L1 - Intro to Pain, Classification and Mechanisms of Pain

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36 Terms

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Definition of Pain

An unpleasant sensory and emotional experience associated with, or resembling that associated with, actual or potential tissue damage

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Impact of Pain

  • Can affect mood, motivation, & cooperation in relation to treatment

  • Can affect emotional life, cognition, relationships

  • Can affect mobility and capacity/energy

  • Can affect work life and financials

  • Overall quality of life

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Why do we experience pain? (6)

  • It’s the body’s warning/defence system

  • Plays a role in mobilisation of escape and avoidance behaviors - and is linked to motor systems (Wall 1999)

  • Triggers mental and physical behaviour to end the physical experience and prevent injury

  • Promotes learning (repetition of harmful behavior less likely)

  • Encourages us to disengage from noxious stimulus

  • Promotes healing process

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4 ways to classify pain

  • Duration

  • Dimensions of pain experience

  • Area of pain distribution

  • Pain mechaninsm

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Two ways to classify pain duration

Acute pain vs Chronic/persistent pain

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Acute Pain

Occurs directly as a result of tissue damage or potential tissue damage, and is a symptom.

  • Lasts less than 3 months

  • Acute pain serves to protect from tissue damage, and if tissue damage occurs, it serves to allow for time to heal

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Response to Acute Pain

  • Immediate - anxiety assures safety from cause eg hopping up after falling

  • Subsequent response

    • Wonder about past present and future implications - may affect motivation

    • Concentration on damage and worry for future consequences - should look for in subjective interview

    • Seeks relief

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Chronic/Persistent Pain

  • Outlasts normal tissue healing time (3-6months)

  • Impairment is greater than would be expected form physical findings or injury

  • Pain occurs in absences of identifiable tissue damage

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3 Different Dimensions of Pain

  • Sensory

  • Cognitive

  • Affective

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Sensory Pain

  • The what and where aspect of the pain/the physical aspects of the pain sensation

  • Eg feeling the throbbing of a headache

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Affective Pain

  • The emotional distress and unpleasantness tied to pain

  • The motivational drive to escape the painful stimulus eg fear, anxiety, despair

  • Eg the fear or frustration accompanying chronic pain, or the anxiety it will never stop

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Cognitive Pain

  • The role of thoughts, attention and evaluation in the pain experience

  • How your mental states nd pain interpretation affects intensity and unpleasantness of pain

  • Eg if you get distracted you might forget about pain

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Areas of Pain

  • Localised

  • Referred/Widespread

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Localised pain

  • pain at the origin of injury or around a specific structure

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Referred/Widespread Pain

Pain felt at areas remote from the origin of pain or far from the involved structure

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Pain Mechanisms (3)

  1. Peripheral Sensitisation/Nociceptive

  2. Neuropathic Pain

  3. Central Sensitisation/Nociplastic Pain

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The 2 inputs based pain mechanisms

  1. Peripheral sensitisation

  2. Neuropathic pain

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The 1 output based pain mechanism

Nociplastic/Central Sensitisation

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Nociceptive Pain

Pain associated with tissue injury or damage or even potential damage

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Nociceptors and their stimuli

Nociceptors are activated by potentially noxious stimuli as a body protective mechanism

  • Thermal, mechanical and chemical stimuli (eg fire, crushing or corrosive acid) all activate nociceptors

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The 7 clinical criteria of peripheral nociceptive pain (3 criteria in the absence of 4 criteria)

  1. Pain localised to area of injury/Recent onset

  2. Clear proportionate mechanical/anatomical nature to aggravating and easing factors

  3. Can be intermittent and sharp with provocation, and may be more constantly dull and achy, or throb at rest

IN THE ABSENCE OF

  1. Pain associated with other dysesthesias

  2. Night pain/disturbed sleep

  3. Antalgic postures/movement patterns

  4. Pain described as burning, shooting, sharp or electric shock like

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Parasthesia vs Dysesthesia

Parasthesia

  • An abnormal sensation that’s not unpleasant/painful

  • eg pins and needles

Dysesthesia

  • abnormal sensation that’s always unpleasant/painful

  • Eg burning, stinging, shooting pain

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Hyperalgesia

Increased pain from a stimulus that normally provokes less pain

Eg abnormally large pain response to a pinch

  • can be a symptom of something larger if there’s no clear cause of injury or if injury is healed

