can influence the other! this is where the off label use of antidepressants and anxiolytics comes in

how do antidepressants work for chronic pain?

pain inhibition relies on serotonin and norepinephrine, chronic pain decreases the effectiveness of descending inhibitory pathways and antidepressants increase serotonin and norepinephrine levels in the synapse, which results in the brain’s ability to suppress pain

what are the primary antidepressants used in chronic pain?

serotonin and norepinephrine reuptake (SNRIs- cymbalta/duloxetine), tricyclic antidepressants (TCAs- elavil/pamelor)

how does context affect pain experience?

study found that focused visual attention to a noxious stimulus matters

can we learn to control activation of brain regions linked with pain perception?

yes. people can learn to voluntarily control activation of localized brain regions associated with pain. study used fMRIs to train participants, and that voluntarily manipulating rostral anterior cingulate cortex activation and mediated pain perception

what is the pain neuromatrix?

refers to the network of brain regions involved in the processing and modulation of pain, integrating sensory, emotional, and cognitive aspects of pain experience. involves somatic, psychological, and social factors and perception

what is the twin peak theory?

suggests that pain perception arises from two processes: a rapid, reflexive response to harmful stimuli and a slower, more cognitive processing that involves the evaluation of the experience and its context. this leads to a larger pain buffer zone that serves to keep tissues safer, and this leads to triggering of pain before there is potential for harm

what is neuropathic pain?

pain that is caused by actual damage or disease impacting the somatosensory nervous system serving the skin, musculoskeletal structures, and viscera

what is peripheral neuropathic pain?

originates from damage or disease impacting peripheral nerve. results from trauma, metabolic diseases, infections, tumors, chronic nerve compression/impingement.

what are examples of peripheral neuropathic pain?

diabetic neuropathy, carpal tunnel syndrome, shingles-related nerve damage

what is the clinical presentation of peripheral neuropathic pain?

distribution of symptoms are more localized. Distribution of pain follows specific peripheral nerve (cutaneous distribution) or dermatomal pattern

what is central neuropathic pain?

originates from lesion or disease process impacting the CNS (brain or spinal cord). examples are stroke, MS, SCI

what is the clinical presentation of central neuropathic pain?

distribution of pain symptoms are more diffuse/widespread, affecting larger region of the body (entire limb, entire side of the body)

what are the hallmark clinical symptoms of neuropathic pain?

persistent, intermittnet, spontaneous pain. Can be intense burning, tingling, or electric shock, sharp, stabbing, shooting pain, “pins and needles”, paresthesias, pain symptoms are spontaneous, which occur in absence of noxious stimulus or trigger/event. May have hyperalgesia, allodynia

what is involved in the pharmacological management of neuropathic pain?

medications are taken for reducing pain intensity, and to enhance the quality of life. First line drugs include antidepressants (SNRIs, TCAs like cymbalta) and antiepileptics/anticonvulsants acting on calcium channels

what is the off label use of antiepileptics for neuropathic pain?

gabapentin (neurotin) and pregabalin (lyrica), commonly used for their ability to stabilize overactive neuronal firing, turns down overactive neurons involved with pain signaling.

what is the mechanisms of action for antiepileptics for neuropathic pain?

they are calcium channel blockers, binds with voltage gated calcium channels on pre-synaptic cells, which decrease the release of excitatory neurotransmitters (glutamate, substance P)

what is phantom limb pain?

theorized to be associated with negative neuroplastic changes in sensory and motor cortices. In the brain there is extensive overlapping of representations of body parts, and when one is removed there is no more use for it so expansion of neighboring areas to the deafferented area. the extent of cortical reorganization is believed to be correlated with severity of the phantom pain.

what are the additional theories for phantom limb pain?

• absence of sensory information from amputated body pain causes neurons in central nociceptive pathway to become overactive.

• maladaptive structural reorganization found at multiple levels of the nervous system, so not just in the motor and sensory cortices

what are treatment interventions for phantom limb pain?

aim to reverse maladaptive cortical reorganization. Can do mirror therapy for neuroplasticity. Can also do graded motor imagery, visual feedback therapy, and virtual reality

what is fibromyalgia?

condition in which individuals have abnormal pain processing, the common central sensitivity syndrome in which pain matrix malfunction disrupting top-down regulation of pain. Etiology is not well understood

how is fibromyalgia diagnosed?

through patient history, physical exam, labs and exclusion of other causes

what is the clinical presentation of fibromyalgia?

widespread/diffuse pain and tenderness, stiffness in muscles and joints, fatigue, mood changes, sleep disturbances, cognitive changes like brain fog

what is complex regional pain syndrome?

typically is triggered by peripheral injury and peripheral sensitization. Sympathetics signaled within the spinal cord, triggering a inflammatory response, exacerbating pain. central sensitization leads to alterations to the somatotopy within VPL of the thalamus or primary somatosensory cortex