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Chapter 8: Neuropathic Pain, Pain Matrix Dysfunction, and Pain Syndromes
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2. Chronic Pain as a Disease
Pain involves inhibitory and excitatory circuits in the CNS that either diminish or amplify pain messages.
Neural mechanisms for regulating pain amplify signals, creating pain in the absence of noxious stimuli in neuropathic pain, pain matrix dysfunction, and pain syndromes.
Pathologic pain has no beneficial biological function.
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3. Four types of Chronic Pain
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Neuropathic Pain
International Association for the Study of Pain defines neuropathic pain as “pain arising as a direct consequence of a lesion or disease affecting the somatosensory system.”
Individuals with genetic codes that produce less of the enzyme that regulates the levels of catecholamine and encephalin are twice as likely to develop neuropathic pain as those who produce more of the enzyme.
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5. Symptoms of Neuropathic Pain
Paresthesia: painless abnormal sensation in the absence of nociceptor stimulation
Dysesthesia: unpleasant abnormal sensation, either evoked or spontaneous
Allodynia: pain evoked by a stimulus that normally would not cause pain
Secondary hyperalgesia: excessive sensitivity to stimuli that are normally mildly painful in uninjured tissue
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6. Five Mechanisms Produce Neuropathic Pain
Ectopic foci
Ephaptic transmission
Central sensitization
Structural reorganization
Altered top-down modulation
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7. Mechanisms of Neuropathic Pain
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Ectopic Foci
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.
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9. Ephaptic Transmission
Cross-talk between axons in regions of demyelination
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10. Central Sensitization
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11. Structural Reorganization
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12. Sites that Generate Neuropathic Pain
Neuropathic pain can arise from abnormal neural activity in the following:
Periphery (e.g., nerve compression in carpal tunnel syndrome)
CNS in response to deafferentation
Dorsal horn
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13. Peripheral Generation of Neuropathic Pain
Injury or disease of the peripheral nerves often results in sensory abnormalities.
Complete nerve resection results in a lack of sensation from that nerve’s receptive field.
Partial damage can result in allodynia and sensations similar to an electric shock.
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14. Peripheral Generation of Neuropathic Pain
Peripheral abnormalities causing neuropathic pain include the following:
Development of ephaptic transmission that occurs in demyelinated regions
Ectopic foci in an injured nerve that occurs at the nerve stump, in areas of myelin damage, or in dorsal root ganglion somas
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15. Central Response to Deafferentation
Deafferentation can be complete or partial.
Neurons in the CNS may become abnormally active when peripheral sensory information is completely absent.
Avulsion of dorsal roots from the spinal cord produces deafferentation and causes an individual to feel burning pain in the area of sensory loss.
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16. Central Response to Deafferentation
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Phantom Pain
Phantom limb sensation refers to individuals who have had a limb amputated but experience sensations that seem to originate from the missing limb.
Phantom sensation that is painful is called phantom pain; reports of this are more rare.
Phantom pain must be differentiated from residual limb pain; treatment for residual limb pain is different than for phantom limb pain
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Central Pain
Central pain is caused by a lesion of the CNS and is usually localized to the area of the body deafferented by the lesion.
Neuropathic central pain refers to burning, shooting, aching, freezing, or tingling pain.
SCI central pain: the thalamus may be the site of pain generation because after a SCI, the neurons in the VPL thalamic nucleus are spontaneously active without input from the spinal cord.
MS central pain depends on the location of the lesion.
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19. Pain Matrix Dysfunction
Top-down regulation of pain is disturbed when the pain matrix malfunctions.
Antinociception is reduced and/or pronociception is intensified; the result is increased pain.
Fibromyalgia, episodic tension-type headache, migraine, and chronic whiplash-associated disorder involve disturbance of top-down regulation of pain.
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Fibromyalgia
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21. Episodic Tension-Type Headache
Criteria for ETTH:
Mild-to-moderate pain, usually bilateral
Lasting 30 minutes to 7 days
Not aggravated by physical activity
Not associated with nausea or vomiting
Photophobia or phonophobia, but not both, may accompany the headache.
Mechanism appears to be supersensitivity to nitric oxide.
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Pain Syndromes
Two syndromes involve other systems in addition to the pain system:
Complex regional pain syndrome involves the somatosensory, autonomic, and motor systems.
Chronic low back pain syndrome involves muscle guarding, disuse, and abnormal movements.
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23. Complex Regional Pain Syndrome
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24. Complex Regional Pain Syndrome
Former names
Causalgia
Shoulder-hand syndrome
Sympathetically maintained pain
Reflex sympathetic dystrophy
Sudeck’s atrophy
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25. Chronic Low Back Pain Syndrome
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26. Surgical Treatment of Chronic Pain
In theory, dorsal rhizotomy should alleviate pain; however, it often fails in practice.
Persistence of pain after spinothalamic tractotomy may be the result of CNS changes in response to the original maintained pain or to pain-mediating fibers traveling in the dorsal columns.
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27. Pharmacological Treatment of Pain
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28. Psychologic Factors in Chronic Pain
Expectations, cognition, and emotions affect the experience of pain.
Anxiety, depression, and catastrophizing predict reactions to pain and the ability to cope with pain.
Amount of pain an individual expects influences the processing in both the medial and lateral pain systems.
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29. Psychologic Factors in Chronic Pain
Therapists must address all three Ds of chronic pain:
Distress
Disuse
Disability
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30. Psychologic Factors in Chronic Pain
Psychologic interventions may decrease activation of the pain system and also improve coping skills.
Relaxation (breathing, muscle relaxation)
Biofeedback
Imagery
Cognitive behavioral therapy
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31. Psychologic Factors in Chronic Pain
Placebo-associated improvement is defined as, “any genuine psychological or physiologic effect which is attributable to receiving a substance or undergoing a procedure, but is not due to the inherent powers of that substance or procedure”.
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32. Psychologic Factors in Chronic Pain
Approaches include:
Providing positive (yet honest) communication about the therapy.
Providing encouragement and education.
Developing trust, compassion, and empathy.
Understanding the person as an individual.
Creating rituals that provide meaning and expectancy for the person.
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33. Conflicts Between Patient and Provider Goals
People with chronic pain often want health care providers to acknowledge them as individuals and to have their pain recognized as biologically based.
Health care providers are frequently more concerned with the diagnosis and treatment than with providing biological explanations for chronic pain.
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34. Conflicts Between Patient and Provider Goals
Most important factor in achieving a positive patient–physical therapist interaction is the therapist’s ability to explain treatment recommendations in a way that is consistent with the patient’s existing beliefs about his or her chronic pain.
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