Neuropathic pain, pain matrix dysfunction, and pain syndromes

Transcription

1 Neuropathic pain, pain matrix dysfunction, and pain syndromes MSTN121 - Neurophysiology Session 3 Department of Myotherapy

2 Session objectives Describe the mechanism of nociceptive chronic pain. Define neuropathic pain, paresthesia, dysesthesia, and central sensitization. Compare central sensitivity syndrome with neuropathic pain. Describe and give examples of central sensitivity syndrome. Describe and give examples of pain syndromes. Describe the mechanisms of the four types of chronic pain. Give examples of each type of chronic pain.

3 Chronic Pain as a Disease Pain is more than a sensation, Pain involves inhibitory and excitatory circuits in the central nervous system (CNS) that either diminish or amplify pain messages. Pain may be nociceptive j.duncan@cavads.com or non-nociceptive Nociceptive pain is due direct stimulation of nociceptors Non-nociceptive pain is pain in the absence of noxious stimuli and includes neuropathic pain, pain matrix dysfunction, and pain syndromes. Pathologic pain has no beneficial biological function. 3 (Lundy-Ekman, 2018, p. 221)

4 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. Symptoms include; 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 4 (Lundy-Ekman, 2018, pp )

5 4 Mechanisms of Neuropathic Pain Mechanisms of nociceptive and neuropathic pain and central sensitivity syndromes. Red indicates activity in the nociceptive pathway. Black indicates that the neuron or part of a neuron is inactive. Green indicates activity in the light touch pathway. A, Normal physiologic function of the pain system: inflammatory chemicals at the site of injury have sensitized peripheral nociceptors, and signals indicating tissue damage travel to the brain. B to E illustrate neuropathic mechanisms: B, Ectopic foci. C, Ephaptic transmission from an Aβ tactile neuron to nociceptive fibers. D, Central sensitization, created by increased excitatory transmitter availability and an increased number of excitatory receptors. E, Structural reorganization, in this case, the retraction of C-fiber proximal endings from nociceptive tract neurons and growth of Aβ tactile endings to synapse with nociceptive tract neurons. F, Central sensitivity syndromes cause changes in pain matrix topdown regulation, with silence of antinociceptive signals and excessive 5 Image (Lundy-Ekman, 2018, p. 223) pronociceptive signals. (Lundy-Ekman, 2018, pp )

6 6 Image (Lundy-Ekman, 2018, p. 223) (Lundy-Ekman, 2018, pp. 223) 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.

7 7 Image (Lundy-Ekman, 2018, p. 223) (Lundy-Ekman, 2018, pp. 224) Ephaptic Transmission Also called cross-talk Occurs in demyelinated regions Occurs as a result of lack of insulation between neurons

8 8 Image (Lundy-Ekman, 2018, p. 223) (Lundy-Ekman, 2018, pp. 224) Central Sensitization Excessive responsiveness of central neurons Develops in response to ongoing nociceptive input, yet the alterations in central neural activity outlast the tissue injury Intense signals from an injury in the periphery may cause central sensitization. Cellular changes that reflect central sensitization include increased spontaneous activity. increased responsiveness to afferent inputs. prolonged after discharge in response to repeated stimuli. Expansion of receptive fields

9 9 Image (Lundy-Ekman, 2018, p. 223) (Lundy-Ekman, 2018, pp. 225) Structural Reorganization Prolonged central sensitization leads to rewiring of connections in the CNS. In dorsal horn, structural changes include withdrawal of C- fiber axon terminals from central nociceptive neurons. Once novel synapses have formed, stimulation of fibers will produce impulses perceived as pain.

