Chronic Pain Differential Diagnostics PDF

Chronic Pain Differential Diagnostics PHTH 539 Differential Diagnosis Week 13 Nov 14, 2024 Rivera Objectives Discriminate between nociception, neurologic and nociplastic pain Compare and contrast the clinical presentation between peripheral and...

Chronic Pain Differential Diagnostics PHTH 539 Differential Diagnosis Week 13 Nov 14, 2024 Rivera Objectives Discriminate between nociception, neurologic and nociplastic pain Compare and contrast the clinical presentation between peripheral and central sensitization patterns Synthesize the neurophysiological properties of chronic pain to the biopsychosocial model of pain management Apply and interpret pain definitions and terminology in a chronic pain patient International Association Study of Pain (IASP) Categories Nociplasti Neuropat c Pain hic Nocieptiv e Pain is multifaceted with pain patterns over Peripheral Mechanism of Pain: Nociceptive (Acute ) Acute pain is inflammatory Substance P is a key mediator of inflammation, released by nerves by noxious stress. Substance P assists in the transmission of pain and is associated with disease processes. Calcitonin gene- related peptide (CGRP) is involved in pain and the inflammatory process  Paradigm Shift in Physical Therapy Pain Management “Physical therapists have a role to provide contemporary education about pain and to Paradigm encourage early engagement of every Shift patient in appropriate evidence-based active pain-management strategies (what the patient can do themselves), rather than solely focusing on the use of passive interventions (what you do for the patient).” (IASP Physical Therapy Curriculum) Shift in concepts in chronic pain management Patient Engageme nt in their Manageme nt Contempor ary Education Evidence Based Pain Management Approach to Pain: A Biopsychosocial and Mechanistic Phys Ther, Volume 98, Issue 5, May 2018, Pages 302–314, https://doi.org/10.1093/ptj/pzy030 The content of this slide may be subject to copyright: please see the slide notes for details.  Chronic Pain The IASP definition addresses both duration and appropriateness, defining chronic pain as pain without apparent biologic value that has persisted beyond the normal tissue healing time (usually taken to be three months) The American College of Rheumatology (ACR) defines chronic pain as widespread or regional pain for at least three months. A few caveats in Nociplastic disease Nociplastic pain can occur with neuropathic and nociplastic pain mechanisms. Neuropathic pain is a risk factor for nociplastic disease For example: a person with a chronic lumbar radiculopathy (9 months) At 9 months began to have mechanical allodynia, touch hypersensitivity and cognitive fatigue  Nociplastic “Arises from altered nociception despite no clear evidence of actual or threatened tissue damage causing the activation of peripheral nociceptors or evidence for disease or lesion of the somatosensory system causing the pain” IASP, 2021  Nociplastic Pain Combination of peripheral and central pain sensitization Hyper-responsiveness to painful and nonpainful sensory stimuli Associated features, including Fatigue Sleep disturbance Cognitive disturbances Hypersensitivity to environmental stimuli Anxiety and depressed mood  Nociplastic Pain Involves peripheral or spinal or central mechanisms Hyperactivity in the brain regions involved in pain Changes in the synapses of pain pathways Decreased brain inhibition of pain transmission Elevated levels of substance P (dorsal horn, Nociplastic: considerations as a disease Nociplastic diagnoses Fibromyalgia Complex regional pain syndrome Irritable bowel syndrome Not always synonymous with “central sensitization” Symptoms of Nociplastic Pain Allodynia : pain due to a stimulus that does not normally provoke pain : mechanical or light touch : cold : heat Sensitivity: increase response of pain receptors to a low threshold tactile sensation : touch (light) : pressure : movement Example: sheets touching skin, fans, putting on your clothes Hyperalgesia: Abnormal or increased pain from a stimulus that provokes pain Example: palpation of area of pain with reports of 8/10  Nociplastic pain (musculoskeletal) (Kosek, 2021) 1. The pain is 1a. Chronic (>3 mo); 1b. Regional (rather than discrete) in distribution*; 1c. There is no evidence that nociceptive pain (a) is present or (b) if present, is entirely responsible for the pain; and 1d. There is no evidence that neuropathic pain (a) is present or (b) if present, is entirely responsible for the pain.