Pain & Pain Control Theory, Slides of Physiology

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PAIN & PAIN CONTROL THEORIES

Managing Pain

What is Pain?

• “An unpleasant sensory & emotional experience associated with actual or potential tissue damage, or described in terms of such damage” – The International Association for the Study of Pain
• Subjective sensation
• Pain Perceptions – based on expectations, past experience, anxiety, suggestions
  • A ffective – one’s emotional factors that can affect pain experience
  • B ehavioral – how one expresses or controls pain
  • C ognitive – one’s beliefs (attitudes) about pain
• Physiological response produced by activation of specific types of nerve fibers
• Experienced because of nociceptors being sensitive to extreme mechanical, thermal, & chemical energy.
• Composed of a variety of discomforts
• One of the body’s defense mechanism (warns the brain that tissues may be in jeopardy)
• Acute vs. Chronic –
  • The total person must be considered. It may be worse at night when the person is alone. They are more aware of the pain because of no external diversions.

Pain Sources

• Fast vs. Slow Pain –
  • Fast – localized; carried through A-delta axons in skin
  • Slow – aching, throbbing, burning; carried by C fibers
  • Nociceptive neuron transmits pain info to spinal cord via

unmyelinated C fibers & myelinated A-delta fibers.

• The smaller C fibers carry impulses @ rate of 0.5 to 2.0 m/sec.
• The larger A-delta fibers carry impulses @ rate of 5 to 30 m/sec.
• Acute vs. Chronic

What is Referred Pain?

• Occurs away from pain site
• Examples: McBurney’s point, Kerr’s sign
• Types of referred pain:
  • Myofascial Pain – trigger points, small hyperirritable areas within a m. in which n. impulses bombard CNS & are expressed at referred pain - Active – hyperirritable; causes obvious complaint - Latent – dormant; produces no pain except loss of ROM
  • Sclerotomic & Dermatomic Pain – deep pain; may originate from sclerotomic, myotomic, or dermatomic n. irritation/injury - Sclerotome: area of bone/fascia that is supplied by a single n. root - Myotome: m. supplied by a single n. root - Dermatome: area of skin supplied by a single n. root

Questions to Ask about Pain

• P-Q-R-S-T format
• Provocation – How the injury occurred & what activities   the pain
• Quality - characteristics of pain – Aching (impingement), Burning (n. irritation), Sharp (acute injury), Radiating within dermatome (pressure on n.)?
• Referral/Radiation –
  • Referred – site distant to damaged tissue that does not follow the course of a peripheral n.
  • Radiating – follows peripheral n.; diffuse
• Severity – How bad is it? Pain scale
• Timing – When does it occur? p.m., a.m., before, during, after activity, all the time
  • P attern: onset & duration
  • A rea: location
  • I ntensity: level
  • N ature: description

Pain Assessment Scales

• Visual & Numeric Analog Scales
• None Severe

• Locate area of pain on a pictures
• McGill pain questionnaire
  • Evaluate sensory, evaluative, &

affective components of pain

• 20 subcategories, 78 words

Types of Nerves

• Afferent (Ascending) – transmit impulses from

the periphery to the brain

• First Order neuron
• Second Order neuron
• Third Order neuron
• Efferent (Descending) – transmit impulses

from the brain to the periphery

First Order Neurons

• Stimulated by sensory receptors
• End in the dorsal horn of the spinal cord
• Types
  • A-alpha – non-pain impulses
  • A-beta – non-pain impulses
    • Large, myelinated
    • Low threshold mechanoreceptor; respond to light touch & low- intensity mechanical info
  • A-delta – pain impulses due to mechanical pressure
    • Large diameter, thinly myelinated
    • Short duration, sharp, fast, bright, localized sensation (prickling, stinging, burning)
  • C – pain impulses due to chemicals or mechanical
    • Small diameter, unmyelinated
    • Delayed onset, diffuse nagging sensation (aching, throbbing)

Third Order Neurons

• Begins in thalamus
• Ends in specific brain centers (cerebral cortex)
  • Perceive location, quality, intensity
  • Allows to feel pain, integrate past experiences &

emotions and determine reaction to stimulus

Descending Neurons

• Descending Pain Modulation (Descending Pain Control

Mechanism)

• Transmit impulses from the brain (corticospinal tract in

the cortex) to the spinal cord (lamina)

• Periaquaductal Gray Area (PGA) – release enkephalins
• Nucleus Raphe Magnus (NRM) – release serotonin
• The release of these neurotransmitters inhibit ascending neurons
• Stimulation of the PGA in the midbrain & NRM in the pons

& medulla causes analgesia.

• Endogenous opioid peptides - endorphins & enkephalins

Sensory Receptors

• Mechanoreceptors – touch, light or deep

pressure

• Meissner’s corpuscles (light touch), Pacinian corpuscles (deep pressure), Merkel’s corpuscles (deep pressure)
• Thermoreceptors - heat, cold
• Krause’s end bulbs ( temp & touch), Ruffini corpuscles (in the skin) – touch, tension, heat; (in joint capsules & ligaments – change of position)
• Proprioceptors – change in length or tension
• Muscle Spindles, Golgi Tendon Organs
• Nociceptors – painful stimuli
• mechanosensitive
• chemosensitive

Nerve Endings

• “A nerve ending is the termination of a nerve fiber in a

peripheral structure.” (Prentice, p. 37)

• Nerve endings may be sensory (receptor) or motor

(effector).

• Nerve endings may be:
  • Respond to phasic activity - produce an impulse when the stimulus is  or , but not during sustained stimulus; adapt to a constant stimulus (Meissner’s corpuscles & Pacinian corpuscles)
  • Respond to tonic receptors produce impulses as long as the stimulus is present. (muscle spindles, free n. endings, Krause’s end bulbs)
  • Superficial – Merkel’s corpuscles/disks, Meissner’s corpuscles
  • Deep – Pacinian corpuscles,

Nociceptors

• Sensitive to repeated or prolonged stimulation
• Mechanosensitive – excited by stress & tissue damage
• Chemosensitive – excited by the release of chemical

mediators

• Bradykinin, Histamine, Prostaglandins, Arachadonic Acid
• Primary Hyperalgesia – due to injury
• Secondary Hyperalgesia – due to spreading of chemical

mediators

Pain Control Theories

• Gate Control Theory

• Central Biasing Theory

• Endogenous Opiates Theory