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Primary and Secondary Hyperalgesia

Primary Hyperalgesia

  • increased sensitivity at the injury site to prevent further tissue damage

Secondary Hyperalgesia

  • increased sensitivity around the injury site as inflammation lowers pH of local tissue (eg red area surrounding small cut)

<p>Primary Hyperalgesia</p><ul><li><p>increased sensitivity at the injury site to prevent further tissue damage</p></li></ul><p>Secondary Hyperalgesia</p><ul><li><p>increased sensitivity around the injury site as inflammation lowers pH of local tissue (eg red area surrounding small cut)</p></li></ul><p></p>
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Allodynia

Pain due to a stimulus that does not normally provokes pain

Eg light touch, pressure or moderate cold and warmth evoke pain

  • seen in patients with lesions of the nervous system for example

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Neuropathic Pain + its 2 subdivisions

Can result anywhere from damage along the neuraxis; peripheral nervous system, spinal or supraspinal nervous system

Subdivided into central neuropathic pain and peripheral neuropathic pain

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Central Neuropathic pain

Pain caused by a lesion or disease of the central somatosensory nervous system

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Peripheral Neuropathic Pain

Pain caused by a lesion or disease of the peripheral somatosensory nervous system

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2 Mechanisms of Nerve ‘Damage’

  • Mechanical Pressure

  • Chemical irritation

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Mechanical pressure causing nerve damage

Mechanical pressure triggers ectopic nerve impulses in damaged nerves by altering ion channel distributions and excitability.

This creates Abnormal Impulse Generating Sites along the axon, which become hyper-excitable and fire spontaneously even in response to non-noxious stimuli

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Chemical irritation and nerve damage

Injury of the nerve can cause ion channels to group at injury and this leads to increased excitability and a loss of potassium channels to modulate/regulate nerve activity

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The 2 symptoms and 1 sign of peripheral sensitisation/neuropathic pain

2 symptoms

  • pain referred in a dermatomal/cutaneous distribution or pattern

  • History of nerve injury, pathology, or a mechanical compromise

1 sign

  • Pain/symptom provocation with mechanical tests eg neurodynamic that move or load neural tissue

Anecdotally

  • descriptors of burning or shooting pain (however this can overlap with central sensitisation)

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6 Conditions associated with neuropathic pain - Central Nervous System

  1. Strokes

  2. Spinal cord injuries

  3. Syringomyelia + Syringobulbia (fluid filled cavity in the spinal cord and brain stem respectively)

  4. Trigeminal and glossopharyngeal neuralgias

  5. Neoplastic and other space occupying lesions

  6. Central pain in multiple sclerosis

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6 Conditions associated with neuropathic pain - Peripheral Nervous System

  1. Nerve compression/entrapment neuropathies

  2. Post traumatic neuropathy

  3. Phantom limb pain

  4. Disease related neuropathies eg diabetic neuropathy

  5. Complex regional pain syndrome

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Central Sesistisation/Nociplastic Pain

PLASTIC=ADAPTED=CENTRAL=BRAIN

Pain that arises from altered Nociceptive despite no clear evidence of actual or threatened tissue damage causing the activiation of nociceptors, OR evidence of disease or lesion of the somatosensory system that would cause this pain.

  • Pain disproportionate to the nature and extent of the injury or pathology, with a disproportionate and unpredictable pattern of response to aggravating and easing factors.

  • Strong association with maladaptive psychosocial factors eg negative emotions, pain behaviours, medical conflict

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Hickam’s Dictum

“A patient can have multiple coincident unrelated disorders”

  • meaning we should treat by focusing on the dominant mechanism of pain