10 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 10 (Lundy-Ekman, 2018, pp )

11 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. 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 (Lundy-Ekman, 2018, p. 226)

12 Central Response to Deafferentation Deafferentation is a disruption to any afferent signals along the somatosensory 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. 12 (Lundy-Ekman, 2018, pp )

13 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. 13 Image (Lundy-Ekman, 2018, p. 227) (Lundy-Ekman, 2018, p. 227)

14 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. Spinal cord injury (SCI) central pain: The thalamus may be the site of pain generation because after a SCI, the neurons in the ventral posterolateral thalamic nucleus are spontaneously active without input from the spinal cord. Multiple sclerosis (MS) central pain depends on the location of the lesion. 14 (Lundy-Ekman, 2018, pp.227-8)

15 Small Fiber Neuropathy Produces partial deafferentation and central sensitization Postherpetic neuralgia, diabetic neuropathy, and Guillain- Barré syndrome cause deafferentation pain due to damage to small-diameter C fibers. Skin biopsy specimens showing density of epidermal nociceptive fibers (arrows) and dermal nerve bundles (arrowheads). A, Biopsy specimen from a healthy control. B, Severe loss of epidermal nociceptive fibers in a biopsy specimen from a patient with diabetic neuropathy. Swelling of the epidermal fiber in B (arrow) indicates axonal degeneration. 15 Image (Lundy-Ekman, 2018, p. 228) (Lundy-Ekman, 2018, pp. 228)

16 Central Sensitivity Syndromes 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 (ETTH), migraine, and chronic whiplash-associated disorder involve disturbance of top-down regulation of pain. The primary cause of these disorders is not a structural lesion and as such they are not included in the neuropathic pain designation. 16 (Lundy-Ekman, 2018, p. 228)

17 Fibromyalgia Tenderness and aching pain, fatigue, sleep disturbances, and abnormal pain processing. FM is neither a subjective pain condition not a psychologic disorder Subjects with fibromyalgia demonstrate biologic amplification of pain signals. Small fiber neuropathy Less grey matter in pain inhibiting areas and stress response areas. Tendency to develop is genetic. Several treatments are effective. 17 (Lundy-Ekman, 2018, pp )

18 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, which sensitizes nociceptive pathways in the CNS 18 (Lundy-Ekman, 2018, p. 229)

19 Migraine Migraine is a neurogenic disorder. Disorders of sensory processing produce a pain matrix malfunction that amplifies nociceptive signals in the trigemino-thalamo-cortical pathway. Characterized by at least two of the following: Unilateral location Pulsating quality Severity interfering with daily activities Aggravation from routine physical activity Cascade of events in migraine proceeds as such: Migraine provocation Excitation of hyperexcitable brainstem neurons Only in people who experience aura: a wave of intense neural activity spreads through cerebral cortex Activation of trigeminal afferents that synapse with trigeminal lemniscus neurons 19 (Lundy-Ekman, 2018, pp )

20 Chronic Whiplash Associated Disorder Whiplash is an injury to the neck resulting from rapid acceleration or deceleration. No damage to the somatosensory system has been identified in chronic whiplash associated disorder; rather, it is considered a pain matrix disorder. 20 (Lundy-Ekman, 2018, p. 231)

21 Pain Syndromes Two syndromes involve other systems in addition to the pain system: CRPS involves the somatosensory, autonomic, and motor systems. Chronic low back pain syndrome involves muscle guarding, disuse, and abnormal movements. 21 (Lundy-Ekman, 2018, p. 232)

22 Complex Regional Pain Syndrome Syndrome of pain, vascular changes, and atrophy Typical signs and symptoms are worst in distal extremity Most frequently follows surgery, fracture, crush injury, or sprain Primary complaint is severe, spontaneous pain, out of proportion to the original injury Red or pale skin Excessive sweating Oedema Joint stiffness and swelling Muscle atrophy Osteoporosis Arthritic changes Spasm / tremor Therapy is essential. Administering drugs via pump allows lower drug doses and increases drug effectiveness. 22 (Lundy-Ekman, 2018, pp )

23 Chronic Low Back Pain Syndrome Transition from acute low back pain to chronic low back pain has been characterized as change in pain etiology from tissue damage to a physiologic impairment consisting of muscle guarding. abnormal movement. disuse syndrome. Brain scans show amplified pain signals in patients with idiopathic chronic low back pain. 23 (Lundy-Ekman, 2018, p. 235)

24 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. Psychologic interventions may decrease activation of the pain system and also improve coping skills. Relaxation (breathing, muscle relaxation) Biofeedback Imagery Cognitive behavioral therapy 24 (Lundy-Ekman, 2018, pp )

25 Psychologic Factors in Chronic Pain (Cont.) Placebo-associated improvement is defined as, any genuine psychologic 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. 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. 25 (Lundy-Ekman, 2018, pp )