† 2. There is a history of pain hypersensitivity in the region of pain. Any one of the following: Sensitivity to touch Sensitivity to pressure Sensitivity to movement Sensitivity to heat or cold  Nociplastic (Musculoskeletal pain) 3. Presence of comorbidities: Any one of the following: Increased sensitivity to sound and/or light and/or odors Sleep disturbance with frequent nocturnal awakenings Fatigue Cognitive problems such as difficulty to focus attention, memory disturbances, etc. 4. Evoked pain hypersensitivity phenomena can be elicited clinically in the region of pain. Any one of the following: Static mechanical allodynia (pain with non-painful stimulation) Dynamic mechanical allodynia Heat or cold allodynia Painful after-sensations reported following the assessment of any of the above alternatives. Possible nociplastic pain: 1 and 4. Probable nociplastic pain: all the above (1, 2, 3, and 4)‡ https://cdn-links.lww.com/permalink/pain/b/pain_2021_05_04_kosek_pain-d-20-0113 0_sdc1.mp4 Nociplastic Pain Two categories: Central Sensitization Peripheral Sensitization Nociplastic Pain: Peripheral or Central Sensitization “Sensitization” refers to a set of physiological processes that may underlie hyperalgesia and allodynia. Peripheral sensitization is defined as “Increased responsiveness and reduced threshold of nociceptive neurons in the periphery to the stimulation of their receptive fields.” Central sensitization is defined as “Increased responsiveness of nociceptive neurons in the central nervous system to their normal or subthreshold afferent input.”  Peripheral sensitization Inflammatory chemical soup All pain is inflammatory Normal hypersensitivity after injury: normal and protective response Allows the tissues to heal Avoids excessive movement Peripheral sensitization is a prolonged hypersensitivity at the site of injury - prolonged chemical soup - stays within the area (localized to the area of injury) Common Presentation: Primary Hyperalgesia: increased sensitivity to a painful stimulation – to heat and mechanical stimlulation  Peripheral Sensitivity is ongoing inflammation of neuro chemicals Receptors are reduced from inflammatory mediators and excitatory transmission at the site of injury  Inflammatory chemical soup: Peripheral S. Specific peripheral receptors become sensitized to the inflammatory chemical during pain. C fibers respond to inflammation and when they become sensitized, they increase their spontaneous, responding to diverse sensory information (mechanical pressure and heat) by inducing pain responses. Instead of reducing with inflammation over a period of time, inflammation remains. Producing mast cells, macrophages, WBCs, similar to a pain response. The nerve receptors set up more pain receptors for pain and the chemical pain soup. Central Sensitization Central Sensitization An amplification of neural signals within the CNS that elicits pain hypersensitivity (Nijs, 2021) Increased responsiveness of nociceptors CNS of encoding of noxious stimulus Primary hyperalgesia Hypersensitivity to stimuli Allodynia Wide spread non-anatomical pain distribution (2ndary hyperalgesia) Unpredictable pain pattern Night pain disturbed sleep Pain irritability  Dorsal horn is a factor in Central Sensitization Central sensitization is a pathologic state: dorsal horn excitability is increased and its gatekeeping function is lost. Increased input by C and Aδ coupled with increased excitability. The modulation of the dorsal horn is transformed by pain input other sensory input. C fibers become dominant.  Connections of the spinothalamic: limbic, PAG and reticula formation Periaqueductal gray (PAG) sends information through the brain - medial prefrontal cortex -hippocampus - involved in pain and stress -hypothalamus (homeostasis) Zhang, 2020 medscape Centralized sensitization can occur with an injury or even without a trigger event. Plastic changes in brain sites within the nociceptive pathway can cause sensitization, for instance at the level of the thalamus or the sensory cortex. Chronic widespread Testing for Central Sensitization M. Kao, 2022 Quantitative Sensory Testing (QST) is an objective method of testing this pain hypersensitivity, where various stimuli are applied to the skin, ranging from vibration, light touch, proprioception and temperature, using standardized testing procedures and validated equipment Sensory Testing for Central Sensitization Sensory testing is of prime importance for the diagnosis of neuropathic pain and CS pain. This includes testing of the function of sensory fibers with simple tools (e.g. a tuning fork for vibration, a soft brush for touch, and cold/warm objects for temperature), which typically assesses the relationship between the stimulus and the perceived sensation. Seek out allodynia, hypersensitivity, mechanical pressure. Sensory Testing for Central Sensitization II Neuropathic pain the location of the sensory dysfunction should be neuroanatomically logical (PN versus dermatome) CS pain it should be spread in non-segmentally related areas of the body and remote from the injured area. Clinical examination in CS pain typically reveals increased sensitivity at sites segmentally unrelated to the primary source of nociception. Questionnaires for Central Sensitization and Behavior Central Sensitization Inventory (CIS) Pain Catastrophizing Scale Brief Illness Perceptions Questionnaire Fear and Avoidance Questionnaire Thoughts for the next Lab: MODULATION OF PAIN Summary Pain is a multifactorial process involving human behavior, pain physiology The field of Physical Therapy is reconceptualizing pain Physical Therapist must identify pain processes in the evaluative process and