Neuropathic Pain, Pain Matrix Dysfunction, and Pain Syndromes Flashcards
What are the four types of chronic pain?
- Nociceptive (mechanical, cancer, burns)
- Neuropathic (nerve entrapment, central pain, neuropathy)
- Pain matrix dysfunction (fibromyalgia, chronic whiplash, headache)
- Pain syndromes (CRPS, chronic LBP syndrome)
pain arising as a direct consequence of a lesion or disease affecting the somatosensory system, which can be anywhere in the somatosensory system (mechanical LBP, cancer, arthritis, burns)
Neuropathic pain
Individuals with genetic codes that produce less of the enzyme that regulates the levels of _______ and ______ are twice as likely to develop neuropathic pain as those who produce more of the enzyme
catecholamine; encephalin
painless abnormal sensation in the absence of nociceptor stimulation (tingling sensations)
Paresthesia
unpleasant abnormal sensation, either evoked or spontaneous (painful)
Dysethesia
pain evoked by a stimulus that normally would not cause pain (usually light touch)
Allodynia
excessive sensitivity to stimuli that are normally mildly painful in uninjured tissue
Secondary hyperalgesia
What are the symptoms of neuropathic pain?
- Paresthesia
- Dysesthesia
- Allodynia
- Secondary hyperalgesia
What are the 5 mechanisms that produce neuropathic pain?
- Ectopic foci
- Ephaptic transmission
- Central sensitization
- Structural reorganization
- Altered top-down modulation
When myelin is damaged, signals from the exposed axon stimulate excessive production of mechanosensitive and chemosensitive ion channels; Channels are inserted into the demyelinated membrane, producing abnormal sensitivity to mechanical and chemical stimuli; Demyelinated regions take on the new, pathologic role of generating action potentials in addition to the normal role of conducting action potentials
Ectopic foci
Cross-talk between axons in regions of demyelination
Ephaptic Transmission
Test where you tap along a nerve, the point where a nerve is injured becomes more sensitive; region where schwann cells are damaged, so insulation between axons is lost and one axon may stimulate its neighbor
Tinel’s sign
Occurs in the CNS; greater peripheral nerve sensitization occurs, so also has greater sensitization in CNS, resulting in increased perception of pain; as intense pain is prolonged, the CNS changes and everything becomes painful, no matter what the peripheral input is; pain does not reverse back to normal input
Central sensitization
Loss of nociceptive neuron from the body; sprouting occurs where touch sensation neuron makes connections with neurons that carry nociceptive information to the brain; hard to get back to normal
Structural reorganization
Antinociceptive pathways are decreased/inhibited/lost, so pain stimulus is increased because pronociceptive signals are not inhibited
Pain matrix dysfunction
Neuropathic pain arise from abnormal activity in the
- Periphery (e.g., nerve compression in carpal tunnel syndrome)
- CNS in response to deafferentation
- Dorsal horn