26 Psychologic Factors in Chronic Pain (Cont.) 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. 26 (Lundy-Ekman, 2018, pp )

27 Four types of chronic pain Image (Lundy-Ekman, 2018, p. 239)

28 Introduction to Examining Cortical Sensory Function MSTN121 - Neurophysiology Session 3 Department of Myotherapy

29 Cortical Sensation Exam 1. Two-Point Discrimination TEST INTERPRETATION Using a bent paper clip, apply a light equal pressure to the two points. Begin with two points further apart than the mean value for that region of the body (see Figure 7-1). Ask the client to close their eyes and tell me whether your feel one point or two points. Move the points closer together until the client states it feels like one point. Measure the distance between the two points and compare that with the mean value of the region. Ability to accurately discriminate in normal ranges indicates the DCML is intact and an inability may indicate DCML lesion or a widening receptive fields either locally or cortically in the somatosensory homunculus. People with diabetic foot ulcers require 14mm before then can discriminate between two points. To prevent anticipation, randomly stimulate with a single point. Only test the hands and feet. For chronic lower back pain, stimulate the region of pain to decipher changes in the cortical sensory perception. Image: (Lundy-Ekman, 2013, p. (Lundy-Ekman, 123) 2018, p. 73 )

30 Cortical Sensation Exam 2. Bilateral Simultaneous Touch TEST INTERPRETATION Touch one limb, then the other then both. Touch the forearms and shins. Ask the client to close their eyes and say left if the left side is touched, right if the right side is touched or both "when both sides are touched. Tests for sensory extinction. Used to determine if the client can attend to both stimuli on both sides of the body simultaneously. If they cannot, it indicates a lesion of the contralateral parietal lobe to the side of the body that where sensory extinction occurs. (Lundy-Ekman, 2013, p. 124)

31 Cortical Sensation Exam 3. Graphesthesia TEST The patients palm should be positioned facing the examiner, with fingers pointed upward as if signalling stop. Ask the client to close their eyes. Ask the patient, Tell me what number I draw in the palm of your hand. Now draw with a fine tipped object on their palm a number. INTERPRETATION Normally the patient is able to correctly identify the number. This tests the dorsal column/ medial lemniscus system and parietal lobe. If touch sensation is intact, yet the patient cannot perform this task, this indicates a lesion in the contralateral parietal cortex or adjacent white matter. (Image: Jarvis, 2016, p. 654) (Lundy- Ekman, 2013, pg.124, Lundy-Ekman, 2018, p. 73

32 Cortical Sensation Exam 4. Stereognosis TEST Ask the client to close their eyes and tell me what this is and then place an easily recognisable object in their hand such as a key or paper clip. INTERPRETATION If touch sensation is intact and yet they cannot identify the object, this indicates a lesion in the contralateral parietal cortex or adjacent white matter. (Lundy-Ekman, 2013, p. 125) (Image: Jarvis, 2016, p. 654)

33 Review Questions 1. In both acute and chronic nociceptive pain what triggers the events that lead to the perception of pain 2. In non-nociceptive pain what triggers the events that lead to the perception of pain 3. List and describe the symptoms of neuropathic pain 4. List and describe the four mechanisms of neuropathic pain 5. What is deafferentation? 6. What is central pain? 7. What diseases are associated with small fibre neuropathy? 8. What is central sensitivity syndrome? 9. Describe the cascade of events in a migraine 10.List the early signs of CRPS

34 Image references Jarvis, C. (2016). Physical Examination & Health Assessment (7 th ed.).missouri: Elsevier. Lundy-Ekman, L.(2013). Neuroscience : Fundamentals for Rehabilitation (4 th ed.). Missouri: Elsevier. Lundy-Ekman, L. (2018). Neuroscience: Fundamentals for Rehanbilitation (5th ed.). Sydney: Elsevier.

35 References Lundy-Ekman, L.(2013). Neuroscience : Fundamentals for Rehabilitation (4 th ed.). Missouri: Elsevier. Lundy-Ekman, L.(2018). Neuroscience : Fundamentals for Rehabilitation (5 th ed.). Missouri: Elsevier.

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